Prevention: Careful fluid management

The best treatment for ACS is prevention. The key to prevention is to recognize patients who are at risk (SIRS, sepsis, ischemia/reperfusion injury followed by large volume resuscitation, major intra-abdominal problem such as trauma, surgery or obstruction), monitor them carefully and intervene prior to end stage complications. Many articles support this approach.[1-6]

The first step is careful fluid management. Under-resuscitation will lead to organ ischemia, increased capillary leak, tissue edema and further elevation of IAP. If the patient is under resuscitated, fluid loading to increase blood flow to the gut and inotropic support to increase cardiac output should begin.[7] Ironically these same methods intended to improve intestinal perfusion may in fact exacerbate ACS through increasing the rate of extravasation of fluid into the abdominal viscera. Therefor over-resuscitation, must be carefully avoided.[8] This fine balance between under and over resuscitation makes assessment of fluid status a critical part of management of patients at risk for ACS and it is complicated by misleading information obtained from fluid status evaluations based on pressure measurements (CVP and PAOP – wedge: See cardiovascular physiology).

Intra-abdominal hypertension -- Treatment options

Given the past focus on the end stage process - the abdominal compartment syndrome - most treatment discussions have emphasized emergent surgical decompression. Based on other commonly treated full blown compartment syndromes – intracranial (epidural or subdural hematoma), thoracic (tension pneumothorax), pericardial (cardiac tamponade), and extremity – all true compartment syndromes are surgical diseases requiring emergent surgical interventions as soon as possible to prevent permanent tissue damage or death. True abdominal compartment syndrome is no different. Failure to provide emergent surgical decompression leads to prolonged severe mesenteric ischemia as well as multiple organ hypoperfusion with its attendant high morbidity and mortality.

On the other hand, intra-abdominal hypertension detected early is amenable to non-surgical interventions. By implementing these options early, abdominal compartment syndrome can be prevented in many patients. To accomplish this, intra-abdominal hypertension must be detected before clinical signs of the abdominal compartment syndrome develop. Newer evidence suggests that intra-abdominal pressure measurements done every one to two hours are necessary to establish a trend and avoid missing a rapid increase in pressure.[9, 10] ICU’s should implement effective, reproducible methods for accomplishing this task. Several companies now manufacture devices that allow noninvasive, rapid and reliable IAP monitoring to occur with little nursing effort. All these devices use either bladder pressure or intra-gastric pressure as surrogates for intra-abdominal pressure. These commercially available systems are the AbViser (www.wolfetory.com), the Foley Manometer (www.holtech-medical.com), the IAP-Monitor (www.spiegelberg.de), and the CiMON (www.pulsion.com).

Once IAP pressures are obtained and a trend is established, treatment options will depend on patient characteristics as well and pressure levels (See treatment algorithm). The first intervention necessary for intra-abdominal hypertension is to ensure optimal fluid resuscitation.[11] Over resuscitation may cause increased edema, while under resuscitation causes prolonged ischemia which worsens capillary leak problems. The complex interactions of intra-abdominal, intrathoracic and intravascular pressures make accurate volume assessment using CVP and PAOP somewhat difficult. End-diastolic volumetric indices and/or echocardiographic indices will improve clinician’s ability to interpret vascular filling. If these are not available, IAP values can be used to correct standard CVP and PAOP measurements to obtain a more accurate reflection of volume status (see correction formula in IAH and hemodynamic monitoring errors section).

Following appropriate volume resuscitation, abdominal blood flow show be optimized.[12] This is reflected in the concept of abdominal perfusion pressure (APP). The concept is essentially identical to that related to cerebral perfusion pressure. Tissue blood flow is directly related to the mean arterial pressure delivered to the tissue (MAP) minus the pressure within the abdominal compartment (IAP): APP = MAP-IAP. Abdominal perfusion pressure, which more accurately reflects actual tissue oxygen delivery may be more predicative of patient outcome that the IAP measurement alone.[12, 13] Once patients are adequately fluid resuscitated, inotropic support to improve tissue blood delivery should be considered if abdominal perfusion pressure is less than 60 mm Hg.[12]

Non-surgical options: Sedation and pain control, gut emptying, paracentesis, neuromuscular blockade, continuous renal replacement therapy, continuous negative abdominal pressure.

If intra-abdominal pressure continues to rise despite optimization of fluid status and abdominal perfusion pressure, numerous other interventions are available. These include sedation and pain control, gut emptying, paracentesis, neuromuscular blockade, continuous renal replacement therapy, and continuous negative abdominal pressure. Sedation and pain control assist in reduction of IAP in any patient suffering from significant pain or agitation. Most patients suffering a severe enough illness to develop IAH should be sedated and pain should be carefully controlled. All patients with rising IAP should also have nasogastric suction considered to remove all excess air and fluid from the intestinal lumen. Simultaneously, stool and other intraintestinal contents should be purged to create a larger volume for expansion of bowel edema. This can be done with cathartics, enemas and rectal tubes. Neuromuscular blockade may further relax the abdominal wall and improve organ perfusion in those situations where sedation is inadequate.[14-17] It works by giving total relaxation to the abdominal and thoracic wall musculature and may buy time for the patient to begin mobilizing fluid. In many situations, dramatic reductions in IAP with substantial increases in urine output and reduction in total body edema are witnessed.[18] However, if capillary leak continues this treatment effect may only have transient effects. Another similar option for reducing IAP is via epidural analgesia. Hakobian and colleagues performed a small study on 11 critically ill postoperative patients where epidural analgesia was began when IAP exceeded 15 mm Hg.(personal communication) They found a reduction in IAP from 15.7 mm Hg to 5.9 mm Hg one hour after institution of epidural analgesia. There was no associated drop in MAP that is often seen with epidural analgesia. They hypothesized that the absence of hypotension and further hemodynamic compromise was due to a decrease of IAP which in turn compensated for decreased preload secondary to medication induced sympathectomy.

Patients with substantial ascites or a large retroperitoneal fluid collection are often amenable to percutaneous drainage of that fluid with substantial reduction in IAP.[19-21] In fact, recent research suggests even in the absence of visible ascites, IAP can be reduced in high risk patients with percutaneous catheter placement. In one small study n 8 patients, Reed et al were able to reduce IAP by 6 mm and increased abdominal perfusion pressure by 16 mm Hg and MAP by 10 mm Hg within 30 minutes of catheter placement in patients whose IAP crossed the 20 mm Hg threshold.[21] Six of these patients did not require decompressive laparotomy, avoiding the need to manage and open abdomen. Survival was 75% (3 of 4) in whom intervention was done early. Paracentesis and drainage of any free fluid visible on ultrasound can be very effective in the burn population as well as liver failure patients and some pediatric cases.[17, 19, 20] It results in an immediate reduction in abdominal contents with a corresponding drop in intra-abdominal pressure as well as an improvement in physiologic parameters such as urine output. Paracentesis often needs to be repeated to maintain a low pressure – making IAP monitoring all that much more important to assist in predicting when the procedure needs to be repeated.

Unfortunately, most patients with intra-abdominal hypertension do not have fluid collections available for drainage. Rather they have substantial interstitial edema present. This edema can be reduced or avoided via two mechanisms in appropriate candidates– colloid infusions and continuous hemofiltration. O’Mara et al found that colloid resuscitation of patients at very high risk of intra-abdominal hypertension (major burn patients) resulted in dramatic reductions in IAP and a trend towards improved outcomes.[22] Oda et al, after substantial investigation into the effects of cytokines on intra-abdominal hypertension, determined that continuous hemofiltration was able to reduce cytokine blood levels as well as intersitial fluid. They predicted that this in combination with colloid infusion to maintain adequate intravascular volume could reduce progression of intra-abdominal hypertension to abdominal compartment syndrome and improve outcome in severe pancreatitis. In a prospective study, they began continuous hemofiltration on all severe pancreatitis patients with IAP of 15 mm Hg or higher.[6] Using this protocol on 17 patients, they successfully reduced cytokine levels and IAP levels (from 15 mm Hg to less than 10) in all their severe acute pancreatitis cases – reducing their historical mortality from 40% down to 6%. Other recently presented abstracts confirm the survival benefits seen with hemofiltration in both pancreatitis cases as well as in patients suffering from severe sepsis.[23-25] Hernandez, et al, who demonstrated a 51% incidence of IAH/ACS in septic shock patients[26] also found that implementation of hemofiltration in hemodynamically unstable sepsis patients failing all other therapy resulted in a dramatic reduction in mortality in those that responded (mortality 21% in rsponders versus 83% in non-responders).[24] Picinni et al, also found a survival advantage to early hemofiltration in septic shock patients, demonstrating a survival improvement and reduced ICU length of stay in those who underwent hemofiltration compared to those who did not (55% survival versus 27.5% survival, LOS 9 days versus 16 days).[25] Clearly, medical interventions for intra-abdominal hypertension exist and early research into their efficacy appears very promising. Larger prospective studies will hopefully be conducted to improve our understanding of these interventions.

Continuous negative abdominal pressure devices have been tested on small groups of patients and are effective at reducing intra-abdominal pressure.[27, 28] However, in their current designs they are not practical for everyday ICU application and further research is needed to ensure they do not cause injury to the abdominal wall and to determine whether they improve physiologic parameters.

Surgical options: Decompressive laparotomy

When all else fails and patients progress from intra-abdominal hypertension to the abdominal compartment syndrome, the patient has progressed from an urgent medical process to a surgical emergency.[29] These patients are suffering from end stage tissue ischemia that has progressed to severe cellular dysfunction with impending cell death. The most appropriate treatment is emergent surgical decompression.[29] Waiting just a few hours will lead to higher incidence of dead bowel and higher mortality. The exact pressure at which abdominal decompression should occur is dependent on a number of host factors including age, underlying co-morbidities and physiologic evidence of developing ACS. With the exception of very high intra-abdominal pressures there are no established guidelines where a definite intervention is necessary. Many experts recommend that the entire clinical picture must be taken into account and one specific pressure cutoff cannot be used.[5, 30] However, since several experts note improved outcomes with decompression at lower pressures, if there is any question it is probably best to err on the side of early decompression.[3, 5, 31]

In the case of trauma laparotomies -- especially after damage control surgery where the patient has had substantial fluid resuscitation, the surgeon should probably just leave the abdomen open. While this results in a reduced risk of ACS, it is not a guarantee. Gracias et al found 25% of surgical patients with their abdomens left open after trauma laparotomies still developed ACS within a relatively short time period.[32] They point out that this complication occurs because no abdomen is truly “open” since all have some type of a dressing. Those patients who developed ACS despite an “open abdomen” did poorly: 60% mortality with ACS versus 7% mortality if ACS did not occur. The authors use this data to emphasize the importance of continued intra-abdominal pressure monitoring in all at risk patients, including “open abdomens” because fluid can re-accumulate in the space beneath the dressing and ACS can develop.

1. Ertel, W., et al., Incidence and clinical pattern of the abdominal compartment syndrome after "damage-control" laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med, 2000. 28(6): p. 1747-53.
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4. Saggi, B.H., et al., Abdominal compartment syndrome. J Trauma, 1998. 45(3): p. 597-609.
5. Ivatury, R.R., H.J. Sugerman, and A.B. Peitzman, Abdominal compartment syndrome: Recognition and management, in Advances in Surgery, J.L. Cameron, Editor. 2001, Mosby. p. 1-19.
6. Oda, S., et al., Management of intra-abdominal hypertension in patients with severe acute pancreatitis with continuous hemodiafiltration using a polymethyl methacrylate membrane hemofilter. Ther Apher Dial, 2005. 9(4): p. 355-61.
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10. Joseph, D.K., et al., Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma, 2004. 57(4): p. 687-95.
11. Malbrain, M.L.N.G. and M.L. Cheatham, Cardiovascular effects and optimal preload markers in intraabdominal hypertension, in Yearbook of Intensive Care and Emergency Medicine, J.L. Vincent, Editor. 2004, Springer-Verlag: Berlin. p. 519-543.
12. Cheatham, M.L., et al., Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma, 2000. 49(4): p. 621-6; discussion 626-7.
13. Malbrain, M.L.N.G., et al., Effect of abdominal perfusion pressure on outcome in mechanically ventilated patients. Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S5 - Abstract 003.
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15. De Waele, J.J., et al., A role for muscle relaxation in patients with abdominal compartment syndrome? Intensive Care Med, 2003. 29(2): p. 332.
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19. Sharpe, R.P., et al., Abdominal compartment syndrome in the pediatric blunt trauma patient treated with paracentesis: report of two cases. J Trauma, 2002. 53(2): p. 380-2.
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21. Reed, S.F., et al., Aggressive surveilance and early catheter directed therapy in the prevention of abdominal compartment syndrome. J Trauma, 2005. 59(2): p. 522, Abstract.
22. O'Mara, M.S., et al., A prospective, randomized evaluation of intra-abdominal pressures with crystalloid and colloid resuscitation in burn patients. J Trauma, 2005. 58(5): p. 1011-8.
23. Maslovsky, O.P. and V.V. Zagorujko, Acute pancreatitis with multiple organ dysfunction syndrome - is high volume hemofiltration helpful? Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S185, Abstract 710.
24. Hernandez, G., et al., High volume hemofiltration in the management of severe hyperdynamic septic shock. Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S185, Abstract 711.
25. Piccinni, et al., Early isovolaemic haemofiltration in oliguric patients with septic shock. Intensive Care Med, 2006. 32(1): p. 80-6.
26. Hernandez, G., et al., Intra-abdominal hypertension in septic shock patients. Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S91, Abstract 339.
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31. Sugrue, M., et al., Temporary abdominal closure: a prospective evaluation of its effects on renal and respiratory physiology. J Trauma, 1998. 45(5): p. 914-21.
32. Gracias, V.H., et al., Abdominal compartment syndrome in the open abdomen. Arch Surg, 2002. 137(11): p. 1298-300.