School of Human Life Sciences, University of Tasmania, Tasmania, AustraliaAustralia
Department of Surgery, Launceston General Hospital Launceston, Tasmania, AustraliaAustralia
University Department of Surgery, European Institute of Oncology, Milan, ItalyItaly
Launceston General Hospital, Intensive Care Unit Launceston, Tasmania, AustraliaAustralia
Department of Surgery, European Institute of Oncology, Milan, ItalyItaly
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Abdominal Compartment Syndrome (ACS) is a potentially lethal condition caused by various events that produce intra-abdominal hypertension. The most common cause is blunt abdominal trauma. Increasing intra-abdominal pressure causes progressive hypoperfusion and ischemia of the intestines and other peritoneal and retroperitoneal structures. Pathophysiological effects include release of cytokines, production of oxygen free radicals, and decreased cellular formation of adenosine triphosphate. These processes may lead to translocation of bacteria from the gut and intestinal edema, predisposing patients to multiorgan dysfunction syndrome. The consequences of abdominal compartment syndrome are profound and affect many vital body systems. Respiratory, hemodynamic, cardiovascular, renal, and neurological abnormalities are signs of abdominal compartment syndrome. Medical management of critically ill patients with raised intra-abdominal pressure should be instigated early to prevent further organ dysfunction and to avoid progression to ACS. Many treatment options are available and are often part of routine daily management in the ICU (nasogastric, rectal tube, prokinetics, enema, sedation, body position). Some of the newer treatments are very promising options in specific patient populations with raised IAP. Nursing care involves vigilant monitoring for early detection, including serial measurements of intra-abdominal pressure.
Keywords: Intra-abdominal hypertension; Abdominal compartment syndrome; Damage control laparotomy; Laparostomy; Open abdomen; Damage con- trol laparotomy
The relatively recent recognition of the IAS/ACS complex has resulted in a profusion of animal and human work on its pathophysiology. Many of the features of the syndrome are still unknown and require a connection with the possibility of the diagnosis, with a routine IAP measurement, (most likely in high-risk cases by continuous technology) and a more liberal policy towards surgical decompression. This view would allow a less prolonged ventilatory, cardiac and renal support and is based on an improved management of the open abdomen and its consequences. Measurement techniques of the IAP and consensus concerning what levels are abnormal are needed, as well as prospective ICU-framed studies, to better assess circulatory filling status utilizing volumetric-modified pulmonary artery catheters and which more accurately define end-organ perfusion and dysfunction. This will be supported by better ‘pathological’ animal models which more directly address the capillary leakage syndrome as part of ACS, which separate the effects of decompression and volume restoration and which distinguish organ from global resuscitation.
We declare that I have no conflict of interest in connection with this paper.
All the authors have no potential or actual personal, political or financial interest in the material, information or techniques described in the paper.