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Abdominal compartment syndrome in children: Experience with three cases
Abdominal Compartment Syndrome in Children: Experience With Three Cases By James M. DeCou, Randel S. Abrams, Richard S. Miller, and Michael W.L. Gauderer Greenville, South Carolina
Background/Purpose: Abdominal compartment syndrome (ACS) is defined as cardiopulmonary or renal dysfunction caused by an acute increase in intraabdominal pressure. Although the condition is well described in adults, particularly trauma patients, little is known about ACS in children. Methods: Three girls, ages 4, 5, and 5 years, were treated for ACS by silo decompression. Each child presented in profound shock, required massive fluid resuscitation, and had tremendous abdominal distension. The first child sustained a thoracoabdominal crush injury, underwent immediate celiotomy for splenic avulsion and a liver laceration, and required decompression 5 hours postoperatively. The second underwent ligation of her bluntly transected inferior vena cava; because of massive edema, her abdominal wall could not be closed, and prophylactic decompression had to be performed. The third presented with shock of unknown
A
BDOMINAL COMPARTMENT syndrome (ACS) is defined as organ system dysfunction—most commonly renal, pulmonary, or cardiovascular—that occurs as a result of an acute increase in intraabdominal pressure. Although the adverse effects of intraabdominal hypertension have been known for more than a century, ACS has only recently been recognized as a lifethreatening but potentially treatable entity, with numerous reports appearing in the trauma and general surgery literature in the last several years.1-7 Pediatric surgeons, in treating infants with abdominal wall defects or stage IV-S neuroblastoma, have long been aware of the problems associated with intraabdominal hypertension. They have been pioneers in the use of prosthetic silos for temporary abdominal decompression and in the clinical use of intraabdominal pressure measurements.8-13 Little has been From the Department of Pediatric Surgery, The Children’s Hospital and the Department of Trauma Surgery, Greenville Hospital System, Greenville, SC. Presented at the 1999 Annual Meeting of the Section on Surgery of the American Academy of Pediatrics, Washington, DC, October 8-10, 1999. Address reprint requests to James M. DeCou, MD, Department of Pediatric Surgery, The Children’s Hospital of Greenville Hospital System, 890 W Faris Rd, Suite 440, Greenville, SC 29605-4253. Copyright 娀 2000 by W.B. Saunders Company 0022-3468/00/3506-0006$03.00/0 doi:10.1053/js.2000.6857
840
etiology, and ACS developed acutely with a bladder pressure of 26 mm Hg.
Results: Respiratory, renal, and hemodynamic function improved immediately in all 3 patients after decompression. Subsequently, each child underwent abdominal wall reconstruction and recovered uneventfully. Conclusions: ACS is a potentially lethal complication of severe trauma and shock in children. To prevent the development of renal or cardiopulmonary failure in these patients, decompression should be considered for acute, tense abdominal distension. J Pediatr Surg 35:840-842. Copyright 娀 2000 by W.B. Saunders Company. INDEX WORDS: Abdominal compartment syndrome, silo decompression.
published, however, on ACS in children beyond the newborn period. In this report, we review the diagnosis and management of ACS in 3 children. CASE REPORTS
Case 1 A 15-kg, 4-year-old girl was pinned under the front tire of a van and sustained a thoracoabdominal crush injury. She was intubated, and chest tubes were placed for bilateral pneumothoraces. Because of hemodynamic instability and a grossly positive diagnostic peritoneal lavage, emergency laparotomy was performed, with the findings of splenic avulsion and a liver laceration. The spleen could not be salvaged; the liver laceration was repaired. Other injuries included femur and clavicle fractures. In addition to crystalloid, she received a total of 16 units of red cells and 4 units of fresh frozen plasma. Postoperatively, she had tense abdominal distension, became oliguric, and had a prolapsed rectum. Her ventilatory requirements increased to a peak inspiratory pressure (PIP) of 55 cm H2O. Five hours after the initial procedure, we decompressed her abdomen and placed a polypropylene mesh silo. Immediately after decompression, her PIP decreased to 35, and her PaO2 increased from 40 to 514. Because of the accompanying crush-related lung injury, she required transfer to another institution for 10 days of extracorporeal membrane oxygenation. She recovered fully and subsequently underwent abdominal wall reconstruction. She is alive and well 4 years later.
Case 2 This case of a 5-year-old girl who sustained a blunt transection of the pararenal vena cava and right renal vein has been reported.14 This massive injury was managed with ligation of both veins. Because of a large retroperitoneal hematoma, bowel edema, and the replacement of
Journal of Pediatric Surgery, Vol 35, No 6 (June), 2000: pp 840-842
ABDOMINAL COMPARTMENT SYNDROME
twice her blood volume, her abdominal wall could not be closed without excessive tension. A polypropylene mesh silo was therefore placed to prevent ACS. After 2 days of diuresis and significantly decreased abdominal distension, the silo was removed and the fascia and skin closed. She recovered fully and is alive and well 2 years after the accident.
Case 3 A 5-year-old girl was transferred to our institution for treatment of shock of unknown etiology, consistent with either septic or toxic shock. In addition to vasopressors, she required a large-volume fluid resuscitation. In less than 24 hours, tense abdominal distension, oliguria, and progressively worsening hypercarbia and hypoxemia developed. Ventilatory requirements progressively increased, with PIP rising from 20 cm H2O to greater than 40 cm H2O. A bladder pressure of 26 mm Hg was measured. Emergent decompressive laparotomy was performed with placement of a polypropylene silo (Fig 1). The liver and spleen appeared congested, and approximately 1 L of tense ascites was drained. Immediately after decompression, the urine output improved significantly, and PIP returned to 20 to 25 cm H2O. After 6 days of steady improvement, the silo could be removed, and the fascia and skin were closed. She made a full recovery and is alive and well 7 months later.
DISCUSSION
The adverse effects of increased intraabdominal pressure were first described in the 1800s, but it was not recognized as a significant clinical problem among general surgery patients until the 1980s.15 Because of improvements in critical care, trauma management, and surgery, more and more critically ill patients are surviving the initial resuscitation, but this resuscitation is complicated potentially by intraabdominal hypertension. The term intraabdominal compartment syndrome, now called abdominal compartment syndrome, was first used by Fietsam et al in 1989.16 Since that time, the diagnosis of ACS is being made more frequently, and there is universal agreement that the only treatment is abdominal decompression.1-7 In early series of adult patients with ACS, there were no survivors without decompression.7
Fig 1. Five-year-old girl (case 3) immediately after decompressive laparotomy and placement of a polypropylene mesh silo.
841
Since the 1940s, when Gross17 first described the treatment of large omphaloceles, pediatric surgeons have been aware of the problems with intraabdominal hypertension. Omphalocele has been called ‘‘a prototype for ACS.’’6 Pediatric surgeons were the first to use prosthetic materials as a temporary closure of the abdominal wall,8 and they were among the first to measure intraabdominal pressures as a guide for reduction of the silo and closure of the abdominal wall.10-12 In addition to their use in the treatment of abdominal wall defects, prosthetic silos have been used in infants for the treatment of stage IV-S neuroblastoma and subcapsular hemorrhage of the liver.9,13,18 Only a few reports, however, discuss the management, beyond the newborn period, of children with ACS caused by trauma or shock.19,20 The most common cause of ACS is severe abdominal trauma complicated by hemorrhage and coagulopathy. Other causes have been described, including ruptured abdominal aortic aneurysm, acute pancreatitis, pelvic fracture, mesenteric thrombosis, intraabdominal abscess, laparoscopic pneumoperitoneum, liver transplantation, and closure of large ventral hernias.1,6,7,16 Even nonabdominal causes, such as extraperitoneal trauma or shock, as in our third case, can lead to ACS when a large fluid resuscitation is required. In addition to renal, pulmonary, and cardiovascular dysfunction, ACS also can lead to bowel ischemia, abdominal wall ischemia with woundhealing problems, venous statis with thrombosis, and increased intracranial pressure.1,3,6,7 The diagnosis of ACS should be considered in any critically ill patient in whom tense abdominal distension develops acutely. A high index of suspicion is necessary. The measurement of intraabdominal pressure is adjunctive information and can be helpful in certain patients, as in our third case. Intraabdominal pressure is determined most commonly and very reliably by measuring bladder pressure, which can be done by instilling 1 mL/kg body weight of sterile saline into the Foley catheter and connecting the end of the catheter to a pressure transducer or a manometer via a 3-way stopcock. The symphysis pubis is used as the zero reference point, and the pressure is measured in millimeters of mercury or centimeters of water (1 mm Hg ⫽ 1.36 cm H2O). The level at which various investigators would decompress the abdomen varies from 15 to 25 mm Hg (20 to 34 cm H2O).3-5,7,15 Other investigators state that the decision to decompress is not determined by a specific pressure measurement but by the physiological consequences of the increased intraabdominal pressure, such as progressive renal or cardiopulmonary insufficiency.4 To prevent ACS in high-risk surgical patients, prophylactic placement of prosthetic mesh is recommended,3 as in our second case. The mesh can remain safely in place
842
DECOU ET AL
for 5 to 7 days, but then should be removed and the fascia closed if significant diuresis and abdominal decompression have occurred. If the fascia cannot be closed by 5 to 7 days, the silo should be removed and a skin graft placed after adequate granulation appears. Later abdominal wall reconstruction then can be performed. From our review of the literature and our limited experience, we have learned several key points in the management of ACS in children. First, a high index of suspicion for ACS is needed in severely injured and critically ill children. Next, prophylactic decompression may be indicated at the time of initial laparotomy for patients in whom abdominal packing is used, who are
coagulopathic, or those who require massive fluid resuscitation. Immediate decompression is necessary in patients with the acute onset of tense abdominal distension combined with progressive oliguria, increased peak inspiratory pressure, or cardiovascular compromise. Lastly, measurement of bladder pressure can be helpful in patients with acute abdominal distension but no organ dysfunction. In these patients, we believe that decompression is indicated for pressures above 25 mm Hg, and we would strongly consider it for pressures between 20 and 25 mm Hg. Further attention and experience are needed to better understand this life-threatening syndrome and to optimize its management in children.
REFERENCES 1. Schein M, Wittmann DH, Aprahamian CC, et al: The abdominal compartment syndrome: The physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 180:745-753, 1995 2. Burch JM, Moore EE, Moore FA, et al: The abdominal compartment syndrome. Surg Clin North Am 76:833-842, 1996 3. Ivatury RR, Diebel L, Porter JM, et al: Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 77:783-800, 1997 4. Eddy V, Nunn C, Morris JA: Abdominal compartment syndrome: The Nashville experience. Surg Clin North Am 77:801-812, 1997 5. Meldrum DR, Moore FA, Moore EE, et al: Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 174:667-673, 1997 6. Watson RA, Howdieshell TR: Abdominal compartment syndrome. South Med J 91:326-332, 1998 7. Saggi BH, Sugerman HJ, Ivatury RR, et al: Abdominal compartment syndrome. J Trauma 45:597-609, 1998 8. Schuster SR: A new method for the staged repair of large omphaloceles. Surg Gynecol Obstet 125:837-850, 1967 9. Schnaufer L, Koop CE: Silastic abdominal patch for temporary hepatomegaly in stage IV-S neuroblastoma. J Pediatr Surg 10:73-75, 1975 10. Wesley JR, Drongowski R, Coran AG: Intragastric pressure measurement: A guide for reduction and closure of the silastic chimney in omphalocele and gastroschisis. J Pediatr Surg 16:264-270, 1981 11. Lacey SR, Bruce J, Brooks SP, et al: The relative merits of various methods of indirect measurement of intraabdominal pressure as
a guide to closure of abdominal wall defects. J Pediatr Surg 22:12071211, 1987 12. Lacey SR, Carris LA, Beyer J, et al: Bladder pressure monitoring significantly enhances care of infants with abdominal wall defects: A prospective clinical study. J Pediatr Surg 28:1370-1375, 1993 13. Lee EW, Applebaum H: Abdominal expansion as a bridging technique in stage IV-S neuroblastoma with massive hepatomegaly. J Pediatr Surg 29:1470-1471, 1994 14. DeCou JM, Abrams RS, Gauderer MWL: Seat-belt transection of the pararenal vena cava in a 5-year-old child: Survival with caval ligation. J Pediatr Surg 34:1074-1076, 1999 15. Kron IL, Harman PK, Nolan SP: The measurement of intraabdominal pressure as a criterion for abdominal re-exploration. Ann Surg 199:28-30, 1984 16. Fietsam R, Villalba M, Glover JL, et al: Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg 55:396-402, 1989 17. Gross R: A new method for surgical treatment of large omphaloceles. Surgery 24:277-292, 1948 18. Kosumi T, Kubota A, Yonekura T, et al: Subcapsular hemorrhage of the liver in a very-low-birth-weight neonate: Survival after decompression laparotomy. Pediatr Surg Int 15:270-271, 1999 19. Stylianos S, Jacir NN, Hoffman MA, et al: Pediatric blunt liver injury and coagulopathy managed with packs and a silo: Case report. J Trauma 30:1409-1410, 1990 20. Stylianos S: Abdominal packing for severe hemorrhage. J Pediatr Surg 33:339-342, 1998
Background/Purpose: Abdominal compartment syndrome (ACS) is defined as cardiopulmonary or renal dysfunction caused by an acute increase in intraabdominal pressure. Although the condition is well described in adults, particularly trauma patients, little is known about ACS in children. Methods: Three girls, ages 4, 5, and 5 years, were treated for ACS by silo decompression. Each child presented in profound shock, required massive fluid resuscitation, and had tremendous abdominal distension. The first child sustained a thoracoabdominal crush injury, underwent immediate celiotomy for splenic avulsion and a liver laceration, and required decompression 5 hours postoperatively. The second underwent ligation of her bluntly transected inferior vena cava; because of massive edema, her abdominal wall could not be closed, and prophylactic decompression had to be performed. The third presented with shock of unknown
A
BDOMINAL COMPARTMENT syndrome (ACS) is defined as organ system dysfunction—most commonly renal, pulmonary, or cardiovascular—that occurs as a result of an acute increase in intraabdominal pressure. Although the adverse effects of intraabdominal hypertension have been known for more than a century, ACS has only recently been recognized as a lifethreatening but potentially treatable entity, with numerous reports appearing in the trauma and general surgery literature in the last several years.1-7 Pediatric surgeons, in treating infants with abdominal wall defects or stage IV-S neuroblastoma, have long been aware of the problems associated with intraabdominal hypertension. They have been pioneers in the use of prosthetic silos for temporary abdominal decompression and in the clinical use of intraabdominal pressure measurements.8-13 Little has been From the Department of Pediatric Surgery, The Children’s Hospital and the Department of Trauma Surgery, Greenville Hospital System, Greenville, SC. Presented at the 1999 Annual Meeting of the Section on Surgery of the American Academy of Pediatrics, Washington, DC, October 8-10, 1999. Address reprint requests to James M. DeCou, MD, Department of Pediatric Surgery, The Children’s Hospital of Greenville Hospital System, 890 W Faris Rd, Suite 440, Greenville, SC 29605-4253. Copyright 娀 2000 by W.B. Saunders Company 0022-3468/00/3506-0006$03.00/0 doi:10.1053/js.2000.6857
840
etiology, and ACS developed acutely with a bladder pressure of 26 mm Hg.
Results: Respiratory, renal, and hemodynamic function improved immediately in all 3 patients after decompression. Subsequently, each child underwent abdominal wall reconstruction and recovered uneventfully. Conclusions: ACS is a potentially lethal complication of severe trauma and shock in children. To prevent the development of renal or cardiopulmonary failure in these patients, decompression should be considered for acute, tense abdominal distension. J Pediatr Surg 35:840-842. Copyright 娀 2000 by W.B. Saunders Company. INDEX WORDS: Abdominal compartment syndrome, silo decompression.
published, however, on ACS in children beyond the newborn period. In this report, we review the diagnosis and management of ACS in 3 children. CASE REPORTS
Case 1 A 15-kg, 4-year-old girl was pinned under the front tire of a van and sustained a thoracoabdominal crush injury. She was intubated, and chest tubes were placed for bilateral pneumothoraces. Because of hemodynamic instability and a grossly positive diagnostic peritoneal lavage, emergency laparotomy was performed, with the findings of splenic avulsion and a liver laceration. The spleen could not be salvaged; the liver laceration was repaired. Other injuries included femur and clavicle fractures. In addition to crystalloid, she received a total of 16 units of red cells and 4 units of fresh frozen plasma. Postoperatively, she had tense abdominal distension, became oliguric, and had a prolapsed rectum. Her ventilatory requirements increased to a peak inspiratory pressure (PIP) of 55 cm H2O. Five hours after the initial procedure, we decompressed her abdomen and placed a polypropylene mesh silo. Immediately after decompression, her PIP decreased to 35, and her PaO2 increased from 40 to 514. Because of the accompanying crush-related lung injury, she required transfer to another institution for 10 days of extracorporeal membrane oxygenation. She recovered fully and subsequently underwent abdominal wall reconstruction. She is alive and well 4 years later.
Case 2 This case of a 5-year-old girl who sustained a blunt transection of the pararenal vena cava and right renal vein has been reported.14 This massive injury was managed with ligation of both veins. Because of a large retroperitoneal hematoma, bowel edema, and the replacement of
Journal of Pediatric Surgery, Vol 35, No 6 (June), 2000: pp 840-842
ABDOMINAL COMPARTMENT SYNDROME
twice her blood volume, her abdominal wall could not be closed without excessive tension. A polypropylene mesh silo was therefore placed to prevent ACS. After 2 days of diuresis and significantly decreased abdominal distension, the silo was removed and the fascia and skin closed. She recovered fully and is alive and well 2 years after the accident.
Case 3 A 5-year-old girl was transferred to our institution for treatment of shock of unknown etiology, consistent with either septic or toxic shock. In addition to vasopressors, she required a large-volume fluid resuscitation. In less than 24 hours, tense abdominal distension, oliguria, and progressively worsening hypercarbia and hypoxemia developed. Ventilatory requirements progressively increased, with PIP rising from 20 cm H2O to greater than 40 cm H2O. A bladder pressure of 26 mm Hg was measured. Emergent decompressive laparotomy was performed with placement of a polypropylene silo (Fig 1). The liver and spleen appeared congested, and approximately 1 L of tense ascites was drained. Immediately after decompression, the urine output improved significantly, and PIP returned to 20 to 25 cm H2O. After 6 days of steady improvement, the silo could be removed, and the fascia and skin were closed. She made a full recovery and is alive and well 7 months later.
DISCUSSION
The adverse effects of increased intraabdominal pressure were first described in the 1800s, but it was not recognized as a significant clinical problem among general surgery patients until the 1980s.15 Because of improvements in critical care, trauma management, and surgery, more and more critically ill patients are surviving the initial resuscitation, but this resuscitation is complicated potentially by intraabdominal hypertension. The term intraabdominal compartment syndrome, now called abdominal compartment syndrome, was first used by Fietsam et al in 1989.16 Since that time, the diagnosis of ACS is being made more frequently, and there is universal agreement that the only treatment is abdominal decompression.1-7 In early series of adult patients with ACS, there were no survivors without decompression.7
Fig 1. Five-year-old girl (case 3) immediately after decompressive laparotomy and placement of a polypropylene mesh silo.
841
Since the 1940s, when Gross17 first described the treatment of large omphaloceles, pediatric surgeons have been aware of the problems with intraabdominal hypertension. Omphalocele has been called ‘‘a prototype for ACS.’’6 Pediatric surgeons were the first to use prosthetic materials as a temporary closure of the abdominal wall,8 and they were among the first to measure intraabdominal pressures as a guide for reduction of the silo and closure of the abdominal wall.10-12 In addition to their use in the treatment of abdominal wall defects, prosthetic silos have been used in infants for the treatment of stage IV-S neuroblastoma and subcapsular hemorrhage of the liver.9,13,18 Only a few reports, however, discuss the management, beyond the newborn period, of children with ACS caused by trauma or shock.19,20 The most common cause of ACS is severe abdominal trauma complicated by hemorrhage and coagulopathy. Other causes have been described, including ruptured abdominal aortic aneurysm, acute pancreatitis, pelvic fracture, mesenteric thrombosis, intraabdominal abscess, laparoscopic pneumoperitoneum, liver transplantation, and closure of large ventral hernias.1,6,7,16 Even nonabdominal causes, such as extraperitoneal trauma or shock, as in our third case, can lead to ACS when a large fluid resuscitation is required. In addition to renal, pulmonary, and cardiovascular dysfunction, ACS also can lead to bowel ischemia, abdominal wall ischemia with woundhealing problems, venous statis with thrombosis, and increased intracranial pressure.1,3,6,7 The diagnosis of ACS should be considered in any critically ill patient in whom tense abdominal distension develops acutely. A high index of suspicion is necessary. The measurement of intraabdominal pressure is adjunctive information and can be helpful in certain patients, as in our third case. Intraabdominal pressure is determined most commonly and very reliably by measuring bladder pressure, which can be done by instilling 1 mL/kg body weight of sterile saline into the Foley catheter and connecting the end of the catheter to a pressure transducer or a manometer via a 3-way stopcock. The symphysis pubis is used as the zero reference point, and the pressure is measured in millimeters of mercury or centimeters of water (1 mm Hg ⫽ 1.36 cm H2O). The level at which various investigators would decompress the abdomen varies from 15 to 25 mm Hg (20 to 34 cm H2O).3-5,7,15 Other investigators state that the decision to decompress is not determined by a specific pressure measurement but by the physiological consequences of the increased intraabdominal pressure, such as progressive renal or cardiopulmonary insufficiency.4 To prevent ACS in high-risk surgical patients, prophylactic placement of prosthetic mesh is recommended,3 as in our second case. The mesh can remain safely in place
842
DECOU ET AL
for 5 to 7 days, but then should be removed and the fascia closed if significant diuresis and abdominal decompression have occurred. If the fascia cannot be closed by 5 to 7 days, the silo should be removed and a skin graft placed after adequate granulation appears. Later abdominal wall reconstruction then can be performed. From our review of the literature and our limited experience, we have learned several key points in the management of ACS in children. First, a high index of suspicion for ACS is needed in severely injured and critically ill children. Next, prophylactic decompression may be indicated at the time of initial laparotomy for patients in whom abdominal packing is used, who are
coagulopathic, or those who require massive fluid resuscitation. Immediate decompression is necessary in patients with the acute onset of tense abdominal distension combined with progressive oliguria, increased peak inspiratory pressure, or cardiovascular compromise. Lastly, measurement of bladder pressure can be helpful in patients with acute abdominal distension but no organ dysfunction. In these patients, we believe that decompression is indicated for pressures above 25 mm Hg, and we would strongly consider it for pressures between 20 and 25 mm Hg. Further attention and experience are needed to better understand this life-threatening syndrome and to optimize its management in children.
REFERENCES 1. Schein M, Wittmann DH, Aprahamian CC, et al: The abdominal compartment syndrome: The physiological and clinical consequences of elevated intra-abdominal pressure. J Am Coll Surg 180:745-753, 1995 2. Burch JM, Moore EE, Moore FA, et al: The abdominal compartment syndrome. Surg Clin North Am 76:833-842, 1996 3. Ivatury RR, Diebel L, Porter JM, et al: Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 77:783-800, 1997 4. Eddy V, Nunn C, Morris JA: Abdominal compartment syndrome: The Nashville experience. Surg Clin North Am 77:801-812, 1997 5. Meldrum DR, Moore FA, Moore EE, et al: Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 174:667-673, 1997 6. Watson RA, Howdieshell TR: Abdominal compartment syndrome. South Med J 91:326-332, 1998 7. Saggi BH, Sugerman HJ, Ivatury RR, et al: Abdominal compartment syndrome. J Trauma 45:597-609, 1998 8. Schuster SR: A new method for the staged repair of large omphaloceles. Surg Gynecol Obstet 125:837-850, 1967 9. Schnaufer L, Koop CE: Silastic abdominal patch for temporary hepatomegaly in stage IV-S neuroblastoma. J Pediatr Surg 10:73-75, 1975 10. Wesley JR, Drongowski R, Coran AG: Intragastric pressure measurement: A guide for reduction and closure of the silastic chimney in omphalocele and gastroschisis. J Pediatr Surg 16:264-270, 1981 11. Lacey SR, Bruce J, Brooks SP, et al: The relative merits of various methods of indirect measurement of intraabdominal pressure as
a guide to closure of abdominal wall defects. J Pediatr Surg 22:12071211, 1987 12. Lacey SR, Carris LA, Beyer J, et al: Bladder pressure monitoring significantly enhances care of infants with abdominal wall defects: A prospective clinical study. J Pediatr Surg 28:1370-1375, 1993 13. Lee EW, Applebaum H: Abdominal expansion as a bridging technique in stage IV-S neuroblastoma with massive hepatomegaly. J Pediatr Surg 29:1470-1471, 1994 14. DeCou JM, Abrams RS, Gauderer MWL: Seat-belt transection of the pararenal vena cava in a 5-year-old child: Survival with caval ligation. J Pediatr Surg 34:1074-1076, 1999 15. Kron IL, Harman PK, Nolan SP: The measurement of intraabdominal pressure as a criterion for abdominal re-exploration. Ann Surg 199:28-30, 1984 16. Fietsam R, Villalba M, Glover JL, et al: Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg 55:396-402, 1989 17. Gross R: A new method for surgical treatment of large omphaloceles. Surgery 24:277-292, 1948 18. Kosumi T, Kubota A, Yonekura T, et al: Subcapsular hemorrhage of the liver in a very-low-birth-weight neonate: Survival after decompression laparotomy. Pediatr Surg Int 15:270-271, 1999 19. Stylianos S, Jacir NN, Hoffman MA, et al: Pediatric blunt liver injury and coagulopathy managed with packs and a silo: Case report. J Trauma 30:1409-1410, 1990 20. Stylianos S: Abdominal packing for severe hemorrhage. J Pediatr Surg 33:339-342, 1998