Abdominal Compartment Syndrome

Abdominal compartment syndrome (ACS) is defined as sustained intra abdominal pressure (IAP) above 20 mmHg, with or without an abdominal perfusion pressure below 60 mmHg, that is associated with new organ dysfunction or failure. Intra abdominal hypertension (IAH) is sustained or repeated IAP of 12 mmHg or above. Normal IAP in a critically ill adult is about 5 to 7 mmHg.

IAH is graded: grade I, 12 to 15 mmHg; grade II, 16 to 20 mmHg; grade III, 21 to 25 mmHg; grade IV, above 25 mmHg. Abdominal perfusion pressure (APP) equals mean arterial pressure minus IAP, and a target of at least 60 mmHg is associated with better survival.

Classification:

• Primary ACS arises from injury or disease within the abdominopelvic region (trauma, ruptured aneurysm, pancreatitis, bowel obstruction, perihepatic packing, retroperitoneal haemorrhage, liver transplantation)
• Secondary ACS arises from conditions outside the abdomen (massive fluid resuscitation, sepsis, burns, capillary leak)
• Recurrent ACS develops again after prior surgical or medical treatment

Pathophysiology is a vicious cycle. Raised IAP reduces venous return and cardiac preload, compresses the inferior vena cava, raises systemic vascular resistance, and elevates the diaphragm, which lowers lung compliance and raises airway pressures.

Renal perfusion falls through direct renal vein and parenchymal compression, causing oliguria. Splanchnic perfusion falls, producing bowel ischaemia, bacterial translocation and visceral oedema, which in turn raises IAP further.

Intracranial pressure rises through increased intrathoracic and jugular venous pressure.

Risk factors include large volume crystalloid resuscitation (above 5 L in 24 hours), massive transfusion, acidosis (pH below 7.2), hypothermia (below 33 degrees C), coagulopathy, sepsis, ileus, mechanical ventilation with high PEEP, obesity, and abdominal packing or tight closure.

The abdomen is tense and distended, although physical examination is unreliable for estimating IAP (sensitivity about 40 to 60%). Clinical manifestations reflect organ dysfunction:

• Cardiovascular: tachycardia, hypotension, falling cardiac output despite elevated filling pressures (central venous pressure and wedge pressure are falsely raised), reduced stroke volume variation reliability
• Respiratory: rising peak and plateau airway pressures, falling tidal volumes, hypoxaemia, hypercapnia
• Renal: oliguria then anuria that is unresponsive to fluid and diuretics, rising creatinine
• Gut: ileus, high gastric residuals, mesenteric ischaemia, elevated lactate
• Neurological: raised intracranial pressure in head injury
• Hepatic: reduced portal flow and impaired clearance
• Abdominal wall: reduced compliance, which delays or compromises primary fascial closure

Any critically ill patient with risk factors who develops new organ dysfunction needs an IAP measurement. Do not wait for classic signs.

• IAP is measured through the bladder. Technique: patient supine, no abdominal muscle contraction, at end expiration; transducer zeroed at the midaxillary line at the level of the iliac crest; instil no more than 25 mL of sterile saline into the empty bladder through the sampling port of a Foley catheter; allow 30 to 60 seconds for detrusor relaxation; read at end expiration. Measure every 4 to 6 hours in at risk patients, and every 1 to 2 hours when IAP is rising or above 15 mmHg. Bladder measurement is unreliable with pelvic fractures, pelvic haematoma, neurogenic bladder or adhesions. Gastric, rectal and inferior vena cava measurements are alternatives.
• Supportive investigations include arterial blood gas and lactate, serum creatinine and urine output, liver function, and ultrasound or CT. CT findings suggestive of ACS include a round belly sign (anteroposterior to transverse diameter ratio above 0.8), bowel wall thickening or hypoperfusion, bilateral inguinal herniation, compressed or flattened vena cava, bilateral renal vein compression, and direct renal compression.

• General principles. The target is to maintain APP at 60 mmHg or above. Escalate measures stepwise as IAP rises and organ dysfunction persists, and move to surgery if medical measures fail. Delay is dangerous.
• Medical (non-operative) measures for IAH, in order:
  1. Improve abdominal wall compliance: adequate sedation and analgesia; remove constrictive dressings or eschar; keep head of bed under 20 to 30 degrees where possible; consider short term neuromuscular blockade (cisatracurium 0.15 mg/kg bolus then 1 to 3 micrograms/kg/min)
  2. Evacuate intraluminal contents: nasogastric tube to low continuous suction; rectal decompression or enemas; neostigmine 2 mg IV over 3 to 5 minutes once mechanical obstruction is excluded; erythromycin 250 mg IV; metoclopramide 10 mg IV every 6 to 8 hours
  3. Evacuate abdominal fluid: percutaneous drainage of ascites or collections (ultrasound guided paracentesis or pigtail drain), which can lower IAP markedly
  4. Correct positive fluid balance: avoid excess crystalloid; use hypertonic or colloid solutions in selected patients; consider diuretics (furosemide) once haemodynamically stable; use continuous renal replacement therapy with ultrafiltration for refractory overload
  5. Optimise organ support: lung protective ventilation with PEEP titration; inotropes for low output; maintain MAP; avoid hypothermia, acidosis and coagulopathy
• Surgical decompression. Decompressive laparotomy is indicated for ACS (IAP above 20 mmHg with new organ failure) refractory to medical management, and should be considered at lower pressures when ischaemia is evident. A midline laparotomy releases pressure promptly, with improvements in blood pressure, urine output and ventilation. Expect a transient reperfusion syndrome (hypotension, hyperkalaemia, acidosis, arrhythmia, cardiac arrest): pre-load the patient with fluid, correct acidosis, hold bicarbonate and calcium ready, and monitor closely.
• Temporary abdominal closure. Options include negative pressure wound therapy with fascial traction (the preferred method, with the best primary fascial closure rates of 60 to 80%), Bogota bag, Wittmann patch, and mesh or sheet closures. The abdomen is kept open, with return to theatre every 24 to 72 hours for washout, until the cause has resolved and swelling subsides. Definitive closure is by delayed primary closure, component separation, absorbable mesh with split thickness skin graft, or planned ventral hernia with later reconstruction. Complications of the open abdomen include enteroatmospheric fistula, bowel injury, fluid and protein losses, and loss of domain.
• Prevention. In damage control surgery, use limited resuscitation, early blood products, packing, and a planned temporary closure. In pancreatitis and burns, restrict crystalloid volumes and aim for early enteral feeding.
• Prognosis. ACS has mortality of 25 to 75% depending on cause and speed of decompression. Survivors may have long term hernia, renal impairment and reduced quality of life.