Aetiology

Intra-abdominal hypertension and ACS share the same aetiology, and the clinical distinctions are points along a continuum. The underlying conditions that produce elevated intra-abdominal pressure (IAP) are divided into primary and secondary causes.

Primary causes are due to decreased abdominal compliance, presence of an intra-abdominal or retro-peritoneal injury, or a pathological process. These are less common than the secondary causes.

  • Decreased abdominal compliance: processes that decrease abdominal compliance (i.e., the elasticity of the abdominal wall and diaphragm), such as severe obesity, burns with abdominal wall eschars, and severe ventilator dyssynchrony with use of accessory muscles, can significantly increase IAP.[5]

  • Intra-abdominal infection/inflammation: infections leading to generalised peritonitis can cause intensive inflammation of the peritoneal surfaces and gut. Significant fluid resuscitation and surgical intervention is often required, which can result in gut oedema and the generation of peritoneal fluid. This is particularly prominent in the paediatric population, where infectious enterocolitis is a significant risk factor for the development of ACS in children.[6] The inflammatory response in severe acute pancreatitis leads to ACS in approximately 40% of cases, with a significant increase in mortality.[7][8]

  • Haemoperitoneum: this can be produced by a ruptured abdominal aortic aneurysm, arterial or venous trauma, or ruptured hepatic tumours. These patients require fluid resuscitation and massive transfusion and will therefore also have gut oedema and ascites. A haemoperitoneum can produce IAPs high enough to cause ACS. However, because fluid resuscitation is instigated early, haemoperitoneum is more commonly seen in combination with ascites and gut oedema.

  • Ileus: any process that decreases or impairs the normal transit of bowel contents (paralytic, mechanical, or pseudo-obstructive ileus) can produce accumulation of luminal contents leading to bowel distension and an increase in IAP.

  • Pneumoperitoneum: this can arise from progression of a pathophysiological process, such as peptic ulcer disease or diverticulitis, that leads to a perforated viscus. It is also intentionally induced prior to laparoscopy, but ACS will only develop if the upper pressure limit is set inappropriately high.

  • Liver cirrhosis: patients with higher amounts of ascites at baseline are at higher risk of developing ACS if abdominal pressure is increased by another cause.

Secondary causes are due to tense ascites or oedema of an otherwise normal bowel.

  • Excess fluid resuscitation is the most common cause of ACS, usually with a significant crystalloid component.[9] In this context 'excess' is defined as more than 3 L of intravenous fluid resuscitation within a 24-hour period. This level of resuscitation is frequently required in patients with sepsis, severe trauma, bleeding, burns, or coagulopathies.[10][11]

  • Massive blood transfusion protocols (>10 units in 24 hours) are also common causes; these are usually given to patients with severe traumatic injury or post-traumatic coagulopathy.

In practice, many primary causes require fluid resuscitation and/or massive transfusion, which further increase gut oedema and the generation of peritoneal fluid. These patients therefore have mixed primary and secondary causes for increased IAP.

Pathophysiology

The abdominal compartment is bound inferiorly by the pelvic floor, circumferentially by the abdominal wall, and superiorly by the diaphragm. Although the diaphragm anatomically divides the chest and abdomen, it is not a rigid barrier and therefore allows pressures to be transmitted from the abdomen to the torso. In normal circumstances, the intra-abdominal pressure (IAP) is 5 to 7 mmHg. However, certain physiological states are associated with a higher IAP, without adverse consequences. This may be seen in pregnant patients and those with a BMI of 30 or above.[2][12] The abdominal compartment is non-expandable, and a rise in IAP therefore impairs blood flow to intra-compartmental tissues. The pathogenesis of ACS evolves in several stages:

  • An underlying process increases IAP, impairing arterial blood flow to intra-abdominal tissues.

  • A threshold pressure is reached at which venous resistance starts to increase, causing venous congestion and a further increase in intra-compartmental pressure. This is a self-propagating cycle.

  • When the IAP is greater than 20 mmHg, capillary perfusion falls, leading to tissue ischaemia. Ischaemia causes capillary leak, leading to increased extravascular fluid loss, a further increase in intra-abdominal volume, and further elevation of IAP. This cycle is also self-propagating.

  • Decreased capillary perfusion results in impaired function of organs within the abdominal compartment. Liver and renal function are impaired. Urine output falls, progressing from oliguria to anuria.

  • Expansion of abdominal volume displaces the diaphragm, decreasing pulmonary compliance and increasing the airway pressure required to maintain tidal volume.

  • Elevated IAP impairs venous return to the heart, decreasing cardiac output and impairing systemic perfusion.

  • Impaired cardiac output and increased intrathoracic pressure from elevated IAP can decrease cerebral venous outflow and decrease cerebral perfusion pressure.[13]

  • Inadequate tissue perfusion leads to multi-organ failure and death.

Classification

Classification according to cause

Primary

  • Due to decreased abdominal compliance (i.e., the elasticity of the abdominal wall and diaphragm), presence of an intra-abdominal or retro-peritoneal injury, or a pathological process.

Secondary

  • Due to tense ascites or oedema of otherwise normal bowel. This is the most common form.

Recurrent

  • Recurrence of abdominal compartment syndrome (ACS) after treatment for either primary or secondary ACS.

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