Blunt Injury Abdomen: Principles and Management

1. INTRODUCTION & EPIDEMIOLOGY

2. MECHANISMS OF INJURY

3. PATHOPHYSIOLOGY OF INJURY

4. CLINICAL ASSESSMENT

4a. History

• Mechanism: speed of impact, seat-belt use, steering wheel deformation, airbag deployment
• Time of injury, pre-hospital vital signs, amount of fluid administered en route
• Comorbidities, anticoagulants, prior abdominal surgery

4b. Physical Examination

5. INVESTIGATIONS

5a. Laboratory

• FBC (serial haematocrit trending), coagulation profile
• Arterial blood gas (base deficit and lactate as markers of shock severity)
• Serum amylase/lipase (pancreatic injury — not sensitive in isolation)
• LFTs, urinalysis
• Group & crossmatch, massive transfusion protocol activation if needed

5b. FAST Examination (Focused Assessment with Sonography for Trauma)

1. Pericardial (subxiphoid)
2. Right upper quadrant — Morison's pouch (hepatorenal space)
3. Left upper quadrant — splenorenal recess
4. Pelvis — pouch of Douglas / rectovesical pouch

Positive FAST = anechoic free fluid in dependent peritoneal spaces = hemoperitoneum

FAST ultrasound: Pelvic view showing free intra-abdominal fluid (hemoperitoneum) as an anechoic black area adjacent to the bladder.

FAST: (a) Free fluid in Morison's pouch between liver and right kidney; (b) perisplenic free fluid — both indicating hemoperitoneum.

5c. CT Abdomen & Pelvis (with IV Contrast)

• Free fluid (hyperdense in acute haemorrhage) — most common finding
• Parenchymal laceration (hypodense), subcapsular haematoma
• Active contrast extravasation ("blush") — indicates ongoing arterial bleeding
• Free air — hollow viscus perforation
• Bowel wall thickening, mesenteric stranding/haematoma — hollow viscus/mesenteric injury
• Pancreatic oedema, disruption of pancreatic duct

CT Abdomen: Axial view showing hypodense perihepatic and perisplenic free fluid consistent with hemoperitoneum after blunt trauma.

CT: Grade III splenic laceration — subcapsular hematoma with parenchymal laceration >3 cm depth.

CT: Grade IV splenic laceration (red arrow) with massive hemoperitoneum (black arrow) in the paracolic gutters.

CT: Pancreatic laceration (hypodense area between body and tail) with free fluid (hemoperitoneum) — Grade III pancreatic injury.

5d. Diagnostic Peritoneal Lavage (DPL)

• Gross blood on aspiration (≥10 mL)
• RBC >100,000/mm³
• WBC >500/mm³ (after 3 hours)
• Bile, bacteria, food fibres

5e. Plain X-rays (Erect CXR & AXR)

• Free gas under the diaphragm — hollow viscus perforation
• Rib fractures (lower left → spleen risk; lower right → liver risk)
• Pelvic fractures
• Lost psoas shadow → retroperitoneal haematoma
• Elevated hemidiaphragm → diaphragmatic rupture or subphrenic pathology

6. ORGAN INJURY GRADING (AAST-OIS Scale)

Liver Injury Scale

Splenic Injury Scale

7. MANAGEMENT — OVERVIEW

FLOWCHART 1 — Blunt Abdominal Trauma (BAT) Algorithm

FLOWCHART 2 — Haemodynamically Stable Patient Decision Flow

8. INITIAL RESUSCITATION (ATLS PRINCIPLES)

Key principle: permissive hypotension (SBP 80–90 mmHg) may be tolerated briefly before definitive haemorrhage control to avoid dilutional coagulopathy — though evidence mandating this practice is still evolving.

• Nasogastric tube decompression (orogastric if midface fracture suspected)
• Urinary catheterisation for hourly urine output monitoring (do not catheterise if blood at meatus)
• Massive Transfusion Protocol (MTP) activated if ≥10 units PRBCs anticipated in 24 h

9. OPERATIVE MANAGEMENT

Indications for Emergency Laparotomy in BAT

Operative Approach

Damage Control Laparotomy (DCL)

• Hypothermia (<35°C)
• Acidosis (pH <7.2, base deficit >–6)
• Coagulopathy (INR >1.5)

1. Phase I — abbreviated laparotomy: Pack bleeding quadrants, control haemorrhage with clamps/sutures (not formal repair), control contamination (staple off perforations), temporary abdominal closure (TAC)
2. Phase II — ICU resuscitation: Correct coagulopathy, hypothermia, acidosis; ventilation, vasopressors, warming
3. Phase III — definitive repair: Return to OR in 24–48 hours for formal bowel anastomosis, vascular repair, abdominal closure

Angioembolisation is a critical adjunct — particularly for ongoing hepatic, splenic, or pelvic arterial bleeding in damage-control patients.

Abdominal Compartment Syndrome (ACS)

10. NON-OPERATIVE MANAGEMENT (NOM)

1. Haemodynamic stability (SBP >90 mmHg, HR <100)
2. Reliable clinical examination (alert, cooperative patient)
3. No peritonitis
4. No hollow viscus injury on CT
5. Institution capable of close monitoring (trauma surgeon, blood bank, OR on standby)

• Blunt spleen injuries: ~80% in adults, 90–95% in children
• Blunt liver injuries: ~95% success for grades I–III

• Serial abdominal examinations (4–6 hourly) by same examiner
• Serial haematocrit (4–6 hourly)
• Strict bed rest; nil by mouth initially
• Repeat CT if clinical deterioration
• Consider angioembolisation for CT "blush" (active arterial bleeding) even in haemodynamically stable patients — avoids laparotomy

11. SPECIFIC ORGAN INJURIES

Spleen

• Most commonly injured organ in BAT
• NOM preferred for grades I–III in stable adults; grades IV–V often require intervention
• Splenic artery angioembolisation (SAE) preserves immunological function and avoids splenectomy
• Splenorrhaphy (repair) preferred over splenectomy when feasible to preserve immunity
• If splenectomy performed → vaccines for Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis + lifelong penicillin prophylaxis (OPSI — Overwhelming Post-Splenectomy Infection)

Liver

• Second most commonly injured solid organ in BAT; most common in penetrating
• 90–95% managed non-operatively
• Complications of liver injury: haemobilia, biloma, delayed haemorrhage, hepatic necrosis, bile duct injury

Pancreas

• Protected retroperitoneally; injury usually requires significant force (handlebar injury in children)
• Main duct integrity guides management:
  • ERCP or MRCP for ductal assessment
  • Grade I–II (no ductal injury): wide external drainage
  • Grade III (distal duct transaction): distal pancreatectomy ± splenectomy
  • Grade IV–V (proximal transaction, ampullary injury): Whipple procedure or damage control + delayed reconstruction

Kidney

• Haematuria (macro or micro) key indicator
• CT urogram gold standard
• Grades I–III: NOM; Grades IV–V: may need embolisation or nephrectomy

Hollow Viscus (Small Bowel, Colon)

• Low incidence (1–5%) but devastating if missed
• Free fluid without solid organ injury on CT = high suspicion for hollow viscus injury
• CT sensitivity only ~80%
• Seat-belt sign, mesenteric stranding, bowel wall thickening are indirect CT signs
• All hollow viscus injuries require operative repair

Diaphragm

• Left-sided rupture 3× more common (liver buttresses right)
• CXR: elevated hemidiaphragm, stomach/bowel loops in chest, NG tube in chest
• CT: best with multiplanar reconstruction
• Repair urgently to prevent strangulation

12. COMPLICATIONS

13. SUMMARY TABLE

KEY POINTS FOR PG EXAM

1. Spleen = most commonly injured organ in BAT; liver = most common in penetrating trauma.
2. FAST is the first bedside tool; CT is the gold standard in stable patients.
3. Clinical examination accuracy in BAT is only 55–65% — do not rely on it alone.
4. Positive FAST + haemodynamic instability = immediate laparotomy — do not waste time with CT.
5. NOM success rate: 80% spleen (adults), 95% liver — requires institutional readiness.
6. Damage control surgery corrects the lethal triad: hypothermia + acidosis + coagulopathy.
7. Free fluid without solid organ injury on CT = hollow viscus injury until proven otherwise.
8. Post-splenectomy: vaccinate against encapsulated organisms + lifelong prophylaxis.
9. Seat-belt sign = strong indicator of hollow viscus and mesenteric injury.
10. Angioembolisation is a modern adjunct that can avoid laparotomy in selected cases.

Blunt Injury Abdomen — Principles & Management

(10-Mark PG Long Answer)

1. INTRODUCTION & EPIDEMIOLOGY

2. MECHANISMS OF INJURY

3. PATHOPHYSIOLOGY

• Solid organ injury → parenchymal laceration → hemoperitoneum → haemorrhagic shock
• Hollow viscus perforation → faecal/biliary peritonitis → sepsis → MODS
• Retroperitoneal injury (pancreas, duodenum, great vessels) → occult presentation, delayed diagnosis
• Diaphragmatic rupture → left-sided 3× more common (liver protects right); may present late with visceral herniation

4. CLINICAL ASSESSMENT

History

• Mechanism, speed of impact, seat-belt use, steering-wheel deformation, airbag deployment
• Pre-hospital vitals, fluids given, time elapsed
• Anticoagulants, prior abdominal surgery, comorbidities

Key Signs

5. INVESTIGATIONS

5a. Laboratory

• Serial FBC (haematocrit trending), coagulation profile (PT/APTT/INR)
• Arterial blood gas — base deficit and lactate as shock markers
• Serum amylase/lipase (pancreatic injury)
• LFTs, urinalysis, group & crossmatch
• Activate Massive Transfusion Protocol (MTP) if ≥10 units PRBCs anticipated in 24 h

5b. eFAST Examination

Limitations: Suboptimal for retroperitoneal and hollow viscus injuries. Negative FAST does not exclude significant injury.

5c. CT Abdomen & Pelvis with IV Contrast

• Sensitivity ~95% for solid organ injuries
• Sensitivity ~80% for hollow viscus injury (imperfect)
• Free fluid without solid organ injury = high suspicion for hollow viscus perforation

5d. Diagnostic Peritoneal Lavage (DPL)

• Gross blood on aspiration (≥10 mL)
• RBC >100,000/mm³
• WBC >500/mm³ (after 3 hours)
• Bile, bacteria, food fibres

5e. Plain Radiographs

• CXR: Pneumothorax, haemothorax, rib fractures, elevated hemidiaphragm, bowel loops in chest
• AXR: Free gas under diaphragm (perforation), loss of psoas shadow (retroperitoneal haematoma), pelvic fractures

6. AAST ORGAN INJURY GRADING

Liver (AAST-OIS)

Spleen (AAST-OIS)

7. MANAGEMENT FLOWCHARTS

FLOWCHART 1 — Master BAT Algorithm (Rosen's Emergency Medicine)

FLOWCHART 2 — Haemodynamically Stable Patient

8. INITIAL RESUSCITATION (ATLS Framework)

Permissive hypotension (SBP 80–90 mmHg) may be tolerated briefly before definitive haemorrhage control to reduce dilutional coagulopathy — prevents clot disruption while awaiting OR.

• NGT decompression (OGT if midface fracture)
• Urinary catheter for hourly urine output (minimum 0.5 mL/kg/h)
• Warming (prevent hypothermia — part of lethal triad)
• Activate MTP early if haemodynamically unstable

9. OPERATIVE MANAGEMENT

Indications for Emergency Laparotomy in BAT

Operative Steps

1. Position: Supine, arms abducted 90°; chest, abdomen, pelvis prepped
2. Incision: Midline laparotomy — xiphoid to pubis
3. Initial control: Four-quadrant packing — control haemorrhage first
4. Systematic exploration: All 9 abdominal regions, retroperitoneum, mesentery
5. Contamination control: Staple/close perforations rapidly
6. Definitive repair or damage control decision

Damage Control Surgery (DCS) — The "Lethal Triad"

• Hypothermia (<35°C)
• Acidosis (pH <7.2, base deficit >−6, lactate >5)
• Coagulopathy (INR >1.5, PT >50% above normal)

Phase I (OR) ─────────────────────────────────────────────────
  │  Haemorrhage control (pack, clip, vascular shunts)
  │  Contamination control (staple off perforations)
  │  Temporary abdominal closure (TAC — Bogotá bag / vacuum)
  ▼
Phase II (ICU) ────────────────────────────────────────────────
  │  Correct hypothermia (warm IV fluids, warming blankets)
  │  Correct coagulopathy (FFP, platelets, cryoprecipitate)
  │  Correct acidosis (resuscitation, vasopressors)
  │  Ventilatory support, renal support
  ▼
Phase III (Return to OR at 24–48 h) ──────────────────────────
     Definitive bowel anastomosis
     Formal vascular repair
     Fascial closure (or staged closure)

Angioembolisation — critical adjunct for ongoing hepatic, splenic, or pelvic arterial haemorrhage; can be performed alongside or instead of operative intervention.

Abdominal Compartment Syndrome (ACS)

• IAP >20 mmHg + new organ dysfunction = ACS
• Monitor with bladder pressure post-laparotomy
• Treat with decompressive laparotomy

10. NON-OPERATIVE MANAGEMENT (NOM)

Prerequisites

1. Haemodynamic stability (SBP >90 mmHg, HR <100)
2. Reliable, evaluable patient (alert, cooperative)
3. No peritonitis
4. No hollow viscus injury on CT
5. Institutional readiness: trauma surgeon available, blood bank, OR on standby

Success Rates

• Blunt splenic injury: ~80% adults, 90–95% children
• Blunt hepatic injury: ~95% for grades I–III

NOM Monitoring Protocol

• Serial abdominal examination every 4–6 hours by same examiner
• Serial haematocrit every 4–6 hours
• Strict bed rest; nil by mouth initially
• Repeat CT if haemodynamic or clinical deterioration
• Angioembolisation for CT "blush" (arterial extravasation) even in stable patients

Failure of NOM → Emergency Laparotomy

• Haemodynamic compromise
• Falling haematocrit despite transfusion
• Worsening abdominal signs
• New peritonitis

11. SPECIFIC ORGAN MANAGEMENT

Spleen

• NOM: grades I–III in stable adults; grades IV–V may need intervention
• Splenic artery angioembolisation (SAE): Preserves immunological function; reduces failure of NOM in high-grade injuries
• Splenorrhaphy (repair) preferred over splenectomy when feasible
• Post-splenectomy: Vaccinate against S. pneumoniae, H. influenzae type b, N. meningitidis + lifelong prophylactic penicillin (prevents OPSI)

Liver

• ~95% managed non-operatively
• Complications: haemobilia, biloma, bile leak, delayed haemorrhage, hepatic abscess
• Angioembolisation for active arterial bleeding
• Surgery: Pringle manoeuvre (hepatoduodenal ligament compression), packing, tractotomy

Pancreas (AAST Grading Guides Management)

Hollow Viscus (Small Bowel / Colon)

• All require operative repair — no NOM
• CT signs: free fluid without solid organ injury, mesenteric stranding, bowel wall thickening, free air
• Small bowel: primary repair (if <50% circumference) or segmental resection + anastomosis
• Colon: primary repair (right/transverse); Hartmann's or diversion for left colon in contaminated field

Kidney

• AAST Grade I–III: NOM (>95% success)
• Grade IV–V: angioembolisation or nephrectomy
• Always perform one-shot IVP (10 mL/kg IV contrast, KUB at 10 min) pre-operatively if time allows, to confirm contralateral kidney function

Diaphragm

• CXR: nasogastric tube in chest, bowel loops above diaphragm, elevated hemidiaphragm
• CT with multiplanar reconstruction: best diagnostic modality
• Repair urgently — risk of visceral herniation and strangulation

12. COMPLICATIONS

13. SUMMARY — THE DECISIVE PIVOT POINT

BLUNT ABDOMINAL TRAUMA
         │
         ▼
   HAEMODYNAMICALLY
      UNSTABLE?
    ┌─────┴─────┐
   YES          NO
    │            │
    ▼            ▼
 eFAST      CT Abdomen/Pelvis
  (+ve)      (Gold Standard)
    │            │
    ▼        ┌───┴────┐
 EMERGENCY  NOM    Laparotomy
 LAPAROTOMY  │    (hollow viscus,
  + DCL    Angio-  peritonitis,
         embolism  failure NOM)

KEY PG EXAM POINTS

1. Spleen = most commonly injured in BAT; liver = most common in penetrating trauma
2. Clinical exam accuracy in BAT = only 55–65% — never rely on it alone
3. FAST + haemodynamic instability = immediate laparotomy — no time for CT
4. CT is gold standard in stable patients; sensitivity ~95% solid organs, ~80% hollow viscus
5. Free fluid without solid organ injury on CT = hollow viscus injury until proven otherwise
6. Seat-belt sign = strong predictor of hollow viscus and mesenteric injury
7. NOM success: ~80% spleen (adults), ~95% liver — institution must be prepared
8. Damage control surgery for lethal triad: hypothermia + coagulopathy + acidosis
9. Angioembolisation — modern alternative/adjunct; avoids laparotomy, preserves organs
10. Post-splenectomy: vaccinate (pneumococcal, Hib, meningococcal) + prophylactic penicillin lifelong