Abdominal trauma

Abdominal trauma is the third leading cause of trauma death and is the injury most commonly missed at the initial assessment. The abdomen is a large cavity holding multiple organs, the physical signs are often subtle, and the bedside imaging is imperfect — so the emergency physician's task divides into three problems: identify intra-abdominal bleeding in the unstable patient (FAST, then theatre), characterise the organ injury in the stable patient (contrast CT), and maintain a high index of suspicion for the hollow viscus and pancreatic injuries that imaging may miss in the first hours.[1]

Blunt and penetrating abdominal trauma

Abdominal trauma is divided by mechanism, and the mechanism predicts which organs are injured. Blunt trauma — the motor-vehicle collision, the fall, the assault, the bicycle handlebar — transfers energy across the abdominal wall and produces solid-organ injury (spleen, liver, kidney) and, with a seat-belt force, the hollow viscus and mesenteric injury. Penetrating trauma — the stab, the gunshot, the shotgun — injures along the track, with hollow viscus and major vascular structures predominant. The examination assesses distension, tenderness, guarding, rigidity and bruising (the seat-belt sign, flank and periumbilical ecchymosis), but examination alone is unreliable and imaging is essential.[1]

Pathophysiology and the lethal triad

Bleeding from a solid organ produces haemorrhagic shock; FAST detects free intraperitoneal fluid only above roughly 200 mL. A hollow viscus tear spills enteric contents and produces peritonitis and sepsis over hours rather than minutes — the injury evolves, which is why a normal initial CT cannot fully exclude it. The seat-belt mechanism compresses bowel against the spine, tearing mesentery and bowel wall, and produces the Chance fracture (a flexion-distraction injury through all three spinal columns) that coexists with a bowel injury in about a third of cases. Sustained shock drives the lethal triad — acidosis, hypothermia, coagulopathy — which is the rationale for damage-control surgery and damage-control resuscitation.[1]

Clinical presentation and the seat-belt sign

Presentation ranges from the alert walking wounded to the moribund. Abdominal pain, distension, tenderness, guarding and rigidity are sought on the secondary survey, but shock may be the only sign: hypotension and tachycardia are haemorrhage until proven otherwise. The seat-belt sign — a transverse band of ecchymosis across the lower abdomen — predicts hollow viscus and mesenteric injury and mandates admission and serial examination regardless of an initially reassuring CT. Shoulder-tip pain (Kehr sign) reflects diaphragmatic irritation from splenic blood. A peritonitic, rigid abdomen suggests a hollow viscus perforation. The retroperitoneal injury and the injured, intoxicated or head-injured patient may have minimal abdominal signs, which is why significant mechanism drives admission and observation even when the examination is soft.[2]

Differential diagnosis

The acutely injured abdomen sorts into three clinical patterns that determine the disposition. Distinguishing them at the bedside is the central decision, because each leads to a different pathway — theatre, laparotomy for contamination, or admission and serial observation. [1]

Bedside assessment

The abdomen is assessed within C (circulation) and E (exposure) of the primary survey, before the detailed secondary survey. Vital signs and the shock grade are recorded, and serial examination is the key to the evolving injury — the single most reliable tool for a missed hollow viscus. Inspect for the seat-belt sign, flank bruising (Grey-Turner) and periumbilical bruising (Cullen) indicating retroperitoneal blood, and distension. Palpate for tenderness, guarding and rigidity. Perform a digital rectal examination for blood and a high-riding prostate (a urethral injury mandates a retrograde urethrogram before catheterisation). Check pelvic stability by gentle lateral compression — never rock the pelvis, and apply a pelvic binder for the open-book fracture. Examine the scrotum and perineum for degloving and urethral blood.[1]

Investigations: FAST, CT and DPL

Three imaging modalities frame the work-up, each answering a different question. FAST (Focused Assessment with Sonography in Trauma) is the bedside ultrasound that answers the one question that matters in the unstable patient: is there free fluid? The four standard views are Morrison pouch (right upper quadrant), the splenorenal recess (left upper quadrant), the subxiphoid pericardial view, and the pouch of Douglas (suprapubic). FAST is highly specific for free intraperitoneal fluid above 200 mL but its sensitivity is only around 60 to 70 per cent — it misses the hollow viscus, the retroperitoneal injury, and the early solid-organ injury before any fluid has extravasated. A positive FAST in the unstable patient indicates intra-abdominal bleeding and mandates immediate laparotomy; CT is not needed. A negative FAST does not exclude injury, and the stable patient with a significant mechanism still requires CT. [1]

Contrast CT is the definitive imaging for the haemodynamically stable patient. It grades the solid-organ injury, identifies active contrast extravasation (the blush), free air (hollow viscus), mesenteric stranding and bowel-wall thickening (hollow viscus and mesenteric injury), and retroperitoneal injury (kidney, duodenum, pancreas). The pancreatic duct should be specifically evaluated when a pancreatic injury is suspected. CT does not exclude a hollow viscus injury that has not yet declared itself, so the patient with a significant mechanism and an equivocal CT is admitted and re-examined. Diagnostic peritoneal lavage (DPL) is now historical: a suprapubic catheter was placed below the umbilicus, the peritoneum lavaged, and the aspirate regarded as positive with more than 10 mL of gross blood or a red-cell count above 100 000 per mL. DPL was highly sensitive for intra-abdominal bleeding but could not characterise the organ or grade the injury, and it has been displaced by FAST at the bedside and CT in the stable patient.[2][1]

Resuscitation and damage-control resuscitation

Resuscitation runs in parallel with the primary survey, not after it. Give high-flow oxygen and establish two large-bore intravenous cannulae (16 G or larger). In the shocked patient activate the massive haemorrhage protocol and resuscitate with blood products in a 1:1:1 ratio of packed red cells, fresh frozen plasma and platelets — crystalloid is minimised because it worsens dilutional coagulopathy and hypothermia. Use permissive hypotension, targeting a systolic pressure of 80 to 90 mmHg until bleeding is controlled; this is contraindicated in traumatic brain injury, where normotension is preserved. Give tranexamic acid 1 g intravenously over 10 minutes within 3 hours of injury, followed by 1 g over 8 hours (CRASH-2). Keep the patient warm to prevent the lethal triad. Provide adequate analgesia with morphine 5 mg intravenously, titrated in 1 to 2 mg increments. Crossmatch at least 4 units of packed red cells. The unstable patient with a positive FAST does not go to CT — they go to theatre for damage-control laparotomy.[1][1]

Splenic injury and non-operative management

The spleen is the most commonly injured organ in blunt abdominal trauma, and the modern standard is non-operative management (NOM) for every haemodynamically stable patient regardless of injury grade — the principle is to treat the patient's physiology, not the radiological grade.[3] NOM comprises admission, bed rest, serial haematocrit and serial abdominal examination, with ICU monitoring for the high-grade injury. Failure of NOM — haemodynamic deterioration or a falling haematocrit — converts to operative management. Splenic angiography with embolisation is indicated for the stable patient with active contrast extravasation (the blush) or a high-grade (AAST grade III or above) injury with a vascular component; it salvages the spleen and preserves immune function. Splenectomy is reserved for the unstable patient, the failure of NOM, or the shattered spleen. Every patient who loses the spleen must receive post-splenectomy prophylaxis: vaccination against the encapsulated organisms — pneumococcus, meningococcus and Haemophilus influenzae type b — ideally at least two weeks before discharge (given as early as possible after injury if discharge is unavoidable), plus lifelong patient education and standby antibiotics for any febrile illness. The anticoagulated patient fails NOM more often and is managed with a lower threshold for embolisation or operation.[3][4]

Management of the liver injury

The liver is the second most commonly injured solid organ in blunt trauma and is managed non-operatively in the stable patient by the same principles as splenic injury, with serial observation and a low threshold for angiographic embolisation of an arterial blush. The unstable patient, or the failure of NOM, undergoes damage-control surgery. Perihepatic packing tamponades most bleeding. The Pringle manoeuvre — clamping the hepatoduodenal ligament to occlude hepatic arterial and portal inflow — controls parenchymal bleeding for up to 30 minutes while repair or packing is completed. Arterial injuries are treated by angioembolisation. The retrohepatic inferior vena cava injury is lethal and is managed by an atrio-caval shunt or venous bypass in a dedicated centre; simple packing and transfer is often the realistic damage-control option.[1]

Management of the hollow viscus injury

A hollow viscus injury — gastric, small-bowel or colonic perforation, or a mesenteric tear with ischaemia — presents with peritonitis or free air, but it often evolves over hours and may be missed on the initial CT, where mesenteric stranding, bowel-wall thickening and a small amount of free air without solid-organ injury are the clues.[2] The seat-belt sign is the warning. The peritonitic patient, or any patient with free air, goes to laparotomy for source control: resection with primary anastomosis or a stoma, and repair of the mesentery. Antibiotics are given within 60 minutes of the decision to operate — ceftriaxone 2 g intravenously plus metronidazole 500 mg intravenously for Gram-negative and anaerobic cover, or piperacillin-tazobactam 4.5 g intravenously as a single broad-spectrum agent.

The damage-control laparotomy

The unstable patient with intra-abdominal bleeding — a positive FAST with hypotension, or a known solid-organ injury with active extravasation and shock — goes to theatre for the damage-control laparotomy, not to CT. The operation has three objectives: control the bleeding by packing, ligation, shunt or the Pringle manoeuvre; control the contamination by resection without anastomosis, stapling and stoma; and leave the abdomen open with a temporary vacuum dressing, deferring all definitive repairs until the lethal triad is corrected in intensive care. A planned second-look laparotomy at 24 to 48 hours re-examines the bowel, completes the repairs and attempts closure. Definitive reconstruction at the index operation in a cold, acidotic, coagulopathic patient is the error this strategy was designed to prevent.[1]

The seat-belt injury: Chance fracture and mesenteric tear

A lap-belt restraint converts the deceleration of a motor-vehicle collision into a flexion force across the upper abdomen and the lower thoracic spine. The seat-belt sign across the lower abdomen is the external marker of this force and carries a significant risk of hollow viscus and mesenteric injury. The Chance fracture is a flexion-distraction injury through all three spinal columns (the anterior and middle columns fail in tension), typically at L1 or L2, and it coexists with a bowel injury in roughly a third of patients — so a Chance fracture on imaging is an explicit prompt to hunt for and observe for a hollow viscus injury, and a bowel injury prompts scrutiny of the thoracolumbar spine. The mesenteric tear may devascularise a segment of bowel and present as ischaemia or a delayed stricture. The management is admission, serial examination, a low threshold for repeat CT, and laparotomy for peritonitis, free air or mesenteric ischaemia.[2]

The anticoagulated trauma patient

The anticoagulated trauma patient is a high-risk subgroup: bleeding is occult, expands while standard coagulation tests are awaited, and non-operative management fails more often — a national analysis confirmed a significantly higher failure rate of splenic NOM in anticoagulated patients.[4] Reverse the anticoagulant early and in parallel with the resuscitation, not after confirmatory testing: for warfarin give vitamin K 10 mg intravenously and prothrombin complex concentrate 25 to 50 IU per kilogram; for dabigatran give idarucizumab; for apixaban or rivaroxaban give andexanet alfa or prothrombin complex concentrate. Maintain a low threshold for CT and repeat imaging, and a lower threshold than usual for operative or angiographic intervention. The full reversal strategy is covered in the dedicated anticoagulated-trauma topic.

Special populations

Pregnancy shifts the viscera, the relative hypervolaemia of pregnancy masks shock until late, and the supine gravid uterus obstructs venous return — tilt the patient 30 degrees to the left, check β-hCG and Rh status, and remember that the foetal-maternal unit tolerates hypotension poorly. Paediatric patients are managed non-operatively even more aggressively: physiological reserve masks shock until late, the small absolute blood volume makes early blood-product resuscitation critical, and FAST is less reliable. Elderly patients have comorbidities, anticoagulation and reduced physiological reserve, lowering the threshold for admission, CT and intervention. The obese patient's signs are masked, and the CT may be technically limited. Every group benefits from the same principle: significant mechanism drives observation regardless of an initially reassuring examination. [1]

Complications and pitfalls

The recurring errors are: sending the unstable patient to CT instead of theatre; accepting a negative FAST as excluding injury (hollow viscus, retroperitoneal, pancreatic); missing the pancreatic injury (lipase may be normal early, and the duct must be evaluated); missing the hollow viscus on the initial CT and discharging the seat-belt-sign patient (admit and observe); under-observing a non-operatively managed solid organ (delayed splenic rupture); forgetting the post-splenectomy vaccination and education; over-resuscitating with crystalloid and worsening the lethal triad; and missing the diaphragmatic injury that presents late with herniation. The abdominal compartment syndrome is a recognised complication after damage-control laparotomy and demands a low threshold for decompression. [1]

Prognosis and disposition

Mortality rises with shock grade, the lethal triad, and associated traumatic brain injury; the delayed diagnosis of a hollow viscus or pancreatic injury carries the highest preventable mortality. The stable patient managed non-operatively is admitted to the ward or HDU for serial haematocrit and abdominal examination; the post-damage-control-laparotomy patient goes to ICU for correction of the lethal triad and a planned second look; and the post-splenectomy patient is discharged with vaccination, standby antibiotics and clear advice to present with any febrile illness. [1]

Evidence and regional guidelines

The management of abdominal trauma is built on ATLS, the European guideline on major bleeding and coagulopathy after trauma (Rossaint 2023) for damage-control resuscitation and tranexamic acid, and the WTA / EAST practice-management guidelines for non-operative management of blunt solid-organ and blunt bowel injury. Recent work refines the CT scoring systems for blunt hollow viscus and mesenteric injury (Granieri 2026), re-emphasises treating the patient's physiology over the radiological grade in solid-organ trauma (Ozcan Siki 2026), and quantifies the failure of non-operative splenic management in the anticoagulated patient (Dhillon 2026). In the ANZ region the Australian and New Zealand Resuscitation Councils align with ATLS.[1][2][3][4][1]

Exam pearls

A candidate who has read only this topic should be able to answer: positive FAST + unstable goes to theatre, never CT; a negative FAST does not exclude a hollow viscus, retroperitoneal or pancreatic injury — admit, observe, repeat; TXA 1 g IV over 10 min within 3 h, then 1 g over 8 h; 1:1:1 PRBC:FFP:platelets, minimise crystalloid; permissive hypotension SBP 80 to 90, not in TBI; the seat-belt sign predicts hollow viscus and mesenteric injury — admit and observe; the Chance fracture coexists with a bowel injury in about a third — examine both; non-operative management is a physiology decision, not a CT-grade decision; post-splenectomy: pneumococcal, meningococcal and Hib vaccination plus lifelong education; the pancreas is missed — evaluate the duct, lipase may be normal early; damage-control laparotomy: control bleeding, control contamination, leave open, correct the lethal triad, return. [1]

Organ injury by mechanism

The mechanism predicts which organs are injured, and the prediction drives the search before imaging confirms it. A solid grasp of the mechanism–organ pairing lets the candidate anticipate injury and hunt for the second injury that the first one obscures. [1]

The eFAST — extended FAST

The extended FAST (eFAST) adds thoracic views to the standard four, and is now the standard bedside study in most trauma centres. The thoracic views detect a pneumothorax (absent lung sliding and comet-tail artefact at the anterior chest in the second to fourth intercostal space) and a haemothorax (dependent anechoic fluid above the diaphragm). The two pleural and two pneumothorax views raise the sensitivity of the bedside ultrasound and reduce the number of chest X-rays and CTs required in the multiply-injured patient.[10]

AAST organ injury grading

The American Association for the Surgery of Trauma (AAST) grading system standardises the description of solid-organ injury and guides the threshold for intervention. Grade I to II is low-grade, III to V high-grade, and VI is the near-complete or complete avulsion that mandates operation. The grade is a communication tool and a research endpoint — the management decision remains physiological, not radiological.[3]

Splenic angiography and embolisation

Splenic artery embolisation (SAE) extends non-operative management to the patient with a contrast blush or a high-grade injury who remains haemodynamically stable. The principle is to occlude the bleeding vessel or reduce the splenic arterial pressure enough for haemostasis while preserving splenic immune function. Proximal embolisation (a coil in the main splenic artery) reduces inflow pressure; distal embolisation (gelatin foam in the intraparenchymal branches) targets a specific bleeding point.[5]

Post-splenectomy care and asplenia precautions

The asplenic patient is at lifelong risk of overwhelming post-splenectomy infection (OPSI) — a fulminant, often fatal septicaemia with encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae type b, Neisseria meningitidis, and Capnocytophaga canimorsus after dog bites). The spleen clears opsonised bacteria and is the principal site of IgM production; without it, the bactericidal response to encapsulated organisms collapses. OPSI mortality is 50 to 70 per cent despite intensive care, so prevention is everything.[6]

Vaccination schedule

Vaccinations are given ideally at least two weeks before an elective splenectomy, but in trauma the spleen is removed first and the vaccines are given 14 days postoperatively — earlier administration during the acute physiological stress impairs the antibody response. [1]

Antibiotic prophylaxis and standby antibiotics

Lifelong oral penicillin V (phenoxymethylpenicillin) 500 mg twice daily is the standard prophylaxis in many guidelines, although some reserve it for the first 2 to 5 years or for high-risk groups (children, the immunosuppressed). Standby (rescue) antibiotics — a supply of amoxicillin 1 g orally (or, in penicillin allergy, a fluoroquinolone) carried by the patient and taken at the first sign of fever, followed by urgent medical care — are the safety net that catches OPSI before it is fulminant. A MedicAlert bracelet, a written care plan, and a clear instruction to present to an emergency department with any febrile illness complete the education.[6]

Penetrating abdominal trauma: selective management

The historic teaching that every anterior penetrating abdominal wound goes to laparotomy has given way to selective non-operative management in the haemodynamically stable patient without peritonitis or evisceration. Stab wounds are explored locally to confirm peritoneal breach; gunshot wounds with a transabdominal trajectory still generally mandate laparotomy, but selected stable patients with tangential or isolated solid-organ injury are managed by CT and observation.[9]

The retroperitoneal injury

The retroperitoneum holds the kidney, ureter, duodenum, pancreas, great vessels, and the colon's retroperitoneal segments — all relatively protected from the FAST, which interrogates the peritoneal cavity. A retroperitoneal haematoma is identified on CT, and its zone predicts the management. Zone I (central, around the great vessels) demands exploration for a vascular injury. Zone II (lateral, kidney and flank) is managed selectively — most blunt renal injuries are observed; a pulsatile or expanding haematoma needs angiography or exploration. Zone III (pelvic) is the pelvic fracture bleed — managed by pelvic binding and angioembolisation, not laparotomy.[1]

Pancreatic and duodenal injury

Pancreatic and duodenal injuries are uncommon but carry the highest morbidity and mortality of the abdominal injuries because they are missed early. The mechanism is compression of the pancreas and duodenum against the spine (handlebar, seat-belt, direct blow). Lipase and amylase may be normal in the first hours; a CT may show only inflammatory stranding. The pancreatic duct is the critical structure — a ductal injury (best seen on MRCP or ERCP, or inferred on contrast CT) changes the management from observation to operative drainage or resection. A combined duodeno-pancreatic injury is the worst-case combination and carries mortality over 30 per cent.[8]

Hollow viscus injury — CT scoring and the seat-belt sign

The hollow viscus injury remains the most commonly missed abdominal injury because it evolves. The CT signs are subtle and additive: free air without solid-organ injury, mesenteric stranding, bowel-wall thickening (over 3 mm), a mesenteric haematoma, and active extravasation into the bowel lumen. Scoring systems (the Biffi, the Malhotra, the AAST mesenteric scale) attempt to quantify the risk, but no score replaces serial examination and a low threshold to re-scan or operate in the patient with a seat-belt sign or worsening pain.[2][9]

Damage-control laparotomy in detail

The damage-control laparotomy is the operation for the patient in extremis — the goal is to survive the operation, not to cure at the first sitting. Definitive reconstruction in the cold, acidotic, coagulopathic patient kills; the abdomen is left open, the lethal triad is corrected in ICU, and the patient returns for a planned re-laparotomy.[7]

Complications of the open abdomen

After a damage-control laparotomy the open abdomen carries its own complications. Abdominal compartment syndrome (bladder pressure over 25 mmHg with new organ failure — renal, respiratory, cardiovascular) demands immediate decompression. Entero-atmospheric fistula forms when exposed bowel mucosa leaks into the wound. Planned ventral hernia is accepted when primary fascial closure fails, to be repaired months later. Fluid sequestration (the third space) is enormous and demands careful fluid balance — the rationale for damage-control resuscitation with blood products and minimal crystalloid. [1]

The diaphragmatic injury

Diaphragmatic injury is missed in around half of cases at the index presentation because the rent is small and the patient is stable. It occurs more often on the left (the liver buttresses the right), from a sudden rise in intra-abdominal pressure (seat-belt, fall) or a penetrating thoracoabdominal wound. The danger is delayed herniation — months to years later, with bowel strangulating through the defect, presenting as bowel obstruction or ischaemia in an unexpected place.[11]

The trauma laparotomy: who and when

The decision to operate is a physiology decision. The candidate must be able to articulate the indication cleanly and immediately. [1]

Pitfalls and high-yield reminders

Red flags