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IAH and ACS: Management

Introduction:

Intra-abdominal hypertension and the abdominal compartment syndrome cause significant morbidity and mortality, and are present a large variety of patients – both medical and surgical.[1-4] In fact, medical patients – specifically those suffering from severe sepsis, have the highest incidence of IAH reported in the literature.[1, 5-7]  Despite the high prevalence of disease in medical patients and extensive literature to the contrary, many physicians and nurses continue to believe that the only treatment for IAH/ACS is surgical decompression – an option they choose not to pursue, therefor ignoring the syndrome all together. In fact, non-operative medical management is the cornerstone to therapy for this syndrome, playing a vital role in both the prevention and the treatment of IAP-induced organ dysfunction.[1, 8] Numerous studies now show that medical management not only improves survival, it prevents progression to full-blown ACS, reduces ICU and hospital length of stay, and results in reduced resource utilization.[9-13] Careful frequent IAP monitoring combined with implementation of medical management for elevated IAP should be implemented in all high-risk patients.

ACS management:

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.

IAH Management:

Properly managing the critically ill patient with IAH requires careful assessment of cardiovascular status with and understanding of the errors that IAP can introduce to hemodynamic data. It requires insight into ventilator management to overcome the reduced chest wall compliance and smaller intrathoracic volumes caused by higher IAP. Careful fluid and vasopressor management are also key since to little fluid will increase intestinal ischemia and cytokine production, while too much will exacerbate the cytokine induced capillary permeability syndrome that occurs in these patients.  To assist clinicians with the complexities of these patients and provide some recommendations for management, the World Society of Abdominal Compartment Syndrome (WSACS) has created both and assessment algorithm and a medical management algorithm that can be downloaded from their web site (http://www.wsacs.org/algorithms.php).  The remainder of this discussion will focus on this management strategy.  

Medical Management:

Download the treatment algorithms now and follow along with this discussion
http://www.wsacs.org/algorithms.php

___________________________________________________

Download Dr. Cheatham’s 2009 review on the topic from the World Journal of Surgery (free)

http://www.springerlink.com/content/72v415n264grv36q/

or -  click here -  for the article

The non-operative management of IAH consists of 5 therapeutic interventions:[1]

1.      Evacuation of contents with the bowel (intraluminal)

2.      Evacuation of extraluminal contents within the abdominal or retroperitoneal space

3.      Improvement of abdominal wall compliance

4.      Optimization of fluid administration (enough but not too much)

5.      Optimization of tissue perfusion

Evacuation of intraluminal contents:

Large volumes of air within the GI tract and ileus are both common occurrences in critically ill patients on ventilators and numerous drug combinations. These intraluminal fluid and gas collections increase the volume within the confines of the abdominal cavity and result in rises in the IAP that can lead to hypoperfusion.  Interventions as simple as nasogastric suction and rectal tube drainage are often very effective in treating these problems and lowering IAH.[8] Administration of prokinetic motility agents can further assist in expelling intraluminal material (erythromycin 200 mg IV q 8 hours, metoclopramide 10 mg IV q 6 hours). If IAP continues to rise and enteral nutrition is running – it may need to be slowed and on rare occasion stopped altogether. On very rare occasions the only intervention for massively distended bowel is colonoscopic decompression or even abdominal surgery.

Evacuation of extraluminal space occupying masses:

Free fluid in the abdomen, retroperitoneal abscess or hematomas – all can increase IAP. Assessment with physical exam, ultrasound and CT can reveal these problems and if IAH develops percutaneous drainage of these fluid collections – whether free fluid in the peritoneum or confined abscesses - is often very effective in reducing IAP, improving organ perfusion and preventing the need for surgical intervention.[11, 16-20]  In fact, even in the absence of visible ascites, IAP can be reduced in high risk patients with percutaneous catheter placement. In one small study in 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.[16, 22, 23] 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.  Very recent data also suggests that drainage of this fluid reduces inflammatory cytokine levels both in the intra-abdominal space as well as in the serum – a therapeutic intervention that may further enhance recovery from the illness.[24]

Photos of intraluminal and extraluminal fluid collections to be drained and reduce intraabdominal pressure

Improve Abdominal Wall Compliance:

As the abdominal wall becomes progressively more distended it can no longer stretch – eventually reaching a compliance threshold past which the pressure within the abdomen increases dramatically.  Muscular tone often lowers this threshold – especially if the patient is in pain or is working against the ventilator.[2, 25]  In fact, IAP fluctuations during mechanical ventilation can be a useful indicator of reduced abdominal wall compliance/tighter abdomen – if there is a large difference between end inspiratory IAP and end-expiratory IAP that patient is developing more serious problems with IAH.[26] Sometimes very simple interventions such as administration of additional pain medication or sedation is all that is needed to reduce IAP.[27] Because body position affects IAP, another easy bedside intervention is to “unfold” the abdomen – straightening out the body (from the 30 degree head of bed elevation) and placing the patient supine with reverse Trendelenburg.[28, 29] Prone positioning also increases IAP and care must be taken on positioning the abdomen during prone positioning to avoid significant bowel ischemia.[30] If medical interventions fail and the patients IAP exceeds 20 mm Hg, a trial of neuromuscular blockade is warranted as there is some published evidence and extensive clinical experience demonstrating the effectiveness of this intervention at higher levels of IAP.[1, 31-34]  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.[35]  However, if capillary leak continues this treatment effect may only have transient effects.  Although muscular weakness is a concern when prolonged neuromuscular blockade is used, this is still worth trying when compared to the morbidity of an open abdomen – an exception might be in the patient on aminoglycoside in whom neuropathy from NMB is more common. Another similar option for reducing IAP is via epidural analgesia. Hakobyan and colleagues performed a small study on critically ill postoperative patients where epidural analgesia was began when IAP exceeded 15 mm Hg.[25] 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.

Improving abdominal wall compliance reduces IAP by shifting the pressure-volume compliance curve to the right

Place patient supine or in reverse Trendelenburg to improve abdominal wall compliance and reduce IAP very easily at the bedside

If IAP rises above 20 mm Hg, a trial of chemical paralysis is warranted as this may reduce IAP, improve renal perfusion and lead to diuresis and persistent IAP reductions.

Optimize fluid resuscitation:

Optimal fluid resuscitation may be the most difficult task in any critically ill patients, and it is made more complicated in the presence of elevated IAP.  In the presence of IAH, many of the hemodynamic parameters are difficult to interpret (see hemodynamic monitoring section) while simultaneously over-resuscitation leads to excessive fluid sequestration in the gut, higher IAP and worse outcomes. The complex interactions of intra-abdominal, intrathoracic and intravascular pressures make accurate volume assessment using CVP and PAOP somewhat difficult. Functional hemodynamic parameters such as SVV and PPV are also effected and less predictive of fluid responsiveness.[36-38] End-diastolic volumetric indices and/or echocardiographic indices will improve clinician’s ability to interpret vascular filling.[37-39] 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).[39]

 Initial adequate resuscitation using standard guidelines should be implemented, but modified as the IAP rises – at which point very careful assessment of further fluid administration using passive leg raising  (or small fluid boluses) while observing pulse pressure variation or beat to beat stroke volume or volumetric data is essential – and difficult.[38, 39] Despite the ongoing controversy of colloid vs crystalloid, patients with IAH probably should be considered for colloid or hypertonic saline fluids boluses rather than isotonic fluids.[1, 40, 41] Never the less, often these patients are fluid overloaded – and judicious removal of this excess fluid will often reduce IAP, improving renal perfusion and function and lead to fluid mobilization and diuresis.[12, 17] One option is to combine diuretics with colloids in an effort to mobilize fluid from the bowel wall and diurese that fluid before the colloids leak into the extravascular space.[42, 43] 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.[40] Another effective method is to institute hemofiltration and remove excess fluid as the IAP is rising but before overt organ failure occurs.[12, 17, 44] 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 interstitial 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.[12] 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%. Mullens found that reducing IAP by fluid removal with hemofiltration and or paracentesis was more effective in treating renal insufficiency than hemodynamic optimization in patients suffering congestive.[17, 45] Other recently presented abstracts confirm the survival benefits seen with hemofiltration in both pancreatitis cases as well as in patients suffering from severe sepsis.[46-48]  Hernandez, et al, who demonstrated a 51% incidence of IAH/ACS in septic shock patients[49] 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 responders versus 83% in non-responders).[47] 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).[48]

Medical management of intraabdominal hypertension and the abdominal compartment syndrome requires optimizing fluid management

In situations where significant fluid overload is present, CVVH with colloid use to maintain intravascular oncotic pressure can have dramatic results in reducing IAP

Optimize tissue perfusion:

Following appropriate volume resuscitation, abdominal blood flow show be optimized.[50] 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.[50, 51] 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.[50, 52]

Medical management of intraabdominal hypertension and the abdominal compartment syndrome requires optimizing tissue perfusion

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.[53] 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.[53] 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.[54, 55] 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.[55-57]

This photos is from a patients with abdominal compartment syndrome who was not making urine, difficult to ventilate and had low abdominal perfusion pressure - medical therapy was too little or ineffective, but surgical therapy was  life saving with immediate improvement in urine output, ventilation and perfusion. Clearly it would be bad for his physiology to try to "stuff" these guts back into the abdomen and suture it closed.

1. 1.      Cheatham, M.L., Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg, 2009. 33(6): p. 1116-22.

   2.      Malbrain, M.L.N.G., 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.

   3.      Reintam, A., et al., Primary and secondary intra-abdominal hypertension-different impact on ICU outcome. Intensive Care Med, 2008. 34(9): p. 1624-31.

   4.      Vidal, M.G., et al., Incidence and clinical effects of intra-abdominal hypertension in critically ill patients. Crit Care Med, 2008. 36(6): p. 1823-31.

   5.      Daugherty, E.L., et al., Abdominal compartment syndrome is common in medical intensive care unit patients receiving large-volume resuscitation. J Intensive Care Med, 2007. 22(5): p. 294-9.

   6.      Regueira, T., et al., Intra-abdominal hypertension: incidence and association with organ dysfunction during early septic shock. J Crit Care, 2008. 23(4): p. 461-7.

   7.      Regueira, T., et al., Intraabdominal hypertension in patients with septic shock. Am Surg, 2007. 73(9): p. 865-70.

   8.      Cheatham, M.L., et al., Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med, 2007. 33(6): p. 951-62.

   9.      Cheatham, M.L. and K. Safcsak, Is the evolving management of IAH/ACS improving survival? Acta Clinica Belgica, 2007. 62, supplement 1: p. Abstract O61.

   10.    Kimball, E.J., et al., A Prospective Evaluation of the Protocolized Management of Intra-abdominal Hypertension and the Abdominal Compartment Syndrome Acta Clinica Belgica, 2009. 64(3): p. 272 (Abstract 110).

   11.    Sun, Z.X., H.R. Huang, and H. Zhou, Indwelling catheter and conservative measures in the treatment of abdominal compartment syndrome in fulminant acute pancreatitis. World J Gastroenterol, 2006. 12(31): p. 5068-70.

   12.    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.

   13.    Ennis, J.L., et al., Joint Theater Trauma System implementation of burn resuscitation guidelines improves outcomes in severely burned military casualties. J Trauma, 2008. 64(2 Suppl): p. S146-51; discussion S151-2.

   14.    Balogh, Moore, and Fa, Intra-abdominal hypertension: not just a surgical critical care curiosity. Crit Care Med, 2005. 33(2): p. 447-9.

   15.    Joseph, D.K., et al., Decompressive laparotomy to treat intractable intracranial hypertension after traumatic brain injury. J Trauma, 2004. 57(4): p. 687-95.

   16.    Latenser, B.A., et al., A pilot study comparing percutaneous decompression with decompressive laparotomy for acute abdominal compartment syndrome in thermal injury. J Burn Care Rehabil, 2002. 23(3): p. 190-5.

   17.    Mullens, W., et al., Prompt reduction in intra-abdominal pressure following large-volume mechanical fluid removal improves renal insufficiency in refractory decompensated heart failure. J Card Fail, 2008. 14(6): p. 508-14.

   18.    Parra, M.W., et al., Paracentesis for resuscitation-induced abdominal compartment syndrome: an alternative to decompressive laparotomy in the burn patient. J Trauma, 2006. 60(5): p. 1119-21.

   19.    Reckard, J.M., et al., Management of intraabdominal hypertension by percutaneous catheter drainage. J Vasc Interv Radiol, 2005. 16(7): p. 1019-21.

   20.    Vikrama, K.S., et al., Percutaneous catheter drainage in the treatment of abdominal compartment syndrome. Can J Surg, 2009. 52(1): p. E19-20.

   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.    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.

   23.    Cleva Rd, R., et al., Acute renal failure due to abdominal compartment syndrome: report on four cases and literature review. Rev Hosp Clin Fac Med Sao Paulo, 2001. 56(4): p. 123-30.

   24.    Kubiak, B.D., et al., Peritoneal negative pressure therapy reduces both peritoneal and systemic inflammation and prevents abdominal compartment syndrome. Acta Clinica Belgica, 2009. 64(3): p. 260 (Abstract 43).

   25.    Hakobyan, R.V. and G.G. Mkhoyan, Epidural analgesia decreases intraabdominal pressure in postoperative patients with primary intra-abdominal hypertension. Acta Clin Belg, 2008. 63(2): p. 86-92.

   26.    Sturini, E., et al., Respiratory variation of intra-abdominal pressure: indirect indicator of abdominal compliance? Intensive Care Med, 2008.

   27.    Hershberger, R.C., et al., Abdominal Compartment Syndrome in the Severely Burned Patient. J Burn Care Res, 2007. Publish Ahead of Print.

   28.    Cheatham, M.L., et al., The impact of body position on intra-abdominal pressure measurement: a multicenter analysis. Crit Care Med, 2009. 37(7): p. 2187-90.

   29.    Vasquez, D.G., G.M. Berg-Copas, and R. Wetta-Hall, Influence of semi-recumbent position on intra-abdominal pressure as measured by bladder pressure. J Surg Res, 2007. 139(2): p. 280-5.

   30.    Hering, R., et al., The effects of prone positioning on intraabdominal pressure and cardiovascular and renal function in patients with acute lung injury. Anesth Analg, 2001. 92(5): p. 1226-31.

   31.    De Laet, I., et al., The effect of neuromuscular blockers in patients with intra-abdominal hypertension. Intensive Care Med, 2007. 33(10): p. 1811-4.

   32.    Macalino, J.U., R.K. Goldman, and J.C. Mayberry, Medical management of abdominal compartment syndrome: case report and a caution. Asian J Surg, 2002. 25(3): p. 244-6.

   33.    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.

   34.    Kimball, E.J., et al., Influence of neuromuscular blockade on intra-abdominal pressure. Critical Care Medicine, 2005. 33(12 supplement): p. A38, Abstract 142-S.

   35.    DeWaele, J.J., et al., A role for muscle relaxation in patients with abdominal compartment syndrome? Intensive Care Med, 2003. 29(2): p. 332.

   36.    Renner, J., et al., Influence of increased intra-abdominal pressure on fluid responsiveness predicted by pulse pressure variation and stroke volume variation in a porcine model*. Crit Care Med, 2009.

   37.    Malbrain, M.L. and I. De Laet, Functional haemodynamics during intra-abdominal hypertension: what to use and what not use. Acta Anaesthesiol Scand, 2008. 52(4): p. 576-7.

   38.    Malbrain, M.L. and I. de Laet, Functional hemodynamics and increased intra-abdominal pressure: same thresholds for different conditions ...? Crit Care Med, 2009. 37(2): p. 781-3.

   39.    Cheatham, M.L. and M.L. Malbrain, Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl, 2007(1): p. 98-112.

   40.    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.

   41.    Oda, J., et al., Hypertonic lactated saline resuscitation reduces the risk of abdominal compartment syndrome in severely burned patients. J Trauma, 2006. 60(1): p. 64-71.

   42.    Umgelter, A., et al., Renal resistive index and renal function before and after paracentesis in patients with hepatorenal syndrome and tense ascites. Intensive Care Med, 2009. 35(1): p. 152-6.

   43.    Umgelter, A., et al., Effects of plasma expansion with albumin and paracentesis on haemodynamics and kidney function in critically ill cirrhotic patients with tense ascites and hepatorenal syndrome: a prospective uncontrolled trial. Crit Care, 2008. 12(1): p. R4.

   44.    Vachharajani, V., et al., Medical Management Of Severe Intra-abdominal Hypertension With Aggressive Diuresis And Continuous Ultra-filtration. The Internet Journal of Emergency and Intensive Care Medicine, 2003. 6(2): p. http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijeicm/vol6n2/ultra.xml.

   45.    Mullens, W., et al., Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol, 2008. 51(3): p. 300-6.

   46.    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.

   47.    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.

   48.    Piccinni, et al., Early isovolaemic haemofiltration in oliguric patients with septic shock. Intensive Care Med, 2006. 32(1): p. 80-6.

   49.    Hernandez, G., et al., Intra-abdominal hypertension in septic shock patients. Intensive Care Medicine, 2005. 31, Supplement 1(134): p. S91, Abstract 339.

   50.    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.

   51.    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.

   52.    Peng, Z.Y., et al., Effects of norepinephrine during intra-abdominal hypertension on renal blood flow in bacteremic dogs. Crit Care Med, 2008. 36(3): p. 834-41.

   53.    Sugrue, Abdominal compartment syndrome. Curr Opin Crit Care, 2005. 11(4): p. 333-8.

   54.    Kimball, E.J., et al., Assessment of the current understanding and clinical management of abdominal compartment syndrome (ACS) among ICU physicians. Critical Care Medicine, 2003. Abstract present at Society of Critical Care Medicine, San Antonio, TX, February 2003.

   55.    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.

   56.    Ivatury, R.R., et al., Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am, 1997. 77(4): p. 783-800.

   57.    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.

   58.    Gracias, V.H., et al., Abdominal compartment syndrome in the open abdomen. Arch Surg, 2002. 137(11): p. 1298-300.

   59.    Ordonez, C., et al., Survival of trauma patients with tertiary abdominal compartment syndrome after damage control laparotomy with open abdomen. Acta Clinica Belgica, 2009. 64(3): p. 283 (abstract 157).