ABSTRACT

Introduction Within any human body compartment a rise in pressure above physiological limits is detrimental. At pressures which still permit axial vessel flow, capillary perfusion may cease to exist resulting in cell death. The physiological sequelae and develop­ ment of signs and symptoms is dependent upon a number of factors, namely perfusion pres­ sure, rate and magnitude of intracompartmental pressure rise, compliance of the compart­ ment, and the reason for the change in compartmental pressure. A rapid exponential rise in intracranial pressure within the rigid skull in a hypotensive patient is rapidly fatal if urgent intervention is delayed, whereas chronic hydrocephalus in a child may have litde, if any, effect on vital organ function. The same principles pertain to the abdomen. During laparoscopy with muscle relaxation LAP may rise acutely to 20 mm Hg or more without any overt interference in organ function.4 Conversely, in a swine model Simon et al showed that if LAP was elevated to 20 mm Hg following a period of haemorrhagic shock and resuscitation, there was a marked decrease in pulmonary function.5 Control animals with similar elevations in LAP but without prior haemorrhage had minimal changes in Pa02/Fi02 ratio. In humans, ACS as a result of rapid accumulation of intra-abdominal fluid has been documented following massive crystal­ loid resuscitation in the absence of intra-abdominal injury,6'9 whereas chronic ascites of up to 15 litres is well tolerated.10 From the above there appear to be certain preconditions for the development of a pathological rise in LAP. The change must be acute and there must be a prior insult which need not necessarily be intra-abdominal.