An elderly man was admitted after a Hartman’s procedure with primary closure for a perforated sigmoid diverticulum with four quadrant peritonitis. Postoperatively, he remained ventilated and noradrenaline dependent. His intra-abdominal pressures gradually rose from 15 to 24mmHg. Urine output was poor, and he required peak pressures of 28cmH2O to achieve 6ml/kg tidal volumes. Vasopressor requirements gradually increased and a diagnosis of abdominal compartment syndrome was made. Medical management was attempted with fluid resuscitation, increased sedation, aspiration of nasogastric tube and neuromuscular blockade. However this did not improve the intra-abdominal pressures so the patient returned to theatre laparostomy and VAC dressing. On return from theatre, intra-abdominal pressures stabilised between 12 and 15mmHg. Noradrenaline requirements fell and urine output improved. The abdomen was closed on day 5 and he was discharged from ICU on day 10.
What non-surgical strategies can be used to reduce intra-abdominal pressure?
Intra-abdominal pressure ( AP) is the steady state pressure within the abdominal cavity and is normally 5-7mmHg in the critically ill patient measured via the bladder in a supine position at end-expiration with the transducer at midaxillary line. Intra-abdominal hypertension ( AH) is a sustained or repeated AP >12mmHg and is graded – V. Abdominal compartment syndrome (ACS) is sustained APs>20mmHg with associated new organ dysfunction/failure as defined by the World Society of Abdominal Compartment Syndrome (1). Primary AH/ACS is associated with injury and disease in the abdomino-pelvic region and secondary AH/ACS refers to causal conditions that are extra-abdominal. There are a wide range of disease
processes that can cause ACS, which includes major burns, major trauma, massive fluid resuscitation and sepsis and shock of any origin. It is more common in medical than surgical intensive care patients. Risk factors are also numerous; acidosis, coagulopathy, hypotension, obesity, PEEP>10 and mechanical ventilation are a few which demonstrate that most intensive care patients have numerous risk factors for developing ACS.
It has been increasingly recognised that a proportion of ACS is iatrogenic from over-resuscitation, sub-optimal control of haemorrhage and primary closure in abdominal trauma to assist with tamponade of solid organs. The incidence of ACS is decreasing with the move to early damage control surgery and primary open abdomens in trauma coupled with more focused and careful fluid resuscitation(2). Mortality from ACS can be as high as 60%.
Gonzalez and Moore have found in their institution that, since the early 2000’s with the introduction of massive transfusion protocols with emphasis on fresh frozen plasma, hypotensive resuscitation and rapid haemorrhage control, they have had a 50% reduction in mortality in their trauma patients and that abdominal compartment syndrome has virtually disappeared(3).
The pathophysiological effects of raised intra-abdominal pressure are widespread and include raised intra-cranial pressure, decreased venous return and therefore cardiac output, increased systemic vascular resistance, decreased mesenteric and hepatic blood flow, liver dysfunction, oedema, bacterial translocation, decreased renal blood flow and increased renal tubular pressure, increased ventilatory pressures and decreased respiratory compliance(4).
Medical management involves therapies in 5 areas: Evacuation of intraluminal contents, Evacuation of intra-abdominal space occupying lesions, improving abdominal wall compliance, Optimizing of fluids and Optimizing perfusion. Intra-luminal contents can be evacuated by nasogastric or rectal tubes (Grade 1D), the use of pro-kinetics (2D) and enemas (1D) and by reducing enteral feeding to trophic levels. Intra-abdominal lesions can be drained percutaneously. Abdominal wall compliance can be improved by adequate analgesia and sedation (Grade 2D), neuromuscular blockade (2D) and consideration of the reverse Trendelenberg position. Fluids are optimised by avoidance of excessive fluid resuscitation (2C), aiming for a negative fluid balance by day 3 (2C), fluid removal by diuresis, hypertonic or colloid fluid resuscitation and haemodialysis. Perfusion is optimised using goal-directed fluid resuscitation using haemodynamic monitoring (1,5). It is noted that the evidence to support the above treatments is poor or very poor using the GRADE system for evidence. The World Society of ACS guidelines could only recommend surgical interventions; medical therapies were either suggestions or had no recommendation e.g. diuretics or renal replacement therapies to mobilize fluid.
There are no randomised controlled trials assessing the effectiveness of most of the medical interventions suggested for the management of abdominal compartment syndrome.
As small amounts of abdominal wall tension may have drastic effects on AP, neuromuscular blockade can decrease AP for a sufficient time to allow other non-operative measures e.g. the removal of excess fluid by diuretics or haemofiltration to be effective and thus avoid an operation(6). It is important that fluid removal does not result in reduced oxygen delivery.
Surgical abdominal decompression should be considered for ACS refractory to medical management and is considered the gold standard of therapy. There is little evidence to support the use of prophylactic ‘open abdomens’ in any patients other than trauma damage control laparotomies (1). Surgical decompression may lead to reperfusion injury and decreases in systemic vascular resistance and thoracic pressures which clinicians need to be wary of (4). A number of these patients can be a challenge to manage following their laparostomy in terms of bowel coverage, prevention and management of fistulas and the management of large ventral hernias, therefore the timing of closure is as important as the timing to surgically treat ACS (7).
A high index of suspicion is required to diagnosing intra-abdominal hypertension, as it is difficult to diagnose clinically and requires the measurement of pressures that is not everyday practice in most intensive care departments. However, An et al would advocate the routine measurement of intra-abdominal pressures in high-risk patients in the intensive care unit (7).
Prevention of abdominal compartment syndrome appears to be the key to management. Apart from the obvious morbidity attached to open laparostomies, medical treatment options such as neuromuscular blockade and avoiding 30 degrees head-up also have potential undesirable consequences such as critical illness neuromyopathies and ventilator- associated pneumonia. Avoidance of excessive fluid resuscitation is paramount, however it is also essential to adequately perfuse organs and achieving that balance can be practically difficult to achieve, particularly as some of the end-points used in fluid resuscitation such as central venous pressure and urine output are independently influenced by intra-abdominal pressure (2). Stroke volume variation may have a role (3).
1) Kirkpatrick AW, Roberts DJ, De Waele J et al. Intra-abdominal hypertension and the abdominal compartment syndrome updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Medicine 2013; 39(7): 1190-206
2) Dries DJ. Abdominal Compartment Syndrome: Towards Less- Invasive Management. Chest 2011; 140(6): 1396-8
3) Gonzalez EA, Moore FA. Resuscitation beyond abdominal compartment syndrome. Current Opinion in Critical Care 2010; 16: 570-4
4) Berry N, Fletcher S. Abdominal Compartment Syndrome. Continuing Education in Anaesthesia, Critical Care and Pain 2012; 3: 110-7
5) Cheatham ML. Nonoperative management of Intraabdominal Hypertension and Abdominal Compartment Syndrome. World Journal of Surgery 2009; 33: 1116-22
6) An G, West MA. Abdominal compartment syndrome: A concise clinical review. Critical Care Medicine 2008; 36(4): 1304-10
7) Cresswell AB. Recognition and management of intra-abdominal hypertension and abdominal compartment syndrome. Emergency surgery 2013; 31(11): 582-7