Decompressive Laparotomy in Abdominal Compartment Syndrome

Decompressive Laparotomy in Abdominal Compartment Syndrome

A 55 yr old man developed severe necrotizing pancreatitis with multiorgan failure. One week into his illness he had developed multiple intra-abdominal collections and had high intra-abdominal pressures. Initial conservative management failed, percutaneous drainage of his collections failed to reduce the abdominal pressures, and he underwent decompressive laparotomy.

What is the evidence behind the current guidelines for the measurement of intra-abdominal hypertension and the use of decompressive laparotomy in the management of Abdominal Compartment Syndrome?

Sam Clark

Intra-abdominal hypertension was first described in the second part of the 19th Century, by Marey (1). Later, Emerson published his seminal article “The intra-abdominal pressure” in 1911(2). In 1940, Sir Henry Ogilvie performed the first decompressive laparostomies help manage significant abdominal trauma(3). However, it wasn’t until 1989 that Fietsam et al first coined the phrase Abdominal Compartment Syndrome(4). The last 150 years of scientific work culminated in the first World Society of Abdominal Compartment Syndrome conference in Noosa (Queensland) in December 2004, a society that continues to develop in size and impact throughout the world.

Both in 2004, and again in 2007, consensus was reached on the certain important definitions that underpin intra-abdominal hypertension and abdominal compartment syndrome. They defined Intra-abdominal pressure (IAP) as the steady state pressure concealed within the abdominal cavity(5,6). Intra-abdominal Hypertension (IAH) was defined by a sustained or repeated pathological elevation in IAP greater than or equal to 12mmHg. IAP can be graded as follows: grade I IAP between 12-15mmHg; grade II IAP between 16-20mmHg; grade III 21-25 mmHg and grade IV IAP over 25mmHg(6). Abdominal Compartment Syndrome (ACS) was defined as a sustained IAP greater than 20 mmHg that was associated with new organ dysfunction or failure(6). They defined a number of potential risk factors for both IAP and ACS including conditions that diminish abdominal wall compliance, increase either intra-abdominal or intra-luminal contents, lead to capillary leak or fluid resuscitation. These conferences were the basis of a number of systematic reviews that were crystallized into practical clinical guidelines for the management of these life-threatening conditions, the most recent of which were published in 2013(6).

One important question related to the management of abdominal compartment syndrome relates to the employment of Decompressive Laparotomy (DL) to reduce IAH and reverse organ dysfunction. The latest WSACS Guidelines recommend the use of DL to reduce IAP in cases of overt ACS compared to strategies that do not use DL in the critically ill adults with ACS in critical care units, which they graded as 1D. De Waele et al conducted a systematic review of papers that examined DL on patients with ACS from 1972 to 2004(11). They included 18 papers with 250 patients, mainly case reports and observational studies. There was no consistent definition of ACS nor was there a consistent indication for DL, with possibilities uncontrolled IAP to raised IAP plus organ dysfunction. There was a significant mortality across the studies (overall being 49.2% and ranging from 22 to 100%). IAP was decreased for all patients receiving DL (mean IAP prior to DL 34.6mmHg to 15.5mmHg), however many patients still had ongoing IAH despite DL leading to persistent or recurrent DL. Secondary outcomes suggested that DL significantly improved cardiac output and in respiratory function though PaO2/FiO2 ratios did not return to normal in any patient. In 5 of 10 studies urine output significantly increased. The lack of control groups in these studies means that it is difficult to assess whether DL is just a measure of severity of disease and their mortality is associated with this fact. The limited detail attached to many of the studies meant that the authors could not fully assess organ function and the markers reported may not have been the most ideal. There was evidence of harm to patients undergoing DL. Risks included lethal reperfusion injury and rebleeding. The authors concluded that there was not a clear consensus for a threshold for DL and recommended further research to elucidate future parameters.

A recent study to examine ACS in patients with acute pancreatitis was a retrospective analysis of 26 patients from a single center undergoing surgical decompression over a six-year period(12). Overall mortality of patients with DL 46% at a median of 25 days post admission (IRQ 18-56 days). They assessed risk factors for fatal outcomes comparing survivors and non-survivors. Significant risks for survivors versus non-survivors were: time to surgical decompression after disease onset (median 1, IRQ1-2 vs. 7, IRQ1-17, p<0.05); preoperative renal failure (36% vs. 75%, p<0.05) and preoperative IAP (33, IRQ 30-36 vs. 28, IRQ 20-34, p<0.05). It is of note that the median IAP was high prior to surgery in the survivor group, perhaps indicating that the non-survivors had indicators of life threatening disease driving the decision to operative and that those risks are less likely to improve with decompression. Interestingly preoperative SOFA scores did not reach significance, but this was only by a small margin. There was some improvement in markers of both respiratory and renal function in approximately half of the patients. They, again, noted significant morbidity attached the resultant open abdomen, including the development of fistulae and infected pancreatic necrosis, which occurred in 46% of patients.

In the systematic review conducted to assist the development of the WSACS guidelines found no RCTs or systematic reviews that compared DL with non DL based strategies(13). The highest quality evidence all came from before-and-after case series, 16 in total, most of which were collected retrospectively (only 3 were prospective). They found results consistent with the earlier review, mortalities ranged from 21.4 to 64% for the varying studies. There was little consistency in the data recorded between the studies and even the methods used to record IAP with a number of studies using large volumes instilled into the bladder. Neither was the reporting of the timing and the indications for DL always well described. The authors did report that most studies showed a significant reduction in IAP especially for patients with very high IAP, and that there was some evidence of improvement in PaO2/FiO2 ratios, reduction in vasopressor requirements. The data over SOFA scores, though limited was not clear with some, but not all studies showing an improvement. They concluded that the evidence base behind DL was limited by bias and by the absence of key data such as RCT comparing conservative with operative management, but that DL was associated with correction or at least partial correction and abnormal patient physiology.


Conclusions:

This case report allowed me to review the guidelines for the management of raised inter-abdominal hypertension and abdominal compartment syndrome, including monitoring, basic conservative management and potential indications for surgical decompression. Closer examination of the evidence suggests that the majority of current clinical consensus derives for a limited and potentially biased evidence base and expert opinion. The evidence for DL is limited and would benefit from mortality data from an RCT as well as potentially trials that examine the timings and indication for the procedure. It may be that DL benefits certain subgroups, for example, those developing ACS rapidly and early in the clinical course or those for very severe IAH yet to develop significant other organ failure.


References

(1) Kron IL, Harman PK, Nolan SP (1984) The measurement of intraabdominal pressure as a criterion for abdominal reexploration. Ann. Surg. 199:28-30.
(2) Emerson H (1911) Intra-abdominal pressures. Arch. Intern. Med. 7:754-784.
(3) Ogilvie WH (1940) The late complications of abdominal war wounds. Lancet. 2: 253-256.
(4) Fietsam RJr, Villalba M, Glover IL, Clark K (1989) Intraabdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Ann. Surg. 55:396-402
(5) Malbrain MLNG, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Zs, Leppaniemi A, Olvera C, Ivatury R, D’Amours S, Wendon J, Hillman K, Johansson K, Kolkman K, Wilmer A (2006) Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Int. Care. Med. 32: 1722-1732
(6) Kirkpatrick A., Roberts D., De Waele J., et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and practical guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med (2013) 39:1190–1206
(7) Kirkpatrick AW, Brenneman FD, McLean RF, Rapanos T, Boulanger BR (2000) Is clinical examination an accurate indicator of raised intra- abdominal pressure in critically injured patients. Can J Surg 43:207–211.
(8) Sun Z., Huang H., & Zhou H. Indwelling catheter and conservative measures in the treatment of abdominal compartment syndrome in fulminant acute pancreatitis. World J Gastrornterol (2006) 21;12(31):5068-5070.
(9) Kirkpatrick A., Roberts D., De Waele J., et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and practical guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med (2013) 39:1190–1206; supplement 8 Measurement of IAP.
(10) Pupelis G., Zeiza K., Plaudis H., & Suhova A. Conservative approach in the management of severe acute pancreatitis: 8-year experience in a single institution. (2008) 10:347-355.
(11) De Waele JJ, Hoste EA, Malbrain ML, (2006) Decompressive laparotomy for abdominal compartment syndrome–a critical analysis. Crit Care 10: R51
(12) Mentula P, Hienonen P, Kemppainen E, Puolakkainen P, Leppaniemi A, (2010) Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Archives of surgery 145: 764-769.
(13) Kirkpatrick A., Roberts D., De Waele J., et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and practical guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med (2013) 39:1190–1206; supplement 22 Should we use decompressive laparotomy for IAH or ACS?.

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