- Email: [email protected]
Abdominal Compartment Syndrome Associated With Capillary Leak Syndrome After Liver Transplantation
Abdominal Compartment Syndrome Associated With Capillary Leak Syndrome After Liver Transplantation W. Zhang, K. Wang, X. Qian, Y. Xia, C. Zheng, X. Zuo, Y. Wang, Q. Cao, X. Wang, and B. Sun ABSTRACT Orthotopic liver transplantation was performed in a 49-year-old man with metastatic liver sarcoma. After surgery, both abdominal compartment syndrome (ACS) and capillary leak syndrome (CLS) developed. Exploratory laparotomy and colon exteriorization were performed. Five days later, a diagnosis of severe CLS was established, and hydroxyethyl starch was infused to prevent leakage of albumin. The patient gradually recovered over 3 weeks. Awareness of ACS and CLS is important to improve outcome because early diagnosis and immediate therapy are essential. Bladder pressure is a key factor in diagnosing ACS, and pressure of 35 mm Hg is an indication for decompressive laparotomy. During the early stage of CLS, hydroxyethyl starch but not albumin should be used to alleviate edema and hypoalbuminemia. BDOMINAL COMPARTMENT syndrome (ACS) is a pathologic state caused by an acute increase in intraabdominal pressure that is sometimes associated with new organ dysfunction or failure. Although it is more frequently recognized in emergency, vascular, and trauma surgery, ACS has not been commonly reported after liver transplantation. Capillary leak syndrome (CLS) is a rare disorder characterized by episodic life-threatening hypotension, hemoconcentration, and hypoalbuminemia. The precise pathophysiologic cause is unknown. We report a case of secondary ACS that was further complicated by CLS in a patient who underwent orthotopic liver transplantation (OLT).
A
CASE REPORT A 49-year-old man was referred to our department with metastatic liver sarcoma. His medical history revealed an ileal smooth-muscle sarcoma, which had been partially resected 7 years previously. He had a dolichosigmoid colon. At OLT performed on day 4 after admission, 2 drains were placed around the liver. The operative procedure was uneventful, and the patient was transferred to our intensive care unit for further management. On arrival in the intensive care unit, the patient’s blood pressure was 120/70 mm Hg, and his heart rate was 104 bpm. At 31 hours after admission, the patient’s abdomen became increasingly distended. Total fluid from the 2 drains was about 800 mL. Five units of red blood cells and 3.5 L of fluid were infused; however, the blood pressure remained low, requiring administration of dopamine, 15 g/kg/min, to maintain blood pressure between 90 –110/ 60 –75 mm Hg. Partial pressure of carbon dioxide was 32 mm Hg, and of oxygen was 59 mm Hg. Anuria developed rapidly. Because
of concerns about his clinical course and distended abdomen, bladder pressure was measured and determined to be 30 mm Hg. Four hours later, bladder pressure had increased to 36 mm Hg. With this sign and clinical symptoms, acute ACS was diagnosed. Because bladder pressure was greater than 35 mm Hg, exploratory laparotomy was performed. Prominent intestinal edema was observed, and the colon was inflated with gas and liquor entericus. The right upper quadrant contained approximately 1000 mL of clotted blood, which was removed. Because of the history of dolichosigmoid, colon exteriorization was performed, and the abdomen was left open and covered with a sterile membrane. A 3-L bag was used for intravenous infusion of nutrition (Fig 1A). Within 7 hours after surgery, renal function had improved, with resumption of diuresis. Ventilation was easily performed within 2 days. Five days later, a partial colectomy was performed with skin-level colostomy, and the abdomen was closed (Fig 1B and C). After colectomy, ascitic fluid was approximately 4000 to 5000 mL, and albumin concentration was 30.3 g/L. Thus, 5% albumin
From the Liver Transplantation Center (W.Z., K.W., X.Q., Y.X., X.W., B.S.) and Department of Intensive Care Medicine (C.Z., X.Z., Y.W., Q.C.), First Affiliated Hospital of Nanjing Medical University, Nanjing, China. This study was supported by grant RC2007057 (to B.S.) from the Jiangsu Province Outstanding Medical Academic Leader Program, Jiangsu Province Key Medical Center. Address reprint requests to Beicheng Sun, MD, PhD, or Xuehao Wang, MD, Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd, Nanjing, Jiangsu 210029, China. E-mail: [email protected]
© 2009 Published by Elsevier Inc. 360 Park Avenue South, New York, NY 10010-1710
0041-1345/09/$–see front matter doi:10.1016/j.transproceed.2009.06.220
Transplantation Proceedings, 41, 3927–3930 (2009)
3927
3928
ZHANG, WANG, QIAN ET AL
Fig 1. A, Colon exteriorization was performed to decrease intra-abdominal pressure. B, Five days after decompression laparotomy, partial colectomy with skin-level colostomy was performed to close the abdomen. C, Tension sutures were used to close the abdomen after skin-level colostomy. was infused to prevent the leak of ascitic fluid and to elevate the plasma albumin concentration. However, ascites increased to 6000 to 7000 mL over the next 3 days (Fig 2A), and the albumin concentration decreased to 13.1 g/L (Fig 2B). The dopamine dose was increased from 8 g/kg/min to 20 g/kg/min to maintain blood pressure at 100/50 mm Hg. Heart rate was 120 to 130 bpm. Physical examination demonstrated bilateral leg edema. Laboratory findings revealed hemoconcentration with hypoproteinemia and acute renal impairment. Considering all of these findings, a diagnosis of CLS was made. During the next 3 days, the patient received more than 8 L of fluid and 4 to 5 L of hydroxyethyl starch (HES; 200/0.5) per day. Dexamethasone was infused to suppress the release of inflammatory factors. The systolic blood pressure returned to normal. Leakage of ascitic fluid decreased, and the albumin concentration increased. Urine volume increased, and the leg edema gradually improved without diuretic therapy. The dosages of intravenous fluids and HES were tapered, and the infusion was terminated 8 days after the diagnosis was made. At 22 days later, the hemoglobin concentration was 12.6 g/dL, and no edema was present. Total serum protein had increased to 5.0 g/dL (albumin, 3.1 g/dL) (Table 1). The patient was discharged with a closed abdomen and with normal serum protein concentration and renal function.
DISCUSSION
Abdominal compartment syndrome is characterized by the presence of acute or subacute intra-abdominal hypertension of relatively brief duration occurring as a result of an
intra-abdominal cause such as abdominal trauma, acute pancreatitis, retroperitoneal hemorrhage, or liver transplantation.1–3 The exact pressure thresholds that signify both intra-abdominal hypertension and correlate with ACS are controversial. Secondary ACS has been defined as occurring in patients without primary intraperitoneal injury, surgery, or intervention. It is evident in up to 0.7% of patients overall4 and in 31% of patients after OLT.5 Orthotopic liver transplantation is associated with several factors that may lead to elevated intra-abdominal pressure such as bowel edema after portal vein clamping, ascites, and donor-recipient graft size mismatch.6 Although conservative measures such as urinary bladder and stomach decompression, sedation, and albumin and diuretic therapy may prove helpful, the best recognized treatment of ACS is decompressive laparotomy.7,8 When these are combined with a surgically amenable mass lesion, as may be seen in acute trauma or liver transplantation, removal/hemostasis and decompression are indicated. Only a decompressed abdomen has been shown to reduce the pulmonary, cardiovascular, renal, and visceral dysfunction associated with ACS.1,7 In the present case, the patient underwent laparotomy. Bowel edema and tympanites were found in the abdomen; thus, we chose to perform colon exteriorization and then partial colectomy. The patient recovered quickly.
ABDOMINAL COMPARTMENT SYNDROME
3929
A
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B $OEXPLQJ/
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C
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Abdominal compartment syndrome primarily affects the respiratory, cardiovascular, and renal systems.2 Oliguria and renal failure caused by ACS, as in the present case, are believed to be related to direct compression of the kidneys, which results in decreased renal perfusion. Recently it has been reported that artificial increase in intra-abdominal pressure through pneumoperitoneum also can substantially reduce blood flow to the liver and kidneys.9 The incidence of portal vein and hepatic artery thrombosis is greater in the presence of increased intra-abdominal pressure, underlining the need for an early diagnosis.10
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Fig 2. After albumin therapy, ascites increased from 3640 mL to 7700 mL (A), albumin concentration decreased from 30.3 g/L to 13.1 g/L (B), and white blood cell count (WBC) increased to 21.3 ⫻ 109/L (C). Hydroxyethyl starch was infused on day 9, and ascites decreased over the next several days, albumin concentration gradually returned to the initial level, and white blood cell counts also returned to normal levels.
This case illustrates the importance of monitoring intraabdominal pressure in all critically ill patients. Intra-abdominal pressure is best and most easily measured using a transurethral probe located in the urinary bladder. By measuring intra-abdominal pressure using the transurethral technique, ACS in patients at risk may be diagnosed at an early stage. Usually, if the bladder pressure is more than 25 mm Hg, the diagnosis of ACS is established, and urinary bladder and gastrointestinal decompression are required. If bladder pressure increases to 35 mm Hg, decompressive laparotomy must be performed. In this case, we monitored bladder
3930
ZHANG, WANG, QIAN ET AL Table 1. Laboratory Values Day Test
Normal Range
⫺1
0
1
3
5
9
10
12
16
22
ALT, g/L Total bilirubin, mol/L Direct bilirubin, mol/L Hemoglobin, g/L Hematocrit Urea, mmol/L Creatinine, mmol/L Total protein, g/L
0–45 6–22 0–6 110–160 0.35–0.58 2.1–7.2 36.0–144.0 60–85
38.7 13.4 2.7 105 0.39 6.8 117.0 58.0
328.0 24.7 12.5 102 0.35 4.55 93.1 40.4
161.0 33.7 16.7 117 0.36 17.2 277.0 47.5
45.3 33.9 14.1 127 0.37 22.67 160.7 45.1
14.3 21.6 10.1 134 0.47 27.6 201.0 53.5
15.9 61.4 31.9 145 0.42 30.3 201.0 29.7
15.3 30.3 15.4 172 0.58 36.9 217.0 21.6
72.5 59.1 37.0 123 0.5 45.98 236.0 39.3
61.2 39.5 24.1 124 0.4 20.7 174.0 40.6
61.0 26.9 15.6 126 0.41 10.4 87.2 50.4
ALT, alanine aminotransferase.
pressure continually, and as soon as it reached 36 mm Hg, decompressive laparotomy was performed, and the patient recovered. Capillary leak syndrome is a rare complication of OLT. It is an unusual condition characterized by episodes of generalized edema, low albumin concentration, and severe hypotension, associated with an episodically elevated capillary permeability. Episodic attacks are characterized by a marked shift of plasma from the intravascular space to the extravascular space. The causes of CLS include trauma, cardiopulmonary bypass, sepsis, systemic inflammatory reaction syndrome, and adult respiratory distress syndrome.11,12 It has been reported that in sepsis, a variety of inflammatory mediators produced by leukocytes such as IL-2, IL-6, and tumor necrosis factor-␣ induce increased microvascular permeability and capillary leakage, which in turn results in interstitial fluid accumulation, loss of protein and tissue edema.13 In the present case, we inferred that the trauma caused by the ACS, the fluid loss as a result of much ascites and subsequent systemic inflammatory reaction syndrome contributed to the CLS. We also observed that the white blood cells multiplied quickly in the early stage of CLS, decreasing to normal levels after treatment (Fig 2C), indicating that white blood cells may have an important role in the process of CLS and that white blood cell counts may be used as a standard for the diagnosis of CLS. Treatment of CLS is supportive and dominated by fluid resuscitation, although it is likely that the fluid resuscitation may itself worsen the edema and organ dysfunction.12 Colloids such as HES, 200/0.5, but not albumin should also be infused because albumin may aggravate the edema and protein loss, according to our experience. Small molecules such as albumin could leak from the blood capillary to the intercellular space and exacerbate the edema, whereas large molecules such as HES do not. In summary, awareness of ACS and CLS is most important to improve outcome because early diagnosis and
immediate therapy are essential. Bladder pressure is a key factor in the diagnosis of ACS; 35 mm Hg is an indication for decompressive laparotomy. During the early stage of CLS, HES but not albumin should be used to alleviate the edema and hypoalbuminemia. REFERENCES 1. Bailey J, Shapiro MJ: Abdominal compartment syndrome. Crit Care 4:23, 2000 2. Mayberry JC: Prevention of the abdominal compartment syndrome. Lancet 354:1749, 1999 3. Handschin AE, Weber M, Renner E, et al: Abdominal compartment syndrome after liver transplantation. Liver Transplantation 11:98, 2005 4. Balogh Z, McKinley BA, Holcomb JB, et al: Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 54:848, 2003 5. Biancofiore G, Bindi ML, Romanelli AM, et al: Intra-abdominal pressure monitoring in liver transplant recipients: a prospective study. Intensive Care Med 29:30, 2003 6. Biancofiore G, Bindi ML, Romanelli AM, et al: Postoperative intra-abdominal pressure and renal function after liver transplantation. Arch Surg 138:703, 2003 7. Hobson KG, Young KM, Ciraulo A, et al: Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 53:1129, 2002 8. Eddy V, Nunn C, Morris JA: Abdominal compartment syndrome. Surg Clin North Am 77:801, 1997 9. Schaefer M, Saegesser H, Reichen J, Kraehenbuehl L: Alterations in hemodynamics and hepatic and splanchnic circulation during laparoscopy in rats. Surg Endosc 15:1197, 2001 10. Seaman DS, Newell KA, Piper JB, et al: Use of polytetrafluoroethylene patch for temporary wound closure after pediatric liver transplantation. Transplantation 62:1034, 1996 11. Marx G: Fluid therapy in sepsis with capillary leakage. Eur J Anaesthesiol 20:429, 2003 12. Mandava S, Kolobow T, Vitale G, et al: Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: an experimental study. Crit Care Med 31:885, 2003 13. Groeneveld AB, Bronsveld W, Thijs LG: Hemodynamic determinants of mortality in human septic shock. Surgery 99:140, 1986
A
CASE REPORT A 49-year-old man was referred to our department with metastatic liver sarcoma. His medical history revealed an ileal smooth-muscle sarcoma, which had been partially resected 7 years previously. He had a dolichosigmoid colon. At OLT performed on day 4 after admission, 2 drains were placed around the liver. The operative procedure was uneventful, and the patient was transferred to our intensive care unit for further management. On arrival in the intensive care unit, the patient’s blood pressure was 120/70 mm Hg, and his heart rate was 104 bpm. At 31 hours after admission, the patient’s abdomen became increasingly distended. Total fluid from the 2 drains was about 800 mL. Five units of red blood cells and 3.5 L of fluid were infused; however, the blood pressure remained low, requiring administration of dopamine, 15 g/kg/min, to maintain blood pressure between 90 –110/ 60 –75 mm Hg. Partial pressure of carbon dioxide was 32 mm Hg, and of oxygen was 59 mm Hg. Anuria developed rapidly. Because
of concerns about his clinical course and distended abdomen, bladder pressure was measured and determined to be 30 mm Hg. Four hours later, bladder pressure had increased to 36 mm Hg. With this sign and clinical symptoms, acute ACS was diagnosed. Because bladder pressure was greater than 35 mm Hg, exploratory laparotomy was performed. Prominent intestinal edema was observed, and the colon was inflated with gas and liquor entericus. The right upper quadrant contained approximately 1000 mL of clotted blood, which was removed. Because of the history of dolichosigmoid, colon exteriorization was performed, and the abdomen was left open and covered with a sterile membrane. A 3-L bag was used for intravenous infusion of nutrition (Fig 1A). Within 7 hours after surgery, renal function had improved, with resumption of diuresis. Ventilation was easily performed within 2 days. Five days later, a partial colectomy was performed with skin-level colostomy, and the abdomen was closed (Fig 1B and C). After colectomy, ascitic fluid was approximately 4000 to 5000 mL, and albumin concentration was 30.3 g/L. Thus, 5% albumin
From the Liver Transplantation Center (W.Z., K.W., X.Q., Y.X., X.W., B.S.) and Department of Intensive Care Medicine (C.Z., X.Z., Y.W., Q.C.), First Affiliated Hospital of Nanjing Medical University, Nanjing, China. This study was supported by grant RC2007057 (to B.S.) from the Jiangsu Province Outstanding Medical Academic Leader Program, Jiangsu Province Key Medical Center. Address reprint requests to Beicheng Sun, MD, PhD, or Xuehao Wang, MD, Liver Transplantation Center, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd, Nanjing, Jiangsu 210029, China. E-mail: [email protected]
© 2009 Published by Elsevier Inc. 360 Park Avenue South, New York, NY 10010-1710
0041-1345/09/$–see front matter doi:10.1016/j.transproceed.2009.06.220
Transplantation Proceedings, 41, 3927–3930 (2009)
3927
3928
ZHANG, WANG, QIAN ET AL
Fig 1. A, Colon exteriorization was performed to decrease intra-abdominal pressure. B, Five days after decompression laparotomy, partial colectomy with skin-level colostomy was performed to close the abdomen. C, Tension sutures were used to close the abdomen after skin-level colostomy. was infused to prevent the leak of ascitic fluid and to elevate the plasma albumin concentration. However, ascites increased to 6000 to 7000 mL over the next 3 days (Fig 2A), and the albumin concentration decreased to 13.1 g/L (Fig 2B). The dopamine dose was increased from 8 g/kg/min to 20 g/kg/min to maintain blood pressure at 100/50 mm Hg. Heart rate was 120 to 130 bpm. Physical examination demonstrated bilateral leg edema. Laboratory findings revealed hemoconcentration with hypoproteinemia and acute renal impairment. Considering all of these findings, a diagnosis of CLS was made. During the next 3 days, the patient received more than 8 L of fluid and 4 to 5 L of hydroxyethyl starch (HES; 200/0.5) per day. Dexamethasone was infused to suppress the release of inflammatory factors. The systolic blood pressure returned to normal. Leakage of ascitic fluid decreased, and the albumin concentration increased. Urine volume increased, and the leg edema gradually improved without diuretic therapy. The dosages of intravenous fluids and HES were tapered, and the infusion was terminated 8 days after the diagnosis was made. At 22 days later, the hemoglobin concentration was 12.6 g/dL, and no edema was present. Total serum protein had increased to 5.0 g/dL (albumin, 3.1 g/dL) (Table 1). The patient was discharged with a closed abdomen and with normal serum protein concentration and renal function.
DISCUSSION
Abdominal compartment syndrome is characterized by the presence of acute or subacute intra-abdominal hypertension of relatively brief duration occurring as a result of an
intra-abdominal cause such as abdominal trauma, acute pancreatitis, retroperitoneal hemorrhage, or liver transplantation.1–3 The exact pressure thresholds that signify both intra-abdominal hypertension and correlate with ACS are controversial. Secondary ACS has been defined as occurring in patients without primary intraperitoneal injury, surgery, or intervention. It is evident in up to 0.7% of patients overall4 and in 31% of patients after OLT.5 Orthotopic liver transplantation is associated with several factors that may lead to elevated intra-abdominal pressure such as bowel edema after portal vein clamping, ascites, and donor-recipient graft size mismatch.6 Although conservative measures such as urinary bladder and stomach decompression, sedation, and albumin and diuretic therapy may prove helpful, the best recognized treatment of ACS is decompressive laparotomy.7,8 When these are combined with a surgically amenable mass lesion, as may be seen in acute trauma or liver transplantation, removal/hemostasis and decompression are indicated. Only a decompressed abdomen has been shown to reduce the pulmonary, cardiovascular, renal, and visceral dysfunction associated with ACS.1,7 In the present case, the patient underwent laparotomy. Bowel edema and tympanites were found in the abdomen; thus, we chose to perform colon exteriorization and then partial colectomy. The patient recovered quickly.
ABDOMINAL COMPARTMENT SYNDROME
3929
A
$VFLWHVP/
'D\
B $OEXPLQJ/
'D\
C
:%&/
Abdominal compartment syndrome primarily affects the respiratory, cardiovascular, and renal systems.2 Oliguria and renal failure caused by ACS, as in the present case, are believed to be related to direct compression of the kidneys, which results in decreased renal perfusion. Recently it has been reported that artificial increase in intra-abdominal pressure through pneumoperitoneum also can substantially reduce blood flow to the liver and kidneys.9 The incidence of portal vein and hepatic artery thrombosis is greater in the presence of increased intra-abdominal pressure, underlining the need for an early diagnosis.10
'D\
Fig 2. After albumin therapy, ascites increased from 3640 mL to 7700 mL (A), albumin concentration decreased from 30.3 g/L to 13.1 g/L (B), and white blood cell count (WBC) increased to 21.3 ⫻ 109/L (C). Hydroxyethyl starch was infused on day 9, and ascites decreased over the next several days, albumin concentration gradually returned to the initial level, and white blood cell counts also returned to normal levels.
This case illustrates the importance of monitoring intraabdominal pressure in all critically ill patients. Intra-abdominal pressure is best and most easily measured using a transurethral probe located in the urinary bladder. By measuring intra-abdominal pressure using the transurethral technique, ACS in patients at risk may be diagnosed at an early stage. Usually, if the bladder pressure is more than 25 mm Hg, the diagnosis of ACS is established, and urinary bladder and gastrointestinal decompression are required. If bladder pressure increases to 35 mm Hg, decompressive laparotomy must be performed. In this case, we monitored bladder
3930
ZHANG, WANG, QIAN ET AL Table 1. Laboratory Values Day Test
Normal Range
⫺1
0
1
3
5
9
10
12
16
22
ALT, g/L Total bilirubin, mol/L Direct bilirubin, mol/L Hemoglobin, g/L Hematocrit Urea, mmol/L Creatinine, mmol/L Total protein, g/L
0–45 6–22 0–6 110–160 0.35–0.58 2.1–7.2 36.0–144.0 60–85
38.7 13.4 2.7 105 0.39 6.8 117.0 58.0
328.0 24.7 12.5 102 0.35 4.55 93.1 40.4
161.0 33.7 16.7 117 0.36 17.2 277.0 47.5
45.3 33.9 14.1 127 0.37 22.67 160.7 45.1
14.3 21.6 10.1 134 0.47 27.6 201.0 53.5
15.9 61.4 31.9 145 0.42 30.3 201.0 29.7
15.3 30.3 15.4 172 0.58 36.9 217.0 21.6
72.5 59.1 37.0 123 0.5 45.98 236.0 39.3
61.2 39.5 24.1 124 0.4 20.7 174.0 40.6
61.0 26.9 15.6 126 0.41 10.4 87.2 50.4
ALT, alanine aminotransferase.
pressure continually, and as soon as it reached 36 mm Hg, decompressive laparotomy was performed, and the patient recovered. Capillary leak syndrome is a rare complication of OLT. It is an unusual condition characterized by episodes of generalized edema, low albumin concentration, and severe hypotension, associated with an episodically elevated capillary permeability. Episodic attacks are characterized by a marked shift of plasma from the intravascular space to the extravascular space. The causes of CLS include trauma, cardiopulmonary bypass, sepsis, systemic inflammatory reaction syndrome, and adult respiratory distress syndrome.11,12 It has been reported that in sepsis, a variety of inflammatory mediators produced by leukocytes such as IL-2, IL-6, and tumor necrosis factor-␣ induce increased microvascular permeability and capillary leakage, which in turn results in interstitial fluid accumulation, loss of protein and tissue edema.13 In the present case, we inferred that the trauma caused by the ACS, the fluid loss as a result of much ascites and subsequent systemic inflammatory reaction syndrome contributed to the CLS. We also observed that the white blood cells multiplied quickly in the early stage of CLS, decreasing to normal levels after treatment (Fig 2C), indicating that white blood cells may have an important role in the process of CLS and that white blood cell counts may be used as a standard for the diagnosis of CLS. Treatment of CLS is supportive and dominated by fluid resuscitation, although it is likely that the fluid resuscitation may itself worsen the edema and organ dysfunction.12 Colloids such as HES, 200/0.5, but not albumin should also be infused because albumin may aggravate the edema and protein loss, according to our experience. Small molecules such as albumin could leak from the blood capillary to the intercellular space and exacerbate the edema, whereas large molecules such as HES do not. In summary, awareness of ACS and CLS is most important to improve outcome because early diagnosis and
immediate therapy are essential. Bladder pressure is a key factor in the diagnosis of ACS; 35 mm Hg is an indication for decompressive laparotomy. During the early stage of CLS, HES but not albumin should be used to alleviate the edema and hypoalbuminemia. REFERENCES 1. Bailey J, Shapiro MJ: Abdominal compartment syndrome. Crit Care 4:23, 2000 2. Mayberry JC: Prevention of the abdominal compartment syndrome. Lancet 354:1749, 1999 3. Handschin AE, Weber M, Renner E, et al: Abdominal compartment syndrome after liver transplantation. Liver Transplantation 11:98, 2005 4. Balogh Z, McKinley BA, Holcomb JB, et al: Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma 54:848, 2003 5. Biancofiore G, Bindi ML, Romanelli AM, et al: Intra-abdominal pressure monitoring in liver transplant recipients: a prospective study. Intensive Care Med 29:30, 2003 6. Biancofiore G, Bindi ML, Romanelli AM, et al: Postoperative intra-abdominal pressure and renal function after liver transplantation. Arch Surg 138:703, 2003 7. Hobson KG, Young KM, Ciraulo A, et al: Release of abdominal compartment syndrome improves survival in patients with burn injury. J Trauma 53:1129, 2002 8. Eddy V, Nunn C, Morris JA: Abdominal compartment syndrome. Surg Clin North Am 77:801, 1997 9. Schaefer M, Saegesser H, Reichen J, Kraehenbuehl L: Alterations in hemodynamics and hepatic and splanchnic circulation during laparoscopy in rats. Surg Endosc 15:1197, 2001 10. Seaman DS, Newell KA, Piper JB, et al: Use of polytetrafluoroethylene patch for temporary wound closure after pediatric liver transplantation. Transplantation 62:1034, 1996 11. Marx G: Fluid therapy in sepsis with capillary leakage. Eur J Anaesthesiol 20:429, 2003 12. Mandava S, Kolobow T, Vitale G, et al: Lethal systemic capillary leak syndrome associated with severe ventilator-induced lung injury: an experimental study. Crit Care Med 31:885, 2003 13. Groeneveld AB, Bronsveld W, Thijs LG: Hemodynamic determinants of mortality in human septic shock. Surgery 99:140, 1986