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Ann Thorac Surg 2008;85:2133-2135. doi:10.1016/j.athoracsur.2007.12.041
© 2008 The Society of Thoracic Surgeons
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Case Reports

Surgical Decompression for Abdominal Compartment Syndrome After Emergency Cardiac Surgery

Annick De Wolf, MD, Jan Poelaert, MD, PhD, Ingrid Herck, MD, Jan J. De Waele, MD, PhD*

Department of Critical Care Medicine, Ghent University Hospital, Ghent, Belgium

Accepted for publication December 14, 2007.

* Address correspondence to Dr De Waele, Intensive Care Unit, Ghent University Hospital, De Pintelaan 185, Ghent, 9000, Belgium (Email: jan.dewaele{at}ugent.be).


   Abstract
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 Abstract
Introduction
 Comment
 References
 
Abdominal compartment syndrome typically occurs in patients after abdominal surgical procedures or trauma. Abdominal compartment syndrome is also increasingly described in conditions not related to abdominal operations, such as fluid resuscitation or burns. We report two patients who required surgical abdominal decompression for abdominal compartment syndrome that developed early after emergency coronary artery bypass graft surgery. No intraabdominal abnormalities were found at operation. Both patients had a protracted clinical course, but they survived and were discharged from the hospital.


   Introduction
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 Abstract
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 References
 
The abdominal compartment syndrome (ACS) is defined as new-onset organ dysfunction resulting from a sustained increase in intraabdominal pressure (IAP) [1]. Most obviously affected is cardiovascular, respiratory, and renal function. Abdominal compartment syndrome is generally understood as a complication that typically occurs after intraabdominal trauma or surgical procedures, but ACS may also develop in patients who have not had an abdominal injury or operation. This entity, termed secondary ACS, appears to be related to resuscitation-induced bowel edema, and ascites [2].

We report two patients who presented with secondary ACS after emergency cardiac surgery and who were successfully treated with decompressive laparotomy.

A 50-year-old man and a 65-year-old man were both successfully resuscitated after an out of hospital cardiac arrest. They underwent urgent coronary artery bypass graft procedures with cardiopulmonary bypass (CPB) and were admitted to the cardiac surgery intensive care unit (ICU).

A few days later, pneumonia developed in both patients that resulted in severe sepsis. Despite massive fluid resuscitation, acute kidney injury developed that required renal replacement therapy. Mechanical ventilation gradually became very difficult during the next few days, requiring high peak inflating pressures, high positive expiratory end-pressure (PEEP), and high fractions of inspired oxygen (FIO 2) to maintain adequate oxygenation.

At first, intraabdominal pressure (IAP) measurements were 17 mm Hg in the first patient and 18 mm Hg in the second patient, but they gradually reached a maximum of 24 and 27 mm Hg, respectively, after a few days, with no effect of neuromuscular blockers.

Because of progressive organ dysfunction, each patient underwent abdominal decompression at 5 and 4 days postoperatively, respectively. Except for bowel wall edema and ascites in the second patient, no intraabdominal abnormalities were noted. The fascia could not be approximated, and a Vicryl mesh (Ethicon, Somerville, NJ) was used. The skin was closed over the Vicryl mesh in both patients.

After surgical decompression, the IAP fell immediately to 14 mm Hg in the first patient and to 12 mm Hg in the second patient. A summary of organ function variables before and after decompressive laparotomy is reported in Table 1.


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  		Table 1 Physiologic Variables Before and 2 Hours After Decompressive Laparotomy
 
In the following days, the ventilatory indicators improved progressively, with decreased peak inflating pressures, PEEP and FIO 2. Initially, there was no effect on urinary output, but renal function gradually improved. Both patients were eventually weaned from the ventilator and discharged from the ICU in good condition, and by then, renal function had also recovered completely. Fascial closure could be achieved in the first patient 14 days after decompressive laparotomy, and the second patient is awaiting abdominal hernia repair.


   Comment
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 Abstract
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 Comment
References
 
Abdominal compartment syndrome is defined as the clinical syndrome of organ dysfunction resulting from sustained elevation of IAP exceeding 20 mm Hg and is the final stage of a continuum of physiologic derangements resulting from increased IAP, also referred to as intraabdominal hypertension (IAH). Abdominal compartment syndrome has been divided into primary, secondary, and recurrent ACS, where primary ACS refers to an intraabdominal cause, secondary ACS has an extraabdominal cause, for example, massive fluid resuscitation leading to intraperitoneal edema; and recurrent ACS occurs after previous treatment for ACS [2]. Organ dysfunction typically includes hemodynamic instability, respiratory insufficiency with impaired gas exchange, and acute renal failure with oliguria as the most prominent signs early in the course of the disease.

The lack of treatment options has often been cited as a reason not to measure IAP [3], but several strategies have been devised to reduce IAP [4]. Various nonsurgical approaches, such as percutaneous drainage of intraperitoneal fluid and neuromuscular blockers [5], have been shown to reduce IAP. If these prove ineffective, decompressive laparotomy has been shown to effectively reduce IAP and improve organ function in critically ill patients [6].

Open abdomen treatment, or laparostomy, was initially intended for patients with diffuse intraabdominal infections [7], but open abdomen treatment—either prophylactic or therapeutic—is becoming more common in the ICU. Several techniques to cover the open abdomen are available [8], but the Bogota bag, prosthetic material, and vacuum systems are most often used.

A Bogota bag is a plastic sheet cut from a sterile 3-L irrigation bag and sewn to the skin or fascia. This system is cheap and offers the advantage that the bowel and abdominal contents can be easily inspected and accessed; however, fluid losses are difficult to control, which makes it a real challenge for the nursing staff. Removable prosthetic materials were used initially in open abdomen treatment of intraabdominal sepsis and are now used for temporary abdominal closure in other circumstances as well; examples are the Wittman patch (Star Surgical, Burlington, WI), which uses two adhering sheets of biocompatible polymeric material. Packing techniques that use suction or a vacuum to control the fluid draining from the open abdomen are increasingly popular. These are simple solutions for the management of an open abdomen and provide easy control and quantification of fluid losses.

In the patients presented, IAH had an important effect on respiratory function, with prompt improvement after decompression. In association with increased IAP, there is a restrictive effect on the lungs with reduction in ventilation. It typically leads to problems with pulmonary compliance with progressive reduction in total lung capacity, functional residual capacity, and residual volume. There is also an adverse effect on efficiency of gas exchange. The clinical picture is manifested by hypoxia, hypercapnia, and increased ventilatory pressure. In our patients, the decompressive laparotomy had no immediate effect on urinary output, probably because the intervention came rather late after the start of IAH.

In these two patients there are two important factors that may play a significant role in the pathophysiology of ACS. First there is an episode of shock that leads to redistribution of blood from splanchnic organs, which in turn causes cellular hypoxia of intestinal tissues. Hypoxia leads to production of cytokines with subsequent vasodilatation and increased capillary permeability with edema. After cellular reperfusion, oxygen free radicals are generated that have a toxic effect on cell membranes. Hypoxia also impairs the cellular sodium-potassium pump, which leads to further cell edema. All this may lead to elevation of the IAP, with further impairment of intestinal perfusion, and the cycle of cellular hypoxia, cell death, inflammation and edema continues. Second, optimization of preloading conditions by important fluid administration probably maintained the vicious circle.

Little is known about the role of extracorporeal circulation in the development of postoperative IAH. Czajkowski and colleagues [9] showed an increase in IAP depending on the degree of hemodilution after the initiation of the CPB. Andrási and colleagues [10] demonstrated a significant impact of CPB with cardiac arrest on the mesenteric circulation in an in vivo canine model of extracorporeal circulation where CPB causes a splanchnic hypoperfusion. Hypothermia and especially rewarming are associated with a release of vasoactive substances, causing vasoconstriction at the microcirculatory level and the gut mucosa, which may lead to bowel edema.

In conclusion, this report demonstrates that ACS can occur outside the typical setting of abdominal surgery or trauma. Patients undergoing CPB may be at risk for postoperative IAH, but the exact incidence of IAH in this setting remains unclear. Further investigations, for instance regarding the risk for IAH caused by the extracorporeal circulation itself, are necessary. A low index of suspicion in these patients is mandatory [11], and in cases of ACS, appropriate actions to decrease IAP should be taken.


   References
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 Abstract
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 Comment
 References
 

  1. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006;32:1722-1732.[Medline]
  2. Kirkpatrick AW, De Waele JJ, Ball CG, Ranson K, Widder S, Laupland KB. The secondary and recurrent abdominal compartment syndrome Acta Clin Belg Suppl 2007:60-65.
  3. De Waele JJ, De laet I, Malbrain ML. Intraabdominal hypertension and abdominal compartment syndrome: we have paid attention, now it is time to understand! Acta Clin Belg Suppl 2007:6-8.
  4. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med 2007;33:951-962.[Medline]
  5. De Laet I, Hoste E, Verholen E, De Waele JJ. The effect of neuromuscular blockers in patients with intra-abdominal hypertension Intensive Care Med 2007;33:1811-1814.[Medline]
  6. De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy for abdominal compartment syndrome - a critical analysis Crit Care 2006;10:R51.[Medline]
  7. Blot S, De Waele JJ. Critical issues in the clinical management of complicated intra-abdominal infections Drugs 2005;65:1611-1620.[Medline]
  8. Sugrue M, D'Amours SK, Kolkman KA. Temporary abdominal closure Acta Clin Belg Suppl 2007:210-214.
  9. Czajkowski M, Dabrowski W. Changes in intra-abdominal pressure during CABG with normovolemic hemodilution Med Sci Monit 2006;12:CR487-CR492.[Medline]
  10. Andrási TB, Buhmann V, Soós P, Juhász-Nagy A, Szabó G. Mesenteric complications after hypothermic cardiopulmonary bypass with cardiac arrest: underlying mechanisms Artif Organs 2002;26:943-946.[Medline]
  11. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, De Waele J, Ivatury R. Abdominal compartment syndrome: it's time to pay attention! Intensive Care Med 2006;32:1912-1914.[Medline]




This Article
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