manual icu

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Royal Adelaide Hospital

Intensive Care Unit

Medical Manual

2012 Edition

http://icuadelaide.com.au/

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FOREWORD

Welcome to Intensive Care.

This manual has been written to facilitate the daily running of the RAH Intensive Care

Unit. It is by no means the definitive answer to all intensive care protocols and

procedures, nor is it designed to be a textbook.

A standardised approach to management is desirable for optimal patient care and safety,

improving communication and understanding between members of the ICU team and

associated specialties. This approach provides a common platform for staff who come

from different countries and training backgrounds.

The manual outlines various Protocols, which represent a standard approach to practice

within the Unit. These have been derived from the available literature, clinical

experience and where appropriate, cost-effectiveness. Guidelines designed to assist in

clinical management are included but patient management will ultimately depend upon

the clinical situation. Consultants may modify these guidelines on consideration of the

nuances of a particular clinical case. Registrars wishing to go outside the guidelines

should discuss this with the Duty Consultant before proceeding.

Assistance is always available from the Duty Consultant and senior nursing staff. Use

your time in the Unit to get the most out of the large clinical caseload. Ask questions

about clinical problems, equipment and procedures with which you are unfamiliar.

There are numerous textbooks, journals and references available in the Unit.

This manual has undergone numerous changes, with contributions from many of the ICU

staff and from other specialty services within the hospital. The contents of this manual

are produced from the consensus views of the senior medical staff. We aim to make the

information in this manual as accurate and consistent with the available evidence as

possible at the time of publication. However no guarantee can be provided that errors do

not exist – please notify the Duty Consultant if you identify any errors of fact.

A/Prof Robert Young

Director

2012 12th

Edition

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CONTENTS

FOREWORD ....................................................................................................................... 2 CONTENTS ......................................................................................................................... 3 PART 1 - ADMINISTRATION .............................................................................................. 6

A. Staffing - Royal Adelaide Hospital ICU ............................................................... 6 B. Rostering and Job Descriptions ............................................................................. 8

Table: Team Duties .............................................................................................. 8 Table: Registrar Shifts ....................................................................................... 10

C. Orientation .......................................................................................................... 11 D. Weekly Programme ............................................................................................. 12

Table: Weekly Unit Programme ........................................................................ 12 E. Admission and Discharge Policies ...................................................................... 13 F. Care for Patients Discharged from ICU for Terminal Care. ............................... 15 G. Clinical Duties in the ICU ................................................................................... 16 H. Documentation .................................................................................................... 19 I. Consent in ICU ................................................................................................... 21 J. ICU Ward Rounds ............................................................................................... 22 K. Clinical Duties Outside of the Intensive Care Unit ............................................. 23 L. Hospital Emergencies ......................................................................................... 28 M. Research in ICU .................................................................................................. 29 N. Information Technology in ICU .......................................................................... 30

PART 2 - CLINICAL PROCEDURES .................................................................................. 31 A. Introduction ......................................................................................................... 31 B. Procedures ........................................................................................................... 31 C. Peripheral IV Catheters ....................................................................................... 32 D. Arterial Cannulation ............................................................................................ 33 E. Central Venous Catheters .................................................................................... 34 F. Urinary Catheters ................................................................................................ 36 G. Epidural Catheters ............................................................................................... 37 H. PICCO Catheters ................................................................................................. 37

Table: PiCCO Values and Decision Tree ........................................................... 38 I. Pulmonary Artery Catheters ................................................................................ 39

Table: Standard Haemodynamic Variables ........................................................ 41 J. Pleural Drainage .................................................................................................. 42 K. Endotracheal Intubation ...................................................................................... 44 L. Weaning Guidelines ............................................................................................ 49

Flowchart: Ventilation Weaning Protocol .......................................................... 50 M. Extubation ........................................................................................................... 50 N. Emergency Surgical Airway Access ................................................................... 52 O. Fibreoptic Bronchoscopy .................................................................................... 53 P. Tracheostomy ...................................................................................................... 54 Q. Cardiac Pacing .................................................................................................... 57 R. Pericardiocentesis................................................................................................ 60 S. Intra-Aortic Balloon Counterpulsation................................................................ 61 T. Gastric / Oesophageal Tamponade Tubes ........................................................... 64

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U. Extracorporeal Membrane Oxygenation .............................................................. 65 PART 3 - DRUGS AND INFUSIONS .....................................................................................66

A. Policy ................................................................................................................... 66 B. Principles of Drug Prescription in Intensive Care ............................................... 67 C. Cardiovascular Drugs .......................................................................................... 67

Table: Cardiovascular Effects of Catecholamines .............................................. 68 Table: Inotropic Agents Used in ICU ................................................................. 69 Table: Vasopressors ............................................................................................ 70 Table: Antihypertensive & Vasodilator Agents .................................................. 71 Table: Antiarrhythmic Agents ............................................................................ 74 Table: Thrombolytics ......................................................................................... 77 Table: Antiplatelet Agents .................................................................................. 78

D. Respiratory Drugs ................................................................................................ 79 Table: Bronchodilators ....................................................................................... 80

E. Sedation, Analgesia and Delirium ....................................................................... 81 Table: Nurse Controlled Sedation Protocol ........................................................ 82 Table: Modified Richmond Agitation Sedation Scale (RASS) .......................... 82 Table: Drugs Associated with Increased Delirium ............................................. 84 Flowchart: Confusion Assessment Method for ICU (CAM-ICU) ..................... 85 Table: Sedatives / Analgesics ............................................................................. 86

F. Muscle relaxants .................................................................................................. 88 Table: Muscle Relaxants .................................................................................... 88

G. Anticoagulation ................................................................................................... 89 Table: HITS Probability Score – ‘4T Score’ ...................................................... 92 Table: Anticoagulants ......................................................................................... 93 Table: Heparin Infusion Protocol ........................................................................ 94 Table: Lepirudin Infusion Protocol ..................................................................... 94

H. Endocrine Drugs .................................................................................................. 96 Flowchart: Blood Glucose Management in ICU ................................................ 97 Table: Insulin Infusion Protocol ......................................................................... 97 Table: Steroid Doses / Relative Potencies .......................................................... 99

I. Renal Drugs - Diuretics ................................................................................... 100 Table: Diuretics ................................................................................................ 101

J. Gastrointestinal Drugs ....................................................................................... 102 Table: GI Drugs ................................................................................................ 103

K. Antibiotics ......................................................................................................... 104 Table: Vancomycin Dosing Schedule .............................................................. 106 Table: Antibiotic Infusion Schedules ............................................................... 107 Table: Peri-operative Antibiotic Prophylaxis ................................................... 109 Table: Perioperative Endocarditis Prophylaxis ................................................. 110 Table: Empiric Antibiotics ............................................................................... 111 Table: Antibiotics for Specific Organisms ....................................................... 113

PART 4 - FLUIDS AND ELECTROLYTES ......................................................................... 114 A. Principles of Fluid Management in Intensive Care............................................ 114

Table: Common IV Solutions ........................................................................... 115 B. Nutrition ............................................................................................................ 116

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Flowchart: Nutritional Therapy Protocol ......................................................... 117 Table: Average Daily Requirements ................................................................ 120 Table: Baxter TPN Solution Options ............................................................... 121

C. Blood Component Therapy ............................................................................... 122 Table: Critical Bleeding (Massive Transfusion) .............................................. 124 Table: Guidelines for the Management of an Elevated INR ............................ 128 Table: Pre-operative Dabigatran Management ................................................. 131 Flowchart: Management of Bleeding Patient on Dabigatran ........................... 132 Table: Blood Transfusion Reactions ................................................................ 135

D. Guidelines for the Management of Electrolytes ................................................ 136 Table: Classification of Lactic Acidosis .......................................................... 144

PART 5 - CLINICAL MANAGEMENT .............................................................................. 147 A. Cardiopulmonary Resuscitation ........................................................................ 148

Flowchart: Basic Life Support ......................................................................... 148 Flowchart: Advanced Life Support .................................................................. 149 Flowchart: Paediatric Cardiorespiratory Arrest ............................................... 150 Induced Hypothermia Post Cardiac Arrest ........................................................ 151

B. Failed Intubation Drill ....................................................................................... 152 Flowchart: Failed Intubation Drill ................................................................... 153

C. Respiratory Therapy .......................................................................................... 154 Table: Oxygen Delivery Devices ...................................................................... 154 Table: Oxygen Delivery Percentage - Nasal High Flow .................................. 156

D. Management of Cardiothoracic Patients ........................................................... 166 Flowchart: Arrest Post Cardiac Surgery ........................................................... 168 Flowchart: Bleeding Post Cardiac Surgery ...................................................... 169 Table: Antibiotic Prophylaxis for Cardiac Surgery .......................................... 170

E. Renal Failure ..................................................................................................... 171 Table: Haemodialysis Solutions ....................................................................... 179 Prismaflex – ST 150 Circuit .............................................................................. 184 Form: Dialysis Data for Drug Overdose .......................................................... 185

F. Neurosurgical protocols .................................................................................... 186 Flowchart: Cerebral Perfusion Pressure Algorithm .......................................... 189 Table: World Federation of Neurosurgeons Classification .............................. 190

G. Microbiology Protocols ..................................................................................... 195 Flowchart: Antifungal Treatment in Immunosuppressed Patients ................... 201

H. Drug Overdose .................................................................................................. 204 Flowchart: The Unconscious, Undetermined Overdose .................................... 207 Graph: Modified Rumack-Matthew Nomogram .............................................. 209 Flowchart: Acute Paracetamol OD - Known Time of Ingestion ...................... 210 Flowchart: Repeated Supratherapeutic Paracetamol Ingestion ........................ 211 Table: N-Acetylcysteine Administration ......................................................... 211

I. Bites and Envenomation ................................................................................... 220 J. Limitation of Therapy ....................................................................................... 221 K. Brain Death and Organ Donation ...................................................................... 221 L. Donation After Cardiac Death (DCD) .............................................................. 226

Table: Contact Phone Numbers ....................................................................... 229

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PART 1 - ADMINISTRATION

A. Staffing - Royal Adelaide Hospital ICU

1. Consultant Medical Staff

Director A/Prof Rob Young

Deputy Director Dr Peter Sharley

Director of Research A/Prof Marianne Chapman

Supervisor of Training Dr Nick Edwards

Consultants Dr Mike Anderson

Dr Stuart Baker

Dr David Clayton

Dr Adam Deane

Dr David Evans

Dr Mark Finnis

A/Prof Arthas Flabouris

Dr Ken Lee

Dr Matt Maiden

Dr Stuart Moodie

Dr Richard Newman

Dr Ben Reddi

Dr Richard Strickland

Dr Krishnaswamy Sundararajan

A/Prof Mary White

Dr Alex Wurm

2. Senior Nursing Staff

Nursing Director: Mr Ian Blight

Clinical Services Coordinators: Ms Deb Herewane

Ms Ros Acott

Ms Tracey Cramey

Mr Michael Schwarz

Mr Steve Wills

Nurse Managers: Ms Ali Coventry

Ms Heather Pile

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3. Administrative Staff

Administrative Manager Ms Melissa Filleti

Resource Accountant Ms Tammy Moffat

Team Leader / Roster Manager Ms Sherridan Clark

Unit Secretary Ms Kristina Gabell

Ward Clerks Ms Ali Fraser

Ms Lisa Migliaccio

Mr Gavin Sain

4. Registrars

a) Three levels of registrars are rostered in the unit:

i) Senior Registrars (SR):

Advanced trainees in the College of Intensive Care Medicine (CICM)

(or equivalent training program)

Have completed or near completed specialist training.

Take “first on-call” at night and experience responsibility at a

consultant level.

The SRs help manage the registrar roster, coordinate registrar

presentations, simulator training and contribute to teaching activities.

ii) Senior Trainees:

Usually CICM trainees (or equivalent)

Rostered according to seniority and experience.

iii) Junior Trainees/RMOs:

Vocational trainees, trainees in other specialist programs

e.g. surgical, physician training, etc

Residents in general rotations.

b) Portfolios are determined by experience and rostering requirements.

c) All registrars, except SRs, will rotate through Units A, B and C.

d) Training positions at Royal Adelaide Hospital:

i) Intensive Care Positions

The College of Intensive Care Medicine has accredited the RAH as a

C24 Unit for training for the fellowship in intensive care (FCICM).

Registered CICM trainees may undertake their full 24 months of core

ICU training at the RAH.

Non-CICM-trainee registrars wishing to gain further postgraduate

experience in intensive care may apply for these positions.

Applications including a current c.v. should be forwarded to:

Dr Alex Wurm. ([email protected])

Trainees in formal training programs are given appointment priority.

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ii) Positions for non-intensive care trainees

Rotations of registrars in these positions are made from the respective

specialty based training programs at the RAH.

Anaesthesia trainees: 1 position (3 or 6 month term).

Physician trainees: 1 position (3 or 6 month term).

Surgical trainees: 1 position (3 or 6 month term).

Emergency Medicine trainees: 2 positions (3 or 6 month term).

iii) Supervisors of Training at Royal Adelaide Hospital:

Intensive Care: Drs Nick Edwards

& Peter Sharley

Medicine: Dr S M Guha

Anaesthesia: Dr I Banks

Surgery: Mr P G Devitt

Emergency Medicine: Dr R Dunn

B. Rostering and Job Descriptions

Table: Team Duties

0800 - 1900

ICU Team A Beds 1-12

Consultant Team A Manages Unit A

Senior Registrar A Manages Unit A, TPN

Registrar A1 (D1) Beds 1-6.

Registrar A2 (D2) Beds 7-12.

ICU Team B Beds 12-24

Consultant Team B Manages Unit B

Senior Registrar B Manages Unit B

Registrar B1 (D3) Beds 13-18

Registrar B2 (D4) Beds 19-24

ICU Team C Beds 25-34

Consultant Team C Manages Unit C

Registrar C1 (D5) Unit C, Beds 25-34.

Registrar C2 (D6)

Duty Intensivist Speed Dial 1650

Bed management, Ward consults

D7 registrar Consults, Code blue, TPN

CICU Consultant Cardiothoracic ICU Consultant

Teaching Consultant Undergraduate and postgraduate teaching

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1830 - 0830

ICU 1st On-Call Consultant / Senior Registrar

Attends evening handover round. On-call for any problems overnight.

ICU 2nd On-Call Consultant Backs-up ICU 1st on-call when required.

Night Registrar 1 (N1) Beds 1-12



Night Senior (NS) Consults, Code blue calls. Oversees beds 1-34, allocates workload

Senior Registrar 1 First Consultant call Wednesday and Saturday

Senior Registrar 2 First Consultant call Thursday and Sunday

NB: The allocation of responsibilities overnight is at the discretion of the registrars present and should be established by mutual agreement between the registrars and consultant on call. It is assumed that all registrars will maintain an awareness of all patients in ICU and will provide assistance in other areas of the ICU if required. Hence the workload should be spread evenly and all registrars should be allowed to have their required (and reasonable) rest periods.

1. Roster Guidelines

a) Rosters are primarily designed to meet training and patient care requirements,

taking into account overall staff numbers and skill-mix.

b) In addition, award requirements, occupational health & safety considerations,

and individuals’ preferences and requests are taken into account.

c) The system is not infallible – if there is a problem with any aspect of the roster,

please notify the ICU secretary as soon as possible.

d) Each roster covers a 4 week period, with the working week commencing on a

Wednesday.

e) Rosters are usually posted two weeks in advance.

f) Where possible you will be rostered two or more days-off following night duty.

g) When rostered to night duty, you are not expected to attend weekly teaching

sessions, as this would result in unsafe work hours.

h) The rostering system utilises a wide variety of different codes as set out in the

following table:

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Table: Registrar Shifts

Abbr Shift Description Times & Meal Breaks Hrs

SR Senior Registrar 08:00-18:00 1x 30min meal break

9.5 D8 Day shift: report to DI

D1,2 Day shift Unit A

08:00-19:00 1x 30min meal break

10.5 D3,4 Day shift Unit B

D5,6 Day shift Unit C

D7 Day shift: consults & Code blue

N1 Night shift Unit A

18:30-08:30 2x 30min meal breaks

13 N2 Night shift Unit B

N3 Night shift Unit C

N4 Night shift: consults & Code blue

A Annual, Study, Exam, Conference leave

@ Request

2. Requesting Shifts

a) Particular shifts or days-off can be entered on a ‘request roster sheet’ that is

posted on the pin-up board opposite the medical staff pigeon holes.

b) The request sheet is collected on the date indicated on the top of the sheet.

c) Requests should also be discussed with the ICU secretary.

(Ph: 8222 5325 or email: [email protected]).

d) Factors to consider when requesting shifts:

i) Requests can significantly complicate the roster and you should therefore

exercise some restraint and not request your entire roster.

ii) If you need to request several shifts please indicate in red, which two are

the most important and priority will be given to these requests.

iii) Requests cannot be granted if they disadvantage other staff, compromise

skill-mix, or overall staffing numbers necessary for the shift.

mailto:[email protected]

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3. Changing/Swapping Shifts

a) If you wish to change a shift after the roster has been posted, you may do so

with the following guidelines:

i) Once the roster is posted, the onus is on the individual to arrange any shift

swaps and these must occur within the same roster period.

ii) You should first endeavour to swap the shift with someone in the same

skill group so that the skill-mix is maintained for the shift.

iii) You must speak to the ICU Secretary for approval (T: 8222 5325 or email:

[email protected]) and then note changes on the rosters

posted in the ward and on the medical pin-up board.

4. Annual Leave

a) Annual leave for medical staff is on a “first come - first served” basis, so book

leave as soon as possible.

b) Only 3 registrars can be on leave at any one time, so before filling in an

application form check that leave is available with the ICU secretary.

c) Please contact the ICU Secretary if you have any questions or concerns about

your roster at anytime.

d) Leave is in accordance with the SA Salaried Medical Officers’ Award (5 weeks

annual and 1 week study leave) and registrars are required to forward a signed

copy of leave requests to the Senior Registrar for rostering purposes.

5. Sick Leave

a) If you are sick and unable to attend work, please contact both:

i) The Duty Intensivist by day, or

Senior Registrar at night (SD: 1650), and

ii) The Roster Manager - Mon-Fri (09:00-16:00)

b) If you can, predict an expected day or night of return to work.

c) Annotate your pay sheet as “sick leave” accordingly.

C. Orientation

1. Registrars commencing duty within the unit at the main RMO changeover dates will

undergo a half-day orientation program.

2. This will include sessions from:

a) The Director of ICU (or delegate)

b) The Director of Research

c) Infectious Diseases / Clinical Microbiology

d) The Acute Pain Service

mailto:[email protected]

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D. Weekly Programme

Table: Weekly Unit Programme

Monday Tuesday Wednesday Thursday Friday

08:00 Handover round Handover round Handover round Handover round Handover round

09:00

Bedside round

Bedside round Bedside round

Bedside round

Bedside round

10:00

11:00

ICU Grand Round ICU Grand Round

12:00 ICU X-ray meeting

Consultant meeting

13:00

Bedside round Primary Exam

Tutorial (1

y trainees)

14:00 Simulator Training Simulator Training

15:00 Audit Journal Club

Clinical Teaching (trainees)

Trainee Tutorial BICMed Course junior registrar

tutorial

16:00

Registrar tutorial (all registrars)

17:00

18:30 Handover round Handover round Handover round Handover round Handover round

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E. Admission and Discharge Policies

1. Admissions Policy

a) Patients are managed by the ICU staff during their stay in ICU.

b) Admission is reserved for patients with actual or potential vital organ system

failures, which appear reversible with the provision of ICU support.

c) All admissions, including transfers and retrievals, must be approved by the

Duty Intensivist (SD: 1650).

d) Resuscitation or admission must not be delayed in imminently life threatening

cases, unless specific advanced directives exist and are clearly documented.

e) Such admissions should be discussed with the Duty Intensivist ASAP.

f) Patients are admitted to ICU under the ‘bed-card’ of the original or taking clinic.

g) MedStar Retrievals

i) Require admission under a parent clinic, who should be aware prior to patient

transfer and notified of the patient’s arrival in the ICU.

ii) Must be discussed with the Consultant when the SR is on 1st call.

h) Clinics requesting elective postoperative surgical beds should book the bed at least

one day in advance and must confirm bed availability with the Duty Intensivist on

the day of surgery, prior to anaesthesia commencing.

i) Admission disputes must be referred to the Duty Intensivist.

2. Discharge Policy:

a) All discharges should be:

i) Approved by the responsible ICU consultant.

ii) Discussed with the parent clinic prior to patient transfer

including discussion of any ongoing or potential problems.

iii) Transferred “In hours”

i.e. prior to 18:00 - unless specifically approved by a consultant.

b) A discharge summary must be completed and a copy filed in the case-notes.

c) All patients on insulin protocols should be referred to the Endocrine Unit prior to

discharge (preferably the day before)

d) Patients discharged on TPN must be entered in the TPN folder in Unit A.

e) Notify the Acute Pain Service of patients discharged under their care.

f) Withdrawal or limitation of therapy is a consultant responsibility.

g) Treatment limitation/non-escalation directives must be discussed with the patient

or patient’s family, the parent clinic and clearly documented prior to discharge.

h) Referral to the Palliative Care should occur pre-discharge where indicated.

3. Deaths Policy:

a) The duty ICU consultant must be informed of all unexpected deaths.

b) The duty ICU registrar must ensure:

i) A death certificate is completed or the Coroner notified

ii) The parent clinic or duty intern is notified

iii) Referring doctors (i.e. GP’s, other specialists / hospitals) are notified.

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c) Where indicated, consent for a post-mortem should be obtained from relatives as

soon as possible.

d) The Coroner must be notified in all cases where death is:

i) A death in custody, e.g. police, corrections, mental health detention.

ii) A death by unusual, unexpected, unnatural, violent or unknown cause.

iii) A death during, as a result of or within 24 hours of a surgical, invasive or

diagnostic procedure, including the administration of an anaesthetic for the

carrying out of the procedure.

iv) The term ‘anaesthetic’ means a local or general anaesthetic and includes a

sedative or analgesic. The following procedures are excluded:

The giving of an intravenous injection

The giving of an intramuscular injection

Intravenous therapy

The insertion of a line or cannula

Artificial ventilation

Cardio-pulmonary resuscitation

Urethral catheterisation

The insertion of a naso-gastric tube

Intra-arterial blood gas collection

Venipuncture for blood collection for testing

Subcutaneous injection or infusion

v) A death within 24 hours of being discharged from a hospital or having

sought emergency treatment at a hospital.

vi) A death of a person under a ‘protected person’ order under the Aged or

Infirm Persons’ Property Act 1940 or the Guardianship and

Administration act 1993.

vii) A death in the course or as a result or within 24 hours of a person receiving

medical treatment to which consent for that treatment has been given under

Part 5 of the Guardianship and Administration act, 1993.

viii) A death of a child subject to a custody or guardianship order under the

Children’s Protection Act 1993.

ix) A death on an aircraft or vessel with a place in South Australia as its place

of disembarkation.

x) A patient death in an approved treatment centre under the Mental Health

Act 1993.

xi) Death of a resident of some (but not all) supported residential facilities

licensed under the Supported Residential Facilities Act. A list of the

relevant facilities is provided in the “Coroner’s Folder” in the nursing bay

stations.

xii) A death in a hospital or treatment facility for the treatment for a drug

addiction.

xiii) If no certificate as to the cause of death has been given to the Registrar of

Births, Deaths and Marriages.

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F. Care for Patients Discharged from ICU for Terminal Care.

1. Preparation for discharge.

a) For the families of dying patients, moving from a familiar environment will add

a level of anxiety and uncertainty, even if it will be to a quieter setting.

b) Handover to the ward treating team should be as comprehensive as possible,

including a social as well as medical history.

c) Families should be supported to accept that there may still be uncertainty about

the patient’s course and the timing of death.

d) Families should be reassured that the focus will be on maintaining comfort.

e) Levels of ongoing active support for the patient, e.g. IV or subcutaneous fluids

should be clarified between ICU staff, the Ward team and family members.

2. Symptom management in terminal care.

a) Physical symptoms that should be considered in planning ongoing care are:

i) Pain – either spontaneous or on movement

ii) Agitation, restlessness

iii) Respiratory tract secretions

iv) In a conscious patient there may be other symptoms

e.g. nausea and vomiting, dyspnoea

v) Prevention of seizures may be a relevant issue

b) If the patient is requiring either analgesia or sedation in ICU, these should be

continued on discharge to the ward.

i) Opioid infusions can be continued as subcutaneous infusions via a pump

(e.g. Graseby® or equivalent)

ii) If sedation is required, midazolam can be administered via subcutaneous

route as a continuous infusion, with an opioid if already in use.

c) If the patient has not required regular opioid or sedation in ICU, the following

PRN orders should be in place prior to discharge:

i) For pain:

Opioid naïve patient - e.g. morphine 2.5-5mg s.c. 2 hrly prn

Opioid tolerant - dose guided by background usage

ii) For agitation, restlessness:

Midazolam 2.5mg - 5mg s.c. 1 hrly prn

iii) For management of secretions:

Hyoscine hydrobromide 400 µg s.c. 3-4 hourly prn

Atropine 600 µg s.c. 3-4 hourly prn

3. Where appropriate, formal consult and involvement of the Palliative Care Service is

encouraged.

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G. Clinical Duties in the ICU

1. Infection Control in ICU

a) Prevention and containment of nosocomial infection is a fundamental principle of

effective medical practice.

b) The critically ill patient is highly vulnerable to nosocomial infection, which results

in significant morbidity, prolonged length of hospital stay, increased cost and

attributable mortality.

c) It is the responsibility of every member of the health care team to ensure

compliance with Hospital and Unit infection control policies. This may include

reminding senior colleagues or visiting teams to conform to basic issues such as

hand-washing or additional precautions.

d) Hand-hygiene remains an established method of effective infection control and

must be strictly performed by all members of the health care team:

i) Aqium hand gel must be used by all staff:

Every time they enter or exit a patient’s cubicle

(defined as the line of the door or curtain of bed space.)

Before wearing gloves

Before and after patient contact

Before and after contact with a patient’s environment

ii) Hand wash with soap where:

Contact with blood or body fluids

Hands are visibly soiled

After removing gloves

iii) Hand wash with chlorhexidine:

Prior to clinical procedures

After contact with patients with multi-resistant organisms

e) Gloves

i) Disposable gloves must be worn for all contact with patient’s bodily fluids,

dressings and wounds.

ii) Gloves must be disposed of within the patient cubicle on leaving

f) Plastic aprons are to be worn:

i) With gross physical contact with the patient (e.g. patient turns)

ii) For “additional precautions” (see below)

g) Additional precautions:

i) The following patients require additional precautions:

Infection or colonisation with:

a. Methicillin Resistant Staph. Aureus

b. Vancomycin Resistant Enterococcus

c. Multiresistant gram negatives

d. Clostridium difficile

Burns

Febrile neutropenia

Immunosuppressed patients as directed by Infection Control

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ii) These patients will normally be managed in either Units A or B.

iii) An “Additional Precautions” sign is placed outside cubicles of patients

identified as infective risks:

Red sign = patient has multi-resistant organism

Blue sign = patient is immunocompromised

iv) New disposable gowns and gloves must be used for each person entering

the cubicle and disposed of within the cubicle upon leaving.

v) Consumable stock within the cubicle should be kept to a minimum.

vi) Notify appropriate staff if patients are transported to theatre, for diagnostic

procedures, or for ambulance transport.

vii) Once the patient has been transferred or discharged, the area should remain

vacant until “terminally cleaned” in accordance with RAH policy.

viii) Environmental swabbing in Intensive Care is conducted as required by

Infection Control staff.

h) Aseptic technique

i) Aseptic technique is to be used for all patients undergoing major invasive

procedures (refer to procedures section).

ii) This includes:

Hand disinfection: surgical scrub with chlorhexidine for >1 minute

Sterile barrier: full gown, mask, hat, gloves and sterile drapes.

Skin preparation with chlorhexidine 2% in 70% alcohol.

i) Sharps disposal

i) The person performing the procedure is responsible for disposal of all

sharps (needles, blades) using the sharp disposal containers.

ii) The nursing staff are not responsible for sharps disposal.

j) “Traffic control”

i) Movement of people through the unit should be kept to a minimum.

ii) This applies equally to visiting clinics and large numbers of relatives.

iii) All visitors are expected to conform to the above infection control

measures and should be tactfully reminded or instructed when necessary.

k) Nominated isolation/quarantine rooms for highly contagious patients:

i) Rooms 3, 4, 5 & 6 - shared air-conditioning

ii) Rooms 21 & 22 - sealed, independent, negative pressure A/C units.

2. Guidelines for admission of a new patient to ICU

a) Handover from the referring doctor. Obtain as much information as possible.

b) Primary survey:

i) Ensure adequate airway, breathing and place the patient on a FiO2 = 1.0 until

a blood gas is done.

ii) Check circulation and venous access.

c) Notify the duty consultant.

d) Secondary survey: fully examine the patient.

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e) Document essential orders:

i) Ventilation

ii) Sedation / analgesia

iii) Drugs, infusions

iv) Fluids

f) Outline the management plan to the nursing staff.

g) Secure appropriate basic monitoring/procedures:

i) SpO2

ii) ECG

iii) Arterial line

iv) IDC, nasogastric tube

v) CVC for the majority

h) Basic investigations as indicated:

i) Routine biochemistry, blood picture and coagulation studies

ii) Group and screen.

iii) Septic screen / microbiology.

iv) Arterial blood gas

v) ECG

vi) CXR (after placement of appropriate lines)

i) Advanced investigations: CT, angiography, MRI, etc

j) Advanced monitoring where indicated: e.g. PA catheter, ICP, PiCCO.

k) Document in case notes. (See below)

l) Notify the parent clinics of patients admitted directly to ICU

NB: this applies particularly to patients who have been retrieved.

m) Clinic Interns and RMOs should clerk hospital admissions direct to ICU.

n) Inform and counsel relatives.

3. Daily management in ICU.

a) Daily investigations:

i) Routine blood tests (U&E, LFT, Mg, Hb, WCC, Plts, ABG) are ordered on

the daily flow chart and signed for on the 11:00 am fluid round.

ii) Coagulation studies, drug levels or other tests are requested as required and

may also be requested on the daily flow chart.

iii) The night duty nurses take the bloods at 06:00 and complete the request form,

which must be signed by the night registrar.

iv) Registrars are responsible for taking blood specimens:

When nursing staff request assistance.

For blood transfusion - the requesting MO must ensure that the labelling

of the request form and specimen matches the patient’s wristband.

19

v) Chest x-rays are ordered after the morning handover round via OACIS.

Routine daily chest x-rays are not performed in ICU

Chest x-rays are performed

a. On admission to ICU (beds 1-24)

b. Following invasive procedures:

i. Endotracheal intubation

ii. Complicated percutaneous tracheostomy

iii. CVC placement (subclavian or jugular)

iv. Nasogastric or IABP placement

c. Suspected pneumothorax

d. At the discretion of the attending doctor

b) Handover ward rounds are at 08:00 and 18:30. These are brief business rounds to

handover essential information to the next team (either day or night) and are

attended by the duty consultant, team registrars and senior nursing staff.

c) Liaison with parent clinics is essential to ensure continuity of management.

Clinics must be informed of significant changes in a patient’s condition or the

requirement for specialist investigations or interventions.

d) Complex investigations (e.g. CT, MRI scans) and procedures should be authorised

by the duty consultant and discussed with the parent clinic where appropriate.

H. Documentation

The following guidelines are designed to facilitate the recording of clear, relevant

information that is essential for continuity of care, audit and medico-legal review.

Entries should establish a balance, being concise but still accurately recording all

relevant information and events.

Specific documentation expected from ICU registrars includes:

1. Admission note for all patients admitted to ICU (Units A, B & C)

2. Daily entry in case notes during admission.

3. Handover summary

4. Discharge summary

5. Death certificates.

1. Admission Notes

a) All patients admitted to Units A & B must have a detailed admission summary.

i) The admitting clinic must be notified by the admitting registrar and invited

to record an admission summary for patients admitted directly to ICU.

This is to ensure that clinics are aware when a patient has been admitted

under their bedcard.

ii) The admission note should incorporate all relevant aspects of the patient’s

medical history, clinical examination and investigation results.

20

b) Complicated Unit C patients require the same detail as Unit A & B patients.

c) Routine postoperative, short stay patients in Unit C do not need detailed

admission notes. In these patients record:

i) Relevant operative & anaesthetic details

ii) Significant comorbidities and history

iii) Anticipated problems

iv) Procedures e.g. epidural, invasive monitoring, TPN

2. Daily case-note entries

a) A daily entry must be made in the case notes.

i) Notes are most efficiently recorded after the 11:00 ward round so that

current results and management plans are recorded

b) Additional notes must be made for the following:

i) Significant changes in physical condition necessitating changes in

management, e.g. renal failure requiring dialysis.

ii) Invasive procedures, e.g. laparotomy, tracheostomy, PAC/CVC insertion

iii) Results of specific investigations or tests, e.g. CT scans, endocrine tests

iv) Changes in policy, e.g. non-escalation of treatment, advance directives.

3. Handover summary

a) Due to the large number of complex patients, an ongoing handover summary

should be established for each patient

b) This facilitates ease of handover between day and night resident staff and for the

duty consultant staff.

c) This is not a formal casenote, nor does it take the place of a thorough review of

each patient and their casenotes. This is meant to be an aide-mémoire to be

updated each shift.

d) This is stored in a specific ICU database available on the PCs in the ICU.

4. Discharge summary

a) All patients transferred from ICU (Units A/B/C) require a Medical Transfer

Summary (MR 42) form completed.

b) This is a single page document outlining all relevant transfer information.

c) The original should be filed in the case notes and a photocopy placed in the

marked box in the Unit B station for filing by the secretary.

d) The duty registrar on the day of transfer is responsible for completing the form.

e) Incomplete or missing summaries will be forwarded to the responsible registrar

for completion.

f) Short term Unit C patients do not require detailed discharge summaries, only

pertinent information relating to their stay.

21

5. Death certificates

a) The following forms need to be completed:

i) RAH Notification and Certification of Death (MR 150.2)

all patients including those reported to the Coroner

ii) Death Certificate ("the yellow form")

do not complete this for deaths reported to the Coroner

iii) First Medical Certificate

do not complete this for deaths reported to the Coroner

b) Deaths notifiable to the Coroner:

i) Contact the Coroner’s office and provide preliminary demographic details

of the deceased.

ii) The Coroner’s office will then fax the Medical Practitioner’s Deposition

form for you to complete and return by fax.

iii) File the original deposition in the patient’s case-notes.

I. Consent in ICU

1. Competent patients:

a) All competent patients undergoing invasive procedures should have a standard

RAH consent form (MR: 60.16) completed and signed by the patient.

2. Incompetent patients (sedation, coma or encephalopathy):

a) Third party consent is not necessary for routine ICU procedures:

i) endotracheal intubation

ii) arterial lines

iii) central venous lines

iv) pulmonary artery catheters

v) transvenous pacing wires

vi) underwater seal drains

vii) jugular bulb catheters

viii) intra-aortic balloon counterpulsation

ix) oesophageal tamponade tubes

x) bronchoscopy

b) However, relatives should be informed prior to the procedure if present.

c) The indications, conduct and complications of the procedure should be

documented in the casenotes.

d) Major invasive procedures such as percutaneous tracheostomy, coronary

angiography, permanent pacemaker insertion or major surgical procedures

require completion of a consent form:

i) Emergency procedures signed by two doctors

ii) Non-urgent procedures by third party consent (next-of-kin).

e) Responsibility for consent lies with the operator performing the procedure.

22

f) ICU staff are not responsible for consent for procedures performed outside of

ICU, e.g. surgical tracheostomy, or PICC lines placed in radiology

g) A person, not necessarily next-of-kin, who has been nominated by the patient as

a medical power of attorney may sign or refuse consent on behalf of the patient.

h) Relatives should always be informed of any non-routine procedures and the

consent issue explained, irrespective of the presence or absence of a medical or

legal power of attorney.

i) If relatives cannot be contacted, emergency life saving treatment should

proceed immediately, with discussion with the Duty Consultant.

J. ICU Ward Rounds

1. Grand rounds

a) Held on Mondays and Fridays are an integral feature of the running of the unit.

b) These are open, multi-disciplinary meetings to discuss management issues and are

a valuable teaching forum.

c) Current x-rays and investigation results are displayed via computer projection.

d) The ward round is attended by:

i) Team A, B, C and Duty ICU consultants and all floor registrars

ii) An infectious diseases consultant

iii) Senior nursing staff

iv) Physiotherapists

v) A pharmacist

vi) A dietician

vii) Invited clinics when appropriate

viii) Medical students

e) Registrars are expected to present their allocated patients and to actively participate

in management discussion.

f) Presentations should be of a standard suitable for a fellowship examination:

i) Should take no more than 5-8 minutes.

ii) Emphasise the relevant and pertinent issues only:

Patient details and demographics.

State day of ICU admission (e.g. Day 6 ICU).

Diagnosis or major problems.

Relevant pre-morbid history pertinent to this admission.

Relevant progress and events in ICU

(deterioration/improvement, procedures, investigations).

Current clinical status (system by system).

Outline features on daily pathology and radiology.

Current plan of management:

a. Medications

b. Further investigations / procedures

c. Discharge planning & prognosis

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2. Bedside patient rounds

a) Are held daily, including grand-round days.

b) Team consultants and registrars review each patient’s condition.

c) Unit A&B flowcharts are re-written daily and include orders for ventilation,

procedures, medications, infusions and fluid therapy.

i) To ensure all aspects of patient care have been considered, the

“FATDOGS” algorithm should be considered in all patients:

F - Feeding & fluids

A - Analgesia & sedation

T - Thromboprophylaxis

D - Drugs – therapeutic & usual

O - Oxygen & ventilation

G - Glucose control

S - Sit out of bed

ii) You need to either write up each one of these each day or have a reason

why you have not.

d) Printed stickers should be used for routine medications and infusions.

e) All orders must be signed by a doctor.

f) Requests for routine blood tests are made on the chart.

g) Patients transferred to the general ward or Unit C

i) Should have the hospital “blue folder” completed.

ii) All medication orders should be re-written

iii) Fluid or nutrition orders for the next 24 hours are prescribed.

iv) Patients started on TPN should have their details entered in the “TPN

folder” kept in Unit A.

h) Similarly, Unit C patients have their charts reviewed, however all medications

and fluids are recorded on the hospital blue treatment folders.

K. Clinical Duties Outside of the Intensive Care Unit

1. Policy regarding outside consults:

a) NB: The Unit must not be left unattended at any time to attend outside calls.

(i.e. at least one registrar must remain on the floor)

b) The consults and code-blue/trauma pagers are carried by the Consults Registrar

(D7) during the day and Night Senior overnight (this may be modified at the

discretion of the 1st on-call consultant / senior registrar).

c) All consults should be addressed as soon as possible.

d) If the ICU workload is heavy, refer ward consults to the DI, who will delegate

appropriately.

e) Notify the senior nurse and fellow registrar(s) when leaving the floor.

f) The following duties accompany the Consults pager (pager no #89 22888*):

i) Ward consults

ii) Requests for Total Parenteral Nutrition (refer to Team A SR)

iii) Requests for retrieval (refer to MedStar)

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g) The following duties accompany the Emergency pager (#33)

i) Code blue calls |

ii) Escalated MET calls | *see (4) below.

iii) Trauma (P1) resuscitation

Trauma pages are subdivided into levels

Attendance by the ICU registrar is only required for Level 1 calls.

h) All consults/MET calls potentially requiring admission to ICU must be

discussed with the Duty Intensivist (DI).

2. Ward Calls

a) Consults regarding potential admissions from the general wards, theatre or ED.

b) Pre-operative consults for potential or booked surgical patients.

c) Advice regarding fluid and electrolyte management, oxygen therapy, sedation and

analgesia (usually referred to APS).

d) Review as requested patients in the:

i) Spinal Injuries Unit with potential respiratory failure.

ii) Burns Unit for airway / breathing assessment, IV access or resuscitation.

e) Requests for venous access:

i) Requests must come from registrar level or above and after reasonable

attempts have been made to obtain IV access.

ii) Radiology provide a PICC line service in working hours.

iii) CVCs are not to be inserted on ward patients.

iv) Should be attended to in a timeframe appropriate to the patient’s condition.

f) Requests for TPN.

3. Total Parenteral Nutrition (TPN)

a) ICU provides a TPN service for the hospital.

b) Requests for TPN are elective (i.e. Mon to Fri: 0800-1800) and should be made

according to recommended indications.

c) Requests are made via the DI or consults registrar.

d) The ‘TPN Folder’ is kept in the Unit A ward station.

e) The Team A Senior Registrar and Consultant will manage:

i) Initial consultation with the requesting clinic.

ii) Recording TPN patients in the “TPN Folder”.

iii) Insertion of a PICC catheter.

iv) Daily:

Review of electrolytes and fluid balance,

Review of the central venous catheter/PICC,

Prescription of TPN orders ± vitamins / trace elements,

Issue a request form for serum electrolytes.

Use pink labels from ICU & leave a spare for labelling of specimen tubes

- this ensures priority in the lab

f) Refer to the section on nutrition in the clinical protocols for indications &

complications.

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4. Code Blue & MET Calls

a) The RAH medical emergency code is “33#”.

i) Upon dialling 33#, switchboard automatically page the following people:

ICU registrar

ICU equipment nurse

Medical registrar

b) These calls are divided into:

i) Code Blue *all calls must be attended immediately

Cardiac &/or respiratory arrest (actual or impending)

Threatened airway

Major haemorrhage

ii) MET calls

Significant clinical deterioration (see MET criteria)

MET calls are not routinely attended by ICU Registrars.

The ICU Registrar should remain immediately available if a MET call

has been activated, so that assistance can be provided to the MET team if

required (e.g. avoid starting procedures such as CVC insertions if the

MET pager has activated).

c) When “33” is displayed on the pager:

i) Dial “33#” on an internal phone.

ii) Switchboard will then state the location of the arrest.

iii) Clearly state who you are (i.e. ICU registrar) and go to the location.

d) Ensure that the ICU staff know where you are going and that the Unit is not left

unattended.

e) At the emergency:

i) This hospital follows the Australian Resuscitation Council guidelines for

cardiopulmonary resuscitation.

ii) The ICU/resuscitation registrar is responsible for initial assessment, securing

the airway and establishing effective ventilation.

iii) Basic life support is done by attending nursing and medical staff and may be

directed by either ICU or medical registrar.

iv) Advanced life support is directed by the more senior registrar present. This is

usually the ICU registrar.

v) Depending on the outcome of the Code Blue, the patient may be admitted to

ICU, CCU or remain on the ward according to standard admission policies.

vi) As a general rule, it is better to admit a patient if previous details are not

immediately available than to prematurely abandon resuscitation.

vii) Document your involvement with the resuscitation in the casenotes.

viii) The home team should be involved or at least informed of their patient’s

condition, including when resuscitation is unsuccessful.

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5. Trauma Calls

a) As in cardiac arrest, a “33#” call is activated for trauma patients who meet

specified trauma criteria. (Refer to trauma directives.)

b) Trauma pages will appear as 2 Levels:

i) Level 1: major trauma requiring immediate attendance / airway support

ii) Level 2: trauma requiring full assessment in ED/Resus.

c) The following people are paged and the level response detailed on the pager:

i) ICU/resuscitation registrar

ii) Trauma Service registrar

iii) Accident and emergency registrar

d) On receiving a Level 1 call the ICU registrar should proceed directly to Resus in

the Emergency Department (ED)

e) Ensure that ICU staff know where you are going and that the Unit is not left

unattended.

f) At the trauma resuscitation:

i) This hospital follows the Early Management of Severe Trauma (RACS)

guidelines.

ii) The team leader is designated by the current Trauma Service Directive (found

on the wall in Resus).

iii) Role of the ICU registrar:

Primarily as a backup for acute life threatening situations in the event that

sufficiently experienced personnel are not available in Resus.

If anaesthetic staff are present in Resus, there is no requirement for ICU

registrars to attend the resuscitation unless specifically requested by these

personnel or the Trauma Director.

If anaesthetic staff are not immediately available, the following role is

indicated until appropriate personnel arrive:

a. Initial airway assessment and management.

b. Establishing effective ventilation

c. Assistance with vascular access and restoration of circulation.

d. Other acute interventions (e.g. UWSD) as required

Once anaesthetic & trauma team members are present and the situation is

under control, return to ICU - do not leave ICU unattended for lengthy

periods of time.

If prolonged resuscitation is anticipated, call in the ICU or Trauma

Consultant and/or delegate to the anaesthetic/resuscitation registrars.

Transportation of trauma patients to CT scan, angiography etc. is the

responsibility of the emergency anaesthetic staff.

ICU registrars must not do prolonged intra-hospital transports for trauma

patients without approval by the duty ICU consultant.

27

iv) General principles:

Document your involvement with the resuscitation in the casenotes

Once the primary survey is completed, proceed to the secondary survey

and order appropriate investigations as per the Trauma team leader.

In critically ill patients, ensure that a suitably qualified person (in terms of

resuscitative skills) remains with the patient at all times. This is

mandatory if the patient is transported from Resus (e.g. to radiology,

ICU, theatre).

Notify ICU staff of pending admissions.

Demarcation disputes are referred to the duty Trauma Consultant.

6. Retrieval Requests

a) Requests for consultation may originate from a number of sources. Namely,

i) The DI phone (SD: 1650)

ii) Other ICU telephones

iii) ICU registrar pager

iv) Other clinics who have been consulted by outside medical officers.

b) All retrieval requests should be referred immediately to the state retrieval

service, MedStar on 82224222.

c) All requests from MedStar for the transfer of patients to the RAH must be

referred to the on-call ICU consultant.

7. Intrahospital transportation of Intensive Care patients

a) All transports must be authorised by the duty ICU consultant.

b) The transport/investigation must be considered in the best interests of the patient.

c) All ventilated and potentially unstable transports need a medical escort.

d) Stable, self-ventilating patients may be transported by an ICU RN

e) If ICU nursing staff are concerned, then a medical escort is required.

f) At no stage must the unit be left uncovered.

g) If the Unit is busy, or transports clash with ward rounds, other personnel may be

deployed to do the transport. This is coordinated by the duty ICU consultant.

h) As a general rule, ICU staff are responsible for transportation of ICU patients.

i) Anaesthesia is responsible for transport of the following ICU patients:

i) Trauma resuscitation patients

ii) Patients to and from theatre

iii) Patients to and from hyperbaric medicine.

j) The transport of patients undergoing prolonged investigations or treatments, (e.g.

MRI, angiographic embolisation, invasive radiological procedures, TIPS) should

be discussed with the Duty ICU consultant and Duty Anaesthetist (SD 1175)

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k) Guidelines

i) Registrars must familiarise themselves with transport monitors, portable

ventilators and infusion pumps.

ii) Inform and discuss the transport with the nursing staff as soon as possible.

iii) Patients must be appropriately monitored during the transport and

observations recorded on the flow chart.

iv) Document any problems which may occur during transport.

v) Ensure that the results of investigations performed (e.g. CT scans etc) are

recorded in the case notes by the appropriate person.

L. Hospital Emergencies

1. The emergency number is 33# : state the nature and location of emergency

2. Fire a) A copy of the hospital emergency procedures (fire, smoke, bomb-threat) is kept in

the P4A and P4C nursing stations.

b) The chief fire and emergency officer is the overall controller during a fire or smoke

emergency (Code Red).

c) Become familiar with the location of fire exits, extinguishers and blankets in ICU

i) Unless small and easily contained do not attempt to fight a fire yourself.

ii) Remove yourself from the immediate vicinity of the fire, alerting other staff

members as indicated, and position yourself behind the automatic fire doors.

iii) The MFS has a 3 minute response time to the RAH.

iv) Wait for the arrival of the Fire Chief and assist in any patient

movement/evacuation only as indicated by the Fire Chief.

d) Role of medical staff:

i) There is no place for “heroic” action - ensure your own safety first!

ii) Wait for the arrival of the MFS.

iii) Assist in patient assessment/management under the coordination of the Fire

Chief.

iv) In the event of a significant fire / smoke hazard, staff will only re-enter the

danger zone in the immediate company of a MFS fire-fighter, with

appropriate breathing apparatus.

29

M. Research in ICU

1. Background:

There is a prolific research programme at the RAH ICU. This research is world

leading in the areas of gastrointestinal motility, nutrient absorption and incretin

hormones in the critically ill.

2. Personnel:

a) Director of Research - A/Prof. Marianne Chapman

b) Research Fellow - Dr Adam Deane

c) Research Manager - Ms Stephanie O’Connor

d) Research Nurses - Ms Justine Rivett

- Mr Luke Chester

- Ms. Alison Ankor

e) Research Scientists - Mr Matthew Summers

- Mr Antony Zaknic

3. There are students studying toward their higher degrees frequently working in the

ICU. These students are strongly supported by the ICU Research Unit. Trainees

interested in undertaking a higher degree are always well received.

4. There are broadly 3 types of research studies occurring in the unit:

a) Locally initiated studies

b) Drug company sponsored studies

c) Studies performed with the ANZICS Clinical Trials Group (see below).

5. Medical and nursing staff are encouraged to become involved in research:

a) Registrars are expected to assist in obtaining consent for ongoing studies.

b) Knowledge of these studies can be obtained from any of the research staff.

c) Further involvement is encouraged and there are supports within the unit to

facilitate research to occur.

d) Because the ICU is a world-leader in several areas, it is advised to leverage on

the expertise and availability of sophisticated methodologies within the group.

However, independent projects, driven by highly committed individuals, will

always be supported.

6. The CICM formal project takes, at a minimum, 12 months to complete.

a) Trainees interested in undertaking a study for their formal project are advised to

approach potential supervisors with sufficient time to complete their project.

b) Potential projects (and initial contact persons) are:

i) Retrospective observational studies (A/Prof Flabouris and Dr Finnis)

ii) Prospective observational studies (Dr Sundarajarajan)

iii) Experimental work using a sheep model (Dr Maiden)

iv) Laboratory based work (Dr Reddi) and

v) Prospective clinical research (A/Prof Chapman and Dr Deane).

30

7. Most projects require prior RAH Research Ethics Committee approval. Your

supervisor will be able to provide details.

8. Completed research projects should be presented at either a local or interstate

scientific meeting.

a) Partial funding is available for staff who present work at approved meetings.

b) Applications should be made to the Coordinator of Research.

c) Eligible meetings include, but are not limited to:

i) ANZICS / ACCCN Annual Scientific Meeting - October.

ii) CICM Annual Scientific Meeting – May/June.

iii) ACCCN (Institute of Continuing Education), Conference. Annual – May.

9. ANZICS Clinical Trials Group (CTG).

a) A national clinical trials group to facilitate multicentre trials in Australia & NZ.

b) World-leading in critical care research and is open to all interested parties.

c) CTG meetings are held once per season, with the main meeting in March.

d) Resource person: A/Prof. Marianne Chapman.

10. If you are unsure of what to do about a patient enrolled in a study, please contact the

relevant staff member regardless of the time of day.

a) Queries about drug company sponsored studies should be directed to the ICU

Research Nurse on-call (SD 1520)

b) Queries relating to a local investigator studies should be directed to the primary

investigator.

N. Information Technology in ICU

a) All consultant and registrar offices and the Registrar Teaching Room are

equipped with PCs, connected to the RAH local area network (LAN).

b) Facilities available through the LAN include:

i) Intranet e-mail accounts

ii) WWW browsing facilities (available on application).

iii) Intranet resources, which are being continuously expanded:

UpToDate®, eMIMS, Medline, Toxnet, etc.

An extensive range of electronic text books

ICU Handover Database

iv) On application registrars will be allocated a username, which will carry

with it an ‘Internet’ e-mail account for the duration of their stay.

c) In addition, many of the consultants have access to the University of Adelaide,

including Barr-Smith Library resources.

d) The Unit has an internet presence at http://www.icuadelaide.com.au/

e) NB: Use of hospital computers to access inappropriate material is not tolerated.

RAH guidelines detail appropriate use.

31

PART 2 - CLINICAL PROCEDURES

A. Introduction

1. Registrars are encouraged to become proficient in all Intensive Care procedures.

2. Invasive procedures should be authorised by a senior registrar or the duty ICU

consultant.

3. Adequate familiarisation and supervision with unfamiliar procedures is essential:

there is always someone available to help.

4. The relative risk vs. benefit of all procedures must be carefully considered.

5. Do not persist if you are having difficulty with the procedure - call for help.

6. Consent for procedures: *refer to Administration / Consent

a) Competent patients undergoing invasive procedures should have a standard

RAH Consent Form (MR:60.16) completed and signed by the patient

b) Third party consent is not necessary for incompetent patients undergoing

routine ICU procedures.

c) Major ICU procedures, such as percutaneous tracheostomy or

enterogastrostomy, require third party or two-doctor consent.

7. The indications, conduct and any complications of the procedure should be clearly

documented in the case notes, in addition to a consent form if this is completed.

8. Discuss the planned procedure with the nursing staff and allow sufficient time for

setting up of trays and equipment.

9. Remember: the nursing staff have extensive experience with these procedures.

10. It is the responsibility of the operator to discard all sharps used in the procedure and

to ensure that they are placed in a sharps disposal container.

B. Procedures

1. Registrars are expected to become proficient in all routine procedures.

2. Where appropriate trainees are expected to learn to place lines both

a) Via surface anatomical landmark, and

b) With ultrasound guidance

3. Whilst ultrasound may aid in delineating the relevant anatomy:

a) Trainees will find themselves in environments where U/S is unavailable

b) The time delay involved in the use of U/S may be clinically deleterious, and

c) There are insufficient data that the use of U/S actually reduces complications.

4. Specialised procedures are done either by the Duty Consultant or strictly under

consultant supervision.

5. Guidelines for the listed routine and specialised procedures are outlined in the

following sections.

32

Routine ICU procedures

Endotracheal intubation

Peripheral venous catheterisation

Arterial cannulation

Central venous catheterisation / PICC line insertion

Urinary catheterisation

Lumbar puncture

Epidural catheterisation

PiCCO Catheter

Pulmonary artery catheterisation

Pleural Drainage

Underwater seal drain insertion

Pleurocentesis

Peritoneocentesis

Nasogastric tube insertion

Specialised ICU procedures

Fibreoptic bronchoscopy

Percutaneous tracheostomy

Cardiac (transvenous) pacing

Pericardiocentesis

Intra-aortic balloon counterpulsation

Oesophageal tamponade tube insertion

Extracorporeal Membrane Oxygenation

C. Peripheral IV Catheters

1. Indications:

a) First line IV access for resuscitation, especially blood transfusion

b) Stable patients where a CVC is no longer necessary

2. Management protocol:

a) Remove/replace all resuscitation lines inserted in unsterile conditions.

b) Generally avoid peripheral IV use in ICU patients and remove if not in use.

c) Use local anaesthesia in awake patients.

d) Aseptic technique:

i) Handwash with AVAGARD® (chlorhexidine 2%) or

MEDISPONGE® (chlorhexidine 4%) + gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)

iii) Dressing: Opsite® or equivalent occlusive dressing

e) Change / remove all peripheral lines after 48 hours.

f) Avoid lower-limb placement in patients with vascular disease.

33

3. Complications a) Infection - local and systemic

b) Thrombosis

c) Extravasation in tissues

D. Arterial Cannulation

1. Indications:

a) Routine measurement of systemic blood pressure in ICU

b) Multiple blood gas and laboratory analysis

c) Measurement of BP during transport of patients in hostile environments


a) Remove and replace lines inserted in unsterile conditions as soon as possible.

b) Brachial and femoral arterial lines should be changed as soon as radial or

dorsalis pedis arteries are available.

c) Aseptic technique:

i) Handwash with AVAGARD® (chlorhexidine 2%) or

MEDISPONGE® (chlorhexidine 4%) + sterile gloves

ii) Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)

d) Local anaesthesia in awake patients.

e) Cannulae:

i) Arrow® radial or femoral kits (Seldinger technique).

ii) 20G Insyte®.

iii) Single lumen 20G CVC (paediatric) for femoral arterial lines.

f) Insertion sites – in order of preference:

radial > dorsalis pedis > femoral > brachial

g) The femoral artery may be the sole option in the acutely shocked patient.

h) Secure with a StatLock® device.

i) There is no optimal time for an arterial line to be removed or changed.

j) IA cannulae are changed/removed in the following settings:

i) Invasive IA line is no longer necessary.

ii) Distal ischaemia

iii) Mechanical failure (overdamped waveform, inability to aspirate blood)

iv) Evidence of local or unexplained systemic infection

k) Measurement of pressure:

i) Transducers should be ‘zeroed’ each nursing shift

ii) Zero reference = the mid-axillary line, 5th intercostal space

l) Maintenance of lumen patency

i) Continuous pressurised (Intraflo®) saline flush at 3ml/hr.

3. Complications

a) Infection

b) Thrombosis / digital ischaemia

c) Vessel damage / aneurysm

d) Haemorrhage / disconnection

34

E. Central Venous Catheters

NB: Registrars should be familiar with the interpretation and limitations of

haemodynamic variables derived from central catheters (CVC, PICCO and PAC) in

critically ill patients.

1. Indications:

a) Standard IV access in ICU patients:

i) Vasoactive infusions

ii) Fluid administration (including elective transfusion)

iii) Hypertonic solutions (TPN, amiodarone, nimodipine, etc.)

b) Monitoring of right atrial pressure (CVP)

c) Venous access for:

i) Pulmonary artery catheterisation (PAC)

ii) Continuous renal replacement therapy (CVVHDF)

iii) Plasmapheresis.

iv) Transvenous pacing.

v) Jugular bulb oximetry.

d) Resuscitation

i) Large bore peripheral IV line(s) are 1st line.

ii) Standard lumen CVCs are not appropriate for acute volume resuscitation.

iii) Consider using a PAC sheath or Vascath if central access is required and

adequate peripheral access is unobtainable.

2. Management protocol: (applies to all types of CVC):

a) Types:

i) The default CVC for all ICU patients is a Cook antimicrobial

impregnated (rifampicin/minocycline) 7F 15 or 20cm 3-lumen catheter.

ii) Non-impregnated catheters inserted outside the ICU should be changed to

an impregnated catheter according to clinical indication.

iii) Dolphin Protect® catheters are used for CVVHDF and plasmapheresis

iv) Pulmonary artery catheter sheath (part of the PAC kit)

v) Dress non-impregnated catheters with a BioPatch®

b) Sites:

i) Preferred site for routine stable patients → SCV > IJV.

ii) Femoral v. access is preferable where:

Dolphin Protect® / CVVHDF

Limited IV access (burns, multiple previous CVC’s),

A thoracic approach is considered hazardous with:

a. Severe respiratory failure from any cause (PaO2/FiO2 < 150)

b. Hyper-expanded lung fields (severe asthma, bullous disease)

c. Coagulopathy (see below)

Inexperienced staff requiring urgent access, where supervision is not

immediately available.

35

c) Coagulopathic patients:

i) INR > 2.0 or APTT > 50s correct with FFP and/or

prothrombinex

ii) INR 1.5-2.0 or APTT 40-50s correct with FFP, or

use IJ or femoral approach

iii) Platelets < 50,000 transfuse 1 pack (5U) platelets

Failure to increment femoral approach or PICC

iv) Uncontrolled coagulopathy femoral approach or PICC

Including recent therapy with Dabigatran

v) Insertion under ultrasound guidance may be preferred.

d) Technique policy

i) Use local anaesthesia in awake patients.

ii) Strict aseptic technique at insertion:

Handwash with AVAGARD® (chlorhexidine 2%) or

MEDISPONGE® (chlorhexidine 4%)

Sterile barrier: gown, sterile gloves, mask, hat

sterile drapes (CVC - Patient Cover)

Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)

iii) Seldinger technique or ultrasound guided insertion – Sonosite®

iv) U/sound guided insertion may be preferred where:

There is an increased complication risk (e.g. bleeding, pneumothorax)

Large bore catheter insertion.

Distorted patient anatomy.

v) CVC Catheter lengths:

15cm - right subclavian or internal jugular

20cm - left subclavian or internal jugular, either side femoral

vi) Secure all lines with a StatLock® device or securely suture

vii) Dressing: non-occlusive dressing

viii) Flush all lumens with saline.

ix) Transduce pressure ASAP post-insertion to exclude arterial placement.

x) Check CXR prior to use (SCV, IJV), except in urgent circumstances

e) Maintenance

i) Routine IV administration set change at 7 days.

ii) Daily assessment for infection irrespective of insertion duration.

iii) Catheters remain as long as clinically indicated and are changed when:

Evidence of systemic infection

a. New, unexplained fever or WCC

b. Deterioration in organ function

c. Positive blood culture by venipuncture with likely organisms

(S. epidermidis, candida spp.), and/or

Evidence of local infection - inflammation or pus at insertion site.

iv) Guidewire exchanges are actively discouraged. They may be indicated in

the following situations, only after discussion with a consultant:

Mechanical problems in a new catheter (leaks or kinks)

Difficult or limited central access (e.g. burns).

36

v) Maintenance of lumen patency

Central venous catheters (pre-printed on the patient flowsheet)

a. Flush unused lumens with 1ml normal saline 8 hourly

Vascath: into each lumen 8 hourly (printed sticker)

a. Withdraw 2ml and discard.

b. Flush with 2ml normal saline.

c. Flush 1.5ml solution (5000U heparin/3ml = 2500U/lumen).

d. NB: Each lumen has it’s internal volume printed on it.

3. Complications:

a) At insertion

i) Arterial puncture – haematoma, thrombosis, embolism

ii) Pneumothorax, haemothorax, chylothorax

iii) Neural injury (phrenic, brachial plexus, femoral nn.)

b) Passage of wire/catheter

i) Arrhythmias

ii) Wire embolism *if this occurs, notify senior staff immediately

iii) Perforation of SVC / RA - tamponade

c) Presence of catheter

i) Catheter infection: rates increase under the following conditions:

Size of catheter - thicker catheters (PAC, Vascaths)

Site of catheter - femoral > internal jugular > subclavian sites

Number of lumens

Nature of fluid through catheters - TPN or dextrose solutions

ii) Thrombosis, HITS secondary to heparin

iii) Catheter / Air embolism

iv) Knotting of catheters (esp. PAC)

v) Pulmonary infarct / arterial rupture (PAC)

NB: Where CVC insertion presents a “significant risk” in a non-urgent

situation, consider insertion of a PICC line as an alternative.

F. Urinary Catheters

1. Standard in all ICU patients

2. Management protocol: a) Aseptic technique at insertion.

i) Hand disinfection: surgical scrub with chlorhexidine for >1 minute

ii) Sterile barrier: gloves and sterile drapes.

iii) Skin prep: chlorhexidene 1%

b) Local anaesthesic gel in all patients.

c) Only BiocathTM catheters should be inserted in ICU & changed 6 weekly.

d) Standard Foley catheters should be changed to a BiocathTM after 14 days.

e) Silastic catheters should be changed after 1 month.

f) Remove catheters in anuric patients and perform intermittent catheterisation

weekly, or as indicated.

37

G. Epidural Catheters

1. Indications

a) Post-operative pain relief (usually placed in theatre)

b) Analgesia in chest trauma.


a) Notify the Acute Pain Service of any epidural placed in ICU.

b) Epidural cocktails should follow the Acute Pain Service protocols

c) Strict aseptic technique at insertion.

d) Daily inspection of the insertion site. The catheter should not be routinely

redressed, except under the advice of the APS.

e) Leave in for a maximum of 5 days and then remove.

f) Remove if:

i) Not in use for > 24 hours, or

ii) Clinical evidence of unexplained sepsis, or

iii) Positive blood culture by venipuncture with likely organisms

(S. epidermidis, candida).

iv) Heparin/Warfarin Protocol

*also see ‘Acute Pain Service Guidelines for Anaesthetists’

3. Complications

a) Hypotension from sympathetic blockade / relative hypovolaemia

i) This usually responds to adequate intravascular volume replacement

ii) Occasionally, a low-dose vasopressor infusion is required

iii) If this is considered, occult bleeding must be excluded.

b) Pruritis, nausea & vomiting, or urinary retention (opioid effects)

c) Post-dural puncture headache

d) Infection: epidural abscess

e) Pneumothorax (rarely)

4. NB: Further guidelines for the management of epidural catheters can be obtained

from “The Acute Pain Service Guidelines for Anaesthetists”. Manuals are stored in

each ICU station.

H. PICCO Catheters

1. Introduction

a) PiCCO uses a combination of thermodilution and pulse waveform analysis to

provide an estimate of cardiovascular status.

b) Trainees should become familiar with the theory of insertion, indications,

interpretation and complications of PiCCO catheters.

c) Indicated in the assessment & response to therapy in shock states.

38

2. Technique

a) A normal CVC line can be used.

b) The peripheral arterial catheter is inserted into a femoral, brachial or axillary

artery using an aseptic Seldinger technique.

c) The pulse waveform analysis of continuous cardiac output is calibrated by

thermodilution according to the device instructions.

d) Calibration should be repeated once per nursing shift and as indicated.

e) Additional measurements of Global End-diastolic Volume Index (GEDI) and

Extravascular Lung Water Index (ELWI) can be made via thermodilution.

3. Below are the normal values and a suggested decision tree from the manufacturer

which should be used as a guide only:

Table: PiCCO Values and Decision Tree

Variable Abbr. Normal Units

Cardiac Index CI 3.0-5.0 l/min/m2

Global End-diastolic Blood Volume Index GEDI 680-800 ml/m2

Intrathoracic Blood Volume Index ITBI 850-1000 ml/m2

Stroke Volume Variation SVV 10 %

Extravascular Lung Water Index* ELWI* 3.0-7.0 ml/kg

39

I. Pulmonary Artery Catheters

1. Policy

a) Insertion of PA catheters must be authorised by the duty consultant.

b) Trainees should become familiar with the theory of insertion, indications,

interpretation and complications of PACs.

c) Insertion of a PAC must never delay resuscitation of a shocked patient.

d) Allow sufficient time for nursing staff to set up insertion trays and transducers.

e) Remove catheters once they are not being routinely used.

f) They may be left in situ for up to 7 days.

2. Indications:

a) Haemodynamic measurements (CO/I, SV/I, SVR/I)

i) Aid to diagnosis and response to therapy of shock states,

e.g. cardiogenic, septic or hypovolaemic

b) Measurement of right heart pressures (RAP, PAP):

i) Acute pulmonary hypertension

ii) Pulmonary embolism

iii) Cardiac tamponade

c) Estimation of preload / left heart filling (PAOP)

i) Intravascular volume status & response to fluid loading

ii) LVF

d) Measurement of intracardiac shunt: (Acute VSD)

e) Derivation of oxygen delivery & utilization variables (VO2, DO2)


a) Insertion protocol as per CVC, with the following features:

i) Sheath introducer (8.5Fr) with side port, haemostatic valve and plastic

contamination shield.

ii) Shared transducer for RAP (proximal) and PAP (distal) lumens

iii) Check competence of balloon and concentric position

iv) Ensure all lumens are flushed with heparinised-saline prior to insertion.

v) Ensure the system is zeroed and an appropriate scale (0-40mmHg) on the

monitor prior to insertion.

vi) Insert the catheter observing changing waveforms (RARVPA) on the

monitor, with the balloon inflated and locked, until catheter displays

pulmonary artery occlusion tracing

Subclavian and left IJ ~ 50cm

Right IJ ~ 40cm

vii) Deflate the balloon and ensure an adequate PA trace reappears.

viii) Adjust the catheter depth until a PAOP trace appears consistently

with 1-1.5ml balloon inflation.

ix) Suture introducer and attach the contamination shield to the hub.

x) Apply a BioPatch® and non-occlusive dressing.

b) Ensure an adequate PA tracing is on the monitor at all times

40

c) “Wedged” tracings must be corrected as soon as possible:

i) Flush distal lumen with 2ml N.Saline

ii) Withdraw the catheter until a PA trace is visible

d) Measurement of pressures:

i) Reference pressures to the mid-axillary line

ii) Measure at end-expiration of the respiratory cycle

iii) Do not disconnect ventilated patients to measure pressures.

iv) Measurement of PAOP:

End expiration: lowest point in ventilated patients, highest point in

spontaneously ventilating patients

Use the “electronic cursor” on monitors after 2-3 respiratory cycles.

Do not use the electronic average of the wedge tracing.

e) Haemodynamic measurements

i) These are routinely performed by the nursing staff, however registrars

should become familiar with the procedure.

ii) Record all measurements in the flow chart in the results folder.

iii) Cardiac outputs:

Injectate: 10ml 5% dextrose @ room temperature

Inject at random times in the respiratory cycle

Take > 3 measurements and ignore values > 10% from average.

iv) Derived variables:

CO/CI and SVR are routinely charted (8 hrly or as indicated).

Other variables including PVR(I), SV(I), L(R)VSWI are recorded in

the haemodynamics flowsheet.

Mixed venous oxygen levels should be measured on a sample taken

from the distal (yellow) port.

Oxygen saturation should be directly measured with co-oximetry.

Derived haemodynamic variables (see table), should be used in

conjunction with clinical assessment.

4. Complications

a) Related to CVC cannulation (see CVC section)

b) Related to insertion/use of a PAC

i) Cardiac perforation

ii) Thromboembolism

iii) Pulmonary infarction ~ 0-1.4% (2 persistent wedging)

iv) Pulmonary artery rupture ~ 0.06-0.2% (mortality 50%)

v) Catheter related sepsis

vi) Endocarditis

vii) Pulmonary valve insufficiency

viii) Catheter knotting

ix) Balloon fragmentation / embolism

x) Tachyarrhythmias

xi) RBBB

41

Table: Standard Haemodynamic Variables

Variable Formula Normal range

Cardiac index CO/BSACI 2.5-5 l/min/m2

Systemic vascular resistance

SVRMAP RAP

CO

79 9. 750-1500

dyn.sec/cm5/m2

Systemic vascular resistance index

79.9CI

RAPMAPSVRI

1400-2400

dyn.sec/cm5/m2

Pulmonary vascular resistance index

9.79CI

PAOPPAPmPVRI

150-250

dyn.sec/cm5/m2

Stroke volume index HRCISVI 33- 47 ml/beat/m2

LV stroke work index 0.0136SVIPAOPMAPLVSWI 50-120 g/m2 / beat

RV stroke work index 0.0136SVIPAOPmPAPRVSWI 25-55 g/m2 / beat

Arterial oxygen content CaO Hb SaO PaO2 2 2134 0003 . . 17-20 ml/100ml

Venous oxygen content CvO Hb SvO PvO2 2 2134 0 003 . . 12-15 ml/100ml

Oxygen delivery index DO I CI CaO2 2 10 550-750 ml/min/m2

Oxygen consumption index VO I CI CaO CvO2 2 2 10 115-160 ml/min/m2

Oxygen extraction ratio O ERVO I

DO I2

2

2

0.24-0.4

Shunt equation 010OvCOcC

CaOOcC

Qt

Qs

22

22

5-15%

End capillary oxygen content

0.003PAO1.01.34HbOcC 22 80-100 ml/100ml

Alveolar gas equation PAO FiO PaCO2 2 2760 47 125 . 100-650 mmHg

42

J. Pleural Drainage

1. Indications:

a) Pneumothorax

b) Tension pneumothorax may require urgent needle thoracostomy

c) Haemothorax

d) Large symptomatic pleural effusion


a) Needle thoracostomy (tension pneumothorax):

i) 14 or 16G cannula placed in mid-clavicular line, 2nd intercostal space

ii) Always place an UWSD following this procedure

b) Pleurocentesis: (pleural effusion)

i) Prior to commencement, ultrasound the chest to confirm the presence of

fluid and indentify/mark an appropriate insertion site.

ii) Strict aseptic technique at insertion:

Handwash with AVAGARD® (chlorhexidine 2%) or

MEDISPONGE® (chlorhexidine 4%)

Sterile barrier: gown, sterile gloves, mask, hat & drape(s)

Skin prep. with SOLU-IV (chlorhexidine 2% / 70% alcohol)

iii) Local anaesthesia in conscious patients.

iv) Seldinger technique:

Pigtail catheter or ThalQuick® 12F kit.

Insert guidewire through needle into pleural space

Insert catheter into pleural space over the wire

Aspirate intermittently with closed system or attach to an UWSD.

v) Record volume removed and send for MC&S, cytology & biochemistry.

vi) Check CXR post-procedure.

c) Underwater seal drainage:

i) Local anaesthesia in awake patients.

ii) Aseptic insertion technique - as above.

iii) Site:

Mid-axillary line, 3-5th intercostal space

Mid-clavicular line, 2nd intercostal space ( air only)

Do not insert drains through old wounds

iv) ICU patients need large drains: 28F catheter or larger

v) Use soft Mallinkrodt tubes in preference to the stiffer Argyle tubes

vi) Remove the trochar from catheter: do not use the trochar for insertion

vii) For the usual lateral ICD, go for the anterior or mid-axillary lines, avoid

the posterior sites as the chest wall is too thick, and there is a danger to

neurovascular structures

viii) Make a 2-3cm skin incision parallel to the ribs (#10 or #15 scalpel)

43

ix) Instruments & technique:

Blunt dissect using short artery forceps, avoid long forceps.

Do not “plunge” into the chest with either instrument.

Access to the intercostal space is by careful blunt dissection of the

intercostal muscles above the rib below.

The chest wall hole must be 2-3 cm wide in order that a finger can be

inserted into the pleural space to identify possible adhesions.

The soft tube should be guided by the intrapleural finger so that the

tube goes in between the finger and chest wall

x) Connect to an underwater seal drain apparatus

xi) Insert 2 purse string sutures:

1 to fasten the tube

1 (‘Z’ or purse-string) to close the skin incision on drain removal.

xii) Insert additional sutures as required to close the external wound.

xiii) Dressing: occlusive dressing (Hypafix)

xiv) Check CXR.

xv) Maintenance

Remove or replace drains inserted in unsterile conditions ASAP.

Leave the drain in situ until:

a. Radiological resolution of pleural collection (air/fluid)

b. No ongoing air-leak (no drain bubbling)

c. Minimal drainage (< 150 ml/24 hrs).

In ventilated patients, consider clamping the drain for 4 hours prior to

removal, providing the patient remains stable and/or post CXR.

Surgically placed drains are the responsibility of the surgeon and

should only be removed in consultation.

3. Complications

a) NB: minimised using the blunt technique

b) Incorrect placement - extrapleural, intrapulmonary, subdiaphragmatic

c) Pulmonary laceration - haemorrhage, fistula

d) Pneumothorax

e) Bleeding

i) local incision, intercostal vessels

ii) lung

iii) IMA (with anterior placement)

iv) Great vessels (rare)

f) Infection

i) Soft tissue

ii) Empyema

g) Mechanical (kinking, luminal obstruction)

44

K. Endotracheal Intubation

1. Policy:

a) Endotracheal intubation in ICU patients is a high risk but vital procedure:

i) Usually an emergency procedure, with limited time.

ii) Usually indicated for acute respiratory failure, or associated with limited

respiratory reserve

iii) Patients may have cardiovascular instability and significant co-morbidities

iv) Patients may have cervical spine or oropharyngeal trauma / surgery

v) Patients are at risk of vomiting and aspirating

vi) Positioning is difficult.

b) Familiarisation with the intubation trolleys, equipment and drugs is essential.

c) Intubation should ideally not be done as a sole operator procedure.

Skilled assistance should always be sought.

d) If you are alone (i.e. after hours): call for help!

i) Expertise in intubation is always available.

ii) Remember emergency anaesthesia staff.

e) The majority of ICU patients mandate rapid sequence induction.

2. Indications a) Institution of mechanical ventilation

b) To maintain an airway

i) Upper airway obstruction

Potential e.g. early burns

Real e.g. epiglottitis, trauma

ii) Patient transportation

c) To protect an airway

i) Patients at risk of aspiration

ii) Altered conscious state

iii) Loss of glottic reflexes

d) Tracheal toilet

3. Techniques

a) Orotracheal intubation is the standard method of intubation in this unit.

b) Nasotracheal intubation may be indicated where:

i) Patients require short-term ventilation and are intolerant of oral ET tubes.

ii) Nasal Fibreoptic intubation may be indicated for:

Oro-maxillary surgery and pathology

Inability to open the mouth:

e.g. intermaxillary fixation, TMJ trauma, rheumatoid arthritis.

Upper airway obstruction and nasal route preferred

iii) Contraindicated in base of skull & LeForte facial fractures

c) Methods:

i) Direct laryngoscopy, C-MAC after rapid sequence induction

ii) Fibreoptic bronchoscopic awake intubation (oral or nasal)

iii) Intubating laryngeal mask – LMA – Fastrac®

45

4. Endotracheal Tubes a) Standard tube:

i) Low pressure, high volume cuff.

ii) Males: 8-9 mm secure at 21-23cm to incisors

iii) Females: 7-8 mm secure at 19-21cm to incisors

iv) Do not cut tubes to less than 26 cm length

b) Double lumen tubes: *rarely indicated in ICU:

i) Lung isolation for broncho-pulmonary fistula, abscess or haemorrhage

ii) Inserted as a temporary manoeuvre prior to definitive therapy

iii) Allow differential lung ventilation

iv) Males: Left 41F

v) Females: Left 39F

vi) NB: right bronchial tubes are harder to correctly site.

vii) Position should be checked with bronchoscope.

c) Intubated patients from theatre may have the following tubes that are not

recommended for prolonged intubation. These tubes must be changed if intubation

is anticipated > 48 hrs and exchange is safe and feasible.

i) Plain PVC tubes - no above cuff suction port

ii) Armoured tubes - risk kinking & obstruction

iii) RAE tubes - difficulty with suction & malposition

5. Protocol for endotracheal intubation in ICU

a) Personnel:

i) Intubation is a 3-4 person procedure - skilled assistance is mandatory

ii) The “top end” intubator coordinates the procedure

iii) One person to administer drugs

iv) One person to apply cricoid pressure (CP) post-induction:

This is routine for all emergency intubations

CP is considered safe in the presence of suspected spinal injury.

CP must be correctly applied - distortion of the larynx and difficulty in

intubation may occur if poorly applied.

v) One person to provide in-line cervical spine immobilisation (trauma and

spinal patients only).

b) Secure adequate IV access

c) Equipment (kept in difficult airway & intubation trolleys in P4-A,B&C).

Ensure the following equipment is available and functional:

i) Adequate light

ii) Oropharyngeal airways

iii) Working suction with a rigid (Yankauer) sucker

iv) Self-inflating hand ventilating assembly and mask

v) 100% oxygen, i.e. working flowmeter at 15 l/min

vi) 2 working laryngoscopes (standard & long blades)

vii) Magill forceps

viii) Malleable introducer and gum-elastic bougie

46

ix) 2 Endotracheal tubes

Normal size + 1 size smaller

Check cuff competence

x) Access to difficult intubation equipment and be aware of the difficult

airway trolley location and its contents.

Be aware of the Failed Intubation Drill.

Airtrach, C-MAC, Heine Flex tip

Intubating Fastrach LMA

Cricothyroidotomy equipment

a. Percutaneous kit or

b. #15 scalpel & #6.0 cuffed ETT

d) Monitoring (on all patients) :

i) SpO2, ETCO2, ECG

ii) Invasive BP *desirable but not essential and must not delay intubation

if urgent

e) Drugs

i) Induction agent - propofol, fentanyl, ketamine, midazolam

ii) Suxamethonium - 1-2mg/kg is the muscle relaxant of choice.

Contraindicated in:

a. Burns > 3 days

b. Chronic spinal injuries (i.e. spastic plegia)

c. Chronic neuromuscular disease (e.g. GBS, motor neurone disease)

d. Hyperkalaemic states. (K+ > 5.5)

Consider Rocuronium (1-2 mg/kg) if Sux. contraindicated

iii) Atropine - 0.6-1.2mg available

iv) Adrenaline - 10ml 1:10000 solution available

f) Procedure: Rapid sequence induction and orotracheal intubation

i) Pre-oxygenate with 100% oxygen for 3-4 minutes.

ii) For patients on mask CPAP/NIV, pre-O2 with the NIV mask

iii) Preload with 250-500ml IV crystalloid

iv) Inotropes may be necessary after induction/intubation

v) Induction agent + suxamethonium

Induction doses in the critically ill must be modified from routine

doses used in general anaesthesia

vi) Cricoid pressure applied (ensure correct positioning)

vii) Direct visualisation of vocal cords and tracheal intubation

viii) Inflation of cuff until airway sealed

ix) Confirmation of ETCO2

x) Chest and gastric auscultation with manual ventilation

xi) Cricoid pressure released

xii) Secure tube at correct length

xiii) Connect patient to ventilator (see default ventilator parameters)

xiv) Ensure adequate sedation ± muscle relaxant

47

xv) Consider insertion of a naso/oro-gastric tube.

Required by the majority of ICU patients.

Insertion will avoid repeating the CXR.

xvi) Chest X-ray

xvii) Confirm blood gas analysis and adjust FIO2 accordingly.

g) Sedation post-intubation:

i) None if comatose or haemodynamically unstable

ii) Propofol ± fentanyl infusions as clinically indicated.

6. Maintenance of endotracheal tubes

a) Securing to face

i) Secure ETT with white tape after insertion.

ii) Ensure that the loop of tape is snug around back of neck but not too tight to

occlude venous drainage should allow 2 fingers under tape.

iii) Re-secure with adhesive tape once CXR check done.

b) Cuff checks

i) Volumetric tests are done following insertion and whenever a leak is

detected: sufficient air to obtain a seal + 1ml

ii) Seal is assessed by auscultation over trachea during normal ventilation.

iii) Manometric tests are inaccurate and do not correlate with mucosal

pressure. These are an adjunct only if cuff malfunction is suspected.

c) Persistent cuff leaks

i) Tubes requiring more than 8ml of air to obtain a seal or if there is a

persistent cuff leak must be examined by direct laryngoscopy as soon as

possible:

Even if taped at the correct distance at the teeth.

Ensure that the cuff has not herniated above the cords

Tube has not ballooned inside the oral cavity and “pulled’ the cuff

above the cords.

ii) Patients at high risk for cuff leaks:

Nasal RAE’s - prone to outward migration

Cut tubes - do not cut tubes < 26 cm

Facial swelling - burns, facial trauma

Patients requiring high airway pressures during ventilation

48

7. Endotracheal tube change protocol a) Ensure adequate skilled assistance, equipment, drugs and monitoring as for de

novo intubation.

b) Procedure

i) Set the FIO2 = 1.0 and change SV modes to SIMV.

ii) Ensure sufficient anaesthesia and muscle relaxation (fentanyl / propofol +

neuromuscular blockade)

iii) Perform laryngoscopy and carefully identify:

Patency of upper airway after suction

Anatomy of larynx

Degree of laryngeal exposure and swelling.

iv) IF clear view of larynx and no or minimal laryngeal swelling:

Application of cricoid pressure by assistant and careful, graded

extubation under direct laryngoscopic vision.

Maintain laryngoscopy and replace tube under direct vision.

v) IF impaired visualisation of larynx:

Re-evaluate the need to change ETT

Use gum elastic or ventilating bougie

Place bougie through tube under direct vision and insert to a length

that would be just distal to the end of the ETT (approximately 30cm

from end of tube)

Have an assistant control the bougie so that it does not move during

movement of the endotracheal tube

Application of cricoid pressure by assistant and careful, graded

extubation

Maintain laryngoscopy and ensure bougie is through the cords on

extubation

Replace tube over bougie and guide through larynx under available

vision.

Inflate cuff, check ETCO2, auscultation and expired tidal volume

Release cricoid pressure.

Secure tube with tape.

49

L. Weaning Guidelines

1. Commencement of weaning is a medical decision.

2. Weaning is contraindicated with any of the following:

a) Unstable ICP (abort weaning if ICP increases)

b) Need for heavy sedation (e.g. upper airway obstruction)

c) Haemodynamic instability

d) Significant bronchospasm

e) High work of breathing.

3. Trial pressure support daily if the patient meets both the following criteria:

a) PaO2/FiO2 ratio > 150

b) Patient can take spontaneous breaths if SIMV resp-rate reduced.

4. Weaning protocol:

a) See the flow diagram following page.

b) Set initial pressure support to maintain adequate VT

i) Start at 10 cmH2O and adjust to:

VT ≤ 6 ml/kg IBW for patients recovering from ARDS.

VT ≤ 8 ml/kg IBW for all others.

IBW Males = 0.91 × (height [cm] – 152.4) + 50

IBW Females = 0.91 × (height [cm] – 152.4) + 45.5

ii) Alternatively, use target VT = 80-100% of set SIMV VT

iii) Allowable PS range = 5-25 cmH2O

If VT cannot be achieved with 25cmH2O, cease trial

c) Assess at 15 and 30 minutes for “weaning success criteria”

d) Assess each hour for suitability to wean PS

e) Once PS has reached minimum (5cmH2O) then wean PEEP to 5cmH2O

f) If PS & PEEP = 5cmH2O then assess for extubation.

5. Weaning Success Criteria:

i) RR < 30/min

ii) SpO2 > 90%

May be set lower with COPD, e.g. >86-88%

iii) FIO2 ≤ 0.5

iv) No respiratory distress as shown by 2 or more of the following:

HR > 120% baseline

Accessory muscle use

Diaphoresis

Paradoxical abdominal movements

Marked dyspnoea

50

Flowchart: Ventilation Weaning Protocol

PaO2/FiO2 > 150

&

PEEP < 10 cmH2O

Pass Fail

NO Weaning Contraindication:

Unstable ICP

Need for heavy sedation

Haemodynamic instability

Significant bronchospasm.

AND

“Start Weaning” Settings: Reduce patient sedation

Reduce SIMV-Rate to 8bpm

Adjust initial PS to target VT

8ml/kg IBW, or

6ml/kg IBW if ARDS

Allowed PS range (5-25 cmH2O)

PEEP remains on previous setting.

Check each 15 minutes -

Weaning Success Criteria: RR < 30/min

SpO2 > 90% (*lower in COPD)

FIO2 ≤ 0.5

No respiratory distress as shown

by 2 or more of the following:

HR > 120% baseline

Accessory muscle use

Diaphoresis

Paradoxical muscle movements

Marked dyspnoea

Assess After Each Hour -

Set Pressure Support Level: If weaning successful after 1st

Hour

cease SIMV

If successful on subsequent hours

decrease PS, as per …

If no previous weaning failure

decrease PS by 4 cmH2O

If previous episode of failure

decrease PS 1-2 cmH2O

If at minimum PS = 5 cmH2O

decrease PEEP by 1-2 cmH2O

Weaning Failure:

IF post PS decrease

return to previous settings

*note change to PS decrease rate

IF post return to settings

set PS to max = 25 cmH2O

IF on maximum PS

return to SIMV settings

IF PSMax or SIMV, patient should

be reviewed by SR or Consultant

Weaning Complete:

If PS = 5 & PEEP = 5 cmH2O

Check ABG

Assess for Extubation – see over.

51

M. Extubation

1. The decision to extubate is made by medical staff, in consultation with either the

senior registrar, fellow or duty consultant.

2. Extubation is to be performed by medical or senior nursing staff, with airway

competent medical staff immediately available.

3. Criteria to predict successful extubation are helpful, however, ongoing success

should never be assumed:

a) FiO2 < 0.5 with PEEP ≤ 5 cmH2O

b) PaO2 > 70 mmHg ** lower values may be appropriate in

SpO2 > 90% chronically hypoxaemic patients

c) RR < 30 with PS ≤ 5cmH2O (Dräger)

d) pH > 7.2

e) No respiratory distress (see over)

f) Patient able to obey commands

g) Patient able to protect airway and cough

h) Patient able to cope with amount of secretions

i) Reason for intubation resolved.

*this may include checking for an air leak with the cuff deflated

4. Early extubation to NIV may be considered for some patients who present with

hypercapnic exacerbation of COPD or pulmonary oedema:

a) Performed with close supervision by senior medical staff.

b) If no improvement after 1-2 hrs, the patient should be considered for

reintubation.

5. Extubation protocol:

a) Ensure equipment, monitoring and adequate assistance is available, as for

intubation

b) Plastic surgical and ENT patients with intermaxillary fixation/wiring require

consultation with the Parent Clinic.

i) A wire cutter must be present in the room at all times.

ii) The parent clinic should be given opportunity to be present during extubation

if the jaws are wired.

c) All patients should receive supplemental oxygen pre/post-extubation.

52

N. Emergency Surgical Airway Access

1. Policy

a) Call for skilled assistance then proceed without delay.

b) Difficult airway & failed intubation trolleys are in areas A, B & C

c) Cricothyroidotomy, percutaneous or surgical, is the recommended procedure for

urgent surgical airway access and emergency oxygenation.

d) Standard percutaneous tracheostomy is not an emergency procedure.

e) Cricothyroidotomy is a temporary airway - arrange a definitive surgical airway

(ENT surgeons) as soon as possible.

2. Indications:

a) Refer to the failed intubation drill in the clinical protocols section.

b) Inability to establish an effective airway following failed laryngoscopy despite:

i) Basic manoeuvres - jaw thrust / chin lift / oral-nasal airways

ii) Attempted LMA insertion

c) Inability to ventilate.

3. Cricothyroidotomy

a) Percutaneous technique

i) Equipment

Cook Melker Emergency Cricothyrotomy Catheter kit (cuffed)

ii) Procedure

Palpate cricothyroid membrane with neck well extended

1cm horizontal incision through skin

Locate tracheal lumen with fluid-filled syringe & needle/cannula

Insert wire through cannula, then remove the cannula over the wire.

Insert dilator/introducer & tube assembly over wire in single motion

Remove wire & introducer leaving the cuffed tube.

Inflate cuff & suction prior to ventilation.

Confirm endotracheal placement with ETCO2 & CXR.

b) Surgical technique

i) Equipment

Size 15 scalpel + handle

Size 6.0 cuffed endotracheal tube

Straight forceps

Oxygen delivery circuit: Laerdal bag

ii) Procedure

Palpate cricothyroid membrane.

2cm horizontal incision through skin and cricothyroid membrane

Insert forceps into wound and open to enlarge the wound

Consider insertion of long blue ventilating bougie into trachea

Insert endotracheal tube, directly into the trachea or over bougie

Remove bougie and connect oxygen circuit

Confirm placement with ETCO2, auscultation and CXR

Perform catheter suction ASAP after adequate oxygenation

53

O. Fibreoptic Bronchoscopy

1. Policy:

a) This is only to be used by skilled personnel and authorised by the duty consultant.

b) Under no circumstances may the bronchoscope be loaned to other clinics.

c) Expertise with bronchoscopy takes time. Registrars are encouraged to approach

the Department of Thoracic Medicine to attend bronchoscopy clinics to become

familiar with the anatomy of the tracheobronchial tree and use of the flexible

fibrescope.

2. Indications:

a) Semi-elective difficult intubation: not used as an aid to failed intubation

b) Luminal obstruction

i) Sputum retention - persistent collapse refractory to physiotherapy

ii) Foreign bodies

iii) Luminal pathology - diagnostic

c) Diagnostic bronchoalveolar lavage (BAL)

3. Protocol for fibreoptic intubation

a) Indication as per endotracheal intubation

b) Procedure

i) All equipment, drugs and monitoring c.f. routine endotracheal intubation

ii) Supplemental oxygen must be given

Routinely via a mask – this may need to be cut to facilitate intubation

May also be given via the suction channel of the bronchoscope

iii) Can be via oral (with bite protection mandatory) or via nasal route

iv) Local anaesthesia / preparation of the airway:

Nasal mucosa - topical 10% lignocaine or 2% amethocaine spray.

Pharynx - viscous lignocaine gargle

Larynx - choice according to operator experience

a. Transtracheal injection and/or direct application through the scope

b. Nebulised - 5 mls 4% lignocaine

c. Superior laryngeal nerve blockade (2-3ml 1-2% lignocaine).

v) Check ET tube cuff

vi) Place a warmed appropriately sized ETT (7mm tube for either sex) into

posterior nasal space.

vii) Insert the scope through the tube under direct vision.

viii) Identify the vocal cords and advance the scope into the trachea.

ix) Advance the ETT over scope into trachea, maintaining view of the tracheal

rings or carina, then remove the scope.

x) Confirm ETT placement by ETCO2, auscultation and CXR.

xi) Administer additional sedation/analgesia to the patient as required.

xii) NB: Suction at least 500ml water through scope immediately following use

and notify the equipment nurse for cleaning ASAP.

54

4. Protocol for BAL a) Diagnosis of nosocomial pneumonia (colonization vs. infection)

b) Other indications – alveolar proteinosis, eosinophilic lung disease, etc.

c) Sufficient reserve to tolerate procedure:

i) Ideally PaO2 > 70 and FiO2 < 0.7

ii) BAL will commonly result in a 10% reduction in PaO2 for up to 24 hours

after procedure

d) Procedure

i) Ensure sufficient sedation & place patient on 100% oxygen

ii) Select lobe to be lavaged from recent CXR

iii) Local anaesthetic gel is contra-indicated (interferes with culture media)

iv) If possible, do not suction through scope prior to lavage (upper airway

bacterial contamination)

v) Pass the scope directly into the selected lobe

vi) Wedge the scope as far as possible – ideally to 3rd generation bronchi

vii) Lavage with 4-6 x 20-40 ml aliquots of sterile normal saline

viii) Aspirate between aliquots and label aliquots accordingly

ix) Send aspirates for quantitative culture and atypical pneumonia screen.

NB: label specimens “Immunocompromised protocol” as indicated.

P. Tracheostomy

1. Policy:

a) Percutaneous tracheostomy (PCT) is the preferred procedure in suitable patients.

b) To be performed only by consultant staff or advanced ICU trainees.

c) Patients must have the option of surgical tracheostomy cleared by the parent

clinic (either medical or surgical). This is a courtesy.

d) The decision to perform a PCT is at the discretion of the ICU consultant.

e) PCT is an elective procedure and has no place in urgent airway access.

2. Indications :

a) The indications for PCT are the same as surgical tracheostomy:

b) Airway maintenance

i) Prolonged intubation, e.g. > 10 days

ii) Laryngeal pathology – this may also be a contraindication to PCT

c) Airway protection

i) Delayed return of glottic reflexes

ii) Tracheal toilet

3. Relative Contraindications to PCT a) Lack of consent - absolute

b) Coagulopathy

i) Platelets: < 100,000

ii) APTT: > 40

iii) INR: > 1.5

55

c) Difficult anatomy - e.g. previous neck surgery, short fat neck

d) Unstable cervical spine injury

e) Grade III or IV intubation (relative – consider use of Glidescope / C-MAC)

f) FIO2 0.6 / PEEP 10cmH2O

4. Procedure:

a) Ensure consent has been obtained and documented.

b) Equipment, monitoring and drugs as per endotracheal intubation

c) Coagulation screen prior to procedure.

d) Bedside procedure light essential.

e) General anaesthesia - the airway operator must be appropriately experienced.

f) Ventilate the patient on 100% oxygen.

g) Tracheostomy equipment:

i) Standard technique: modified Cook Ciaglia kit using the “Blue Rhino”

ii) Tracheostomy tubes

EVAC® aspirating tubes are standard for all tracheostomies.

a. Includes patients having surgical tracheostomies

b. Ensure that an EVAC tube goes with the patient to theatre.

Patients who have non-aspirating tracheostomy tubes in place (e.g.

from CTSU or other hospitals) must have these tubes changed to an

EVAC tube as soon as safe and feasible. This is usually 4-5 days post-

tracheostomy.

Other tubes:

a. Foam cuffed tubes - patients with tracheomalacia or persistent air

leaks

b. Uncuffed tube (usually #6.0) used in weaning

c. Fenestrated tube: these are either cuffed or un-cuffed with a

fenestration to allow patients to talk.

d. XLT – extended length tubes: useful for patients with marked

neck or soft tissue swelling.

h) Insertion technique:

i) Aseptic technique.

ii) Goggles are essential for both the operator and anaesthetist

iii) Local anaesthetic infiltration (2% lignocaine + 1:200000 adrenaline) over

the pretracheal rings.

iv) Check the tube cuff, lubricate and insert the dilator into the tube.

v) 1.5-2cm horizontal incision over 1st or 2nd tracheal ring

vi) Pretracheal tissue blunt dissection down to fascia

*look for anterior jugular vein and ligate if identified.

vii) Insert a 14G IV cannula mounted on a syringe with saline into trachea and

aspirate through saline/water to confirm intratracheal placement.

viii) Removal the stylet and reconfirm intratracheal placement by aspirating air

via the IV cannula

ix) Insert the guide-wire through the IV cannula and remove the cannula.

56

x) Insert the small pre-dilator over the wire into the trachea and make a hole

large enough to accommodate the main dilating instrument.

xi) Blue Rhino® graduated 1-step dilator:

Lubricate with water, not gel

Place the dilator and guide cannula (white) over the wire, noting:

a. The black marker on the guide at the proximal end of the Rhino

b. The silver marker on the wire at the proximal end of the guide

Slowly insert to the required ETT size, ensuring that both markers

(wire and guide) remain in alignment at the proximal end.

xii) Remove the dilator leaving the white guide cannula on the wire and insert

the tracheostomy tube & dilator over the wire/guide into the trachea

xiii) Remove the dilator and wire, inflate the cuff and suction the trachea

xiv) Ventilate and confirm ETCO2 - self-inflating bag or ventilator

xv) Secure tracheostomy tube with tapes.

xvi) Obtain a CXR post procedure.

xvii) Document the procedure in the case notes and complete a separate

operation note.

5. Complications (of tracheostomy)

a) Loss of the airway *immediately re-intubate the patient orally

b) Bleeding

c) False passage

d) Pneumothorax

e) Cricoid cartilage fracture

f) Laryngeal dysfunction

g) Tracheal stenosis

h) Infection

6. Prolonged care of tracheostomy a) Cuff checks

i) Volumetric (sufficient air to obtain a seal) tests are done following

insertion and whenever a leak is detected with a manual hyperinflation

once per nursing shift.

ii) Manometric tests are inaccurate and do not correlate with mucosal

pressure. These are an adjunct only if cuff malfunction is suspected.

b) Tube changes - routine change at 28 days.

c) Aspirate EVAC tube 2 hourly or more frequently if > 10ml supraglottic

secretion per hour.

57

Q. Cardiac Pacing

1. Policy:

a) If inserted by ICU staff, the procedure is only to be performed by consultant

staff or advanced vocational trainees under supervision.

b) Become familiar with the theory of insertion, indications, interpretation and

complications of TVP.

2. Indications:

a) Medical pacing with adrenaline or transthoracic pacing may be adequate to treat

some symptomatic bradycardias and has obviated the need for prophylactic

pacing in high-risk patients. NB: particularly for retrievals.

b) Any sustained symptomatic bradycardia which does not respond to medical

treatment, or predisposes to a malignant ventricular arrhythmia.

Note: pacing is indicated by the haemodynamic consequences of the rhythm,

not the arrhythmia per se.

c) Ventricular tachycardias (especially polyphasic) may respond to overdrive

suppression pacing.

d) Following cardiac surgery in high-risk patients (epicardial leads):

i) Valve replacement / repair (especially mitral).

ii) VSD repair / papillary muscle rupture.

iii) Acute myocardial infarction.

3. Types: a) Semi-rigid, bipolar pacing lead (VVI) inserted under image intensification

(standard TVP at RAH)

b) Epicardial leads

i) Placed during cardiac surgery in high risk patients

ii) Usually unipolar ventricular, but may be bipolar, atrial or ventricular:

check the operative note and liaise with the surgeon.

c) Balloon flotation leads - ECG or pressure guided catheters

d) Paceport PA catheters

4. Paceport PA protocol

a) VVI mode only

b) Ensure a ventricular demand pacemaker box is available

c) Insert the Paceport PA catheter using standard technique (see PAC section)

d) A pressure transducer should be attached to the RV as well as the distal port

e) The RV port should be 1-2cm distal to the tricuspid valve

i) In some patients the catheter may wedge before the RV port is in the RV in

these cases an alternate technique should be used

f) Attach the adapter to the RV port

g) Insert probe to the reference mark

h) Connect distal electrode to V lead of ECG and advance until ST elevation

indicates contact with the endocardium (usually 4-5cm)

i) Secure the probe and connect side port to a saline flush

58

j) Commence pacing

k) Check adequate capture and sensing (see next section)

59

5. Semi-rigid Wire protocol: (VVI lead)

a) Strict aseptic technique

b) Image intensification

c) Local anaesthesia where appropriate

d) Insertion protocol:

i) 6F peel away sheath or PAC introducer

ii) Right IJ vein is the preferred route, then left subclavian.

NB: if permanent pacing is likely then avoid subclavian placement.

iii) Under I-I control, feed the wire until the tip just stops on the RV wall

iv) Connect to the control box (switched off)

v) Set output and sense to their minimum value, and rate 20bpm faster than

the patient's own rate (or 70bpm, whichever is greater).

vi) Turn the generator on and gradually increase the output while watching the

ECG for capture.

vii) If there is no capture or a high output is required:

Place on demand mode

Turn output right down, advance or reposition the wire slightly

Try to capture again. An ideal capture setting is ~ 2 mA

Ensure wires are not exposed and tape both sides

viii) Suture the wire and apply an occlusive dressing

ix) Arrange a post-insertion CXR.

x) Always be aware of the risk of tamponade even when pacing has been

unsuccessful.

e) Daily check:

i) Battery strength

ii) Capture: set the output 2x higher than threshold for safety.

6. Flotation Catheter Insertion

a) These may be inserted either “blind”, under ECG guidance (standard

recommendation), or via pressure guidance for catheters having an infusion

lumen (c.f. PA catheter insertion).

b) Aseptic technique & local anaesthesia where appropriate

c) Insertion protocol:

i) 6F peel away sheath, do not use a PAC introducer as these will leak

ii) Attach V5 lead of an ECG to the distal electrode of catheter & monitor

iii) Note P then QRS wave-form changes as the catheter advances to the RV

iv) Advance catheter another 2cm, deflate the balloon & advance 1cm

v) Connect to the pulse generator (switched off)

vi) Set output and sense to their minimum value, and rate 20 bpm faster than

the patient's own rate.

vii) Turn the generator on and gradually increase output while watching the

ECG for capture.

viii) If there is no capture or a high output is required - see (5.d.vii) above

ix) Suture the wire and apply an occlusive dressing

x) Arrange a post-insertion CXR.

60

R. Pericardiocentesis

1. Policy

a) This procedure must be authorised by an ICU consultant and performed by

consultant staff, trainees under supervision, or cardiology.

b) Confirmation of pericardial effusion or tamponade with echocardiography is

required prior to the procedure, except in peri-arrest situations.

c) Liaison with cardiology is essential.

2. Indications

a) Symptomatic pericardial effusion (tamponade).

b) Although advocated in EMST (ATLS), this procedure has limited utility in

traumatic pericardial tamponade.

3. Procedure

a) Strict aseptic technique.

b) Local anaesthetic infiltration in an awake patient.

c) This procedure should be performed under ultrasound guidance.

d) Technique: Seldinger technique and insertion of a pigtail catheter

i) Insert needle on syringe at 45° from the horizontal axis and aim for tip of

left shoulder

ii) Advance slowly and aspirate until confirmation by aspirating blood or serous

fluid

iii) Insert catheter using Seldinger technique over guidewire.

iv) Confirm placement by aspiration and/or echocardiography

v) Check CXR (pneumothorax)

vi) Suture and occlusive dressing if leaving for > 24 hours.

4. Complications

a) Cardiac tamponade!

b) Arrhythmias

c) Myocardial laceration

d) Pneumothorax, pneumopericardium

e) Liver laceration

61

S. Intra-Aortic Balloon Counterpulsation

1. Policy:

a) The ICU consultant should be involved in the decision to insert an IABP

b) Only to be performed by a consultant or advanced vocational trainee under

supervision.

c) Become familiar with the theory of insertion, indications, interpretation and

complications of IABP.

2. Indications :

a) As a mechanical bridge prior to, and/or following myocardial revascularization

or transplantation:

b) Ischaemic heart disease

i) Low cardiac output states following cardiac surgery

ii) Cardiogenic shock: in association with angiography and revascularization

(PTCA, stent or CAVG)

iii) Acute mitral incompetence (papillary muscle rupture) or VSD following

AMI pending operative repair.

c) Myocardial disease

i) Severe myocardial contusion

ii) Severe myocarditis

iii) Cardiomyopathy

iv) Severe -blocker overdose.

3. Contra-indications: a) Aortic regurgitation

b) Aortic dissection

c) Severe peripheral vascular disease

d) Tachyarrhythmias (relative)

e) Coagulopathy (relative)

4. Procedure protocol

a) Strict aseptic technique

b) Check IABP function prior to insertion:

i) Adequate helium cylinder volume

ii) Arterial pressure manifold: referenced & zeroed to mid-axillary line

iii) Dedicated 5 lead ECG connected to IABP

iv) Turn on and leave in standby mode

v) Initial settings:

ECG sense: 1:3 ratio

Augmentation: minimum (pre-insertion only)

Inflate and deflate times: zero

62

c) Insertion procedure:

i) Local anaesthesia in awake patients

ii) Scrubbed assistant recommended

iii) Select size (by patient’s height)

< 152cm 25ml balloon

152 – 162cm 34ml balloon

162 – 183cm 40ml balloon

>183cm 50ml balloon

iv) Femoral artery insertion of a 12F introducer, Seldinger technique.

v) Check the length for balloon catheter insertion, using the angle of Louis

(level of T4) as the surface landmark, prior to insertion.

vi) Insert the balloon to the level of T4.

The double black marker on the balloon catheter must be visible

This indicates that the balloon has fully exited the sheath.

vii) Connect to pressure transducer and pump.

viii) Press the [IAB Fill] button to fill the balloon & wait for completion.

ix) Press the [Assist/Standby] button to start the pump.

x) Start on minimal augmentation and increase to maximum.

NB: subsequent augmentation should not be set below 50%

xi) Suture in place and cover with an occlusive dressing.

xii) Set timing:

Check balloon inflation against pressure wave:

set to peak of dicrotic notch.

Check balloon deflation against ECG:

prior to QRS complex and

observe decrease in end diastolic pressure.

Check diastolic augmentation on pressure wave.

Select augmentation ratio: *standard = 1:1

d) Maintenance

i) Check CXR post insertion:

tip of IABP below T4 (carina) & origin of the left subclavian artery

ii) Neurovascular obs of insertion site, lower limbs and left arm hourly.

iii) Nurse at < 30° elevation.

iv) Document pump timing (ratio) and adequacy of augmentation.

v) Assess haemodynamic response: CI, MAP, SVR, filling pressures, CXR.

vi) Ensure clear balloon tubing is exposed:

Monitor condensation (due to rapid helium shuttling), or

Blood in tubing (balloon rupture).

e) Timing during arrhythmias

i) Ectopics: keep on ECG trigger, system will automatically deflate on

ectopic

ii) Tachycardia > 160/min :

Reduce augmentation (equal to patient systole)

Decrease ratio to 1:2 if reducing augmentation is not adequate

63

iii) Atrial fibrillation: move deflate slide to extreme right to deflate on R wave

(not required on newer pumps)

iv) VT or VF: defibrillate or cardiovert as required, the IABP is isolated

v) Cardiac arrest (no output) start ECM

Effective output: set on pressure trigger to synchronise balloon

inflation with ECM

No output: set internal mode for a fixed rate of 40 bpm + 20ml

augmentation

f) Weaning:

i) Commence when patient’s haemodynamics have improved.

ii) Methods:

Reducing ratio from 1:1 to 1:2 to 1:3 and / or

Reduce augmentation. NB: minimum balloon inflation 50%

g) Removal of catheter

i) Notify cardiac / vascular surgeons

ii) Cease heparin infusion 3 hours prior to removal

iii) Disconnect IABP tubing: do not aspirate the balloon

iv) Withdraw balloon up to (but not into) the introducer sheath. Even empty

the used balloon will not fit into the sheath, and may rupture if attempted.

v) Remove the sheath and balloon as single unit, applying pressure

immediately.

vi) Use Femostop® local pressure during catheter removal:

Remove IABP catheter with Femostop at 60-80mmHg

Inflate dome to 20mmHg above systolic as catheter is fully withdrawn

Reduce pressure by 15mmHg at 10-15 min intervals

If bleeding occurs, reinflate the Femostop to the previously effective

pressure and recommence cyclic pressure reduction

Remove Femostop and apply a firm dressing

vii) 10-20% may require surgical repair to the artery.

5. Complications:

a) Limb ischaemia – thrombotic or embolic

b) Bleeding at the insertion site or systemically

c) Infection

d) Aortic dissection

e) Occlusion of origins of aortic arch vessels if too high

f) Occlusion of renal/splanchnic vessels if too low

g) Thrombocytopaenia

h) Balloon rupture: gas embolism

i) Femoral artery aneurysm

64

T. Gastric / Oesophageal Tamponade Tubes

1. Policy:

a) Ensure the Gastroenterology Unit are informed.

b) The ICU consultant must be involved in the decision to insert an oesophageal

tamponade tube.

c) All patients should be intubated prior to insertion and managed in ICU.

i) High risk torrential regurgitation of blood into the airway

ii) Should only be undertaken by an experienced operator.

d) Major complications following insertion of tamponade tubes have been reported

to occur in 15%, particularly if inserted by inexperienced clinicians.

2. Indications:

a) Upper gastro-intenstinal variceal haemorrhage.

i) Temporising measure while awaiting endoscopy, TIPSS and / or surgery.

ii) The tamponade tubes are used in conjunction with an octreotide infusion.

3. Types of tubes:

a) Minnesota: oesophageal and gastric balloons and 2x aspirating ports

b) Sengstaken: oesophageal and gastric balloons and gastric aspirating port

c) Linton: gastric balloon and aspirating port

4. Procedure:

a) Preferably use a bulk & frame bed to allow application of traction.

b) Prior to insertion:

i) Check both balloons for leaks.

ii) Inflate the gastric balloon with 300ml of air and record pressure reading

with a manometer.

iii) Deflate all balloons completely and lubricate the tube.

c) Estimate insertion length = bridge of nose to earlobe + nose to xiphoid process.

d) Insert via nose or mouth, under direct vision using a laryngoscope.

e) Must ensure gastric balloon is not in the oesophagus.

i) Perform urgent x-ray to tube is adequately in the stomach.

ii) NB: inflating the gastric balloon in the oesophagus is virtually 100% fatal!

f) Inflate the gastric balloon in 50ml increments up to 300ml while monitoring the

balloon pressure.

i) If the balloon pressure ≥ 5mmHg above the pre-insertion pressure then

incorrect (oesophageal) placement is probable

ii) This mandates deflation of the balloon and reinsertion of the tube.

g) Pull back until resistance is felt as the balloon rests against the gastric fundus.

h) Note the measurement at the lips and apply gentle traction with 500ml bag of

fluid on a rope and pulley system.

65

i) Inflation of the oesophageal balloon is usually not required.

i) If bleeding continues despite adequate placement of the gastric balloon and

optimizing medical therapy, consider inflating oesophageal balloon.

ii) It should only be inflated after discussion with the ICU consultant.

iii) Inflate oesophageal balloon to 40 mmHg and reduce pressure by 5mmHg

once bleeding is controlled.

j) Recheck position on x-ray once balloons inflated and traction applied.

k) After 12-24 hours, the balloons should be deflated to check for ongoing

bleeding.

U. Extracorporeal Membrane Oxygenation

1. Extra Corporeal Membrane Oxygenation (ECMO) is a method of oxygenating

blood in cases of overwhelming respiratory failure (veno-venous ECMO) or

temporary circulatory support in reversible cases of refractory cardio-respiratory

failure (veno-arterial ECMO).

2. ECMO policies and protocols are a separate document to this ICU manual and can

be accessed on the RAH ICU website (www.icuadelaide.com.au).

3. Any requests for ECMO support must be immediately directed to the ICU

consultant.

4. ECMO circuit and equipment must not be altered without ICU consultant and/or

perfusionist supervision.

66

PART 3 - DRUGS AND INFUSIONS

A. Policy

1. Patients admitted to the ICU must have a complete drug history documented:

a) Premorbid and current medications

*see pharmacy’s drug listing within the patient’s medical records.

b) Previous adverse drug reactions and allergies

*if known the basis for that allergy.

c) Note potential drug interactions.

2. Charting of drugs and infusions is to be done by ICU medical staff.

a) Parent clinics must not write on the ICU flowchart.

b) Therapeutic changes suggested by the home team must be communicated to the

appropriate ICU medical staff for consideration prior to charting.

3. All changes to drug and fluid orders must be written and signed for on the flowchart.

a) Nursing staff must be notified of such changes.

b) Verbal orders alone are neither sufficient nor legal.

4. All drugs, infusions and fluids are reviewed and transcribed at least daily.

5. Printed labels for commonly used infusions and drugs should be used where possible.

6. Standardisation of infusion concentrations is essential for the prevention of drug

errors. Infusion concentrations should not be changed (e.g. ‘double strength’) from

the protocols outlined below.

7. Vasoactive or hypertonic infusions (e.g. TPN) must be administered through a

dedicated lumen of a CVC or PICC.

8. Vasoactive infusions must not be used in the general wards, other than for patients en

route to ICU and who are being continuously monitored.

9. All antibiotics written on the ICU flowchart must also have an indication of either:

a) Date started and due date for review/completion, or

b) Duration and position in course, e.g. “Day 4/7”.

10. Patients cleared for discharge from ICU must have all appropriate drugs, infusions and

fluids prescribed on the standard hospital forms, prior to discharge. Where

appropriate, old drug charts should be re-written.

11. Patients discharged on TPN must have their details entered in the TPN folder (stored

in the Unit A office area).

12. Any changes to acute pain drug regimens in patients under the care of the Acute Pain

Service should be done in consultation with the Acute Pain Service.

13. Any proposed changes to specialty type drugs, e.g. immunosuppressives,

anticoagulants, antiplatelet agents, etc should be discussed with home teams.

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B. Principles of Drug Prescription in Intensive Care

1. Drugs should be prescribed according to Unit protocols and guidelines.

2. Critically ill patients have altered pharmacokinetics and pharmacodynamics, with the

potential for toxicity and drug interactions.

3. Where possible:

a) Use drugs that can be titrated or prescribed to an easily measured endpoint.

b) Use drugs that can be measured to monitor therapeutic drug levels.

c) Avoid drugs with narrow therapeutic indices (e.g. digoxin, theophylline),

particularly in patients with associated hepatic or renal dysfunction.

d) Cease a drug if there is no apparent benefit.

e) If two drugs are of equal efficacy, choose the cheaper drug as the cost of drugs in

ICU is significant.

4. Prescribe using generic drug names only.

5. When there is a medication change (e.g. replacing an antibiotic for another, alteration

in drug dose, ceasing a drug) then some indication as to the reason behind doing so

should be made within the patient’s medical records or drug chart.

6. A Clinical Pharmacist conducts a daily review (Mon-Fri) of ICU drug charting,

attends grand ward-rounds and is available for consultation. This is an invaluable

service and should be utilized accordingly.

C. Cardiovascular Drugs

1. Inotropes

Inotropes (specifically catecholamines) are frequently used in ICU. There are varied

prescription practices and preferences for these drugs, mostly based upon the reported

pharmacological effects of the different agents.

a) General principles:

i) Defence of BP in the critically ill forms the basis of haemodynamic

resuscitation and organ perfusion.

Must be interpreted in the context of the patient’s pre-morbid BP

Particularly in renovascular hypertension or cerebrovascular disease.

ii) Hypovolaemia is the most common cause of hypotension and low cardiac

output in ICU and must be assiduously monitored and corrected.

iii) The main indications for the use of inotropes are to increase myocardial

contractility, heart rate and/or vascular tone.

iv) The use of inotropes requires regular haemodynamic monitoring:

Arterial line and CVC are mandatory

Where indicated - PAC, PiCCO, Vigileo CO or ultrasound.

v) No single inotrope (or mixture) has been shown to be superior to another.

vi) There is marked inter-individual variation in the response to inotropes:

Pre-existing chronic illness, genetic variation

Co-administration of other drugs

Qualitative and quantitative changes in adrenergic receptor kinetics.

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vii) Prolonged exposure to catecholamine infusions can produce adrenergic

receptor down-regulation and tachyphylaxis.

b) Catecholamines

i) Receptor effects may be unpredictable, however, in general:

-adrenergic effects predominate at low doses, and

-adrenergic effects at higher doses.

ii) It is impossible to predict the dose range for an individual patient.

iii) Prescription on a body weight basis (µg/kg/min) is of little clinical utility.

iv) Infusions should be started at a low rate (3-5 µg/min) and titrated to a set

clinical response, e.g. MAP (not systolic)

v) There is no well established maximal dose.

vi) Regular assessment should be made of both global (pH, lactate) and

regional effects (urine output/creatinine clearance, limb perfusion).

c) Phosphodiesterase inhibitors (milrinone)

i) Inhibition of PDE3 increases intracellular cAMP and calcium, causing:

an increase in myocardial contractility

systemic and pulmonary vasodilatation, and

improved diastolic relaxation (lusitropy)

ii) Any resultant hypotension (due to systemic vasodilatation) usually

responds with the addition of a vasopressor (e.g. noradrenaline).

iii) Phosphodiesterase inhibitors have longer half-lives than catecholamines,

are less titratable and their half-life is prolonged with renal failure.

Table: Cardiovascular Effects of Catecholamines

Agent

1 effects 2 effects 1 effects 2 effects

Chronotropy

Dromotropy

Inotropy

Inotropy Vasodilatation Bronchodilatation

glucose/lactate

Inotropy Vasoconstriction

Inotropy Vasoconstriction

Adrenaline Noradrenaline Dopamine

effects predominate at low dose

effects predominate at high dose

Dobutamine + + (+) -

Isoprenaline + (+) - -

+ = strong effect (+) mild effect - = no effect

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Table: Inotropic Agents Used in ICU

Agent Standard Infusion Uses

Noradrenaline 6 mg / 100 ml 5% dextrose (ml/hr = µg/min)

First line drug in septic shock Maintenance of blood pressure

Adrenaline 6 mg / 100 ml 5% dextrose (ml/hr = µg/min)

Cardiopulmonary resuscitation Acute severe asthma Anaphylaxis Cardiogenic shock Maintenance of blood pressure Medical pacing

Dobutamine 500 mg / 100 ml 5% dextrose (ml/hr approx µg/kg/min)

Primarily a vasodilator, weak inotropic action Traditionally used in cardiogenic shock or low

output, high afterload states or when filling pressures high

Often used in combination with noradrenaline

Dopamine 400 mg / 100ml 5% dextrose (ml/hr approx µg/kg/min)

Maintenance of blood pressure No advantage over adrenaline/noradrenaline “Renal dose” dopamine is not used Endocrine side effects

Isoprenaline 6 mg / 100 ml 5% dextrose (ml/hr = µg/min)

Vasodilator, chronotrope (rarely used) Symptomatic bradycardia

Levosimendan 12.5 mg / 250 mL 5% dextrose Loading dose: 6-12µg/kg/10min Infusion: 0.05-0.2 µg/kg/min NB: Loading dose may cause

marked hypotension, may be omitted or reduced.

Calcium sensitizer Increases myocardial contractility in an oxygen

efficient manner and dilates coronary and systemic vessels

Role in Intensive Care not established

Milrinone 10mg / 100 ml 5% dextrose Loading dose: 50µg/kg/20 min Infusion: 0.5 µg/kg/min*

Cardiogenic shock due to diastolic failure Pulmonary hypertension following valve

replacement Catecholamine induced down regulation

*Standard milrinone prescription for 70 kg patient: Loading dose: 3500 µg = 35 ml over 20 minutes Maintenance: 2100 µg/hr = 20 ml/hr.

2. Vasopressor agents

a) General principles

i) Vasopressors usually act directly on the peripheral vasculature and are

primarily used to acutely elevate BP

ii) The most common cause of hypotension in ICU patients is hypovolaemia.

iii) Pressor agents should not be used as an alternative to fluid resuscitation.

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b) Indications (in ICU)

i) Tissue infiltration with local anaesthesia

ii) Topically prior to nasal intubation

iii) Hypotension following sympathetic block (e.g. epidural anaesthesia)

iv) Hypotension refractory to large doses of catecholamines (vasoplegia):

Consider relative hypoadrenalism

Consider use of vasopressin

c) Complications

i) Rebound hypertension

ii) Vagal reflex bradycardia

iii) Tachyphylaxis

Table: Vasopressors

Agent Standard Infusion / Dose Uses

Metaraminol 10mg / 10ml 5% dex: titrate Potent short acting vasoconstrictor

Ephedrine 30mg / 10ml 5% dex: titrate Synthetic indirect sympathomimetic. Commonly used in anaesthesia, little

benefit over adrenaline.

Vasopressin 20units/20ml 5%dex: 1.8mls/hrs (0.03u/min)

Noradrenaline resistant hypotension. May be useful in septic shock and post

cardiac bypass for catecholamine resistant hypotension

3. Antihypertensive agents


i) The most common cause of hypertension in ICU patients is sympathetic

drive due to pain, agitation, drug withdrawal or delirium. These should be

treated with adequate sedation, anxiolytics and/or analgesia.

ii) Patients in the recovery phase of acute renal failure are often hypertensive.

This usually represents the resetting of endogenous neurohumoral

mechanisms and as such does not routinely require treatment.

iii) Hypertension following an intracranial event (haemorrhagic or ischaemic)

is common and the underlying mechanism dictates therapy. A high BP

may be tolerated in ischaemic stroke, c.f. the setting of SAH with an

unclipped aneurysm, where treatment would be paramount.

iv) Target therapy should be titrated against the patient’s premorbid BP.

v) In the absence of adverse effects, the maximal therapeutic dose of a

selected agent should be used prior to commencing a second or third agent.

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b) Indications

i) Acute

Perioperative control of BP in “at risk” patients.

Hypertensive crisis (malignant hypertension)

Pre-eclampsia / eclampsia

Phaeochromocytoma

Untreated aneurysm or vascular injury,

e.g. intracranial aneurysm, ruptured/dissected aorta

ii) Other indications for vasodilators

Reduction of afterload in CCF or valvular disease

Adjunct to passive warming in hypothermia

iii) Chronic

Sustained essential hypertension

Ischaemic heart disease

Cerebrovascular disease

c) Complications – are many, but in relation to ICU patients:

i) Hypotension

First-dose effect / especially in hypovolaemia

ii) Reflex tachycardia

iii) Tachyphylaxis

iv) Pulmonary vasodilatation shunt and hypoxaemia

v) Cyanide toxicity (SNP)

vi) Angioedema – especially ACEI

vii) Deterioration in renal function

viii) Electrolyte disturbances

Table: Antihypertensive & Vasodilator Agents

Agent Infusion & Dose Uses

Glyceryl trinitrate (GTN)

30mg / 100ml 5%D (non PVC bottle and giving set) Range 2-25 ml/hr First line drug in RAH ICU Can be given topically.

Mainly venodilation: Useful in cardiac ischaemia Less predictable control of BP than SNP Tachyphylaxis develops within 24-48hr

will need additional agents for persistent BP

Sodium nitroprusside (SNP)

50mg / 250 ml 5%D Range 3-40 ml/hr

Rapid control of hypertensive crises. Tachyphylaxis and metabolic acidosis may imply

cyanide toxicity (total dose > 1.5mg/kg/24 hrs)

Phentolamine 10mg / 10ml 5%D: titrate Pure -blockade, short acting antihypertensive

Hydralazine 5-10 mg as bolus 20-40 mg 6-8 hourly

Short to medium term IV agent.

Often use with -blockers to control reflex tachycardia Useful in renovascular hypertension

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Amlodipine 5-10mg oral bd Long acting oral Ca++ antagonist. Caution in renal impairment

Captopril Start low dose ~ 5-6.25mg

up to 50mg orally 8 hrly Syrup: 5mg/ml or tablets Acute hypertension: 5-25mg sublingually prn

Treatment of hypertension Left ventricular dysfunction, esp post-MI Left ventricular failure Diabetic nephropathy Caution in renovascular disease and renal failure

Perindopril Start 2.5mg daily

up to 10mg daily orally

Phenoxybenzamine Oral : 10mg/day and increase until postural hypotension IV : 1mg/kg/day dilute to 200-500ml 1/3 dose over 1/24 2/3 dose over 1/24

Long acting, non-competitive -blocker Preoperative preparation of phaeochromcytoma Idiosyncratic hypotension may occur

Prazosin Start with 0.5mg, and increase up to 5mg tds orally

-blocker Potent antihypertensive agent Prominent first dose effect

Metoprolol Oral: 25-100mg bd IV: 1-2mg bolus every 2-3 minutes up to 10 mg.

High sympathetic drive states: neurogenic BP All grades of hypertension, inc renovascular Cardiac ischaemia Control of reflex tachycardia with vasodilators Thyroid crisis Caution in poor LV function, asthma Mainly eliminated by hepatic metabolism

Esmolol Loading dose 0.5 mg/kg Infuse 100mg/10ml and titrate

Ultra-short acting -blocker Useful as trial for patients with poor LV function. Adjunct to vasodilators post cardiac surgery

Clonidine 25µg boluses of up to 150µg/24hrs Oral: 75µg bd

up to 150-300µg tds.

Acute, centrally mediated hypertension Useful post cardiac surgery Withdrawal states Care with hepatic or renal dysfunction Rebound hypertension with chronic use Sedation, especially 1st dose

Dexmedetomidine 400 µg in 40mls load 1µg/kg over 20min infuse 1-5ml/hr

Selective alpha-2-agonist Acute, centrally mediated hypertension Not a first line drug. Selected use by senior medical staff only Sedation

MgS04 5-10 mmol loading Infuse at 4-12 mmol/hr Target plasma [Mg] ~ 1.5-2 mmol/L

Pre-eclampsia / eclampsia Phaeochromocytoma Sympathetic overdrive in tetanus

Propanalol Portal hypertension

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4. Antiarrhythmics


i) Prior to administration of antiarrhythmic agents, optimise correction of the

following:

Hypovolaemia

Metabolic abnormalities

a. K+, Mg++, Ca++, HPO4=

b. Hypoxaemia, hypo/hyper-carbia, alkalosis/acidosis

Myocardial ischaemia or cardiac failure (especially post-cardiac

surgery)

Pain and agitation.

ii) All antiarrhythmic drugs are potentially arrhythmogenic.

iii) Virtually all depress myocardial contractility.

iv) Antiarrhythmics drugs are indicated with:

Actual or potential haemodynamic compromise, or

Susceptible patients with myocardial ischaemia.

v) Consider anticoagulation if AF > 48 hours

vi) More than one antiarrythmic may be required

b) Indications

i) Termination of an acute arrhythmia

ii) Prophylaxis against recurrence

iii) Rate control

iv) Enhance efficacy of cardioversion

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Table: Antiarrhythmic Agents

Agent Infusion & Dose Uses

Amiodarone Acute use: 900mg / 250ml 5%D: Load 100ml / 1 hr (5mg/kg) Infuse 10 ml/h for 24-48 hrs (15mg/kg/day) Bolus Dose 150-300mg Chronic: 200-400 mg IV/oral daily

Rapid AF / flutter or MAT Monomorphic ventricular tachycardia Generally does not suppress contractility Can cause acute hypotension if given too rapidly Less proarrhythmic than most other drugs

Causes QTc, but rarely Torsade de pointes Renal excretion is minimal – no need to change dose

in renal failure Long term side-effects rare in short-term use. Interference with digoxin kinetics and assay. Interference with thyroid function tests.

Magnesium 5-10 mmol IV slow bolus Infuse at 2-5 mmol/hr. 2.4g MgSO4 = 10 mmol Mg++

Acts principally as a calcium blocker Useful in SVT and Torsade de pointes

Verapamil 5-10 mg IV slow bolus Conversion atrial flutter SR SVT

Digoxin Loading dose: 0.5-1 mg IV. Maintenance: 62.5-250 µg IV/day Levels: 0.6–1.0 mmol/l

Ventricular rate control in rapid AF (usually 2nd line to amiodarone in critically ill)

Narrow therapeutic index esp in renal failure and

metabolic abnormalities ( K+, Mg, PO4, alkalosis) Proarrhythmic potential high in critically ill patients Minimal inotropic effect in critically ill patients Hypokalaemia potentiates effects

Metoprolol 1-2 mg IV bolus (up to 10 mg) 25-100 mg oral bd

Used in high sympathetic drive states : neurogenic hypertension, hyperthyroidism

Control of reflex tachycardia with vasodilators Caution in poor LV function, asthma Mainly hepatic metabolism

Sotolol 10-80 mg IV slow bolus (10-15 min)

Class III and -blocking actions Supraventricular tachyarrhythmias

Conversion AF/flutter SR Low pro-arrhythmic potential

Adenosine 6-12 mg IV push Diagnosis / conversion of SVT

Lignocaine 0.4% solution = 4mg/ml : 60 ml/hr (4mg/min) for 1-2 hrs 45 ml/hr for 2-4 hrs 30 ml/hr for 2-4 hrs

2nd line drug after amiodarone Sustained, recurrent VT No longer routinely used for prophylaxis for VT VF resistant to defibrillation (now questioned) Potent negative inotrope, pro-convulsant

Flecanaide 1 mg/kg slow IV push 100 mg oral BD (max of 300 mg/day)

SVT AV nodal re-entrant tachycardia WPW Ventricular dysrythmias

Phenytoin 15 mg/kg loading / 1 hr 300 mg/day (level 40-80 mmol/l)

Digoxin toxicity Tricyclic induced malignant arrhythmias

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5. Thrombolytic Therapy

a) All patients with acute MI are potential candidates for primary angioplasty:

i) Cardiology must be notified as early as possible.

ii) The duty cardiologist will decide between primary angioplasty,

thrombolysis and medical management.

b) Indications

i) Acute myocardial infarction

Thrombolysis is standard in the management of AMI unless primary

angioplasty is performed.

a. No specific age limit

b. Onset within 12hrs (potentially 24hrs) of presentation

i. Benefit is inversely proportional to delay in thrombolysis,

therapy should be considered a “medical emergency”

ii. Late therapy may be inappropriate for “small” infarcts.

c. ECG evidence of acute infarction:

i. ST segment 2mm in 2 adjacent chest leads, or

ii. ST segment 1mm in 2 adjacent limb leads, or

iii. New LBBB

iv. Posterior infarction (R in V1 + ST in V2)

d. No benefit has been demonstrated for patients with ST-depression,

T-wave inversion, or a normal ECG.

The patient should be advised of the potential risks and benefits.

ii) Haemodynamically unstable pulmonary embolism.

An unequivocal diagnosis is necessary (spiral CT or angiogram).

Tenecteplase is preferred in life threatening pulmonary embolism.

iii) Ischaemic Cerebrovascular Accident

Within 4.5 hrs of onset of symptoms

CT head: confirming CVA and excluding intracranial haemorrhage

Oedema on initial CT head is associated with a higher incidence of

bleeding

In consultation with a neurologist according to RAH protocol.

c) Contraindications:

i) Absolute:

Active internal bleeding or bleeding diathesis.

Recent head/facial trauma, major trauma or surgery within 3 months.

Previous intracerebral haemorrhage.

Known structural cerebral vascular lesion or malignant intracranial

neoplasm

CVA within 3 months.

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ii) Relative:

Lack of verbal informed consent.

Prolonged CPR (> 10 mins) and/or traumatic resuscitation

History of poorly controlled hypertension

Uncontrolled hypertension at presentation: systolic >180mmHg

and/or diastolic >110mmHg

CVA greater than 3 months

Other intracranial disease, including dementia

Diabetic proliferative retinopathy.

For streptokinase or anistreplase - a prior exposure (>5 days

previously) or allergic reaction to these drugs

Major Surgery within 3 weeks.

Active peptic ulceration or other GI bleeding within 2-4 weeks

Non-compressible vascular puncture/injury.

Pregnancy.

d) Complications

i) Reperfusion arrhythmias

ii) Bleeding (cerebral haemorrhage 0.5%)

iii) Anaphylaxis/anaphylactoid reactions: hypotension, rash, bronchospasm

e) Routine follow-up

i) ECG at 1 and 4 hours post TNK

ii) Cardiac enzymes 6, 12 and 24 hours post infusion

iii) If ST-elevation persists ≥ 1 hr post-TNK,

contact cardiology regarding “rescue angioplasty”.

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Table: Thrombolytics

Drug Dose Protocol

Tenecteplase TNK

Single dose: 1. 0.5 mg/kg over 10 sec 2. non-glucose containing line 3. flush line with N.Sal pre & post

Maximum dose = 50mg (=10,000U)

Aspirin 150mg pre-Rx, then daily Enoxaparin 30mg IV prior to TNK Enoxaparin 1mg/kg sc bd

(if renal function normal) If renal impairment consider heparin IV

instead of enoxaparin.

Alteplase

Bolus Dose = 15 mg. Infusion (1) = 0.75 mg/kg over 30 min (max of 50mg), then Infusion (2) = 0.5 mg/kg over 60 min (max of 35mg) Therapeutic Heparin Infusion - per RAH protocol.

Observe vital signs and neurological observations every 30 minutes for the first 6 hours post infusion then hourly for the next 16 hours

Repeat BP more frequently if elevated Keep BP <180/105

Alteplase in Pulmonary Embolus

0.9 mg/kg intravenously (max 90mg) 10% as a bolus, then remainder over 60 min

Heparin 5000U IV pre-TNK Heparin infusion: APTT > 50-80 secs

Bleeding protocol:

Monitor: APTT PT / INR Fibrinogen level Euglobulin clot lysis time

Apply local pressure (if possible) Reverse heparin with protamine Cryoprecipitate 10 units + FFP 2 units Defibrination or intracranial bleed:

tranexamic acid 10 mg/kg over 20 minutes then 1mg/kg/hr infusion

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6. Antiplatelet Agents

Table: Antiplatelet Agents

Agent Usual dose Indications/Comments

Aspirin 75-150 mg Post acute coronary syndrome Other thrombotic cardiac event Post TIA / stroke

Clopidogrel 75mg orally daily 300mg oral loading dose pre-PTCA (then 75mg daily)

Irreversibly modifies platelet ADP receptor, inhibiting aggregation

Uses: prevention of vascular ischaemic events e.g. MI, CVA, PTCA

ReoPro (abciximab)

Bolus: 0.25mg/kg IV over 1 min, 10mins before PTCA

Infusion: 0.125µg/kg/min IV for 12hrs. (max rate = 10µg/min)

Only to be ordered by Cardiology Binds to platelet glycoprotein IIb/IIIa receptor,

inhibiting platelet aggregation and thrombus formation

Primarily used with PTCA Used with aspirin and heparin

(target ACT >200sec) Increased risk of major bleeding and

thrombocytopaenia

Tirofiban (aggrastat)

Bolus: 0.4 µg/kg/min for 30 mins Maintenance: 0.1 µg /kg/min for at least 48hrs NB: reduce doses by 50% with severe renal insuff. (e.g. creat clearance <30ml/min)

Only to be ordered by Cardiology Blocks glycoprotein IIb/IIIa receptor Short half-life (1.4-1.8 hrs) Uses: unstable angina, non-Q wave MI Use with heparin and aspirin Continue through angiography, and for 12-24hrs

post-PTCA Check platelet count 6hrs post-bolus, then at

least daily. If <90,000 cease and contact cardiology

SEs: bleeding (major 1.4%), thrombocytopenia, fever

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D. Respiratory Drugs

1. Inhaled bronchodilators

a) General Principles:

i) Relieve bronchoconstriction.

ii) They are not routinely used in all ventilated patients.

iii) Not all wheeze is bronchoconstriction – consider other pathology such as

upper airway obstruction, pulmonary oedema, consolidation.

iv) Regularly review:

Patients symptoms.

Work of breathing (i.e. respiratory rate, accessory muscle use).

Wheeze.

Airway pressures.

End-tidal CO2.

Blood gases.

b) Indications:

i) Asthma.

ii) Chronic obstructive pulmonary disease (COPD).

iii) Bronchospasm 2° to infection, aspiration or during mechanical ventilation,

not primarily due to airway secretions.

iv) For the treatment of hyperkalaemia (nebulised salbutamol only).

c) Metered dose inhalers:

i) MDIs are the default therapy for ICU patients.

ii) Can be administered via a MDI adaptor on the ventilator circuit.

d) Nebulised medication:

i) Nebulsied medications are best avoided due to the risk of aerosolising airway

secretions and suboptimal delivery of drug to smaller airways.

ii) Nebulisers are used only if inadequate response to 10 puffs of MDI.

iii) Continuous nebulised bronchodilators can be administered in status

asthmaticus.

2. Parenteral therapy

a) Indications:

i) Adjunctive therapy for patients with acute severe asthma or COPD not

responding to maximum dose inhaled bronchodilators.

b) Complications

i) Tachyarrhythmias.

ii) Hypokalaemia.

iii) Hyperglycaemia.

iv) Lactic acidosis.

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Table: Bronchodilators

Drug Infusion / dose Clinical uses

Salbutamol MDI Usual Dose - 2 puffs 4 hrly. Max Dose - 10 puffs every 15 minutes.

First line bronchodilator. Default method of administration.

Salbutamol (nebulised) Usual Dose - 5mg every 1-4 hours. Max Dose - 20mg every hour (i.e. continuous nebs).

Bronchospasm refractory to MDI. Severe hyperkalaemia.

Ipratropium MDI Usual Dose – 2 puffs 6hrly Max Dose - 4 puffs hrly as required.

Acute Asthma. Chronic obstructive pulmonary disease. Bronchorrhoea. Ipratroprium

(nebulised) Usual Dose - 500ug 8 hrly. Max Dose - 500ug hrly as required.

Adrenaline (nebulised) Max Dose – 1mg every 15 minutes. Severe bronchospasm unresponsive to continuous salbutamol nebs.

Salbutamol (IV) 6 mg / 100 ml 5%D (ml/hr = µg/min) Load = 200ug over 1 minute. Infusion = 5-20ug/min

Acute severe asthma Acute severe asthma unresponsive to

continuous inhaled bronchodilators + systemic steroids.

Adrenaline (IV) 6 mg / 100 ml 5%D (ml/hr = µg/min) Infusion = 1-20 ug/min

Acute severe asthma unresponsive to continuous inhaled bronchodilators + systemic steroids.

Titrate until blood pressure rises..

Aminophylline 1000mg / 100ml 5%D Loading 5-7mg/kg, Infuse 2-4ml/hr (1gm/day)

Levels: 55-110 mol/l

Unproven efficacy in acute asthma / COAD. Narrow therapeutic index.

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E. Sedation, Analgesia and Delirium

1. Sedation and Analgesia

a) Adequate analgesia and anxiolysis are primary management goals in ICU.

b) Pain and anxiety are associated with significant adverse effects:

i) Hypertension, tachycardia

ii) Increased myocardial and cerebral oxygen consumption

iii) Gastric erosions

iv) Intracranial hypertension

v) Increased catabolism

vi) Delirium

c) Sedatives and analgesics are also associated with adverse effects:

i) Respiratory depression

ii) Prolonged ventilation and complications (e.g. nosocomial infections)

iii) Delirium

iv) Hypotension

v) Gastroparesis, ileus and resultant feed intolerance

vi) Increased cost & ventilator days

d) Sedation protocol for ICU patients:

i) Important to obtain a reasonable balance between the awake, distressed

patient and the patient that is oversedated.

ii) Sedation should be given by infusion ± boluses to maintain constant levels

rather than peaks and troughs

iii) Titrate infusions to clinical effect: there is marked inter-individual variability

and absolute doses are of little value

iv) Sequential increases in infusion rate, without the use of a bolus dose,

increases the risk of over-sedation as steady-state is reached (5 half-lives)

v) The half-life for fentanyl increases with the duration of infusion (context-

sensitive half-time), so time to steady-state may be greatly prolonged.

vi) Grimacing alone is not a reliable sign and may only indicate awareness or

reflex activity.

vii) Patients with an encephalopathy, renal or hepatic impairment are likely to

require significantly less or no sedation.

viii) Prescribe the desired sedation level (RASS = 0 to -5) in the box on the ICU

flow chart.

ix) In the absence of a contraindication, sedation should be held daily from 0800

for all patients, except those prescribed a sedation score of - 4 or -5.

e) PCA or epidurals are considered when the patients are awake, in cooirdination

with the Acute Pain Service.

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Table: Nurse Controlled Sedation Protocol

Over-sedated Hold the infusion until the patient reaches the prescribed level If ongoing sedation is required, recommence at half the previous

infusion rate.

Under-sedated Use a bolus of sedation/analgesia and increase rate according to

dose range prescribed. If insufficient repeat until a satisfactory sedation level is attained.

Infusions should not be titrated to responses during high-intensity stimuli, e.g. suction. In these situations, bolus sedation should be provided.

Table: Modified Richmond Agitation Sedation Scale (RASS)

Score Term Description

+4 Overtly combative / violent Immediate danger to staff

+3 Very agitated, pulls or removes tube(s) or catheter(s) Aggressive

+2 Agitated, frequent non-purposeful movement Fights ventilator

+1 Restless, anxious Movements not aggressive or vigorous

0 Alert and calm Eyes open spontaneously

-1 Not fully alert but responds easily to voice or light touch. Sustained awakening & eye contact >10 seconds

-2 Responds easily to voice or light touch. Difficulty staying awake & eye contact <10 seconds

-3 Difficult to rouse, responds to voice or touch with movement or brief eye opening No eye contact

-4 No response to voice or touch. Movement or eye opening to physical stimulation (discomfort / tracheal suction)

-5 No response to voice or physical stimulation Weak or absent cough on tracheal suction

2. Delirium

a) Delirium: “an acute, reversible organic mental syndrome with disorders of

attention and cognitive function, increased or decreased psychomotor activity and

a disordered sleep wake cycle”.

b) An independent predictor of longer ICU stay and increased mortality.

c) Three forms characterised:

i) Hyperactive - agitated, paranoid

ii) Hypoactive - withdrawn, quiet, paranoid

iii) Mixed - combination of above

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d) Hypoactive delirium is under recognised, especially without specific screening.

e) Patients with a modified RASS score ≥ -3 will be screened for delirium by

nursing staff using the CAM-ICU (see below):

i) Adaptation of the ‘Confusion Assessment Method’ for non-verbal patients.

ii) Sensitive and specific tool and if positive the patient likely has delirium.

iii) Should be assessed and a management plan formulated daily.

f) Prevention:

i) Provide appropriate analgesia and anxiolysis, avoiding oversedation

ii) Hold sedation daily until the patient wakes RASS > -1,

unless contraindicated, i.e. patients prescribed RASS -4 / -5

iii) When possible correct physiological disturbances

Hypoxia, acidosis, electrolyte imbalance

Drug withdrawal (nicotine, alcohol, opiates, benzodiazepines)

iv) After prolonged infusion opiates may require weaning rather than abrupt

cessation

v) Provide psychological support and orientation

Encourage patient participation in treatment

Repeatedly orientate the patient in time, place and person

Involve relatives in reassuring patient if possible

Consider papers, television etc. to help orientate patient during the day

vi) Provide an unambiguous environment

vii) Allow an environment for sleep (minimal noise, light etc. at night)

If possible do not performing invasive procedures at night

Minimise nocturnal interventions when clinically safe.

Perform RASS concurrent with GCS assessment.

Use nocturnal sedation as a last resort

viii) Maintain competence

Maintain activity levels and promote early mobilisation

Make sure glasses, hearing aids etc. available for use

Consider interpreters for non English speaking patient

ix) Minimise use of drugs associated with delirium. (see table below)

If appropriate consider sedation with a central α-2 agonist

g) Management of Delirium

i) Identify and treat predisposing factors:

Pain

Metabolic and haemodynamic instability

Infection

Drug interactions and withdrawal

CNS disorders (stroke, abscesses, seizures, tumours)

Renal, cardiac, hepatic, GI failure

Myocardial ischaemia

Ventilator dysynchrony

Immobilisation

Frustration / Anxiety

84

ii) Minimise use of drugs associated with delirium:

Table: Drugs Associated with Increased Delirium

Analgesics Codeine Morphine Fentanyl

Antiemetics Prochlorperazine

Corticosteroids Dexamethasone Hydrocortisone Prednisolone

Antidepressants Amitriptyline Paroxetine

Antimuscarinic Atropine Hyoscine

Hypnotics Diazepam Midazolam Thiopentone

Anticonvulsants Phenytoin Phenobarbital

Cardiovascular Atenolol Digoxin Dopamine Lignocaine

Antihistamines Chlorphenamine Promethazine

Antipsychotics Chlorpromazine

Misc. Furosemide Ranitidine

iii) Pharmacotherapy

Limited evidence pharmacotherapy shortens duration of established

delirium however may be necessary for behavioural control

Drug choice should be individualized and therapy short term.

Recommended agents (see table below) include:

a. Haloperidol

b. Olanzapine

c. Dexmedetomidine /clonidine

d. Quetiapine, Chlorpromazine

Benzodiazepines are best avoided unless indicated for rapid sedation or

treatment of GABA withdrawal syndromes, e.g. delirium tremens.

One agent should be titrated to maximal safe dose (or onset of adverse

effect) before introduction of a second agent.

iv) Physical Restraint – see following.

3. Physical Restraint – for emergency medical treatment

a) The use of restraints can be humane and effective while facilitating diagnosis and

treatment and preventing injury to the patient and medical staff.

b) Restraint may be indicated when a professional and proper approach, including

verbal techniques are unsuccessful.

c) Patients may be restrained under either:

i) The Mental Health Act (1993): when a patient requires immediate treatment

for a mental illness including drug and alcohol induced delirium

ii) The Consent to Medical Treatment and Palliative Care Act (1995): when a

patient over 16 years of age requires treatment for an immediate risk to life

or health and is incapable of giving consent

85

d) The process requires:

i) Examination by two doctors (when available) to confirm the patient is

incapable of giving consent. A person can be deemed incapable when they

are unable to comprehend, retain and judge information relating to the

consequences of having or not having treatment

ii) This can be demonstrated by positive CAM-ICU

iii) Documentation in the case-notes of the patient’s incapability and a treatment

plan for the condition, detailing the need for temporary restraint.

e) Identification and treatment of the illness precipitating the mental incapability

f) The doctor to be acting in good faith and in accordance with professional

standards in order to preserve or improve quality of life

g) Regular reassessment of the need for physical restrain is required and restraints

must be removed if a patient regains mental competence (ie the delirium resolves,

which may be evidenced by a negative CAM-ICU)

h) If the patient has a guardian they should be notified of the need for restraint as

soon as possible.

i) A Form 1 need only be completed if the patient is detained under The Mental

Health Act (1993). In this instance it is necessary to inform the Psychiatry team.

j) A patient with the capacity to make reasonable decisions and who poses no threat

to himself or others cannot be confined or restrained without their permission.

Doing so is illegal. If patient deemed to be competent poses a significant threat

security and the police should be called

k) On ICU discharge ensure a plan regards cessation of agents used to manage

delirium is documented and communicated verbally to the home team.

Flowchart: Confusion Assessment Method for ICU (CAM-ICU)

86

Table: Sedatives / Analgesics

Drug Infusion/dose Clinical uses

Propofol 10mg/ml (neat solution) Initial rate 3-5ml/hr Titrate against effect Maximum 4mg/kg*/hr (*estimate lean weight)

First line sedation in combination with fentanyl Anaesthesia for minor procedures where prompt return of

consciousness is required (e.g. tracheostomy, CVC) Potent myocardial depressant/vasodilator No analgesic effect.

Fentanyl 100-200 µg IV bolus Infusion: 20-200 µg/hr (neat solution)

First line analgesic Potent medium acting narcotic with relative

haemodynamic stability Combined with propofol for sedation Useful for ICU procedures.

Morphine and Midazolam

morphine 60mg + midazolam 30mg per 50ml 5% dextrose Rate: 1-10 ml/hr

Second line sedation - consider if propofol contraindicated or causing adverse effects (eg hypotension)

Review rate/sedation at least daily Effects prolonged in renal failure

Morphine 1-5 mg IV, sc prn, or PCA per protocol

Alternative analgesic to fentanyl Caution in renal failure

Diazepam IV: 2-10 mg prn Orally: 5-20mg bd-qid*

First line in acute alcohol or benzodiazepine withdrawal Larger doses may be required esp. delirium tremens Avoid in delirium not related to alcohol/benzo withdrawal

Epidural cocktail (APS protocol)

Fentanyl 5µg/ml and Bupivacaine 0.1% or Ropivacaine

Standard epidural analgesic regimen Plain bupivacaine may be used (0.25%) Maximal duration 4 days unless indicated Rate: age related doses (per APS)

Dexmedetomidine 400 µg in 40mls load 1µg/kg over 20min infuse 0.2-0.7 ug/kg/hr

Selective central alpha-2-agonist Short term sedation / weaning from ventilation / delirium /

withdrawal states Selected use by senior medical staff only

Agents Primarily Used in Agitation/Delirium

Haloperidol 0.5-2.5 mg IV prn Max dose: 10mg

First line major tranquilliser Delirium, agitation Esp. in opioid / benzodiazepine withdrawal.

blocker : may cause hypotension

QTc, seizures, extrapyramidal ettects

Chlorpromazine 2.5-5 mg IV prn 2nd / 3rd line agent for delirium More sedating, unpredictable & longer acting Vasodilator

Olanzapine (off-label)

5-10mg SL or orally (2.5-5mg in the elderly) Maximum dose 10mg BD

Increase delirium (central cholinergic effect) QTc prolongation Reduced seizure threshold Extrapyramidal effects Metabolism (CYP-1A2) is reduced by Ciprofloxacin

Quetiapine (off-label)

50-100mg enterally BD QTc prolongation Reduced seizure threshold.

Metabolism (CYP-3A4) with fluconazole, erythromycin

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4. Analgesia in Awake Patients – See APS Intranet Guidelines

ACUTE PAIN SERVICE

SC AND ORAL OPIOIDS – INITIAL DOSES

Age (yrs) SC morphine/oxycodone

(mg) Oral oxycodone*

(mg)

15 – 39 7.5 – 12.5 15.0 – 25.0

40 – 59 5.0 – 10.0 10.0 – 20.0

60 – 69 2.5 – 7.5 5.0 – 15.0

70 – 85 2.5 – 5.0 5.0 – 10.0

> 85 2.0 – 3.0 2.5 – 5.0

Recommended dose interval: 2 hourly prn * ↓ if pain not severe

Acute Pain Service (APS) contact numbers

Mon-Fri: 0830-1730 pager 22556

After 1730 hrs SD 1175

W/E & Pub Hol via Switch

Notes:

▪ Suggest start in middle of dose range; upper limit of dose range can be increased if analgesia is inadequate, sedation score is less than -2 and resp rate > 8 /min (first check that doses are correct/ have been given as ordered)

▪ Sedation score - 2 = responds easily to voice or light touch but difficulty staying awake, eye contact maintained < 10 seconds

Simple analgesia:

▪ Unless contraindicated, paracetamol is best ordered for all patients and on a regular rather than prn basis

Dose equiv. SC (mg) Oral (mg)

Morphine 10 30

Oxycodone 10 20

Fentanyl 150 microgram -

Buprenorphine 400 microgram (patch) 800 microgram (SL)

88

F. Muscle relaxants

1. General principles

a) These agents have a limited role in ICU and must not be used unless the patient is

adequately sedated (modified RASS -4 / -5).

b) Non-depolarising agents (except rocuronium) should not be used for emergency

(rapid sequence induction) endotracheal intubation.

2. Indications

a) Depolarising: suxamethonium

i) First line agent for emergency endotracheal intubation

b) Non-depolarising: rocuronium, vecuronium, atracurium

i) Acute control of ventilation post-intubation

ii) Patient transport / retrieval on Oxylog ventilator who cannot be managed

by other means

iii) Selected patients with poor lung compliance who are difficult to ventilate

following “heavy” sedation

iv) With anaesthesia for procedures: tracheostomy, bronchoscopy

3. Complications

a) Hyperkalaemia, bradycardia (suxamethonium)

b) Sympathetic overdrive, particularly in under-sedated patients

c) Adverse outcome in head injury when used as a measure to control ICP

d) Use of non-depolarising relaxants may be associated with increased risk of critical

illness polyneuropathy, especially with concomitant use of steroids.

Table: Muscle Relaxants

Relaxant Dose Comment

Suxamethonium 100-200 mg or 1-2 mg/kg

1st line agent in Rapid Sequence Induction (RSI) Consider pre-treatment with atropine (0.6-1.2mg) if

potential bradycardia Contraindicated in burns (>3 days), chronic spinal and

neuromuscular disease, hyperkalaemic states (K+ > 5.5) Caution in any patient with any central or peripheral

muscle weakness including critical illness related weakness

Rocuronium 0.6 mg/kg 1.0 mg/kg for RSI

First line non-depolarising agent in ICU Rapid onset (60secs) 2nd line agent in RSI = alternative to suxamethonium Duration of action : 30-40 minutes

Vecuronium 4-10mg IV prn 2nd line non-depolarising agent in ICU Duration similar to rocuronium Cardiostable, low incidence of allergy

89

G. Anticoagulation


a) All patients on systemic anticoagulation must have an APTT, INR and CBP

performed daily.

2. Indications

a) Acute systemic anticoagulation:

i) As a general rule, heparin infusions are used in critically ill patients:

Allows monitoring/titration to a therapeutic APTT.

Provision for reversal if indicated (e.g. procedures, bleeding).

ii) Enoxaparin is effective but more difficult to use in critically ill patients:

Inability to monitor activity

Dose variation in renal disease and

Inability to reverse effect.

iii) Indications:

Proven venous or arterial thromboembolism

Acute coronary syndromes

Prosthetic heart valves:

a. Prior to commencement of oral anticoagulants

b. During an acute illness, where oral anticoagulation is relatively

contraindicated.

AF in patients complicated by emboli < 70 years.

AF for more than 48 hours, in which cardioversion is being considered

Extracorporeal circuits e.g. CVVHDF, ECMO

iv) RAH Heparin Protocol – see below

b) Partial anticoagulation

i) low dose IV heparin (500 u/hr)

ii) IV prostacyclin

c) Warfarin

i) The kinetics of warfarin are highly variable in the critically ill.

ii) Normally only used in stable long term patients

iii) Prosthetic valves (mitral > aortic valves)

iv) Previous thromboembolism

v) Maintenance of thromboprophylaxis in high risk patients (# pelvis)

90

3. Protocol for DVT/VTE prophylaxis

All patients must have a documented plan for DVT prophylaxis

a) Mechanical prophylaxis i) TED stockings

All patients except those with:

a. Significant PVD

b. Significant lower limb trauma, cellulitis, dermatitis or oedema

c. Peripheral venous or arterial access on lower limb(s)

d. For most of the above patients, a single TED should be used on

the unaffected limb

TED stockings can be used in patients with proven DVT to decrease

the incidence of post DVT thrombophlebitis

Continue until the patient can mobilise effectively

ii) Sequential calf compression devices

SCCD’s have an additive effect to other forms of DVT prophylaxis.

Patients unable to use chemoprophylaxis or at high risk are given

priority.

In patients without DVT prophylaxis > 24 hrs consider a lower

limb ultrasound to exclude DVT prior to application of SCCD’s

b) Chemoprophylaxis

i) Enoxaparin or heparin should be charted for all patients unless

contraindicated and continued throughout their ICU stay

ii) For patients with a high risk of bleeding, communication with the relevant

surgical teams (neurosurgery, spinal, ophthalmology, etc) is essential.

iii) Enoxaparin 40 mg s/c daily is the default agent.

Start on day 1 or as early as possible especially in high risk patients.

Potential accumulation in renal failure

Not routinely monitored (anti-Xa level).

iv) Unfractionated (UF) Heparin 5000U s/c b.d.-t.d.s

Used in patients with a high risk of bleeding or renal failure

Shorter duration of action and ease of reversal.

v) Enoxaparin 60 mg s/c daily (20mg mane + 40mg nocte)

Considered for high risk patients:

a. Pelvic or long bone fractures

b. Significant spinal injury or paralysis

c. Previous PTE/DVT

Routine monitoring is not necessary.

vi) No other DVT protocols are to be used except post-pelvic surgery

Adjusted dose heparin protocol may be used

See “VTE Prophylaxis in Orthopaedics” on the RAH Intranet

vii) Cease prophylaxis for significant bleeding or suspected HITS - see below

91

viii) Absolute and relative contraindications for heparins:

Significant active haemorrhage

High risk of bleeding

a. Coagulopathy - DIC, thrombocytopenia, liver failure, etc.

b. Post-surgical - neuro, spinal, eyes

c. Major trauma - TBI with parenchymal lesions, liver/spleen

Known or suspected adverse reaction to heparin

a. Documented or suspected HITS, known heparin allergy

Patients already on therapeutic anticoagulation

c) IVC filter

i) In high risk patients with ongoing contraindications to chemoprophylaxis,

an IVC filter can be considered.

4. Perioperative anticoagulation in patients on Warfarin

a) Heparin infusion

i) First choice in ICU

ii) Effect is more readily monitored and reversed.

b) Where heparin is contraindicated, consider danaparoid or consult haematology.

5. Protocol for Heparin Induced Thrombocytopaenia Syndrome (HITS)


i) HITS is a prothrombotic disorder caused by platelet-activating antibodies

ii) An intense hypercoagulable state often complicated by venous and arterial

thrombosis

iii) Risk factors

Duration of therapy *see 4T table

Type of Heparin UFH > LMWH

Type of patient postsurgical > medical > pregnancy

b) Diagnosis

i) The 4T Score ‘pre-test probability’ of HITS

Points - 0, 1, or 2 for each of 4 categories (see table)

Maximum possible score = 8

a. High risk 6-8 points

b. Intermediate risk 4-5 points

c. Low risk 0-3 points

If probability is intermediate or high do a HIT screen for antibodies.

If high probability cease heparin immediately pending test results

ii) HIT Screen

ELISA detects antibodies against heparin and PF4.

Also detects other non-HIT heparin-Ab, therefore lower specificity

If ELISA positive then test further with a "functional assay",

serotonin release assay (SRA)

iii) Lower limb doppler U/S

92

Table: HITS Probability Score – ‘4T Score’

Risk Factor 2 Points 1 Point 0 Points

Thrombocytopenia Platelet fall >50% Nadir >20

Platelet fall 30-50% or >50% fall due to surgery or nadir 10-19

Platelet fall <30% Nadir <10

Timing of onset of platelet fall (or other sequelae of HITS)

Day 5-10 or Day 1 with heparin in last 30 days

> Day 10 or timing unclear or < Day 1 with heparin in last 31-100 days

< Day 4 No recent heparin

Thrombosis or other sequelae

Proven new thrombosis, skin necrosis or Anaphylactoid reaction after IV heparin bolus

Progressive or recurrent thrombosis, erythematous skin lesions, suspected thrombosis, asymptomatic upper limb DVT

None

OTher cause of platelet fall

None Possible Definite

Pre-test probability score: High (6-8) | Intermediate (4-5) | Low (0-3)

a) Treatment principles

i) Two Do’s

Do stop all heparin (including flushes, LMWH, etc )

Do start an alternative non-heparin anticoagulant in therapeutic doses.

a. Lepirudin - difficult to use, or

b. Danaproid - may cross react

c. Discuss with haematology

ii) Two Don’ts

Don’t administer warfarin acutely and if warfarin has already been

administered, give vitamin K

Don’t give prophylactic platelet transfusions

iii) Two Diagnostics

Test for HIT antibodies

Investigate for lower limb DVT

93

6. Anticoagulants

Table: Anticoagulants

Drug Infusion / Dose

Warfarin

Variable dose Daily INR See age-adjusted Warfarin loading protocol on the RAH intranet. NB. This is meant only as a guide, and was developed for non-

critically ill patients, whose pharmacodynamics may differ significantly from the intensive care population.

Heparin (infusion) 25000u/50ml = 500u/ml See below: titrate against APTT: Cease 4-6 hours prior to surgical procedures

Heparin (subcut) 5000 u subcut bd <70 kg 5000 u subcut 8 hrly >70 kg or high risk DVT

Enoxaparin (Clexane®)

Prophylaxis: 40mg subcut daily 20mg subcut daily if Creat clearance < 30ml/min

“High risk” 20mg mane 40mg nocte Treatment:

1mg/kg subcut bd - lean body mass 1mg/kg subcut once daily if CrCl < 30ml/min

Prostacyclin (infusion)

Dose: 0.2-0.6 µg/kg/hr 500µg (+10ml diluent): add to 40ml NSal = 10µg/ml solution Start at 2ml/hr and monitor platelet count May cause hypotension

Danaparoid sodium (Orgaran®) Infusion

IV loading dose: < 60kg 1500 U 60-75 kg 2250 U 75-90 kg 3000 U > 90 kg 3750 U

Infusion: 2250U of danaparoid in 250ml 5% dextrose: 44 ml/hr (400 U/hr) x 4 hours 33 ml/hr (300 U/hr) x 4 hours 22 ml/hr (200 U/hr)

Adjust dose to anti-Xa levels (target 0.5-0.8 anti-Xa U/ml) Long half life (25 hrs): cease early if changing to oral anticoagulants

Danaparoid (subcut) 750 U 8-12 hourly

Lepirudin Complex see below

Dabigatran See below

94

Table: Heparin Infusion Protocol

Weight (kg) 45-55 56-65 66-75 76-85 86-95 >95

Bolus (U) 3,500 4,200 4,900 5,600 6,300 7,000

Infusion (U/hr) 900 1,100 1,250 1,400 1,600 1,800

Infusion adjustment

APTT IV bolus Stop Infusion Rate Change Repeat APTT

< 37 5,000 units 400u/hr 6 hrs

38-64 200u/hr 6 hrs

65-110 No change Daily

111-130 50u/hr 6 hrs

131-140 30 min 100u/hr 6 hrs

141-150 60 min 150u/hr 6 hrs

> 150 120 min or APTT <150

200u/hr 2 hrs

Note: Infusion: 25,000 units in 50ml syringe = 500U/ml Check first APTT 6 hrs after bolus dose

Table: Lepirudin Infusion Protocol

CrCl (ml/min) Bolus Dose Maintenance Infusion

mg/kg/hr % original dose

> 60 0.4 mg/kg (max 44mg)

0.1 (max 11mg/hr) 100%

45-60 0.2 mg/kg 0.05 50%

30-44

None

0.025 25%

15-29 0.01 10%

< 15 0.005 5%

CVVHDF 0.01 10%

95

7. Lepirudin

a) Recombinant direct thrombin inhibitor

b) Dose range varies by a factor of 20x

i) Care must be used in determining the precise dose

ii) Renally excreted and must be carefully monitored in the critically ill

c) NB: a bolus dose is only used if patient has life threatening thrombus

8. Dabigatran

a) Competitive direct thrombin inhibitor.

b) Used as an oral alternative to warfarin.

c) Current indications include:

i) Atrial fibrillation

ii) VTE prophylaxis following major orthopaedic surgery.

d) Renally cleared with a half-life 12-14 hrs.

e) Monitoring

i) INR cannot be used to monitor efficacy or toxicity.

ii) APTT provides an approximate indication of the level of anticoagulation

iii) A normal APTT suggests that drug is unlikely to be present in significant

concentration.

iv) APTT of > 80 seconds suggests that drug is present in excess.

f) No specific antidote is available to reverse effect.

i) For severe bleeding, supportive strategies are recommended, including

transfusion of fresh whole blood, or fresh frozen plasma.

ii) Dialysis may be indicated in patients with prolonged APTT particularly if

renal function is impaired.

iii) The role of prothrombinex and rFVIIa is unclear.

iv) For advice under these circumstances contact the on-call Haemostasis

Service through Transfusion on 8222 5430 or 8222 5431.

96

H. Endocrine Drugs

1. Insulin

a) Indications:

i) Diabetic emergencies – DKA and hyperosmolar coma

ii) Treatment of hyperkalaemia

50% dextrose 50ml, plus Actrapid 10U

iii) Perioperative diabetic patients (both insulin and non-insulin dependent)

iv) General ICU patients

Hyperglycaemia 10 mmol/l or glycosuria in acute illness:

a. Maintaining BGL 6-10mmol/l is recommended for all critically ill

patients

b. Majority of ICU patients will require insulin using this protocol.

c. NB: This protocol is not designed for patients with diabetic

ketoacidosis and is a guideline only.

d. Some patients will require individual manipulation of dose.

Subcutaneous sliding scale insulin:

a. Is inadequate for most critically ill patients and should be avoided.

b. May be used in a small number of less critically ill patients, who

have a limited requirement for exogenous insulin.

c. A regular dose of subcutaneous intermediate/long-acting insulin,

adjusted according to BGL may be suitable in some ICU patients.

b) ICU Insulin Protocol – see following page.

i) Target BGL = 6-10mmol/l.

ii) Blood for testing should ideally be:

Sampled from the arterial line rather than capillary (finger prick), as the

former is more accurate in the critically ill.

Measured via the blood gas analyser, c.f. bedside glucometer.

iii) Protocol Precautions:

If insulin rate ≥ 8 U/hr and the BGL remains high, measurement may

be erroneous take a sample from another site and measure in the

blood gas analyser.

Consider holding the infusion if feed or glucose infusions are stopped.

Potassium level

a. Administration of insulin reduces K+ levels.

b. Check K+ on ABG specimen at least twice daily and more often if

the insulin infusion rate is high or changing acutely.

c. If [K+] < 3.5 mmol/l

KCl ~ 30 mmol over 1h via a pump.

97

Flowchart: Blood Glucose Management in ICU

Table: Insulin Infusion Protocol

BGL Bolus Starting infusion

Subsequent infusion Repeat BGL

mmol/l Units IV Units/hr Units/hour Hours

>15 2 2 Increase by 1 1

10.1-14.9 1 1 Increase by 1 1

8-10 0 0 If BGL dropping continue current rate. If static or rising increase by 0.5

1

5-7.9 0 0 Continue current rate If BGL dropping for 2 consecutive hrs decrease rate by 0.5.

1 (2hrly if BGL stable for 6 hrs)

3.5-4.9 0 0 Cease 1 (4hrly if off insulin>6hrs)

<3.5 Call MO 0 Cease 1

c) Discharge Management:

i) Pre-discharge, cease insulin infusion for at least 4 hours and check BGL

ii) Order BGL to be checked 8 hourly on the ward

iii) Refer to the RAH intranet documents:

Insulin Protocol for Patients Discharged from ICU.

Diabetes Management Guidelines.

iv) Liaise with Endocrinology as indicated.

Target BGL = 6-10mmol/l Perform BGL on Admission

BGL = 6-10mmol/l

BGL > 10 mmol/l Commence Protocol

Perform BGL 4hrly

98

2. Diabetes insipidus: protocol for DDAVP a) Diabetes insipidus may occur in the following situations:

i) Post ablative pituitary surgery

ii) Severe head injury, esp. anterior cranial fossa #, trauma

iii) Evolving brain death

iv) Lithium administration

b) Indications for DDAVP

i) Acute perioperative management (24-48hrs) of DI following pituitary

surgery is usually fluid based – the use of DDAVP is rarely indicated.

ii) Persistent polyuria in the absence of diuretics > 300ml/hr for > 3hrs

iii) Altered conscious state, inability to detect thirst or take oral fluids

iv) Low urine osmolality in the presence of high plasma osmolality

v) Pre-existing hyperosmolar state or predisposition to pre-renal failure where

persistent polyuria may exacerbate this.

c) DDAVP Prescription

i) Dose 1-2µg s.c. bd as required. (4µg is excessive)

ii) Adjust maintenance fluids according to the response

d) Maintenance fluids should be prescribed in the usual manner, according to

volume status, renal function and osmolality.

e) Presumptive or proven brain death:

i) DI should be treated early (i.e. as soon as polyuria occurs)

ii) Delayed administration of DDAVP can result in significant electrolyte

abnormalities, which may influence the organ donation process.

3. Steroids

a) Indications

i) Pre-existing steroid therapy:

Wide variety of indications, doses and durations of therapy.

The need to continue steroids, with or without dose adjustment, should

be assessed.

ii) ICU conditions where steroid therapy may be beneficial. :

Addisonian crisis

Anaphylaxis

Asthma, Chronic obstructive pulmonary disease

Bacterial meningitis - esp. pneumococcal prior to antibiotics

Croup, post-extubation laryngeal oedema

Fulminant vasculitis

Hypercalcaemia

Idiopathic thrombocytopenic purpura

Myasthenic crisis

Myxoedema coma / Thyroid storm.

Organ transplantation

Pneumocystis jurovecii pneumonia

99

iii) Conditions where supporting data are variable and the decision to administer

steroids should be made on a case-by-case basis

Sepsis

ARDS

b) Contra-indications / non-indications

Active infection

Acute head injury

Guillain-Barré syndrome

Fat embolism syndrome

c) Relative drug potencies

Table: Steroid Doses / Relative Potencies

Drug Equivalent dose (mg)

Glucocorticoid activity

Mineralocorticoid activity

Hydrocortisone 100 1 1

Prednisone 25 4 0.3

Methylprednisolone 20 4 0

Dexamethasone 4 30 0

Cortisone acetate 125 0.8 0.8

Fludrocortisone 1 10 250

d) Limitations of a random cortisol

i) Marked fluctuation in plasma cortisol in the critically ill.

ii) The ‘normal’ range in critical illness is not defined.

iii) There is no consensus ‘cut-off’ value below which insufficiency is present.

e) Limitations of total cortisol

i) Free cortisol is the bioactive fraction of cortisol

ii) Large variation in total cortisol assay results when the same specimen is

tested in different laboratories and using different assays

iii) Peripheral tissue-specific glucocorticoid resistance is not tested

f) Conventional (high-dose) short synacthen test (HDSST)

i) Synacthen concentrations are supraphysiological

ii) Published data likely overestimate the incidence of adrenal insufficiency,

as most studies did not excluded patients on etomidate.

iii) The low-dose SST may be more a better predictor of outcome.

iv) Insufficient data to support the routine use in patients with septic shock.

v) Should only be performed if there is suspicion of hypoadrenalism

Hyperkalaemia/hyponatraemia

Hypoglycaemia

Refractory acidosis

Catecholamine resistance

100

I. Renal Drugs - Diuretics


a) Oliguria in acutely ill patients is frequently a manifestation of:

i) Hypovolaemia – relative or absolute

ii) Decreased cardiac output

iii) Direct renal toxicity, or

iv) A combination of these factors.

b) Therapy should be directed toward causative factors and not maintenance of urine

output by the administration of a diuretic agent.

c) Urine output, in the absence of diuretic use, represents one of the best markers of

end-organ perfusion and is a useful guide to clinical management.

d) Diuretics should never be used to treat oligo/anuria, they are only a treatment for

fluid overload

2. Indications

a) Symptomatic fluid overload

i) Pulmonary oedema / CCF

ii) Cor pulmonale

b) Hyperaldosterone states: ascites

c) Chronic renal failure

3. Contraindications

a) Hypovolaemic and/or Na+-depleted states

b) Known drug hypersensitivity (esp. sulphonamide group)

4. Complications a) Hypovolaemia

b) Hyperosmolar states

c) Potentiation of renal failure - 2° to hypovolaemia

d) Electrolyte disturbance especially K+, Mg, PO4, metabolic alkalosis

e) Natriuresis and kaliuresis will alter urine electrolytes and osmolality for 24-48

hrs post dose.

101

Table: Diuretics

Drug Infusion/dose Clinical uses

Frusemide 40-250 mg/day IV / oral

First line, potent loop diuretic Doses may be increased in diuretic dependence

K+, Mg, PO4, metabolic alkalosis common

Acetazolamide 250-500 mg IV tds Carbonic anhydrase inhibitor Alkaline diuresis with HCO3

- excretion Used for severe metabolic alkalosis after

correction of hypovolaemia: K+, Mg++, PO4=

Post-hypercapnic alkalosis

Spironolactone 25-100 mg oral bd Potassium sparring diuretic Often given with loop and thiazide diuretics Indicated as part of a chronic treatment regimen

for left ventricular failure Use in acute LVF is less certain May be of use in patients with ascites, particularly

if secondary hyperaldosteronism is a feature. Careful administration is required in patients with

impaired renal function.

Mannitol 20% solution / 200 mg/ml Dose 100 ml prn (20g) (0.5g/kg is too much!!)

Potent osmotic diuretic May cause - initial hypervolaemia

- late hypovolaemia - hyperosmolal state - osmolal gap.

Maintain measured osmolality < 300 mosmol/l Limited role in suspected acute life-threatening

intracranial hypertension as a bridge to definitive surgical therapy.

Limited (unproven) roles in rhabdomyolysis, transfusion reactions, myoglobinuria for renal protection

102

J. Gastrointestinal Drugs

1. Stress ulcer prophylaxis

a) Routine ‘stress ulcer prophylaxis’ is not indicated:

i) Low prevalence of clinically significant bleeding due to stress ulceration

ii) No evidence of survival benefit with use of stress ulcer prophylaxis

iii) Possible increased incidence of VAP and/or clostridium difficile infection

b) Pantoprazole may be considered in patients at high risk.

c) Patients on pre-existing therapy (with PPIs or H2-blockers) should be continued

d) Patients with clinically suspected GI bleeding should commence on a PPI

e) Enteral feeding should be commenced as soon as possible.

2. Acute GI bleeding

a) Definition

i) Overt bleeding

Blood in the NGT

Haematemesis or malaena

ii) Plus either:

MAP > 20 mmHg

Hb 20 g/L in 24 hours

Required 2 units blood transfusion in 24 hrs

iii) Blood in the NG tube is frequently due to local erosion and by itself does not

constitute clinically significant GI bleeding.

b) Management

i) Resuscitation - ABC

ii) Correct coagulopathy

iii) Cease heparin / anticoagulants

iv) Commence PPI - pantoprazole 40 mg bd/tds.

v) Endoscopy sclerotherapy

vi) If the source is not identified and with ongoing bleeding, consider:

Labelled red cell scan

Angiography (+/-embolisation), or

Colonoscopy.

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3. GI drugs

Table: GI Drugs

Drug Dose Clinical uses

Metoclopromide 10 mg IV 6 hrly, prn Persistent vomiting, nausea Large gastric aspirates

(in combination with erythromycin)

Erythromycin 100-200 mg IV bd Large gastric aspirates (in combination with metoclopramide)

Droperidol 0.625 mg IV prn Potent, effective antiemetic Minimal side effects

Tropisetron 2 mg IV / oral daily Use if anticholinergic side effects are to be avoided.

Ondansetron 4 mg IV prn / 12 hrly Second line, antiemetic (not available at RAH)

Ranitidine 50 mg 8hrly IV 150-300 mg daily po

Stress ulcer prophylaxis Peptic ulcer disease Does not prevent acute rebleeding Reduce dose in renal failure.

Pantoprazole Acute RX: 40 mg IV bd/tds Maint. RX: 40 mg daily

First line RX for peptic ulceration Refractory peptic ulcer, ulcerative oesophagitis Z-E syndrome Upper GI bleeding

Octreotide Bolus: 50 g IV

Varices: 50 g / hr

Fistulae: 100-200 g sc 8-hrly

Variceal bleeding (as effective as sclerotherapy)

Enteric, pancreatic fistulae Sulphonylurea overdose Severe secretory diarrhoea, e.g. post-chemo

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K. Antibiotics

1. Policy

a) Prescription of antibiotics must conform to RAH guidelines.

b) The over-prescription and irrational use of antibiotics is associated with the

development of bacterial resistance, nosocomial infection and drug related

morbidity

c) All antibiotics must be reviewed daily and where appropriate, discussed with

Infectious Diseases or Clinical Microbiology.

d) Record the day and expected course of antibiotics in the left-hand margin of the

drug chart, e.g. ‘D4/7’ = day 4 of a 7 day course.

e) Record date, test and results (including sensitivities) in the “results folder”.

2. Principles of antibiotic prescription

a) The treatment of infection consists of (in order of priority)

i) Adequate resuscitation

ii) Source control drainage of infected collections, etc.

iii) Relevant samples for microbiological and/or histological analysis

iv) Routine cultures:

Blood - 2 sets at different times from venous stabs

Urine

Sputum

Any other suspicious site

v) Prompt administration of

Rational empiric antibiotics

Culture-directed antibiotics

NB: time to effective ABx treatment affects outcome.

b) General indications for antibiotics:

i) Prophylaxis for invasive procedures and operations

Proven indications

a. Abdominal surgery which involves a breach of the colonic mucosa

(traumatic or elective), or draining an infected cavity

b. Selected obstetrical and gynaecological procedures:

i. Caesarean section with ruptured foetal membranes

ii. Vaginal hysterectomy

c. Insertion of a prosthetic device

d. Compound fractures

e. Amputation of gangrenous limb

Unproven but recommended

a. Lacerations penetrating into periosteum or into joint cavities

b. Crush injuries

c. Insertion of a neurosurgical shunt

d. Cardiac valve replacement

e. Arterial prosthesis

105

ii) Empirical antibiotics

Obtain as many cultures as possible before antibiotics commenced.

Should be commenced early in critically ill patients

Should be rationalised according to gram stain & culture results.

iii) Specific infections where the organisms is known

c) Complications of antibiotics

i) Antibiotic effect related

Bacterial resistance

Nosocomial infection

Pseudomembranous colitis

ii) Systemic reactions

Skin rashes

Anaphylactoid / anaphylactic reactions

iii) Specific organ toxicities, e.g.

Interstitial nephritis, ATN

Seizures

Marrow suppression, thrombocytopaenia

QT prolongation

iv) Cost

d) Gentamicin / Tobramycin

i) Where possible, the aminoglycosides should be used for a limited duration

and therapy changed to a suitable alternative when possible.

ii) Pharmacodynamic properties

Concentration-dependent killing peak:MIC ~ 10:1

Significant post-antibiotic effect

iii) Toxicity

Nephrotoxicity - non-oliguric renal failure

Ototoxicity - permanent, vestibular or auditory

iv) Dosing

All dosing is by estimated Lean Body Weight (LBW):

a. Male: kg 50 + 0.9×(height - 150cm)

b. Female: kg 45 + 0.9×(height - 150cm)

Initial Dose: 5-7 mg/kg *irrespective of renal function

a. Measure level 6-10 hrs post-dose

b. Liaise with ICU Pharmacist (Pg: 22916), or

Drug Information (Ext: 25546) re further dose requirements.

c. Do not use the standard dosing normogram in ICU patients.

Synergistic gentamicin, e.g. tds dosing in endocarditis

a. Measure pre-dose trough levels

b. Aim for < 1.0 mg/L to avoid toxicity.

106

e) Vancomycin i) Pharmacology

Time-dependent killing max 24h-AUC:MIC ratio

Moderate post-antibiotic effect

Renally cleared Plasma t½ 4-6 hrs

ii) Toxicity

Ototoxicity < 2%

Nephrotoxicity - very rare (20 case reports 1956-84)

*probably non-existent with current preparations

‘Red-man’ synd. rate of IV administration.

iii) Preference in ICU is for continuous infusion, c.f. interval dosing.

More constant plasma levels & efficacy

Reduced ‘red-man’ syndrome

Irritant to veins, dilute to 250ml

Daily drug levels until stable

*assessment of CrCl in critical illness is sub-optimal.

iv) For patients on CRRT or CrCl < 20ml/min

Intermittent Dose = 1.0g slow IV when levels < 15mg/l

v) For patients transferring to the ward, see RAH intranet guidelines.

Table: Vancomycin Dosing Schedule

Renal Function CrCl

> 60 ml/min CrCl

20-60ml/min CrCl < 20 ml/min

CRRT

Initi

al D

osin

g

Loading dose IV 25 mg/kg (max 2.0g) | Slow infusion (1/24)

in All Patients

Infusion Rate 2.0-4.0g / 24 hrs 1.0g / 24 hrs Not indicated

Infu

sio

n D

ose

Adj

ustm

ent

Vanc Level *Daily levels until stable

< 15mg/L§ Dose 1.0g/day§ Dose 0.5g/day§

Not indicated

15-20mg/L Dose 500mg/day Dose 250mg/day

Target Level = 20-25mg/L Cont Current Infusion Rate

> 30mg/L Hold 12 hrs

Recheck Level Hold 12 hrs

Recheck Level

§In critically unwell patients with low levels, consider giving a further bolus dose 0.5-1.0g in addition to increasing the rate.

Do NOT use if

CrCl < 60 ml/min

107

Table: Antibiotic Infusion Schedules

Antibiotic IV Loading All Patients

Max Hrs Stability

1Standard Infusion Dose (per 24 hrs) Renal Function

CrCl > 60 ml/min CrCl ~ 20-60ml/min CrCl < 20 ml/min CRRT

Vancomycin2 1.0-2.0g 24 1.0-4.0g/day – Per Levels Not indicated

Penicillin G 1.2-1.8g 12 4.8-14.4g 4.8-9.6g 2.4g 4.8-9.6g

Amoxycillin 1.0-2.0g 6 4.0-12.0g 4.0-6.0g 2.0g 4.0-12.0g

Flucloxacillin 1.0-2.0g 24 4.0-12.0g 4.0g 4.0-12.0g

Piperacillin 4.0g 24 12.0-16.0g 8.0g 12.0-16.0g

Tazocin 4.5g 24 13.5g 9.0g 13.5g

Ceftriaxone 1.0g 24 1.0-4.0g

Ceftazidime 1.0-2.0g 24 3.0-6.0g 2.0-4.0g 1.0-2.0g 2.0-4.0g

Meropenem 1.0-2.0g 8 3.0-6.0g 1.0-2.0g 0.5g 2.0g

1 Standard Infusion Orders: 24 Hrs Dose in 100ml {N.Saline | 5%Dext.} @ 4ml/hr (per Max Hrs Stability) 12 Hrs (Dose / 2) in 100ml {N.Saline | 5%Dext.} @ 8ml/hr 8 Hrs (Dose / 3) in 100ml {N.Saline | 5%Dext.} @ 12ml/hr 6 Hrs (Dose / 4) in 100ml {N.Saline | 5%Dext.} @ 16ml/hr 2 Vancomycin should be diluted into 250mls if given via a peripheral line. Loading dose over at least 60 mins, or 10mg/min.

*NB: Add the reconstituted solutions to a 100mL bag of compatible fluid, having first removed an equivalent volume of solution, i.e. so the final total volume of the bag remains 100ml, then administer over the required interval.

108

3. Ventilator associated pneumonia (VAP) a) Significant cause of mortality and morbidity in ICU

b) Clinical diagnosis based upon the presence of a number of the following:

i) New CXR infiltrates (hard to see in patients with ARDS)

ii) New clinical chest signs

iii) Increasing oxygen requirement

iv) Increased purulent sputum

v) Indications of systemic sepsis:

Increased/decreased WCC

Fever

Hypotension

c) Treatment

i) Sputum culture

ii) Commence antibiotics immediately

Tazocin 13.5g/24hrs &

Gentamicin 5mg/kg on day 1, then as per levels

If gentamicin contraindicated, ciprofloxacin 200-400mg b.d.

In patients with known MRSA or ICU stay > 5days

a. Add vancomycin

b. Stop if no gram positive organisms seen on micro

iii) Review sputum culture

If no organism and not on ABx consider another diagnosis

De-escalate to narrow spectrum therapy ASAP

Normal treatment 5-7 days except pseudomonas sp. then 10-14 days

4. Antibiotic prophylaxis

a) Peri-operative (Table)

i) Ongoing prophylactic therapy is required for selected post-operative

patients in ICU.

ii) Refer to individual protocols for recommendations on pre-operative

antibiotic prophylaxis.

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Table: Peri-operative Antibiotic Prophylaxis

Specialty Procedure Antibiotics

Orthopaedics Elective cases Cefazolin 1g IV 8h x 3 doses

Traumatic wounds Involving bone or joint

compound fractures

Cefazolin 1g IV 8h x 2 days

+ severe tissue damage + myonecrosis + vascular injury

Cefazolin 1g IV 8h x 2 days + Gentamicin 5 mg/kg IV daily x 2 days + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days

Abdominal Surgery Colorectal Cefazolin 1 gm ± gentamicin 3 mg/kg + Metronidazole 500mg IV single doses

Biliary surgery Gentamicin 3 mg/kg x 1 dose, or cefazolin 1g x 1 dose

Vascular surgery Elective cases + severe bowel injury + myonecrosis or

vascular injury Amputation

Cefazolin 1g IV 8h x 3 doses + Gentamicin 5 mg/kg LBW IV daily x 2 days

+ Metronidazole 500 mg IV bd x 2 days + Benzyl pen. 3 g IV stat, 1.2 g IV 6h x 2 days

Cefazolin 1g IV 8h x 3 doses + Metronidazole 500 mg IV bd x 2 doses

Neurosurgery CSF leak / # Skull base None: treat only if signs of meningitis

Craniotomy / ICP insertion Cefazolin 1g IV at induction

Head & neck, thoracic

Craniofacial with breach of nasal or oral mucosa

Cefazolin 1g IV 8h x 3 doses + Metronidazole 500 mg IV bd x 2 doses

Cardiac Surgery See Section “Management of Cardiothoracic Patients”

110

Table: Perioperative Endocarditis Prophylaxis

111

Table: Empiric Antibiotics

Infection Type / Comment Antibiotics

Pneumonia

Community acquired Immunocompetent Admitted to ICU / HDU

(i.e. respiratory failure)

Azithromycin 500mg IV daily, plus *Ceftriaxone 1 IV daily

For treatment failure, consider Moxifloxacin 400mg IV daily ± Flucloxacillin 1g 6h (if high suspicion of S.aureus)

*Default ICU therapy differs from the RAH standard protocol (penicillin + gentamicin) due to the wide variability in renal function in ICU patients and the inability to use baseline creatinine as a marker of renal function.

Ventilator associated Hospital acquired

Tazocin 4.5g IV 8 hrly or 13.5g/day + Gentamicin 5 mg/kg IV daily

Consider Vancomycin 1g b.d. IV See above

Immunocompromised host Contact ID

Aspiration

No antibiotics without evidence of proven infection.

With proven infection Benzyl penicillin 1.2g IV 6 hrly, plus

metronidazole 500 mg IV 12 hrly

Exacerbation of COPD

No clinical signs of pneumonia Treat as community acquired pneumonia

Epiglottitis Usually H. influenzae Ceftriaxone 1 g IV daily

Meningitis/ encephalitis

Suspected bacterial Usually: meningococcus

pneumococcus, or H. influenzae

Ceftriaxone 2g IV 12 hrly, plus Penicillin 1.8g to 2.4g IV 4 hrly

Dexamethazone 10mg IV before or with the first dose of antibiotic then 6hrly for 4 days

Not definitely bacterial Consider Acyclovir 10mg/kg IV 8hrly

Urinary tract infection

Without systemic sepsis in patients with a urinary catheter

No treatment. Remove / change catheter

With systemic sepsis Amoxycillin 2g IV 6 hrly, plus gentamicin 5mg/kg IV daily, or

Ceftriaxone 1gm IV daily if unable to tolerate gentamicin

Intra-abdominal sepsis

Faecal peritonitis Perforated viscus

Amoxycillin 2 gm IV 6 hrly + Gentamicin 5 mg/kg IV daily + Metronidazole 500 mg IV bd x 7 days

Recurring intra-abdominal sepsis or failed Rx with above

Consult ID/Clinical Microbiology

Pancreatitis No CT evidence of necrosis No antibiotics

Significant CT necrosis Tazocin 4.5g IV 8 hrly

Biliary sepsis

Acute cholecystitis Ascending cholangitis

Amoxycillin 1 g IV 6 h + Gentamicin 5 mg/kg/d IV x 7 days

Amoxycillin 2 gm IV 6 h + Gentamicin 5 mg/kg/d IV

Previous biliary tract surgery or known biliary obstruction

add Metronidazole 500mg IV BD x 7 days

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Gynae sepsis

Septicaemia secondary to PID Amoxycillin 2g IV 6 h + Gentamicin 5 mg/kg IV dly + Metronidazole 500 mg IV bd x 5 days

Suspected S. aureus infection Lincomycin 1.2g IV bd + Gentamicin 5 mg/kg IV dly x 7 days

Suspected Bacterial Endocarditis

Community acquired Benzyl penicillin 1.8 g IV 4 h + Gentamicin 1 mg/kg IV tds ± Flucloxacillin 2g IV qid

Hospital acquired Prosthetic valve, or Penicillin allergic

Vancomycin 1g IV bd + Gentamicin 1 mg/kg IV tds

3 sets of blood cultures, and review at 48 hrs Manage pre-dose trough levels for gentamicin <1 mg/L to avoid toxicity

Fungal Septicaemia

Suspected candidiasis Amphotericin 0.5-1 mg/kg/day, or Fluconazole 400 mg IV daily

(in non-neutropaenic patients)

Suspected aspergillosis Voriconazole IV/oral 6mg/kg BD loading for 24 hours, then 4mg/kg BD or

Caspofungin 70mg IV daily loading for 24 hours, then 50mg daily

1. Consult ID for all proven fungaemias 2. Remove all potential sources of infection (lines, catheters, etc) 3. Monitor renal / hepatic function during the course of antifungal therapy. 4. Adjust the amphotericin dose in renal insufficiency, or consider the use of fluconazole if

appropriate 5. Voriconazole levels can be monitored for toxicity and clinical responses. 6. IV voriconazole is contraindicated in patients with CrCl < 30mL/min due to accumulation

of the excipient

Burns No antibiotics without evidence of bacterial infection

Cutaneous infections

Wound infection + signs of systemic sepsis

Benzylpenicillin 1.8 g IV 4 h + Flucloxacillin 1-2 g IV 6 h or

Cefazolin 1g IV 8h

Synergistic gangrene Necrotising fasciitis In addition to surgery

± hyperbaric oxygen

Meropenem plus

Lincomycin 600 mg IV 8 hrly, or Clindamycin 600 mg IV 8 hrly

Consider IV-Ig 2.0g/kg total dose (3 days)

Severe oral infections Penicillin 1.2 g IV 4-6 hourly + Metronidazole 500 mg IV bd

Line sepsis

Patient not overtly septic Remove unnecessary, old or clinically suspect lines & send for culture.

Blood cultures by venipuncture No antibiotics

Patient overtly septic Prosthetic valve / arterial graft High risk patient

Vancomycin 1 g IV BD until blood culture results available

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Table: Antibiotics for Specific Organisms

Organism 1st choice 2nd choice

Pneumococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1 IV dly

Staphylococcus aureus Flucloxacillin 2 gm IV 6 h Vancomycin 1gm IV bd or Cefazolin 1-2g IV 8h

Meningococcus Benzyl penicillin 1.2g IV 4-6 h Ceftriaxone 1g IV dly

Meningococcus contacts Ciprofloxacin 500mg po x 1dose Rifampicin 600mg po bd x 2 days

MRSA Vancomycin 1g IV bd Consult ID

Enterococcus Amoxycillin 1-2 g IV 6 h (+ Gentamicin 5 mg/kg if SBE)

Vancomycin 1g IV dly (+ Gentamicin 5mg/kg if SBE)

Gp A Strep. With Shock

Benzylpenicillin 1.8g 4 hrly IV + Lincomycin 1.2g IV bd + Intragam 2.0g/kg total dose (3 days)

Consult ID Cease IG when pt. improves

Haemophilus influenzae Ceftriaxone 1g IV daily Amoxycillin 1-2 g IV 6 h (if sensitive)

H. influenzae contacts (meningitis)

Rifampicin 600 mg oral bd x 4 days Ceftriaxone 1g IM dly x 2 doses

E. Coli Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly

Enterobacter Gentamicin 5 mg/kg IV dly Meropenem 500mg IV 8h

Klebsiella Gentamicin 5 mg/kg IV dly Ceftriaxone 1g IV dly

Pseudomonas aeruginosa Piperacillin 4 g IV 8 hrly + Gentamicin 5-7 mg/kg IV dly

Choice based on sensitivity results: Ceftazidime 2g IV 8hrly or Tazocin 4.5g IV 8hrly PLUS Gentamicin 5-7 mg/kg IV daily or Ciprofloxacin 400mg IV bd

Legionella spp. Moxifloxacin 400mg IV daily Azithromycin 500mg IV daily

Mycoplasma pneumoniae Erythromycin 1g IV 6h

Pneumocystis jurovecii Co-trimoxazole 15-20 ml IV 6 h + methylpred 40mg bd x 5d, methylpred 40mg die x 5d, methylpred 20mg die x 11d,

Pentamidine isethionate 4 mg/kg/day IV + methylprednisolone 40mg 6 hrly x 7days

Clostridium difficile: 1. Mild / moderate 2. Severe, or relapse post RX

Cease antibiotics 1. Metronidazole 400 mg o tds

(or 500mg IV if npo) x 7-10 days

2. Repeat above

Consult ID or Clinical Micro. Treatment options are: Bacitracin 25,000U 6hrly 7-10d or Vancomycin 125mg po 6hrly 7-10d

Clostridial infection (Polymicrobial Infection)

Benzylpenicillin 1.8g IV 4 hrly + Gentamicin 5 mg/kg IV dly + Metronidazole 500 mg IV bd + surgical debridement

hyperbaric oxygen

Lincomycin 600 mg IV 8 hrly + Gentamicin 5 mg/kg IV daily

114

PART 4 - FLUIDS AND ELECTROLYTES

A. Principles of Fluid Management in Intensive Care

1. All fluids, infusions are reviewed daily and rewritten:

a) On the ICU flowchart (Units A & B), or

b) In the IV Fluid chart in the ward folder (Unit C).

2. Assessment of volume status and fluid balance:

a) Clinical markers

i) Skin turgor, mucous membranes, capillary refill, peripheral perfusion

ii) HR, BP, Urine output

iii) CVP, PAOP

iv) PiCCO catheter - GEDI, ELWI, stroke volume variability.

v) CXR, interstitial oedema

vi) Echo – IVC distensibility index, LVOT-VTI variability

b) Biochemical markers

i) Serum Na+, Cl-, osmolality

ii) Urea / creatinine (± ratio)

iii) Bicarbonate

iv) Haematocrit

c) Charted fluid balance (notoriously inaccurate!)

i) Total intake including drug & infusion volumes

ii) Total output including urine output, drains, NG losses, blood loss

iii) Insensible losses due to pyrexia, transcellular shifts, etc.

(NB: usually impossible to quantify accurately)

3. Fluids should be considered in two components:

a) Maintenance fluids

i) Usually crystalloids - 5% dextrose, 4% dextrose + 1/5 N.Saline

- N.Saline

- Hartmann’s, CSL

ii) Usual volumes: 25-30 ml/kg/day 80-120 ml/hr

iii) TPN (refer to guidelines)

b) Replacement / resuscitation fluids

i) N.saline should be used for most fluid resuscitation.

Equivalent to 4% albumin for resuscitation

Better for patients with head trauma.

ii) Colloid - 4% albumin, gelofusine

May be considered for fluid resuscitation in selected patients.

Greater cost, no demonstrable advantage.

Should be avoided in patients with traumatic brain injury.

iii) Blood and components as indicated according to NH&MRC guidelines.

iv) Crystalloid replacement is usually used for excessive renal, enteric and

burns losses (see below).

v) Hyperchloraemia may be harmful so consider the use of fluids with other

anions, e.g. Hartmann’s.

115

4. Composition of commonly used fluids (1000ml solution):

Table: Common IV Solutions

Solution Na+ K+ Cl- Ca++ Lact. Gluc. Osm. Prot.

N Saline 150 150 300

N/2 Saline 75 75 150

N/5 Sal. + 4% Dex. 30 30 40 g 282

5% Dextrose 50 g 278

Hartmann’s 131 5.0 111 2 29 280

Gelofusine (500ml) 77 60 274 20g

Albumex 4% (500ml) 70 62.5 25g

5. Fluid management in burns patients

a) The RAH Burns Unit uses the modified Parkland regimen.

b) This is a guide - other clinical markers such as urine output, heart rate, blood

pressure, CVP, serum sodium and osmolality, and haematocrit must be taken

into account.

c) As a result, both solution composition and administration rate may have to be

modified in order to maintain the above parameters within normal ranges.

d) Protocol:

i) Assess the patient’s % burn surface area (%BSA) using an accurate chart.

ii) Assess patient weight (kg).

iii) Formula:

First 24 hours = total fluid (as Hartmann’s solution):

Wt. x %BSA burn x 4.0 ml

a. give ½ the total fluid during first 8 hours post-burn

b. give ½ the total during the subsequent 16 hours

Second 24 hours fluid is given as Albumex 4%

Wt x %BSA burn x 0.5 ml

Other maintenance fluid is given according to the above physiological

parameters

The primary endpoint of fluid resuscitation is generally accepted to be

a urine output 0.5-1 ml/kg/hr

Catecholamines:

a. Should be commenced only when adequate volume replacement is

unable to maintain a satisfactory urine output, or there is

associated myocardial failure.

b. The duty consultant or SR should be consulted prior to use.

iv) Commence enteral feeding as soon as possible.

116

B. Nutrition

1. Enteral nutrition

a) Enteric feeding is the preferred mode of nutritional support and should be

considered in all patients as soon as possible after admission.

b) Advantages

i) Early EN in trauma patients has been associated with improved outcome.

ii) Use of the gut decreases mucosal atrophy, which may reduce bacterial

translocation thereby reducing the incidence and duration of sepsis.

iii) The incidence and severity of gastric erosions and stress ulceration may be

reduced.

iv) Cheaper than TPN

v) CVC complications (especially infection) are reduced or avoided.

c) Disadvantages

i) Regurgitation / aspiration

ii) Nosocomial pneumonia

iii) Diarrhoea (other causes are more likely than enteral feeding)

d) Indications

i) As soon as possible in all intubated / tracheostomised patients, where

admission and duration of intubation is expected to be > 24-48 hours.

ii) Patients with an operative jejunostomy may commence feeding within 6

hours of placement.

e) Contraindications

i) Gastrointestinal (including oesophageal) perforation, gastrointestinal

fistulae, bowel obstruction, ileus.

ii) Recent bowel anastomosis is not a contraindication – however, discussion

with the surgical team is essential.

iii) Absent bowel sounds are not a contraindication.

f) Protocol (see feeding protocol at bedside)

i) Liaise with the dietician (who will order feeds) during the fluid round.

ii) Outline any problems: e.g. hyperkalaemia, renal failure, osmolality

iii) Place a 12F or larger nasogastric tube (to allow reliable aspiration)

iv) Use orogastric tubes in patients with anterior and middle cranial fossa #

v) Check the position of the feeding tube with x-ray prior to use.

Attach label to NG tube, and

Document in notes that the position of the tube has been checked.

vi) Nurse the patient at 30-45° head up.

vii) Commence feed at 80 ml/hr continuously according to the protocol.

viii) Aspirate all NG and PEG tubes 6 hrly

ix) Do not aspirate jejunostomies, naso-duodenal/jejunal tubes or PEJs

117

x) Flush jejunostomy/gastrostomy tubes with 20ml N.saline 6hrly.

Aspirate < 250 ml:

a. Return aspirate to stomach

b. If {rate < max} then increase rate by 20 ml/hr

c. Repeat aspiration at 6hrs and

If {aspirate < 250 ml} then rate to max (usually 80-100 ml/hr)

Aspirate > 250 ml:

a. Return 250 ml

b. Halve the feed rate (not less than 20 ml/hr)

c. Continue to aspirate 6 hrly

d. Consider prokinetics:

i. Metoclopramide 10 mg IV 6 hrly, plus

Erythromycin 100-200 mg IV bd

ii. Continue until tolerating feed for > 72hrs,

then cease and observe

iii. Recommence as needed

e. Reduce narcotic administration if possible.

Aspirates > 250 ml while receiving prokinetics, consider:

a. Post-pyloric feeding tube

i. Using the Cortrak® device, or

ii. Endoscopically placed by the GI Unit

b. Feeding jejunostomy

c. Nasogastric naloxone 4-8mg tds

d. TPN.

xi) Consider a PEG, PEJ or feeding jejunostomy in long term patients

e.g. Guillain Barré or severe head injury

xii) Cease feeds 4 hrs prior to extubation, tracheostomy, ET tube change.

xiii) There is no requirement to cease feeds until immediately prior to going to

theatre, unless:

Surgical procedure on the GIT

Planned for tracheostomy or ETT change.

xiv) Remember to modify insulin dose when feeds are reduced or ceased.

2. Enteral Protocol - See over page.

Flowchart: Nutritional Therapy Protocol

118

Patients expected to be mechanically ventilated for > 48h should have enteral nutrition (EN) commenced within 24 h of admission to ICU

Insert NET, confirm position by XR and confirm suitability for commencement of feeds

Commence feeds Osmolite 1 ml/kg/h (1 kcal/ml @ max 80 ml/h) (unless pt fluid restricted)

Pts unsuitable for EN should be considered for TPN if EN unlikely for > 5 days. Include; short gut, GI fistulae, contraindication to placing NET, GIT perforation.

Referral to Dietitian for Nutritional Ax Weekdays - ICU Dietitian will review ICU / SDU pts daily and chart max recommended feeding rate on daily obs chart. Contact ICU Dietitian on Pg 1342 if any concerns / queries. Weekends - Nursing T/L should be advised of new NET / changes to existing regimens. On call Dietitian should be contacted (SD 1156 / 0401711460) and advised of - new ICU / SDU NET feeds; changes to existing regimens; pt transfers. Cover (when ICU Dietitian on leave) - Clinical Dietetics should be contacted (Pg 1342) and advised of all NEW ICU / SDU NET feeds and changes to existing regimens.

If GRV remains high (i.e. 2 aspirates ≥ 250 ml within

12 h) consider post-pyloric feeding

Do NOT aspirate post pyloric feeding tubes. Monitor pt for signs of intolerance including abdominal distension, constipation, diarrhoea or vomiting. Notify physician of concerns.

Feeding interruptions • Do not hold feeds for

routine nursing care, bedside procedures or diagnostic tests unless specified.

• No need to fast prior to surgery unless ETT to be removed, i/o tracheostomy, tracheostomy change or GIT surgery.

• If fasting for theatre, commence fast when pt called to theatre. Or fast for 4 hr prior to r/o ETT, i/o tracheostomy, tracheostomy change or surgery on gut lumen.

• EN and insulin to cease during time in OT and restart at same rate as when discontinued.

• Cease feeds 4hr prior to planned

extubation.

Check Gastric residual volume (GRV) every 6 h for ALL gastric tubes, document on chart.

Do NOT aspirate post pyloric tubes.

GRV < 250 ml return aspirate, continue feed

regimen (if not at goal increase rate

by 20 ml/h)

GRV ≥ 250 ml return 250 ml,

halve feed rate, commence prokinetics

Prokinetics Both Metoclopramide 10mg QID IV and Erythromycin 100 - 200mg BD IV Metoclopramide not recommended for use in head injury pts.

Refer Pt to Dietitian for Nutritional Ax

Consider TPN if unable to place post pyloric tube

Jejunostomy feeds should commence at rate of 1 ml/kg/h or as recommended by Dietitian and flushed 20 ml N saline QID.

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3. Post-pyloric feeding protocol:

a) Commence feed at 1ml/kg/hr, up to a maximum 80 ml/h.

b) No need to cease feed for any procedures, other than GI surgery.

c) Consider placement of a NG tube to aspirate and ensure an empty stomach.

4. Parenteral Nutrition


i) TPN may be harmful in critically ill patients.

ii) Enteral nutrition is preferred and TPN should only be considered for patients

in whom this is not possible.

iii) Supplementing EN with TPN is not beneficial and should be avoided.

iv) Refer to ‘Clinical Duties Outside ICU’, regarding the responsibilities and

management of ward patients receiving TPN.

v) TPN is usually ordered by the Unit A Senior Registrar, under the supervision

of Dr Adam Deane.

vi) IV access may be via a CVC or PICC line, with the latter being preferred.

vii) TPN for ICU patients is prescribed during the midday fluid round.

viii) Patient being discharged from ICU on TPN must be entered into the TPN

folder in Unit A.

b) Indications for TPN in the patient who cannot be fed enterally are:

i) GIT Failure > 7-10 days and expected duration of support > 5-7 days.

Prolonged post-operative ileus

Enteric fistulae

ii) Short GIT syndrome following major intestinal resection.

c) Complications of TPN:

i) Depression of immune function, esp. in cancer patients

ii) Intestinal villous atrophy

iii) Metabolic imbalance

Electrolyte disturbances ( K+, HPO4=, Mg++)

Glucose intolerance: hyperglycaemia and glycosuria

Hyperosmolar dehydration syndrome

Rebound hypoglycaemia on cessation of TPN

Hyperbilirubinaemia

CO2 production, esp. in COPD patients

iv) Central venous access complications

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d) Protocol

i) On commencement:

Add the following orders to the patient's drug folder:

a. Cernevit MV 1 ampoule IV daily.

b. Trace elements 1 ampoule daily

c. Vitamin K 10 mg IV weekly

d. Commence insulin:

i. Initial dose = 5U s.c. qid *hold if BGL < 10

ii. Check BGL qid

iii. Adjust the dose on subsequent days guided by BGLs

iv. “Sliding Scale” regimens are no longer used.

Commence TPN solution at a lower rate (40ml/hr) in “starved” patients

a. Potential movement of K+ / HPO4= into cells with re-feeding

b. May cause acute severe hypokalemia and hypophosphataemia.

Slowly increase to desired rate, usually 60-80 ml/hr.

Dietician will provide a calculated energy requirement as a guide

ii) Daily:

Review the patient, CVC site, biochem, BGL chart and fluid balance.

Prescribe TPN selecting the most appropriate “option” from the table

below.

These bags are pre-prepared and must not be altered, i.e. no further

additives. Patients requiring K+, PO4 and fluids etc. above the quantities

provided must receive these in a separate line/infusion.

iii) Intralipid

Commence TPN with lipid-free solutions (#3, #4)

Lipid is indicated if the period of malnutrition > 4 weeks or if the patient

is hyperglycaemic.

Table: Average Daily Requirements

Water 30-40 ml/kg/day

Calories 25-30 kcal/kg/day 1. Glucose: 2g/kg/day @ 4.1 kcal/g 2. Fat: 2g/kg/day @ 9 kcal/g

Protein 0.5-2.0 g/kg/day 1. 2:5 essential:total amino acids 2. 150:1 kcal:g N2 (non-nitrogen kcal)

Sodium 1.0 mmol/kg/day

Potassium 1.0 mmol/kg/day Dependent on renal function

Phosphate 0.2 mmol/kg/day Dependent on renal function

Vitamins B groups daily B12, Folate, A, D, E, K weekly

Trace elements as required.

Replacement solutions

1. Urine 2. Nasogastric/ileostomy 3. Pancreatic/biliary fistulae

1. ½ Normal saline ± KCl 10 ml/L 2. ½ Normal saline ± KCl 10 ml/L 3. Hartmann’s solution

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Table: Baxter TPN Solution Options

Composition Baxter Option 1

With Lipid With Potassium

Baxter Option 2 With Lipid

No Potassium

Baxter Option 3 No lipid

With Potassium

Baxter Option 4 No Lipid

No Potassium

Total Volume (ml) 2000 2100 2000 2100

Glucose (gm) 250 250 500 500

Lipids (gm) 100 100 0 0

Energy (kcal) 2270 2270 2300 2300

Protein (gm) 100 100 100 100

Nitrogen (gm) 16.5 16.5 16.5 16.5

Na+ (mmol) 73 73 73 73

K+ (mmol) 60 0 60 0

Mg++ (mmol) 5 5 5 5

HPO4= (mmol) 37.5 7.5 30 0

Cl- (mmol) 70 110 70 110

Acetate (mmol) 150 82 150 82

Solution shelf life 12 mths room T 6 mths room T 12 mths room T 6 mths room T

1. Lipid source is Clinoleic 20% which comprises olive oil 80% and soya oil 20%. 2. Multivitamin and trace elements to be given separately from TPN. 3. Nothing may be added to TPN bags. 4. All solutions come in triple phase bag and have light protection cover.

NB: Specialised prescription TPN can be ordered via pharmacy, e.g. when large daily potassium requirements are not feasibly administered by 10mmol/100ml bags and the standard 60mmol/2L TPN.

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C. Blood Component Therapy

1. Indications

a) Blood component therapy should only be given if benefit outweighs the risk

b) The decision to transfuse should be based on clinical assessment, disease course

and response to previous transfusion as well as [Hb] levels.

c) Potential risks including

i) Mis-identification / acute transfusion reaction

ii) Bacterial / viral infection

iii) Transfusion associated acute lung injury (TRALI)

iv) Transfusion associated circulatory overload (TACO)

v) Immune modulation (this and TRALI are probably the most significant)

d) The best way to reduce the risk of blood component therapy is to reduce

requirements

i) Minimise unnecessary blood sampling

ii) Minimise blood loss during procedures

iii) Consider nutritional and iron stores state

2. Red Blood Cells

a) Elective *as per NHMRC / ASBT guidelines.

i) Use of RBCs at Hb > 100g/L is likely to be inappropriate

ii) Use of RBCs at Hb < 70g/L is likely to be appropriate but in some

asymptomatic patients a lower threshold may be acceptable

iii) At Hb 70-100g/L clinical assessment of risk versus benefit is required.

iv) The following criteria may indicate RBC transfusion is indicated

Significant ongoing bleeding present or anticipated.

Clinical signs of impaired oxygen transport such as dyspnoea,

tiredness/weakness, angina, syncope.

Cardiac ischaemia or cardiac failure due to anaemia.

v) Order as “Red cells” or RBCs on the ICU or ward fluid chart

vi) “Type & Screen” specimens are held for 10 days for compatibility testing.

vii) For transfusion, a new specimen is needed for cross-match every 72 hours.

b) Resuscitation

i) Abnormal bleeding is usually surgical and requires urgent surgical and/or

radiological intervention.

ii) A full cross-match takes 30 minutes if marked urgent (not including the

time for transfer of blood); this should be performed if possible while

volume is replaced with crystalloid or colloid.

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iii) If blood is required faster than this, the request “Time Required” box

should be marked:

“Desperate” *group O Rh(D)-ve blood is issued immediately

(see massive transfusion protocol)

“10 minutes” *group-specific (ABO/Rh-D) but without full

compatibility testing

“30 minutes” urgently processed, fully crossmatched blood

NB: The requesting MO accepts full responsibility for these (*)

iv) Blood replacement should start immediately in the setting of:

Rapid blood loss leading to hypovolaemia and shock.

Blood loss estimated or anticipated to exceed 20-25% of blood

volume, i.e. 1000-1500 ml in a normal adult.

3. Massive Transfusion Protocol

a) Definition:

i) Loss of one blood volume within a 24 hr period.

ii) Alternative, more practical definitions:

≥ 50% blood volume loss within 3 hr, or

≥ 150 ml/min rate of loss.

b) The RAH massive transfusion protocol should be activated as soon as the need

is identified

c) Correction of critical bleeding requires simultaneous approach to:

i) Control the source of bleeding

ii) Contact key personnel required for haemorrhage control

iii) Maintain blood volume

iv) Prevent hypothermia and acidosis

d) Principles

i) Trauma patients with critical bleeding are coagulopathic on presentation

ii) Prevention of further coagulopathy with aggressive management is much

more effective than delayed treatment

iii) Acidosis and hypothermia worsen coagulopathy

e) On identification:

i) Take blood and place in red bags for:

CBE, Group and match

Extended Coags

ii) Notify transfusion medicine on 47*

iii) Dispatch blood samples ASAP

iv) Transfusion will provide products in “Massive Transfusion Packs”

v) Notify transfusion when bleeding controlled

f) Tranexamic acid

i) Routinely used in trauma only as per CRASH2

ii) Triggers modified for local use (see Chart)

iii) Dose 1g over 10 minutes then 1g over 8 hours

iv) Delivered with first MTP pack

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Table: Critical Bleeding (Massive Transfusion)

Procedure Comments

Laboratory investigations

Samples to Blood Bank for T&S CBE, INR, APTT, fibrinogen Biochemical profile, blood gases etc. Repeat CBE, INR, APTT, Fib

after blood component infusion, or every 4 hrs until stable.

Take samples at earliest opportunity as results may be affected by colloid infusion.

Mis-identification is commonest transfusion risk.

May need to give components before results available.

Use “Massive Transfusion–Priority Processing” labels with ‘Red bag’ to alert lab for speedy processing.

Suitable RBC Un-crossmatched group O Rh(D) negative in extreme emergency until blood group known, then group-specific.

Then fully crossmatched blood when time permits.

To prevent hypothermia by the use of blood warmer and/or rapid infusion device.

Employ intra-op blood salvage if available and appropriate.

Rh(D) positive is acceptable if patient is male or post-menopausal female.

Laboratory will complete compatibility testing after issue.

Further compatibility test not required after replacement of 1 blood volume (8–10 units).

Blood-warmer indicated if flow rate >50 ml/kg/hr in adult.

Salvage contraindicated if wound heavily contaminated.

Platelets Anticipate platelet count <50x109/L after 2 x blood volume replacement.

Target platelet count: >100x109/L for multiple/CNS trauma or if platelet function abnormal.

Target >50x109/L for other situations.

FFP (10-15 ml/kg – 1 litre or 4 units for an adult)

Aim for INR <1.5 and APTT <40 secs. Allow for 30 min thawing time. Consider extended life plasma

INR >1.5 and APTT >40 secs correlates with increased surgical bleeding.

Keep Ca++>1.13mmol/L

Cryoprecipitate (2-4 units)

Replace fibrinogen. Aim for fibrinogen >1.0 g/L. Allow for 30 min thawing time.

Fibrinogen <0.5 strongly associated with microvascular bleeding.

Fresh whole blood Request hospital Blood Bank to contact ARCBS on-call MO.

Anticipated major blood loss in elective patients with platelet or coagulation abnormalities. Continued significant bleeding even after use of conventional component therapy. Role in haemostasis controversial.

Recombinant FVIIa (Novoseven) Dose ~ 90 μg/Kg

Obtain approval from consultation with senior Surgeons / Anaesthetists / Intensivists and Haematologists / ARCBS on-call MO.

May be considered when the patient’s condition continues to deteriorate to likely haemorrhagic death

Usually as a desperate effort after other measures fail.

See Massive Transfusion Protocol

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4. Platelets a) Standard dose is “Platelets - 1 Adult Pack”

b) Prophylactic transfusion before surgery or other “at risk” procedures:

i) Platelet count < 50 × 109/L or

ii) Platelet count > 50 × 109/L

with evidence of inherited or acquired (drug-induced) platelet dysfunction

c) Prophylactic transfusion in marrow failure:

i) Platelet count < 10 × 109/L, or

ii) Higher levels with clinical evidence of bleeding or other risk factor

d) Therapeutic transfusion for uncontrolled haemorrhage:

i) As per the massive transfusion protocol

ii) Platelet count < 50 × 109/L

iii) Platelet count < 100 × 109/L with microvascular bleeding

iv) Irrespective of platelet count with evidence of platelet dysfunction.

e) Platelet dysfunction can contribute to bleeding with a normal platelet count

f) ITP: Only if life-threatening bleeding is present.

5. Fresh Frozen Plasma (FFP) a) Prophylactic transfusion before surgery or other invasive procedure that could

result in significant bleeding:

i) Urgent correction of prolonged INR or APTT in warfarin overdose or

vitamin K deficiency (see below)

ii) Correction of prolonged INR or APTT in liver disease

iii) Correction of inherited coagulation factor deficiencies where specific

coagulation factor concentrates are not available

b) Therapeutic transfusion for uncontrolled haemorrhage in:

i) Warfarin overdose

ii) Liver disease

iii) Vitamin K deficiency

iv) Inherited coagulation factor deficiencies where specific coagulation factor

concentrates are not available

v) DIC

c) Plasma exchange in TTP & related syndromes

d) As per the massive transfusion protocol

e) Post massive transfusion with coagulopathy:

i) INR > 1.5, or

ii) APTT > 40 seconds

6. Extended Life Plasma

a) Recent regulatory changes allow transfusion laboratories to used thawed FFP

for up to 5 days.

b) By using thawed FFP the product can now be provided immediately, c.f. the

standard 20-30 minute delay normally involved in thawing.

c) Five day thawed FFP will be labelled ‘Extended Life Plasma’

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Table: Guidelines for the Management of an Elevated INR

Clinical Setting Action

INR < 5.0 Bleeding absent

Lower the dose or omit the next dose of warfarin. Resume therapy at a lower dose when the INR approaches therapeutic range. If the INR is only minimally above therapeutic range (up to 10%), dose reduction

may not be necessary.

INR ~ 5.0–9.0* Bleeding absent

Cease warfarin; consider reasons for INR and patient-specific factors. If bleeding risk is high, give vitamin K1 (1.0–2.0mg orally or 0.5–1.0mg IV) †. Measure INR within 24 hrs, resume warfarin at a reduced dose once INR is in

therapeutic range.

INR > 9.0 Bleeding absent

Where there is a low risk of bleeding Cease warfarin, give 2.5–5.0mg vitamin K1 orally or 1.0mg IV Measure INR in 6-12 hrs & resume warfarin at a reduced dose once INR < 5.0. Where there is high risk of bleeding‡ Cease warfarin, give 1.0mg vitamin K1 IV. Consider Prothrombinex-HT (25–50 IU/kg) and FFP (150–300mL) Measure INR in 6-12 hrs, resume warfarin at a reduced dose once INR < 5.0.

Any clinically significant bleeding where warfarin induced coagulopathy is considered a contributing factor

Cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, as well as Prothrombinex-HT (25–50 IU/kg) and fresh frozen plasma (150–300mL), assess patient continuously until INR < 5.0, and bleeding stops.§ or

If fresh frozen plasma is unavailable, cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, and Prothrombinex-HT (25–50 IU/kg), assess patient continuously until INR < 5.0, and bleeding stops.§ or

If Prothrombinex-HT is unavailable, cease warfarin therapy, give 5.0–10.0mg vitamin K1 intravenously, and 10–15mL/kg of fresh frozen plasma, assess patient continuously until INR < 5.0, and bleeding stops.§

* Bleeding risk increases exponentially from INR 5 to 9, INR ≥ 6 should be monitored closely. † Vitamin K effect on INR can be expected within 6-12 hours. ‡ Examples of patients with a high bleeding risk:

active gastrointestinal disorders (such as peptic ulcer or inflammatory bowel disease) those receiving concomitant antiplatelet therapy those who underwent a major surgical procedure within the preceding two weeks, and those with a low platelet count.

§ In all situations carefully reassess the need for ongoing warfarin therapy.

From consensus guidelines Australian Society of Thrombosis and Haemostasis 2004

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7. Cryoprecipitate

a) Bleeding and fibrinogen < 1.0 g/L in:

i) DIC.

ii) Massive transfusion.

iii) Hereditary hypofibrinogenaemia.

b) 10U of cryoprecipitate will plasma fibrinogen by ~ 1.0g/l

c) Standard dose = 8U for hypofibrinogenaemia.

8. DDAVP

a) Standard dose = 0.3-0.4µg/kg intravenously over 30 mins

b) Increases factors VIII:C, VIII:vWF and platelet adhesion.

c) Indications: actual, or significant risk of bleeding with,

i) Haemophilia A

ii) type I von Willebrand's disease

iii) Post cardio-pulmonary bypass (check with surgeon)

iv) Clinical scenarios where platelet dysfunction is likely

Uraemia

Drugs - aspirin, clopidogrel

9. Recombinant activated factor VII (rFVIIa, NovoSeven)

a) TGA approved indications

i) Haemophilia patients with antibodies to factor VIII

ii) Glanzmann's thrombasthenia with antibodies to GPIIb-IIIa and/or HLA,

and who have past or present refractoriness to platelet transfusions

iii) Patients with congenital factor VII deficiency

b) Effective in improving coagulopathies associated with trauma, major surgery,

and organ transplantation = ‘off-label’ indications.

c) No risk of virus transmission and contains no human protein

d) Binds to tissue factor (TF) activating both factors IX and X.

i) High doses activate factor X on the surface of activated platelets

ii) Has both TF-dependent and TF-independent effects

e) Recommended dose for the treatment of a severe coagulopathy 90µg/kg

f) Acts within a few minutes and has a half-life of about 2.5 hours.

g) Requires consultant/haematology approval because of high cost and absence of

current TGA approval for these indications.

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10. Dabigatran Clinical Guidelines

a) General Information

i) Dabigatran etexilate (Pradaxa) is a pro-drug of dabigatran

ii) Reversible direct thrombin inhibitor

iii) Onset of anticoagulant effect within 30 minutes after oral administration

iv) Peak plasma concentration and effect within 2-3hrs.

v) Usual half-life: 12-14 hrs

vi) Renally cleared, ClCr < 30 ml/min t½ > 24 hrs.

b) Effect on Laboratory Coagulation Parameters

i) Monitoring is not routinely required

ii) No direct relationship between coagulation tests and therapeutic effect.

iii) Thrombin time (TT)

Particularly sensitive to dabigatran

A normal TT excludes clinically significant dabigatran levels.

iv) Activated partial thromboplastin time (APTT)

Shows best correlation with plasma levels

Increasing APTT occurs with dabigatran concentration.

a. Usual peak concentration APTT ~ 2x control

b. Trough levels (12 hrs post dose) ~ 1.5x

A normal APTT suggests that minimal drug is present

A significantly prolonged APTT suggests drug excess:

a. APTT > 65s at trough (12 hrs post-dose) or

b. APTT > 80s at any time.

v) Prothrombin time (PT)

At therapeutic concentrations (50-200 ug/L) dabigatran has little effect

on PT and therefore INR.

INR results therefore do not reflect anticoagulant activity.

At supra-therapeutic concentrations the INR may be 2.0.

c) Dabigatran Assay

i) Haemoclot dabigatran assay has been established by SA Pathology

ii) A “dabigatran level” should be requested on the pathology form and the

timing of the last dabigatran dose given.

iii) A single citrate tube is required. For further information ring 8222 3918.

d) Dabigatran and other anticoagulants

i) When converting patients from warfarin do not commence dabigatran

until the INR is < 2.0.

ii) For patients on dabigatran commencing parenteral anticoagulation, wait

12 hours (CrCl ≥ 30 mL/min) or

24 hours (CrCl < 30 mL/min) after the last dose.

iii) For patients receiving a parenteral anticoagulant commencing dabigatran

LMWH (b.d.) commence dabigatran 0-2 hours before the next dose of

LMWH was to have been administered

Heparin infusion - commence dabigatran on cessation of infusion.

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e) Peri-operative dabigatran management

i) The requirement to cease anticoagulation should be assessed

ii) If cessation is required, the timing will be dependent upon renal function

and the bleeding risk associated with the procedure.

Table: Pre-operative Dabigatran Management

Renal Function (CrCl ml/min)

Half-life dabigatran (hrs)

Timing of discontinuation prior to surgery

Standard bleeding risk High bleeding risk

> 80 13.4 24 hrs 2-4 days

> 50 to 80 15.3 24 hrs 2-4 days

> 30 to 50 18.4 At least 2 days 4 days

30* 27.2 2-5 days > 5 days

NB: *Ongoing treatment with dabigatran should be reviewed as use in patients with a CrCl < 30ml/min is contra-indicated.

f) Bridging therapy with parenteral anticoagulation

i) Pre-operative bridging is not required in the majority of patients.

ii) Post-operative bridging

The onset of therapeutic anticoagulation after administration of

dabigatran is rapid (within 1-2 hrs)

Caution should be exercised in restarting within 48-72 hrs following

high bleeding risk procedures

Alternative parenteral prophylactic anticoagulation may be warranted

(eg subcutaneous enoxaparin) in the time period prior to resuming

dabigatran, depending on the procedure performed.

g) Epidural and other regional anaesthesia/analgesia and dabigatran

i) LP, spinal, epidural and some forms of major regional block should not be

performed within 24 hrs post-dabigatran, longer with renal dysfunction.

ii) Dabigatran should not be administered to patients with an epidural catheter

in-situ (and some regional analgesia catheters – discuss with anaesthetist).

iii) Dabigatran should be delayed 4 hrs following performance of an

epidural, spinal, LP, regional block or after catheter removal.

h) Emergency procedures

i) Surgery or invasive procedures should be delayed at least 12 hrs post-dose

ii) An urgent APTT +/- dabigatran level can be requested and bleeding risks

are small providing:

normal APTT or

dabigatran level < 50 ug/L.

iii) See guideline for management of bleeding in patients receiving dabigatran

for details regarding the treatment of surgical bleeding.

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Flowchart: Management of Bleeding Patient on Dabigatran

Moderate bleeding – reduction in Hb ≥ 20g/L, transfusion of ≥ 2 units of red cells

Severe bleeding – bleeding in critical area or organ (intraocular, intracranial, intraspinal, compartment

syndrome, retroperitoneal or pericardial), hypotension not responding to resuscitation.

* This is an off license use of rVIIa (NovoSeven) and the risk of thrombotic complications when rVIIa is

used for this indication is unclear. The use of rVIIa is supported by laboratory data however clinical

evidence supporting an improvement in clinical outcomes is still lacking.

Bleeding Patient on Dabigatran

Initiate Standard Resuscitation Procedures as Required

Urgent bloods:

FBC, APTT, PT, TT and dabigatran level* E, C&U, Creatinine

*2 x citrate tubes + time of last dose of dabigatran.

STOP DABIGATRAN THERAPY

Mild Bleeding

- Local haemostatic measures.

- Delay next dose of dabigatran or discontinue if felt appropriate by prescribing physician.

Moderate Bleeding

- Consult critical bleeding on-call haematologist via transfusion. (25430/25431)

- Consider oral charcoal administration if dabigatran ingestion < 2 hrs prior.

- Local haemostatic measures

o Mechanical compression

o Consider seeking an opinion regarding surgical intervention

- Maintain adequate hydration to aid drug clearance.

- Transfusion support

o Packed cell transfusion as indicated by Hb and ongoing bleeding

o Consider platelet transfusion if platelets < 70 x 109/L or if taking antiplatelet therapy.

o Consider 25U/kg prothrombinex if INR > 1.5.

o If ongoing bleeding resulting in clinical instability despite above measures consider

rVIIa* +/- dialysis as described as for severe bleeding.

Severe Bleeding

- Consult critical bleeding on-call

haematologist via transfusion.

(25430/25431)

- Consult ICU or if necessary other appropriate facility.

- Institute measures as for moderate to severe bleeding.

- Administer rVIIa 90 ug /kg

(rounded up to nearest mg), and

consider repeat dose at 30

minutes, if no response.*

- Consider dialysis particularly indicated if high drug level as indicated by excessively

prolonged aPTT > 80 secs or

dabigatran level > 200 ug/L and/or impaired renal function.

Consider dose of rVIIa immediately prior to vascular access if significantly prolonged aPTT.

4 hrs of haemodialysis will reduce

drug level by approx. 60%.

- Neither rVIIa nor dialysis is likely to improve outcome in patients with a normal aPTT or a dabigatran level of < 50 ug/L

133

11. Disseminated intravascular coagulation (DIC)

a) Definition

i) DIC occurs when the balance of the haemostatic and fibrinolytic systems

becomes disordered. It occurs in response to severe pathophysiological

stimuli and is a part of multisystem organ dysfunction (often associated

with ARDS and acute renal failure). It is characterised by:

Microthrombi formation causing microvascular obstruction

Consumption of platelets and clotting factors

Abnormal fibrinolysis

b) DIC screen:

i) Complete blood picture

microangiopathic haemolytic anaemia with red cell fragmentation

haemolysis

thrombocytopenia

ii) Extended coagulation screen:

prolongation of TCT, APTT, PT

hypofibrinogenaemia

low factor VIII

excess fibrinolysis with elevated FDPs

iii) Liver and renal function tests

c) Treatment

i) Treatment of the underlying cause

ii) Replacement of blood components in the bleeding patient

FFP - based on INR/APTT

cryoprecipitate - for marked fibrinogen deficiency

iii) Controversial therapies (following consultant approval only)

heparin, fibrinolytics (tPA)

anti-fibrinolytics (EACA)

11. Blood transfusion reaction protocol

a) Plasma can cause reactions ranging from mild pruritus, erythema and urticaria

through to severe flushing, hypotension, fever, angioedema, bronchospasm and

fulminant anaphylaxis.

b) Suspected Reaction Protocol

i) Stop the transfusion immediately – do not disconnect the IV line.

ii) Recheck the patient identification on the blood product pack label against

the patient’s wristband and verbally with the patient if possible.

iii) If there is an unexplained discrepancy, discontinue the transfusion and

treat as per (iv, v below)

iv) Mild Reactions

Temp. < 1.5º C

Mild or no hives or rash.

Action - slow the rate and continue transfusing the same unit of blood.

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v) Severe Reactions

Severe hives and/or a rash.

Temp. > 1.5°C and is the only clinical sign or symptom

Action

a. Consider an antihistamine and antipyretic

b. Cease and then restart transfusing the same unit of blood after

approximately 20 minutes.

If there are further signs & symptoms of a reaction

discontinue & order a transfusion reaction investigation

If there is a sudden and acute change in the patient’s condition, e.g.

cyanosis, bad headache, backache, or significant change in pulse or

blood pressure for no apparent clinical reason

discontinue & order a transfusion reaction investigation

vi) Investigation of a transfusion reaction:

A transfusion reaction investigation form (IMVS 224) should be

completed and sent to Transfusion Medical Unit (TMU) with:

a. A description of the relevant clinical findings and vital signs

b. A post-reaction 10ml EDTA blood specimen, preferably from a

vein other than that used for transfusion

c. Any used or unused blood packs and the attached IV set(s).

If there is a major reaction, it is also recommended that the first urine

specimen voided after reaction is saved, and patient’s urine output

over the next few hours is recorded.

Further blood samples for biochemical assays, coagulation tests, and

cultures will be needed.

Administration of incompatible blood constitutes a Sentinel Event.

vii) Haemovigilance

The IMVS and RAH are participating in the ‘Blood Safe’

haemovigilance scheme, an adverse incident reporting system aimed at

the quality and safety improvement of transfusion practices.

Contact the Transfusion Safety RN (Pager: 1575, Tel: 22975)

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Table: Blood Transfusion Reactions

Type Signs & Symptoms Treatment Prevention

Febrile non-haemolytic transfusion reaction (FNHTR)

Pyrexia (> 1°C rise) Rigors/chills Anxiety

Withhold transfusion. Mild fever without other symptoms may be treated by slowing infusion. An antipyretic may be helpful. Investigate as for suspected HTR if the reaction is significant.

Consider use of leucodepleted red cells or platelets if a recurrent problem.

Circulatory Overload Distended cervical veins. Pulmonary oedema Dyspnoea. Headache. Heaviness in limbs.

Discontinue. Institute treatment for fluid overload, e.g. diuretic

Give all fluids slowly to patients with compromised cardiac or renal status. Use red cell concentrates. If anticipated, give diuretic.

Allergic Flushing Urticaria, itchy hives Facial oedema

Slow rate of flow. Consider anti-histamine. Watch for laryngeal oedema and development of anaphylaxis.

When anticipated, use prophylactic antihistamines.

Anaphylaxis Dyspnoea from laryngeal oedema or bronchospasm, sometimes cyanosis and collapse

Discontinue transfusion immediately. Institute treatment for anaphylaxis, e.g. Adrenalin, steroids

Use of Medi-Alert wristband in proven IgA deficient patients.

Acute Haemolytic Transfusion Reaction (HTR)

Pyrexia Rigors/chills Lumbar pain Pain along vein Jaundice Haemoglobinuria Oliguria – later uraemia

Discontinue transfusion immediately. Get expert advice immediately. Save all used packs, blood samples. Save all urine. Collect fresh blood samples.

Extreme care in collecting the correct blood sample for T&S. Careful compatibility testing by laboratory. Careful method for storing & labelling blood. Careful identification of the correct recipient.

Infected blood Bacterial sepsis with hyperpyrexia Pain in limb & chest Headache Pallor Burning pain along vein Low blood pressure Rapid pulse Profound collapse & shock

Discontinue transfusion immediately. Acute medical emergency – get advice immediately. Save used packs, all blood samples, with labels. Save all urine. Anti-shock treatment and antibiotics.

Storage at correct temp. Do not remove from refrigerator until immediately before transfusion

Non-cardiogenic pulmonary oedema. Transfusion related acute lung injury (TRALI): rare

Dyspnoea ARDS picture within 6 hours after transfusion.

Maintain blood pressure & cardiac output with fluid support. May require ventilatory support.

Difficult, usually in the setting of multiparous blood donor with anti-recipient-WBC antibodies.

NB: See RAH Intranet, Transfusion Medicine (http://rahadm05v.had.sa.gov.au/)

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D. Guidelines for the Management of Electrolytes


a) Total body water (60% total body weight):

i) intracellular fluid : predominant ions : K+, PO42-

ii) extracellular fluid:

75% interstitial fluid: predominant ions : Na+, Cl-

25% plasma volume (PV)

b) Osmotic equilibrium is maintained by Na+/K+ pump

i) ECF ions therefore reflect total osmolality:

Calculated osmolality 2×Na+ + urea + glucose

ii) Magnesium is a cofactor for this pump

c) Most electrolyte disturbances in critically ill patients relate to changes in the

distribution and concentrations of the predominant ECF and ICF ions.

d) As a general rule, changes in one ion will be reflected in the associated cation or

anion.

e) Electrolyte disturbances should be considered in terms of the following groups:

i) Erroneous results

Lab error

Bloods taken from a drip arm

Haemolysed specimen - traumatic (old IA lines), delayed samples

Osmolar agents

ii) Decreased or increased losses: usually

Renal

Extra renal: GIT, skin losses

iii) Transcellular shifts.

iv) Decreased or increased intake

f) Treatment should be directed at the underlying cause.

g) Rapid correction of electrolyte disturbances may be deleterious.

h) One electrolyte disturbance may be predictive of another electrolyte disturbance

e.g. K+ often associated with Mg+

i) The following paragraphs outline the common electrolyte disturbances.

137

2. Hyponatraemia: Na+ < 130 mmol/l

a) Aetiology / classification

i) Misleading result

Isotonic - Hyperlipidaemia

- Hyperproteinaemia

Hypertonic - Hyperglcaemia

- Mannitol, glycerol, glycine or sorbitol excess

ii) Water Retention

Renal Failure

Hepatic Failure

Cardiac Failure

SIADH

Drugs

Psychogenic polydipsia

iii) Water retention / Salt depletion

Post-operative, post-trauma

Patients with excess fluid losses given inappropriate replacement

Cerebral salt-wasting syndrome

Adrenocortical failure

Diuretic excess

b) Diagnosis & Management:

i) Factitious: ignore and manage underlying condition then recheck Na+

ii) Misleading:

Hyperglycaemia: BGL 10 mmol/l [Na+] 3 mmol/l

a. Hyponatraemia per se is real, but treatment is directed at the

underlying cause, where correction of the hyperglycaemia will

correct the plasma [Na+]

b. NB: Total body Na+ deficit may co-exist with diuresis in DKA

Mannitol:

a. [Na+] early, then diuresis & late [Na+] are more problematic

b. Maintain adequate plasma volume with N.saline initially

Alcohols: permeate solutes, [Na+] less problematic

iii) Hypovolaemic states:

Restore volume with colloid or normal saline according to clinical

markers: urine output, plasma [Na+], RAP

Aim for slow Na+ correction: 2 mmol/l/hr, unless seizures.

Urine Na+ is uninterpretable after diuretics or catecholamines for 24hrs

138

iv) Hypervolaemic states: *most common clinically

Fluid restriction < 15 ml/kg/day

a. “Water Excess” ~ (140 - Na+ )/140 × (Wt × 0.6)

e.g., 70kg patient with plasma [Na+] = 120 mmol/l:

= (140 - 120)/140 × (70kg × 0.6)

= 6 litres

b. Will slowly correct excess - ADH group & “reset osmostat”

c. Treat the underlying cause - CCF, nephrotic synd., ascites

v) SIADH

Causes

a. Ectopic ADH production by tumours

e.g. small cell bronchogenic tumour

b. CNS disorders

e.g. tumour, abscess, trauma, SAH etc

c. Pulmonary diseases

e.g. TB, pneumonia, abscess etc

Diagnosis

a. Hypo-osmolar hyponatraemia

b. Urine osmo > plasma osmo

c. Urine Na+ > 40 mosm/l

d. Normal endocrine, renal, hepatic, cardiac function

e. No diuretics or drugs affecting ADH secretion

f. Corrected by water restriction alone

Management: fluid restriction

vi) Severe Symptomatic Hyponatraemia : fitting, or decreased consciousness

Resuscitation / ABC

Consider anticonvulsants - phenytoin, benzodiazepines

Hypertonic saline (3%) may be indicated

a. Always discuss use with the Duty Consultant

b. Correct [Na+] rapidly only to ~ 120mmol/l

Thereafter, slow correction with N.saline over 24-36hrs ( 2 mmol/l/hr)

Treat the underlying cause.

3. Hypernatraemia: Na+ > 145 mmol/l

a) Hypernatraemia is always a hyperosmolar state

b) Most body fluids have a [Na+

] < plasma net water loss

c) Aetiology / classification:

i) Water depletion / inadequate replacement

Renal

a. Diuretics, glycosuria

b. ARF/CRF, partial obstruction

c. Central diabetes insipidus

i. Post traumatic head injury or surgery

ii. CNS infection, tumour, granulomatous disease, GBS

139

d. Nephrogenic diabetes insipidus:

i. 1° : congenital renal resistance to ADH

ii. 2° : hypokalaemia, hypercalcaemia, lithium, multiple

myeloma, sickle cell anaemia, nephrocalcinosis, amyloid

GIT losses - diarrhoea, vomiting, fistulae, SBO

Respiratory - IPPV with dry gases

Skin losses

a. Fever, high ambient temperature

b. Vasodilatory states

c. Exfoliative skin disorders, burns

d. Thyrotoxicosis

Unconsciousness

“Reset osmostat”

ii) Salt gain - Na+ gain > H2O gain

Iatrogenic

a. Most common cause

b. Excess “normal saline” ~ 150 mmol/l [Na+]

c. NaHCO3, feeding formulae, TPN

Mineralocorticoid excess:

a. Conn's, Cushing's syndromes

b. Steroid excess

d) Management

i) Hypovolaemic states

Restore volume according to clinical markers:

BP, HR, urine output, RAP

a. Hartmann’s solution - slightly hypo-osmolar

b. Colloid: initial resuscitation, severe hypovolaemic states

ii) Slow Na+ correction: 2 mmol/l/hr

Water deficit: ~ (Na+ - 140)/140 × (B.Wt × 0.6)

e.g. 70 kg patient, with plasma [Na+] = 160 mmol/l

~ (160-140)/140 × (70 × 0.6)

~ 6.0 litres

1 litre water replacement will reduce [Na+] ~ 3-4 mmol/l

In addition to basal fluid requirements & ongoing losses

Replace over a 24-48 hr period with 5% dextrose

Monitor [Na+] regularly

Manage aetiological causes

Cease causal drugs and inappropriate IVT

DDAVP for central DI only ~ 1-2 µg s.c.

140

4. Hypokalaemia: K+ < 3.0 mmol/l plasma

K+ < 3.5 mmol/l serum

a) Aetiology / classification:

i) Compartmental / transcellular shift

Alkalaemia pH ~ 0.1 [K+]pl ~ 0.5 mmol/l

Catecholamines / salbutamol

Insulin / anabolism - refeeding effect

Hypomagnesaemia - ICF K+ depletion

Toxic / poisoning - barium, toluene

Familial periodic paralysis

Hypothermia

ii) Reduced intake - urine [K+] < 20 mmol/L

Starvation

TPN

iii) Increased clearance/losses

Renal - urine [K+] > 20 mmol/L

a. Diuretics distal tubular flow

i. Loop agents - frusemide, bumetanide

ii. PT agents - acetazolamide, mannitol

iii. Early DT - thiazides

b. Steroids / Mineralocorticoid excess

i. Conn’s, Cushing’s, Bartter’s syndrome

ii. Ectopic ACTH - Small cell Ca lung

- Pancreatic, thymus carcinoma

iii. Exogenous steroids

c. Drugs

i. Anionic drugs - antibiotics (penicillins, amphotericin)

ii. High dose gentamicin

iii. Lithium

d. Hypomagnesaemia, Hypocalcaemia

e. RTA I, II

GIT losses

a. Villous adenoma

b. Ureterosigmoidostomy

c. Fistulae, malabsorption syndromes

d. Diarrhoea, Laxatives

Skin losses

b) Management:

i) Treat underlying cause

ii) Correct hypovolaemia: volume contraction will potentiate both alkalosis

and hypokalaemia

iii) Always add Mg++

normomagnesaemia is essential for correction of hypokalaemia

iv) Look for and treat concurrent hypophosphataemia

141

v) Potassium preparations

KCl: 10 ml = 10 mmol/l

KH2PO4: 10 ml = 10 mmol/l

K-acetate: 5 ml at 5 mmol/ml

25 mmol K+ + 25 mmol acetate (bicarbonate)

5. Hyperkalaemia: K+ > 5.0 mmol/l serum

K+ > 4.5 mmol/l plasma

a) Aetiology / classification:

i) Artefactual

Drip arm specimen

Tourniquet / Haemolysed specimen (extravascular)

Thrombocytosis > 750,000

Leukocytosis > 50,000

ii) Compartmental / transcellular shift

Acidosis pH ~ 0.1 [K+] ~ 0.5 mmol/l

Insulin deficiency: DKA

NB: normo- or hypo-kalaemia in the presence of severe DKA is

associated with a marked total body K+ deficit, which must be

addressed prior to correction of the acidaemia.

Familial periodic paralysis

Suxamethonium

Digoxin, -blocker overdose

Fluoride poisoning

ECF tonicity

a. Water moves from cells → [K+]ICF and passive diffusion

b. Seen with large doses of mannitol given rapidly (1.5-2.0 g/kg)

c. Hyperkalaemia of DKA is due to this in addition to the acidaemia

& insulin deficiency

iii) Cellular disruption / death

Tissue breakdown

Rhabdomyolysis, haemolysis (intravascular), ischaemia / reperfusion

Severe burns

Tumour lysis syndrome, leukaemia

iv) Increased intake - rarely a problem unless impaired renal function

Massive transfusion

Direct IV/oral

Drugs (penicillins)

142

v) Reduced clearance

Acute renal failure

a. Any cause for distal tubular flow, or distal NaCl delivery

b. Hypoaldosteronism

i. Mineralocorticoid deficiency, Addison’s

ii. K+ is multifactorial - K+ICF K+

ECF

- distal tubular flow

- DT aldosterone effect

Type IV RTA

ACE Inhibitors

Potassium sparing diuretics

a. aldosterone antagonists - spironolactone

b. distal Na+ channel inhibitors - amiloride, triamterene

b) Management:

i) The clinical scenario will dictate treatment

ii) Acute K+ > 6.0 mmol/l is a medical emergency

iii) Associated with acute ECG changes, or haemodynamic compromise:

In following order (not mixed together),

CaCl2 10 ml IV stat

NaHCO3 50-100 ml IV stat

Glucose 50% 50g + Insulin 20 units

Salbutamol nebs continuously

iv) Refractory or persistent:

CVVHDF

intermittent dialysis

v) Chronic K+ or slow rate of rise or no ECG changes:

Resonium 30g oral / PR 8 hourly

vi) Address aetiological factors

vii) Normalise renal function / volume status

6. Acid base disturbances

a) Acid base disturbances in ICU are frequently mixed disorders

b) Correction of these should be directed at the underlying cause and maintenance

of cardiopulmonary homeostasis.

c) Primary correction of an acid base disturbance with acid or alkali is seldom

required.

143

7. “Rules of thumb” *these are approximations only

a) Primary metabolic disturbances: last 2 digits of pH will reflect PaCO2

i) Met Acid to min 7.10 e.g. pH 7.25 PaCO2 25 mmHg

ii) Met alkalosis to max 7.60 e.g. pH 7.57 PaCO2 57 mmHg

b) Primary respiratory acidosis:

i) HCO3 ~ 1mmol/l per 10mmHg PaCO2 above 40 to max 30

c) Primary respiratory alkalosis

i) HCO3 ~ 2.5mmol/l per 10mmHg PaCO2 below 40 to min 18

d) Chronic respiratory acidosis

i) HCO3 ~ 4mmol/l per 10mmHg PaCO2 above 40 to max 36

8. Metabolic acidosis

a) Assessment of metabolic acidosis must include the anion gap:

Anion Gap = [Na+ + K

+] - [Cl

- + HCO3

-] ~ 12-17 mmol/l

Unmeasured cations Unmeasured anions

Mg++ ~ 1.2 mmol/l Albumin ~ 15 mEq/l

Ca++ ~ 2.2 mmol/l H2PO4- ~ 2 mmol/l

IgG Small HSO4- ~ 1 mmol/l

Organic ~ 5 mEq/l

~ 7.0 mEq/l ~ 23 mEq/l

b) This allows sub-classification of metabolic acidosis into raised or normal anion

gap acidoses.

i) Beware a low [Alb] in critically ill lowering the measured AG

ii) Measurement of chloride in the lab is highly variable

iii) Assessment of the AG must be viewed within the clinical context.

c) Aetiology of raised anion gap:

i) Renal failure - H2PO4- , HSO4

- (rarely AG > 23)

ii) Lactic acidosis - types A&B

* normal AG does not exclude a lactic acidosis

iii) Ketoacids - -OH-butyrate, acetoacetate

- diabetes mellitus, starvation, alcohol

iv) Rhabdomyolysis - organic acids

v) Drugs / poisons:

Aspirin - salicylate, lactate, ketones

Paracetamol - lactate, pyroglutamate

Ethanol - acetoacetate, lactate

Methanol - formate (formaldehyde), lactate

Paraldehyde - formate, acetate, lactate, pyruvate

Ethylene glycol - oxalate

Xylitol, Sorbitol - lactate

Fructose - lactate

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Table: Classification of Lactic Acidosis

Type A Type B Drug induced Hereditary

Severe exercise Seizures Cardiac arrest Shock Hypoxia Anaemia

Thiamine deficiency Diabetes Hepatic failure Renal failure Infection Leukaemia, lymphoma Pancreatitis Short bowel syndrome

Phenformin Metformin Ethanol Methanol Salicylates IV fructose Xylitol Sorbitol

G6PD deficiency Fructose-1,6-DP-deficiency

d) Aetiology of low or normal anion gap:

i) Hyperchloraemic metabolic acidosis

Resolving renal failure

Resolving DKA

Renal tubular acidosis / carbonic anhydrase inhibitors

Mineralocorticoid deficiency

Pancreatic, enteric fistulae

Ureterosigmoidostomy

IV HCl, NH4Cl, Arginine

ii) Metabolic alkalosis due to HCO3- gain

iii) Hypoalbuminaemia

iv) Myeloma - IgG has positive charge, 's AG

v) Increased Mg++ or Ca++ (rarely)

vi) Artefactually elevated Cl-

vii) ? Hyperlipidaemia

e) Management

i) High anion gap

Treat the underlying cause

No indication for NaHCO3

ii) Normal anion gap

Treat the underlying cause.

Replace HCO3 serum level and losses

a. Approx. deficit = (24 - [HCO3]) × (Wt. × 0.6) mmol/l

e.g. for a 70kg patient with a [HCO3] = 4 mmol/l

deficit = (24 - 4) × (70 × 0.6)

= 840 mmol (= ml of standard bicarb solution)

b. Replace 1/3-1/2 of this amount then remeasure blood gases.

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9. Metabolic alkalosis a) Aetiology / classification

i) Common causes:

Diuretics

Vomiting

Post-hypercapnia > 48 hours

Commonly associated with hypovolaemia and/or hypokalaemia

however, actual causation by these is debated

ii) Increased proton losses: acid loss is either renal or GIT

Renal

a. Na+ reabsorption (hypovolaemia, dehydration, etc.)

b. Cushing's syndrome, exogenous steroids

c. Hyperaldosteronism 1° / 2°

d. Bartter's syndrome (JGA hyperplasia)

e. Liddle's syndrome

f. Hypercalcaemia / hypomagnesaemia nephrogenic DI

g. Drugs: steroids, diuretics, carbenoxolone

GIT

a. N/G suctioning, protracted vomiting

b. Diarrhoea

iii) Increased bases

Administration of NaHCO3

Metabolism of exogenous acid anions - citrate, lactate, acetate

Milk/alkali syndrome

Renal conservation of HCO3- - acidosis, hypercarbia

iv) Factors tending to maintain an alkalosis

Any fluid loss replaced with insufficient Na+ ↑ H+ excretion

(contraction alkalosis)

Hypovolaemia

Hypokalaemia, hypochloraemia, hypomagnesaemia

Chronic hypercapnia

Mild chronic renal failure

b) Management

i) Correct hypovolaemia

*normal ECF volume is essential for the correction of alkalosis

ii) Inotropic support of cardiac output and GFR

iii) Correct K+, Mg++, HPO4=

iv) Consider acetazolamide if the alkalosis is persistent - provided the above

are corrected.

146

10. Respiratory acidosis

a) Aetiology

i) Any cause of hypoventilation respiratory failure (see diag.)

A. Respiratory centre / CNS

B. Upper motor neuron / spinal cord

C. Anterior horn cell

D. Lower motor neuron

E. Neuro-muscular junction

F. Respiratory muscles

G. Elasticity/compliance of lungs/chest wall

H. Structural integrity of chest wall & pleural cavity

I. Increased airways resistance – intra/extrathoracic

ii) May be acute or chronic

b) Management

i) Restore ventilation / manage underlying cause(s)

ii) No indication for HCO3

2. Respiratory alkalosis

b) Aetiology

i) Early hypoxia, shock or hypotension

ii) Anxiety, hysteria, neurogenic hyperventilation

iii) PTE

iv) Hepatic failure

v) Prescribed hyperventilation (rarely indicated)

c) Management

i) Treat underlying cause

ii) Neurogenic hyperventilation is a marker of severity of head injury

147

PART 5 - CLINICAL MANAGEMENT

The following protocols are designed to facilitate clinical management of patients in the

Intensive Care.

These protocols may vary from other ICUs and do not represent the sole approach to

patient management. However, they do represent a standardised approach which has

evolved in this ICU over the years.

Each clinical scenario is managed according to the particular situation and individual

patient - it is neither practical nor appropriate to apply rigid policies to clinical

situations. However, as clinical medicine is at times more art than a science, these

protocols are designed to assist in areas that are unfamiliar and to standardise

approaches by all staff members of the Unit.

The following protocols are outlined.

A. Cardiopulmonary resuscitation

B. Failed intubation drill

C. Respiratory therapy

D. Management of cardiothoracic patients

E. Renal failure

F. Neurosurgical protocols

G. Microbiology protocols

H. Drug overdose

I. Bites and Envenomation

J. Withdrawal of therapy

K. Organ donation and brain death

148

A. Cardiopulmonary Resuscitation

Flowchart: Basic Life Support

149

Flowchart: Advanced Life Support

150

Flowchart: Paediatric Cardiorespiratory Arrest

151

Induced Hypothermia Post Cardiac Arrest

1. Aim: To improve CNS outcome by actively cooling to a TCore 32-34°C

2. Inclusion Criteria

a) Non-traumatic cardiac arrest with return of spontaneous circulation

a) Unconscious, intubated and ventilated

b) Absence of an immediately correctable cause for coma

c) TC > 34.5°C

4. Exclusion Criteria

a) Cardiac arrest related to trauma or intracranial injury

b) Ongoing CPR and/or persistent cardiovascular instability

c) Cardiology consultation need for acute intervention

d) Criteria that preclude 40mls/kg of cold Hartmann’s solution,

e.g. acute pulmonary oedema, TC < 34.5°C

e) Time from cardiac arrest to ED > 12 hrs

f) Pregnancy – relative C/I

5. Procedure - Initial Treatment Protocol

a) ECG and routine blood tests as indicated

b) Record core temperature (TC): rectal, oesophageal or bladder catheter

c) Ensure adequate IV access (1x 16G)

d) Document neurological function, specifically:

i) Pupillary responses to light

ii) Response to painful stimuli (all limbs), vocalization

iii) Reflexes – gag, conjunctival, lash, tendon & plantar

e) Hartmann’s (Temp. 4°C) / Bolus 40mls/kg. / Infuse @ 100ml/min.

f) Maintain MAP 80-100mmHg (relative to premorbid BP)

g) Maintain K+ 4-5mmol/L and Mg++ 0.8-1.2mmol/L

h) If TC > 35°C after 1 hour, add surface cooling (cooling blanket / packs)

i) If patient is shivering and/or goal TC not achieved:

i) Midazolam (0.05mg/kg bolus, repeat every 5 min as required)

ii) Midazolam (1-5mg/hr) or Propofol infusion as clinically indicated.

iii) If sedation ineffective, consider a non-depolarizing muscle relaxant

6. Observations

a) Maintain TC 32-34°C for 12-24 hrs from the time of achieving goal temp.

b) To increase temp. (T < 31.5°C), use heated air blanket until 33°C

c) To decrease temp. (T > 34.5°C), use cold packs, cooling blanket, sedation and

then consider using non-depolarizing muscle relaxants

7. Complications

a) Arrythmia

b) Reduced cardiac index / increased peripheral resistance.

c) Ongoing cardiac instability may necessitate stopping the hypothermia protocol.

d) Hyperglycaemia

8. Aftercare

a) At 24 hrs cease all active cooling and allow passive rewarming.

b) If temp increases < 1°C per 4 hours then rewarm actively to temp > 36°C

c) Once TC > 35°C, cease sedation and muscle relaxants

152

B. Failed Intubation Drill

1. Following rapid sequence induction in ICU we are generally committed to securing

the airway by some means. Allowing the patient to wake-up in the event of a failed

intubation is rarely practical.

2. Risk of failed intubation in ICU is higher than in the operating theatre.

3. Before intubating, you MUST have a contingency plan for a difficult airway/failed

intubation.

4. After hours, remember the anaesthesic staff may be available to assist.

5. Ensure all equipment is working and that the ETCO2 monitor provides a reliable

waveform.

6. Ensure adequate IV access with running intravenous fluids.

7. Ensure ready access to vasopressors and resuscitation drugs.

8. Always have the difficult intubation trolley at hand.

9. Visually confirm that each individual piece of airway equipment is immediately

available and operational.

10. ICU patients have limited O2 reserves and desaturate quickly.

a) If initial intubation attempts fail, or the patient desaturates significantly, ensure

you can manually ventilate the patient.

b) Failure to achieve manual ventilation is an absolute emergency

“can’t intubate + can’t ventilate”

11. If an intubation technique fails, move on quickly to an alternative.

12. There are a range of airway devices available to help secure the airway.

a) Guedel airway / Nasopharyngeal airway

b) Bougie

c) C-Mac

d) Laryngeal Mask / Intubating Laryngeal Mask

e) Cricothyroidotomy

f) Jet insufflation

g) Bronchoscopy (for anticipated difficult intubations)

13. You must be familiar with the devices you plan to use in the case of a failed

intubation.

14. Airway equipment and intubating manikins are available for practice in the

registrar’s room.

153

Flowchart: Failed Intubation Drill

Oxygenate/ventilate

Committed to

Intubation

Best Attempt

Laryngoscopy

ILMA +/-

Bronchoscope

Failure to

Ventilate

Crico-

Thyroidotomy

FURTHER

ATTEMPTS USING

ADVANCED DEVICE

McCoy / Flextip

C-MAC

Airtraq

Intubate

Intubate

Call for help

No CALL

EMERGENCY

Failure or

SpO2 < 88%

Yes

154

C. Respiratory Therapy

1. Respiratory Failure

a) Definition = failure of efficient gaseous exchange and/or effective ventilation.

i) Type 1 Respiratory Failure

Hypoxaemia, PaO2:FiO2 < 300 mmHg

i.e. failure to oxygenate

ii) Type 2 Respiratory Failure

Hypercapnoea, PaCO2 > 50 mmHg, with a pH < 7.35

i.e. failure to ventilate

2. Oxygen Delivery Capacity

Table: Oxygen Delivery Devices

Apparatus/Device Oxygen Flow (l/min) Approx. FIO2 (%)

Nasal catheters 2 - 6 25-40%

Semi - rigid masks (e.g. Hudson, CIG)

5 6 8 10 12

35 50 55 60 65

Venturi type mask (e.g. Ventimask, Accurox)

2 - 8 24 - 50

Nasal High Flow (humidified circuit)

30-50 l/min 21 - 95

Reservoir plastic masks (Non-rebreathing mask)

6 - 15 FiO2 = 21% + 4% per l/min

Closed Circuits e.g. IPPV, NIV

Variable 21 - 100

Oxylog 1000 and 2000 Oxylog 3000

Variable

Variable

Airmix : 60 No airmix : 100

40 - 100

a) The FiO2 delivered to the patient by an “open circuit” will depend on the

patient’s peak inspiratory flow rate (PIFR).

b) The higher the PIFR, the higher the O2 flow required to provide a given FiO2.

155

3. Humidification

a) All ventilated patients must have adequate humidification of inspired gases for

optimal mucociliary function and conservation of temperature.

b) Optimal humidification requires:

i) Delivery of gas to the trachea at a constant temperature (32-36ºC).

ii) Relative humidity 75-100%.

iii) No increase in circuit resistance.

iv) No increase in circuit dead space.

v) Applicable to spontaneous and controlled ventilation.

vi) Sterile inspired gas

c) Types of humidifiers available

i) Heat/moisture exchangers (HME)

First line humidification.

Effective for most patients.

Incorporates a bacterial and viral filter.

Cannot be used with nebulised drugs.

Secretions increase resistance and reduce HME efficacy. Change to

wet circuit (FP) in patients with bronchorrhoea or mucous inspissation.

Single use & change every 48 hrs, or as required.

ii) Fisher Paykel (FP) evaporative humidifier (wet circuit)

Bronchorrhoea or mucous inspissation.

Hypothermic or heat-loss susceptible patients (e.g. burns).

Ventilation anticipated for more than 48 hrs.

Set chamber to 40°C.

iii) Inspiron (aerosolised T-piece).

Relatively inefficient humidification.

Allows variable FiO2 : 0.21-0.7

4. Nasal High-Flow Oxygen

a) NHF delivers high gas flows through a unique Optiflow™ nasal cannula.

b) Critical to NHF is the delivery of optimal humidity to allow delivery of high

flows directly into the nares.

c) This provides greater patient comfort while optimising mucociliary clearance.

d) Main benefits of NHF:

i) Delivery of up to 100% oxygen.

Actual FiO2 will depend upon the patient’s breathing pattern

ii) Anatomical dead space flushed.

iii) Positive airway pressure (2-5cmH2O) throughout the respiratory cycle.

iv) Improved mucociliary clearance.

156

Table: Oxygen Delivery Percentage - Nasal High Flow

O2% 30 LPM 40 LPM 50 LPM

O2 Air O2 Air O2 Air

30 4 26 5 35 6 44

40 7 23 10 30 12 38

50 11 19 15 25 18 32

60 15 15 20 20 25 25

70 19 11 25 15 32 18

80 22 8 30 10 38 12

90 26 4 35 5 44 6

100 30 0 40 0 50 0

5. Mechanical Ventilation

a) Mechanical ventilation is one of the mainstays of intensive care medicine.

b) There are 2 main types of mechanical ventilation:

i) Non-invasive ventilation.

ii) Invasive ventilation.

c) An understanding of the types of mechanical ventilation, indications,

complications, practical aspects of mechanical ventilators and their use in

respiratory failure is essential.

d) Registrars should familiarise themselves with the ventilators, understand the

default settings and common modes of ventilation.

e) All changes to ventilation orders must be recorded on the flowchart and

conveyed to the bedside nurse.

f) All ventilator alarms must be addressed immediately.

g) Any changes to alarm settings must be relayed to the bed-side nurse.

6. Non-Invasive Ventilation

a) Definition: Mechanical positive pressure respiratory support in the absence of

tracheal intubation (e.g. via a face mask, nasal mask, head piece/box)

b) Modes

i) Continuous positive airway pressure (CPAP)

ii) Bi-level positive airway pressure (BiPAP).

c) Indications

i) As an adjunct to weaning from ventilation (e.g. extubation to NIV).

ii) Acute exacerbation of COAD.

iii) Cardiogenic pulmonary oedema.

iv) Obstructive sleep apnoea / obesity hypoventilation syndrome.

v) Post-extubation hypoxia due to pulmonary oedema or atelectasis.

vi) Febrile neutropaenia with pulmonary infiltrates.

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d) Prerequisites

i) Adequate glottic reflexes should be present to protect from aspiration -

moribund patients require intubation where appropriate.

ii) Patients receiving CPAP or BiPAP are generally managed in Units A&B.

iii) Selected patients may be managed in Unit C.

e) Complications

i) Inadequate ventilation.

ii) Mask leaks.

iii) Aerophagia, gastric distension, vomiting, aspiration.

iv) Claustrophobia and mask intolerance.

v) Pressure necrosis of nasal bridge.

vi) Dry secretions.

vii) Barotrauma.

viii) Reduced preload and hypotension.

ix) Raised intracranial and intraocular pressure.

7. Non-Invasive Ventilators

a) BiPAP® Vision

i) Microprocessor controlled.

ii) Nasal, face & full head masks can be used.

iii) IPAP = Inspiratory positive airway pressure.

iv) EPAP = Expiratory positive airway pressure (PEEP).

v) Pressure support = IPAP - EPA

vi) Monitors machine pressure against proximal airway (mask pressure) to

ensure effective delivery of pressure despite circuit leaks.

vii) Need to calibrate for tubing and mask.

viii) Uses internal algorithm for respiratory cycling and leak adjustment.

ix) Liquid crystal displays:

IPAP, EPAP, Rate, FiO2.

VT, Vmin, PIP, Insp. time/total cycle time.

Leak (patient & total), % patient triggered breaths.

Graphical display of pressure, volume & flow.

x) Operation:

Machine starts up in mode previously used.

Press [Mode] hard key to display CPAP or S/T mode

Press [Activate New Mode] soft key to select the new mode.

Select soft key parameters displayed & turn adjustment knob

accordingly.

CPAP Mode - Default settings

a. CPAP 5cmH2O, FiO2 1.0

S/T Mode - Default settings

a. IPAP 15cmH2O, EPAP 5cmH2O

b. FiO2 1.0, Rate 12, TInsp 1 sec, IPAP rise time 0.1 sec

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b) CPAP via Dräger EVITA®

i) Operation:

Select “Non-Invasive” Mode

Default settings:

a. Pressure support 10 cmH2O (above PEEP)

b. PEEP 5 cmH2O

c. Inspiratory time 4 sec

d. Trigger 5 L/min

Adjust Press Support and Rise Time to provide the assisted breaths.

8. Indications for Invasive Ventilation

a) Respiratory Failure.

b) Intubated for airway protection.

c) Severe metabolic disturbance with altered conscious state.

9. When to institute invasive ventilation

a) Clinical assessment is the most sensitive assessment of respiratory failure.

b) Do not delay the initiation of ventilatory support pending results, blood gases or

mechanical measurements in the following settings:

i) Threatened airway.

ii) Fatigue / exhaustion.

iii) Failure of secretion clearance.

iv) Overt respiratory failure.

v) Speech impairment due to dyspnoea.

vi) Reduced GCS in the absence of other causes.

c) Objective measurements are adjuncts to clinical assessment:

i) RR > 35 bpm

ii) VC < 15 ml/kg

iii) SpO2 < 90% on 15L O2

iv) PaCO2 > 60 mmHg (with pH < 7.2)

10. Modes of Ventilation in ICU

a) Synchronised intermittent mandatory ventilation (SIMV).

i) Default ventilation setting at RAH.

ii) Prescribed tidal volume.

iii) Airway pressure is variable.

b) Pressure control ventilation (PCV).

i) Prescribed peak pressure.

ii) Tidal volume is variable.

iii) High sedation requirements, occasional use of muscle relaxants.

c) Pressure Support Ventilation (PSV) + PEEP

i) Spontaneous ventilation mode for patients with adequate respiratory drive,

respiratory mechanics and strength.

ii) Commonly used when weaning from ventilation.

iii) Requires patient effort to initiate ventilatory assistance.

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11. Optimising Ventilation

a) Optimise oxygenation:

i) Use the lowest FiO2 to achieve an ‘adequate’ SpO2 or PaO2.

e.g. SpO2 > 95% and/or PaO2 > 80 mmHg.

ii) Lower values may be appropriate with chronic lung disease.

b) Optimise PaCO2:

i) Adjust relative to pre-morbid PaCO2.

ii) Consider permissive hypercapnia in patients with poor lung compliance.

c) Optimise patient-ventilator interface:

i) Reduce work of breathing through the ETT and ventilator circuit.

ii) Pressure support.

iii) Automatic Tube Compensation (ATC).

iv) Appropriate trigger threshold.

v) Adequate expiratory time.

vi) Prevent gas trapping: measurement and manipulation of auto-PEEP

vii) Patient positioning.

d) Optimise sedation and analgesia.

i) Review the need for sedation daily.

ii) Calculate the RASS score for each patient daily.

iii) Order depth of sedation on the ICU obs chart.

iv) Always assess suitability for ceasing sedation.

e) Minimise volutrauma (barotrauma)

12. Complications of Mechanical Ventilation

a) Haemodynamic.

i) Reduced preload.

ii) Increased RV afterload unmasked hypovolaemia.

b) Respiratory.

i) Ventilator Associated Pneumonia (VAP).

ii) Volutrauma / Barotrauma Ventilator associated lung injury.

iii) Patient ventilator dys-synchrony.

c) Metabolic.

i) Post-hypercapnoeic metabolic alkalosis.

ii) SIADH.

d) Raised intracranial and intraocular pressure.

e) Need for sedation

i) Reduced patient mobility DVT, pressure sores, weakness

ii) Reduced joint movement.

f) Local pressure effects from intubation, tracheostomy or face masks.

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13. Drager EVITA 2 Ventilator

a) The Evita 2 are the default ventilator at the RAH.

b) Modes: SIMV, PCV, Pressure Support, CPAP, APRV.

c) Non-invasive ventilation modes are also available.

d) Specific features:

i) Auto flow: automated adjusted inspiratory flow according to lung

mechanics during controlled ventilation.

ii) Rise time: manual adjustment in all modes.

iii) 100% O2 suction button: delivers 100% oxygen for 3 minutes.

iv) Programmable default parameters.

v) Flow and Pressure-Volume loops.

vi) Preset emergency and apnoea ventilation parameters.

vii) Automatic tube compensation to assist weaning.

viii) Automated respiratory mechanics:

Static and dynamic compliance.

Automated estimation of auto-PEEP and occlusion pressure (P0.1).

Inspiratory airway resistance.

Negative inspiratory pressure.

Vital capacity.

e) SIMV

i) Default settings: SIMV: 600×12, PS = 5 / PEEP = 5, FiO2 = 1.0

ii) Select mode: SIMV.

iii) FiO2 = 1.0

iv) VT = 0.6 L

v) Rate = 12 bpm

vi) PS = 5 cmH2O

vii) PEEP = 5 cmH2O

viii) Rise time = 0.2 secs

ix) Adjust TInsp I:E ratio 1:2 (default 1.7 secs)

x) “Extra settings” mode

Flow trigger = 5 l/min

Backup ventilation (CMV) : Off

f) PC (Pressure control)

i) Default settings PInsp = 30×12, PEEP = 5, FiO2 = 1.0, I:E=1:2

ii) Select mode: PCV+

iii) Select total inspired level of pressure (PInsp) = 30 cmH2O

iv) Rate = 12

v) Rise time = 0.2 secs

vi) PS = 5 cmH2O

vii) PEEP = 5 cmH2O

viii) FiO2 = 1.0

ix) Adjust TInsp I:E ratio 1:2 (default 1.7 secs)

x) Do not exceed total inspired pressure > 40 cmH2O

xi) Tidal volume is determined by respiratory compliance.

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g) Pressure Support (PS) + PEEP

i) Total inspiratory pressure, when using PS on the Evita, is the dialed value

plus dialled PEEP value

ii) Mode = CPAP

iii) Rise time = 0.2 secs

iv) PS = 10 cmH2O

v) PEEP = 5 cmH2O

vi) FiO2 = 1.0

h) I:E Ratio

i) Alteration of the I:E ratio is potentially hazardous and should only be done

following discussion with the duty consultant.

i) Measurement of auto-PEEP

i) Not accurate if patient effort, patients should be well sedated / paralysed.

ii) Measurement of intrinsic PEEP at end expiration + closed airway.

iii) Press the [Special Procedure] button & select [PEEPi].

iv) Press [Start] to begin the automatic 7sec manoeuvre.

v) Read off the PEEPi and trapped gas volume (VTrap)

vi) The value displayed includes applied PEEP, so:

vii) auto-PEEP = PEEPi - applied PEEP

j) Measurement of occlusion pressure (P0.1)

i) Measurement of the negative airway pressure generated in the first

100msec of inspiration against an occluded airway.

ii) Reflects diaphragmatic effort and neuromuscular drive.

iii) Normal value 3-4 mbar.

iv) Press [Special Procedure] button.

v) Select P0.1 and press [Start] to measure value.

k) Always examine the flow, pressure and volume vs time loops

i) Upper/lower airway obstruction.

ii) Recruitable lung.

iii) Increased airway resistance.

iv) Dynamic hyperinflation

e.g. flow does not return to baseline before the next breath

v) Sudden reversal of flow / pressure which does not trigger a breath may

indicate wasted patient effort.

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14. RAH – ARDS Ventilation

a) Initial Ventilator Set-up and Adjustments (Dräger)

i) Mode: SIMV + PS

ii) Resp. Rate: 18 bpm

iii) Insp. Flow Rate: Autoflow

iv) Tidal Volume: 6 ml/kg IBW

b) Tidal Volume Settings are determined by calculated Ideal Body Weight

i) Males = 0.91 × (height [cm] – 152.4) + 50

ii) Females = 0.91 × (height [cm] – 152.4) + 45.5

iii) Calculate IBW and VT = 6 x IBW

c) Adjust RR to achieve the pH goals according to ABG’s.

i) After any RR change, check the I:E ratio and TInsp.

ii) Target I:E Ratio 1:1 – 1:3

iii) Maintain TInsp 0.8 sec.

d) Adjust VT according to inspiratory plateau pressure (PPlat) goals.

i) Target PPlat < 30cmH2O

ii) Check PPlat with a 2 sec inspiratory pause every 4 hrs and after each change

in PEEP or VT.

iii) Method (Dräger): [Measurements] + press [Insp Hold] for 0.5sec

PPlat will appear on the screen for 1 sec.

iv) PPlat > 30cmH2O

VT by 1 ml/kg IBW steps (min VT = 4ml/kg IBW).

v) PPlat < 25cmH2O and VT < 6ml/kg IBW

VT by 1ml/kg IBW.

vi) NB: Observe spontaneous tidal volumes and adjust PS downwards if

volumes generated are higher than the calculated goal VT.

e) Adjust FiO2 & PEEP according to SpO2 and PaO2.

i) Goal PaO2 = 55-80mmHg

or SpO2 = 88-95%.

ii) Use the table (right) to adjust FiO2 / PEEP combinations

for the target PaO2 range required, e.g.

If FiO2 = 0.4 / PEEP = 5 and the PaO2 = 54,

PEEP to 8 cmH2O

If FiO2 = 0.9 / PEEP = 14 and the SpO2 = 99%

FiO2 to 0.8

f) Other therapies that may improve oxygenation.

i) Recruitment Manoeuvres

ii) Prone Ventilation

iii) Nitric Oxide / Nebulised prostacylcin.

iv) ECMO

None proven – see over.

FiO2 PEEP

0.3 5

0.4 5

0.4 8

0.5 8

0.5 10

0.6 10

0.7 10

0.7 12

0.7 14

0.8 14

0.9 14

0.9 16

1.0 16

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15. Recruitment Manoeuvres

a) Recruitment of under-ventilated alveoli may be achieved by prolonged

inspiration with higher inspiratory pressures and higher PEEP.

b) There are a variety of strategies employed.

c) These should only be performed following discussion with the consultant.

d) Contraindications to a LRM include the following:

i) Mean BP < 60mmHg despite fluids/vasopressors

ii) Active air leak through thoracostomy tube, i.e. broncho-pleural fistula

iii) Pneumatoceles, subpleural cysts, or pericardial or mediastinal emphysema

iv) Subcutaneous emphysema not related to trauma, surgical or ICU

procedures

e) Early termination of a LRM is mandatory if any of the following develop:

i) SpO2 < 85%

ii) HR < 60 or > 140

iii) New arrhythmia - except isolated supraventricular extrasystoles

iv) New air leak through thoracostomy tube

v) Fall in mean BP < 60 mmHg

16. Prone Ventilation.

a) May improve oxygenation

b) Has never been shown to improve ICU survival from ARDS

c) Risky and labour intensive intervention.

d) Should only be considered and undertaken under direct consultant supervision.

17. Nitric Oxide / Nebulised Prostacylcin.

a) Both can improve oxygenation but do not improve survival from ARDS

b) Nitric Oxide is not currently provided in ICU at RAH

c) Nebulized prostacylcin should only be commenced per the duty consultant.

18. Extra-Corporeal Membrane Oxygenation (ECMO)

a) ECMO can be used to provide either:

i) Oxygenation in cases of overwhelming respiratory failure (veno-venous

ECMO)

ii) Circulatory support in reversible cases of refractory overwhelming cardio-

respiratory failure (veno-arterial ECMO).

b) ECMO services commenced at the RAH in 2009, and continue to evolve.

c) Any cases for potential ECMO support will be discussed in detail prior to

initiation, and will be supervised closely by duty ICU consultant.

d) The ECMO circuit and equipment must not be altered without ICU consultant

and/or perfusionist supervision.

e) The policies, protocols and procedures for ECMO are contained in a manual

that is attached to the ECMO machine and available online.

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19. Weaning From Ventilation


i) No mode of weaning has been demonstrated to be superior to another.

ii) Short-term patients with acute resolution of respiratory failure (e.g. post-

operative, drug overdose, trauma) may be rapidly weaned and extubated.

iii) Long-term patients with multiple intercurrent problems take longer and

effectively “go at their own pace”.

iv) See – Flowchart: Ventilation Weaning Protocol (p50)

b) Clinically important determinants for weaning from ventilation

i) Resolution of the process requiring ventilation.

ii) No new CXR abnormality.

iii) Completion of therapeutic options that require ventilation

e.g. debridements, operations.

iv) Appropriate conscious state - cooperative patient.

v) Appropriate peripheral motor function.

vi) Adequate analgesia.

vii) Haemodynamic stability.

viii) Metabolic, acid-base stability.

c) Methods

i) Spontaneous effort is required for the patient to be weaned.

ii) SIMV with reducing RR and VT in conjunction with PSV and PEEP.

iii) Use PSV + PEEP alone once the patient’s spontaneous rate is sufficient to

prevent a respiratory acidosis.

iv) T-piece weaning: intermittent T-piece and positive pressure support.

v) Non-invasive bi-level ventilation.

d) “Objective” measurements

i) Adjuncts to the assessment of weaning success.

ii) Respiratory rate and tidal volume are the most sensitive:

Rate ( f ) < 30/min

VT > 5 ml/kg

f /VT < 100 (rapid shallow breathing index)

PaO2/FiO2 > 200 and PEEP < 10 cmH2O

PaCO2 < 60 mmHg

pH > 7.3

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20. Extubation Protocol

a) The duty consultant or SR must be involved in all decisions to extubate.

b) In case of urgent re-intubation, ensure equipment, monitoring and adequate

assistance is immediately available.

c) Extubation is preferentially done during daytime working hours and is a

medical responsibility.

d) Extubation criteria:

i) Return of adequate conscious state to maintain adequate protective

laryngeal reflexes and secretion clearance.

ii) Adequate pulmonary reserve.

iii) Adequate cuff leak if upper airway surgery or airway swelling.

iv) Ability to be re-intubated.

v) Resolution of reason why patient was intubated.

e) Beware of patients with inter-maxillary fixation and wiring.

i) Home team must be aware of planned extubation.

ii) Wire cutters must be present during extubation.

f) All patients must receive supplemental oxygen post extubation.

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D. Management of Cardiothoracic Patients

1. General Principles

a) The following guidelines apply to elective post-cardiac surgical patients.

b) These are only guidelines and each individual consultant will manage the

patients as is clinically indicated.

2. Respiratory:

a) Following surgery use the following default ventilator settings:

i) FIO2 =1.0

ii) SIMV 12 × 600, PS 10cmH2O, PEEP 5cmH2O.

b) After the first ABG, adjust the FIO2 to maintain a PaO2 > 80mmHg

c) Wean from ventilation according to past history, surgery performed and current

clinical status

d) Suggested extubation criteria:

i) Temperature > 36C

ii) Awake, able to obey commands

iii) Adequate analgesia

iv) Cardiovascular stability on minimal inotropes

(< 10µg/min noradrenaline or adrenaline)

v) Adequate gaseous exchange:

PaO2 > 80 mmHg on FIO2 0.5, PEEP 5cm

vi) Bleeding: drain losses < 100 ml/hr

e) Respiratory failure post-extubation secondary to collapse / consolidation is

common.

i) Ensure good analgesia and frequent, effective physiotherapy

ii) CPAP may be required in the first 48 hours.

f) Patients with poor LV function / recurrent acute pulmonary oedema are prone to

extubation failure and may benefit from the use of ACE inhibitors or inodilators

prior to extubation.

3. Post-operative bloods:

a) Check CBE, U&E, Mg, ACT, APPT, INR and ABGs on all patients.

b) Maintain [K+] > 4.0 mmol/l

4. Hypotension ± increasing inotrope requirements may occur for a variety of reasons:

a) Hypovolaemia

i) Return any remaining pump blood as soon as possible.

ii) Correct fluid/blood losses as appropriate

iii) Check ECG

b) Low cardiac output states

i) Noradrenaline is the first choice vasopressor.

ii) Low dose dobutamine (to improve regional blood flow to splanchnic/renal

vascular beds), may also be considered.

iii) Adrenaline can be used for severely impaired ventricles.

167

iv) If required vasoactive agent > 20µg/min and increasing, and the patient is

euvolaemic, consider:

Echo to exclude tamponade, AMI, papillary muscle rupture, or VSD.

PA catheter insertion or pulse contour CO measurement, e.g. Vigileo.

v) Consider pacing (either epicardial or transvenous) if hypotension is rate

related (HR < 60). A-V sequential pacing is the ideal mode (DDD)

vi) Consider IABP if hypotension persists despite inotropes.

vii) Consider milrinone or dobutamine for patients with predominantly

diastolic cardiac failure or pulmonary hypertension.

c) Tamponade

i) This is a medical emergency.

ii) If suspected, the cardiothoracic surgeon must be notified immediately.

iii) Diagnosis:

Refractory hypotension despite adequate volume replacement and

inotropic support

Cessation / reduction of blood coming from drains

Perform urgent CXR if time available. Globular heart shadow on CXR

and muffled heart sounds may be present but are unreliable signs

Diastolic equalisation of right-sided pressures on PA catheter insertion

Echocardiographic evidence of tamponade.

iv) Treatment

Support MAP with aggressive volume and inotropic support.

Ensure sufficient blood is cross-matched ( 6 units)

If stable, reopening in theatre is the preferred treatment

In emergency situations the chest may need to be opened in ICU.

d) Tension pneumothorax


ii) If a pleural drain is already present, quickly exclude obstruction/kinking.

iii) Otherwise, needle decompression followed by insertion of an underwater

seal drain.

e) Cardiac arrest


ii) The resuscitation guidelines are different from standard BLS/ALS.

iii) A major and important difference is that in patients who arrest following

cardiac surgery, chest compressions should only be commenced if the

sternotomy cannot be performed within 3 minutes.

iv) See guidelines below.

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Flowchart: Arrest Post Cardiac Surgery

5. Hypertension

a) MAP should be kept at approximately 70 mmHg for the first 24-36 hrs.

b) This may vary according to the patient’s pre-morbid BP.

c) Management:

i) Ensure adequate analgesia

ii) Nitroprusside or GTN: titrate to maintain MAP ~ 70 mmHg.

iii) If nitroprusside infusion > 40-50 ml/hr (2 µg/kg/min), consider:

Metoprolol: 1-2 mg IV, (if no contraindication)

Clonidine: 25-50 µg IV (up to 300µg/24 hrs)

Hydralazine: 10-20 mg IV

Captopril: 6.25-12.5mg 2 hourly PRN (up to 150mg/24 hrs)

Ventricular FibrillationVentricular Tachycardia

AsystoleProfound Bradycardia

HR < 30

Pulsless ElectricalActivity

DC shock(3 attempts)

+/- Amiodarone

Atropine 3 mg IVPace : Invasively (If Wires Present)

Noninvasively

If paced turn OFF to exclude Ventricular Fibrillation

- Internal Defibrillation- Internal Cardiac Massage

- Relieve Tamponade (If Present)

- Internal Cardiac Massage - Relieve Tamponade (If present)

- Internal Cardiac Massage - Relieve Tamponade (If present)

Resuscitation of a Patient Who Arrests Post Cardiac Surgery

Assess rhythm Hand ventilate (Administer FiO2 100% with Bag mask/ETT turn OFF PEEP. Auscultate chest to exclude tension pneumothorax)

Commence Advanced Life Support If an IABP in situ change to pressure trigger

No CPR or Precordial thump

Activate 4 Key Roles in Emergency ResternotomyCPR if Resternotomy expected to take longer than 3 minutes

Perform Resternotomy

Adapted From: Dunning J, et al. Guideline for resuscitation in cardiac arrest after cardiac surgery. European Journal of Cardiothoracic Surgery, 2009

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6. Management of Bleeding

Flowchart: Bleeding Post Cardiac Surgery

7. Sedation/Analgesia:

a) Propofol if required

b) Fentanyl IV boluses PRN while on ventilator

c) Morphine or fentanyl subcutaneously post-extubation

d) Paracetamol IV or po 4/24 PRN for first day then 6/24 if no contraindication

e) Oxycodone po 4/24 PRN in appropriate dose from second post-op day

Transfuse RC to maintain Hb > 80g/L

INR > 1.5 or APTT > 45 sec

give 3-4 units FFP

Fib < 1.0g/L

give 5 bags (apheresed) of cryoprecipitate

Platelet <100 x 109/L or prolonged by pass time

or pre-op clopidogrel

give 1 bag of platelet (pooled/apheresed)

Treat acidosis, hypocalcaemia, hypothermia

Resend CBP/coag screen

Discuss with haematologist or activate MTP

Consider DDAVP (0.3 mcg/kg) but must discuss with surgeon

Excessive bleeding post-op: > 200 mL/hr for 3-4 hrs, or > 1500 mL total loss Or, as per Surgeon’s advice

If ACT = 145-159s 25mg protamine once only

ACT > 160s 50mg protamine once only

IF Bleeding Continues +

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8. Anticoagulation / DVT prophylaxis:

a) Heparin 5000U s/c 8 hrly - all patients.

i) Start 6-12 hours post-op in the absence of excessive bleeding.

b) Aspirin 300mg daily - following coronary artery grafts.

i) Start at the same time as the heparin.

ii) Give via NG/OGT or S/L if the patient remains intubated.

c) Commence patients with mechanical valve replacements on warfarin (5mg

nocte) from the second post-operative day if extubated.

d) Discuss anticoagulation requirements for tissue valves with the surgeon.

e) Patients with a mitral valve replacement ventilated > 48hrs may require

heparinisation as will patients in AF for > 48hrs.

9. Antibiotic prophylaxis:

10. Other Drugs

a) Calcium Channel Blockers. Following radial artery grafts, diltiazem (30mg po

tds) may be required from first postoperative day. Discuss with surgeon.

b) Stress ulcer prophylaxis not routinely indicated unless the patient has pre-

existing peptic ulcer disease.

c) Insulin is managed as per the general ICU protocol.

11. Minimally Invasive Mitral Valve Repairs

a) These are performed through a right sided mini-thoracotomy with the patient

on femoro-femoral bypass

b) Patients may have a “pain buster” placed perioperatively for analgesia

c) Management is as for other cardiothoracic patients.

d) Clarify with surgeon if warfarin is to be given postop. This may vary with

exact type of repair, use of annuloplasty ring, heart rhythm etc.

Table: Antibiotic Prophylaxis for Cardiac Surgery

Cardiac Surgery - CABG

Non-allergic, or Type 3 Penicllin allergy –

delayed rash only

Cefazolin 2g IV + Gentamicin 240mg 30min pre-incision, then

Cefazolin 1g IV post-onset-bypass, then Cefazolin 1g IV 8 hourly for 24 hours Gentamicin 240mg day 1 post-op

(omit if CrCl < 60 ml/min)

Penicillin allergy – Type 1 Vancomycin 1g (1.5g > 80kg) + Gentamicin 240mg 30min pre-incision, then

Vancomycin 500mg, 6hrs post bypass Gentamicin 240mg day 1 post-op


Cardiac valve surgery Vancomycin 1g (1.5g > 80kg) + Gentamicin 240mg 30min pre-incision, then

Vancomycin 500mg, 6hrs post bypass Gentamicin 240mg day 1 post-op


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E. Renal Failure

1. Background

a) The mortality from acute renal failure remains high:

i) 8% in isolation

ii) ≤ 70% when associated with other organ or system failures.

b) Patients who die with acute renal failure, usually die from the underlying cause

rather than ARF itself.

c) There is a spectrum of renal dysfunction with variable definitions of what

constitutes “Renal Failure”.

d) Bellomo has proposed the following definitions:

Creat Creat Urea Urea UO / d

Normal 15-70 2-6 >800

Acute Renal Impairment > 120 > +60 > 8 > +4 <800

Acute Renal Failure > 240 > +120 > 12 > +8 <400

e) Approx. 30% of ICU patients have pre-existing renal impairment.

f) Patients at high risk of developing ARF are those with:

i) Pre-existing renal impairment (creatinine > 120).

ii) Severe sepsis

iii) Hypertension

iv) Diabetes

v) Arteriovascular disease

vi) Heart failure

vii) Large contrast media loads

g) The minimum urine output required to excrete the

obligatory solute load 0.5 ml/kg/hr.

h) ARF can be “oliguric” or “non-oliguric”.

i) Non-oliguric renal failure has a better prognosis.

j) Duration of ARF is variable and depends upon resolution of the underlying

injury, severity of the injury and pre-morbid renal function.

k) Consequences of ARF:

i) Fluid overload.

ii) Uraemia – encephalopathy, platelet dysfunction, pericardial effusions.

iii) Acidaemia.

iv) Electrolyte derangements – K+, PO4=, HCO3

-

v) Accumulation of pro-inflammatory cytokines (theoretical)

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2. Pathogenesis – ARF in critically ill patients is usually multifactorial.

a) Pre-Renal

i) The most common cause of renal failure in ICU.

ii) Aetiologies:

Low cardiac output states

Hypovolaemia.

Vasodilation - sepsis, vasodilators

Renal vasoconstriction - NSAIDs

Renal artery obstruction - stenosis, embolus, post-surgical

iii) Reduced renal blood flow

GFR and renal function

angiotensin-II and glomerular efferent arteriolar constriction

blood flow to the renal medulla

If maintained, then ischaemic renal injury occurs (e.g. ATN).

b) Renal

i) Acute Tubular Necrosis.

Ischaemic - see above

Nephrotoxic - drugs, contrast, myoglobin, sepsis

ii) Interstitial Nephritis - infections, drugs

iii) Vascular disease - renal vein occlusion, HUS, vasculitis

iv) Glomerulonephritis

c) Post-Renal

i) Obstruction of the renal collecting system leads to GFR.

ii) Must be considered in unexplained renal failure.

iii) Cannot be reliably ruled out clinically and hence requires imaging.

iv) Ensure a bladder catheter is inserted and draining freely.

v) Aetiologies:

Drugs - opiates, anticholinergics

Pelvic neoplasms.

Retroperitoneal collections (e.g. blood, pus, fibrosis).

Pregnancy.

Prostatic Obstruction

Renal calculi

d) Specific Renal Failure Syndromes i) Increased intra-abdominal pressure (IAP)

Effects at all levels - pre-renal, renal and post-renal

May consider decompression when IAP > 20 mmHg with ARF.

ii) Hepato-Renal Syndrome - predominantly pre-renal

albumin, vasodilatation, splanchnic shunting

diuretics for oedema, lactulose, diarrhoea, intra-abdo pressure

iii) Rhabdomyolysis - pre-renal, renal and post-renal

iv) Ineffective plasma volume

e.g. nephrotic syndrome, liver failure, cardiac failure.

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3. Renal Investigations

a) Blood tests

i) Creatinine

Logarithmic (inverse) relationship with GFR.

Can lose up to 60% renal function and maintain a “normal” creatinine.

Conversely in severe renal failure, a small decrease in renal function

can cause large rises in serum creatinine.

Lags behind the evolution of renal injury.

Insensitive where muscle mass is low – elderly, wasting diseases

ii) Creatinine clearance (ClCr)

ClCr slightly overestimates GFR due to tubular secretion

Estimated on IMVS biochemistry (eGFR) from single specimen

creatinine, thus has same inaccuracies as creatinine

Measured ClCr requires min 8 hour urine collection

iii) Urea

Less accurate indicator of GFR than creatinine

Modified by diet, catabolic state, GIT blood, liver disease

iv) Electrolytes - Na+, K+, HPO4=, ABGs.

v) GN screen - ESR, C3, C4, ANA, RhF, ANCA, anti-GBM.

vi) Haemolysis screen - RBC frags, LDH, haptoglobins, bilirubinaemia.

b) Urine

i) M, C&S - infection must always be excluded

ii) Myoglobin

iii) Urinary electrolytes

impossible to interpret with diuretic or natriuretic agents (CAs).

iv) Urinary sediment

Epithelial cell casts - ATN

RBC / WBC casts - GN

Eosinophils - interstitial nephritis

Crystals - oxalate (e.g. ethylene glycol)

- urate (e.g. tumour lysis)

c) Imaging

i) Ultrasound

Exclude urinary tract obstruction.

Doppler studies can assess renal artery and venous flows

ii) CT Renal Tract (non-contrast) – highlights renal stones and masses.

iii) IVP - rarely required given availability of U/S and CT.

iv) DMSA scan - a static radionuclide scan to reveal kidney structure.

v) MAG3 scan - a dynamic radionuclide scan

- renal function, collecting system obstruction, ATN.

d) Biopsy

i) Glomerulonephritis

ii) Interstitial nephritis

iii) Infiltration

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4. Renal protection

a) Established renal protection strategies

i) Fluid resuscitation to maintain circulating blood volume.

ii) Haemodynamic support of MAP and CO using inotropes

adrenaline, noradrenaline, dobutamine

iii) Exclusion of post-renal obstruction

check IDUC, renal tract U/S, nephrostomy

iv) Avoidance / close monitoring of nephrotoxic drugs

aminoglycosides, amphotericin

contrast agents

ACE inhibitors

NSAIDs

v) Prompt detection & treatment of urinary infection.

b) Unproven strategies for renal protection

i) N-acetyl cysteine

ii) Frusemide infusion / high dose

iii) Mannitol infusion / intermittent

iv) HCO3- for rhabdomyolysis.

v) Aminophylline infusion

vi) Calcium channel blockers

vii) Clonidine

c) Contrast Prophylaxis

i) Best evidence is to use HCO3-

ii) Add 150ml 8.4% NaHCO3 to 850ml 5% Dextrose.

iii) Run at 3ml/kg the hour prior to contrast administration,

then continue at 1ml/kg/hr for 6 hours

d) Low Dose Dopamine

i) May temporarily increase urine output

ii) Does not reduce the incidence of dialysis dependent renal failure or

mortality. (ANZICS CTG).

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5. Indications for renal replacement therapy

a) Symptomatic or refractory:

i) Acidosis

ii) Hyperkalaemia

iii) Fluid overload - e.g. pulmonary oedema

iv) Uraemia - urea > 35 mmol/l or symptomatic

b) Severe sepsis / developing oliguric renal failure

c) Diuretic resistant pulmonary oedema.

d) Drug removal (see Dialysis in Overdose)

e) The decision to commence RRT should be discussed with the duty consultant.

f) RRT is generally initiated early before serious complications develop.

g) The choice of RRT modality depends on patient’s type and severity of illness,

equipment availability and local expertise.

h) The renal unit should be notified “early” of patients who are potential long-term

dialysis candidates.

6. Renal Replacement Therapy Principles

a) Haemofiltration.

i) Convective solute and fluid removal down a hydrostatic pressure gradient

to form an ultrafiltrate (UF).

ii) Clears middle molecules (> 500D) and fluid.

iii) UF formation is dependent on the pressure gradient and membrane

characteristics (effective pore size & surface area).

iv) Predilution replacement of ultrafiltrate with balanced salt solution

increases the availability of urea for convective transfer by favouring its

movement from red cells.

b) Haemodialysis.

i) Diffusion of solute down a concentration gradient across a semi-permeable

membrane, running dialysate fluid counter-current to blood flow

ii) Clears urea, creatinine, electrolytes (i.e. small molecules).

iii) Solute clearance is adjusted by changing the dialysate fluid solute

concentration, blood and dialysate flow rates.

iv) Intermittent HD (IHD)

Utilised if the patient is stable and requires longer-term dialysis.

Takes 3-5 hours using higher blood flows of 300 ml/min

Fluid removal occurs quickly, not tolerated in unstable patients.

Performed by the Renal Unit.

v) Sustained Low Efficiency Dialysis (SLED)

Similar to standard IHD but occurs over 8-12 hours

Lower blood and dialysate flow rates.

Well tolerated by the critically ill.

Used in some ICUs (not the RAH) for nursing and cost reasons.

Although better tolerated than IHD in the critically ill, there is little

evidence to confirm equipoise with CVVHD/F in terms of outcomes.

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c) Continuous veno-venous haemodiafiltration (CVVHDF).

i) Standard form of continuous renal replacement therapy in this Unit.

ii) The combination of ultrafiltration and dialysis improves solute clearance.

iii) Advantages of CVVHDF over conventional intermittent haemodialysis:

Effective and more flexible control over fluid balance.

Greater cardiovascular stability.

Does not require attendance of Renal Unit staff.

May have a role in modification of the septic response.

Some trials suggest improved patient mortality (not proven).

Allows patients to receive continuous protein rich diet.

7. Complications of CVVHDF

a) Hypothermia.

b) Prolonged exposure to heparin: incidence of HITS, bleeding

c) Prolonged venous access: infection, thrombosis, vascular injury

d) Prolonged exposure to extracorporeal membrane: thrombocytopenia

e) Air embolism.

f) Increased nursing workload.

g) Electrolyte imbalance: hypomagnasemia, hypophosphataemia

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Diagram: CVVHDF Circuit

Heparin

UltrafiltrateReplacement

To Patient

DialysateSolution

Effluent

DeaerationChamber

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8. CVVHDF Equipment

a) Dialysis catheters

i) Priority of site placement and optimal catheter length:

R.IJ R.SC L.IJ L.SC Femoral

15cm 15cm 20cm 20cm 25cm

ii) Use Dolphin Protect® high flow catheter guided as above

iii) Heparin lock all catheter lumens 8 hourly when not in use

5000U in 3 mls, divided equally into both lumens.

b) Filters

i) Older filters were made from cellulose and would often initiate an

inflammatory response (i.e. “membrane reaction”).

ii) Membranes are now synthetic (polycarbonate, polyacrylonitrile)

iii) These are more permeable and biocompatible

iv) Standard filter = Prisma® AN69:

Membrane = acrylonitrile

Membrane thickness = 50m.

Surface area = 1m2 /1.5m2 (RT-150)

(larger filters 1.2–2m2 allow blood flow and clearance)

Blood volume in set = 150ml

c) Dialysis machine settings

i) The PrismaFlex® is the standard dialysis machine at the RAH

ii) Older “Prisma” machines are still in use but are being phased out.

d) For patients on ECMO

i) CVVHDF can be performed via the ECMO circuit without additional Vas-

Cath placement.

ii) Must be discussed with ICU consultant supervising ECMO

9. Prescribing CVVHDF

a) Orders for the PrismaFlex or Prisma® should be written on a standard sticker.

b) The following variables require assessment/prescription for CVVHDF.

c) Haemofiltration solution (“replacement”).

i) Standard solution = Gambro Phoxilium.

ii) Hemosol B-Zero will remain available when required for:

A [K+] < 4 mmol/l (e.g. severe hyperkalaemia), or

A phosphate free solution (e.g. tumour lysis syndrome)

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Table: Haemodialysis Solutions

Phoxilium Haemosol B-zero

Volume 5 L 5 L

HCO3- mmol/l 30 32

K+ mmol/l 4 -

Na+ mmol/l 140 140

Cl- mmol/l 115.9 109.5

HPO4= mmol/l 1.2 -

Mg++ mmol/l 0.6 0.5

Ca++ mmol/l 1.25 1.75

Lactate mmol/l - 3

iii) Flow rate 1000-2000 ml/hr (higher rates in catabolic patients)

iv) Ultrafiltration rate target 25 ml/kg/hr (averaged over 24hrs)

v) Standard is to deliver replacement pre-filter (termed pre-blood pump

fluid), but may be given post-filter if required (e.g: some toxidromes)

vi) When given pre-filter on the PrismaFlex®, still require at least 100ml/hr

replacement post-filter for the deaeration chamber to function properly.

d) Dialysis solution

i) Gambro® Phoxilium (or Hemosol B-zero if indicated)

ii) Rate = 500-2000 ml/hr (higher rates if marked electrolyte abnormalities)

e) Blood flow rate

i) On commencing CVVHDF, gradually increase blood flow as tolerated by

patient haemodynamics

ii) Target rate: 250ml/min *limited by machine/access pressures.

f) Anticoagulation

i) Blood passing through the filter activates the clotting cascade.

ii) Anticoagulation is often required to prolong “filter life”

iii) Circuit is primed with heparin 5,000U

iv) No ongoing anticoagulation is required for patients with coagulopathy

v) Systemic anticoagulation (if no contra-indications exist)

Heparin 5000 units stat, then continue at 500-1000 units/hr

Heparin is infused into the circuit pre-filter

Check APTT after 6 hrs and then daily if stable

End-point is “filter life” rather than a therapeutic APTT (i.e. if filter is

working and APTT < 45sec, there is no need to increase heparin dose)

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vi) Regional anticoagulation

Citrate (see citrate protocol)

Heparin

a. Utilised when:

Maintenance of filter life is problematic.

Systemic anticoagulation and citrate are contraindicated

No contraindication to heparin administration.

b. The circuit still needs to be primed with heparin

c. Heparin is administered pre-filter as above

d. Protamine 5-10 mg/hr post-filter

e. Check APTT 6 hourly after any dose changes.

vii) For patients with heparin induced thrombocytopenia (HIT) consider

Danaparoid or lepirudin (systemically, not into circuit – see protocol)

Prostacyclin 5 ng/kg/min (see protocol)

g) Fluid removal

i) Determine how much fluid should be removed from the patient.

ii) Consider its effects on patient haemodynamics

iii) The amount of fluid removed is the difference between the effluent and the

dialysate plus replacement fluid volumes

h) Potassium

i) Gambro® Phoxilium contains 4 mmol/l potassium and will not require

additional potassium

ii) Haemosol B-zero solution contains no potassium.

Supplementary K+:

a. Required for all patients, except in the initial management phase

of marked hyperkalaemia

b. Should to be added to both the replacement & dialysate bags

Plasma K+ < 4.0 mmol/l = 20 mmol / bag

Plasma K+ 4.1 – 4.8 mmol/l = 15 mmol / bag

Plasma K+ 4.9 - 5.5 mmol/l = 10 mmol / bag

Plasma K+ 5.5 – 6.0mmol/l = 5 mmol / bag

Plasma K+ > 6.0 = 0 mmol / bag

c. K-Acetate can be used in severe acidosis:

Acetate is effectively metabolised to HCO3- via the liver

Vial = 25mmol/5ml, dose = 3-4mls per 5L bag

iii) Target plasma [K+] = 3-4mmol/L

i) Drug prescription

i) Consult Antibiotic Guidelines / Pharmacy regarding antibiotic dosing

e.g. meropenem, ciprofloxacin, fluconazole

ii) Monitor drugs that are renally cleared and potentially toxic

e.g. gentamicin, vancomycin, digoxin

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10. Citrate Anticoagulation for Renal Replacement Therapy

a) Rationale:

i) Anticoagulation of the extracorporeal circuit improves life of dialysis

filters resulting in improved ‘dose’ of dialysis, less patient blood loss and

probable cost efficiency.

ii) When systemic anticoagulants are contraindicated it is possible to use

citrate to provide regional anticoagulation of the dialysis circuit without

altering patients coagulation

b) Indication:

i) CRRT is indicated

ii) Systemic anticoagulation is contraindicated and filter life is inadequate

c) Requirements

i) Appropriate high flow vascular access

ii) Gambro Prismaflex dialysis machine

iii) Gambro dialysis fluids

Dialysate: Prism0cal

PBP fluid: Prismocitrate 10/2

Post filter replacement: 0.9% saline

iv) Dedicated central access for calcium infusion

(not required if using Prismaflex software v6.1 – see below)

d) Process

i) Prior to priming the mode of anticoagulation is set to Citrate.

ii) The Prismaflex software will display the steps necessary to prime the

circuit

Pre-blood pump (PBP) fluid (coded white) is Prismocitrate 10/2

Dialysate (coded green) is Prism0cal, a zero calcium, zero potassium,

bicarbonate (32mmol/l) buffered dialysate.

Post filter replacement (coded purple) is normal saline, a 1 liter bag

can be hung on the central hook

iii) At completion of the priming process the Prismaflex displays:

Flow rates:

a. Reduce dialysate to 1000ml/hr

b. Reduce replacement to 100ml/hr

c. Confirm “post replacement” is set

The commencement citrate concentration should be set at 2.5mmol/l

(current default 3.0mmol/l)

Confirm final prescription and dialysis dose

iv) Commence calcium infusion and dialysis simultaneously

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v) Ionized calcium should be checked 30 min post-commencement, both

Post-filter (blue port)

a. Target ionized calcium: 0.3-0.5mmol/l

b. If > 0.5mmol/l [citrate] by 0.3-0.5mmol/l

c. If < 0.3mmol/l [citrate] by 0.3-0.5mmol/l

d. The usual citrate concentration range is 1.5-4.0mmol/l

Arterial

a. Target ionized calcium: 0.9-1.1 mmol/l.

b. Calcium replacement should be commenced with dialysis.

c. If [Ca2+] < 0.9 or there is a strong downward trend

commence infusion via CVC: CaCl 10% 4ml/hr.

d. After calcium is commenced arterial levels should be checked

hourly until stable.

e. Infusion rates should be adjusted by 1ml/hr until arterial calcium

is in the target range

f. If dialysis is ceased the calcium infusion should be stopped.

g. The Prismaflex will display an alert to this effect

(software v6.1 will automatically cease calcium infusion)

vi) Post-filter and arterial calcium should be monitored 2 hourly until stable

then checked 8 hourly

vii) With Prismaflex software v6.1 (due 2012)

Calcium replacement occurs via the ‘heparin syringe’ on the

Prismaflex using a Gambro algorithm.

Separate replacement is unlikely to be necessary.

Check Ca2+ via arterial analysis 8 hourly.

e) Complications

i) Hypocalcaemia:

Calcium is removed via:

a. Clearance of citrate:Ca2+ complexes during haemofiltration

b. Dialysis against calcium free dialysate

In the presence of citrate bound calcium fraction falls and may be as

low as 20%.

The systemic binding of calcium to citrate contributes to a small

degree, however this component reverts as citrate is metabolised.

Unless using Prismaflex software v6.1, separate replacement of

calcium via a CVC is recommended – see above.

ii) Hypercalcaemia:

May occur due to excess calcium replacement.

Corrected by monitoring and appropriate titration of CaCl.

iii) Acidosis:

Possible in advanced liver failure due to accumulation of citric acid.

Citrate anticoagulation is relatively contraindicated in liver disease.

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iv) Alkalosis:

Citrate enters the citric acid cycle and end products of metabolism are

CO2 and bicarbonate.

A small increase in bicarbonate and pH is expected over days.

Citrate overdose may result in metabolic alkalosis.

Estimated 40-70% of citrate is cleared via a high flux dialyser, hence

does not enter the systemic circulation.

Significant alkalosis requires a reduction in citrate dose or cessation of

citrate. This is uncommon.

v) Hypophosphataemia

Prolonged filter life and high pre-dilution flow rates may result in a

high dose of dialysis being delivered.

Associated with an increased risk of hypophosphataemia.

Phosphate should be checked twice daily and replaced appropriately.

Once stable daily monitoring is acceptable.

vi) Hypomagnasaemia

Mg2+ may be chelated by citrate and hypomagnasaemia is common.

Mg2+ should be checked twice daily (with phosphate) and replaced

appropriately

11. Dialysis in Overdose

a) Institution of dialysis for a life-threatening overdose is a consultant decision.

All cases are to be discussed with the ICU Consultant on call

b) There are a number of drugs effectively cleared by extracorporeal techniques

i) These agents are generally small, hydrophillic molecules with low protein

binding and volume of distribution

ii) The kinetics of many agents change in overdose (eg valproate) and

therefore discussion with the ICU Consultant and Toxicologist is required

iii) Common agents cleared by dialysis include:

Lithium

Toxic alcohols

Sodium Valproate

Carbamazepine

Atenolol / Sotalolol

Salicylates

iv) There are a number of other less common agents potentially amenable to

clearance via dialysis but requiring special consideration

eg. paraquat, procanamide, methotrexate, chloral hydrate

c) Institution of dialysis is more likely to be effective in the absorption phase when

a drug is concentrated in plasma than after distribution to tissue.

d) Standard ICU dialysis guidelines (ie. dialysis stickers) are designed for gradual

clearance of uraemic toxins and are not ideal for use in overdose

184

e) The aim of diafiltration in overdose is to optimize clearance by maximizing

extracorporeal blood flow, dialysate gradient and occasionally transmembrane

pressure gradient.

i) For this reason all patients should be treated with the Prismaflex,

not the older Prisma machines, with an ST-150 circuit

ii) An appropriate size femoral dialysis catheter should be inserted to allow

blood flow rates > 250ml/min (ideally 300ml/min)

f) Diafiltration of life threatening overdose should commence as follows:

Prismaflex – ST 150 Circuit

Mode CVVHDF

Blood Flow Rate *increase as tolerated 300 ml/min

Dialysate Phoxilium or Hemosol BO 4000 ml/hr

Pre-blood pump Replacement Phoxilium or Hemosol BO 100 ml/h

Post Filter Replacement Phoxilium or Hemosol BO 2000 ml/hr

Anticoagulation Heparin 500u/ml 1-2 ml/hr

g) Potassium should be added to both dialysate and replacement when using

Hemosol BO unless overdose is associated with severe hyperkalaemia.

h) At high dialysis doses it must be remembered that

i) Hypomagnasaemia and hypophosphataemia (if using Hemosol BO) are

common and occur rapidly. Levels should be checked twice daily and

replaced as indicated

ii) Clearance of many therapeutic drugs is increased and dose adjustment may

be necessary

iii) Levels of other antidotes may be altered (e.g. ethanol) and where possible

need regular monitoring

i) Conventional intermittent haemodialysis may be preferable:

i) Dialysate flow rates and early clearance of small molecules are greater.

ii) If not readily available, institution of CVVHDF is indicated even though

extraction ratios are generally lower, total body clearance is often greater

on CVVHDF.

j) Data on clearance of toxins using CVVHDF and modern membranes is sparse.

For this reason samples should be taken for drug levels as per the form below:

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Form: Dialysis Data for Drug Overdose

Estimated Time of Overdose:

Drug/s & Estimated Dose:

Blood Flow Rate: Dialysis Flow Rate:

Replacement Flow Rate: Fluid Balance:

Haematocrit:

Arterial Pre-filter Post-filter Effluent Urine

0 hrs (Pre-dialysis)

2 hours

4 hours

8 hours

12 hours

186

F. Neurosurgical protocols

1. Neurotrauma in ICU

a) Close liaison and communication with the neurosurgeons is essential for the

coordinated management of acute head injuries.

b) ICU management of the neurotrauma patient includes:

i) Acute trauma resuscitation

ii) Liaison and coordination with other clinics in the multi-trauma patient.

iii) Cardiopulmonary / renal / metabolic homeostasis.

iv) Maintenance of cerebral homeostasis – see CPP algorithm

v) Transport for imaging

c) Principles of ICU management:

i) Ventilation

Maintain normoxia: PaO2 > 80 mmHg

Ventilation to normocapnia: PaCO2 35-40 mmHg

ii) Haemodynamics:

Fluid maintenance

a. Maintain euvolaemia

b. Crystalloid depending upon Na+ and measured osmolality

c. Avoid dehydration if patients become polyuric (DI / mannitol)

Maintain cerebral perfusion pressure:

a. CPP 60–70 mmHg

i. A lower threshold may be tolerable in some patients

ii. Must be discussed with the ICU Consultant

b. MAP 80 mmHg in the absence of ICP measurement

c. NB: use inotropes if required once euvolaemic

Avoid interference with cerebral venous return

a. Nurse patients at 30° head-up elevation

b. Neutral head position

c. Avoid circumferential ETT ties, etc.

iii) Osmotherapy

Should be discussed with the ICU Consultant

Indications for osmotherapy prior to ICP monitoring are:

a. Unequivocal signs of intracranial hypertension prior to imaging or

evacuation of an intracranial mass lesion

b. Threatened transtentorial/brainstem herniation, or

c. Progressive CNS deterioration not due to systemic pathology.

Hypertonic saline

a. Fewer complications c.f. mannitol.

b. Standard dose: 20ml of 20%NaCl

c. Slow IV push through a CVC

d. Osmolality should not exceed 320mosmol/l

187

Mannitol

a. Patient must be euvolaemic and normotensive (relative to pre-

morbid BP) before the administration of mannitol

b. Osmolality (measured) should not exceed 320mosmol/l

i. Mannitol and alcohol cause an osmolal gap

ii. calculated measured osmolality

c. Standard dose = 0.25g/kg

i. 1.25ml/kg of 20% mannitol

ii. Duration of action is variable (90min – 6hrs)

d. A urinary catheter is essential.

iv) Seizure prophylaxis - indications:

Closed head injury with structural damage

(intracerebral or paraxial haematomas)

Penetrating head injuries

Depressed skull fracture

Pre-existing epilepsy

Phenytoin prescription:

a. 15 mg/kg loading over 30 minutes

b. 300 mg iv daily or 400mg NG x 7 days only

c. Monitor levels: therapeutic 40-80mol/l

v) Antibiotics - indications:

Insertion of ICP monitoring catheters: cefazolin 1g stat

Base of skull fractures: antibiotics are not indicated in the absence of

signs of meningitis

Nosocomial infections: as per infectious diseases guidelines.

vi) Sedation:

Consider the use of propofol in patients where regular review of CNS

status is required (majority of patients)

Control large sympathetic swings with fentanyl (100-200µg IV)

Many opioids have been demonstrated to increase ICP and should not

be used as sole therapy to control intracranial hypertension.

The use of muscle relaxants is relatively contraindicated and must be

discussed with the ICU Consultant.

Consider -blockade or clonidine in labile neurogenic hypertension.

vii) Nutrition:

Establish enteral feeding as soon as feasible

Maintain BGL in the normal range by insulin infusions if necessary.

Hyperglycaemia is common in the acute phase and may precipitate a

hyperosmolar state with resultant polyuria.

viii) Stress ulcer prophylaxis is not routinely indicated (see protocol)

188

ix) Thromboprophylaxis:

All patients should have TED stockings and SCCDs applied within

8hrs of admission unless contra-indicated.

Pharmacological thromboprophylaxis is relatively contraindicated in

the first 72 hrs after injury or surgery or if there is ongoing bleeding.

Thromboprophylaxis may be commenced when indicated following

discussion with Neurosurgery

In patients at high risk of VTE or with contra-indications to

mechanical prophylaxis, consideration should be given to early

insertion of a caval filter

x) Avoid hyperthermia.

d) Monitoring of head injured patients:

i) Cardiorespiratory:

In addition to routine ICU monitoring ETCO2 is recommended

a. Interpret with caution & calibrate with PaCO2 when,

i. Change in ventilation

ii. Sudden rise in ICP

b. Adjust ETCO2 to PaCO2 35-40 mmHg

ii) Neurological:

ICP monitoring

a. At the RAH ICP monitors are inserted by neurosurgeons

b. Indications:

i. Severe CHI (GCS < 8) and an abnormal CT scan, or

ii. GCS < 8 and two of

Age > 40 yrs

Focal motor signs

Hypotension after volume resuscitation

iii. Brain swelling following evacuation of intracranial

haematoma

iv. Intracerebral haematomas where the decision to operate will

depend on ICP

v. Polytrauma patients in whom cerebral status cannot be

adequately assessed (e.g. patients requiring ventilation)

vi. Rarely in non-traumatic raised ICP

Meningitis / encephalitis

Hepatic failure.

Ventricular drain and external pressure monitor:

a. Closed system

b. CSF for M,C&S as clinically indicated

c. Set height for drainage according to neurosurgical consultation.

d. Preferred for ICP monitoring in CHI

189

Flowchart: Cerebral Perfusion Pressure Algorithm

THERAPY FAILURE: ICP > 20 mmHg for > 10min or CPP < 60 mmHg

1. Ensure accurate MAP, ICP and where relevant, SjO2 readings 2. Immediately correct hypovolaemia and hypoxia

3. Ensure normocarbia: PaCO2 35-40 mmHg 4. Ensure adequate sedation 5. Consider drainage 2-5ml CSF if intraventricular catheter in situ 6. Exclude contributing factors

Neck position / venous obstruction

30º head-up position

Fever, Seizures 7. Commence osmotherapy with hypertonic saline or mannitol and notify ICU

Consultant 8. Consider short-term hyperventilation whilst arranging urgent CT 9. Consider neuromuscular blockade 10. Notify neurosurgeon on-call

Non-Surgical Lesion

1. Attempt to maintain CPP > 60 mmHg with fluids / inotropes 2. Consider additional therapies after discussion with Duty ICU Consultant:

Propofol / barbiturate coma

Hypothermia

Neurosurgical referral for decompressive crainectomy

Initial Therapy to Optimise CPP

1. Maintain euvolaemia with IV fluids 2. Ensure appropriate sedation

3. Commence inotropes to maintain CPP 60-70 mmHg (MAP-ICP) 4. Maintain normocarbia, PaCO2 35-40 mmHg

Surgical Lesion

Immediate Neurosurgical Consultation

URGENT CT Head

Scan

190

2. Aneurysmal Subarachnoid Haemorrhage

Table: World Federation of Neurosurgeons Classification

Grade GCS Motor Deficit

I 15 Absent

II 13-14 Absent

III 13-14 Present

IV 7-12 Present or absent

V 3-6 Present or absent

a) Principles of ICU management:

i) Priorities:

Monitoring of airway and adequacy of ventilation

Maintenance of adequate cerebral perfusion

maintain appropriate MAP (relative to premorbid BP)

Monitoring of conscious state (GCS)

Early diagnosis and treatment of causes of reduced GCS

a. Rebleed from aneurysm (notify neurosurgeon)

b. Hydrocephalus (notify neurosurgeon)

c. Vasospasm

d. Seizure

ii) Monitoring:

ECG, SpO2, Invasive BP

ICP in patients with a ventricular drain in situ:

a. May be set at a level (usually 10 cm) above head and/or

b. Connected to monitor transducer

c. CSF culture as clinically indicated

b) Anticonvulsants: as clinically indicated

c) Angiographic Coiling

i) Prefered approach for selected, amenable aneurysms:

Less invasive procedure

Better outcomes at 12 months c.f. clipping

ii) Performed in radiology under sedation (provided by anaesthesia)

iii) May still require insertion of an EVD for hydrocephalus.

iv) Post-procedure management in P4-C as for operative patients.

d) Operative therapy:

i) Early (within 48 hrs): usual practice at RAH

Advantages (proposed): prevention of rebleeding, reduction of

vasospasm, prevention of ischaemia

Disadvantages: high risk of rupture, difficult dissection

ii) Late (after 11 days)

Advantages: easier procedure, opportunity to monitor.

Disadvantages: re-rupture, prolonged risk of vasospasm

191

e) Prevention and treatment of vasospasm

i) Specific drug therapy:

Nimodipine:

a. Indications

i. CT proven SAH

ii. IV preferably through central line (2 mg/hr)

*may be given through a peripheral IV

iii. Change to oral as soon as possible (60mg 4hrly)

b. Complications: hypotension (may require cessation of nimodipine)

Statins (simvastatin 80mg daily) may reduce the incidence of

radiological vasospasm and improve outcomes following SAH.

ii) Triple H therapy (hypertension / hypervolaemia / haemodilution):

Has no role in the prevention of vasospasm

prophylactic HHH therapy may be harmful

It is imperative to avoid hypotension and hypovolaemia.

Patients should have fluid therapy targeted at maintaining euvolaemia.

iii) Euvolaemic hypertension

May be indicated in selected patients with proven vasospasm post-

aneurysmal clipping / coiling.

Induced hypertension must be titrated to a mean arterial pressure:

systolic BP is not an accurate indicator of cerebral perfusion pressure.

Principles:

a. Discuss with ICU consultant prior to initiating therapy

b. Intra-arterial pressure monitoring is mandatory

c. Maintain IV volume

i. Continue IV filling until clinically euvolaemic

ii. Avoid volume overload (pulmonary congestion/oedema)

iii. Monitor electrolytes 8 hrly normal osmolality and [K+].

d. Commence noradrenaline titrated to:

i. MAP > 90mmHg, or

ii. MAP > 10mmHg above premorbid baseline

(for known hypertensive patients), or

iii. MAP 5-10mmHg > “defined MAP”

On occasions there may be neurological improvement at a

certain MAP titrate therapy 5-10mmHg above this

iv. Reset target MAP if high doses (> 10g/min) are required, or

if polyuria, arrhythmias or other complications ensue.

Complications:

a. Pulmonary oedema, hypoxia

b. Cardiac arrhythmias, myocardial ischaemia

c. Polyuria, electrolyte disturbances

iv) Chemical (papaverine / verapamil) or balloon angioplasty

Limited role in angiographically proven vasospasm

Requires transport for angiography and may be performed on

consecutive days.

192

2. Status epilepticus a) Definition:

i) Continuous seizure activity > 30 minutes duration, or

ii) Sequential seizures (≥ 2) without recovery of consciousness.

b) Principles of ICU management

i) Assessment of airway and adequacy of ventilation

Intubate and ventilate if appropriate

Avoid muscle relaxants after intubation

ii) IV access

iii) Control of seizures:

Midazolam: 1-10 mg/hr via infusion, or

Diazepam: 10-20 mg IV prn

Phenytoin: 18 mg/kg load, then 300 mg daily

check for previous administration

therapeutic levels 40-80mol/l

If refractory, liaise with neurologists and consider:

a. Clonazepam 1-2 mg IV prn or by infusion 0.5-2 mg/hr

b. Valproate 200-500mg NG/IV 8 hrly

c. Levetiracetam (Kepra) 500mg NG 8 hrly

d. Thiopentone infusion

i. Loading dose: 5mg/kg of 25mg/ml solution

(2500mg / 100ml N.sal)

ii. Infusion: 1-3 mg/kg/hr

(~ 150 mg/hr or 6 ml/hr)

e. Obtain EEG and consider EEG monitoring

iv) Look for a cause and treat appropriately:

CT scan with contrast if unclear

Previous epilepsy / poor compliance

Intracranial pathology:

a. Vascular (haemorrhage, thrombosis), spasm

b. Infection (consider LP if no evidence of raised ICP on CT)

c. Tumour

Extracranial pathology:

a. Check electrolytes: especially Na+, Ca++, Mg++, K+, PO4=

b. Metabolic: exclude hypoglycaemia, thiamine deficiency

c. Toxic ingestion.

Infection

Severe hypertension

c) Maintenance of homeostasis / seek and treat complications

i) Ensure adequate hydration: maintenance fluids according to

creatinine/urea, Na+ and osmolality

ii) Ensure adequate urine output: prolonged seizures may be associated with

rhabdomyolysis

iii) Evaluate for joint dislocations and occult fractures

193

4. Exclusion of Traumatic Cervical Spinal Injury

a) Safe practices are vital to prevent secondary damage to the cord

b) Spinal immobilisation should be practiced in all patients with;

i) significant distracting injury or injury above the clavicles

ii) altered conscious state for any reason (head injury, alcohol, drugs etc)

iii) neck pain or tenderness

iv) abnormal neurological signs or symptoms

v) NB:

Hard collars allow up to 73% of normal flexion and extension – and so

still need appropriate spinal care even if in place.

Soft collars do not provide effective C-spine immobilisation.

c) Clinically clearing the C-spine requires all of the following criteria to be

fulfilled;

i) normal conscious state, with no drugs or alcohol onboard

ii) no neck pain or tenderness

iii) no abnormal neurological signs or symptoms

iv) no significant distracting injury, or significant injury above the clavicles

and then,

v) normal head control (unassisted)

vi) pain-free movement

d) If all of these are confirmed, the hard-collar can be removed, and the C-spine

cleared.

e) If the C-spine cannot be clinically cleared for any reason, radiology needs to be

performed (the majority of patients seen in Trauma Resus)

f) Virtually all patients presenting to Trauma Resus require a trauma series of

adequate AP, lateral, and odontoid C-spine plain views

g) A complete series of 3 plain views will still miss up to 7% of C-spine injuries –

hence the importance of clinically clearing (if possible) the C-spine even if the

Xrays appear normal.

h) If the C-spine cannot be clinically cleared following normal plain films,

maintain spinal precautions and liaise with the Trauma Registrar.

i) Clearing the C-spine in the patient with altered conscious state:

i) If drugs, alcohol or minor closed head injury are the problem, they are

often resolved within 12 hours – maintain spinal precautions until that

stage, and then assess clinically

ii) If the patient is unlikely to become clinically assessable and clearable

within 12-24 hours (most intubated ICU patients):

Perform a complete plain Xray series in ED, and:

Perform a limited CT;

a. C0-2 in all, during first visit to scanner

b. CT any suspicious areas on the plain films

c. CT may be required to visualise cervicothoracic junction

or d. CT entire cervical spine with 3-D reconstructions (the current

recommendation)

194

If these films are all documented normal, the collar may be removed

and the C-spine cleared ‘as per RAH protocol’.

Any ongoing concerns are referred to the Trauma and/or Spinal

Registrar

j) Flexion-extension views of the C-spine must not be performed, unless ordered

by the Spinal Unit, with the Spinal Fellow in attendance

k) As with the C-spine, the thoracolumbar spine should be imaged in all patients in

whom it can not be clinically assessed. This should be done prior to arriving in

ICU. If CT chest and abdomen have been performed, these images can be used

to assess and clear the thoracic and lumbar spines.

l) 25% with a spinal injury at one level will have a second non-contiguous injury.

Therefore, if a fracture is found anywhere in the spine, the entire spine should

be Xrayed

m) Spinal Xrays should ideally be performed in an Xray area (Trauma Resus Room

or Xray Dept) prior to ICU admission.

n) The quality of spinal Xrays performed in ICU is usually very poor

o) The Trauma Registrar must document the status of spinal clearance on the

Trauma Form

p) Steroid use in acute spinal cord injury is not currently recommended by the

Spinal Injuries Unit.

q) The RAH Trauma Service Procedures, Practices and Guidelines (TSPPG) on

‘Acute Spinal Injury Management’ is available on the RAH Intranet and

contains more detail.

195

G. Microbiology Protocols

1. Policy

a) Sepsis is the most common cause of death in critically ill patients.

b) The prompt diagnosis and treatment of infection in critically ill patients is both

important and difficult.

c) Sepaia must be aggressively sought and promptly treated with source control

(where indicated) and appropriate antibiotics.

d) Simple preventative measures are the most important factors in the containment

of nosocomial infection and minimisation of bacterial resistance:

i) Compulsory hand washing and/or use of alcohol hand-gel by all staff

ii) Attention to aseptic technique for invasive procedures

iii) Attention to invasive procedure protocols as outlined in this manual

iv) Avoidance of over-prescription of antibiotics

e) Regular routine microbiological examination in critical care patients is not cost

effective. Investigations should only be ordered on specific indications.

f) Septic screens must follow the guidelines below.

2. Definitions

a) Systemic Inflammatory Response Syndrome (SIRS)

i) Describes the inflammatory process that occurs in response to a variety of

clinical insults resulting in a clinical picture suggestive of “sepsis”

ii) The syndrome includes at least 2 of the following:

temperature > 38° or < 36° C

heart rate > 90 bpm

respiratory rate > 20 bpm, or

PaCO2 < 32 mmHg

WCC > 12,000/mm3, or

< 4,000/mm3, or

> 10% immature (banded) neutrophils

iii) SIRS is non-specific and may be due to non-infectious causes:

Trauma, Post-operatively after major surgery

Haemorrhagic shock, post blood transfusion

Pancreatitis

Burns

Drug reactions

Intracranial pathology, esp. intraventricular or thalamic blood

b) Sepsis: the presence of SIRS 2° to infection

c) Septic shock: decreased vital organ perfusion/function 2° to sepsis

d) Nosocomial infection is defined as infection that occurs during hospitalisation

that was neither present, nor incubating on admission.

e) Colonisation is defined as the presence of microorganisms that do not elicit an

inflammatory response.

196

3. Septic screen a) Routine, performed only on the clinical suspicion of sepsis:

i) New pyrexia

ii) WCC, WCC, or Platelets

iii) Deterioration in gaseous exchange or pH

iv) Cardiovascular instability

Hypotension / relative hypovolaemia

Increased or new inotrope requirement

v) Oliguria or increased creatinine

b) Screen:

i) Urine - C&S

ii) Tracheal aspirate - urgent gram stain, C&S

iii) Blood culture x2

iv) Any other drainage fluid as indicated, e.g. wound, pleural etc.

c) Other

i) Fungal cultures

ii) Pleural fluid, CSF

iii) Sinus x-rays

iv) Bronchoscopy specimens (BAL)

d) Urine:

i) UTI in a catheterised patient is defined as:

> 105 bacteria + positive culture of organisms, plus

> 500 WBC/HPF.

ii) Bacteria and white cells are a normal finding in a catheterised patient

iii) Treatment with antibiotics will not result in clearance of colonisation and

is only indicated for systemic involvement.

iv) The only effective treatment is catheter removal.

v) Bladder wash-out may reduce bacterial load / infective risk.

e) Tracheal aspirate:

i) Cultures often grow mixed colonising oral flora:

Gram positive cocci - S. aureus and S. pnuemoniae

Gram negative bacilli - H. influenzae

Yeast - Candida sp.

ii) Antibiotics will not result in a clearance of colonisation and are only

indicated for invasive (local or systemic) infection.

f) Blood cultures:

i) Esily contaminated by skin organisms, careful technique required:

Clean the skin with an alcohol or betadine swab

Clean the top of culture medium bottle with an alcohol swab and

allow to completely dry before injecting.

Use a sterile needle and aseptic technique during venipuncture

Inject blood immediately into bottle with same needle - do not touch

the needle.

ii) Blood cultures are best taken by clean venipuncture.

iii) Skin organisms grown from a single bottle are usually a contaminant but

must be interpreted in the context of the patient.

197

4. Investigation of pneumonia

a) Community acquired pneumonia:

i) Usual organisms: S. pneumoniae, H. influenzae

ii) Less commonly:

Bacterial: Legionella sp., Gram neg bacilli, S. aureus

Viral: Influenza A, B, Parainfluenza, Adenovirus, RSV

Other : Mycoplasma pneumoniae,

Chlamydia psittaci (birds),

Coxiella burnetti (sheep or cattle),

TB, Chlamydia pneumoniae

iii) Investigations

Haematology - High (> 15000) or Low (< 3000) WCC

- coagulopathy

Biochemistry - note renal function and LFTs

CXR

ABGs

Microbiology: * prior to antibiotic Rx where possible

a. Blood cultures x 2

b. Endotracheal aspirate

i. M,C&S + urgent gram stain

ii. Legionella culture

iii. Respiratory viral Ag (PCR) & culture

NB: If not intubated, then collect a nasopharyngeal aspirate

for respiratory viruses

c. Urine - L. pneumoniae 1 Ag

* only where high index of suspicion or outbreak

d. Pleural fluid - M,C&S

b) Healthcare associated pneumonia – Immunosuppressed Host:

i) Possible organisms

As above plus

a. Bacterial: Nocardia

b. Viral: CMV, HSV, varicella zoster

c. Fungal: candida, cryptococcus, aspergillus

d. Protozoal: pneumocystis jirovecii (PCP)

Consider non-infective causes of a similar picture e.g. ARDS

ii) Investigations: * As per above, plus

Label request “Immunosuppressed Protocol”

Sputum or tracheal aspirate of limited value

Consider BAL if initial cultures negative

HIV serology

iii) Treatment prior to microbiological diagnosis: refer to antibiotic guidelines

& discuss with ID.

198

c) Nosocomial pneumonia in ICU

i) Principles:

Accurate diagnosis and treatment are important but difficult.

Incidence: 20% of all ICU patients

70% of patients with ARDS

major cause of death in patients with ARDS

Clinically indistinguishable from pulmonary fibrosis, alveolar

haemorrhage, atelectasis and other causes of lung infiltrates

Clinical diagnosis, including use of tracheal aspirate, has poor

sensitivity and specificity

Appropriate antibiotics do improve outcome

Empiric broad-spectrum antibiotics are potentially harmful.

ii) Consider nosocomial pneumonia when:

New and persistent CXR changes

Tachycardia, tachypnoea

Fever or hypothermia - temperature >37.5 or <35.5

Leucocytosis or leucopaenia - WCC: >10 or < 4 x 109/l

Purulent sputum

Deterioration in lung function

iii) Confirmation of pulmonary infection:

Tracheal aspirate → MC&S

Preliminary results to direct therapy may be obtained on gram stain

Consideration should be given to obtaining pulmonary samples by

bronchoalveolar lavage (or open lung biopsy) for patients with:

a. Persistent signs of pneumonia

b. Inadequate response to antibiotics

c. Inabililty to obtain adequate tracheal aspirates, or

d. To exclude non-infectious causes of respiratory failure

e.g. interstitial fibrosis or alveolar haemorrhage

Septic screen including blood cultures should also be performed.

199

5. Vascular catheter sepsis a) Refer to the invasive procedures section

b) Suspect line sepsis when:

i) Evidence of systemic infection

New, unexplained fever

Unexplained or in WCC

Deterioration in organ function

Positive blood culture by venipuncture with likely organisms

(coagulase negative staph, candida), and/or

ii) Evidence of local infection - inflammation or pus at the insertion site

iii) The following patients are more susceptible to line infections:

Prolonged vascular access (> 7-10 days)

→ exponential increase in line infection after 4 days.

Endovascular infection (SBE, prosthetic graft infection)

Cutaneous infection

Burns

Severe intra-abdominal infection (pancreatitis)

Deep-seated infections (empyema / abscess)

iv) The incidence of line sepsis with the antibiotic impregnated lines is around

1% and most of these are due to Candida spp.

c) Protocol

i) Take blood cultures from a peripheral vein

ii) Positive blood cultures from the line may only indicate colonisation so

blood culture bottles must be carefully labelled as to site of sampling

Common organisms in line sepsis are normal skin flora

e.g. Staph spp., C. albicans

In ICU gram negative organisms can also be involved

iii) On suspicion of line sepsis the line should be removed

iv) The tip of the catheter should be sent for culture

Avoid contamination of the catheter tip with skin organisms

Skin should be cleaned thoroughly with alcohol, allowing at least one

minute drying time, before removing the catheter

v) Catheter related bloodstream infection is defined as infection where the

same organism is grown from the blood and from the catheter tip

d) Treatment

i) Removal of the line will usually clear low-virulence organism

bacteraemias, e.g. S. epidermidis

ii) Antibiotics are indicated, even if blood culture negative, when:

The patient is high risk - e.g. joint or endovascular prosthesis

Infection with a virulent organism, e.g. S. aureus

Signs of sepsis continue after catheter removal

iii) If ongoing sepsis occurs, additional blood cultures should be taken prior to

starting antibiotics

iv) Refer to antibiotic guidelines.

200

e) Further venous access:

i) Reassess the need for ongoing central access, consider PICC line

ii) Whenever possible:

Wait 24 hours before reinsertion

Select a different insertion site

iii) Guidewire exchanges are not performed unless:

Mechanical problems in a new catheter (leaks/kink & < 4 days old)

Difficult or limited central access (e.g. burns)

6. Bacterial Meningitis

a) Steroids should be started before antibiotics in all patients with a high

probability of bacterial meningitis.

i) No demonstrated benefit given post-antibiotics.

ii) Should occur in A&E / pre-retrieval - check on admission

b) Dose: dexamethasone 10mg 6 hrly for 4 days

c) Antibiotics are as per ID guidelines

7. Fungal infections a) General principles

i) The incidence of systemic fungal infections in ICU patients has increased:

Increased numbers of immunosuppressed patients admitted to ICU

The use of broad-spectrum antibiotics, and

Prolonged use of intravascular catheters

ii) Fungaemia is an indication to commence antifungal therapy.

iii) Whilst candidaemia is associated with significant mortality, systemic

infections can occur with negative blood cultures.

b) Risk factors for candidaemia and disseminated candidiasis:

i) Neutopaenia

ii) Long term CVC use

iii) Candida colonization

iv) Broad spectrum antibiotics

v) Haemodialysis

vi) Immunosuppressants

c) Antifungal prophylaxis

i) Systemic prophylaxis is not recommended for general ICU patients

ii) Solid organ transplant patients do not require prophylaxis

iii) Posaconazole prophylaxis is effective and tolerated in bone marrow

transplant and neutropaenic cancer patients

d) Prophylaxis and treatment are as per the RAH guidelines – see flowchart in

following page, or RAH intranet

201

Flowchart: Antifungal Treatment in Immunosuppressed Patients

202

8. Necrotising soft tissue infections a) General principles

i) This is a generic group of patients with life threatening infections

involving combinations of mucocutaneous, fascial and myofascial planes

ii) These infections represent a medical emergency: patients may present with

severe septic shock and rapidly developing multiple organ failure

iii) In rapidly progressive infections, local signs of inflammation may

underestimate the degree of underlying tissue necrosis

iv) Usually due to one or more of the following organisms:

Anaerobes - clostridium spp, bacteroides

Gram positives - group A streptococcus, staphylococcus

Gram negatives - enteric organisms

b) Management protocol:

i) Appropriately trained personnel, familiar with the severity of the patient's

condition and with appropriate resuscitative equipment, must accompany

these patients during all phases of their management

ii) The hallmarks of management involve a detailed multidisciplinary

approach coordinated by the duty Intensive Care consultant and involving

the following:

The duty ID consultant must be notified as soon as possible.

Prompt and effective resuscitation, restoration of vital organ perfusion

and control of metabolic emergencies (e.g. hyperkalaemia,

hypoglycaemia, coagulopathy). This is coordinated by the Intensive

Care team and must not significantly delay surgery.

Early, aggressive and repeated surgical debridement.

a. Patients with necrotising soft tissue infections must be reviewed

by a plastic surgical consultant (not trainee) ASAP.

b. The Duty Anaesthetist must be notified as soon as surgery is

planned.

Prompt identification of organisms with early prescription of

appropriate empirical, then specific antibiotics as required (refer

empirical and specific antibiotics section).

Immune Globulin (IV-Ig)

a. Clearest evidence in Gp A Strep infections.

b. Should be used in conjunction with clindamycin

c. Liaise with ID in all cases & confirm if to be used

d. Standard regimen over 3 days:

i. 1.0g/kg Day1

ii. 0.5g/kg Days 2&3

e. “Rescue Therapy”

i. May be considered in cases where surgery would prove

devastating, or where surgery is unduly delayed

ii. Dose: 2.0g/kg as single bolus over 3-6hrs.

NB: This may be > 3000ml IV-Ig

203

Hyperbaric oxygen is an adjunctive therapy in selected patients:

a. HBO must not delay debridement and resuscitation must be

maintained during treatments.

b. Indications for hyperbaric oxygen:

i. Progressive bacterial (clostridial) gas gangrene.

ii. Selected patients with severe multisystemic disease not

responding to resuscitation, antibiotics and surgery.

c. The number of HBO treatments on a given day will depend on the

stability of the patient, availability of staff and timing of surgery.

d. As a general rule, patients undergoing surgical debridement will

return to ICU following surgery for stabilisation and assessment

prior to subsequent transfers for HBO. This will be co-ordinated

by the duty Intensive Care and hyperbaric medicine consultants.

204

H. Drug Overdose


a) The majority of drug overdoses are poly-pharmaceutical and respond to general

supportive measures.

b) Overall, early mortality is low and usually relates to cardiorespiratory arrest.

c) Following admission, morbidity relates primarily to aspiration pneumonitis, or a

delay in definitive respiratory care.

d) There is a poor correlation between depth of coma and preservation of glottic

reflexes. Accordingly, if there is any doubt the patient should be intubated.

e) Antidotes such as naloxone or flumazenil:

i) Should generally not be used as alternatives to supportive measures

ii) Are not to be used to facilitate gastric lavage or charcoal administration

iii) The main utility is in aiding diagnosis of the underlying cause of coma

- small doses only are required

iv) Usefulness in treatment is limited by their short half-lives

v) Continuous infusion is required where ongoing therapy is contemplated

vi) Both agents may initiate a withdrawal syndrome or unmask to the toxicity

of co-ingestants.

vii) In the case of flumazenil these effects may be life threatening.

f) ICU/HDU admission criteria following an overdose may include:

i) Intubated patients

ii) Reduced GCS with potential airway compromise

iii) Uncontrolled seizures

iv) Persistent hypotension

v) ECG criteria:

Ventricular or supraventricular tachyarrhythmias

Sinus tachycardia > 140/min with tricyclics or thyroxine

AV block 2nd or 3rd degree

QTC interval > 0.5s

QRS interval 0.12s

Acute RBBB

vi) Metabolic disturbance requiring HDU-level of care

vii) Requirement for extracorporeal elimination

2. Gastrointestinal Decontamination

a) A variety of approaches have been used historically in an attempt to reduce the

dose absorbed following an oral ingestion.

b) There is minimal evidence for improved survival or shortened duration of

toxicity, particularly when applied to unselected patients.

c) The decision to use decontamination requires individual patient risk-benefit

analysis. Appropriate patients and modalities should be selected, and

gastrointestinal decontamination should never proceed to the detriment of

resuscitative and supportive care.

205

d) Gastric lavage

i) Largely historical

ii) Formal lavage (large bore tube placement, water instillation and aspiration)

should not be performed.

iii) For intubated patients, an orogastric or nasogastric tube of appropriate

(standard) size should be inserted, and any gastric content aspirated

iv) No additional fluid should be instilled via the tube.

e) Charcoal

i) Charcoal aspiration has a high morbidity and mortality:

Adequate airway reflexes must be present, or

If there is any doubt the patient should be intubated

ii) For appropriate ingestions administer:

1g/kg body weight (to a maximum of 100g) stat

25g 4 hourly x 3 doses - slow release medications

- drugs with enterohepatic circulation

Cease administration should an ileus develop.

iii) Indications:

Presentation < 1hr from ingestion

a. Compound bound by charcoal

b. Ingestion expected to cause significant morbidity or mortality.

Presentation > 1hr, consider administration for:

a. Salicylates

b. Slow release or enteric coated preparations

c. Agents which delay gastric emptying, and

d. Drugs with enterohepatic circulation.

iv) Charcoal is ineffective for:

Elemental metals and their salts

Hydrocarbons and alcohols

Acids or alkalis

v) With multiple dose charcoal administration, constipation is likely and the

addition of sorbitol may be considered. (NB. Sorbitol may interfere with

the adsorptive capacity of charcoal.)

f) Whole bowel irrigation

i) Use of polyethylene glycol solution to decontaminate the bowel.

ii) Use restricted to life threatening overdoses where:

The agent is a slow release or enteric coated preparation

The agent is not expected to be bound by charcoal.

A good outcome is not expected with supportive care and antidote

administration alone.

The patient presents before the advent of severe toxicity

206

iii) May be potentially useful following:

Iron overdose > 60mg/kg

Slow release potassium chloride > 2.5mmol/kg

Major slow release verapamil or diltiazem ingestion

Symptomatic arsenic trioxide ingestion

Lead ingestion

Body packers (heroine)

iv) Contraindications

Good outcome expected with standard care

Uncooperative patient

Uncontrollable vomiting

Reduced GCS or seizures expected in subsequent 4 hours

Ileus or bowel obstruction

Intubated patients (relative)

v) Technique

Polyethylene glycol solution (standard endoscopy bowel prep.)

Administer via correctly placed nasogastric tube at 2L/hour

(25ml/kg/hr in children)

To minimize vomiting start at a slower rate & titrate up as tolerated

Administer metoclopramide to enhance gastric emptying

Be prepared for explosive diarrhoea

- sit on commode or place effluent tube for example

Continue until rectal effluent is clear or an ileus/abdominal distension

occurs.

3. Osmolal Gap

a) OG = Measured – calculated osmolality

b) Calculated Osmo = 2×[Na + K] + Gluc + Urea + ethanol

c) Baseline osmolar gaps are highly variable in the normal population.

d) Evaluation of potential toxic alcohol ingestion requires serial assessments over

time looking for a characteristic pattern with worsening acidaemia, increasing

anion gap and decreasing osmolar gap.

e) Single measurements may confirm an ingestion but are not reliable in excluding

it.

207

Flowchart: The Unconscious, Undetermined Overdose

Investigation:

Blood Urine

Biochem:

Electrolytes

Glucose

Renal

LFTs

Coags

Urine drug

screens rarely

influence

management and

should be used

sparingly

Drug levels:

Paracetamol

routinely

Others as

indicated

only

Other ECG

ABG

Measured

osmolality

Arterial Blood Gas

RESUSCITATION (ABCDEFG)

1. Airway

2. Breathing

3. Circulation

4. Don’t Ever Forget Glucose

Consider:

1. Glucose 50%

2. Naloxone

3. Thiamine

History:

1. Patient

2. Relatives

3. SAAS Crew

Examination:

1. Clinical toxidromes

2. Trauma

3. Nerve palsies

4. Pressure areas

5. Preganacy?

NO Metabolic Acidosis

1. Sedatives

2. Hypnotics

3. Paracetamol

4. Theoplylline

5. Anticholinergics

6. Antihistamines

7. Antipsychotics

8. Antidepressants

9. Anticonvulsants

10. Lithium

11. Organophosphates

Metabolic Acidosis

Normal Anion Gap

1. Acid ingestion

2. Toluene sniffing

3. Bicarbonate loss

Raised Anion Gap

+

Osmolal Gap§

OG < 10

Salicylates

Cyanide

Carbon monoxide

Lactic acidosis

Iron

Isoniazid

Metformin

OG > 10

Methanol

Other alcohols

208

4. Specific therapies / protocols

a) Paracetamol: Acute overdose

i) Defined as a single ingestion, or staggered ingestion occurring over 8

hours or less.

ii) If the time of ingestion can be defined risk assessment and the decision to

treat may be based upon the modified Rumack-Matthew nomogram (use

the initial ingestion time as the assumed total ingestion time when plotting

staggered ingestions occurring over < 8hrs).

iii) Potentially hepatotoxic dose in a fit adult is > 200 mg/kg (or > 10g)

iv) Markedly less in high risk individuals:

Chronic alcoholics and the malnourished

Pre-existing liver disease

Those taking cytochrome P450 inducing medications

v) The risk of hepatic injury without NAC (N-acetylcysteine) is predicted by

plotting a level taken 4-15 post ingestion on the Rumack-Matthew

nomogram.

vi) The probability, with a 4hr drug level, is:

1-2% < 1320 µmol/L (200mg/L)

30% ~ 1320-1980 µmol/L (200-300mg/L)

90% > 1980 µmol/L (> 300mg/L)

vii) The risk of hepatic impairment with NAC is determined primarily by the

time from overdose to commencement of NAC:

Survival is 100% where NAC is commenced within 8 hours

Benefit is reduced if NAC commenced at 8-24 hours

Benefit is not confirmed if commenced beyond 24 hours, except in the

setting of hepatic failure.

viii) The administration of NAC is indicated in the following settings (refer to

flowcharts on following pages):

Patients who present within 8 hours of ingestion and have a 4-8 hour

level falling above the treatment line

All patients presenting 8-24 hours post-ingestion

*may be ceased if the subsequent level is non-toxic and transaminases

are normal

Patients presenting beyond 24 hours post-ingestion with detectable

paracetamol and elevated transaminases

Unknown time of ingestion (follow the >8 hour scenario in Box 3)

Late presenters with clinical or biochemical evidence of hepatic injury

ix) For repeated supra-therapeutic ingestions see “Flowchart: Repeated

Supratherapeutic Paracetamol Ingestion” for management guidelines.

209

x) For sustained released paracetamol preparations:

Start NAC if > 200mg/kg or 10gm (whichever is less) ingested.

Use paracetamol levels to determine the need for NAC.

a. Check serum levels at 4 hours and repeated 4 hours later.

b. If either level > nomogram line, continue or commence NAC.

c. NAC may be discontinued if both levels < nomogram line

xi) NAC may be ceased in the following settings:

Patients in whom NAC was commenced < 8 hrs post-ingestion who

are clinically well and without hepatic tenderness at the completion of

the 20 hour infusion (no further investigation required)

Patients in whom NAC was commenced > 8 hrs post-ingestion who

are clinically well and have normal transaminases at the completion of

the 20 hour infusion. Those whose transaminases are abnormal at this

time should continue an infusion at 100mg/kg/16 hrs until

transaminases and INR (tested 12-24 hourly) are falling.

xii) Consultation with liver transplant services (FMC) for consideration of

transplant should commence with any of the following high risk criteria:

INR > 3.0 at 48 hours or > 4.5 at any time

Oliguria or creatinine > 200 µmol/L

Acidosis with pH < 7.3 after resuscitation

Ongoing hypotension with systolic BP < 80mmHg

Hypoglycaemia

Severe thrombocytopenia

Encephalopathy (any degree)

xiii) The default position, if in doubt, should be to treat with NAC.

xiv) Toxicological advice should be sought if there are any uncertainties.

Graph: Modified Rumack-Matthew Nomogram

210

Flowchart: Acute Paracetamol OD - Known Time of Ingestion

*from Daly FFS, Fountain JS, Murray L, Graudins A, Buckley NA. Guidelines for the management of paracetamol poisoning in Australia and New Zealand – explanation and elaboration (Consensus Statement). MJA 2008; 188: 296-301.

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Flowchart: Repeated Supratherapeutic Paracetamol Ingestion

Table: N-Acetylcysteine Administration

NAC 150mg/kg in 200mls of 5% dextrose over 30 minutes

NAC 50 mg/kg in 500mls of 5% dextrose over 4 hours

NAC 100mg/kg in 1000mls of 5% dextrose over 16 hours

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b) Lithium - Acute overdose

i) Generally produces significant GIT symptoms with nausea, vomiting,

abdominal pain and diarrhoea.

ii) Ingestion < 25g in the setting of normal renal function is benign

iii) Ingestion > 25g may cause more significant GIT toxicity

iv) Neurotoxicity is rare with good supportive care and hydration

v) Renal impairment, dehydration and sodium depletion cause a reduction in

renal lithium excretion and increase the risk of delayed neurotoxicity

vi) Patients presenting late with established neurotoxicity should be managed

as for chronic toxicity, and have similar long term morbidity

vii) Lithium levels > 5mmol/L 4-8 hrs post ingestion are not uncommon

viii) Treatment

Normal saline rehydration

Maintenance of urine output > 1ml/kg/hr

ix) Haemodialysis is reserved for:

Those with established or worsening renal failure, and

Those presenting late with established neurotoxicity

c) Lithium - Chronic poisoning:

i) The clinical features of chronic toxicity are primarily neurological

ii) Develops when renal lithium excretion is impaired for any reason

iii) Serum lithium levels correlate poorly with clinical toxicity

iv) Neurotoxicity may persist well after lithium levels return to normal.

v) The Hansen-Amdisen classification may be used to grade severity:

Grade 1 (mild): tremor, weakness, ataxia, hyperreflexia

Grade 2 (moderate): stupor, rigidity, hypertonia, hypotension

Grade 3 (severe): myoclonus, convulsions, coma

vi) Cardiac effects can occur in late toxicity following the establishment of

neurological features, which includes rhythm disturbances, A-V delay,

heart block and non-specific ST segment and T wave abnormalities

vii) Lithium levels

Confirm a diagnosis but should not be used to grade severity

Are useful serially to monitor response to therapy

viii) Principles of therapy

Careful correction of fluid and sodium balance

Cease lithium and any medications that may impair excretion

Monitor urine output, renal function, electrolytes and lithium levels

ix) Indications for haemodialysis

Neurotoxicity and a serum level > 2.5 mmol/L

Grade 3 neurotoxicity regardless of level

Pre-existing renal or cardiac disease preventing the achievement of an

adequate urine output with hydration alone

Repeated haemodialysis treatments may be required

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d) Opioids i) Produce CNS and respiratory depression, often just above analgesic doses

ii) Death is usually due to respiratory failure, either primary effect or

compounded by aspiration, and good supportive care ensures survival

iii) Some opioids may possess additional cardiac and neurologic toxicity

- e.g. dextropropoxyphene, tramadol, pethidine

iv) Controlled release preparations may cause delayed and prolonged toxicity

v) Treatment is generally supportive

vi) Naloxone (50 to 100µg IV repeated as needed)

Useful for diagnostic purposes

Can assist in the management of airway and breathing

May result in a withdrawal syndrome

vii) If repeated naloxone boluses are required to ensure a protected airway,

intubation is the preferred method of ongoing management

viii) If a naloxone infusion is established:

Initial hourly requirement is generally half the effective dose used over

the preceding hour, i.e. that required to achieve airway protection and

adequate tidal volumes

Infusions require constant observation/assessment

Hospital deaths have occurred due to inadequate observation

e) Carbon monoxide

i) CO is a common cause of poisoning death

ii) Most deaths occur pre-hospital.

iii) Acute effects are due to tissue hypoxia

iv) Those that arrive at hospital alive should survive.

v) In-hospital management involves supportive care and identification of

those at risk of long term neuropsychiatric sequelae

vi) Delayed neurological effects are secondary to unrelated and incompletely

understood mechanisms

vii) HbF binds CO more avidly than HbA, and the foetus is at particular risk

viii) Self poisonings involve high concentration, short term exposures, and are

associated with fewer long-term sequelae than industrial and domestic

exposures (low concentration, prolonged exposures)

ix) High risk features for delayed neurological sequelae:

Loss of consciousness or coma

Persisting neurological deficit (e.g. confusion)

Cerebellar signs

Metabolic acidosis

Myocardial ischaemia

Age > 55yrs

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x) Treatment options

Normobaric oxygen at high flow via non rebreather mask

a. Continue until all symptoms resolve

b. Pregnant women to continue for 24 hours with concomitant foetal

assessment

Hyperbaric oxygen

a. May be indicated in patients with 1 or more high risk factors

b. Indications and effectiveness are controversial

f) Cyanide

i) Acute cyanide poisoning is rare, dramatic and lethal

ii) Removal from the source of exposure, good resuscitative care and selective

antidote use provide the best chances of survival

iii) Most deaths will occur pre-hospital, and those who arrive alive in hospital

post-inhalational exposure are likely to survive with supportive care.

iv) Risks to those involved in care delivery are negligible.

v) Decontamination should involve removal of clothes and washing of skin

with soap and water.

vi) Cyanide levels are not available in a timely manner and do not aid

management

vii) Serum lactate levels parallel cyanide levels and may be used as a proxy

marker of exposure

viii) A lactate level > 10 mmol/L correlates with a toxic cyanide level

(in the absence of an alternative cause for elevation)

ix) Management should proceed along normal resuscitative lines with the

delivery of 100% oxygen

x) Consider using an antidote in the following settings:

Altered mental state

Seizures

Hypotension

Significant and persisting metabolic acidosis (lactic)

xi) Antidote choice and administration

100% oxygen in all cases

Hydroxocobalamin (1st line)

a. 5g in 200mls of 5% dextrose over 30 minutes

b. Repeat in 15 minutes if no improvement

Sodium thiosulphate (adjunct to Hydroxocobalamin, or 2nd line)

a. 12.5g IV

b. Repeat dose at 30 minutes if acidosis persists

Sodium nitrite

a. 300mg IV over 3 minutes

b. Follow immediately with sodium thiosulphate

c. Half dose may be repeated in 30 minutes if required

d. Monitor methaemoglobin (must not exceed 40%)

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g) Toxic alcohols i) A variety of alcohols (methanol, ethylene and diethylene glycol etc) are

used as industrial solvents, cleaning agents and reactants.

ii) Accidental ingestions are rarely of sufficient volume to cause toxicity

iii) Deliberate ingestion is associated with severe metabolic acidosis,

multiorgan dysfunction and potentially death.

iv) Cause an initial “ethanol like” intoxication followed by a progressive

metabolic acidosis and compound specific end-organ toxicities, e.g.

Retinal toxicity/blindness (methanol)

Acute renal failure (multiple agents)

Seizures (multiple agents)

Refractory hypotension (multiple agents)

Delayed neurological sequelae (diethylene glycol)

v) Diagnosis is based upon a history suggestive of ingestion and a

characteristic evolution of metabolic acidosis

Initially: osmolar gap (OG) + normal pH and anion gap (AG)

Evolution of acidosis with pH, OG and AG

Variability in osmolar gap amongst the normal population is such that

a single assessment of acid-base, AG and OG is insufficient to

exclude significant exposure (although it may confirm it)

vi) Specific treatment

Ethanol

a. Commence ASAP, regardless of symptomatology, in all with:

i. Acidosis, or

ii. An elevated OG (with or without acidosis),

b. Check baseline BAL, if > 0.1g/dl a loading dose is not required

c. Titrate to BAL 0.1-0.2g/dL while on dialysis

d. May be given orally (via NGT) or by IV infusion

e. Oral protocol *avoid in ICU if possible

i. Loading dose of 1.8ml/kg of 43% ethanol

(4 x 30ml vodka shots for a 70 kg adult)

ii. Maintenance infusion of 0.2-0.4 ml/kg/hr

(1 x 40ml vodka shot per hour)

f. Intravenous protocol

i. Loading dose: 8ml/kg of 10% ethanol

ii. Maintenance: 1-2ml/kg/hr of 10% ethanol

g. Actual requirements vary widely between individuals, and serial

blood alcohol assessments are required to ensure a level within the

target range

h. If on CVVHDF, then safer to dialyse against desired [ETOH]

i. 0.1g/dl = 5ml ETOH / 5l Bag (inc. replacement)

ii. first bag may be run at 0.2g/dl = 10ml ETOH / 5l bag

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Haemodialysis (HD)

a. Significantly more efficient at clearing alcohols than CVVHD

b. Indications

i. Serum pH < 7.3

ii. Serum bicarb < 20 mEq/L

iii. Worsening acidosis or vital signs despite supportive care and

ethanol infusion

Folate 50mg IV QID or folinic acid

Thiamine 300mg IV daily

& pyridoxine 50mg QID for ethylene glycol poisoning

Correct hypocalcaemia (if symptomatic) & hypomagnesaemia

h) Organophosphorous agents

i) Includes the organophosphates (OP) and carbamates (CM)

ii) Similar initial presentation

iii) Most deaths occur as a consequence of respiratory failure

iv) OPs as a group have greater lethality

Form a covalent bond with serine esterase enzymes

In contrast to the competitive bond formed by CM.

v) There is great variability amongst the OPs in terms of enzyme aging,

toxicity profiles, and pralidoxime responsiveness

vi) High quality supportive care and aggressive use of antidotes is necessary to

ensure survival.

vii) The diagnosis is essentially clinical:

Muscarinic features - diarrhoea, emesis, urination

- miosis, lacrimation, salivation

- bronchorrhoea, bronchospasm

- bradycardia, hypotension

Nicotinic features - fasciculation, tremor, weakness

- respiratory muscle paralysis

- tachycardia, hypertension

CNS features - agitation, seizures, coma

- delayed neuropsychiatric effects

viii) Cholinesterase levels:

Plasma cholinesterase levels fall more rapidly and recover more

quickly than RBC cholinesterase levels, they are useful in confirming

exposure but do not correlate with toxicity.

RBC cholinesterase levels correlate better with toxicity and response

to therapy, but take longer to perform (limiting their clinical utility)

ix) Decontamination

Resuscitation must not be delayed by external decontamination

procedures

These agents do not vapourise at atmospheric pressure

There is no risk to care providers from inhalational exposure

The characteristic odour is due to a hydrocarbon solvent, which may

cause headaches & eye irritation, but is otherwise harmless

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Staff should wear impermeable gowns, gloves, glasses and facemasks

Care should be delivered in a well ventilated setting

The patient’s clothing should be removed and the skin washed with

soap and water

x) Treatment

Ventilatory and CVS support as indicated

Atropine

a. Reverses muscarinic effects only – it will not reverse paralysis!

b. Titrate 1.2 mg at 5 min intervals (doubling the dose every 5 min)

until signs of successful atropinisation are noted

i. Drying of secretions

ii. Resolution of bradycardia

iii. Clear chest

c. Over 10-20mg, or infusions of up to 5 mg/hr may be required in

severe poisoning.

d. Typically commenced at 10-20% of loading dose per hour.

e. NB: HR and pupil size are not useful for clinical monitoring after

nerve agent exposure

Diazepam IV

a. Treatment of seizures

b. Reduces the incidence of neuropsychiatric sequelae

c. Regular dosing is recommended.

Pralidoxime Iodide

a. Efficacy is unclear and is likely to be compound specific

b. Default is to give ASAP

c. Not required for documented carbamate ingestion (although not

contraindicated)

i. 1g IV over 30 minutes

ii. 500 mg/hr for 24 hours

iii. May be ceased at 24 hours in the absence of nicotinic or

muscarinic features. The benefit of continuing beyond 24

hours is unclear and warrants specialist consultation.

i) Calcium Channel Blockers

i) Of the common slow release formulations, verapamil and diltiazem

frequently cause profound CVS collapse 4-16 hrs post-ingestion.

ii) Other agents within the class rarely cause major toxicity

iii) Onset of toxicity may be delayed:

Up to 2 hours post-ingestion of the standard preparation, and

Up to 16 hours after ingestion of the SR formulation

iv) Ingestion of >10 tablets of verapamil SR or diltiazem SR may cause

serious toxicity

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v) The key issues in management are:

Identification of patients at risk

Judicious use of the pre-toxicity window of stability

Consideration of GIT decontamination options

(including whole bowel irrigation), and

A graduated approach to developing or established toxicity

vi) Risk of serious toxicity is significantly increased by:

Co-ingestion of other cardiac medications, and

Underlying cardiac disease or advancing age

vii) Graduated response to hypotension: failure to achieve stability at each step

should prompt immediate initiation of the next

Fluid load with 10-20 ml/kg isotonic crystalloid (avoid overload)

Calcium load

a. Calcium gluconate - 60ml of 10% solution, or

b. Calcium chloride - 20ml of 10% solution

c. Commence an infusion to keep calcium levels > 2.0mEq/L

Atropine to a total of 1.8mg

Catecholamine infusion effects are variable in terms of:

a. Central - negative inotropic & chrontropic effects

- Adrenaline is an appropriate 1st line agent

b. Peripheral - reduced vascular tone

-Noradrenaline 1st line agent

c. Do not persist with escalating inotrope doses in the setting of

continued instability

High dose insulin & dextrose / euglycaemia

a. Most effective when used early.

b. Glucose

i. Bolus 25g (50 mL of 50% solution)

unless hyperglycaemia (BGL > 22 mmol/L) present

ii. Infusion 25 g/h IV titrated to maintain euglycaemia

c. Actrapid insulin

i. 1 IU/kg bolus

ii. Infusion 0.5 IU/kg/h

titrated every 30 min to a maximum of 5-10 IU/kg/h

d. Monitor:

i. Glucose - every 20 min for first hour, then every 1 h

ii. Potassium - replace only if < 2.5 mmol/L and there is a

source of potassium loss

e. Therapeutic end points:

i. BP > 90mmHg, HR > 60, resolution of acidaemia

ii. Adequate urine output (1-2 mL/kg/h)

iii. QRS interval < 120 ms

iv. Improved mentation

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viii) Seek guidance from Clinical Toxicologist (via switchboard or Poisons

Information Centre) or ICU consultant staff regarding protocol

ix) Cardiopulmonary bypass, ECMO, cardiac pacing and intra-aortic balloon

pumps have been used successfully as extraordinary manoeuvres

j) Beta Blockers

i) Usually minimal toxicity and require only simple supportive care.

ii) By contrast overdoses of sotalol or propranolol may be life threatening

iii) In addition to class 1 and 2 effects (bradycardia, conduction blocks and

hypotension)

Propranolol

a. Na+ channel blocking effects wide complex arrhythmias

b. Highly lipid soluble enters the CNS (coma and seizures)

Sotalol

a. Blocks cardiac K+-channels

b. Causing QT prolongation and torsades de pointes

iv) The clinical response to overdose is highly variable, but the threshold for

severe toxicity from propranolol may be as low as 1g

v) With the exception of sotalol and slow release preparations, toxicity is

usually apparent within a few hours post-ingestion

vi) PR prolongation in the absence of bradycardia is an early marker of

toxicity

vii) Approach to immediate life threatening symptoms:

Bradycardia and hypotension

a. Atropine

b. Adrenaline

c. Noradrenaline

d. Glucagon 5-10mg bolus & 1-5mg/hr infusion (cumbersome), or

e. High dose insulin dextrose euglycaemia

(targeting impaired contractility)

Wide QRS

a. Sodium bicarbonate bolus 1-2 mEq/kg

b. Repeat as required

c. Intubate and hyperventilate targeting serum pH 7.5 to 7.55

Torsades de pointes

a. Isoprenaline

b. Magnesium

c. Overdrive pacing

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k) Tricyclic Antidepressants (TCAs) i) Tricyclic antidepressant use has escalated after an initial reduction

secondary to SSRI introduction

ii) TCAs remain a significant cause of toxicological morbidity and mortality

iii) Poisoning rapid onset CNS and CVS toxicity

peak between 4-6 hrs post ingestion

Dose > 10mg/kg is potentially life threatening

Dose > 30mg/kg is expected to cause severe cardiotoxicity and coma.

Prompt intubation, hyperventilation and sodium bicarb administration

at the onset of major toxicity is life saving.

iv) The investigation of choice is the 12 lead ECG, with diagnostic and

prognostic features including:

Prolongation of the PR and QRS intervals

Terminal R wave in aVR

Increased R/S ratio (>0.7) in aVR

QRS > 100 ms is predictive of seizures

QRS > 160 ms is predictive of ventricular tachycardia

v) The approach to resuscitative management includes the following:

Prompt intubation and hyperventilation (to serum pH 7.5-7.55) at the

onset of CNS depression

Ventricular arrhythmias are unlikely to respond to defibrillation:

a. NaHCO3 ~ 2 mmol/kg IV every 2 minutes until perfusing rhythm

restored. (Most effective when used in combination with

hyperventilation)

b. Lignocaine is a 2nd line agent if arrhythmias persist despite pH.

Hypotension is managed with crystalloid and alkalinisation followed

by noradrenaline

Seizures are managed with benzodiazepines (*avoid phenytoin)

I. Bites and Envenomation

1. Up to date and detailed information on envenomation may be found at the

toxinology website http://www.toxinology.com/ managed by the Women’s &

Children’s Hospital

2. Medical advice for doctors can be sought by contacting the clinical toxinologist,

A/Prof Julian White via the WCH switchboard (Ph: 81617000)

3. Emergency cases are seen through the Emergency Departments of major hospitals,

while less urgent cases are seen after discussion with the treating doctor.

http://www.toxinology.com/

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J. Limitation of Therapy

a) Limitation may involve either withholding and/or withdrawal of life supporting

therapies.

b) There is no ethical or legal distinction between these processes.

c) Limitation may involve challenging ethical and legal issues; however, in patients

with no realistic chance of meaningful recovery, decisions to limit life-sustaining

therapies are both clinically and ethically indicated.

d) Assisted suicide and euthanasia are medically and ethically distinct from limitation

of therapy, are illegal in SA and should never occur.

e) The administration of medication to relieve the suffering of a dying patient is

imperative, even though a side-effect may be to hasten the onset of the patient’s

death. Such therapy is legally distinct from euthanasia.

f) Approximately 70% of all RAH-ICU deaths involve some limitation of therapy.

g) Absolute requirements for limitation of therapy are:

i) Medical consensus, including the treating ICU and admitting clinical teams

ii) Clear and open discussion with the patient, family or next of kin regarding

this consensus medical opinion; and, an ‘absence of objection’ to this

proposed management direction.

iii) Clear documentation in the patient’s medical record, along with a description

of the process by which the decision was made.

h) Counselling patients and families in limitation of therapy requires clarity and

sensitivity to ensure that all parties understand and accept the plan of management.

i) The concerns and wishes of the patient and family are important considerations.

j) The overriding goal is to provide the best care possible for the patient. This may be

to concentrate on palliation, rather than life sustaining therapies.

k) The decision to limit treatment is a consultant responsibility.

l) Refer to the CICM Policy Document IC-14

http://www.cicm.org.au/policydocs.php

K. Brain Death and Organ Donation

1. Reference: ANZICS Statement on Death and Organ Donation http://www.anzics.com.au/death-and-organ-donation

2. For further information, trainees should liaise with the ‘Organ Donation Hospital

Medical Directors’:

a) Dr David Evans

b) Dr Stewart Moodie

c) Dr Peter Sharley

d) Dr Alex Wurm

http://www.cicm.org.au/policydocs.php

http://www.anzics.com.au/death-and-organ-donation

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3. Declaration of brain death a) This is an absolute requirement prior to ‘beating-heart’ organ donation

b) Declaration must be made by two members of the ICU staff:

i) The Duty ICU consultant, and

ii) Another ICU doctor (more than 5yrs qualified with appropriate experience).

c) The declaration of brain death may be by either clinical or imaging certification.

4. Clinical certification of brain death

a) The procedure is completed on a Certification of Brain Death form (MR150.0) and

documented in the case notes.

b) Record the time of onset of coma

i) Last time the patient showed response such as breathing, pupil reaction or

coughed on suction.

ii) This can be determined from the nursing observations

c) Pre-conditions:

i) A recognised irreversible cause of coma must be identified.

ii) Potentially reversible causes of coma have been excluded:

Hypotension

Hypothermia *core temp must be > 35ºC

Drugs or poisons.

Neuromuscular blocking drugs

Metabolic or endocrine disturbance including:

a. Deranged renal or hepatic function

b. Hyperglycaemia, hypoglycaemia, thyroid function

c. Electrolyte disturbances

iii) Ability to perform examination of:

Cranial nerves

Apnoea testing (e.g. not severely hypoxaemia or high cervical injury)

d) Clinical confirmation of absent brain stem function

i) Performed separately by 2 doctors, with the first test at least 4 hours after the

onset of coma (longer in the case of hypoxaemic/ischaemic injuries).

ii) Absent pupillary responses to light, both direct and consensual

iii) Absent corneal reflexes

iv) Absent vestibulo-ocular reflex

No nystagmus on injection of 20ml iced water into the ear

Check tympanic membranes prior to this procedure

Occulo-cephalic reflexes are often tested, but are not formally required

v) Absent gag / cough reflex.

vi) Absent response to pain in the cranial nerve distribution.

vii) Apnoea following disconnection from the ventilator:

Pre-oxygenate patient with 100% oxygen

Disconnect ventilator and connect to bag with 100% O2 at 1-2 l/min

Confirm PaCO2 > 60mmHg and pH < 7.30 (with PaO2 > 60mmHg)

Continuously look for apnoea clinically

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e) The following are compatible with Brain Death

i) Spinal reflexes

ii) Sweating, blushing and tachycardia

iii) Normal BP without pharmacological support

iv) Absence of Diabetes Insipidus

f) The 2 practitioners may choose to be present at each examination, however,

each must perform and be responsible for one of the 2 examinations

g) From the onset of coma until the second set of testing, there should be a

continuous period of observation by nursing staff

h) Families may benefit from witnessing the clinical testing for brain death

i) The time of death is the time when certification of brain death is completed – i.e.

on completion of the second examination and documentation in the case notes.

j) There is no legal requirement for certification of persons not considered for

organ donation, however this is encouraged as it can assist in counselling

relatives and the subsequent cessation of inappropriate medical intervention.

5. Imaging (Non-clinical) certification of brain death

a) Consider when clinical examination is “consistent with” brain death, however, the

preconditions (2c) for clinical certification cannot be met.

b) Demonstrated absence of cerebral blood flow is therefore required.

c) Ideally there should be a period of observation of 4 hours to increase the likelihood

that no flow will be demonstrated.

d) Absence of cerebral blood flow may be established by either:

i) Radionuclide cerebral perfusion scan (Tc99 HMPAO).

ii) 4 vessel cerebral angiography (rarely performed at the RAH)

e) Certification of brain death is by 2 clinicians, (not including the doctor who

performed the imaging investigation) who have considered the onset and cause of

coma, the clinical examination and the results of the investigation performed.

6. Organ donation


i) Any patient who is, or may become brain dead is a potential donor. There are

no automatic exclusion criteria.

ii) All potential donors should be offered the opportunity to donate

iii) Notify the Donor Coordinator from Donate Life, SA (Ph: 82077117) when a

potential donor is identified.

b) Criteria for brain dead organ donation

i) The patient has been declared brain dead

*for donation after cardiac death see below.

ii) Usually, no patient history of:

HIV, untreated bacterial, fungal or viral infection.

IV drug abuse

Malignancies other than primary brain tumours and minor skin lesions.

Treatment with hormones of human pituitary origin.

Dementia (or family history of dementia).

Disease of the donor organ

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iii) All brain dead patients should be discussed with the Donor Coordinator,

regardless of relative contraindications.

c) Procedure:

i) Organ donation should not be discussed with the family until brain death has

been certified and the family informed.

ii) Family approaches regarding donation prior to the patients death should be

referred to the consultant

iii) Counselling families with regard to brain death and organ donation requires

considerable compassion, knowledge, skill and time. While this is primarily a

consultant responsibility, advanced trainees are encouraged to participate in

the process under supervision.

iv) The wishes of the patient and family are paramount.

v) A “donor kit” is kept in the cupboard in P4A which contains a check-list, plus

all the forms and specimen bottles required.

vi) Following consent for organ donation, blood should be sent for:

HTLV-1, HIV 1 + 2

HBsAg, HBsAb, HBcAb, HCV

CMV-IgG, EBV, RPR

Group and X-match

Tissue typing – volume of blood varies according to blood group

Mark the request forms: “Urgent – Organ Donor, cc: Donate Life”

vii) Coronial approval will be sought by the Donor Coordinator where required.

viii) The RAH Designated Officer may give permission for donation if all efforts

to find relatives have failed.

ix) It is the responsibility of ICU medical staff to provide either a death certificate

or report to the coroner. Time of death is the time of second certification.

x) Notification of the recipient and procuring teams (which may come from

interstate) and coordination of operating theatre time, collation of results and

investigations are dealt with by the Donor Coordinator(s)

xi) Donor coordinators may seek assistance from ICU staff with ordering

investigations.

xii) The following investigations are normally required:

Recent ECG

Recent CXR

Echocardiography

ABG

d) Management of the organ donor:

i) The situation is time critical as it is not possible to stabilise a brain dead

patient indefinitely.

ii) Aim to ensure perfusion and protection of all organs for donation to achieve

the optimal outcome for all recipients

iii) Avoid focused management strategies aimed at single organ systems

225

iv) Ventilation:

Adequate oxygenation: PaO2 > 60 mmHg | FIO2 < 0.5

Adequate ventilation: PaCO2 35-45 mmHg

Prevention of atelectasis and lung recruitment is important.

v) Cardiovascular instability:

Common around the time of cerebral herniation (coning).

Hypertensive episodes should be treated with short acting agents.

Maintain MAP > 70 mmHg:

a. Adequate volume loading prior to using inotropes.

b. If CVC present: CVP 8-14mmHg

c. High dose inotropic support may reduce organ viability.

vi) Aim for a urine output > 0.5ml/kg/hr

vii) Maintain normothermia:

Established hypothermia can be difficult to manage.

Prevention is preferred, using active warming devices if necessary.

viii) Check biochemistry and maintain normal electrolytes.

ix) Diabetes insipidus

Common but not universal in the setting of brain death

Treatment should commence on clinical suspicion and not be delayed for

confirmatory results.

Hypernatraemia adversely affects liver transplant outcomes.

DDAVP 1-2 µg IV bd

x) Evidence for hormonal resuscitation is conflicting. Steroids and vasopressin

should be considered if hypotension is refractory.

xi) Consider non-depolarising muscle relaxants if spinal reflexes persist, as these

may be disconcerting for relatives and attending carers.

7. Tissue Donation

a) All patients who die in the ICU may become tissue donors.

b) Tissues donated include:

i) Corneas

ii) Heart valves

iii) Bones

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L. Donation After Cardiac Death (DCD)

1. Introduction

a) DCD provides an option where there is a strong desire for organ/tissue donation;

however, the patient is unlikely to progress to brain death.

b) In all circumstances, the decision to withdraw life sustaining therapy is made

independent & prior to any consideration of organ donation.

c) DCD may be considered when:

i) A patient is planned for withdrawal of active therapy.

ii) The patient and/or their representative(s) support organ/tissue donation.

iii) Preferably age ≤ 65 (c.f. donation after brain death)

iv) Cardiac standstill is probable within 90 minutes of withdrawal:

Liver and Pancreas 30 minutes

Kidneys 60 minutes

Lungs 90 minutes.

v) There is good underlying organ function

vi) Normal contraindications to donation are absent

e.g. malignancy, active infection etc. (consult donor coordinator)

d) If a patient is likely to progress to brain death - this is preferred to DCD.

2. Determining the patient’s wishes

a) As for all organ donations, the pre-morbid wishes of the patient are paramount.

b) The Australian Organ Donor Register may assist with decision making.

c) DCD can be difficult for families, relevant issues include but are not limited to:

i) The discussion of donation prior to patient death

ii) Families may change their mind at any time without reason or question.

iii) Logistic requirements which inevitably delay the withdrawal process.

iv) Reasonable escalation of supports may occur, however if the patient becomes

too unstable donation may not occur.

v) The requirement for ante-mortem testing and interventions.

vi) Consent should be sought and rationale provided for ante mortem therapies

intended solely to aid donation.

vii) The immediate transfer of the deceased following death for organ

procurement and effective “removal” from the family.

viii) Difficulty in predicting the time of death.

ix) A significant risk of donation not proceeding, depending upon timing.

x) If the patient does not die within the organ suitability times, then palliative

care will continue in ICU and possibly the ward.

xi) There may be unknown medical reasons why donation cannot occur.

d) Under some circumstances (such as complex difficult decisions to withdraw

therapy) it may not be appropriate to include discussion about DCD.

e) A plain language statement on DCD is available from the Donate Life website.

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3. Process of DCD

a) The process will be governed by the duty ICU consultant, in conjunction with the

Organ and Tissue Donor Coordinator (OTDC - pager 83781671) and Organ

Donation Hospital Medical Director as required.

b) If “reportable” under the Coroner’s Act:

i) The treating ICU team should complete the required documentation.

ii) The OTDC will seek “in principle” approval for donation and notify the

Coroner’s representative between death and donation.

c) Withdrawal is best done as planned event in working hours.

d) The organ retrieval teams must not be involved in direct patient care before death.

4. Ante-Mortem Interventions

a) Ongoing supportive care prior to donation is rational and accepted.

b) Escalation of care, for the sole purpose of facilitating donation, is less clear.

c) The following may be considered excessive in most circumstances:

i) CPR

ii) Massive use of blood products

iii) Escalating organ support in the setting of deteriorating physiology

d) For invasive interventions, such as bronchoscopy or biopsy, discussion/consensus

with the next of kin is recommended .

e) Interventions directly aimed at the organ donation process i.e. of benefit to the

recipient but not the patient, may be considered when unlikely to cause harm

e.g. antibiotics or steroids.

f) High dose heparin with intra-cerebral pathology or ante-mortem cannulation for

organ perfusion are not considered acceptable.

g) Advice can be sought from the Organ Donation Hospital Medical Director

5. Care of the dying patient

a) Use of sedative and analgesic drugs should be in accordance with the standard

practice of good palliative care.

b) Locality

i) There is no suitable location in the current theatre suite so withdrawal should

occur in ICU with transport to theatre after death.

ii) An appropriate route should be pre-identified and kept clear.

iii) Normally there will be an OTDC with both the theatre and ICU teams.

iv) Withdrawal should not occur until there is direct communication from the

ODTC that theatre is ready.

c) Monitoring

i) HR, BP (IA), SpO2 and respiratory rate

ii) Alarms should be disabled.

iii) Remote monitoring may be preferable.

iv) Warm ischaemic time is considered to be from when SBP ≤ 50 mmHg.

v) All timing is recorded by the OTDC in the ICU.

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d) Determination of Death

i) Death is considered “irreversible” in the context of DCD when 5 minutes

have passed since circulation ceased.

Best determined by loss of a pulsatile waveform on IABP.

ECG monitoring may be used along with clinical signs.

ii) A note including the time of death should be documented in the patient’s case

notes declaring death prior to organ procurement surgery.

iii) Should death not occur in the required time the family and organ retrieval

teams should be informed and standard comfort care continued.

iv) The family may wish to view their relative following organ procurement; this

can be facilitated by the OTDC.

See the 2010 Organ and Tissue Donation and Transplant Authority (AOTDTA) http://www.donatelife.gov.au/the-authority/national-protocol-for-donation-after-cardiac-death

http://www.donatelife.gov.au/the-authority/national-protocol-for-donation-after-cardiac-death

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Table: Contact Phone Numbers

ICU Secretary Ph: 8222 5325

MedStar Ph: 8222 4222

F: 8222 2826

Organ Donor Coord T: 8207 7117

Duty Intensivist SD: 1650 Pg: 8378 1671

M: 0434 605 903

Transfusion IMVS Ext: 25430 / 25431

Consults Pager Pg: #89 22888 Transfusion RN

Pg: #89 1575

Emergency Pg: #33 Ext: 22975

Massive Transfusion 47*

Duty Anaesthetist SD: 1175

APS Pg: #89 22556 WCH Toxicology T: 8161 7000

ICU Research RN SD: 1520

ICU Dietician

SD: 1156

M: 0401 711 460

Pg: 1342

manual icu

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