Abdominal Compartment Syndrome
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Direct answer
Intra-abdominal pressure above 20 mmHg with new organ dysfunction defines abdominal compartment syndrome (ACS); pressures sustained above 12 mmHg define intra-abdominal hypertension (IAH), graded I to IV (12–15, 16–20, 21–25, over 25). Bedside measurement through the urinary catheter — instilling about 25 mL of saline into the bladder and reading end-expiratory pressure — makes this a diagnosis any surgical ward can make, and it must be actively sought in the high-risk: damage-control laparotomy patients, massive resuscitation, burns, pancreatitis and sepsis. Organ effects arrive in a predictable order — reduced urine output and falling cardiac output before the airway pressures climb — and decompressive laparotomy with an open abdomen is the definitive treatment, reinforced by medical measures (neuromuscular blockade, nasogastric and rectal decompression, fluid discipline) at lower grades.
What you must remember
- Normal intra-abdominal pressure is roughly 5–7 mmHg in the resting adult; the World Society of the Abdominal Compartment Syndrome (WSACS) definitions are the reference standard.
- Grading of IAH: Grade I 12–15 mmHg, Grade II 16–20, Grade III 21–25, Grade IV above 25; ACS is IAH above 20 mmHg with new organ failure (a clinical state, not a number alone).
- Bladder technique: 25 mL saline instilled with the patient supine, transducer zeroed at the iliac crest, read at end-expiration in mmHg — the bladder acts as a passive conduit when the detrusor is relaxed.
- Organ effects: oliguria (renal venous compression and reduced cardiac output) is early and proportionate; then reduced venous return and raised airway pressures — the combination of oliguria, high airway pressures and a tensely distended abdomen after resuscitation is the classical triad.
- Abdominal perfusion pressure = mean arterial pressure minus intra-abdominal pressure; resuscitation targets an APP of at least 50–60 mmHg, sometimes achievable without surgery.
- Risk factors: massive fluid resuscitation (the classic "secondary" ACS after burns or trauma with a normal abdomen initially), damage-control closure under tension, pancreatitis, ileus, peritonitis, liver transplantation, obesity, and high-insufflation laparoscopy.
- Management ladder: medical first — sedation and neuromuscular blockade, nasogastric and rectal tubes, positioning, diuretics or renal replacement for fluid overload; then percutaneous catheter drainage of collections; decompressive laparotomy for established ACS, leaving the abdomen open under a temporary closure.
- Prophylaxis after damage-control surgery: avoid forced fascial closure under tension; a planned open abdomen with negative-pressure therapy reduces ACS and fistula risk.
How to work through it
Twelve hours after damage-control packing for a liver injury, a ventilated patient who received 14 units of blood and 8 litres of crystalloid becomes oliguric, peak airway pressures climb, and blood pressure requires escalating noradrenaline — while the abdomen is tense and the temporary closure taut. The team measures bladder pressure: 26 mmHg end-expiratory. Cross-check the physiology: abdominal perfusion pressure of 50 mmHg barely clears the threshold; the chest radiograph shows elevated hemidiaphragms. This is Grade IV IAH with organ failure — ACS. Immediate steps: paralysis in the already sedated patient, gastric and rectal decompression, and a low threshold for returning to theatre, because the definitive move is reopening the temporary closure, evacuating packs and oedema, and leaving the abdomen open with a negative-pressure dressing. In the ICU afterwards, the game is prevention of recurrence: fluid restriction or removal, enteral nutrition held to tolerance, and surveillance bladder pressures until closure. The counter-scenario is "secondary" ACS in a burnt child with a soft abdomen at admission: two days of massive resuscitation, then oliguria and rising airway pressures with a newly tense abdomen — the lesson being that ACS appears in patients whose abdomens were never opened, which is why high-risk groups need scheduled pressure measurement rather than a watched-for tense abdomen.
Where students slip
Two measurement slips recur: quoting pressures in centimetres of water (mixing units — the definitions are in mmHg) and describing a bladder measurement with a large instillation volume or during diuresis, both of which distort the reading. Clinically, the favourite error is waiting for the "classical tense abdomen" in a sedated, ventilated patient — in the ICU the presentation is physiological: oliguria plus rising airway pressures plus falling cardiac output. The second error is conceptual — confusing ACS (pressure plus new organ dysfunction) with mere IAH (pressure alone). Third, decompression timing: writing "decompress when convenient" loses the mark — established ACS is a surgical emergency in which hours of delay are irreversible renal and gut ischaemia.
Frequently asked questions
How is intra-abdominal pressure measured at the bedside?
Through a urinary catheter: instil about 25 mL saline into the bladder, zero the transducer at the iliac crest, and read end-expiratory pressure in mmHg — the validated indirect method.
What distinguishes intra-abdominal hypertension from abdominal compartment syndrome?
IAH is a sustained pressure above 12 mmHg (graded I–IV); ACS is pressure above 20 mmHg with new organ dysfunction — oliguria, respiratory compromise or circulatory failure — making it a clinical syndrome, not a number.
Which patients need routine pressure monitoring?
Damage-control laparotomy patients, massive resuscitation for trauma or burns, severe pancreatitis, sepsis with ileus, and those with closed abdomens under tension after emergency surgery.
What is abdominal perfusion pressure and its target?
Mean arterial pressure minus intra-abdominal pressure; a target of at least 50–60 mmHg guides resuscitation and vasopressor use before resorting to decompression.
Why does urine output fall early in ACS?
Because raised pressure compresses renal veins and parenchyma and reduces cardiac output by impeding venous return — oliguria is the first sign and reverses promptly after decompression.