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Original article – OA 20
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND? G. Plantefeve, R. Hellmann, O. Pajot, M. Thirion, G. Bleichner, H. Mentec Key words: intra-abdominal hypertension, abdominal compartment syndrome, intraabdominal sepsis, peritonitis, ICU
ABSTRACT Background: Abdominal compartment syndrome and intra-abdominal hypertension are frequently associated with peritonitis. The aim of this study is to establish the relationship between intraabdominal hypertension and intra-abdominal sepsis especially in critically ill patients. Methods: Relevant information was identified through a Medline search (1966-October 2006). The terms used were “intra-abdominal sepsis”, “peritonitis”, “abdominal compartment syndrome”, “intra-abdominal hypertension” and “relaparotomy for sepsis”. The search was limited to English- and French-language publications. Results: Only a few clinical trials exist on this specific topic. Further investigations are required to define the incidence of intra-abdominal hypertension in intra-abdominal sepsis, and the prognostic impact of this setting and finally the potential
––––––––––––––– Réanimation Polyvalente, Hôpital Victor Dupouy, Argenteuil, France Address for correspondence: Dr. Gaëtan Plantefeve Service de Réanimation Polyvalente Centre Hospitalier Victor Dupouy 69, rue du Lieutenant Colonel Prudhon 95100 Argenteuil France Tel: +33 1 34 23 14 45 & +33 1 34 23 25 50 Fax: +33 1 34 23 27 91 E-mail: [email protected]
Acta Clinica Belgica, 2007; 62-Supplement 1
specific treatment. Abdominal compartment syndrome is more likely linked to the abdominal surgery than to peritonitis itself. Conclusion: Intra-abdominal pressure monitoring can be valuable in critically ill patients with suspicion of persisting intra-abdominal sepsis after surgical peritonitis treatment.
INTRODUCTION The increase of intra-abdominal pressure (IAP) above 12 mmHg defines intra-abdominal hypertension (IAH) (1). Abdominal compartment syndrome (ACS) is a lifethreatening condition defined as a combination of this abnormal increase in IAP with at least one new organ failure (2). Different mechanisms may be involved in the IAP elevation. Abdominal or pelvic trauma are most commonly associated with IAH and ACS, but less common causes such as space-occupying lesions as neoplasms, obstructed intestines with distension or retroperitoneal edema may also be involved. Finally, peritonitis and intra-abdominal sepsis can influence the IAP, because of bowel distension, ascites or parietal muscle contraction. The aim of this study was to review the literature in order to determine the relationship between intra-abdominal sepsis and IAH or ACS. We focused on four questions: 1) Do IAH or ACS occur in peritonitis before surgery? 2) Does a specific risk for IAH exist in this population after surgery? 3) How can the increased IAP be explained in this setting? Finally, 4) what are the consequences of IAH for patients with peritonitis?
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND?
METHODS
HOW CAN PERITONITIS BE A CAUSE OF IAH/ACS
Relevant studies were retrieved from Medline. The search was performed using the terms “intra-abdominal sepsis”, “peritonitis”, “abdominal compartment syndrome”, “intra-abdominal hypertension” and “relaparotomy for sepsis”, and studies published between January 1966 though October 2006 were included in the analysis. The search was limited to English-language and French-language publications.
According to the abundant literature and reinforced by the recent International Consensus of the World Society of Abdominal Compartment Syndrome (WSACS), intra-abdominal sepsis is one of the risk factors for IAH (2). The most common circumstance for increased IAP seems to be in cases in which patients require large amounts of fluid and have undergone extensive intra-abdominal dissection. The infectious process is localized in the abdominal cavity (primary ACS) and many factors could participate to the increased IAP: ascites, localized or multiple abscesses, ileus and bowel distension, visceral edema or pancreatitis (2). Faecal contamination or peritonitis may lead to even more inflammation and, therefore, edema in the peritoneal space. Although no clinical or animal study has demonstrated that any of these factors has a predominant effect that could lead to ACS, it seems obvious from clinical practice that these factors may be involved. However, the cumulative effects are probably responsible for elevated IAP: these factors undoubtedly are partly responsible for elevated IAP, but in the individual patient, the importance can be different. On the other hand, peritonitis remains an important cause of severe sepsis en septic shock. The resuscitation of septic shock requires massive fluid perfusion as described in secondary ACS (2). As reported in trauma patients, we can logically extrapolate that vascular expansion increases visceral edema and decreases abdominal wall compliance (13). The gut is particularly susceptible to global ischemia and shock-induced low-flow states with severe local and distant effects. Bowel ischemia followed by reperfusion leads to increased microvascular permeability resulting in bowel edema. In the presence of IAH, gut dysfunction resulting in bacterial translocation may play an important role in the development multiple organ failure in critically ill patients. Delayed intestinal transit, increased permeability, and decreased epithelial resistance can also contribute to gut edema formation even without mucosal ischemia/reperfusion (14). Experimentally, a slight increase in IAP to 12 mmHg is able to create microvascular disorders and capillary edema (15). A prospective study was recently performed in 73 patients already operated for major abdominal surgery (16). Patients with decreased gastric intramucosal pH (pHi) lower than 7.32 had more frequently IAH and abdominal sepsis. No relationship could be found between these last two parameters. However, the strong association between IAP and pHi suggests mucosal
RESULTS Numerous reviews described peritonitis or intraabdominal sepsis as causes of ACS (3). In a survey conducted among American trauma surgeons, the authors reported that peritonitis or faecal contamination were factors associated with the development of elevated IAP or ACS (4). A few years later, the American survey performed among members of the Society of Critical Care Medicine (SCCM) confirmed this (5), and intra-abdominal sepsis was listed as a clinical cause of IAH or ACS. In a small cohort of 8 patients suffering from ACS, one patient develops ACS in a context of peritonitis and intra-abdominal haemorrhage (6). In a prospective study in a trauma centre in Denver, Meldrum et al report 14% of ACS (21 patients among 145 patients requiring laparotomy). Among them, 11 suffered from ACS due to digestive tract injury with bowel perforation (7). In a large cohort of 1190 surgical admissions, 19 ACS are identified but no patient has intra-abdominal sepsis (8). In the largest prospective study on IAH, 36 patients suffer from abdominal infection among the 265 patients studied (9). Unfortunately, the authors did not provide the exact number of patients who developed IAH or ACS. Among 97 patients included in a multicentre prospective study on IAH prevalence in ICU, 10 (10.3%) had abdominal infection (10). Among these ten patients, eight patients had IAP over 12 mmHg. Therefore, in the literature, peritonitis as a cause of ACS appears to be only of minor importance. One explanation is the underestimation of IAH/ ACS associated with intra-abdominal sepsis (11). In a study of yeast peritonitis, Dupont et al noted that IAP was not monitored routinely (12), and no specific article focused on this topic. The exact incidence of IAH or ACS in patients undergoing surgery for intra-abdominal infections and peritonitis is unknown.
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splanchnic hypoperfusion caused by IAH. The impaired intestinal barrier function may result from splanchnic ischemia. Many patients with peritonitis develop increased abdominal wall rigidity. The increase in abdominal wall muscular tone may be voluntary in response to or in anticipation of the abdominal examination or involuntary because of the peritoneal irritation. Interestingly, one could expect that the IAP increase is due to this parietal rigidity, however this hypothesis remains to be elucidated. The efficacy of muscular blocking agents to resolve ACS strengthens this hypothesis (17). In the clinical presentation of peritonitis, the abdomen is often distended. Acute tension pneumoperitoneum can occur in case of bowel perforation, which could lead to IAH in a similar way as the pneumoperitoneum during laparoscopy (18). Peritonitis is associated with hypoactive or absent bowel sounds. This finding reflects a generalized ileus. In Ogilvie’s syndrome or bowel occlusion, IAH has also been reported (19). In case of intra-abdominal abscesses, the consequences on IAP are not clear. The slow, progressive increase in volume of the abscess possibly doesn’t increase the IAP. As reported in chronic IAH, the pressure increases but probably not to levels that can induce ACS (2).
CLINICAL PRESENTATION OF ACS IN THE CONTEXT OF PERITONITIS In peritonitis, septic shock is usually associated with renal, respiratory and coagulation dysfunctions. Especially in ICU patients, the inflammatory response and the bacterial infection itself can mimic the clinical signs of ACS. In a small cohort of five cases, Williams reports a very demonstrative case (20). A young man is hospitalized for trauma, and fifteen days postoperative after primary splenectomy and fractures repair, the patient develops oliguria, hyperlactatemia, and increased white blood cells count. With an IAP measured of 42 mmHg, ACS is diagnosed. The relaparotomy found a faecal peritonitis due to perforated sigmoid colon. It is very difficult to conclude on the temporal relationship between clinical course and ACS. Both the peritonitis and the ACS may be revealed by organ failure and abdominal distension as in this case. The first diagnosis here is probably the peritonitis before ACS. In many ICU patients, the diagnosis of ACS may not be coined because bladder pressure is seldom measured, despite the fact that surgical critical care physicians were aware of the
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problem (5). Finally, the need for surgery can treat the two syndromes at the same time: peritonitis and ACS. Except for patients treated with laparoscopy, the preoperative diagnosis of ACS associated with peritonitis seems futile. However, during the postoperative period, the situation is markedly different. The worsening of the physiological status has been described on the first postoperative day after surgical treatment for peritonitis (21). However, when organ failure persists, the questions of an ongoing intra-abdominal sepsis (new or unknown bowel perforation, necrosis or abscesses) and the need for relaparotomy should be considered. In these patients, IAP monitoring should be standard of care. During the postoperative period after surgical treatment of peritonitis, the IAP can increase from 12 mmHg to 19 mmHg (22). The ACS may worsen the prognosis of peritonitis in this setting, however actually no data are available to support this hypothesis. A small clinical study described four cases of postoperative abdominal re-exploration, none of which had intra-abdominal sepsis (23). However, the authors suggest the use of the IAP value as a criterion for abdominal re-exploration. In another small study on five collected cases, IAP is used to decide to re-explore the abdominal cavity (20). Two patients had intra-abdominal sepsis discovered during the laparotomy. The first report of a prospective study (just published as an abstract) used IAP as predictive factor for persistent intra-abdominal sepsis after peritonitis (24). With a small sample size (37 patients), an IAP threshold of 12 mmHg had a positive predictive value of 80% to detect ongoing intra-abdominal sepsis. Hence elevated IAP can point to peritonitis, this is especially relevant in sedated critically ill patients. A larger multicenter study on peritonitis and IAH/ACS is required. A recent study demonstrated that planned relaparotomy for treatment of severe intra-abdominal infection was better than on-demand for two reasons: better efficiency to eradicate infection and prevention of postoperative ACS (22). Sixty five patients were prospectively included in two hospitals (31 planned relaparotomy and 34 on-demand relaparotomy). Daily monitoring of IAP with bladder pressure was performed. IAH occurred in both groups. The IAP reached 19.2 ± 5.2 mmHg in the on-demand group and 12.4 ± 4.6 mmHg in the planned group (p=0.009). The mortality was significantly increased in the on-demand group (58.8% versus 29%, p=0.024). After adjustment for severity score (APACHE II) and sex, the relative risk of an on demand approach for mortality becomes nonsignificant (RR, 1.79; p=0.178). Because this study was not
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND?
randomized and because the result was not adjusted to IAP, it is impossible to conclude on the impact of IAH on mortality. However, it is interesting to note the large difference of IAP values between the groups. An explanation can be that the planned relaparotomy prevents an increase in IAP. However, the superiority of planned relaparotomy has not been proven, and the results of the above mentioned study are not very convincing. The difference may lie in the use of an open abdomen treatment, which may be more frequent, or the fact that postoperative fluid collections are drained more adequately in the planned relaparotomy group. Previous studies also reported more complications in planned relaparotomy patients.
IAH AS A RISK FACTOR FOR INTRAABDOMINAL SEPSIS The International Consensus reports intra-abdominal infection, abscesses, and peritonitis as risk factors for IAH and/or ACS (2). No study clearly demonstrates a relationship between IAH/ACS and induction of peritonitis. However, two major points must be noted. First, experimental studies argue for an increased alteration of gut microcirculation (16, 25). In a rat model of IAH, Kologlu et al explore the impacts of faecal peritonitis compared to gradually increased IAP (4 to 18 mmHg) (26). The healing of colonic anastomoses is comparable between IAH and faecal peritonitis. Secondly, experimental studies in animals demonstrate an increased risk of bacterial translocation from the intestinal tract when IAH occurs (27, 28). The bacterial translocation may participate to intra-abdominal infection (29).
CONSEQUENCES OF IAH/ACS IN INTRAABDOMINAL SEPSIS In experimental literature, few specific models study the association between intra-abdominal sepsis and IAH or ACS (30, 31). Because the best surgical technique for peritonitis treatment (laparotomy versus laparoscopy) still remains subject to debate, surgeons use animal models to explore the impact of carbon dioxide pneumoperitoneum. According to this literature, ACS may worsen the clinical course of abdominal sepsis especially when the decompression is delayed and probably when the IAH is high and remains high for a
longer period of time (31, 32). In a rat model with gastric perforation-induced peritonitis, a slight increase in IAP (4mmHg) was induced with carbon dioxide 12h after the perforation and lasting for 60 minutes (33). Despite this, the mesothelial cells of parietal peritoneum suffered from premature distortion and disintegration on scanning electronic-microscopic analysis. Previously, an increased severity of peritonitis related to gastric perforation and caecostomy has been demonstrated after carbon dioxide pneumoperitoneum in rat (32, 34). In a rabbit model, Gurtner et al compared one group with peritoneal inoculation of bacteria alone, one group with bacterial peritonitis and IAH (12 mmHg during one hour) and a last group with IAH alone (30). Probably because the level of IAP was low and maintained for only a short period of time, bacteraemia, endotoxaemia, mean arterial pressure and heart rate were similar for peritonitis alone or combined with IAH. Similarly, when pneumoperitoneum is maintained for one hour, at a level of 15 mmHg with helium or carbon dioxide, no difference was reported in inflammatory response according to white blood count, C-reactive protein, TNF and bacteraemia (35). Balci et al apply an IAP of 25 mmHg on rats with intra-abdominal sepsis (107 E.coli injected intraperitoneally) (31). All clinical parameters worsened when IAH was applied: decreased peripheral oxygen saturation, increased heart rate and increased body temperature. In all these models, the IAH was not maintained for many hours after the intraabdominal infection but only for a short period of time. This resembles more a laparoscopic procedure than the IAH related with intraabdominal sepsis. In clinical practice, ACS becomes only apparent at higher levels of IAP than reported experimentally. In these animal models, the IAH induced by a pneumoperitoneum with carbon dioxide only reflects the surgical procedure but not all the other causes leading to IAH (ascites, ischemia/reperfusion, bowel distension and edema).
SPECIFIC TREATMENT FOR PERITONITIS ASSOCIATED WITH ACS The surgical management of peritonitis is based on three principles: elimination of the source of infection, reduction of bacterial inoculum in the peritoneal cavity and finally prevention of persistent or recurrent intraabdominal infection. Some authors consider that another principle is also an important objective: avoid postoperative IAH and ACS, therefore decompression
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should be included in the source control concept (22). As APP is reduced in case of IAH/ACS, it is logical to say that intestinal anastomoses are at risk for hypoperfusion, which may lead to perforation at a later stage. Therefore an open abdomen treatment should be considered in critically ill patients (e.g. high APACHE scores) at laparotomy, as these may be at risk for subsequent IAH/ACS. The prevention of postoperative IAH/ACS is possible if parietal tension is avoided. Specific techniques can be used as delayed fascia closure or absorbable mesh prosthesis (36). Enterostomy can be performed even with temporary abdominal closure as sterile intravenous bag (“Bogota bag”) (37).
8.
9.
10.
11.
12.
CONCLUSIONS 13.
Presumably because of a lack of general clinical awareness and because of the severity of peritonitis itself, clinical data on IAH and ACS during intra-abdominal sepsis are scarce. Many questions remain unsolved: is intraabdominal sepsis commonly associated with IAH? Should IAP be monitored in all patients with abdominal sepsis? What is the best and safe treatment for patients with IAH? Is IAH an indication for relaparotomy? Further investigations are definitely required, but it seems that IAH and abdominal sepsis are two of a kind…
REFERENCES 1. Malbrain ML, Deeren D, De Potter TJ. Intra-abdominal hypertension in the critically ill: it is time to pay attention. Curr Opin Crit Care. 2005; 11: 156-71. 2. Malbrain M, Cheatham ML, Kirkpatrick AW, et al. Results from the International Conference of Experts on Intra-Abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med. 2006; 32: 1722-32. 3. Schulman C. Abdominal compartment syndrome mimicking sepsis. Infect Med. 2000; 17: 746- 57. 4. Mayberry J, Goldman R, Mullins R, Brand D, Crass R, Trunkey D. Surveyed opinion of American trauma surgeons on the prevention of the abdominal compartment syndrome. J Trauma. 1999; 47: 509-14. 5. Kimball D, Rollins M, Mone M, et al. Survey of intensive care physicians on the recognition and management of intra-abdominal hypertension and abdominal compartment syndrome. Crit Care Med. 2006; 34: 2340-8. 6. Cullen D, Coyle J, Teplick R, Long M. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989; 17: 118-21. 7. Meldrum DR, Moore FA, Moore EE, Franciose RJ, Sauaia A, Burch JM. Prospective characterization and selective management of
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the abdominal compartment syndrome. Am J Surg. 1997; 174: 667-72; discussion 672-3. McNelis J, Soffer S, Marini CP, et al. Abdominal compartment syndrome in the surgical intensive care unit. Am Surg. 2002; 68: 18-23. Malbrain ML, Chiumello D, Pelosi P, 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: 315-22. Malbrain ML, Chiumello D, Pelosi P, et al. Prevalence of intraabdominal hypertension in critically ill patients: a multicentre epidemiological study. Intensive Care Med. 2004; 30: 822-9. Marvin R, McKinley B, McQuiggan M, Cocanour C, Moore AF. Nonocclusive bowel necrosis occurring in critically ill trauma patients receiving enteral nutrition manifests no reliable clinical signs for early detection. Am J Surg. 2000; 179: 7-12. Dupont H, Bourichon A, Paugam-Burtz C, Mantz J, Desmonts J. Can yeast isolation in peritoneal fluid be predicted in intensive care unit patients with peritonitis. Crit Care Med. 2003; 31: 7527. McNelis J, Marini CP, Jurkiewicz A, et al. Predictive factors associated with the development of abdominal compartment syndrome in the surgical intensive care unit. Arch Surg. 2002; 137: 133-6. Moore-Olufemi S, Xue H, Attuwaybi B, et al. Resuscitation-induced gut edema and intestinal dysfunction. J Trauma. 2005; 58: 264-70. Samel ST, Neufang T, Mueller A, Leister I, Becker H, Post S. A new abdominal cavity chamber to study the impact of increased intraabdominal pressure on microcirculation of gut mucosa by using video microscopy in rats. Crit Care Med. 2002; 30: 1854-8. Sugrue M, Jones F, Lee A, et al. Intraabdominal pressure and gastric intramucosal pH: is there an association? World J Surg. 1996; 20: 988-91. De Waele JJ, Benoit D, Hoste E,Colardyn F. A role for muscle relaxation in patients with abdominal compartment syndrome? Intensive Care Med. 2003; 29: 332. Fraipont V, Lambermont B, Ghaye B, et al. Unsual complication after percutaneous dilatational tracheostomy: pneumoperitoneum with abdominal compartment syndrome. Intensive Care Med. 1999; 25: 1334-5. Gorecki P, Kessler E, Schein M. Abdominal compartment syndrome from intractable constipation. J Am Coll Surg. 2000; 190: 371. Williams M, Simms HH. Abdominal compartment syndrome: case reports and implications for management in critically ill patients. Am Surg. 1997; 63: 555-8. Paugam-Burtz C, Dupont H, Marmuse J, et al. Daily organ-system failure for diagnosis of persistent intra-abdominal sepsis after postoperative peritonitis. Intensive Care Med. 2002; 28: 594-8. Rakic M, Popovic D, Rakic M, et al. Comparison of on-demand vs planned relaparotomy for treatment of severe intra-abdominal infections. Croat Med J. 2005; 46: 957-63. Kron IL, Harman PK, Nolan SP. The measurement of intra-abdominal pressure as a criterion for abdominal re-exploration. Ann Surg. 1984; 199: 28-30. Plantefeve G, Lasocki S, Khaleq K, et al. La pression intra-abdominale permet-elle de prédire un sepsis intra-abdominal persistant après péritonite sévère? Réanimation. 2005; 14: S129.
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND?
25. Schwarte LA, Scheeren TW, Lorenz C, De Bruyne F, Fournell A. Moderate increase in intraabdominal pressure attenuates gastric mucosal oxygen saturation in patients undergoing laparoscopy. Anesthesiology. 2004; 100: 1081-7. 26. Kologlu M, Sayek I, Kologlu LB, Onat D. Effect of persistently elevated intraabdominal pressure on healing of colonic anastomoses. Am J Surg. 1999; 178: 293-7. 27. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome. J Trauma. 1997; 43: 852-5. 28. Gargiulo NJ, 3rd, Simon RJ, Leon W, Machiedo GW. Hemorrhage exacerbates bacterial translocation at low levels of intra-abdominal pressure. Arch Surg. 1998; 133: 1351-5. 29. Widdison A, Karanjia N, Reber H. Routes of spread of pathogens into the pancreas in a feline model of acute pancreatitis. Gut. 1994; 35: 1306-10. 30. Gurtner G, Robertson C, Chung S, Ling T, Ip S, Li A. Effect of carbon dioxide pneumoperitoneum on bacteraemia and endotoxaemia in an animal model of peritonitis. Br J Surg. 1995; 82: 844-8. 31. Balci C, Akbulut G, Karabekir H, Karagoz F, Sungurtekin H. Comparison of SPO2, heart rate and body temperature values in abdominal compartment syndrome in a rat model with intraabdominal sepsis and intraabdominl hypertension. Saudi Med J. 2006; 27: 1254-7.
32. Bloechle C, Emmermann A, Treu H, et al. Effect of pneumoperitoneum on the extent and severity of peritonitis induced by gastric ulcer perforation in the rat. Surg Endosc. 1995; 9: 989901. 33. Bloechle C, Kluth D, Holstein A, et al. A pneumoperitoneum perpetuates severe damage to the ultrastructural integrity of parietal peritoneum in gastric perforation-induced peritonitis in rats. Surg Endosc. 1999; 13: 683-8. 34. Ipek T, Paksoy M, Colak T, Polat E, Uygun N. Effects of carbon dioxide pneumoperitoneum on bacteremia and severity of peritonitis in an experimental model. Surg Endosc. 1998; 12: 432-5. 35. Clary E, Bruch S, Lau C, et al. Effects of pneumoperitoneum on hemodynamic and systemic immunologic responses to peritonitis in pigs. J Surg Res. 2002; 108: 32-8. 36. Mayberry J, Mullins R, Crass R, Trunkey D. Prevention of abdominal compartment syndrome by absorbable mesh prosthesis closure. Arch Surg. 1997; 132: 957-62. 37. Alfici R, Ashkenazi I, Kessel B, Zut N, Sternberg A. Temporary bowel diversion using the Bogota bag (Hadera stoma): technical details. J Am Coll Surg. 2004; 199: 344-6.
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Original article – OA 20
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND? G. Plantefeve, R. Hellmann, O. Pajot, M. Thirion, G. Bleichner, H. Mentec Key words: intra-abdominal hypertension, abdominal compartment syndrome, intraabdominal sepsis, peritonitis, ICU
ABSTRACT Background: Abdominal compartment syndrome and intra-abdominal hypertension are frequently associated with peritonitis. The aim of this study is to establish the relationship between intraabdominal hypertension and intra-abdominal sepsis especially in critically ill patients. Methods: Relevant information was identified through a Medline search (1966-October 2006). The terms used were “intra-abdominal sepsis”, “peritonitis”, “abdominal compartment syndrome”, “intra-abdominal hypertension” and “relaparotomy for sepsis”. The search was limited to English- and French-language publications. Results: Only a few clinical trials exist on this specific topic. Further investigations are required to define the incidence of intra-abdominal hypertension in intra-abdominal sepsis, and the prognostic impact of this setting and finally the potential
––––––––––––––– Réanimation Polyvalente, Hôpital Victor Dupouy, Argenteuil, France Address for correspondence: Dr. Gaëtan Plantefeve Service de Réanimation Polyvalente Centre Hospitalier Victor Dupouy 69, rue du Lieutenant Colonel Prudhon 95100 Argenteuil France Tel: +33 1 34 23 14 45 & +33 1 34 23 25 50 Fax: +33 1 34 23 27 91 E-mail: [email protected]
Acta Clinica Belgica, 2007; 62-Supplement 1
specific treatment. Abdominal compartment syndrome is more likely linked to the abdominal surgery than to peritonitis itself. Conclusion: Intra-abdominal pressure monitoring can be valuable in critically ill patients with suspicion of persisting intra-abdominal sepsis after surgical peritonitis treatment.
INTRODUCTION The increase of intra-abdominal pressure (IAP) above 12 mmHg defines intra-abdominal hypertension (IAH) (1). Abdominal compartment syndrome (ACS) is a lifethreatening condition defined as a combination of this abnormal increase in IAP with at least one new organ failure (2). Different mechanisms may be involved in the IAP elevation. Abdominal or pelvic trauma are most commonly associated with IAH and ACS, but less common causes such as space-occupying lesions as neoplasms, obstructed intestines with distension or retroperitoneal edema may also be involved. Finally, peritonitis and intra-abdominal sepsis can influence the IAP, because of bowel distension, ascites or parietal muscle contraction. The aim of this study was to review the literature in order to determine the relationship between intra-abdominal sepsis and IAH or ACS. We focused on four questions: 1) Do IAH or ACS occur in peritonitis before surgery? 2) Does a specific risk for IAH exist in this population after surgery? 3) How can the increased IAP be explained in this setting? Finally, 4) what are the consequences of IAH for patients with peritonitis?
ABDOMINAL COMPARTMENT SYNDROME AND INTRAABDOMINAL SEPSIS: TWO OF THE SAME KIND?
METHODS
HOW CAN PERITONITIS BE A CAUSE OF IAH/ACS
Relevant studies were retrieved from Medline. The search was performed using the terms “intra-abdominal sepsis”, “peritonitis”, “abdominal compartment syndrome”, “intra-abdominal hypertension” and “relaparotomy for sepsis”, and studies published between January 1966 though October 2006 were included in the analysis. The search was limited to English-language and French-language publications.
According to the abundant literature and reinforced by the recent International Consensus of the World Society of Abdominal Compartment Syndrome (WSACS), intra-abdominal sepsis is one of the risk factors for IAH (2). The most common circumstance for increased IAP seems to be in cases in which patients require large amounts of fluid and have undergone extensive intra-abdominal dissection. The infectious process is localized in the abdominal cavity (primary ACS) and many factors could participate to the increased IAP: ascites, localized or multiple abscesses, ileus and bowel distension, visceral edema or pancreatitis (2). Faecal contamination or peritonitis may lead to even more inflammation and, therefore, edema in the peritoneal space. Although no clinical or animal study has demonstrated that any of these factors has a predominant effect that could lead to ACS, it seems obvious from clinical practice that these factors may be involved. However, the cumulative effects are probably responsible for elevated IAP: these factors undoubtedly are partly responsible for elevated IAP, but in the individual patient, the importance can be different. On the other hand, peritonitis remains an important cause of severe sepsis en septic shock. The resuscitation of septic shock requires massive fluid perfusion as described in secondary ACS (2). As reported in trauma patients, we can logically extrapolate that vascular expansion increases visceral edema and decreases abdominal wall compliance (13). The gut is particularly susceptible to global ischemia and shock-induced low-flow states with severe local and distant effects. Bowel ischemia followed by reperfusion leads to increased microvascular permeability resulting in bowel edema. In the presence of IAH, gut dysfunction resulting in bacterial translocation may play an important role in the development multiple organ failure in critically ill patients. Delayed intestinal transit, increased permeability, and decreased epithelial resistance can also contribute to gut edema formation even without mucosal ischemia/reperfusion (14). Experimentally, a slight increase in IAP to 12 mmHg is able to create microvascular disorders and capillary edema (15). A prospective study was recently performed in 73 patients already operated for major abdominal surgery (16). Patients with decreased gastric intramucosal pH (pHi) lower than 7.32 had more frequently IAH and abdominal sepsis. No relationship could be found between these last two parameters. However, the strong association between IAP and pHi suggests mucosal
RESULTS Numerous reviews described peritonitis or intraabdominal sepsis as causes of ACS (3). In a survey conducted among American trauma surgeons, the authors reported that peritonitis or faecal contamination were factors associated with the development of elevated IAP or ACS (4). A few years later, the American survey performed among members of the Society of Critical Care Medicine (SCCM) confirmed this (5), and intra-abdominal sepsis was listed as a clinical cause of IAH or ACS. In a small cohort of 8 patients suffering from ACS, one patient develops ACS in a context of peritonitis and intra-abdominal haemorrhage (6). In a prospective study in a trauma centre in Denver, Meldrum et al report 14% of ACS (21 patients among 145 patients requiring laparotomy). Among them, 11 suffered from ACS due to digestive tract injury with bowel perforation (7). In a large cohort of 1190 surgical admissions, 19 ACS are identified but no patient has intra-abdominal sepsis (8). In the largest prospective study on IAH, 36 patients suffer from abdominal infection among the 265 patients studied (9). Unfortunately, the authors did not provide the exact number of patients who developed IAH or ACS. Among 97 patients included in a multicentre prospective study on IAH prevalence in ICU, 10 (10.3%) had abdominal infection (10). Among these ten patients, eight patients had IAP over 12 mmHg. Therefore, in the literature, peritonitis as a cause of ACS appears to be only of minor importance. One explanation is the underestimation of IAH/ ACS associated with intra-abdominal sepsis (11). In a study of yeast peritonitis, Dupont et al noted that IAP was not monitored routinely (12), and no specific article focused on this topic. The exact incidence of IAH or ACS in patients undergoing surgery for intra-abdominal infections and peritonitis is unknown.
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splanchnic hypoperfusion caused by IAH. The impaired intestinal barrier function may result from splanchnic ischemia. Many patients with peritonitis develop increased abdominal wall rigidity. The increase in abdominal wall muscular tone may be voluntary in response to or in anticipation of the abdominal examination or involuntary because of the peritoneal irritation. Interestingly, one could expect that the IAP increase is due to this parietal rigidity, however this hypothesis remains to be elucidated. The efficacy of muscular blocking agents to resolve ACS strengthens this hypothesis (17). In the clinical presentation of peritonitis, the abdomen is often distended. Acute tension pneumoperitoneum can occur in case of bowel perforation, which could lead to IAH in a similar way as the pneumoperitoneum during laparoscopy (18). Peritonitis is associated with hypoactive or absent bowel sounds. This finding reflects a generalized ileus. In Ogilvie’s syndrome or bowel occlusion, IAH has also been reported (19). In case of intra-abdominal abscesses, the consequences on IAP are not clear. The slow, progressive increase in volume of the abscess possibly doesn’t increase the IAP. As reported in chronic IAH, the pressure increases but probably not to levels that can induce ACS (2).
CLINICAL PRESENTATION OF ACS IN THE CONTEXT OF PERITONITIS In peritonitis, septic shock is usually associated with renal, respiratory and coagulation dysfunctions. Especially in ICU patients, the inflammatory response and the bacterial infection itself can mimic the clinical signs of ACS. In a small cohort of five cases, Williams reports a very demonstrative case (20). A young man is hospitalized for trauma, and fifteen days postoperative after primary splenectomy and fractures repair, the patient develops oliguria, hyperlactatemia, and increased white blood cells count. With an IAP measured of 42 mmHg, ACS is diagnosed. The relaparotomy found a faecal peritonitis due to perforated sigmoid colon. It is very difficult to conclude on the temporal relationship between clinical course and ACS. Both the peritonitis and the ACS may be revealed by organ failure and abdominal distension as in this case. The first diagnosis here is probably the peritonitis before ACS. In many ICU patients, the diagnosis of ACS may not be coined because bladder pressure is seldom measured, despite the fact that surgical critical care physicians were aware of the
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problem (5). Finally, the need for surgery can treat the two syndromes at the same time: peritonitis and ACS. Except for patients treated with laparoscopy, the preoperative diagnosis of ACS associated with peritonitis seems futile. However, during the postoperative period, the situation is markedly different. The worsening of the physiological status has been described on the first postoperative day after surgical treatment for peritonitis (21). However, when organ failure persists, the questions of an ongoing intra-abdominal sepsis (new or unknown bowel perforation, necrosis or abscesses) and the need for relaparotomy should be considered. In these patients, IAP monitoring should be standard of care. During the postoperative period after surgical treatment of peritonitis, the IAP can increase from 12 mmHg to 19 mmHg (22). The ACS may worsen the prognosis of peritonitis in this setting, however actually no data are available to support this hypothesis. A small clinical study described four cases of postoperative abdominal re-exploration, none of which had intra-abdominal sepsis (23). However, the authors suggest the use of the IAP value as a criterion for abdominal re-exploration. In another small study on five collected cases, IAP is used to decide to re-explore the abdominal cavity (20). Two patients had intra-abdominal sepsis discovered during the laparotomy. The first report of a prospective study (just published as an abstract) used IAP as predictive factor for persistent intra-abdominal sepsis after peritonitis (24). With a small sample size (37 patients), an IAP threshold of 12 mmHg had a positive predictive value of 80% to detect ongoing intra-abdominal sepsis. Hence elevated IAP can point to peritonitis, this is especially relevant in sedated critically ill patients. A larger multicenter study on peritonitis and IAH/ACS is required. A recent study demonstrated that planned relaparotomy for treatment of severe intra-abdominal infection was better than on-demand for two reasons: better efficiency to eradicate infection and prevention of postoperative ACS (22). Sixty five patients were prospectively included in two hospitals (31 planned relaparotomy and 34 on-demand relaparotomy). Daily monitoring of IAP with bladder pressure was performed. IAH occurred in both groups. The IAP reached 19.2 ± 5.2 mmHg in the on-demand group and 12.4 ± 4.6 mmHg in the planned group (p=0.009). The mortality was significantly increased in the on-demand group (58.8% versus 29%, p=0.024). After adjustment for severity score (APACHE II) and sex, the relative risk of an on demand approach for mortality becomes nonsignificant (RR, 1.79; p=0.178). Because this study was not
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randomized and because the result was not adjusted to IAP, it is impossible to conclude on the impact of IAH on mortality. However, it is interesting to note the large difference of IAP values between the groups. An explanation can be that the planned relaparotomy prevents an increase in IAP. However, the superiority of planned relaparotomy has not been proven, and the results of the above mentioned study are not very convincing. The difference may lie in the use of an open abdomen treatment, which may be more frequent, or the fact that postoperative fluid collections are drained more adequately in the planned relaparotomy group. Previous studies also reported more complications in planned relaparotomy patients.
IAH AS A RISK FACTOR FOR INTRAABDOMINAL SEPSIS The International Consensus reports intra-abdominal infection, abscesses, and peritonitis as risk factors for IAH and/or ACS (2). No study clearly demonstrates a relationship between IAH/ACS and induction of peritonitis. However, two major points must be noted. First, experimental studies argue for an increased alteration of gut microcirculation (16, 25). In a rat model of IAH, Kologlu et al explore the impacts of faecal peritonitis compared to gradually increased IAP (4 to 18 mmHg) (26). The healing of colonic anastomoses is comparable between IAH and faecal peritonitis. Secondly, experimental studies in animals demonstrate an increased risk of bacterial translocation from the intestinal tract when IAH occurs (27, 28). The bacterial translocation may participate to intra-abdominal infection (29).
CONSEQUENCES OF IAH/ACS IN INTRAABDOMINAL SEPSIS In experimental literature, few specific models study the association between intra-abdominal sepsis and IAH or ACS (30, 31). Because the best surgical technique for peritonitis treatment (laparotomy versus laparoscopy) still remains subject to debate, surgeons use animal models to explore the impact of carbon dioxide pneumoperitoneum. According to this literature, ACS may worsen the clinical course of abdominal sepsis especially when the decompression is delayed and probably when the IAH is high and remains high for a
longer period of time (31, 32). In a rat model with gastric perforation-induced peritonitis, a slight increase in IAP (4mmHg) was induced with carbon dioxide 12h after the perforation and lasting for 60 minutes (33). Despite this, the mesothelial cells of parietal peritoneum suffered from premature distortion and disintegration on scanning electronic-microscopic analysis. Previously, an increased severity of peritonitis related to gastric perforation and caecostomy has been demonstrated after carbon dioxide pneumoperitoneum in rat (32, 34). In a rabbit model, Gurtner et al compared one group with peritoneal inoculation of bacteria alone, one group with bacterial peritonitis and IAH (12 mmHg during one hour) and a last group with IAH alone (30). Probably because the level of IAP was low and maintained for only a short period of time, bacteraemia, endotoxaemia, mean arterial pressure and heart rate were similar for peritonitis alone or combined with IAH. Similarly, when pneumoperitoneum is maintained for one hour, at a level of 15 mmHg with helium or carbon dioxide, no difference was reported in inflammatory response according to white blood count, C-reactive protein, TNF and bacteraemia (35). Balci et al apply an IAP of 25 mmHg on rats with intra-abdominal sepsis (107 E.coli injected intraperitoneally) (31). All clinical parameters worsened when IAH was applied: decreased peripheral oxygen saturation, increased heart rate and increased body temperature. In all these models, the IAH was not maintained for many hours after the intraabdominal infection but only for a short period of time. This resembles more a laparoscopic procedure than the IAH related with intraabdominal sepsis. In clinical practice, ACS becomes only apparent at higher levels of IAP than reported experimentally. In these animal models, the IAH induced by a pneumoperitoneum with carbon dioxide only reflects the surgical procedure but not all the other causes leading to IAH (ascites, ischemia/reperfusion, bowel distension and edema).
SPECIFIC TREATMENT FOR PERITONITIS ASSOCIATED WITH ACS The surgical management of peritonitis is based on three principles: elimination of the source of infection, reduction of bacterial inoculum in the peritoneal cavity and finally prevention of persistent or recurrent intraabdominal infection. Some authors consider that another principle is also an important objective: avoid postoperative IAH and ACS, therefore decompression
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should be included in the source control concept (22). As APP is reduced in case of IAH/ACS, it is logical to say that intestinal anastomoses are at risk for hypoperfusion, which may lead to perforation at a later stage. Therefore an open abdomen treatment should be considered in critically ill patients (e.g. high APACHE scores) at laparotomy, as these may be at risk for subsequent IAH/ACS. The prevention of postoperative IAH/ACS is possible if parietal tension is avoided. Specific techniques can be used as delayed fascia closure or absorbable mesh prosthesis (36). Enterostomy can be performed even with temporary abdominal closure as sterile intravenous bag (“Bogota bag”) (37).
8.
9.
10.
11.
12.
CONCLUSIONS 13.
Presumably because of a lack of general clinical awareness and because of the severity of peritonitis itself, clinical data on IAH and ACS during intra-abdominal sepsis are scarce. Many questions remain unsolved: is intraabdominal sepsis commonly associated with IAH? Should IAP be monitored in all patients with abdominal sepsis? What is the best and safe treatment for patients with IAH? Is IAH an indication for relaparotomy? Further investigations are definitely required, but it seems that IAH and abdominal sepsis are two of a kind…
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