Does monitoring and intervention change outcomes?

While we still await level 1 evidence in terms of several multicenter randomized controlled trial outcome studies, there is a very large volume of outcome data that is fairly compelling. First, the data is very clear from large studies that there is a correlation between elevated intra-abdominal pressure and worse outcome in terms of organ failure, ICU length of stay and mortality. Malbrain et al in 2005 demonstrated this conclusively in a multicenter trial showing even "mild" elevations of IAP (>12 mmHg) lead to worse outcomes probably due to the prolonged organ ischemia that occurs. Sugrue et al in 1999 showed elevated IAP (over 18 mm Hg) was an independent predictor of renal failure, ranking up with hypotension, age and sepsis. Tao studied 23 pancreatitis patients with ACS. Of them 18 underwent rapid decompressive laparotomy and 5 did not. The mortalities were 16.7% versus 80% - a dramatic difference. Pupelis prospectively collected IAP and outcome data on pancreatitis patients and also found significant differences in outcomes. Those patients IAP less than 18 mm Hg had no mortality, 19% incidence of MODS/SIRS and mean ICU length of stay of 9 days whereas patients with IAP greater than 18 mm Hg had 36% mortality, 64% incidence of MODS/SIRS and mean ICU length of stay of 21 days. These authors conclude - "Routine measurement of the intra-abdominal pressure is rational in the clinical setting of the ICU and gives additional criteria for the evaluation of the clinical course and the effectiveness of the treatment." Biancofiore prospectively followed 108 liver transplant patients and noted that those who developed elevated intra-abdominal pressures had substantially higher incidences of death, renal failure and the need for permanent dialysis. The conclude – "The critical IAP values" with the best sensitivity specificity, were 23 mm Hg for postoperative ventilatory delayed weaning (P <.05), 24 mm Hg for renal dysfunction (P <.05), and 25 mm Hg for death (P <.01). "Many, many studies show similar correlations in patients with liver failure, trauma, pancreatitis, sepsis, ruptured aneurysms, etc."

So can we impact these outcomes through prevention or treatment (monitor, detect and intervene)?  The answer is yes and more and more studies to support this conclusion.  There are multiple case series and case reports showing situations where dieing patients had their outcomes reversed by interventions that reduced IAP once the abdominal compartment syndrome was recognized.  However, there are also numerous interventional studies on larger groups demonstrating you can improve outcomes in a group overall if you measure IAP and intervene aggressively. Ten years ago Ivatury showed that prophylactic interventions to reduce IAH/ACS in major trauma cases led to dramatic outcome improvement (ACS reduction from 52% to 22%, death reduction from 36% to 11%). Joseph et al noted that IAP monitoring and treatment with laparotomy was instrumental in improving outcome in their neurotrauma/stroke patients with elevated ICP - they now advocate aggressive IAP monitoring and interventions in all patients with ICP bolts. Oda demonstrated that aggressive IAP monitoring with early CRRT once IAP increased to more than 15 mm Hg (using a filter specifically designed for removal of cytokines) in cases of severe pancreatitis resulted in a huge reduction in their traditional mortality (>30% down to 6%). Sun et al, in a prospective randomized trial, were able to cut hospital length of stay in half and reduce pancreatitis mortality from 20% to 10% using IAP monitoring to guide interventional strategies.

Despite all this information, it needs to be very clear that treatment for IAH and ACS does not guarantee a good outcome. As demonstrated by both Oda and Sun, it is much better to detect this syndrome in the early stages (IAH) and intervene in an urgent medical fashion prior to the onset of overt organ failure (ACS). Patients who end up with ACS are extremely ill, often requiring emergent therapies including very invasive surgery and many die no matter what the clinician does to intervene. However, there is clear evidence that intervention for both IAH and for ACS definitely improves outcomes in some patients who would otherwise die.

Below is a brief summary of many of these articles:

Randomized Controlled trials:

Sun, World J Gastro 2006 - pancreatitis
These authors randomized their fulminant acute pancreatitis patients into two groups. Both groups received routing non-operative care including hemofiltration. The study group also had their IAP monitored and had a continuous indwelling paracentesis catheter placed to drain off excess cytokine rich peritoneal fluid (even if none was visible). Groups were compared for changes in APACHE II scores, length of hospitalization and survival to hospital discharge. The interventional group did much better in all parameters – APACHE II scores dropped significantly by day 2, hospital length of stay was half (15 days vs. 28 days) and mortality was half (10% vs. 20%).

Interventional before and after studies:
Ivatury, J Trauma 1998- Trauma surgery
70 damage control laparotomy patients comparing open vs. closed abdomen treatment. First 25 had facial closure – 52% developed abdominal compartment syndrome and 39% died. Last 45 cases were treated with open abdomen, 22% developed abdominal compartment syndrome and 10.9% died.

Oda, Ther Apher 2005 - Pancreatitis
Traditional mortality for severe acute pancreatitis in this ICU was over 25%. These authors sought to reduce this mortality by early aggressive continuous hemofiltration in patients who developed IAP of 15 mmHg or higher. They prospectively entered 17 patients and were able to dialyze off interleukin 6 (an inflammatory cytokine) as well as excess extravascular water, resulting in a drop in intra-abdominal pressure in all patients to less than 10 mm Hg and a 94% survival rate.

Rasmussen, J Vasc Surg 2002 – Aortic Aneurysm surgery
Study comparing treatment of ruptured aortic aneurysm with open abdomen vs. closure and re-opening if IAH developed. 35 patients were initially treated with open abdomen after ruptured AAA repair – mortality 51%, multiple organ failure 11%. 10 patients were closed primarily and developed ACS requiring decompressive surgery – mortality 70%, multiple organ failure 70%.

Tao, J Huazhong Univ Sci Technolog Med Sci 2003 - Pancreatitis 23 cases of severe acute pancreatitis who developed abdominal compartment syndrome. 18 were treated with aggressive intervention and early decompressive surgery – 16.7% mortality. 5 were observed, no ACS intervention – 80% mortality.

Observational outcome studies

Malbrain, Crit Care Med, 2005 – Mixed ICU population outcome
Prospective, multi-center trial looking at incidence and outcome of patients with sub-acute intra-abdominal hypertension of only 12 mm Hg or more (a level that reduces essential organ perfusion but does not cause the abdominal compartment syndrome). 265 patients were entered. In patients with an IAP < 12 mm Hg the mortality was 22.2%, (lower APACHE quartiles mortality <3%). In cases with IAP > 12 mm Hg the mortality was 38.8% (lower APACHE quartiles mortality 15-30%).

Pupelis: Acta Chir Belg 2002 - Pancreatitis
37 cases of severe acute pancreatitis observed for outcome. 26 cases maintained IAP less than 18 mm Hg – no mortality, 19% MODS, 9 day ICU LOS 11 cases with IAP over 18 mm Hg – 36% mortality, 64% MODS, 21 day ICU LOS

Biancofiore, Transplant Proc 2004 – Liver transplant
108 liver transplant cases observed for outcome. 32% developed IAP > 18 mm Hg, 1/3 developed acute renal failure, 9% required permanent dialysis, mortality higher. 68% never developed IAH, 8% had acute renal failure, none required permanent dialysis

Raeburn, Am J Surg 2001 – Trauma surgery
77 patients with damage control surgery. 36% developed IAP over 20 mm Hg – these patients had longer LOS, longer ventilator times, higher incidence of MOF, higher mortality

Joseph, J Trauma 2004 – Neurotrauma with elevated ICP
17 patients with intractable ICP (mean 30 mm Hg) despite maximal intervention including removal of upper skull in 14. Mean IAP was 27 mm Hg. All had decompressive laparotomy to treat their ICP. 100% had ICP reduction to a mean of 17 mm HG. 11 of 17 had persistently lower ICP and all lived with "good neurologic outcomes." Authors now "routinely measure intra-abdominal pressure every 2-4 hours" and conclude that decompression should occur before obvious symptoms of abdominal compartment syndrome.

Ejike, Critical Care Medicine 2005 – General Pediatric ICU
17.6% of mechanically ventilated pediatric patients had abdominal compartment syndrome (defined as IAP > 12 mm Hg plus 2 organ failures). In this group the median IAP was 18 mm Hg, the mean ICU length of stay was 13 days and the mortality was 33.3%. The remaining children did not have ACS, their mean length of stay was 6 days and their mortality was 2.4%.

Cipolla, Am Surg 2005
20 patients with complicated abdominal surgery managed with an open abdomen and an algorithm for treatment based on intra-abdominal pressures. Predicted mortality was 73% based on simplified acute physiology scores. Actual mortality was 5.9%.

Reintam, Intensive Care Medicine 2005 – General ICU outcome
113 patients were monitored for IAP over 12 mm Hg. In those with IAP > 12 mm Hg the mortality was 50%, whereas those with normal IAP had mortality of 18%. Odds ratio of death with IAP over 12 mm Hg was 9.2 in medical ICU patients, and 1.4 in surgical patients.