Case of the Month #22

Christopher Shaw

A 60 year old man is admitted to the intensive care unit with spontaneous bacterial peritonitis on a background of alcoholic liver disease. He is treated with appropriate antibiotics. However, following admission to the unit he continues to deteriorate and requires intubation. He becomes hypotensive requiring fluid resuscitation and vasopressor support, oliguric and requires high ventilatory pressures. Examination reveals decreased air entry bibasally, with a firm, distended and tense abdomen.

What condition is important to consider?

Intra-abdominal Hypertension & Abdominal Compartment Syndrome

Pressure within the abdomen in critically ill patients is normally 5-7 mmHg1 with the abdomen being considered a ‘closed box’ with walls which are both rigid (costal arch, spine, pelvis) and flexible (abdominal wall and diaphragm)2. Intra-abdominal hypertension (IAH) occurs when abdominal pressures > 12 mmHg are sustained or are recurrent3. If pressure continues to rise, abdominal compartment syndrome (ACS) may occur, which is defined as abdominal pressures > 20 mmHg with evidence of end organ dysfunction/ failure2,3.

How is intra-abdominal hypertension classified?

IAH is common in the intensive care unit and depending on case mix can affect up to 50% of patients, with ACS affecting up to 8%. IAH can be graded on the basis of intra-abdominal pressures (IAP):

● Grade I: 12-15 mmHg 

● Grade II: 16-20 mmHg

● Grade III: 21-25 mmHg

● Grade IV: >25 mmHg

Measurement of IAP may be performed either directly or indirectly. Direct pressure measurement occurs via a peritoneal transducer, while indirect measurement (most commonly used) involves transduction of a urinary catheter, zeroed at the intersection of the iliac crest in the mid-axillary line. The patient should be supine, without muscle contractions for an accurate measurement1.

What are the causes of IAH?

The causes of IAH are myriad, and as a result a simple classification system is helpful. They can be divided into:

  1. Those that increase intra-abdominal volume
    • a)Intra-luminal causes include ileus, severe constipation or added colonic volume (such as may occur as result of clostridium difficile infection).
    • b)Extra-luminal increases include free fluid, blood or air. Imaging is often necessary to investigate these causes.
  2. Those that decrease abdominal wall compliance
    • a)Abnormalities in body habitus (namely obesity).
    • b)Effects of abnormalities within the abdominal wall itself.
    • c)Effects of other pathology/ treatment on abdominal wall compliance such tight abdominal wall closure post-surgery, pronation or burn eschars. Pathology that increases capillary wall leakage, such as sepsis and pancreatitis, may also contribute. It is worth noting that large volume resuscitation can result in capillary leak, and as such it is one of the biggest risk factors for the development of IAH.

Why is IAH clinically important?

IAH can result in multi-organ failure, often related to reduced perfusion (Abdominal perfusion pressure (APP) = Mean Arterial Pressure (MAP) – IAP). Sub-clinical organ injury can develop at IAPs as low as 12-15 mmHg1. As IAP rises, organ dysfunction will become more evident and is often proportional to the level of IAP. Organs affected include2:

  • Respiratory – basal atelectasis, high airway pressures and difficulty ventilating due to splinting of the diaphragm.
  • Cardiovascular – a multifactorial decrease in cardiac output may occur, secondary to increased afterload, decreased preload (due to decreased venous return), increased CVP, increased intrathoracic pressure and can result in physical deformation of the heart itself. All the above will reduce cardiac output and by extension blood pressure.
  • Renal – Acute kidney injury and oliguria may occur when pressures reach 15mmHg.
  • Gastro-intestinal – Ischaemia due to decreased perfusion pressure to organs.
  • Hepatic – dysfunction can start at an IAP of as low as 10 mmHg, with decreased hepatocellular blood flow, decreased portal venous flow and increased portal collateral circulation, decreased lactate clearance and altered glucose handling.
  • Neurological – cerebral perfusion pressure decreases as a result of increased intra-thoracic pressure, causing functional cerebral venous outflow obstruction and may precipitate cerebral oedema.

How is IAH managed?

The decision to treat IAH should be taken after considering a combination of – (a) the overall pressure and (b) it’s impact that pressure is having on the patient. Based on this, management of IAH should involve three key questions:

  1. Is an intervention required?
    • The decision to intervene in a case of IAH will be guided by the degree of resultant organ dysfunction. Patients with higher pressures but improving organ function may not require intervention initially, and especially so if these interventions carry risks themselves (for example, sedation requiring intubation or decompressive laparotomy). However, if IAP is elevated or rising and impacting organ function, intervention will be required.
  2. How urgent is the intervention?
    • The urgency of the intervention will be determined by the IAP, the rate of pressure increase and its effects on organ function. Slowly rising pressures allow time for more delayed interventions, while precipitous rises in pressure with organ dysfunction will require urgent intervention – this can rapidly become life threatening should ACS develop. Stepwise management should be instituted, although immediate decompression may be indicated in the event of refractory cardiovascular or respiratory failure3.
  3. What is the most appropriate intervention?
    • The best intervention will be determined by the cause. A multi-modal approach may be favourable to a single intervention in isolation. IAP should be measured every four-six hours3 and excessive fluid administration3 should be avoided.  IAP should be targeted to <15 mmHg1. Management strategies can be divided into:
      • Intra-luminal volume reduction – Evacuation of gut contents, through the use of prokinetics & enemas. Although nasogastric tubes and rectal tubes may be beneficial, these will only decompress the most proximal and distal aspects of the gastrointestinal tracts.
      • Extra-luminal volume reduction – May be amenable to percutaneous drainage as a temporising measure while other treatments take effect.
      • Abdominal wall compliance improvement – Depends on the cause – Prone patients can be supinated if clinical condition allows, while burn patients with IAH may be amenable to escharotomy to reduce the abdominal constriction. Sedation and muscle relaxation may be required to reduce muscular tone in the abdomen and thus increase compliance.
      • Optimise fluid therapy and organ perfusion – Goal directed fluid therapy and monitoring1 to target an APP >60 mmHg2.
      • Decompressive laparotomy – A definitive treatment for ACS3, which has considerable morbidity so should be reserved for cases of treatment failure. When performed, it may result in an extensive reperfusion syndrome. Close monitoring of IAPs should occur post-operatively to monitor for recurrence of ACS.

Key Messages

  • It is important to be vigilant and consider IAH as it can present insidiously in critically ill patients – consider when a distended abdomen is present and organ dysfunction worsens.
  • Do not rely on the IAP as a sole indicator of whether IAH is present.
  • Treatment is multi-factorial with no one strategy correct for all causes.
  • Decompressive laparotomy is an aggressive treatment with significant morbidity attached.


  1. De Laet IE, Malbrain, MLNG, De Waele JJ. A Clinician’s Guide to Management of Intra-abdominal Hypertension and Abdominal Compartment Syndrome in Critically Ill Patients. Crit Care 2020;24(1)97.
  2. Papavramidis TS, Marinis AD, Pliakos I, Kesisoglou I, Papavramidou N. Abdominal compartment syndrome – Intra-abdominal hypertension: Defining, diagnosing, and managing. J Emerg Trauma Shock 2011;4(2): 279-291.
  3. World Society of the Abdominal Compartment Syndrome. WSACS Algorithms. Available at