- Email: [email protected]
Abdominal Compartment Syndrome in a Pediatric Patient With Cloacal Exstrophy
ARTICLE IN PRESS
Pediatric Case Reports Abdominal Compartment Syndrome in a Pediatric Patient With Cloacal Exstrophy Caleb E. Cooper, Alfred P. Kennedy, Jr., and D. Preston Smith We present a rare complication of abdominal compartment syndrome (ACS) in a child undergoing complex urologic reconstruction. A 10-year-old female born with the abdominal wall defect cloacal exstrophy who had previously undergone multiple abdominal procedures then developed findings consistent with ACS following a complex Mitrofanoff procedure. Although intravesical pressures were not documented because of the nature of her reconstruction, her ACStype findings were (1) abdominal pain, (2) melena, (3) pulmonary hypoinflation, (4) renal insufficiency, (5) tachycardia, and (6) segmental ischemic small bowel. Management consisted of abdominal decompression, segmental bowel resections, and wound vacuum-assisted-closure management. Patient was eventually discharged home. UROLOGY ■■: ■■–■■, 2016. © 2016 Elsevier Inc.
A
bdominal compartment syndrome (ACS) is a rare result of raised intra-abdominal pressure and can occur in postsurgical patients. High intraabdominal hypertension (IAH), usually above 25 mmHg, can lead to abdominal compartment syndrome with possible multiorgan dysfunction.1 The pressure from ACS on the inferior vena cava causes poor blood circulation and restricts blood flow to organs within the abdominal cavity.2 Pulmonary, cardiovascular, renal, splanchnic, musculoskeletal, and central nervous systems can all be affected.3 The development of ACS in burn and trauma patients is more understood than when it occurs in postoperative patients. Regardless of the cause, the diagnosis and prompt treatment of IAH are key factors to avoidance of ACS and multiorgan dysfunction. We present a case of a 10-year-old female born with the abdominal wall defect cloacal exstrophy. Because cloacal exstrophy is associated with significant urologic, intestinal, neurologic, and orthopedic deformities, multiple and sometimes complex surgical procedures are required.4 Abdominal surgical management can be complicated in these patients, given the tension from the abdominal wall defect, associated medical conditions, and the adhesions from multiple abdominal procedures. The reported patient had previously undergone multiple abdominal procedures and underwent a complex Mitrofanoff and ureteral
Financial Disclosure: The authors declare that they have no relevant financial interests. From the Pediatric Urology, East Tennessee Children’s Hospital, Knoxville, TN; and the Pediatric Surgery, Geisinger Health System, Danville, PA Address correspondence to: D. Preston Smith, M.D., F.A.A.P., F.A.C.S., F.S.P.U., Pediatric Urology, East Tennessee Children’s Hospital, 2100 Clinch Ave. MOB Suite 120, Knoxville, TN 37916. E-mail: [email protected] Submitted: December 5, 2015, accepted (with revisions): February 16, 2016
© 2016 Elsevier Inc. All rights reserved.
reimplantation procedure 6 days prior to developing complications and symptoms most likely related to ACS.
CASE HISTORY A very muscular 10-year-old female born with cloacal exstrophy, neurogenic bladder, and underlying renal insufficiency underwent a complex redo Mitrofanoff procedure (Monti iliocystostomy) and redo-ureteral reimplantation. Following a bowel preparation, she underwent the above procedures through a previous Pfannenstiel incision using a short segment of ileum. Although limited adhesiolysis was required, the procedure was uncomplicated. The nasogastric tube was inadvertently removed at the termination of the procedure. Over the next several days, the patient developed increasing abdominal pain, vomiting, intermittent oliguria, and one episode of melena. Aggressive intravenous crystalloid fluid replacement and insertion of nasogastric tube failed to provide improvement. She then developed tachycardia and worsening renal insufficiency. Abdominal and chest radiographs revealed partial small bowel obstruction and hypoinflation of lungs with bronchovascular crowding (Fig. 1). Exploratory laparotomy was pursued and discovered that in addition to ischemia around the distal ileal anastomosis, multiple proximal ischemic segmental small bowel lesions (skip lesions) were noted that were distant from the resected ilium and surgically manipulated small bowel. The patient’s abdomen was not closed and wound vacuum-assisted closure management was required. Several surgical procedures were required and multiple small bowel resections were necessary for segmental necrotic bowel. The patient was discharged home on total parental nutrition 78 days after the initial surgery. Eventually, bowel continuity was returned and she is now back to baseline and using the Mitrofanoff channel. Table 1 outlines the risk factors for our patient’s development of ACS. http://dx.doi.org/10.1016/j.urology.2016.02.025 0090-4295
1
ARTICLE IN PRESS Table 1. Risk factors in the development of abdominal compartment syndrome (ACS) Risk Factors for Developing ACS 1. 2. 3. 4. 5. 6.
Abdominal wall defects/Cloacal exstrophy Muscular abdominal wall Previous surgery/Adhesions Absence of nasogastric tube Aggressive intravenous fluid replacement Underlying renal insufficiency
DISCUSSION Despite being described 100 years ago, ACS was reported as a new clinical diagnosis in the 1980s. The recognition of both ACS and IAH has improved our understanding of the devastating effects these occurrences can have on the abdomen.5 ACS is a rare occurrence with significant effects in postoperative patient’s physiology. Early IAH is common but can lead to ACS-related multiorgan dysfunction. The results of ACS can cause a patient mortality rate to range from 30% to 60%.6 ACS can be caused by several confounding factors that increase pressure within the abdominal cavity or restrict the compliance of the abdominal wall. Ascites, edema, hemorrhage, visceral enlargement, ileus or bowel obstruction, and trauma are common causes for increased pressure or space-occupying factors that increase pressure within the abdomen. Abdominal wall compliance can be affected by congenital abdominal wall abnormalities (omphalocele, exstrophy), scar, musculature, dressings, and tissue edema. Prevention of ACS is possible by the use of tension-free abdominal mesh closures or staged closure that is commonly used in neonates with omphalocele.7 Diagnosis of suspected IAH and ACS is not complicated and usually
Figure 1. Abdominal and chest radiographs revealed partial small bowel obstruction and hypoinflation of lungs with bronchovascular crowding.
2
measured via Foley bladder catheter pressure measurements. Nonsurgical management is mostly directed to appropriate fluid resuscitation to avoid edema while preserving perfusion and decompressing space occupation within the abdominal cavity. Paracentesis, surgical drainage, nasogastric tube and Foley catheter insertion, and removal of abdominal dressings are all common nonsurgical considerations to improve clinically significant IAH. Decompressive laparotomy can be life saving and is also commonly necessary when conservative management fails. We hypothesize that ACS is a plausible cause for our patient born with a severe abdominal wall defect to develop several skip lesions of necrotic small bowel distant from the surgical site. High intra-abdominal pressures leading to poor perfusion of select areas perhaps compromised by adhesions and fixed space certainly could lead to ischemic bowel. Our patient never received preoperative vasopressors; therefore, it is likely that the “skip” small bowel necrotic segments were due to decreased bowel perfusion and adhesions in a very confined noncompliant abdominal compartment. Adhesiolysis and surgical manipulation were not the sole causes of this patient’s complication as most of the necrotic bowel segments were remote from the surgically manipulated tissues. Although we never investigated preoperatively for the increased abdominal pressure via standard bladder catheter pressure monitoring, the clinical presentation and findings intraoperatively certainly support the diagnosis of ACS. Our concern is whether conventional bladder catheter pressure monitoring would have been reliable or placed our recent procedure at risk because this patient had just undergone significant bladder surgery and had a history of a neurogenic bladder.8 Medical management (nasogastric tube, bladder catheter) has been used in several cases to attempt the immediate reduction of IAH. Nasogastric decompression is a common protocol used in patients undergoing major abdominal surgery.9 Our case resulted in the error of removal of the nasogastric tube once surgery was completed. Without a nasogastric tube, the patient was still NPO. Error of early omission of the nasogastric tube was predicted to be contributory to the cause of the resulting abdominal compartment syndrome because swallowed air and fluids accumulated, causing increased intra-abdominal pressure. Also, underlying renal insufficiency and aggressive intravenous crystalloid infusions contributed to tissue edema and abdominal pressure. Preoperatively, our patient’s abdomen was very muscular because she ambulated on one leg due to a congenital extremity deformity. Her muscularity along with a tight abdomen cavity from previous cloacal exstrophy closure certainly decreased her abdominal wall compliance. Surgical decompression and aggressive medical management quickly improved her clinical status. The necrotic bowel segments were resected and eventually bowel continuity was established. Our patient received delayed abdominal closure along while implementing vacuum-assisted closure management, which is a standard surgical consideration when faced with presumed ACS. This surgical method has been shown to be the most UROLOGY ■■ (■■), 2016
ARTICLE IN PRESS effective way of reversing ACS vs noninvasive methods, allowing for improved patient survival.10
CONCLUSION ACS is still associated with high mortality rates, leaving early recognition of high intra-abdominal pressure as the key to the prevention of organ dysfunction in a clinical setting. Medical management to avoid high intra-abdominal pressures should be optimized in patients at risk. Patients with abdominal wall defects, such as those with cloacal exstrophy, should be considered at risk and monitored postoperatively for IAH and even ACS when clinical parameters change.
References 1. Suzuki T, Okamoto T, Hanyu K, Suwa K, Ashizuka S, Yanaga K. Repair of Bochdalek hernia in an adult complicated by abdominal compartment syndrome, gastropleural fistula and pleural empyema: report of a case. Int J Surg Case Rep. 2014;5:82-85.
UROLOGY ■■ (■■), 2016
2. Cheatham ML. Abdominal Compartment Syndrome: pathophysiology and definitions. Scand J Trauma Resusc Emerg Med. 2009;17:10. 3. DeCou JM, Abrams RS, Miller RS, Gauderer MWL. Abdominal compartment syndrome in children: experience with three cases. J Pediatr Surg. 2000;35:840-842. 4. Miranda ME, Piçarro C, Campos BA, et al. Cloacal exstrophy associated with gastroschisis: case report of a rare association with favorable outcome. J Pediatr Surg Case Rep. 2015;3:107-110. 5. De Waele JJ, Malbrain ML, Kirkpatrick AW. The abdominal compartment syndrome: evolving concepts and future directions. Crit Care. 2015;19:211. 6. Newcombe J, Mathur M, Ejike C. Abdominal compartment syndrome in children. Crit Care Nurse. 2012;32:51-61. 7. Mohapatra B. Abdominal compartment syndrome. Indian J Crit Care Med. 2004;8:26-32. 8. Papavramidis TS, Marinis AD, Pliakos I, Kesisoglou I, Papavramidou N. Abdominal compartment syndrome—intra-abdominal hypertension: defining, diagnosing, and managing. J Emerg Trauma Shock. 2011;4:279-291. 9. Dinsmore JE, Maxson RT, Johnson DD, Jackson RJ, Wagner CW, Smith SD. Is nasogastric tube decompression necessary after major abdominal surgery in children? J Pediatr Surg. 1997;32:982-985. 10. Cheatham ML. Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg. 2009;33:1116-1122.
3
Pediatric Case Reports Abdominal Compartment Syndrome in a Pediatric Patient With Cloacal Exstrophy Caleb E. Cooper, Alfred P. Kennedy, Jr., and D. Preston Smith We present a rare complication of abdominal compartment syndrome (ACS) in a child undergoing complex urologic reconstruction. A 10-year-old female born with the abdominal wall defect cloacal exstrophy who had previously undergone multiple abdominal procedures then developed findings consistent with ACS following a complex Mitrofanoff procedure. Although intravesical pressures were not documented because of the nature of her reconstruction, her ACStype findings were (1) abdominal pain, (2) melena, (3) pulmonary hypoinflation, (4) renal insufficiency, (5) tachycardia, and (6) segmental ischemic small bowel. Management consisted of abdominal decompression, segmental bowel resections, and wound vacuum-assisted-closure management. Patient was eventually discharged home. UROLOGY ■■: ■■–■■, 2016. © 2016 Elsevier Inc.
A
bdominal compartment syndrome (ACS) is a rare result of raised intra-abdominal pressure and can occur in postsurgical patients. High intraabdominal hypertension (IAH), usually above 25 mmHg, can lead to abdominal compartment syndrome with possible multiorgan dysfunction.1 The pressure from ACS on the inferior vena cava causes poor blood circulation and restricts blood flow to organs within the abdominal cavity.2 Pulmonary, cardiovascular, renal, splanchnic, musculoskeletal, and central nervous systems can all be affected.3 The development of ACS in burn and trauma patients is more understood than when it occurs in postoperative patients. Regardless of the cause, the diagnosis and prompt treatment of IAH are key factors to avoidance of ACS and multiorgan dysfunction. We present a case of a 10-year-old female born with the abdominal wall defect cloacal exstrophy. Because cloacal exstrophy is associated with significant urologic, intestinal, neurologic, and orthopedic deformities, multiple and sometimes complex surgical procedures are required.4 Abdominal surgical management can be complicated in these patients, given the tension from the abdominal wall defect, associated medical conditions, and the adhesions from multiple abdominal procedures. The reported patient had previously undergone multiple abdominal procedures and underwent a complex Mitrofanoff and ureteral
Financial Disclosure: The authors declare that they have no relevant financial interests. From the Pediatric Urology, East Tennessee Children’s Hospital, Knoxville, TN; and the Pediatric Surgery, Geisinger Health System, Danville, PA Address correspondence to: D. Preston Smith, M.D., F.A.A.P., F.A.C.S., F.S.P.U., Pediatric Urology, East Tennessee Children’s Hospital, 2100 Clinch Ave. MOB Suite 120, Knoxville, TN 37916. E-mail: [email protected] Submitted: December 5, 2015, accepted (with revisions): February 16, 2016
© 2016 Elsevier Inc. All rights reserved.
reimplantation procedure 6 days prior to developing complications and symptoms most likely related to ACS.
CASE HISTORY A very muscular 10-year-old female born with cloacal exstrophy, neurogenic bladder, and underlying renal insufficiency underwent a complex redo Mitrofanoff procedure (Monti iliocystostomy) and redo-ureteral reimplantation. Following a bowel preparation, she underwent the above procedures through a previous Pfannenstiel incision using a short segment of ileum. Although limited adhesiolysis was required, the procedure was uncomplicated. The nasogastric tube was inadvertently removed at the termination of the procedure. Over the next several days, the patient developed increasing abdominal pain, vomiting, intermittent oliguria, and one episode of melena. Aggressive intravenous crystalloid fluid replacement and insertion of nasogastric tube failed to provide improvement. She then developed tachycardia and worsening renal insufficiency. Abdominal and chest radiographs revealed partial small bowel obstruction and hypoinflation of lungs with bronchovascular crowding (Fig. 1). Exploratory laparotomy was pursued and discovered that in addition to ischemia around the distal ileal anastomosis, multiple proximal ischemic segmental small bowel lesions (skip lesions) were noted that were distant from the resected ilium and surgically manipulated small bowel. The patient’s abdomen was not closed and wound vacuum-assisted closure management was required. Several surgical procedures were required and multiple small bowel resections were necessary for segmental necrotic bowel. The patient was discharged home on total parental nutrition 78 days after the initial surgery. Eventually, bowel continuity was returned and she is now back to baseline and using the Mitrofanoff channel. Table 1 outlines the risk factors for our patient’s development of ACS. http://dx.doi.org/10.1016/j.urology.2016.02.025 0090-4295
1
ARTICLE IN PRESS Table 1. Risk factors in the development of abdominal compartment syndrome (ACS) Risk Factors for Developing ACS 1. 2. 3. 4. 5. 6.
Abdominal wall defects/Cloacal exstrophy Muscular abdominal wall Previous surgery/Adhesions Absence of nasogastric tube Aggressive intravenous fluid replacement Underlying renal insufficiency
DISCUSSION Despite being described 100 years ago, ACS was reported as a new clinical diagnosis in the 1980s. The recognition of both ACS and IAH has improved our understanding of the devastating effects these occurrences can have on the abdomen.5 ACS is a rare occurrence with significant effects in postoperative patient’s physiology. Early IAH is common but can lead to ACS-related multiorgan dysfunction. The results of ACS can cause a patient mortality rate to range from 30% to 60%.6 ACS can be caused by several confounding factors that increase pressure within the abdominal cavity or restrict the compliance of the abdominal wall. Ascites, edema, hemorrhage, visceral enlargement, ileus or bowel obstruction, and trauma are common causes for increased pressure or space-occupying factors that increase pressure within the abdomen. Abdominal wall compliance can be affected by congenital abdominal wall abnormalities (omphalocele, exstrophy), scar, musculature, dressings, and tissue edema. Prevention of ACS is possible by the use of tension-free abdominal mesh closures or staged closure that is commonly used in neonates with omphalocele.7 Diagnosis of suspected IAH and ACS is not complicated and usually
Figure 1. Abdominal and chest radiographs revealed partial small bowel obstruction and hypoinflation of lungs with bronchovascular crowding.
2
measured via Foley bladder catheter pressure measurements. Nonsurgical management is mostly directed to appropriate fluid resuscitation to avoid edema while preserving perfusion and decompressing space occupation within the abdominal cavity. Paracentesis, surgical drainage, nasogastric tube and Foley catheter insertion, and removal of abdominal dressings are all common nonsurgical considerations to improve clinically significant IAH. Decompressive laparotomy can be life saving and is also commonly necessary when conservative management fails. We hypothesize that ACS is a plausible cause for our patient born with a severe abdominal wall defect to develop several skip lesions of necrotic small bowel distant from the surgical site. High intra-abdominal pressures leading to poor perfusion of select areas perhaps compromised by adhesions and fixed space certainly could lead to ischemic bowel. Our patient never received preoperative vasopressors; therefore, it is likely that the “skip” small bowel necrotic segments were due to decreased bowel perfusion and adhesions in a very confined noncompliant abdominal compartment. Adhesiolysis and surgical manipulation were not the sole causes of this patient’s complication as most of the necrotic bowel segments were remote from the surgically manipulated tissues. Although we never investigated preoperatively for the increased abdominal pressure via standard bladder catheter pressure monitoring, the clinical presentation and findings intraoperatively certainly support the diagnosis of ACS. Our concern is whether conventional bladder catheter pressure monitoring would have been reliable or placed our recent procedure at risk because this patient had just undergone significant bladder surgery and had a history of a neurogenic bladder.8 Medical management (nasogastric tube, bladder catheter) has been used in several cases to attempt the immediate reduction of IAH. Nasogastric decompression is a common protocol used in patients undergoing major abdominal surgery.9 Our case resulted in the error of removal of the nasogastric tube once surgery was completed. Without a nasogastric tube, the patient was still NPO. Error of early omission of the nasogastric tube was predicted to be contributory to the cause of the resulting abdominal compartment syndrome because swallowed air and fluids accumulated, causing increased intra-abdominal pressure. Also, underlying renal insufficiency and aggressive intravenous crystalloid infusions contributed to tissue edema and abdominal pressure. Preoperatively, our patient’s abdomen was very muscular because she ambulated on one leg due to a congenital extremity deformity. Her muscularity along with a tight abdomen cavity from previous cloacal exstrophy closure certainly decreased her abdominal wall compliance. Surgical decompression and aggressive medical management quickly improved her clinical status. The necrotic bowel segments were resected and eventually bowel continuity was established. Our patient received delayed abdominal closure along while implementing vacuum-assisted closure management, which is a standard surgical consideration when faced with presumed ACS. This surgical method has been shown to be the most UROLOGY ■■ (■■), 2016
ARTICLE IN PRESS effective way of reversing ACS vs noninvasive methods, allowing for improved patient survival.10
CONCLUSION ACS is still associated with high mortality rates, leaving early recognition of high intra-abdominal pressure as the key to the prevention of organ dysfunction in a clinical setting. Medical management to avoid high intra-abdominal pressures should be optimized in patients at risk. Patients with abdominal wall defects, such as those with cloacal exstrophy, should be considered at risk and monitored postoperatively for IAH and even ACS when clinical parameters change.
References 1. Suzuki T, Okamoto T, Hanyu K, Suwa K, Ashizuka S, Yanaga K. Repair of Bochdalek hernia in an adult complicated by abdominal compartment syndrome, gastropleural fistula and pleural empyema: report of a case. Int J Surg Case Rep. 2014;5:82-85.
UROLOGY ■■ (■■), 2016
2. Cheatham ML. Abdominal Compartment Syndrome: pathophysiology and definitions. Scand J Trauma Resusc Emerg Med. 2009;17:10. 3. DeCou JM, Abrams RS, Miller RS, Gauderer MWL. Abdominal compartment syndrome in children: experience with three cases. J Pediatr Surg. 2000;35:840-842. 4. Miranda ME, Piçarro C, Campos BA, et al. Cloacal exstrophy associated with gastroschisis: case report of a rare association with favorable outcome. J Pediatr Surg Case Rep. 2015;3:107-110. 5. De Waele JJ, Malbrain ML, Kirkpatrick AW. The abdominal compartment syndrome: evolving concepts and future directions. Crit Care. 2015;19:211. 6. Newcombe J, Mathur M, Ejike C. Abdominal compartment syndrome in children. Crit Care Nurse. 2012;32:51-61. 7. Mohapatra B. Abdominal compartment syndrome. Indian J Crit Care Med. 2004;8:26-32. 8. Papavramidis TS, Marinis AD, Pliakos I, Kesisoglou I, Papavramidou N. Abdominal compartment syndrome—intra-abdominal hypertension: defining, diagnosing, and managing. J Emerg Trauma Shock. 2011;4:279-291. 9. Dinsmore JE, Maxson RT, Johnson DD, Jackson RJ, Wagner CW, Smith SD. Is nasogastric tube decompression necessary after major abdominal surgery in children? J Pediatr Surg. 1997;32:982-985. 10. Cheatham ML. Nonoperative management of intraabdominal hypertension and abdominal compartment syndrome. World J Surg. 2009;33:1116-1122.
3