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Original Article |

Abdominal Compartment Syndrome in the Open Abdomen FREE

Vicente H. Gracias, MD, FCCP; Benjamin Braslow, MD; Jon Johnson, MD; John Pryor, MD; Rajan Gupta, MD; Patrick Reilly, MD; C. William Schwab, MD
[+] Author Affiliations

From the Division of Traumatology and Surgical Critical Care, Department of Surgery, University of Pennsylvania School of Medicine, Philadelphia.


Arch Surg. 2002;137(11):1298-1300. doi:10.1001/archsurg.137.11.1298.
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Background  Multiple methods exist to manage in the intensive care unit the patient with an open abdomen. An increasingly common method is the vacuum packed technique. This method accommodates considerable expansion of intra-abdominal contents and should obviate the potential development of the abdominal compartment syndrome (ACS). Despite this, some patients with these temporary abdominal dressings will go on to develop ACS. For the purpose of this study we have defined this clinical entity as the open abdomen ACS.

Hypothesis  Patients with an open abdomen who develop ACS have a poor prognosis. Fluid requirements and resuscitative indices may predict which of these patients will develop open abdomen ACS.

Methods  A retrospective review was performed of patients with trauma who had an open abdomen treated with vacuum packed dressings at our urban level I trauma center. Over 1 year (July 1, 1999-June 30, 2000), 5 patients managed with an open abdomen developed ACS. These patients were compared with 15 consecutive patients with an open abdomen who did not develop clinical ACS during that same period. Fluid resuscitation, base deficit, pH, lactate level, systolic blood pressure, prothrombin time, temperature, peak inspiratory pressure, and PCO2 were abstracted. The Fisher exact test was used for statistical analysis.

Results  In patients managed with an open abdomen, ACS developed between 1.5 and 12 hours (mean [SD], 7.5 [3.9] hours) after placement of the vacuum packed dressing. The base deficit, pH, peak inspiratory pressure, PCO2, and lactate level were more abnormal and the crystalloid requirements were significantly higher in the ACS group. The systolic blood pressure, temperature, and prothrombin time did not differ between groups. Three patients with ACS developed a second episode of ACS. Mortality in the ACS group was 3 (60%) of 5 patients vs 1 (7%) of 15 patients in the control group.

Conclusions  Management of the open abdomen with the temporary abdominal closure does not prevent the development of ACS. Mortality is high when ACS occurs in this scenario. Severe physiologic derangement and high crystalloid requirements may predict which patients will develop ACS.

ABDOMINAL compartment syndrome (ACS), first suggested in 1863 by Marey, is a term used to describe a constellation of physiologic sequelae of increased intra-abdominal pressure (IAP) or intra-abdominal hypertension (IAH).1 It is characterized by a tensely distended abdomen, elevated IAP and peak airway pressure, impaired ventilation associated with hypoxia and hypercarbia, decreased urine output, increased systemic vascular resistance, and decreased cardiac output. Although ACS may be associated with many clinical scenarios, it is often seen in the patient with trauma who has multiple injuries following aggressive fluid resuscitation. Patients with trauma who require lengthy operative procedures often develop the triad of hypothermia, acidosis, and coagulopathy. Abbreviated or (damage-control) staged laparotomy is used to allow adequate correction of these conditions with a set period of resuscitation in the surgical intensive care unit (ICU) prior to definitive repair and closure of the abdominal wall.2 To preserve the fascia, to provide ease of surgical reexploration, and to prevent the development of ACS in this high-risk subset of patients, many temporary abdominal closure techniques have been used. These techniques include towel clip skin closure (leaving fascial edges unapproximated), a sterile intravenous bag open and sewn to fascial edges (Bogata bag), or synthetic patch placement sutured to fascial edges. More recently the vacuum-pack technique has come into favor.3 This technique has proven to be efficient and allows for safe transport and even prone positioning of the patient if needed.4 Despite these attempts to obviate IAH by maintaining the abdomen open, we have observed that some patients with these temporary abdominal closures will go on to develop ACS. For this article we have defined this clinical entity as open abdomen ACS. The purposes of this article are to determine if any resuscitation indices might help predict the patients at risk of developing ACS in the open abdomen and to define its associated mortality.

A retrospective review of patients with an open abdomen treated with vacuum packed dressings was performed at our urban, level I trauma center. The vacuum packed dressing used has been well described in the literature5,6 and consists of a large antimicrobial incise drape (Ioban; 3M Health Care, St Paul, Minn) sheet held adherent side up as a sterile blue surgical towel is placed on top. The edges of the towel are then enfolded by the antimicrobial incise drape. This dressing is then placed subfascially with the antimicrobial incise drape side facing the peritoneal cavity to ensure that the bowel is in contact with a nonadherent surface. Two flat Jackson-Pratt drains are then laid alongside the subfascially placed antimicrobial incise drape–towel dressing and their tails brought out through separate skin stab wounds cephalad to the upper apex of the incision. A second large antimicrobial incise drape sheet is then placed adherent side down over the abdomen and the intra-abdominal antimicrobial incise drape–towel dressing. No effort is made to approximate skin edges or force the abdominal wall edges together. Concurrently, the drains are placed to low-pressure, continuous wall suction creating a vacuum. The drains allow controlled egress of fluid and the layered plastic dressing maintains a sterile, waterproof barrier.

Bladder pressures above 25 mm Hg defined IAH. Abdominal compartment syndrome was diagnosed using this bladder pressure threshold, as well as the other following clinical factors: tensely distended abdomen, elevated peak airway pressures, impaired ventilation associated with hypoxia and hypercarbia, decreased urine output, increased systemic vascular resistance, and decreased cardiac output. Over a 1-year period from July 1, 1999, through June 30, 2000, five patients with open abdomen and vacuum packed temporary abdominal closure who developed ACS (study group) were compared with 15 consecutive patients with open abdomen and vacuum packed temporary abdominal closure who did not develop ACS (control group). Total fluid resuscitation volume, base deficit, pH, lactate levels, systolic blood pressure, prothrombin times, temperature, peak inspiratory pressures, and PCO2 were abstracted. The Fisher exact test was used for statistical analysis when appropriate. All values are given as mean (SD).

From July 1, 1999, through June 30, 2000, one hundred thirty-six laparotomies for patients with trauma were performed at the University of Pennsylvania Hospital, Philadelphia. Twenty patients who required management with an open abdomen and vacuum packed temporary abdominal closure were identified. Five of these patients with an open abdomen and vacuum packed temporary abdominal closure developed ACS. During the same period, 15 consecutive patients with open abdomen with temporary abdominal closure did not develop ACS. The demographics of the 2 groups (ie, mean age, sex, mean Injury Severity Score, and mechanism of injury) are given in Table 1. No demographic data varied significantly between the 2 groups.

In patients with an open abdomen, ACS occurred between 1.5 and 12 hours (mean, 7.5 [3.9] hours) after arrival in the surgical ICU. Bladder pressures were not routinely checked in the control group as it is not our clinical practice to check this factor in the absence of clinical suspicion, ie, a tensely distended abdomen. Therefore, no comparison of this value between the 2 groups was possible. All patients with an open abdomen having the diagnosis of ACS had bladder pressures higher than 25 mm Hg prior to reopening the abdomen. Base deficit, pH, and lactate levels on surgical ICU admission were significantly worse in the ACS group (Table 2). Systolic blood pressure, temperature, and prothrombin time did not differ between groups. The peak inspiratory pressure, PCO2, and intravenous fluids infused prior to abdominal decompression in the ACS group were then compared with the values in the control group during the first 12 hours of surgical ICU admission (Table 3). All were significantly worse in the ACS group.

Table Graphic Jump LocationTable 2. Comparison of Open Abdomen ACS Control Group and ACS Study Group Factors on Arrival in the Surgical Intensive Care Unit*
Table Graphic Jump LocationTable 3. Comparison of Open Abdomen ACS Control Group and ACS Study Group Factors During the First 12 Hours of Surgical Intensive Care Unit Admission*

Analysis predecompression and postdecompression of the ACS group demonstrated an improvement in peak inspiratory pressure (46 [9] cm H2O to 36 [4] cm H2O), base deficit (9.2 [3.6] mmol to 5.7 [0.7] mmol), and urine output (64 [56] mL/h to 242 [164] mL/h). None of these factors achieved statistical significance with P values of .064, .065, and .070, respectively. Postdecompression data were compiled over a 12-hour period. Peak inspiratory pressure and urine output were measured on hourly intervals following decompression. Base deficit was checked within 1 hour of decompression and frequently thereafter. Improvements in all 3 factors were noted immediately following decompression. Three patients in the ACS group developed a second episode of ACS. Mortality in the control group was 7% (1/15) vs a mortality of 60% (3/5) in the ACS group.

Abdominal compartment syndrome has a reported incidence of 6% in patients with severe abdominal and/or pelvic trauma undergoing emergency laparotomy.7 The exact pathogenesis of ACS is still unknown. Abdominal compartment syndrome usually occurs within hours of arrival into the surgical ICU and causes severe disturbances of renal, respiratory, and cardiovascular functions and can increase intracranial pressure in patients with severe head trauma.8 Compromised splanchnic blood flow leads to bowel ischemia and significant acidosis.9 Subsequently, increased mucosal permeability and bacterial translocation seem to play a role in the development of multiple system organ failure.10,11 Attempts at reducing the incidence of IAH and ACS have led to the use of open abdomen techniques. Evolution of this concept has led to greater usage of the damage-control staged laparotomy and the avoidance of primary closure of fascia.1,12,13 This entails the placement of a synthetic material (ie, Bogota bag [an opened, empty, sterile intravenous fluid bag], polyglactin 910 knitted mesh [Vicryl mesh; Ethicon, Somerville, NJ], Whitman Patch [Starsurgical, Inc, Burlington, Vt, and others) to serve as coverage for exposed abdominal contents.

Over the last 5 years, the use of the vacuum packed technique for temporary abdominal dressings has gained wider accepance.14 At our institution, it has supplanted all other closure techniques at the initial laparotomy. This dressing allows rapid and expedient temporary abdominal coverage and considerable increase in abdominal volume. Controlled egress of fluid from the abdomen is allowed, and a sterile barrier is maintained, while providing a durable dressing for possible prone position ventilation.3

Management of the patient with open abdomen using the vacuum packed technique has been thought to prevent the occurrence of IAH by increasing the volume of the pseudoabdomen. We have demonstrated that a subset of patients with an open abdomen and temporary abdominal closures is still at risk of developing ACS. This entity may, in fact, be due to the efficiency with which the vacuum packed dressing is able to contain the abdominal volume and allow subsequent IAP increases associated with ongoing resuscitation requirements and capillary leak, third-space mobilization, and visceral edema.15 Temporary abdominal closure methods, although helpful, may not always provide the capacity to further increase the abdominal volume needed to prevent an increase in IAP, and thus, continued monitoring for ACS is required.

Physiologic factors and fluid requirements in the surgical ICU may predict which patients will develop ACS. Previous data reported and confirmed in our study warned that inordinately high volumes of crystalloid infusion, specifically more than 10 L, may be a risk factor for ACS.11,16,17 As we have also demonstrated, continued monitoring of IAP, base deficit, PCO2, and lactate level may lead to earlier identification of ACS and intervention. Patients with an open abdomen who develop IAH must be treated immediately to prevent ACS and its associated extreme mortality. For those who have a vacuum packed dressing in place, treatment of IAH can be achieved by incising the external antimicrobial incise drape to allow for further expansion of the neoabdominal wall and more eventration of abdominal viscera prior to placement of a new sterile antimicrobial incise drape.

Management of the open abdomen with the vacuum-pack closure technique does not obviate against the development of ACS. Mortality is high when ACS occurs in this setting. Physiologic factors and crystalloid requirements in the surgical ICU may predict which patients will develop this ominous syndrome. Ongoing vigilant monitoring of IAP is mandatory in this patient population to recognize IAH and treat it expediently.

Accepted for publication June 29, 2002.

Corresponding author: Vicente H. Gracias, MD, FCCP, Division of Traumatology and Surgical Critical Care, Department of Surgery, University of Pennsylvania School of Medicine, 3440 Market St, First Floor, Philadelphia, PA 19104-3335 (e-mail: graciasv@uphs.upenn.edu).

Ivatury  RRSugerman  HJ Abdominal compartment syndrome: a century later, isn't it time to pay attention? Crit Care Med. 2000;282137- 2138
Moore  EE Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg. 1996;172405- 410
Johnson  JWGracias  VHSchwab  CW  et al.  Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma. 2001;51261- 271
Schiller  HJReilly  PMAnderson  HLSchwab  CW The "open abdomen" is not a contra-indication to prone positioning for severe ARDS (abstract). Chest. 1996;110142S
Rotondo  MFSchwab  CWMcGonigal  MD  et al.  "Damage control": an approach for improved survival in exsanguination penetrating abdominal injury. J Trauma. 1993;35375- 382discussion 382-383.
Rotondo  MFZonies  DH The damage control sequence and underlying logic. Surg Clin North Am. 1997;77761- 777
Ertel  WOberholzer  APlatz  AStocker  RTrentz  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;281747- 1753
Saggi  BHSugerman  HJIvatury  RRBloomfield  GL Abdominal compartment syndrome. J Trauma. 1998;45597- 609
Agusti  MElizalde  JIAdalia  RCifuentes  AFontanals  JTaura  P Dobutamine restores intestinal mucosal blood flow in a porcine model of intra-abdominal hypertension. Crit Care Med. 2000;28467- 472
Schein  MWittmann  DHAprahamian  CCCondon  RE The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg. 1995;180745- 753
Ivy  MEAtweh  NAPalmer  JPPossenti  PPPineau  MD'Aiuto  M Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma. 2000;49387- 391
Meldrum  DRMoore  FAMoore  EEFrançiose  RJSauaia  ABurch  JM Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174667- 673
Offner  PJde Souza  ALMoore  EE  et al.  Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma. Arch Surg. 2001;136676- 681
Barker  DEKaufman  HJSmith  LACiraulo  DRichart  CLBurns  RP Vacuum pack technique of temporary abdominal closure: a 7-year experience with 112 patients. J Trauma. 2000;48201- 207
Cheatham  MLWhite  MWSagraves  SGJohnson  JLBlock  EF Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49621- 627
Biffl  WLMoore  EEBurch  JMOffner  PJFrançiose  RJJohnson  JL Secondary abdominal compartment syndrome is a highly lethal event. Am J Surg. 2001;182645- 648
Maxwell  RAFabian  TCCroce  MADavis  KA Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma. 1999;47995- 999

Figures

Tables

Table Graphic Jump LocationTable 2. Comparison of Open Abdomen ACS Control Group and ACS Study Group Factors on Arrival in the Surgical Intensive Care Unit*
Table Graphic Jump LocationTable 3. Comparison of Open Abdomen ACS Control Group and ACS Study Group Factors During the First 12 Hours of Surgical Intensive Care Unit Admission*

References

Ivatury  RRSugerman  HJ Abdominal compartment syndrome: a century later, isn't it time to pay attention? Crit Care Med. 2000;282137- 2138
Moore  EE Staged laparotomy for the hypothermia, acidosis, and coagulopathy syndrome. Am J Surg. 1996;172405- 410
Johnson  JWGracias  VHSchwab  CW  et al.  Evolution in damage control for exsanguinating penetrating abdominal injury. J Trauma. 2001;51261- 271
Schiller  HJReilly  PMAnderson  HLSchwab  CW The "open abdomen" is not a contra-indication to prone positioning for severe ARDS (abstract). Chest. 1996;110142S
Rotondo  MFSchwab  CWMcGonigal  MD  et al.  "Damage control": an approach for improved survival in exsanguination penetrating abdominal injury. J Trauma. 1993;35375- 382discussion 382-383.
Rotondo  MFZonies  DH The damage control sequence and underlying logic. Surg Clin North Am. 1997;77761- 777
Ertel  WOberholzer  APlatz  AStocker  RTrentz  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;281747- 1753
Saggi  BHSugerman  HJIvatury  RRBloomfield  GL Abdominal compartment syndrome. J Trauma. 1998;45597- 609
Agusti  MElizalde  JIAdalia  RCifuentes  AFontanals  JTaura  P Dobutamine restores intestinal mucosal blood flow in a porcine model of intra-abdominal hypertension. Crit Care Med. 2000;28467- 472
Schein  MWittmann  DHAprahamian  CCCondon  RE The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg. 1995;180745- 753
Ivy  MEAtweh  NAPalmer  JPPossenti  PPPineau  MD'Aiuto  M Intra-abdominal hypertension and abdominal compartment syndrome in burn patients. J Trauma. 2000;49387- 391
Meldrum  DRMoore  FAMoore  EEFrançiose  RJSauaia  ABurch  JM Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg. 1997;174667- 673
Offner  PJde Souza  ALMoore  EE  et al.  Avoidance of abdominal compartment syndrome in damage-control laparotomy after trauma. Arch Surg. 2001;136676- 681
Barker  DEKaufman  HJSmith  LACiraulo  DRichart  CLBurns  RP Vacuum pack technique of temporary abdominal closure: a 7-year experience with 112 patients. J Trauma. 2000;48201- 207
Cheatham  MLWhite  MWSagraves  SGJohnson  JLBlock  EF Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49621- 627
Biffl  WLMoore  EEBurch  JMOffner  PJFrançiose  RJJohnson  JL Secondary abdominal compartment syndrome is a highly lethal event. Am J Surg. 2001;182645- 648
Maxwell  RAFabian  TCCroce  MADavis  KA Secondary abdominal compartment syndrome: an underappreciated manifestation of severe hemorrhagic shock. J Trauma. 1999;47995- 999

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