Abdominal Compartment Syndrome

📘 1 · Washington Manual of Critical Care

A Pressure You Have to Measure to Find

The abdomen is a closed compartment, and like any compartment its pressure can rise until it strangles the organs within it and beyond it. Intra-abdominal hypertension (IAH) is a sustained intra-abdominal pressure ≥12 mmHg; abdominal compartment syndrome (ACS) is a sustained pressure >20 mmHg accompanied by new organ dysfunction. The diagnosis is easy to miss because the clinical examination — a tense, distended abdomen — is unreliable; the only way to find it is to measure the pressure, almost always via the bladder. In the deteriorating patient with a swollen abdomen after resuscitation, surgery or pancreatitis, measuring the intra-abdominal pressure should be routine.

Summarised from the Washington Manual of Critical Care — Abdominal Compartment Syndrome.

Grade I

IAP 12–15 mmHg

Grade II

IAP 16–20 mmHg

Grade III

IAP 21–25 mmHg

Grade IV

IAP >25 mmHg

ACS = sustained IAP >20 mmHg + new organ dysfunction/failure. Normal IAP in the critically ill is ~5–7 mmHg. Abdominal perfusion pressure (APP) = MAP − IAP; a target APP ≥60 mmHg is often used.

📗 2 · Marino's The ICU Book, 5th Edition (2025)

One Pressure, Every Organ System

Raised intra-abdominal pressure does not confine its damage to the abdomen. It pushes the diaphragm up, splinting the lungs and driving up airway pressures; it compresses the inferior vena cava and reduces venous return and cardiac output; it throttles renal blood flow to produce oliguric acute kidney injury; it reduces gut and hepatic perfusion; and, transmitted to the chest, it raises intracranial pressure. A patient with abdominal compartment syndrome therefore presents as a puzzle of simultaneous failing systems — high ventilator pressures, falling urine output and hypotension — that resolves the moment the abdomen is decompressed.

Summarised from Marino PL. The ICU Book, 5th Ed — Intra-abdominal Hypertension.

🔬 How raised IAP fails the organs

↑ IAPFluid, oedema, ileus, haemorrhage, packing, ascites → tense abdomen

Lungs ↑ diaphragm → ↑ airway pressure, hypoxia, hypercapnia

Cardiac IVC compression → ↓ venous return → ↓ output, hypotension

Renal ↓ renal perfusion → oliguric AKI

Splanchnic gut/hepatic ischaemia, ↑ lactate

CNS ↑ intrathoracic pressure → ↑ ICP

ACSMulti-organ dysfunction that reverses on decompression

📗 Marino — measure it right, at end-expiration, supine

Bladder pressure is the standard: instil ~25 mL saline into the bladder via the urinary catheter, transduce, and read at end-expiration, fully supine, with the transducer zeroed at the iliac crest/mid-axillary line, and the abdominal muscles relaxed.
It is a sustained pressure that matters — measure serially and trend, don't act on a single spuriously high reading (coughing, straining, an unrelaxed patient).
Beware the "secondary" ACS — it occurs without an abdominal injury, from massive fluid resuscitation (burns, sepsis, pancreatitis) causing bowel-wall and mesenteric oedema; capping the crystalloid load is prevention.

📋 3 · Measuring & Managing IAP

Evidence-Based Management (WSACS)

Measure IAP in at-risk patients WSACS

Have a low threshold to measure bladder pressure in patients with risk factors: massive fluid resuscitation, abdominal surgery/trauma, severe acute pancreatitis, burns, bowel obstruction/ileus, intra-abdominal sepsis, tense ascites, liver failure, or prone positioning. Measure serially (e.g. 4–6 hourly) if IAH is present, and calculate APP (MAP − IAP). Physical examination is unreliable — the number, not the belly, makes the diagnosis.

Medical management first — five levers to lower IAP STRONG

Try the non-surgical measures before laparotomy: (1) evacuate intraluminal contents — nasogastric/rectal decompression, prokinetics, stop enteral feed; (2) evacuate space-occupying lesions — percutaneous drainage of ascites/collections/blood; (3) improve abdominal wall compliance — adequate sedation/analgesia, remove constricting dressings, consider neuromuscular blockade, avoid head-up >20–30°; (4) optimise fluids — avoid over-resuscitation, use balanced fluids, consider diuresis/ultrafiltration to achieve neutral-to-negative balance; (5) optimise perfusion — support MAP to keep APP ≥60 mmHg.

Decompressive laparotomy for refractory ACS definitive

Surgical decompression (decompressive laparotomy with a temporary/open abdomen) is the definitive treatment for overt ACS with organ dysfunction refractory to medical measures — it produces an immediate fall in IAP and reversal of the organ failure. The abdomen is left open with a temporary closure (e.g. negative-pressure dressing) and managed toward staged/delayed closure. Do not delay decompression in a patient failing from established ACS while persisting with medical measures.

Prevent it — the resuscitation you give matters

Much ACS is iatrogenic "secondary" ACS from over-resuscitation. Use balanced, goal-directed fluid resuscitation, avoid crystalloid excess (especially in burns, pancreatitis and septic shock), consider damage-control surgery leaving the abdomen open when massive visceral oedema is anticipated, and measure IAP early so rising pressures are caught before organ failure.

🇮🇳 Indian Context

The common Indian settings for ACS are severe acute pancreatitis, major abdominal trauma and surgery, intra-abdominal sepsis (perforation peritonitis, which is very common), major burns, and massive fluid resuscitation — often in units where IAP is not routinely measured, so ACS is under-recognised. The single most useful practice change is cheap and universal: measure bladder pressure with the existing urinary catheter and a simple manometer/transducer in any at-risk deteriorating patient. Emphasise avoiding crystalloid over-resuscitation (a preventable cause), aggressive medical measures (NG decompression, prokinetics, drainage of ascites/collections), and not delaying decompressive laparotomy when organ failure is established — the surgery is definitive and widely available.

🩺 4 · Measures & Doses

The Toolkit for Lowering IAP

Measure	Lever	How	Notes
Bladder pressure measurement	Diagnosis	Instil ~25 mL saline via catheter, transduce, read end-expiration supine (zero at iliac crest)	Serial & sustained; calculate APP = MAP − IAP
Nasogastric / rectal decompression + prokinetics	Evacuate intraluminal contents	NG tube, flatus tube; metoclopramide/erythromycin; stop feed	First-line, low-risk
Percutaneous drainage	Evacuate space-occupying fluid	Drain ascites, collections, blood (image-guided)	Can avert laparotomy if fluid-dominant
Sedation / analgesia ± neuromuscular blockade	Improve abdominal wall compliance	Deepen sedation; short NMB trial	Relaxing the wall lowers IAP; avoid prolonged NMB
Fluid optimisation	Reduce volume overload	Avoid over-resuscitation; diuresis/ultrafiltration for neutral-negative balance	Prevention is better than cure
Vasopressor to defend APP	Optimise perfusion	Support MAP for APP ≥60 mmHg	Perfusion target while lowering IAP
Decompressive laparotomy	Definitive	Open abdomen + temporary closure (NPWT)	For refractory ACS with organ failure — don't delay

🗺 5 · Clinical Flowchart

IAH / ACS — Measure, Medicalise, Decompress

Suspect & measure

At-risk + deteriorating (rising airway pressures, falling urine, hypotension, high lactate)
Measure bladder pressure — don't rely on the examination; calculate APP

Grade it & define ACS

IAH grade I–IV; ACS = sustained IAP >20 mmHg + new organ dysfunction
Start serial monitoring (4–6 hourly) and target APP ≥60 mmHg

Apply the five medical levers

Evacuate luminal contents · drain fluid collections · improve wall compliance (sedation ± NMB)
Optimise fluids (avoid overload) · defend perfusion pressure

Reassess — is organ dysfunction reversing?

Falling IAP + improving urine/ventilation/haemodynamics → continue medical management
Refractory ACS with organ failure → decompressive laparotomy (open abdomen)

Manage the open abdomen & prevent recurrence

Temporary closure (NPWT), staged/delayed closure; nutrition; fluid stewardship
Continue IAP monitoring — recurrence can occur even after decompression

⚠️ 6 · Common Mistakes

Common Mistakes in ACS

❌ Mistake 1 — Diagnosing ACS by feeling the abdomen

Physical examination is unreliable for intra-abdominal pressure. If you don't measure the bladder pressure, you will miss it — measurement should be routine in at-risk patients.

❌ Mistake 2 — Missing multi-organ ACS as separate problems

High airway pressures, oliguria and hypotension occurring together in a distended patient are one problem — raised IAP — and they reverse together on decompression.

❌ Mistake 3 — Over-resuscitating with crystalloid

Excess fluid causes bowel-wall and mesenteric oedema and secondary ACS. Use balanced, goal-directed resuscitation and cap the crystalloid load in burns, pancreatitis and sepsis.

❌ Mistake 4 — Measuring pressure incorrectly

A reading taken sitting up, mid-inspiration, or in a straining patient is falsely high or low. Measure supine, at end-expiration, with the transducer zeroed at the iliac crest and the patient relaxed.

❌ Mistake 5 — Persisting with medical measures in established ACS

Once organ failure from ACS is refractory to medical management, delaying decompressive laparotomy costs organs and lives. The surgery is definitive.

❌ Mistake 6 — Forgetting recurrence after decompression

ACS can recur even with an open abdomen. Continue IAP monitoring and fluid stewardship after decompression.

🎓 7 · Exam Pearls — DrNB / PDCC / IFCCM / EDIC

Exam Pearls

Q: Define IAH and ACS.
IAH = sustained IAP ≥12 mmHg; ACS = sustained IAP >20 mmHg with new organ dysfunction/failure. Normal IAP in the critically ill is ~5–7 mmHg.

Q: How is IAP measured?
Bladder (intravesical) pressure — instil ~25 mL saline via the urinary catheter, transduce, read at end-expiration, supine, zeroed at the iliac crest/mid-axillary line with the abdomen relaxed.

Q: What is abdominal perfusion pressure?
APP = MAP − IAP; a target of ≥60 mmHg is commonly used.

Q: Name the organ effects of raised IAP.
↑ airway pressures/hypoxia (lungs), ↓ venous return/output (cardiac), oliguric AKI (renal), gut/hepatic ischaemia (splanchnic), ↑ ICP (CNS).

Q: What are the medical measures to lower IAP?
Evacuate luminal contents, drain fluid collections, improve abdominal-wall compliance (sedation ± NMB), optimise fluids (avoid overload), and defend perfusion pressure.

Q: What is the definitive treatment of refractory ACS?
Decompressive laparotomy with an open abdomen and temporary closure.

Q: What is secondary ACS?
ACS without an intra-abdominal injury — from massive fluid resuscitation (burns, sepsis, pancreatitis) causing visceral oedema; prevented by avoiding over-resuscitation.

📚 8 · References

References

Kirkpatrick AW, Roberts DJ, De Waele J, et al. (WSACS). Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines. Intensive Care Med. 2013;39:1190–1206.
De Waele JJ, Malbrain MLNG, Kirkpatrick AW. The abdominal compartment syndrome: evolving concepts and future directions. Crit Care. 2015;19:211.
Malbrain MLNG, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and ACS: Definitions. Intensive Care Med. 2006;32:1722–1732.
Marino PL. The ICU Book, 5th Edition. Intra-abdominal Hypertension. Wolters Kluwer; 2025.
Washington Manual of Critical Care, 4th Edition. Kollef MH, Witt CA (eds). Abdominal Compartment Syndrome. Wolters Kluwer; 2023.