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.