batch 1b.pdf

Signs & Symptoms

Swelling & tenderness inthe abdomen

Fever & Chills

Loss of Appetite

Nausea & Vomiting

Increased breathing &Heart Rates

Shallow Breaths

Low BP

Limited Urine Production

Inability to pass gas orfeces

Exam :

The usual sounds made bythe active intestine andheard during examinationwith a stethoscope will beabsent, because theintestine usually stopsfunctioning.

The abdom may be rigidand boardlike

Accumulations of fluid willbe notable in primary dueto ascites.

Evaluation

Lab :

Blood Test

Samples of fluid from

the abdomen

CT Scan

Chest X-rays

Peritoneal lavage.

th/

Hospitalization is

common.

Surgery is often

necessary to remove thesource of infection.

Antibiotics are

prescribed to control theinfection & intravenoustherapy (IV) is used torestore hydration.

Stomach/duodenum – Perforation

Presentation :

abdominal pain

Pain on palpation

Release pain

rigidity

peritonism, shock

Air under diaphragm onX-ray

Treatment

resuscitateantibiotics,

repair

Mekanisme Sekresi Asam lambung

optimized by optima

Blunt Abdominal Trauma

The most commonly injured organs

Spleen

Liver

Retroperitoneum

small bowel

kidneys

Bladder

Colorectum

Diaphragm

pancreas

32. Shock

Cardiogenic shock - a major component of the the

mortality associated with cardiovascular disease (the

#1 cause of U.S. deaths)

Hypovolemic shock - the major contributor to early

mortality from trauma (the #1 cause of death in those

< 45 years of age)

Septic shock - the most common cause of death in

American ICUs (the 13th leading cause of death overall

in US)

Shock: Definitions

Kumar and Parrillo (1995) - ―The state in which

profound and widespread reduction of effective tissue

perfusion leads first to reversible, and then if

prolonged, to irreversible cellular injury.‖

Shock: Classification

Hypovolemic shock - due to decreased circulating blood volume in

relation to the total vascular capacity and characterized by a reductionof diastolic filling pressures

Cardiogenic shock - due to cardiac pump failure related to loss of

myocardial contractility/functional myocardium or structural/ mechanicalfailure of the cardiac anatomy an characterized by elevations ofdiastolic filling pressures and volumes

Extra-cardiac obstructive shock - due to obstruction to flow in the

cardiovascular circuit and characterized by either impairment of diastolicfilling or excessive afterload

Distributive shock - caused by loss of vasomotor control resulting in

arteriolar/venular dilatation and characterized (after fluid resuscitation)by increased cardiac output and decreased SVR

Hypovolemic

Hemorrhagic

Trauma

Gastrointestinal

Retroperitoneal

Fluid depletion

(nonhemorrhagic)

External fluid loss

Dehydration

Vomiting

Diarrhea

Polyuria

Interstitial fluid redistribution

Thermal injury

Trauma

Anaphylaxis

Increased vascular

capacitance (venodilatation)

Sepsis

Anaphylaxis

Toxins/drugs

CARDIOGENIC

Myopathic

Blunt Cardiac Injury (trauma)

Myocarditis

Cardiomyopathy

Post-ischemic myocardial

stunning

Septic myocardial depression

Pharmacologic : Calcium

channel blockers

Mechanical

Valvular failure (stenotic or

regurgitant)

Hypertropic cardiomyopathy

Ventricular septal defect

Arrhythmic

Bradycardia

Tachycardia

EXTRACARDIAC OBSTRUCTIVE

Impaired diastolic filling

(decreased ventricular preload)

Direct venous obstruction (vena

cava)

intrathoracic obstructive

tumors

Increased intrathoracic pressure

Tension pneumothorax

Mechanical ventilation (with

excessive pressure or volumedepletion)

Asthma

Decreased cardiac compliance

Constrictive pericarditis

Cardiac tamponade

Impaired systolic contraction

(increased ventricular afterload)

Right ventricle

Pulmonary embolus (massive)

Acute pulmonary

hypertension

Left ventricle

embolus

Aortic dissection

DISTRIBUTIVE

Septic (bacterial, fungal, viral, rickettsial)

Toxic shock syndrome

Anaphylactic, anaphylactoid

Neurogenic (spinal shock)

Endocrinologic

Adrenal crisis

Thyroid storm

Toxic (e.g., nitroprusside, bretylium)

• Cutaneous vasoconstriction vs. vasodilation.

• Mental Changes: anxiousness, agitation, indifference,

CLINICAL MARKERS OF SHOCK

l

kj

• Brachial systolic blood pressure: <110mmHg

• Sinus tachycardia: >90 beats/min

• Respiratory rate: <7 or >29 breaths/min

• Urine Output: <0.5cc/kg/hr

• Metabolic acidemia: [HCO3]<31mEq/L or base

deficit>3mEq/L

• Hypoxemia: 0-50yr: <90mmHg; 51-70yr: <80mmHg;>71yo<70mmHg; K

lethargy, obtundation

Etiologyofshock example CVP CO SVR VO2sat

preload hypovolemic low low high low

contractility cardiogenic high low high low

afterload distributive

Etiology & Hemodynamic Changes in Shock

ETIOLOGYOF

SHOCK

EXAMPLE CVP CO SVR VO2SAT

AFTERLOAD DISTRIBUTIVE

HyperdynamicSeptic Low/High High Low High

HypodynamicSeptic Low/High Low High Low/High

Neurogenic Low Low Low Low

Anaphylactic Low Low Low Low

Etiology & Hemodynamic Changes in Shock

(Afterload)

HYPOVOLEMIC SHOCK• Decreased preload->small ventricular end-diastolic

volumes -> inadequate cardiac generation of pressure andflow

• Causes:

• bleeding: trauma, GI bleeding, ruptured aneurysms,

hemorrhagic pancreatitis

• protracted vomiting or diarrhea

• adrenal insufficiency; diabetes insipidus

• Dehydration

• third spacing: intestinal obstruction, pancreatitis,cirrhosis

Hypovolemic Shock

Signs & Symptoms: Hypotension, Tachycardia, MSchange, Oliguria, Deminished Pulses.

Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lacticacid and PCWP

Treatment: ABCs, IVF (crystalloid), Trasfusion Stemongoing Blood Loss

SEPTIC/INFLAMMATORY SHOCK

Mechanism: release of inflammatory mediators leading to

1. Disruption of the microvascular endothelium

2. Cutaneous arteriolar dilation and sequestration of blood incutaneous venules and small veins

Causes:

1. Anaphylaxis, drug, toxin reactions

2. Trauma: crush injuries, major fractures, major burns.

3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis,

meningitis, cholangitis, pyelonephritis, necrotic tissue,pancreatitis, wet gangrene, toxic shock syndrome, etc.

Septic/Inflammatory Shock

Signs: Early– warm w/ vasodilation, often adequate urine

output, febrile, tachypneic.

Late-- vasoconstriction, hypotension, oliguria,

altered mental status.

Monitor/findings: Early—hyperglycemia, respiratory

alkylosis, hemoconcentration,WBC typically normal or low.

Late – Leukocytosis, lactic acidosis

Very Late– Disseminated Intravascular

Coagulation & Multi-OrganSystem Failure.

Tx : ABCs, IVF, Blood cx, ABX, Drainage (ie abscess)

pressors.

CARDIOGENIC SHOCK

Mechanism: Intrinsic abnormality of heart -> inability todeliver blood into the vasculature with adequate power

Causes:

1. Cardiomyopathies: myocardial ischemia, myocardial infarction,cardiomyopathy, myocardiditis, myocardial contusion

2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture,septal defects, aortic stenosis

3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrialfibrillation, atrial flutter, ventricular fibrillation)

4. Obstructive disorders: PE, tension peneumothorax, pericardialtamponade, constrictive pericaditis, severe pulmonary hypertension

Cardiogenic Shock

Characterized by high preload (CVP) with low CO

Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria

Monitor/findings: CXR pulm venous congestion, elevated CVP,

Low CO.

Tx: CHF– diuretics & vasodilators +/- pressors.

LV failure – pressors, decrease afterload,

intraaortic ballon pump &

ventricular assist device.

NEUROGENIC SHOCK

Causes:

1.Spinal cord injury

2.Regional anesthesia

3.Drugs

4.Neurological disorders

Mechanism: Loss of autonomic

innervation of the cardiovascular system(arterioles, venules, small veins, includingthe heart)

Neurogenic Shock

Characterized by loss of vascular tone & reflexes.

Signs: Hypotension, Bradycardia, Accompanying

Neurological deficits.

Monitor/findings: hemodynamic instability, test

bulbo-carvernous reflex

Tx: IVF, vasoactive medications if refractory

33. FOREHAND FRACTURE

Montegia Fracture Dislocation

It is a fracture of the proximal

1/3rd of the Ulna with

dislocation of head of radius

anteriorly. Posteriorly or

laterally

Head of Radius dislocates

same direction as fracture

It requires ORIF or it will

redisplace

Montegia : Lateral displacement

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Galliazi Fracture

It is a fracture of distal

Radius and dislocation ofinferior Radio- Ulnar joint

Like Montegia fracture if

treated conservatively itwill redisplace

This fracture appeared in

acceptable position afterreduction and POP

Greenstick Fractures

Colles‘ Fracture

Most common fracture in Osteoporoticbones

Extra-Articular : 1 inch of distal Radius

Results from a fall on dorsi flexed wrist

Typical deformity : Dinner Fork

Deformity is : Impaction, dorsal displacement

and angulation, radial displacement andangulation and avulsion of ulnar styloidprocess

Colles‘ Fracture

optimized by optima

# distal 1‘‘ Impaction ,Dorsal displacement

and dorsal tilt

Colles‘ Fracture

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Smith Fracture

Smith Fracture

Almost the opposite of Colles‘ fracture

Much less common compared to colles‘

Results from a fall on palmer flexed wrist

Typical deformity : Garden Spade

Management is conservative : MUA and Above

Elbow POP

34. LOW BACK PAIN

Herniated Nucleus Pulposus

The progressive

degeneration of a disc, or

traumatic event, can lead

to a failure of the annulus

to adequately contain the

nucleus pulposus

This is known as herniated

nucleus pulposus (HNP) or

a herniated disc


Symptoms

Back pain

Leg pain

Dysthesias

Anesthesias


Varying degrees

Disc bulge

Mild symptoms

Usually go away with

nonoperative treatment

Rarely an indication

for surgery

Extrusion (herniation)

Moderate/severe symptoms

Nonoperative treatment


Diagnosis

Magnetic resonance imaging(MRI)/patient exam

Nonoperative Care

Initial bed rest

Nonsteroidal anti-

inflammatory (NSAID)medication

Physical therapy

Exercise/walking

Steroid injections


Surgical care

Failure of nonoperative

treatment

of 6 weeks in Minimumduration

Can be months

Discectomy

Removal of the

herniatedportion of the disc

Usually through a small

incision

High success rate


Cauda Equina Syndrome

Caused by a central disc

herniation

Symptoms include bilateral

leg pain, loss of perianal

sensation, paralysis of the

bladder, and weakness of

the anal sphincter

Surgical intervention in

these cases is urgent

Spondylolisthesis

Gradation of

spondylolisthesis

Meyerding‘s Scale

Grade 1 = up to 25%

Grade 2 = up to 50%

Grade 3 = up to 75%

Grade 4 = up to 100%

Grade 5 >100%

(complete dislocation,

spondyloloptosis)

Spondylolisthesis

Symptoms

Low back pain

With or without buttock or

thigh pain

Pain aggravated by standing

or walking

Pain relieved by lying down

Concomitant spinal stenosis,

with or without leg pain, maybe present

Other possible symptoms

Tired legs, dysthesias,

anesthesias

Partial pain relief by leaning

forward or sitting

Spondylolisthesis

Diagnosis

Plain radiographs

CT, in some cases with

leg symptoms

Nonoperative Care

Rest

NSAID medication

Physical therapy

Steroid injections

Spondylolisthesis

Surgical care

Failure of nonoperative

treatment

Decompression and fusion

Instrumented

Posterior approach

With interbody fusion

Spondylolysis

Spondylolysis

Also known as pars defect

Also known as pars fracture

With or without

spondylolisthesis

A fracture or defect in the

vertebra, usually in the

posterior elements—most

frequently in the pars

interarticularis

Spondylolysis

Symptoms

Low back pain/stiffness

Forward bending

increases pain

Symptoms get worse

with activity

May include a stenotic

component resulting in

leg symptoms

Seen most often in athletes

Gymnasts at risk

Caused by repeated strain

Spondylolysis

Diagnosis

Plain oblique radiographs

CT, in some cases

Nonoperative care

Limit athletic activities

Physical therapy

Most fractures heal without

other medical intervention

Spondylolysis

Surgical care

Failure of nonoperative treatment

Posterior fusion

Instrumented

May require decompression

Ankylosing spondilitis

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35. ABDOMINAL INJURIES

Causes

injuries to the

abdomen, pelvis

and genitalia are

generally caused by

accidents involving

high kinetic energy

and acceleration or

deceleration forces

Open vs. Closed Injuries

Abdominal injuries can beeither open or closed

Open injuries are caused bysharp or high velocityobjects that create anopening between theperitoneal cavity and theoutside of the body

Closed injuries are causedby compression traumaassociated withdeceleration forces andinclude:

contusions

ruptures

lacerations

shear injuries

Hollow and Solid Organs

The type of injury will depend on whether the organ injured issolid or hollow.

hollow organs include:

stomach

intestines

gallbladder

bladder

solid organsinclude:

liver

spleen

kidneys

when hollow organsrupture, their highlyirritating andinfectious contentsspill into theperitoneal cavity,producing a painfulinflammatory reactioncalled peritonitis

damage to solid organssuch as the liver can causesevere internal bleeding

blood in the peritonealcavity causes peritonitis

when patients injure solidorgans, the symptoms ofshock may overshadowthose from peritonitis

Abdominal Injuries

Hollow Organ Injuries Solid Organ Injuries

Abdominal Injuries

Abdominal injuries canbe obvious, such as anopen wound, or subtle,such as a blow to theflank that initiallycauses little pain, butdamages the liver orspleen

Suspect abdominalinternal injury in anypatient who has apenetrating abdominalwound or has sufferedcompression trauma tothe abdomen

Liver

Largest organ in abdominalcavity

Right upper quadrant

Injured from trauma to: Eighth through twelfthribs on right side ofbody

Upper central part ofabdomen

Suspect liver injury when:

Steering wheel injury Lap belt injury Epigastric trauma

After injury, blood and bileleak into peritoneal cavity Shock

Peritoneal irritationManagement:

Resuscitation Laparotomy and repairor resection.

Avulsion of pedicle isfatal

Spleen

Upper left quadrantRich blood supply

Slightly protected by organssurrounding it and by lower ribcage Most commonly injured organ

from blunt trauma Associated intraabdominal

injuries commonSuspect splenic injury in:

Motor vehicle crashes Falls or sports injuries

involving was an impact to thelower left chest, flank, orupper left abdomen

Kehr’s sign

Left upper quadrant painradiates to left shoulder

Common complaint withsplenic injury

Management :

Resuscitation.

Laparotomy (repair, partialexcision or splenectomy)

Observation in hospital forpatients with sub-capsularhaematoma

Stomach/duodenum

Not commonly injured by blunt trauma

Protected location in abdomen

Penetrating trauma may cause gastric transection or

laceration

Signs of peritonitis from leakage of gastric contents

Diagnosis confirmed during surgery

Unless nasogastric drainage returns blood

Stomach/duodenum

Presentation :

abdominal pain

rigidity

peritonism, shock

Air under diaphragm onX-ray

Treatment Antibiotics

resuscitate

repair

Presentation :

Haematemesis +/-

Melaena

Severity

Increased PR>90

Fall BP<100

Treatment :

transfusion

inject DU

Perforation Bleeding

36. ILEUS

Introduction and Definitions

Accounts for 5% of all acute surgical admissions

Patients are often extremely ill requiring prompt

assessment, resuscitation and intensive monitoring

Obstructive ileus

A mechanical blockage arising from a structural abnormality

that presents a physical barrier to the progression of gut

contents.Paralytic Ileus

is a paralytic or functional variety of obstruction

Obstruction is: Partial or complete

Simple or strangulated

Pathophysiology I

8L of isotonic fluid received by the small intestines (saliva,stomach, duodenum, pancreas and hepatobiliary )7L absorbed

2L enter the large intestine and 200 ml excreted in the faeces

Air in the bowel results from swallowed air ( O2& N2) and bacterialfermentation in the colon ( H2, Methane & CO2),

600 ml of flatus is releasedEnteric bacteria consist of coliforms, anaerobes and strep.faecalis.

Normal intestinal mucosa has a significant immune role

Distension results from gas and/ or fluid and can exert hydrostaticpressure.In case of BO Bacterial overgrowth can be rapid

If mucosal barrier is breached it may result in translocation of bacteria andtoxins resultingin bactaeremia,septaecemia and toxaemia.

Pathophysiology II

Obstruction results in:

1.

2.

3.

4.

5.

6.

7.

8.

Initial overcoming of the obstructionby increased paristalsisIncreased intraluminal pressure by fluid and gasVomitingsequestrationof fluid into the lumen from the surroundingcirculationLymphatic and venous congestion resultingin oedematous tissuesFactors 3,4,5 result in hypovolaemia and electrolyte imbalanceFurther: localised anoxia,mucosal depletion necrosisand perforationand peritonitis.Bacterial over growth with translocation of bacteria and it’s toxinscausingbacteraemia and septicaemia.

Decompresswith NGTReplace lost fluid

Correct electrolyteabnormalities

Recognisestrangulation andperforation

Systemic antibiotics.

Colonic

• Preexisting change in

bowel habit

•Colicky in the lower

abdomin

•Vomiting is late

•Distension prominent

•Cecum ? distended

Distal small bowel

•Pain: central and colicky

•Vomitus is feculunt

•Distension is severe

•Visible peristalsis

•May continue to pass

flatus and feacus before

absolute constipation

High

•Pain is rapid

•Vomiting copious and

contains bile jejunal content

•Abdominal distension is

limited or localized

•Rapid dehydration

1. History

The Universal Features

Colicky abdominal pain, vomiting, constipation (absolute), abdominal

distension.

Complete HX ( PMH, PSH, ROS, Medication, FH, SH)

Persistent pain may be a sign of strangulation

Relative and absolute constipation

Luminal Mural Extraluminal

F.Body

Bezoars

Gallstone

FoodParticles

A.lumbricoides

Neoplasms

lipoma

polyps

leiyomayoma

hematoma

lymphoma

carcinoid

carinoma

secondaryTumors

Crohns

TB

Stricture

Intussusception

Congenital

Postoperative

adhesions

Congenital

adhesions

Hernia

Volvulus

Causes- Small Bowel

2. Examination

Others

Systemic examination

If deemed necessary.

•CNS

•Vascular

•Gynaecological

•muscuoloskeltal

Abdominal

•Abdominal distension

and it‘s pattern

•Hernial orifices

•Visible peristalsis

•Cecal distension

•Tenderness, guarding

and rebound

•Organomegaly

•Bowel sounds

–High pitched

–Absent

•Rectal examination

General

•Vital signs:

P, BP, RR, T, Sat

•dehydration

•Anaemia, jaundice, LN

•Assessment of vomitus if

possible

•Full lung and heart

examination

Initial Management in the ER

Resuscitate:

Air way (O2 60-100%)

Insert 2 lines if necessary

IVF : Crytloids at least 120 ml/h. (determined by estimated fluid loss and

cardiac function).Add K+ at 1mmmol/kg

Draw blood for lab investigations

Inform a senior member in the team.

NPO.

Decompress with Naso-gastric tube and secure in position

Insert a urinary catheter (hourly urinary measurements) and start a fluid

input / output chart

Intravenous antibiotics (no clear evidence)

If concerns exist about fluid overloading a central line should be inserted

Follow-up lab results and correction of electrolyte imbalance

The patient should be nursed in intermediate care

Rectal tubes should only be used in Sigmoid volvulus.

Indications for Surgery

Immediate intervention:

Evidence of strangulation (hernia….etc)

Signs of peritonitis resulting from perforation or

ischemia

Paralytic Ileus

Associated with the following conditions:

Postoperative and bowel resection

Intraperitoneal infection or inflammation

Ischemia

Extra-abdominal: Chest infection, Myocardia infarction

Endocrine: hypothyroidism, diabetes

Spinal and pelvic fractures

Retro-peritoneal haematoma

Metabolic abnormalities:

Hypokalaemia

Hyponatremia

Uraemia

Hypomagnesemia

Bed ridden

Drug induced: morphine, tricyclic antidepressants

Clinical Findings

Clinical features

Is there an under lying cause?

Is the abdomen distended but tenderness is not marked.

Is the bowel sounds diffusely hypoactive.

Radiological features:

Is the bowel diffusely distended

Is there gas in the rectum

Are further investigasions (CT or Gastrografin studies) helpful

in showing an obstruction.

Does the patient improve on conservative measures

37. BURN INJURY

Burn Injuries

Potential complications

Fluid and Electrolyte loss Hypovolemia

Hypothermia, Infection, Acidosis

catecholamine release, vasoconstriction

Renal or hepatic failure

Formation of eschar

Complications of circumferential burn

Burn Injuries

An important step inmanagement is todetermine depth andextent of damage todetermine where and howthe patient should betreatedDepth Classification Superficial Partial thickness Full thickness

Thermal burn Skin injury Inhalation injury

Chemical burn Skin injury Inhalation injuryMucous membraneinjury

Electrical burn Lightning

Radiation burn

Burn Classifications

1st degree (Superficial burn)

Involves the epidermis

Characterized by reddening

Tenderness and Pain

Increased warmth

Edema may occur, but no

blistering

Burn blanches under pressure

Example - sunburn

Usually heal in ~ 7 days


2nd degree

Damage extends through the

epidermis and involves the dermis.

Not enough to interfere with

regeneration of the epithelium

Moist, shiny appearance

Salmon pink to red color

Painful

Does not have to blister to be 2nd

degree

Usually heal in ~7-21 days


3rd degree

Both epidermis and dermis are

destroyed with burning into SC fat

Thick, dry appearance

Pearly gray or charred black color

Painless - nerve endings are destroyed

Pain is due to intermixing of 2nd

degree

May be minor bleeding

Cannot heal and require grafting

Burn Injuries

Often it is not possible to predict the exact depth of

a burn in the acute phase. Some 2nd degree burns

will convert to 3rd when infection sets in. When in

doubt call it 3rd degree.

Body Surface Area Estimation

Rule of Nines

Adult

Palm Rule

Body Surface Area Estimation

Rule of Nines

Peds

For each yr over 1 yoa,

subtract 1% from head

and add equally to legs

Palm Rule

38. ARTERIAL DISEASE

Arterial Disease

Raynaud phenomenon is a

vasospastic disease of the digital

arteries; occurs in susceptible

people when exposed to cool

temperatures or during emotional

stress.

Symptoms:

numbness,

paresthesias, or

Pain

Raynaud's syndrome is used to

encompass both the primary &secondary conditions causing

Raynaud phenomenon.

Vasospasm of digital arteriesobliterates the lumen

Inhibited blood flow triphasic colorresponse

fingers blanch to a distinct white as bloodflow is interrupted

cyanosis, related to local accumulation ofdesaturated hemoglobin

ruddy color as blood flow resumes

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Brunicardi FC. Schwartz principles of surgery. 8th ed. McGraw-Hill; 2004.

Arterial Disease

Raynaud disease:

Predominantly woman ages 20-40

Mechanism:

sympathetic discharge in

response to cold,

vascular sensitivity to adrenergic

stimuli, or

Raynaud phenomenon:

may appear as a component of otherconditions.

Causes: connective tissue diseases

(scleroderma & SLE) arterial occlusive disorders. carpal tunnel syndrome, thermal or vibration injury.

In patients with connective tissuediseases/arterial occlusive disease: thedigital vascular lumen is largelyobliterated by sclerosis or

Treatment:

sympathetically mediatedvasoconstriction.

footwear.• Preventing vasospasm with CCB or alpha

blocker.Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

39. Urine Incontinence

40. Urethral Trauma

Anterior Urethral Trauma

Position : Distal fromurogenital diagphram

Etiology :

Straddle Injury

Instrumentation

Clinical Signs :

Blood from urethral meatus

Hematom, perineal pain

Urinary retenstion

Radiology : urethrogram

Therapy :

Sistostomyimmediate repair

Tanagho EA, et al. Smith‘s general urology. 17th ed. McGraw-Hill; 2008.

Tanagho EA, et al. Smith‘s general urology. 17th ed. McGraw-Hill; 2008.

Urethral Trauma

Posterior Urethral Trauma

Etiology Pelvic bone fracture

Clinical Symptoms Blood from meatus Urinary retention Pain, hematom on pubic region

Radiology Pelvic Photo Urethrogram

Therapy Sistostomy Repair 3-4 days later.

41. Pericardial Disease

Etiology of cardiac tamponade:

neoplastic, postviral, & uremicpericarditis.

Acute hemorrhage into

pericardium:

blunt/penetrating chest

trauma,

rupture of the left

ventricular free wallfollowing MI,

dissecting aortic aneurysm

Pulsus Paradoxusdecreased of SBP ≥10 mmHg during inspiration

Thorax expansion duringinspiration

Intrathoracic pressure becomemore negative

Facilitates venous return &right ventricle filling

Increase in RV sizediminishes LV filling

In cardiac tamponade, the normal

situation (left diagram) is

exaggerated because both ventricles

share a reduced, fixed volume as a

result of external compression by the

tense pericardial fluid.

Pulsus paradoxus may also be

manifested by other conditions in

which inspiration is exaggerated,

including severe asthma & COPD.

LV stroke volume & systolicblood pressure decline slightly

McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006.

Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000.

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Management:

ABC‘s with c-spine control

as indicated

High Flow oxygen

Cardiac Monitor

Large Bore IV access

Rapid Transport

What patient needs is

pericardiocentesis

Cardiac Tamponade

Pericardiosentesis

Using aseptic technique, Insert atleast 3‖ needle at the angle of theXiphoid Cartilage at the 7th rib

Advance needle at 45 degreetowards the clavicle whileaspirating syringe till blood returnis seen

Continue to Aspirate till syringe isfull then discard blood andattempt again till signs of no moreblood

Closely monitor patient due tosmall about of blood aspiratedcan cause a rapid change in bloodpressure

42. COMPARTMENT SYNDROME

Compartment Syndrome

A condition in whichincreased pressure withina limited spacecompromises thecirculation and functionof the tissues within thatspace.

Elevated tissue pressurewithin a closed fascialspace

Reduces tissue perfusion- ischemia

Results in cell death -

necrosis

True Orthopaedic Emergency

Compartment Syndrome

Etiology

Compartment Size tight dressing; Bandage/Cast

localised external pressure; lying on limb

Closure of fascial defects

Compartment Content Bleeding; Fx, vas inj, bleeding disorders

Capillary Permeability;

Ischemia / Trauma / Burns / Exercise / Snake Bite /Drug Injection / IVF

optimized by optima

optimized by optima

Compartment SyndromeEtiology

Fractures-closed and

open

Blunt trauma

Temp vascular

occlusion

Cast/dressing

Closure of fascial

defects

Burns/electrical

Exertional states

IV/A-lines

Intraosseous IV(infant)

Snake bite

Arterial injury

Compartment SyndromeDiagnosis

Pain out of proportion

Palpably tense compartment

Pain with passive stretch

Paresthesia/hypoesthesia

Paralysis

Pulselessness/pallor

Clinical Evaluation

―Pain and the aggravation of pain by passive

stretching of the muscles in the compartment in

question are the most sensitive (and generally the

only) clinical finding before the onset of ischemic

dysfunction in the nerves and muscles.‖

Clinical Evaluation

Pain – most important. Especially pain out of

proportion to the injury (child becoming more and

more restless /needing more analgesia)

Most reliable signs are pain on passive stretching

and pain on palpation of the involved compartment

Other features like pallor, pulselessness, paralysis,

paraesthesia etc. appear very late and we should

not wait for these things.

Willis &Rorabeck OCNA 1990

Compartment SyndromePressure Measurements

Infusion

manometer

saline

3-way stopcock(Whitesides, CORR

1975)

Catheter

wick

slit wick

Arterial line

16 - 18 ga.Needle

(5-19 mm Hg higher)

transducer

monitor

Stryker device

Side port needle

Compartment SyndromeEmergent Treatment

Remove cast or dressing

Place at level of heart

(DO NOT ELEVATE to optimize perfusion)

Alert OR and Anesthesia

Bedside procedure

Medical treatment

Surgical Treatment

optimized by optima

Fasciotomy

Casts and tightbandagesremove or

loosen anyconstrictingbandages

All compartments !!!

PEMBAHASAN ANAK

43. Ikterus Neonatorum

Bayi perempuan (neonatus), kuning

Lahir cukup bulan, APGAR 5/8

Ibu B Rh-, ayah O Rh+

Hb 15, bilirubin total 8, golongan darah O

Metabolisme bilirubin

Bilirubin

Tidak terkonjugasi:

Bilirubin indirek

Tidak larut dalam air

Berikatan dengan albumin

untuk transport

Komponen bebas larut

dalam lemak

Komponen bebas bersifat

toksik untuk otak

Terkonjugasi:

Bilirubin direk

Larut dalam air

Tidak larut dalam lemak

Tidak toksik untuk otak

Ikterus neonatorum

Secara umum penyebabnya:

Meningkatnya produksi bilirubin akibat hemolisis

Kurangnya albumin sebagai alat transport

Penurunan uptake oleh hati

Penurunan konjugasi bilirubin oleh hati

Penurunan ekskresi bilirubin

Peningkatan sirkulasi enterohepatik

Setiap penyakit yang menyebabkan hemolisis yang

berlebihan atau gangguan pada metabolisme/ekskresibilirubin biasanya akan menyebabkan ikterus

Ikterus fisiologis vs non fisiologis

Ikterus fisiologis:

Awitan terjadi setelah 24 jam

Memuncak dalam 3-5 hari, menurun dalam 7 hari (pada NCB)

Ikterus fisiologis berlebihan ketika bilirubin serum puncak adalah 7-15 mg/dl pada NCB

Ikterus non fisiologis:

Awitan terjadi sebelum usia 24 jam

Tingkat kenaikan > 0,5 mg/dl/jam

Tingkat cutoff > 15 mg/dl pada NCB

Ikterus bertahan > 8 hari pada NCB, > 14 hari pada NKB

Tanda penyakit lain

Gangguan obstruktif menyebabkan hiperbilirubinemia direk.Ditandai bilirubin direk > 2 mg/dl. Penyabab: kolestasis, atresiabilier, kista duktus koledokus.

Kemungkinan besar: inkompatibilitas ABO, Rh, penyakit hemolitik, atausferositosis. Penyebab lebih jarang: infeksi kongenital, defisiensi G6PD

Ikterus yang berkembang cepat setelah usia 48 jam

Kemungkinan besar: infeksi, defisiensi G6PD. Penyebab lebih jarang:inkompatibilitas ABO, Rh, sferositosis.

20

18

16

14

12

10

8

6

4

2

0

hari 1 hari 2 hari 3 hari 4 hari 5 hari 6 hari 7

Ikterus yang berkembang cepat pada hari ke-1

fisiologis

non- fisiologis

Daerah tubuh

Muka

Dada/punggung

Perut dan paha

Tangan dan kaki

Kadar bilirubin (mg/dl)

4 -8

5 -12

8 -16

11-18

Telapal tangan/kaki >15

Penyakit Keterangan

InkompatibilitasABO Adanyaaglutininibuyangbersirkulasididarahanak

terhadapaglutinogenABOanak.

InkompatibilitasRh Adanyaantibodiibuyangbersirkulasididarahanak

terhadapantigenRhanak.Jarangpadaanakpertama.

Hematomadarah

ekstravaskuler

Akibatprosespersalinan.

DefisiensiG6PD PenyakitterkaitkromosomX.EnzimG6PDberfungsiuntuk

melindungieritrositdarikerusakanoksidatif.

Sferositosisherediter Terdapatdefekproteinmembranyangmenyebabkan

instabilitaseksoskeletoneritrosit

Polisitemia Peningkatanpembentukaneritrosityangmenyebabkan

peningkatandestruksieritrosit

Penyebab hemolisis

44. Perdarahan pada neonatus

Bayi usia 2 hari

BAB berdarah, muntah darah, petekie

Persalinan ditolong dukun

Stadium Characteristic

EarlyHDN Occurswithin2daysandnotmorethan5daysoflife.Baby

bornofmotherwhohasbeenoncertaindrugs:anticonvulsant,

antituberculousdrug,antibiotics,VKantagonistanticoagulant.

ClassicHDN Occursduring2to7dayoflifewhentheprothrombincomplex

islow.ItwasfoundinbabieswhodonotreceivedVKPor

VKsupplemented.

VitKdeficiency Occurswithin2daysandnotmorethan5daysoflife.Definite

etiologyinducingVKPisfoundinassociationwithbleeding:

malabsorptionofVKiegutresection,biliaryatresia,severe

liverdisease-inducedintrahepaticbiliaryobstruction.

LateHDN/APCD Acquiredbleedingdisorderinthe2weekto6monthageinfant

causedbyreducedvitaminKdependentclottingfactor(II,VII,

IX,X)withahighincidenceofintracranialhemorrhageand

respondstoVK.

Hemorrhagic disease of newborn (HDN)

Acquired prothrombrin complex deficiency (APCD)

45. Anemia

Anak perempuan, usia 2 tahun, pucat, rewel, nafsu

makan berkurang

Gizi kurang, anemia, atrofi papila lidah, tidak ada

hepatosplenomegali & limfadenopati

Hb 6,2; leukosit 8.000; Ht 19,5%; tro 350.000;

MCV 62; MCH 21; MCHC 28

Parameter Kadarnormal Satuan

Hb 6bln-2thn:10,5-13,5

2-6thn:11-14,7

6-12thn:11,5-15,5

12-18thn:13-16(L);12-16(P)

g/dL

Ht 2thn:33-42 %

Leukosit 2thn:6000-17.500 /μL

Trombosit 150.000-400.000 /μL

MCV 2thn:70-86 fL

MCH 2thn:23-31 pg/sel

MCHC 2thn:30-36 %Hb/sel

Hipokrom: MCH ˂ normal

Mikrositik: MCV ˂ normal

Hiperkrom: MCH ˃ normal

Makrositik: MCV ˃ normal

Red Cell MorphologyPenyakit (tambahan)

Hereditary, Lipid

disorders,

splenectomy

Hb C disease, post

splenectomy

Myeloid metaplasia

Uremia, following

heparin injection, def

pyruvate kinase

Thalassemia, anemia

megaloblastic, iron

deficiency

Stage IronDepletion

I

IronDeficiency

II

IDA

III

IronStore

(Ferritin)

SerumIron Normal

Hb Normal Normal MCV,MCHMCHC

Anemia defisiensi Fe

Penyebab:

Peningkatan kebutuhan (pemakaian Fe , infeksi berulang)

Perdarahan kronik

Asupan diet kurang

Malabsorpsi

Kurangnya cadangan besi (prematur, gemelli, anemia pada ibu hamil)

46. Hemophilia

Bayi perempuan, usia 4 bulan, perdarahan

Riwayat keluarga +

Hb 11,2; leukosit 7.500; trombosit 300.000; BT 2‘;

PT 12‖; aPTT 70‖

Didiagnosis hemofilia A

Kaskade koagulasi

aPTT

PT

47. Congenital Heart Disease

Congenital HD

Acyanotic

With ↑ volumeload:

- ASD

- VSD

- PDA

- Valve

regurgitation

1. Nelson‘s textbook of pediatrics. 18th ed.

2. Pathophysiology of heart disease. 5t ed.

With ↑ pressureload:

- Valve stenosis

- Coarctation ofaorta

Cyanotic

With ↓pulmonary blood

flow:

- ToF

- Atresiapulmonal

- Atresiatricuspid

With ↑pulmonary blood

flow:

- Transpositionof the great

vessels

- Truncusarteriosus

Tekanan di dalam Jantung

Acyanotic Congenital HD:General Pathophysiology

With↑ volume load

The most common: left to right shunting

Blood back into the lungs

Fluid leaks into the interstitial space &

alveoly

High level of ventricular output ->↑sympathetic nervous system

If left untreated, ↑ volume load willincrease pulmonary vascular resistance

Clinical Findings

e.g. ASD, VSD, PDA

↓ compliance &↑ work of breathing

Pulmonary edema, tachypnea, chest

retraction, wheezing

↑ Heart rate & stroke volume

↑Oxygen consumption -> sweating,irritability, FTT

Remodelling: dilatation & hypertrophy

Eventually leads to EisenmengerSyndrome


Acyanotic Congenital HD:General Pathophysiology

Clinical Findings

Dilatation happened in the later stage

Severe pulmonic stenosis in newborn

right-sided HF (hepatomegaly,peripheral edema)

Severe aortic stenosis left-sided(pulmonary edema, poor perfusion) &

right-sided HF

With↑ pressure load

Obstruction to normal blood flow:pulmonic stenosis, aortic stenosis,

coarctation of aorta.

Hypertrophy & dilatation of ventricularwall

Defect location determine thesymptoms


Cyanotic Congenital HD

The degree of cyanosis depends on:

the degree of obstruction to pulmonary blood flow

If the obstruction is mild:

Cyanosis may be absent at rest

These patient may have hypercyanotic spells during condition of stress

If the obstruction is severe:

Pulmonary blood flow may be dependent on patency of the ductus arteriosus.

When the ductus closes hypoxemia & shock

Cyanotic lesions with ↓ pulmonary blood flow must include both:

an obstruction to pulmonary blood flow & a shunt from R to L

Common lesions:

Tricuspid atresia, ToF, single ventricle with pulmonary stenosis

Abnormal ventricular-arterialconnections:

- TGA

Total mixing of systemic venous &pulmonary venous within the heart:

- Common atrium or ventricle

- Total anomolous pulmonary venousreturn

Cyanotic Congenital HD

Cyanotic lesions with ↑ pulmonary blood flow is notassociated with obstruction to pulmonary blood flow

Cyanosis is caused by:

- Truncus arteriosus


Ventricular Septal Defect

VSD:Pathophysiology & Clinical Findings

Ph/: increased of 2nd heart sound


Flow across VSD

Over flow across mitral valve

LA, LV, RV volume overload

High systolic pressure & highflow to the lungs pulmonary

hypertension

Pansystolic murmur & thrillover left lower sternum.

If defect is large 3rd heart sound& mid diastolic rumble at the apex.

ECG: Left ventricular hypertrophyor biventricular hypertrophy,

peaked/notched P wave

Ro: gross cardiomegaly

Dyspnea, feeding difficulties, poorgrowth, profuse perspiration,

pneumonia, heart failure.

Duskiness during crying or infection

VSD:

Pathophysiology & Clinical Findings

cardiomegaly with prominence of

both ventricles,

the left atrium, &

the pulmonary artery.

pulmonary vascular marking


Atrial Septal Defect

Overflow in the right side ofheart

Enlargement of the RA & RV

Dilatation of the pulmonary artery

The LA may be enlarged

ASD:Pathophysiology & Clinical Findings

The degree of L-to-R shunting is dependent on:

- the size of the defect,

- the relative compliance of the R and L ventricles, &

- the relative vascular resistance in the pulmonary & systemic circulations

Infant has thick & less compliant RV minimal symptoms

As children grow older: subtle failure to thrive, fatigue, dyspneu oneffort, recurrent respiratory tract infection

Pulmonary vascular resistance may begin to increase in adulthood

reversal of the shunt & cyanosis



Increased flow into right side ofthe heart & lungs

Constant increased ofventricular diastolic volume

Increased flow across tricuspidvalve

Increased flow acrosspulmonary valve

Ro:

- enlargement of RV, RA, &pulmonary artery

- increased vasvular marking

Wide, fixed 2nd heart soundsplitting

Mid-diastolic murmur at thelower left sternal border

Thrill & systolic ejection murmur, bestheard at left middle & upper sternalborder

Flow across the septal defect doesn’t produce murmur because the pressuregap between LA & RA is not significant



size of the main pulmonary

artery

size of the right atrium

size of the right ventricle

(seen best on the lateral view

as soft tissue filling in the lower

& middle retrosternal space).


2. Essentials of Radiology. 2nd ed.

Patent Ductus Arteriosus

Coarctasio of Aorta

Tetralogi Fallot

48.Tropic Infection:

typhoid fever

Etiology:Salmonella typhosa

Clinical features: Step ladder fever in

the first week, thepersist

Abdominal pain

Diarrhea/constipation

Headache

Coated tongue

Hepatosplenomegaly

Rose spot

Harrison‘s principles of internal medicine. 18th ed.

• Muscle tenderness in the muscles

Tropic Infection: leptospirosis

Infection through themucosa or wounded skin

Proliferate in thebloodstream or

extracellularly within organ

Disseminatehematogenously to all

organs

Multiplication can cause:

• Hepatitis, jaundice, & hemorrhage in the liver• Uremia & bacteriuria in the kidney• Aseptic meningitis in CSF & conjunctival or scleral hemorrhage in the aqueous humor


Lauralee S. Human physiology. From cells to system.

49. Electrolyte: Natrium regulation

Sodium functions:

fluid balance (the major

factor in extracellular

osmolality)

nerve impulse

generation &

transmission

(neuromuscular

function).

Electrolyte: hyponatremia

Many symptoms of

hyponatremia are associated

with the hypotonic hydration.

The most common symptoms:

• Headache

• Nausea

• Disorientation

• Tiredness

• Muscle cramps

Johnson JY. Fluids and Electrolytes demystified. 2008

Electrolyte: hyponatremia

Natrium concentration is influenced by the balance of natrium &

water in the body.


Electrolyte: hypernatremia

Hypernatremia can affect

brain cells and cause

neurologic damage,

resulting in

Confusion

Paralysis of the muscles

of the lungs

Coma

Even death

Hypernatremia

Fluid moves out of the cells

Cell dehydration with shrinkage

Dry tissues dry mucous membrane, lossof turgor, & thirst

Johnson JY. Fluids and Electrolytes demystified. 2008

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