Dig Dis Sci DOI 10.1007/s10620-014-3240-1
STANFORD MULTIDISCIPLINARY SEMINARS
Acute Gastric Dilation and Necrosis as a Late Complication Following Laparoscopic Nissen Fundoplication Jordan M. Cloyd • Alexander Moskovitz John Stevenson
•
Received: 29 May 2014 / Accepted: 29 May 2014 Springer Science+Business Media New York 2014
Case Presentation and Evolution One year prior to the present admission, a 58-year old woman underwent a laparoscopic para-esophageal hernia repair using mesh and a Nissen fundoplication. Her postoperative course was notable for dysphagia that had required two endoscopic dilations. On the day of admission, she presented to the emergency department with acute onset of severe abdominal pain, distension, nausea and inability to vomit. On physical examination, she appeared toxic and in respiratory distress. Her abdomen was distended, firm, with marked, diffuse tenderness. Her lower extremities demonstrated progressive mottling to the level of her waist. Scant dark urine was present in her Foley catheter. Her laboratory values were notable for a WBC of 22,000/lL lactate of 3.8 mmol/L, creatinine of 0.9 mg/dL, INR of 2.1 and lipase of 32,038 U/ L. Urgent plain radiographs demonstrated massive gastric dilation (Fig. 1). Despite multiple attempts, a nasogastric tube could not be placed. An urgent CT scan demonstrated gastric and small bowel distension, small bowel pneumatosis, portal venous gas, free intra-abdominal fluid, gallstones and peri-pancreatic inflammation (Fig. 2). She was taken emergently to the operating room for exploratory laparotomy. Portions of the stomach and small intestine appeared ischemic although potentially salvageable. Her fundoplication was intact. Although no obvious
intestinal obstruction was identified, significant retroperitoneal edema and a compartment syndrome were confirmed. The stomach was decompressed, a gastrostomy tube was placed, and a cholecystectomy was performed. The abdomen was then temporarily closed, and patient was taken to the intensive care unit. Two days later, she underwent a second look operation and esophagoscopy. Full thickness gastric necrosis and small bowel ischemia were noted. An increase in retroperitoneal inflammation and saponification was also observed. A proximal subtotal gastrectomy and small bowel resection with anastomosis were performed, while a short segment of antrum was left over in order to place a decompressing gastrostomy tube. The patient was left in discontinuity with an esophageal stump and adjacent drains. A feeding jejunostomy tube was placed, and the abdomen was closed using a bridging biologic mesh. The patient was kept with nothing by mouth with a cervical pharyngotomy tube in the esophageal pouch waiting for the intra-abdominal inflammation to subside and nutrition to improve. A split thickness skin graft was placed to hasten secondary healing of the abdominal bed. Nine months into her hospitalization, she underwent completion gastrectomy and successful reconstruction with Roux-en-y esophagojejunostomy. Two months later, she was discharged home eating solid food with tube feed supplementation.
Discussion J. M. Cloyd (&) Department of Surgery, Stanford University, 300 Pasteur Dr, MC5641, Stanford, CA 94305, USA e-mail: [email protected] A. Moskovitz J. Stevenson Kaiser Permanente Santa Clara Medical Center, Santa Clara, CA, USA
First described in 1833, acute gastric dilation (AGD) may be caused by polyphagia, electrolyte abnormalities, diaphragmatic herniation and volvulus, medications, intestinal obstructions, trauma or other conditions [1]. The exact cause in our patient is unknown; possibilities include distal small bowel obstruction from adhesions or massive ileus
123
Dig Dis Sci
Fig. 1 Plain supine radiograph upon presentation, demonstrating massive gastric dilation
related to severe gallstone pancreatitis. In a patient status post-fundoplication, increased intra-gastric pressure from distal obstruction tightens the competent fundoplication wrap, prohibiting emesis, creating in essence a closed loop obstruction and worsening AGD. With increasing gastric distension, abdominal compartment syndrome may occur, as in this patient. Without prompt intervention, acute kidney injury, respiratory failure and other physiologic insults ensue. The most feared complication of AGD, though, is gastric necrosis. Because of its rich arterial blood supply, the stomach is very resistant to ischemia [2]. When intra-gastric
pressure exceeds 20 cm Hg, however, venous congestion coincides with arterial insufficiency that can lead to mucosal ischemia and eventually full thickness gastric necrosis. Although rare, gastric necrosis is associated with an exceedingly high mortality rate, worsened by delays in diagnosis or intervention. Prompt nasogastric decompression is the preferred initial management. When concern for ischemia exists, urgent laparotomy is imperative. AGD and gastric necrosis following laparoscopic fundoplication were first reported in two toddlers who had developed adhesive small bowel obstructions; both patients expired shortly after surgery [3]. Two previous cases of gastric necrosis have been reported in adults following fundoplication: One was managed with total gastrectomy and immediate Roux-en-Y esophago-jejunostomy, and the other patient expired with comfort care measures [4, 5]. In this patient, immediate reconstruction following gastrectomy was not performed due to hemodynamic instability and ongoing pancreatitis. Instead, delayed reconstruction after several months of conservative treatment with esophageal pouch decompression, wound care and enteral feeds was undertaken [6]. The tightness of the wrap is strongly considered at the time of fundoplication with surgeons needing to balance the risk of recurrent GERD with the potential for postoperative dysphagia. The gas-bloat syndrome is an ill-defined entity that affects some patients after a tight fundoplication. It typically presents with post-prandial bloating, early satiety, flatulence and the inability to belch or vomit [7]. In addition to contributing to gas-bloat symptoms, a wrap that is too tight may increase the risk for AGD. Previous work in canine models found that those with tighter fundoplication were unable to vomit after insufflation of air and
Fig. 2 Axial computed tomography images demonstrating a gastric dilation, portal venous gas (small arrow) cholelithiasis (large arrow) and b small intestinal dilation, retroperitoneal edema (small arrow) and compressed kidneys (large arrow)
123
Dig Dis Sci
were at higher risk for gastric dilation, infarction and death, suggesting that a looser fundoplication is preferable [8]. Regardless of the tightness of the fundoplication wrap, a high index of suspicion for AGD in patients who have undergone previous antireflux surgery is critical to avoiding further complications. Prompt placement of a nasogastric tube is mandatory when AGD is suspected or confirmed. If laparotomy is required and gastric necrosis is encountered, gastrectomy is typically indicated with immediate or delayed reconstruction based on the patient’s clinical status.
Key Messages •
• •
Acute gastric dilation may be caused by polyphagia, electrolyte abnormalities, diaphragmatic herniation and volvulus, medications, intestinal obstructions, trauma or other conditions and represents a medical-surgical emergency Placement of a nasogastric tube is mandatory for decompression. Laparotomy may be required and if gastric necrosis is found, a gastrectomy is indicated
References 1. Todd SR, Marshall GT, Tyroch AH. Acute gastric dilatation revisited. Am Surg. 2000;66:709–710. 2. Edlich RF, Borner JW, Kuphal J, Wangensteen OH. Gastric blood flow. I. Its distribution during gastric distention. Am J Surg. 1970;120:35–37. 3. Glick PL, Harrison MR, Adzick NS, Webb HW, DeLorimier AA. Gastric infarction secondary to small bowel obstruction: a preventable complication after Nissen fundoplication. J Pediatr Surg. 1987;22:941–943. 4. Patuto N, Acklin Y, Oertli D, Langer I. Gastric necrosis complicating lately a Nissen fundoplication. Report of a case. Langenbecks Arch Surg. 2008;393:45–47. 5. Barker JA, Burnett H, Carlson GL. Gastric necrosis complicating acute gastric dilatation after Nissen fundoplication. BMJ Case Rep. 2011. doi:10.1136/bcr.02.2011.3811. 6. Bass KD, Meagher DP Jr, Haase GM. Gastric necrosis after fundoplication: a novel approach for esophageal preservation. J Pediatr Surg. 1998;33:1720–1722. 7. Richter JE. Gastroesophageal reflux disease treatment: side effects and complications of fundoplication. Clin Gastroenterol Hepatol. 2013;11:465–471. 8. Donahue PE, Larson GM, Stewardson RH, Bombeck CT. Floppy Nissen fundoplication. Rev Surg. 1977;34:223–224.
123
STANFORD MULTIDISCIPLINARY SEMINARS
Acute Gastric Dilation and Necrosis as a Late Complication Following Laparoscopic Nissen Fundoplication Jordan M. Cloyd • Alexander Moskovitz John Stevenson
•
Received: 29 May 2014 / Accepted: 29 May 2014 Springer Science+Business Media New York 2014
Case Presentation and Evolution One year prior to the present admission, a 58-year old woman underwent a laparoscopic para-esophageal hernia repair using mesh and a Nissen fundoplication. Her postoperative course was notable for dysphagia that had required two endoscopic dilations. On the day of admission, she presented to the emergency department with acute onset of severe abdominal pain, distension, nausea and inability to vomit. On physical examination, she appeared toxic and in respiratory distress. Her abdomen was distended, firm, with marked, diffuse tenderness. Her lower extremities demonstrated progressive mottling to the level of her waist. Scant dark urine was present in her Foley catheter. Her laboratory values were notable for a WBC of 22,000/lL lactate of 3.8 mmol/L, creatinine of 0.9 mg/dL, INR of 2.1 and lipase of 32,038 U/ L. Urgent plain radiographs demonstrated massive gastric dilation (Fig. 1). Despite multiple attempts, a nasogastric tube could not be placed. An urgent CT scan demonstrated gastric and small bowel distension, small bowel pneumatosis, portal venous gas, free intra-abdominal fluid, gallstones and peri-pancreatic inflammation (Fig. 2). She was taken emergently to the operating room for exploratory laparotomy. Portions of the stomach and small intestine appeared ischemic although potentially salvageable. Her fundoplication was intact. Although no obvious
intestinal obstruction was identified, significant retroperitoneal edema and a compartment syndrome were confirmed. The stomach was decompressed, a gastrostomy tube was placed, and a cholecystectomy was performed. The abdomen was then temporarily closed, and patient was taken to the intensive care unit. Two days later, she underwent a second look operation and esophagoscopy. Full thickness gastric necrosis and small bowel ischemia were noted. An increase in retroperitoneal inflammation and saponification was also observed. A proximal subtotal gastrectomy and small bowel resection with anastomosis were performed, while a short segment of antrum was left over in order to place a decompressing gastrostomy tube. The patient was left in discontinuity with an esophageal stump and adjacent drains. A feeding jejunostomy tube was placed, and the abdomen was closed using a bridging biologic mesh. The patient was kept with nothing by mouth with a cervical pharyngotomy tube in the esophageal pouch waiting for the intra-abdominal inflammation to subside and nutrition to improve. A split thickness skin graft was placed to hasten secondary healing of the abdominal bed. Nine months into her hospitalization, she underwent completion gastrectomy and successful reconstruction with Roux-en-y esophagojejunostomy. Two months later, she was discharged home eating solid food with tube feed supplementation.
Discussion J. M. Cloyd (&) Department of Surgery, Stanford University, 300 Pasteur Dr, MC5641, Stanford, CA 94305, USA e-mail: [email protected] A. Moskovitz J. Stevenson Kaiser Permanente Santa Clara Medical Center, Santa Clara, CA, USA
First described in 1833, acute gastric dilation (AGD) may be caused by polyphagia, electrolyte abnormalities, diaphragmatic herniation and volvulus, medications, intestinal obstructions, trauma or other conditions [1]. The exact cause in our patient is unknown; possibilities include distal small bowel obstruction from adhesions or massive ileus
123
Dig Dis Sci
Fig. 1 Plain supine radiograph upon presentation, demonstrating massive gastric dilation
related to severe gallstone pancreatitis. In a patient status post-fundoplication, increased intra-gastric pressure from distal obstruction tightens the competent fundoplication wrap, prohibiting emesis, creating in essence a closed loop obstruction and worsening AGD. With increasing gastric distension, abdominal compartment syndrome may occur, as in this patient. Without prompt intervention, acute kidney injury, respiratory failure and other physiologic insults ensue. The most feared complication of AGD, though, is gastric necrosis. Because of its rich arterial blood supply, the stomach is very resistant to ischemia [2]. When intra-gastric
pressure exceeds 20 cm Hg, however, venous congestion coincides with arterial insufficiency that can lead to mucosal ischemia and eventually full thickness gastric necrosis. Although rare, gastric necrosis is associated with an exceedingly high mortality rate, worsened by delays in diagnosis or intervention. Prompt nasogastric decompression is the preferred initial management. When concern for ischemia exists, urgent laparotomy is imperative. AGD and gastric necrosis following laparoscopic fundoplication were first reported in two toddlers who had developed adhesive small bowel obstructions; both patients expired shortly after surgery [3]. Two previous cases of gastric necrosis have been reported in adults following fundoplication: One was managed with total gastrectomy and immediate Roux-en-Y esophago-jejunostomy, and the other patient expired with comfort care measures [4, 5]. In this patient, immediate reconstruction following gastrectomy was not performed due to hemodynamic instability and ongoing pancreatitis. Instead, delayed reconstruction after several months of conservative treatment with esophageal pouch decompression, wound care and enteral feeds was undertaken [6]. The tightness of the wrap is strongly considered at the time of fundoplication with surgeons needing to balance the risk of recurrent GERD with the potential for postoperative dysphagia. The gas-bloat syndrome is an ill-defined entity that affects some patients after a tight fundoplication. It typically presents with post-prandial bloating, early satiety, flatulence and the inability to belch or vomit [7]. In addition to contributing to gas-bloat symptoms, a wrap that is too tight may increase the risk for AGD. Previous work in canine models found that those with tighter fundoplication were unable to vomit after insufflation of air and
Fig. 2 Axial computed tomography images demonstrating a gastric dilation, portal venous gas (small arrow) cholelithiasis (large arrow) and b small intestinal dilation, retroperitoneal edema (small arrow) and compressed kidneys (large arrow)
123
Dig Dis Sci
were at higher risk for gastric dilation, infarction and death, suggesting that a looser fundoplication is preferable [8]. Regardless of the tightness of the fundoplication wrap, a high index of suspicion for AGD in patients who have undergone previous antireflux surgery is critical to avoiding further complications. Prompt placement of a nasogastric tube is mandatory when AGD is suspected or confirmed. If laparotomy is required and gastric necrosis is encountered, gastrectomy is typically indicated with immediate or delayed reconstruction based on the patient’s clinical status.
Key Messages •
• •
Acute gastric dilation may be caused by polyphagia, electrolyte abnormalities, diaphragmatic herniation and volvulus, medications, intestinal obstructions, trauma or other conditions and represents a medical-surgical emergency Placement of a nasogastric tube is mandatory for decompression. Laparotomy may be required and if gastric necrosis is found, a gastrectomy is indicated
References 1. Todd SR, Marshall GT, Tyroch AH. Acute gastric dilatation revisited. Am Surg. 2000;66:709–710. 2. Edlich RF, Borner JW, Kuphal J, Wangensteen OH. Gastric blood flow. I. Its distribution during gastric distention. Am J Surg. 1970;120:35–37. 3. Glick PL, Harrison MR, Adzick NS, Webb HW, DeLorimier AA. Gastric infarction secondary to small bowel obstruction: a preventable complication after Nissen fundoplication. J Pediatr Surg. 1987;22:941–943. 4. Patuto N, Acklin Y, Oertli D, Langer I. Gastric necrosis complicating lately a Nissen fundoplication. Report of a case. Langenbecks Arch Surg. 2008;393:45–47. 5. Barker JA, Burnett H, Carlson GL. Gastric necrosis complicating acute gastric dilatation after Nissen fundoplication. BMJ Case Rep. 2011. doi:10.1136/bcr.02.2011.3811. 6. Bass KD, Meagher DP Jr, Haase GM. Gastric necrosis after fundoplication: a novel approach for esophageal preservation. J Pediatr Surg. 1998;33:1720–1722. 7. Richter JE. Gastroesophageal reflux disease treatment: side effects and complications of fundoplication. Clin Gastroenterol Hepatol. 2013;11:465–471. 8. Donahue PE, Larson GM, Stewardson RH, Bombeck CT. Floppy Nissen fundoplication. Rev Surg. 1977;34:223–224.
123
