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Frequently Asked Questions >>
IAH and ACS: Effects on patient outcome
There a numerous articles and case studies that note patients who are dying or extremely ill have had dramatic recoveries when they undergo abdominal decompression and their ACS resolves. A good example of a case series is the article by DeCou."[1] This article discusses 3 pediatric cases suffering from various disease processes who were near death until they had abdominal decompression and all three are now "alive and well."
There are other larger studies that show a clear correlation between death and organ failure in cases that are not treated for ACS versus those that are treated. One article by Ivatury looked at outcomes in patients who suffered severe abdominal trauma requiring damage control surgery. Patients early on in the data bank had their abdominal fascia closed, while those later were taken to the ICU with an open abdomen.[2] In those with facial closure, 52% developed ACS with pressures over 25 mm Hg and 36% overall died (and the number with multiple organ failure was 3 times greater than in the open abdomen group). In the open abdomen group, 22% developed ACS and 11% died -- a far lower mortality and far lower organ failure rate.
A more recent study was conducted on medical patients suffering severe pancreatitis.[3] In this study 23 patients were identified with ACS. Of them 18 underwent 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 with IAP less than 25 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 25 mm Hg had 36% mortality, 64% incidence of MODS/SIRS and mean ICU length of stay of 21 days.[4] 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.[5] They 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).
Sugrue proved conclusively that renal failure rate is directly correlated with increasing IAP.[6] (See IAH and Renal for in depth discussion)
Cipolla noted that by leaving abdomens open in high risk trauma patients, he was able to reduce predicted mortality from 73% to 5.9%.[7] He felt this was directly related to a decrease in incidence of ACS and reduced multisystem organ failure.
Malbrain and colleagues recently published a large, prospective study that investigated the incidence of intra-abdominal hypertension (IAH) and its impact on patient outcome in a mixed population of ICU patients.[8] 265 patients from 14 ICUs in 6 countries were included over a 1-month period and had intra-abdominal pressure measured on admission and recurrently during the first 7 days of their ICU stay.
They found that:
- The incidence of IAH > 12 mm Hg was 32.1%
- The development of IAH > 12 mm Hg during ICU stay was an independent predictor of mortality (relative risk 1.85; 95% CI 1.12-3.06; p=.01).
- Patients with IAH had a 38.8% mortality
- Patients without IAH had a 22.2% mortality
- IAH > 12 mm Hg remained a predictor of mortality even after patient stratification into APACHE II score quartiles. In fact, those patients with lower APACHE II scores who had IAH had dramatically higher mortality than those without IAH (see figure).
- There was no difference regarding the diagnostic category for intensive care admission (medical or surgical) and the presence of IAH. It was just as common in medical ICUs as in surgical ICUs.
- Independent predictors of IAH > 12 mm Hg were:
Fluid resuscitation with > 3.5 liters of colloid or crystalloid within the first 24 hours.
- Ileus
- Abdominal surgery
- Liver dysfunction (liver cirrhosis or failure with ascites)
These results provide some very insightful information regarding IAH that has not been well discussed in previous literature. In the past, most articles focused on the abdominal compartment syndrome (very high IAH plus organ failure) as the clinical syndrome that causes death. This article, however, focused not on ACS but on the development of IAH at a fairly low level (IAP > 12 mm Hg). They found that consistent sub-ACS level intra-abdominal hypertension was a predictor of mortality. These results show that full-blown ACS is not necessary to cause death, only persistently elevated intra-abdominal hypertension. This finding is graphically demonstrated in the figure, which shows that in patients with relatively low APACHE II scores (Quartiles I and II) those without IAH had almost no mortality while those with IAH had mortality approaching 30%.
The authors of this study conclude:
"The presence of IAH should be considered as an organ dysfunction for which specific diagnostic and therapeutic (medical or surgical) interventions are needed."
"Due to the possible impairment of every organ system and the high prevalence and incidence of IAH either in generally critically ill patients or in surgical patients, we suggest that clinicians measure the IAP in all patients in the first days after intensive care admission."
In an accompanying editorial, Drs. Balogh and Moore add similar conclusions[9]:
"We strongly advocate that all high-risk patients should be monitored for IAH. This effort would include all shock resuscitation patients regardless of the type of shock and any patients who had intestinal or whole body ischemia-reperfusion, major abdominal surgery, major trauma and burns, and major (especially abdominal) infection."
"Once IAH is recognized, intermittent IAP measurements (every 4-6 hours) are not sufficient since ACS develops in high-risk patients within that time frame, and once the abdominal compartment is in the steep portion of its pressure-volume curve, IAPs can increase suddenly and can be easily missed."
To date no one has randomized patients with ACS to be treated versus not treated. This may never occur due to the overwhelming evidence of high mortality for untreated ACS and the ethical problem associated with randomization of patients into a group that does not get treated.
Despite all this information, it needs to be very clear that treatment for ACS does not guarantee a good outcome. Patients who end up in and ICU are CRITICAL and many die no matter what the clinician does to intervene. However, there is clear evidence that intervention for ACS definitely improves outcomes in some patients who would otherwise die.
Figure: This figure demonstrates that as APACHE score increase, so does mortality regardless of whether the patient has IAH or no IAH. However, patients with low APACHE scores -- in the lower 2 quartiles - are predicted to survive (as they do in those without IAH -- white boxes) yet those with elevated intra-abdominal pressure over 12 mm Hg have a substantial mortality.[8]
References
- DeCou, J.M., et al., Abdominal compartment syndrome in children: experience with three cases. J Pediatr Surg, 2000. 35(6): p. 840-2.
- Ivatury, R.R., et al., Intra-abdominal hypertension after life-threatening penetrating abdominal trauma: prophylaxis, incidence, and clinical relevance to gastric mucosal pH and abdominal compartment syndrome. J Trauma, 1998. 44(6): p. 1016-21; discussion 1021-3.
- Tao, J., et al., Diagnosis and management of severe acute pancreatitis complicated with abdominal compartment syndrome. J Huazhong Univ Sci Technolog Med Sci, 2003. 23(4): p. 399-402.
- Pupelis, G., et al., Clinical significance of increased intraabdominal pressure in severe acute pancreatitis. Acta Chir Belg, 2002. 102(2): p. 71-4.
- Biancofiore, G., et al., Intraabdominal pressure in liver transplant recipients: incidence and clinical significance. Transplant Proc, 2004. 36(3): p. 547-9.
- Sugrue, M., et al., Intra-abdominal hypertension is an independent cause of postoperative renal impairment. Arch Surg, 1999. 134(10): p. 1082-5.
- Cipolla, J., et al., A proposed algorithm for managing the open abdomen. Am Surg, 2005. 71(3): p. 202-7.
- Malbrain, M.L., et al., Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study. Crit Care Med, 2005. 33(2): p. 315-22.
- Balogh, Z. and F.A. Moore, Intra-abdominal hypertension: Not just a surgical critical care curiosity. Crit Care Med, 2005. 33(2): p. 447-9.
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