Viva Voce: Traumatic Brain Injury for Emergency Medicine Doctors

SECTION 1 - Classification & GCS

• Mild TBI (mTBI/concussion): GCS 13-15
• Moderate TBI: GCS 9-12
• Severe TBI: GCS 3-8

1. Loss of consciousness (LOC) for less than 30 minutes
2. Loss of memory for events before or after the accident (post-traumatic amnesia <24 hours)
3. Any alteration in mental state at the time of the accident (dazed, disoriented, confused)
4. Focal neurologic deficit(s), which may or may not be transient

1. Somatic - headache, dizziness, balance problems, vertigo, tinnitus, photophobia, nausea/vomiting
2. Cognitive - impaired memory/concentration, delayed language comprehension, slowed/repetitive speech
3. Emotional - irritability, sadness, anxiety, depression
4. Sleep-related - insomnia or fatigue (the full spectrum)

SECTION 2 - Anatomy & Pathophysiology

• S - Skin
• C - Connective tissue (subcutaneous, with a rich blood supply including hair follicles)
• A - Aponeurosis (galea - tough fascia containing occipitofrontalis muscle)
• L - Loose areolar tissue (allows subgaleal hematomas to become large as blood dissects easily through this layer; also the plane of scalp avulsions)
• P - Pericranium (periosteum)

• Activation of inflammatory responses
• Imbalances in ion concentrations (especially potassium efflux and calcium influx)
• Increased excitatory amino acids (notably glutamate - excitotoxicity)
• Dysregulation of neurotransmitter synthesis/release
• Mitochondrial dysfunction and impaired energy metabolism
• Production of free radicals

• No Hypoxia (SpO2 >95%, PaO2 >60 mmHg)
• No Hypotension (maintain adequate MAP/CPP)
• Normothermia (avoid hyperthermia)
• Normocapnia (PaCO2 35-45 mmHg)
• Euvolemia (avoid fluid deficits)
• Euglycemia (avoid hypo- and hyperglycemia)

SECTION 3 - Types of Intracranial Injury

1. Emergent non-contrast CT head
2. Immediate neurosurgical consultation
3. Resuscitate - protect airway (intubate for GCS ≤8 or deteriorating)
4. Reduce ICP if signs of herniation: osmolar therapy (mannitol or hypertonic saline), brief controlled hyperventilation as bridge
5. Definitive treatment is emergent surgical evacuation

• Acute SDH: Hyperdense (bright white) crescent on CT
• Subacute SDH (1-3 weeks): Isodense (may be hard to detect, look for midline shift and gyral effacement)
• Chronic SDH (>3 weeks): Hypodense (dark/CSF-like) crescent

SECTION 4 - Skull Fractures

• Battle's sign - post-auricular ecchymosis (mastoid bruising, >24 h to develop)
• Raccoon eyes (periorbital ecchymosis) - bilateral periorbital bruising
• Hemotympanum - blood behind the tympanic membrane
• CSF otorrhea or rhinorrhea - clear fluid from ear or nose (test with glucose or beta-2 transferrin)
• Hearing loss, facial nerve palsy

• Intracranial air (pneumocephalus)
• Association with an overlying scalp laceration (open/compound fracture - risk of meningitis/abscess)
• Depressed fractures - risk of dural laceration and underlying brain injury
• Linear fractures overlying the temporal bone - risk of EDH

SECTION 5 - Neuroimaging Decision Rules

• High-risk (for neurosurgical intervention): GCS <15 at 2h post-injury, suspected open/depressed skull fracture, any sign of basal skull fracture, vomiting ≥2 episodes, age ≥65
• Medium-risk (for brain injury on CT): retrograde amnesia ≥30 min, dangerous mechanism (pedestrian vs. vehicle, ejected from vehicle, fall >1 m)

• Criteria for CT: evidence of skull fracture, scalp hematoma, altered LOC, neurologic deficit, altered alertness, abnormal behavior, coagulopathy, age ≥65

• Basal cisterns (normal=0; compressed=1; absent=2)
• Midline shift (no shift ≤5mm=0; shift >5mm=1)
• Epidural mass lesion (present=0; absent=1)
• Intraventricular or subarachnoid blood (absent=0; present=1)

SECTION 6 - Airway Management in TBI

• GCS ≤8 or deteriorating neurologic status
• Loss of airway protective reflexes
• Respiratory failure/distress
• Requirement for ventilatory support or ICP-directed management

• In-line cervical spine immobilisation (remove collar only during laryngoscopy, then reapply)
• Confirm tube placement with chest radiograph or US and exclude pneumothorax
• RSI preferred - use agents that do not raise ICP
• Avoid post-intubation hypoxia and hypotension
• After intubation: target PaCO2 35-45 mmHg (normocapnia); avoid prophylactic hyperventilation

• Current recommendation: Target normocapnia (PaCO2 35-45 mmHg) in all severe TBI patients.
• Prophylactic hyperventilation is contraindicated - especially in the first 24 hours when CBF is often critically low.
• Therapeutic hyperventilation (PaCO2 30-35 mmHg) is acceptable only as a short-term bridge to definitive therapy (e.g., craniectomy) in life-threatening herniation.
• If used, jugular venous oxygen saturation (SjO2) or brain tissue O2 partial pressure (BtpO2) monitoring is advised to detect ischemia.

SECTION 7 - ICP Management

• ICP monitoring is recommended for severe TBI; treatment threshold is ICP >20 mmHg
• Cerebral perfusion pressure (CPP) = MAP - ICP; target CPP 50-70 mmHg (adults); 40-50 mmHg (pediatric)
• Head of bed elevation to 30 degrees
• Osmolar therapy:
  • Mannitol 0.25-1 g/kg IV q6h (max serum osmolality 320 mOsm/kg); onset within minutes, peaks at ~60 minutes, lasts 6-8 hours. Avoid in hypotension (potent diuretic; risk of renal failure)
  • Hypertonic saline (HTS) 23.4%, 30-60 mL q6h via central line (max Na 160 mEq/L); 3% NaCI peripherally is acceptable; preferred over mannitol in hypovolemia
• Avoid:
  • Prophylactic hyperventilation (PaCO2 <30 mmHg)
  • Prophylactic hypothermia (not recommended)
  • Corticosteroids (harmful in TBI - increased mortality)
  • Fentanyl and midazolam boluses during ICP crises (pediatric guideline)

SECTION 8 - Seizures in TBI

• Early post-traumatic seizures occur within the first 7 days and are more common in severe TBI
• Seizure prophylaxis is recommended in severe TBI to prevent early seizures
• Agents: Phenytoin (fosphenytoin) or Levetiracetam (increasingly preferred due to better tolerability)
• Prophylaxis is given for the first 7 days after injury only
• Prophylaxis beyond 7 days is not indicated as it does not prevent late post-traumatic epilepsy
• Late seizures (>7 days) indicate established post-traumatic epilepsy and require long-term antiepileptic therapy

SECTION 9 - Penetrating Head Trauma

• Intracranial path: Projectiles crossing the midline, passing through the ventricles, or reaching the posterior fossa carry extremely high mortality
• Projectile velocity: High-velocity wounds have greater mortality
• Missile size and fragmentation: Large or fragmenting missiles are usually fatal
• Tissue cavity: Bullet creates a cavity up to 10x its diameter; low-velocity missiles can deflect erratically
• Clinical factors: Increasing age, suicide attempt, lower GCS, bilateral mydriasis, dural penetration, bihemispheric/multi-lobar injury

SECTION 10 - Special Populations

• Cerebral atrophy creates more space within the cranial vault, allowing larger amounts of blood to accumulate before clinical deterioration becomes apparent
• Higher incidence of anticoagulant/antiplatelet use (warfarin, DOACs, aspirin, clopidogrel) - increases hemorrhage risk and worsens outcomes
• Lower physiologic reserve
• Even patients with seemingly minor mechanisms (low-velocity falls) may have significant intracranial pathology
• A low threshold for CT is recommended regardless of symptoms in elderly patients on anticoagulants

• Larger, heavier cranial vault relative to body mass predisposes to greater cervical torque on impact
• Unfused sutures make the skull more pliable but can transmit forces causing parenchymal injury without fracture
• Less myelinated brain with higher water content = greater susceptibility to shearing forces and diffuse axonal injury (DAI)
• Higher risk of post-traumatic seizures
• Brain is more sensitive to secondary injury from hypoxia/hypotension
• Scalp lacerations can cause significant hemodynamic compromise relative to smaller blood volume

SECTION 11 - Herniation Syndromes

• Ipsilateral dilated, fixed pupil (CN III compression - first sign)
• Contralateral hemiparesis (ipsilateral cerebral peduncle compression)
• Cushing's triad (hypertension, bradycardia, abnormal respirations) = late and ominous sign of brainstem compression
• Decorticate posturing (injury above midbrain) progressing to decerebrate posturing (midbrain lesion)

1. Secure airway (intubate)
2. Osmolar therapy: mannitol 1 g/kg IV or 23.4% HTS 30-60 mL IV
3. Brief hyperventilation (PaCO2 30-35 mmHg) as a bridge - not prophylactically
4. Emergent neurosurgical consultation for decompressive craniectomy or hematoma evacuation
5. Reverse any coagulopathy

SECTION 12 - Disposition

• Worsening headache (progressive)
• Repeated vomiting
• Increasing confusion or altered consciousness
• One pupil larger than the other or not reacting to light
• Seizures
• Weakness or numbness in limbs (new focal neurologic signs)
• Drainage of clear fluid from nose or ears
• Inability to be woken up

SECTION 13 - Diffuse Axonal Injury

• CT may be normal or show petechial hemorrhages at gray-white junctions, corpus callosum, or brainstem
• MRI is more sensitive and shows lesions in these regions (GRE/SWI sequences best)
• Classic presentation: immediate LOC after trauma with a CT that appears disproportionately normal relative to clinical severity
• MRI has prognostic value during subsequent care and assists in directing rehabilitation

SECTION 14 - Quick Clinical Pearls

1. Normal GCS does not exclude significant injury - over 10% of patients who eventually become comatose initially present with GCS 15
2. Lucid interval ≠ only EDH - SDH can also have a lucid interval; always image
3. Elderly patients on anticoagulants - image regardless of mechanism or symptoms; delayed hemorrhage is common
4. Do not give corticosteroids - increases mortality (CRASH trial)
5. Do not prophylactically hyperventilate - causes cerebral ischemia
6. Treat hypotension aggressively - even one episode of SBP <90 mmHg doubles mortality in TBI
7. Avoid secondary transfers through non-neurosurgical centres when possible
8. Tangential GSW with GCS 15 still has 25% risk of intracranial hemorrhage - always CT

1. Did the patient sustain a blunt force mechanism or whiplash-type acceleration-deceleration event?
2. At any point after injury, was there any alteration in mental status - confusion, disordered awareness (dazed, disoriented, "seeing stars," slowed thinking), amnesia (retrograde or anterograde), or loss of consciousness?

Viva Voce: Tension Pneumothorax for Emergency Medicine Doctors

SECTION 1 - Definitions & Classification

• Progressive increase in intrapleural pressure
• Mediastinal shift to the contralateral side
• Compression of mediastinal venous structures and the contralateral lung
• Impaired venous return to the heart
• Progressive cardiovascular collapse and death if untreated

1. Simple/Closed pneumothorax - No communication with the atmosphere, no mediastinal shift. Usually from rib fracture or alveolar rupture. An isolated simple pneumothorax rarely causes severe symptoms unless it occupies >40% of the hemithorax (in a patient without pre-existing cardiopulmonary disease).
2. Communicating/Open pneumothorax ("sucking chest wound") - A defect in the chest wall creates communication with the atmosphere. Most common in combat injuries or gunshot wounds. Paradoxical collapse on inspiration and expansion on expiration, creating large functional dead space.
3. Tension pneumothorax - One-way valve mechanism causes progressive air accumulation under pressure, leading to mediastinal shift, venous compression, haemodynamic compromise, and death.

SECTION 2 - Pathophysiology

• During inspiration: Negative intrathoracic pressure draws air through the defect into the pleural space
• During expiration: The defect seals, trapping the air inside

• Ipsilateral lung collapse
• Mediastinal shift to the contralateral side
• Compression of the contralateral lung - worsening hypoxemia
• Compression of mediastinal venous structures (SVC, IVC) - impairs venous return to the heart
• Reduced cardiac output → haemodynamic collapse → cardiac arrest

• Chest trauma (rib fractures, penetrating injuries) - most common traumatic cause
• Mechanical ventilation with positive-pressure ventilation - converts a simple or occult pneumothorax to tension
• CPR - rib fractures from compressions lacerate lung parenchyma; positive-pressure ventilation then increases intrapleural pressure
• COPD/airway obstruction - additional air forced into the pleural cavity during expiration due to outflow obstruction
• Spontaneous pneumothorax (especially secondary spontaneous pneumothorax in COPD)
• Iatrogenic causes - central line placement (subclavian, internal jugular), thoracentesis, mechanical ventilation
• Stab wounds - delayed pneumothorax for up to 6 hours post-injury

1. Positive pressure directly increases intrapleural pressure, converting a simple/occult pneumothorax into tension
2. Rib fractures from CPR can lacerate lung parenchyma, creating the one-way valve
3. An occult pneumothorax (detected on CT but not apparent clinically) can rapidly convert to tension when positive-pressure ventilation is started
4. The earliest sign in this scenario is an increase in resistance to ventilation (rising peak airway pressures), followed by falling blood pressure and rising CVP

SECTION 3 - Clinical Features

• T - Tracheal deviation (to the contralateral side - a late sign)
• H - Hypotension
• O - Oxygen desaturation/hypoxia
• M - Mediastinal shift
• A - Absent/decreased breath sounds (ipsilateral)
• S - Subcutaneous emphysema (may be present); Shock; raised JVP/distended neck veins

• One or more of these signs may be absent, particularly in the presence of hypovolaemia (JVP may not be elevated)
• Tracheal deviation is a late sign - its absence does not rule out tension pneumothorax
• Hypotension is a late finding in spontaneous tension pneumothorax
• Patients on positive-pressure ventilation are more likely to be hypoxic, hypotensive, and in cardiac arrest than spontaneously breathing patients

• Blood pressure falls
• Central venous pressure (CVP) rises
• Oxygen saturations drop
• Cardiac arrest can follow rapidly

SECTION 4 - Diagnosis

• Tintinalli's, Chapter 261

• Rosen's, Chapter 63

• Absent lung markings on the affected side
• Increased radiolucency (air density) lateral to the pleural line
• Tracheal deviation away from the affected side (contralateral)
• Mediastinal shift to the contralateral side
• Depression of the ipsilateral hemidiaphragm
• Contralateral shift of the cardiac silhouette

• Absent lung sliding sign - normally, the two pleural layers sliding against each other during respiration produces a shimmering "ants marching in a line" appearance on M-mode. This movement is absent in pneumothorax
• Absent B-lines (comet tail artefacts) - their absence supports pneumothorax
• Stratosphere (barcode) sign on M-mode - replaces the normal "seashore sign" when lung sliding is absent

• Lung point (transition point) - where normal lung sliding transitions to absent lung sliding. This is 100% specific for pneumothorax but less sensitive

• Chest radiography misses 17-80% of pneumothoraces on upright and supine films respectively
• CT is the gold standard for detection
• In most patients, detection of an occult pneumothorax has minimal clinical significance and does not improve outcome
• Critical exception: Patients who require intubation and positive-pressure ventilation - the occult pneumothorax can rapidly convert to a tension pneumothorax, making detection and prophylactic treatment crucial
• Similarly, patients taken to the operating room are at risk for conversion to tension pneumothorax under anaesthesia

• Haemothorax - similar presentation but dull percussion, not hyper-resonant
• Cardiac tamponade - Beck's triad: hypotension, JVP elevation, muffled heart sounds; no absent breath sounds; treated by pericardiocentesis
• Right mainstem bronchial intubation - unilateral absent breath sounds but no haemodynamic collapse; trachea not deviated
• Massive pulmonary embolism - haemodynamic collapse, no chest signs
• Acute severe asthma/severe bronchospasm - bilateral signs
• Diaphragmatic hernia - bowel sounds in chest

SECTION 5 - Management

1. Clinical diagnosis - do not delay for imaging
2. Immediate decompression:
   • In the ED: Tube thoracostomy (or finger thoracostomy) is the definitive treatment
   • Needle decompression is a temporizing measure - it should be followed promptly by tube thoracostomy
3. Reassess after decompression: clinical improvement (haemodynamic stability, improved oxygenation) confirms the diagnosis
4. Chest X-ray post-procedure to confirm tube position and lung re-expansion
5. POCUS in equivocal cases to confirm pneumothorax before intervention

• Insert a large-bore IV catheter (14-16 gauge in adults; 18 gauge in children) of adequate length (at least 3-5 cm in adults)
• The needle is inserted until air escapes under positive pressure
• Remove the needle, leave the catheter open to air until definitive tube thoracostomy is completed

• 2nd intercostal space at the midclavicular line (MCL) - traditional anterior approach (superior border of the 3rd rib to avoid neurovascular bundle)
• 4th/5th intercostal space at the anterior axillary line (AAL) - lateral approach preferred by Rosen's as more accessible, avoids pectoral muscle bulk, and reduces risk of insufficient catheter length in obese patients

• Standard IV catheters may be insufficient length to penetrate the pleural space, especially in obese patients or those with thick chest walls - the catheter kinks or fails to reach the pleura
• In this situation: proceed directly to finger thoracostomy or tube thoracostomy
• Needle decompression is a temporizing measure only - it does not replace tube thoracostomy

• Suspected tension pneumothorax in a critically ill patient, especially when needle decompression has failed or is likely to be inadequate (e.g., obesity)
• As an equally expeditious alternative to needle decompression in the ED when equipment is available
• Traumatic cardiac arrest where bilateral decompression may be performed rapidly

1. Prep and drape; local anaesthetic if time allows
2. Incision over the superior border of the lower rib (to avoid the neurovascular bundle running under the rib above)
3. Blunt dissection through subcutaneous tissue and intercostal muscles into the pleural space
4. Insert finger to confirm pleural entry and clear any clots
5. Insert chest tube (large-bore 28-32 Fr for adults with haemothorax; smaller for simple pneumothorax) directed posteriorly and superiorly
6. Connect to underwater seal drain or flutter valve
7. Secure and check lung re-expansion on CXR

SECTION 6 - Special Situations

• Three sides are sealed (creating a flutter-valve effect)
• One side is left open to allow air to exit but not enter
• The patient is then given supplemental oxygen

1. Immediate search for reversible causes using eFAST (extended FAST): cardiac tamponade, tension pneumothorax, massive haemoperitoneum, cardiac activity
2. Bilateral needle or finger thoracostomy should be performed early in traumatic cardiac arrest to exclude bilateral tension pneumothorax
3. The decision for ED thoracotomy should also be considered:
   • Strongest indication: penetrating chest trauma with witnessed signs of life on arrival or during transport
   • No survivors in blunt arrest without field pulse/respiration - ED thoracotomy not indicated

• Air travel: Reduced cabin pressure at altitude can cause air in the pleural space to expand (Boyle's Law - pressure decreases, volume increases), converting a stable residual pneumothorax into a tension pneumothorax
• Underwater diving: Rapid ascent causes gas to expand; descent increases risk of air trapping
• Timing: Follow-up imaging (chest X-ray) is required to confirm complete resolution before resuming either activity
• For recurrent pneumothorax, surgical intervention (pleurodesis, apical bullectomy) should be discussed before any return to high-risk activities

• Tube malposition (most common) - tube in fissure, outside pleural space, too far in
• Pleural space infection - empyema; risk increases with traumatic vs sterile technique
• Pain at the chest tube site
• Re-expansion pulmonary oedema - rare, occurs after rapid re-expansion of a large or long-standing pneumothorax
• Re-expansion hypotension - rare
• Injury to intercostal neurovascular bundle - if tube placed below rather than above the rib
• Lung laceration
• Diaphragmatic injury if tube inserted too low

SECTION 7 - Disposition & High-Yield Pitfalls

1. Do not wait for CXR before treating - the diagnosis is clinical; delays cause cardiac arrest
2. Do not rely on tracheal deviation - it is a late and often absent sign
3. Do not overlook flat neck veins - hypovolaemia masks JVP elevation; absence of distended neck veins does not exclude tension
4. Needle decompression is not definitive - it is a bridge to tube thoracostomy; always follow with a chest tube
5. Standard IV catheters may be too short - especially in obese patients; failure to decompress should prompt immediate finger/tube thoracostomy
6. Occult pneumothorax + intubation = risk - anticipate and plan for conversion to tension before starting positive-pressure ventilation
7. Open wound three-sided dressing - never fully occlude a sucking chest wound; this converts it to tension
8. Do not insert chest tube through the wound - risk of tube tracking into lung or diaphragm

Viva Voce: Acute Abdominal Injury for Emergency Medicine Doctors

SECTION 1 - Epidemiology & Overview

• Abdominal trauma accounts for 15-20% of all trauma deaths
• The liver is the most frequently injured abdominal organ overall; however, the spleen is the most frequently injured intra-abdominal organ from sports accidents
• The small intestine, colon, and liver are the most likely organs injured in penetrating trauma
• In blunt trauma, the spleen is the most commonly injured solid organ (in ~two-thirds of cases, it is an isolated organ injury); the liver is the second most common
• Firearm injuries are the third largest cause of trauma-related death in the US, accounting for ~15% of trauma deaths; they have the highest case fatality rates across every age group compared with other mechanisms
• Stab wounds occur nearly as often as gunshot wounds, but GSWs account for ~90% of penetrating trauma mortality

SECTION 2 - Anatomy & Pathophysiology

• Anterior abdomen: Between the anterior axillary lines, from the costal margins to the groin creases
• Low chest: Nipple line (4th ICS anteriorly) / inferior scapular tip (7th ICS posteriorly) down to the inferior costal margins - overlaps with the abdomen because the diaphragm can reach the 4th ICS anteriorly and 6th ICS laterally/posteriorly during expiration
• Flank: Between anterior and posterior axillary lines bilaterally, from the inferior scapular tip to the iliac crest
• Back: Posterior axillary lines from the inferior scapular tip to the iliac crest

1. Compressive forces - direct crushing of solid organs (spleen, liver) against the spine or ribs
2. Shearing/stretching forces - tearing at fixed points (e.g., ligament of Treitz - junction of fixed and mobile bowel, a common site of mesenteric and small bowel injury; hepatic veins; renal pedicle)
3. Acceleration-deceleration forces - e.g., rapid deceleration in MVC causes the pancreas to be compressed across the spine; liver/spleen tear at vascular pedicles

SECTION 3 - Clinical Assessment

• Up to 45% of blunt trauma patients with a benign initial abdominal exam are subsequently found to have intra-abdominal injuries
• The following all impair abdominal assessment:
  • Head injury (altered consciousness)
  • Alcohol or drug intoxication
  • Distracting injuries (even isolated extremity injuries can suppress signs of intra-abdominal injury)
  • Spinal cord injury (loss of pain sensation)
  • Language barriers
• Young, healthy patients can compensate for significant haemorrhage before vital signs change
• Elderly patients may be on beta-blockers/CCBs blunting tachycardia, and on anticoagulants increasing injury risk
• Retroperitoneal injuries do not cause peritoneal signs at all (no rebound/guarding)
• A normal-appearing abdomen does not exclude serious intra-abdominal injury

• Abdominal tenderness, distention, guarding, or rigidity (peritonism)
• Seatbelt sign - abdominal wall bruising from lap belt; associated with hollow viscus and mesenteric injuries (especially "seatbelt syndrome": lumbar Chance fracture + bowel injury)
• Cullen's sign - periumbilical bruising (retroperitoneal haemorrhage, delayed sign)
• Grey Turner's sign - flank bruising (retroperitoneal haemorrhage, delayed sign)
• Kehr's sign - left shoulder tip pain on lying flat (diaphragmatic irritation from splenic injury/free blood under left hemidiaphragm)
• Evisceration - bowel or omentum protruding through wound; associated with up to 80% incidence of major intraperitoneal injury
• Rectal bleeding - suggests colonic laceration
• Blood at the urethral meatus - strongly suggests genitourinary injury
• Haemodynamic instability with no external blood loss - suspect intra-abdominal haemorrhage

• Presence of abdominal pain, tenderness, distension, or external signs of trauma
• Mechanism with high likelihood of causing abdominal injury
• Suspicious lower chest, back, or pelvic injury (any of these can involve the abdomen)
• Inability to tolerate a delayed diagnosis - elderly patients, those on anticoagulants, patients with liver cirrhosis/portal hypertension
• Presence of distracting injuries
• Altered consciousness or sensorium - CNS injury, intoxicating substances

SECTION 4 - Diagnostic Tools

• Morrison's pouch (hepatorenal recess) - most dependent RUQ space
• Splenorenal recess (LUQ)
• Pouch of Douglas (pelvic/suprapubic) - most dependent pelvic space
• Pericardial window - cardiac tamponade
• Bilateral lung fields - pneumothorax, haemothorax

• Rapid, accurate, non-invasive, portable, no radiation, no contrast
• Greatest benefit: Rapid identification of free intraperitoneal fluid in the hypotensive patient with blunt trauma
• Detects as little as 100-200 mL of free fluid
• Has largely replaced DPL in North American trauma centres

• Cannot identify the exact source of free fluid
• Cannot evaluate the retroperitoneum well
• Cannot detect solid organ parenchymal damage (lacerations without free fluid)
• Cannot detect diaphragmatic defects
• Operator-dependent; limited in obesity, subcutaneous air, or excessive bowel gas
• Cannot distinguish haemoperitoneum from ascites
• Should NOT be used as a "rule-out" test for significant intra-abdominal trauma

• Precisely identifies and localises specific organ injuries
• Most accurate for solid visceral lesions
• Quantifies and differentiates the amount and type of free fluid
• Detects active extravasation (blush of contrast = active arterial haemorrhage - may need angioembolisation)
• Evaluates the retroperitoneum (pancreas, duodenum, kidneys, great vessels)
• Detects free intraperitoneal air better than plain X-rays (small amounts from hollow viscus injury)
• Evaluates for spinal, bony pelvic, and thoracic injuries simultaneously
• Guides decision between operative vs. nonoperative management

• Oral contrast is not used in trauma CT (risk of aspiration, delays assessment)
• IV contrast only is standard
• Risk of contrast-induced nephropathy is lower with modern low-osmolar agents; mitigated by IV fluid hydration
• CT cannot be used in the haemodynamically unstable patient - go to the OR/eFAST instead

• Chest X-ray: Screens for haemothorax, pneumothorax, and mediastinal widening; increasingly replaced by e-FAST for these indications
• Pelvic X-ray (AP): Identifies significant pelvic disruptions; indicated in haemodynamically unstable patients or those with unstable pelvic examination; can be omitted in stable patients proceeding to CT
• Abdominal X-ray: Shows location and presumed track of projectiles in GSW/shotgun injuries; of little value in blunt or stab trauma if CT is planned
• Free air under the diaphragm can be detected on upright CXR or left lateral decubitus, but small amounts (especially from small bowel) are better seen on CT
• Bony fractures on plain film (lower ribs, lumbar transverse processes, pelvic fractures) should raise suspicion for nearby visceral injury

• Centres where ultrasound equipment is not available or the clinician is untrained in FAST
• Diagnostic peritoneal aspiration (DPA) - simpler, using just the aspiration step - still used in some algorithms for unstable patients with pelvic fractures when FAST is equivocal

SECTION 5 - Specific Organ Injuries

• The most commonly injured solid organ in blunt trauma
• Injury often results from left lower rib fractures or direct epigastric/left flank blow
• Signs: left upper quadrant tenderness, Kehr's sign (left shoulder tip pain from diaphragmatic irritation), haemodynamic instability
• Splenic injuries are graded I-V (AAST grading); CT with IV contrast identifies grade, laceration extent, and active extravasation
• Nonoperative management (NOM) is the standard for haemodynamically stable patients: success rate ~95% in patients with normal sensorium and no peritonitis
• In elderly patients, NOM success rate ranges from 62-85%
• Surgical consultation required for all grades
• Angioembolisation is used for higher-grade injuries (Grade III-V) with active extravasation
• Delayed splenic rupture can occur days to weeks after the initial injury - warn patients on discharge
• Infectious mononucleosis predisposes to splenic rupture after trivial trauma

• The most frequently injured abdominal organ overall and second most common in blunt trauma
• Often results from right lower rib fractures or deceleration injury
• Signs: RUQ tenderness, referred right shoulder pain, haemodynamic instability
• CT grades liver injuries (AAST I-VI); identifies lacerations, haematomas, and active extravasation
• NOM success rate ~95% in haemodynamically stable patients without peritonitis
• Active extravasation on CT (contrast "blush") may require angioembolisation
• Hepatic injuries at high risk for haemorrhage in both blunt and penetrating trauma
• Delayed rupture of hepatic haematoma can occur
• Hepatic venous injuries (retrohepatic vena cava) carry very high mortality

• Incidence is 1-12% - uncommon compared to solid organ injuries
• Causes: direct crushing of bowel between seatbelt and spine; rapid deceleration tearing mesentery at fixed points (ligament of Treitz)
• Seatbelt sign should prompt aggressive evaluation for HVI
• Symptoms may be delayed - peritoneal contamination by gastric acid causes immediate pain; bacterial contamination of the bowel causes delayed peritonitis (hours to days)
• CT may show free intraperitoneal air or free fluid without solid organ injury - highly suspicious for HVI
• Haemorrhage from mesenteric injury may be minimal and not apparent on exam

• Delays in diagnosis and operative management are directly associated with increased mortality
• CT can miss HVI in up to 15-20% of cases initially
• Serial abdominal examinations are essential

• Infrequent (only ~4% of abdominal trauma) but associated with significant morbidity and mortality
• Mechanism: rapid deceleration causing compression of the pancreas (specifically the body) across the spine
• Classic mechanisms: handlebar injury in cyclists, unrestrained driver striking steering column
• Often asymptomatic initially - delayed presentation is common
• Retroperitoneal location means no peritoneal signs early
• Serum amylase and lipase may be elevated but are insensitive early
• CT is primary diagnostic tool but can underestimate injury acutely; MRI/MRCP or ERCP may be needed
• Main complications: pseudocyst formation, pancreatic fistula, abscess

• Retroperitoneal location makes diagnosis challenging - contents may not spill into the peritoneum
• Mechanism: high-velocity deceleration (also handle-bar injury)
• Presentation: may be relatively asymptomatic initially
• As a duodenal haematoma expands: signs of gastric outlet obstruction develop - abdominal pain, distension, and vomiting
• Duodenal rupture: contents are contained within retroperitoneum, so peritoneal signs are absent; missed by studies investigating only the peritoneum
• Fever and leucocytosis herald development of abscess or sepsis
• CT is the primary diagnostic tool but MRCP or upper GI series may be needed

• Uncommon: 0.5-5% of thoracoabdominal injuries
• Blunt trauma: sudden massive increase in intraperitoneal pressure causes radial tears (usually left-sided as the liver protects the right hemidiaphragm)
• Penetrating trauma (low chest or upper abdomen): both sides equally at risk
• Diagnosis is frequently delayed in blunt trauma due to concomitant severe injuries
• CT has variable sensitivity/specificity (as low as 60%/70%); missed by initial imaging
• Clinical clue: bowel sounds heard in the chest; bowel or stomach seen in the chest on CXR
• Left-sided diaphragmatic injury with stomach/bowel in the left chest is an indication for immediate operative intervention
• Delayed diagnosis leads to herniation or strangulation of abdominal contents, with mortality rates up to 50%

SECTION 6 - Penetrating Abdominal Trauma

• Haemodynamic compromise - preeminent indication; patient to OR without further diagnostic studies
• Unequivocal peritoneal signs - rebound, rigidity, guarding (highest positive predictive value for therapeutic laparotomy)
• Evisceration - associated with 80% incidence of major intraperitoneal injury; most surgeons proceed to laparotomy. Exception: isolated omental evisceration without viscus evisceration and negative FAST may be managed conservatively
• Left-sided diaphragmatic injury (stomach/bowel in chest on CXR)
• GI haemorrhage via nasogastric tube/rectal bleeding

• Local wound exploration (LWE) in a non-obese patient with a single anterior wound - infiltrate with local anaesthetic, visualise each tissue layer under direct vision
• If peritoneum clearly NOT violated + negative e-FAST + no other injury: treat as local abdominal wall injury and discharge
• If peritoneal entry confirmed or end of wound not found: further evaluation (CT, admission)

• CT scanning, serial physical examinations, or laparoscopy depending on clinical scenario and institutional resources

• Wound infiltrated with local anaesthetic containing adrenaline (for haemostasis)
• The wound is carefully visualised through each successive tissue layer
• Blind probing with digits, instruments, or cotton-tipped swabs is unreliable unless the peritoneal cavity is obviously freely entered
• The wound may need to be extended to allow adequate visualisation

• Only applicable to anterior abdominal stab wounds (not back, flank, or chest wounds where deep exploration risks neurovascular or pleural injury)
• Impractical when there are multiple wounds
• Not applicable in obese patients - layers too thick to explore adequately
• Cannot be performed in the thoracic cage area due to risk to neurovascular structures and pleura
• Cannot determine if there is an intraperitoneal injury - only whether the peritoneum has been penetrated

SECTION 7 - Indications for Laparotomy

1. Refractory hypotension in a patient with a positive e-FAST for hemoperitoneum AND the absence of an unstable pelvic fracture (pelvic fracture bleeding is retroperitoneal and may not require laparotomy)
2. Obvious peritonitis with a positive e-FAST
3. Evidence of intra-abdominal injury on e-FAST in the context of other life-threatening injuries requiring transfer to the OR (e.g., uncontrollable chest haemorrhage)

• Success rate is ~95% in patients with normal sensorium, no peritonitis, and no haemodynamic compromise
• Requires an institution with trauma surgeons, experienced nursing staff, adequate blood resources, and interventional radiology with angioembolisation capability

• Haemodynamic stability
• Normal sensorium (reliable clinical monitoring)
• No peritonitis
• CT characterisation of the injury grade
• Access to immediate operative intervention if needed

• Haemodynamic deterioration
• Need for blood transfusion exceeding acceptable parameters
• CT showing active contrast extravasation not amenable to angioembolisation
• Peritoneal signs developing

SECTION 8 - Special Situations

• Operative intervention for abdominal haemorrhage generally takes precedence over head injury management, as exsanguination is immediately fatal
• The key principle: "A patient with known haemoperitoneum whose vital signs cannot be stabilised should undergo laparotomy to avoid exsanguination"
• However, management is highly complex and multispecialty - trauma surgery, neurosurgery, and anesthesia must make joint decisions
• e-FAST is invaluable to rapidly characterise both injuries
• Delay for extensive radiology in a haemodynamically unstable patient is not appropriate
• Laparotomy may be performed with simultaneous neurosurgical monitoring or intervention where resources allow

• Bowel evisceration (protrusion of bowel or omentum through an abdominal wound) is associated with up to an 80% incidence of major intraperitoneal injury
• Most trauma surgeons proceed directly to exploratory laparotomy

1. Remove any significant particulate matter or dirt
2. Attempt to replace bowel contents intra-abdominally if possible (may not be possible with significant bowel oedema or small defect)
3. Cover exposed bowel and the abdominal defect with a moist dressing
4. Cover with plastic wrap or fluid-impervious dressing to minimise insensible fluid loss and heat loss
5. Establish IV access and administer IV fluids as needed
6. Administer IV antibiotics in preparation for surgery

• Seatbelt syndrome: A triad of abdominal wall bruising + hollow viscus injury (small bowel, colon, or mesentery) + lumbar Chance fracture (flexion-distraction fracture of the lumbar spine)
• Risk of bowel or mesenteric injury is significantly increased when a seatbelt sign is present
• These injuries may have delayed presentation with symptoms developing hours after the initial assessment
• CT may initially miss small bowel injuries - free fluid without solid organ injury is highly suspicious
• Serial abdominal examinations are mandatory
• A low threshold for operative exploration is appropriate if clinical concern persists despite initially negative imaging

SECTION 9 - Key Pitfalls & High-Yield Clinical Pearls

1. Normal abdominal exam ≠ no injury - up to 45% of blunt trauma patients with benign initial exam have intra-abdominal injuries on further evaluation
2. Negative FAST ≠ no abdominal injury - FAST cannot rule out retroperitoneal injuries, diaphragmatic tears, or solid organ injuries without free fluid; do not use it as a rule-out test
3. Seatbelt sign must prompt hollow viscus workup - serial exams and low CT threshold
4. Stab wound to the low chest = possible abdominal injury - 50% of GSWs to the low chest have intraperitoneal injuries; approach thoracoabdominal injuries systematically
5. Delayed haemorrhage - splenic and hepatic injuries can rupture days after initial injury; warn patients on discharge after NOM
6. Diaphragmatic injury is frequently missed - low CT sensitivity; always check for bowel in the chest on CXR/CT
7. Retroperitoneal injuries give no peritoneal signs - pancreatic, duodenal, and retroperitoneal vascular injuries are clinically silent; need CT to detect
8. Do not delay laparotomy for imaging in haemodynamically unstable patients with positive e-FAST
9. Infectious mononucleosis predisposes to spontaneous or traumatic splenic rupture with trivial mechanisms - take a careful history
10. Occult coagulopathy - patients on warfarin, DOACs, or antiplatelet agents can sustain serious intra-abdominal haemorrhage from seemingly minor trauma

• Both pelvic fractures and intraperitoneal injuries can cause haemodynamic instability
• Key distinction: Pelvic fracture haemorrhage is retroperitoneal; it will appear as a positive pelvic e-FAST but without free intraperitoneal fluid in Morrison's pouch or the splenorenal recess
• A negative peritoneal FAST in a patient with an unstable pelvic fracture suggests retroperitoneal (pelvic) as the bleeding source - pelvic binder + haemostasis (angioembolisation, pelvic packing)
• A positive peritoneal FAST (free intraperitoneal fluid) in a haemodynamically unstable patient with a pelvic fracture suggests both sources of bleeding - laparotomy takes precedence to control intraperitoneal haemorrhage, followed by pelvic stabilisation
• Diagnostic peritoneal aspiration (DPA) may be used to confirm intraperitoneal haemorrhage when e-FAST is equivocal
• This is multispecialty decision-making requiring trauma surgery input