Abdominal compartment syndrome

Contents

Overview

Abdominal compartment syndrome (ACS) is a sustained rise in intra-abdominal pressure (IAP) above 20 mmHg associated with new or progressive organ dysfunction. It is a potentially reversible but life-threatening condition that demands early recognition and a systematic management approach.

Intra-abdominal hypertension (IAH) — defined as IAP ≥12 mmHg — is common in critically ill patients and precedes ACS. Not all patients with IAH develop ACS, but untreated IAH that progresses causes multiple organ failure.

Pathophysiology

Normal IAP is 5–7 mmHg and may be slightly higher in obese patients. It is generated by the compliance of the abdominal wall and the volume of intra-abdominal contents.

Rising IAP compresses abdominal viscera and vasculature, impairs diaphragmatic excursion, and increases thoracic pressure. The abdominal perfusion pressure (APP = MAP − IAP) falls as IAP rises. An APP below 50 mmHg is associated with organ ischaemia and predicts mortality more reliably than IAP alone.

The pathological cascade involves:

  1. Compression of the inferior vena cava and portal vein, reducing venous return to the right heart
  2. Elevated thoracic pressure, further reducing venous return and increasing right ventricular afterload
  3. Impaired cardiac output
  4. Direct renal vein compression and reduced renal arterial perfusion
  5. Mesenteric and bowel wall ischaemia, with mucosal barrier disruption and bacterial translocation
  6. Raised intracranial pressure from impaired cerebral venous drainage via elevated thoracic pressure

Aetiology

Primary ACS: Arises from abdominal or pelvic pathology — major abdominal trauma, haemoperitoneum, peritonitis, bowel obstruction, pancreatitis, abdominal aortic aneurysm repair.

Secondary ACS: Arises from conditions outside the abdomen, typically large-volume fluid resuscitation causing bowel oedema and retroperitoneal oedema. Sepsis and burns are common causes.

Recurrent ACS: Recurrence after initial resolution, often after temporary abdominal closure.

Risk factors include massive fluid resuscitation, ileus, mechanical ventilation with high PEEP, and obesity.

Measurement and Classification

Standard measurement: Intravesicular (bladder) pressure is the gold standard. The technique involves:

  1. Patient supine
  2. Instil 25 mL of sterile saline via a urinary catheter
  3. Connect pressure transducer zeroed at the iliac crest (mid-axillary line in the supine position, at the level of the symphysis pubis per WSACS guidance)
  4. Measure at end-expiration

Values should be taken in the supine position; head elevation, abdominal wall muscle tension (agitation, coughing), and PEEP all increase the recorded pressure.

WSACS grading of IAH:

Grade IAP
I 12–15 mmHg
II 16–20 mmHg
III 21–25 mmHg
IV >25 mmHg

ACS is diagnosed when IAP exceeds 20 mmHg and there is associated new organ dysfunction.

Organ Effects

Cardiovascular: Reduced venous return (IVC compression), increased right ventricular afterload from raised intrathoracic pressure, reduced cardiac output. CVP and PAOP may be elevated but do not reflect preload accurately in this context.

Respiratory: Diaphragm displacement causes reduced functional residual capacity, atelectasis, reduced compliance, and increased peak and plateau pressures. Hypoxia and hypercapnia follow.

Renal: Combination of reduced cardiac output, direct renal parenchymal compression, and renal vein compression reduces GFR and urine output. Oliguria with IAP >20 mmHg and anuria with IAP >30 mmHg are recognised thresholds.

Gastrointestinal: Mesenteric venous congestion and arterial hypoperfusion cause mucosal ischaemia, impaired gut motility, and risk of bacterial translocation.

Neurological: Raised intracranial pressure occurs via impaired cerebral venous outflow secondary to elevated thoracic and central venous pressure.

Management

Management follows a stepwise approach from medical optimisation to surgical decompression.

Medical Management

Improve abdominal wall compliance:

  • Adequate sedation and analgesia to reduce abdominal wall muscle tension
  • Neuromuscular blockade in refractory cases — can reduce IAP by 10–15 mmHg
  • Avoid excessive head-of-bed elevation (>30° increases IAP)

Evacuation of intraluminal contents:

  • Nasogastric tube on free drainage
  • Prokinetics to treat ileus (metoclopramide, erythromycin)
  • Rectal tube for lower bowel distension
  • Colonoscopic decompression in megacolon

Evacuation of abdominal fluid:

  • Paracentesis or ascitic drainage if ascites is contributing
  • Radiologically guided drainage of localised collections

Fluid balance optimisation:

  • Avoid ongoing positive fluid balance; reassess fluid requirements critically
  • Target euvolaemia or negative balance once haemodynamics allow
  • Diuretics or ultrafiltration if fluid-overloaded

Ventilator management:

  • Raised IAP requires increased airway pressure to overcome reduced thoracic compliance
  • Monitor plateau pressure and compliance carefully

Surgical Management

Decompressive laparotomy is indicated when IAP exceeds 20 mmHg with organ dysfunction that does not respond to optimised medical management.

A midline laparotomy is performed and the abdomen left open using temporary abdominal closure (TAC). Vacuum-assisted closure (VAC) systems (e.g., ABTHERA) maintain abdominal domain, prevent evisceration, manage effluent, and allow repeated access. The patient returns to theatre every 48–72 hours for reassessment, lavage, and planned primary closure when abdominal oedema has resolved.

Open abdomen management requires specialist input and is associated with significant complications including enteroatmospheric fistula and hernia. Early planned closure reduces these risks.

Viva Questions

How do you measure intra-abdominal pressure and what are the diagnostic thresholds?

Intra-abdominal pressure is measured via the intravesicular route using a urinary catheter. With the patient supine, 25 mL of sterile saline is instilled into the bladder. The catheter is connected to a pressure transducer zeroed at the iliac crest, and the reading is taken at end-expiration. Normal IAP is 5–7 mmHg. Intra-abdominal hypertension is defined as a sustained IAP of 12 mmHg or higher, graded I to IV by the WSACS. Abdominal compartment syndrome is diagnosed when IAP exceeds 20 mmHg and there is new or worsening organ dysfunction attributable to raised pressure. The abdominal perfusion pressure (MAP minus IAP) is a clinically useful derived value — an APP below 50 mmHg correlates with organ ischaemia and mortality, and may be a more reliable treatment target than IAP alone.

What are the organ-specific effects of raised intra-abdominal pressure?

Raised intra-abdominal pressure affects multiple organ systems simultaneously. Cardiovascular effects include reduced venous return from IVC compression, impaired cardiac output, and increased afterload from raised intrathoracic pressure — CVP and PAOP may be paradoxically elevated and should not be used to guide fluid management. Respiratory effects include diaphragmatic splinting, reduced lung compliance, atelectasis, and hypoxaemia; airway pressures rise and the risk of barotrauma increases. Renal effects are mediated by direct parenchymal compression, renal vein compression, and reduced renal perfusion pressure; oliguria typically develops above an IAP of 20 mmHg. Gastrointestinal effects include mesenteric venous congestion and arterial underperfusion causing mucosal ischaemia and bacterial translocation. Raised intrathoracic pressure impairs cerebral venous drainage, increasing intracranial pressure.

When would you recommend decompressive laparotomy for ACS?

Decompressive laparotomy is indicated when ACS is confirmed — IAP above 20 mmHg with new organ dysfunction — and does not respond to a systematic trial of medical management. Medical measures should be pursued in parallel and rapidly: sedation and neuromuscular blockade to improve abdominal wall compliance, nasogastric and rectal decompression, paracentesis if indicated, and optimisation of fluid balance. If these measures fail to reduce IAP or improve organ function within a reasonable timeframe, surgical decompression is required. The decision should not be delayed excessively; progressive ACS with worsening renal failure, increasing ventilatory requirements, or haemodynamic deterioration warrants urgent surgical review. The abdomen is left open with temporary abdominal closure, typically using a vacuum-assisted system. Planned closure is attempted within 24–72 hours in subsequent return trips to theatre once oedema and inflammation have resolved.