Postoperative gastric dilatation causing abdominal compartment syndrome

  • Ahmad Mahajna1,

    Affiliated with

    • Sharon Mitkal1 and

      Affiliated with

      • Michael M Krausz1Email author

        Affiliated with

        World Journal of Emergency Surgery20083:7

        DOI: 10.1186/1749-7922-3-7

        Received: 19 March 2007

        Accepted: 31 January 2008

        Published: 31 January 2008

        Abstract

        Objective

        To study the effect of postoperative gastric dilatation on intra-abdominal pressure (IAP).

        Design and setting

        Single case report from a primary teaching hospital.

        Patients and methods

        A 72-year-old woman demonstrated a sudden respiratory and cardiovascular collapse following resection of a retroperitoneal sarcoma. This collapse was caused by abdominal compartment syndrome due to gastric dilatation.

        Results

        The patient was re-explored, an enormously distended stomach was found with the nasogastric tube situated in a small sliding hernia which prevented drainage of the distended stomach. Re-positioning of the nasogastric tube, allowed the decompression of the stomach and the patient's condition immediately improved.

        Conclusion

        Acute abdominal distention following major abdominal surgery may result from acute gastric dilatation, leading to oliguria and increased airway pressures. Untreated gastric dilatation can cause abdominal compartment syndrome.

        Introduction

        Abdominal compartment syndrome (ACS) is defined as an increased intra-abdominal pressure (IAP > 20 mmHg) in combination with single or multiple organ dysfunction which was not previously present [13]. This condition affects multiple organ systems in graded fashion [4]. Early identification and abdominal decompression are essential in the management and treatment of this difficult situation, otherwise, it leads to multiple organ failure and ultimately, death [5]. Increased intra-peritoneal volume conditions are the most common source of elevated IAP [6, 7]. Extrinsic compression of the abdomen by burn eschars [8], pneumatic anti-shock garments [9], tight abdominal closure [10], massive volume resuscitation for any reason, and inflation of the peritoneum by CO2 in laparoscopic surgery can also lead to increased IAP [11]. We present a rare case of abdominal compartment syndrome caused by postoperative gastric dilatation in 72-year-old woman.

        Case presentation

        A 72-year-old woman was addmitted for elective resection of retroperitoneal sarcoma. The diagnosis was done by CT scan and pathological confirmation by explorative laparotomy 3 weeks before in another institution. At operation complete resection of the tumor was performed. Following surgery the patient was admitted to the intensive care unit. On arrival she was stable hemodynamically, her blood pressure was 135/80 mmHg and heart rate was 95 beats/min. During the first day the patient was mechanically ventilated on Fio2- 0.4, Vt- 600 ml, and a rate of 12/min. The peak airway pressure was 21 cmH2o and the mean airway pressure was 10 cmH2o. Her blood gases were within the normal range.

        After 24 hours, the patient was extubated. Following extubation, her abdomen became gradually tenser and distended, with increasing abdominal discomfort. A nasogastric tube was placed but no fluid or air was obtained. Since no suspicion regarding the nasogastric tube's place was araised, chest x-ray was not obtained. The patient gradually developed hemodynamic instability and was treated with crystalloid transfusions but her blood pressure dropped continuously to 70/40 mmHg and her pulse rate increased to 140 beats/min. The ECG showed no signs of ischemia and her hematocrit was 28%. The patient was re-intubated and mechanicaly ventilated with great difficulty. At a Vt of 550 ml, a rate of 12/min, with a peak airway pressure of 42 cmH2o and mean airway pressure of 22 cmH2o. Her condition deteriorated rapidly, with no response to crystalloid and blood transfusion, and aggressive use of vasoactive agents. The abdomen was massively distended despite the use of muscle relaxants and the patient became anuric. IAP measured via a Foley bladder catheter according to the modified Kron technique described by Malbrain et al. [12], was 31 mmHg. As the patient presented a life threatening condition, she was taken immediately for re-exploration without any further diagnostic or therapeutic measures. She underwent laparotomy which revealed a minimal amount of intraperitoneal fluid but an enormously distended stomach. The nasogastric tube was situated in a small sliding hernia and did not drain the distended stomach. The nasogastric tube was flushed and re-positioned, allowing the deflation of the stomach. After deflation, the patient's condition immediately improved. The blood pressure rose to 140/70 mmHg, the heart rate decreased to 104/min, and the urine output increased to 300 ml/hr. Vasopressor agents were stopped. The peak airway pressure dropped to 21 cmH2O and the mean airway pressure dropped to 8 cmH2O. The repeated postoperative IAP measurements were within the normal limits. The postoperative course was complicated by line sepsis, treated by line removal, broad-spectrum antibiotics and vasoactive agents with a favorable response. The patient was discharged from hospital after 10 days in good condition.

        Discussion

        The World Society of the ACS (WSACS) has recently developed consensus definitions outlining standards for IAP measurement as well as diagnostic criteria for IAH and ACS based upon both the best available clinical evidence and expert opinion.

        Acute and rapid elevation in intra-abdominal pressure exceeding 12 mmHg is considered to be pathologically elevated and has been termed intra-abdominal hypertension [10]. IAH is graded as follows: grade I: IAP 12–15 mmHg, Grade II: IAP 16–20 mmHg, Grade III: IAP 21–25 mmHg, and grade IV: IAP > 25 mmHg.

        ACS is defiened as a sustained IAP > 20 mmHg (with or without an APP < 60 mmHg) that is associated with new organ dysfunction or failure [13, 14].

        The phrase abdominal compartment syndrome was first used by Kron et al. [12] in the early 1980s to describe the physiologic effects of intra-abdominal hypertension complicating a ruptured aortic aneurysm surgery. However, most of our knowledge about this entity has evolved over the past few years [4, 5, 15].

        ACS can develop in both nonsurgical and surgical patients, either preoperatively or postoperatively. Although the incidence of the ACS was found to range between 5% and 15% of trauma patients [16], an increased IAP (18 mmHg) was observed in up to 41% of surgical patients [17]. ACS is most commonly diagnosed in patients sustaining abdominal or pelvic trauma, or suffering some other intra-abdominal hemorrhagic catastrophe. Less common etiologic factors include retroperitoneal hematoma or edema, bowel obstruction, ascites, and necrotizing pancreatitis [4, 18].

        Sustained elevation of intra-abdominal pressure causes increased intrathoracic pressure and abnormalities in pulmonary dynamics, increased afterload, decreased venous return, decreased cardiac output, and decreased perfusion to the kidneys and intestinal mucosa [1921].

        Early recognition and prompt intervention are essential to optimize a patient's outcome. The management and treatment of ACS is not difficult once the diagnosis is considered, but diagnosis is many times obscured in critically ill or shocked patients.

        Therefore, a high index of suspicion is needed in any patient who acutely develops tense abdominal distention combined with one or more of the following: decreased cardiac output, oliguria progressing to anuria, and respiratory failure with high ventilatory pressures.

        The diagnosis of IAH and ACS is dependent upon the accurate and frequent measurement of IAP. Recent prospective studies that evaluated the factors evolving IAH and ACS suggested that there is no specific type of patient or disease or treatment that reliable indicates when IAP needs to be measured, or when the measurement is not necessary in a mixed ICU population. Therefore, IAP should be routinely measured, for the initial overall evaluation of ICU patients [3].

        According to the consensus recommendations of the World Society of the ACS, a baseline IAP measurement should be obtained if two or more risk factors for IAH/ACS are present, and serial IAP measurements should be performed throughout the patient's critical illness, if IAH is present [14].

        To the best of our knowledge, no case of postoperative gastric dilatation causing ACS has been described. Mook et al. [22] described a case of ACS caused by distended stomach due to duodenal ulcer bleeding.

        Conclusion

        Deterioration of the patients' condition following a major abdominal surgery should raise a suspicion of gastric dilatation, especially in cases of distended abdomen, oliguria and increased airway pressures. Postoperative untreated gastric dilatation may cause abdominal compartment syndrome. Measurement of IAP should be done promptly in these patients. When increased IAP is present, the correct placement of the nasogastric tube must be carefully confirmed to avoid unnecessary surgery.

        Declarations

        Authors’ Affiliations

        (1)
        Department of Surgery A, Rambam Medical Center, and the Bruce Rappaport, Faculty of Medicine, Technion-Israel Institute of Technology

        References

        1. Johna S, Taylor E, Brown C, Zimmerman G: Abdominal compartment syndrome: dose intra-cystic pressure reflect actual intra-abdominal pressure? A prospective study in surgical patients. Crit Care 1999, 3:135–138.View ArticlePubMed
        2. Malbrain ML: Intra-abdominal pressure in the intensive care unit: clinical tool or toy? In Yearbook of intensive care and emergency medicine. Edited by: Vincent JL. Springer. Berlin Heidelberg New York; 2001:547–585.
        3. Malbrain ML, Chiumello D, Pelosi P, Wilmer A, Brienza N, Malcangi V, Bihari D, Innes R, Cohen J, Singer P, Japiassu A, Kurtop E, De Keulenaer BL, Daelemans R, Del Turco M, Cosimini P, Ranieri M, Jacquet L, Laterre PF, Gattinoni L: Prevalence of intra-abdominal hypertension in critically ill patients: a multicentre epidemiological study. Intensive care Med 2004, 30:822–829.View ArticlePubMed
        4. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL: Abdominal compartment syndrome. J Trauma 1998, 45:597–609.View ArticlePubMed
        5. Biffl WL, Moore EE, Burch JM, Offner PJ, Franciose RJ, Johnson JL: Secondary Abdominal compartment syndrome is a highly lethal event. Am J Surg 2001, 182:645–648.View ArticlePubMed
        6. Luca A, Cirera I, Garcia-Pagan JC, Feu F, Pizcueta P, Bosch J, Rodes J: Hemodynamic effects of acute changes in intra-abdominal pressure in patients with cirrhosis. Gastroenterology 1993, 104:222–227.PubMed
        7. Celoria G, Steingrub J, Dawson JA, Teres D: Oliguria from high intra-abdominal pressure secondary to ovarian mass. Crit Care Med 1987, 15:78–81.View ArticlePubMed
        8. Greenhalgh DG, Warden GD: The importance of intra-abdominal pressure measurements in burned children. J Trauma 1994, 36:685–690.View ArticlePubMed
        9. McSwain NE: Pneumatic antishock garment: State of the art 1998. Ann Emerg Med 1988, 17:506–525.View ArticlePubMed
        10. Morris JA, Eddy VA, Blinman TA, Rutherford EJ, Sharp KW: The staged celiotomy for trauma. Ann Surg 1993, 217:576–585.View ArticlePubMed
        11. Lenz RJ, Thomas TA, Wilkins DG: Cardiovascular changes during laparoscopy. Anesthesia 1976, 31:4–12.View Article
        12. Malbrain ML: Different techniques to measure intra-abdominal pressure (IAP): Time for a critical re-appraisal. Intensive Care Med 2004, 30:357–371.View ArticlePubMed
        13. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D'Amours S, Wendon J, Hillman K, Johansson K, Kolkman K, Wilmer A: Results from the international Conference of Experts on Intra-abdominal hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006,32(11):1722–1732.View ArticlePubMed
        14. Cheatham ML, Malbrain ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh Z, Leppäniemi A, Olvera C, Ivatury R, D'Amours S, Wendon J, Hillman K, Wilmer A: Results from the international Conference of Experts on Intra- abdominal hypertension and Abdominal Compartment Syndrome. II. Recommendations. Intensive Care Med 2007,33(6):951–962.View ArticlePubMed
        15. Ivatury RR, Diebel L, Porter JM, Simon RJ: Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 1997, 77:783–800.View ArticlePubMed
        16. Ertel W, Oberholzer A, Platz A, Stocker R, Trentz O: 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, 28:1747–1753.View ArticlePubMed
        17. Sugrue M, Jones F, Deane SA, Bishop G, Bauman A, Hillman K: Intra-abdominal hypertension is an independet cause of postoperative renal impairment. Arch Surg 1999, 134:1082–1085.View ArticlePubMed
        18. Burch JM, Moore EE, Moore FA, Franciose R: The abdominal compartment syndrome. Surg Clin North Am 1996, 76:833–842.View ArticlePubMed
        19. Schein M, Wittmann DH, Aprahamin CC, Condon RE: The abdominal compartment syndrome: the physiologic and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 1995, 180:745–753.PubMed
        20. Rasmussen IB, Berggren U, Arvidsson, Ljungdahl M, Haglund U: Effects of pneumopretoneum on splanchnic hemodynamics: an experimental study in pigs. Eur J Surg 1995, 161:819–826.PubMed
        21. Simon RJ, Friedlander MH, Ivatury RR, DiRaimo R, Machiedo GW: Hemorrhage lowers the threshold for intra-abdominal hypertension-induced pulmonary dysfunction. J Trauma 1997, 42:398–403. intra-abdominal pressure.View ArticlePubMed
        22. Mook W, Huslewe-Evers R, Ramsay G: Abdominal compartment syndrome. Lancet 2002, 360:1502.View ArticlePubMed

        Copyright

        © Mahajna et al. 2008

        This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://​creativecommons.​org/​licenses/​by/​2.​0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

        Advertisement