case presentation mr. golf unknown critical care academics 11 february 2013

Case presentation

Mr. Golf Unknown

Critical Care Academics 11 February 2013

• 28 Year male, community assault-pt put alight and assualted with sjambok

• Injuries include:

• 30% , 3rd degree burns to face, abdomen, chest, arms, legs + inhalation burns(soot in mouth)=total of 40%

• Bilateral mandible fractures, subdural- and subarachnoid hemorraghes and cerebral oedema

• Diffuse soft tissue injuries with rhabdomyolyis

i Examination on admission

Vital signs:

- BP: 113/89mmHG

- Pulse: 119 b/min

- Temp: 35°

- RR : 22b/min

- Pulse Oximetry: 98%

• Physical examination

- GCS 7/15 (E1 M5 V2), pupils dilated

but reactive

- Abdomen: no signs of acute abdomen or injury

- Resp: no signs of resp compromise/distress (intubated due to low GCS and inhalation burns)

- 30% burns arms, legs, abdomen, face

• Biochemistry:

- Sodium: 139 mmol/l

- Potassium: 3,8 mmol/l

- Chloride: 105 mmol/l

- Urea: 5,6 mmol/l

- Creatinine: 124 mmol/l

- Myoglobin: 2322 uq/l

- CK: 4052 u/l

- CK-MB: 48,9 ug/l

- Trop I: 71ng/

- HB: 13,8 g/dl

- WCC: 10, 42

- Platelets: 404

- CRP: 138 ng/l

- INR 1,53

- PCT 7,9 ug/l

• Arterial bloodgas

- pH : 7,45

- paO2 : 133,7mmHg

- paCo2 : 40,0 mmHg

- P/F ratio : 232 mmHg

- SaO2 : 98%

- HCO3 : 20,9 mmol/l

- Lactate : 4.0 mmol/l

• Patient intubated and ventilated in casualty-SIMV (vol control)

• Myoglobin regime initiated 6 hours post injury

• FAST –no free fluid, no abdominal pathology

• Fluid resuscitation acc to Parkland formula (4ml/kg/% burns)

• Admitted to SICU 12 hours post-injury

• Progress in SICU

- Extradural ICP monitered =25 mmHg, pt sedated and paralysed, anti-convulsants started

- Early enteral nutrition initiated

- Wounds cleaned and dressed with Flamazine

- Day 4 post admission- new opacification + pleural effusion left lower lobe + pyrexia

- WCC decreased to 0,38, CRP 304, PCT 4,5

- Confirmed HIV + status

- Haemodynamic instability-vasopressor support required

- Severe sepsis , septic burns to lower limbs

• Below-knee R + forefoot amputation L done to obtain source control

• Pseudomas, coagulse - Staph cultured on LUKI, yeast on CVP

• Meronem, Teicoplanin , Colistin started, Amphotericin B added later

• No response after days, still severe LRTI-necrotising pneumonitis, pneumothorax developed and ICD placed

Currently:

• Day 11 Meronem +Teioplanin +Colistin, Amphotericin B day 6, necrotising pneumonitis-minimal response, still septic, deranged LFT’s

• Minimal neurological improvement - GCS=5/10 (M4, E1)

• Still ventilated, haemodynamically unstable, pyrexial

• Arterial blood gas

- ph: 7,41

- FiO2:40%

- P/F ratio: 186

- PaO2: 74

- PaCo2:36

- HCO3: 23

- HB : 8,7

- BE: -1,5

- lactate: 1

- Bili total: 26

- Bili conj: 16

- Alb<10

- GGT: 253

- ALP: 156

- ALT: 159

- AST:338

• Biochemistry

- Na: 137

- K: 4,2

- Cl: 106

- Urea: 5,2

- Creatinine: 49

- WCC 5,36

- PCT 3,6

- CRP 217

- INR 1,49

• Endpoints of discussion

- Fluid resuscitation/ management of burns patient

- Pathophysiology of rhabdomyolysis

- Myoglobin regime

- Management of severe head injury

- Nutrition in critical care- severe head injury and burns

RhabdomyolysisRhabdomyo = striped muscle

Lysis = dissolution

CausesTrauma

Exertion

Hypoxia

Genetic defects

Infections

Body temperature changes

Metabolic and electrolyte disorders

Drugs and toxins

Idiopathic

RhabdomyolysisRhabdomyo = striped muscleLysis = dissolution

CausesTrauma

Exertion

Hypoxia

Genetic defects

Infections



Drugs and toxins

idiopathic

CausesTrauma

Exertion

Hypoxia

Genetic defects

Infections



Drugs and toxins

idiopathic

Burns

Most serious complication : AKI

Rhabdomyolysis + AKI : 59 percent †Rhabdomyolysis – AKI : 22 percent †

AKI KILLS

Pathogenesis of AKI in rhabdmyolysis

Renal vasocontstriction volume depletion: due to fluid sequestration damaged muscle

Vascular mediators released from muscle.

Tubule obstructionMyoglobin – Tamm Horsfall complex in acidic conditions

Direct toxicityMyoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

Treatment Start/Stop:Bosh et al. NEJM july 2009

When to treat?Use plasma CK. Do not use plasma Myoglobin.

No consensus about CK cutoff : 15000IU ?

Take other factors into acount : CRF, sepsis, ...

What about myoglobinuria as a marker?

When to stop treating? Upon disappearance of myoglobinuria.

No CK or myoglobin cutoff values discribed in current literature.

Treatment / Prevention

Renal vasocontstriction volume depletion: due to fluid seaquestrationin damaged muscle




Treatment of volume depletion

Early and agressive volume replacementOnly retrospective data, Shimazu et al. , Gunal et al.

... but expert consensus.

What fluid? Studies only done with saline and ringers.

Ringers group needed more HCO3- (Cho et al.)

consensus to use saline

• What is agressive?

Very vague recommendations (NEJM july 2009) : On average 400cc / h

200 – 1000cc / h depending on setting and severity

While monitoring hemodynamic status

Target urine output of 3 ml / kg

Treatment of acidosis: NaHCO3+?

No Evidence based proof for this practice (Homsi et al., Brown et al.)

... But attractive rationaleNo Tamm Horsfall – myoglobin complex formation

Prevents redox reactions

Prevents vasoconstriction due to methemoglobin

Counteracts saline hyperinfusion acidosis

Recommendation : (NEJM 2009)If urinary pH < 6.5 alternate saline with saline + 100mmol NaHCO3+

Stop if no effect on urinary pH in 4-6h

Flushing away the obstruction?Volume repletion !!

Diuretics

Mannitol :

No evidence based proof (Homsi et al, Brown et al.)

... But attractive rationale

Prevents hypovolemia (‘draws sequestrated fluid back in circulation)

Free radical scavenging effects

Flushing effect

Recomendation (NEJM 2009): consider mannitol

Lasix:

Only flushing effect

No evidence based proof

Recommendation: (NEJM 2009)

use only if indicated due to other reasons than rhabdomyolysis.

Antioxidants

Pentoxyifilline, Vitamin E, Vitamin C

Case reports, case series, in vitro studies

May be justified, but not enough evidence. (Vanholder et al, Huerta et al)

Treatment overview

Early and agressive volume replacement with saline.

Average 400cc/h

Target urinary output : 3cc/kg/h

Monitor hemodynamic status

Add HCO3- if urinary pH < 6.5

Consider mannitol

In case of Hyperkalemia, oliguria, volume overload, metabolic acidosis dialyse (with high flux filter?)

Treatment pitfalls

Late treatment, underresuscitation

Overresuscitation , especially in anuric/oliguric patients.

Hyperkalemia

Take home message SBAH

Resuscitate early and aggressively.

... but don’t get carried away either, if patient is anuric or oliguric, don’t drown the patient and call the nepfrologist.

Do not use myoglobin, Use CK.

Check electrolytes.

Resuscitation of the Burns Patient

Initial Assessment and TreatmentAirway Management

Fluid Resuscitation

Wound Management

Secondary Survey

Complications

Initial assessment and treatment

Initial treatment and assessment occurs simultaneously with resuscitation.

Primary management includes stabilizing airway +C-spine, assess for inhalation burns, ?resp distress, ?intubation , breathing, circulation (ABCDE).

Add algorithm

Fluid resuscitation

Rapid, aggressive fluid resuscitation to

-reconstitute intravascular volume

-maintain end-organ perfusion

Determine fluid requirements by considering following:

Age

Severity of burns-depth and percentage burns

Co-morbidities

Associated injuries

Parkland formulaFluid requirements in first 24 hours= 4ml/kg body weight for each % TBSA (superficial burns excluded)

Adapt formula to personal requirements: 2-4ml/kg body weight for each% TBSA as this pt was fluid overloaded

First half given over initial 8 hours

Second half given over following 16 hours

Choice of fluid- crystalloid in form of RL- colloids and hypertonic saline not advised

Step down to 5%dex, 0,45% saline with 20mEq KCL in each vacoliter when adequate resus achieved.

Blood transfusions not advised if HB > 8mg/ dL (with transfusion threshold of 10mg/dL). In this case not indicated.

Monitor fluid statusNB!!!! Confirming adequate resus response, more important than adherence to Parkland formula( in this case myglobin regime +fluid resus should’ve been adapted to pt’s fluid requirements)

Maintain urine output at 0,5ml/kg/hour

Clinical signs of volume status

-pulse rate <110b/min (normovolemia), > 120b/min (hypovolemia)

-distal pulses

-pulse pressure

-straight-leg-rise test etc.

-vigileo, venous sats, serum lactate levels

Monitor hourly for first 24 hrs and ADJUST ACCORDINGLY!!!

PREVENT OVER-RESUSCITION!!!!!! increased incidence of compartment syndromes, pulmonary oedema etc.

Immediate wound care and cooling

Pain management

Intravenous morphine advised

Consider benzodiazepines in severe anxiety

Second survey and managementLaboratories- FBC,U+E, glucose, venous blood gas, ABG, CXR, Myoglobin levels, CK, serum lactate levels

Tetanus immunization

Topical antibiotics-silver sulfadiadize most commonly used

Wound management-irrigation soap + water, debridement,

Metabolism/nutrition

-Start feeding as soon as resus underway (increased wound healing and shorter hospitalization)

-Glucose monitoring (strict glucose control @ 8-10mmol/l)

-Anabolic steroids

Modulating catabolic responseGlycemic control( 8-10mmol/l)

Beta blockers

Preventable complications

Hypothermia

Compartment syndromes

In this case PULMONARY OEDEMA!

DVT-routine thromboembolic prophylaxis

Heparin-induced thrombocytopenia

Stress ulcers-routine prophylaxis

Adrenal insufficiency

case presentation mr. golf unknown critical care academics 11 february 2013

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