Arnold H. Belgraier, Senior Attending Surgeon, St. Luke's- Roosevelt Hospital, New York, NY, Assistant Clinical Professor of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY
Arnold H. Belgraier, MD Senior Attending Surgeon
St. Luke’s-Roosevelt Hospital
New York, NY
Assistant Clinical Professor of Surgery
College of Physicians and Surgeons
New York, NY
Petersen’s internal hernia occurs posterior to a gastroenteric anastomosis. Although rare, this hernia was well known during the 75 years in which chronic peptic ulcer disease was commonly treated by gastric resection and gastrojejunostomy. Since elective surgery for chronic peptic ulcer disease is now uncommon, a whole generation of surgeons may not be familiar with Petersen’s hernia at a time when this defect is making a resurgence because of the increasing popularity of Roux-en-Y gastric bypass to treat morbid obesity. Early recognition of this potentially serious condition is essential.
In the undisturbed abdominal cavity, the transverse colon acts as a partition between the stomach above and the small intestine below. Once a gastroenteric anastomosis is constructed, a potential space for internal herniation is created posterior to the limbs of the small intestine. The risk for herniation exists whether the anastomosis is ante- or retrocolic and whether the gastrojejunostomy is nonresectional or performed after a partial or subtotal gastrectomy.
In 1900, the European literature included a report by Petersen on the occurrence of an internal hernia after partial gastrectomy and gastrojejunostomy.1 Soon thereafter, similar reports appeared in the American literature. Throughout the greater part of the 20th century, there were frequent updates on Petersen’s hernia, and by 1974, 178 cases had been reported.2 This span of about 75 years was the era when peptic ulcer disease and its complications were common and every general surgeon was familiar with performing antrectomy, truncal vagotomy, gastrojejunostomy, or subtotal gastrectomy in conjunction with gastrojejunostomy, since these were the most popular and effective treatments for chronic peptic ulcer disease. Although Petersen’s hernia was rare despite the millions of gastric resections that had been performed, it was an appreciated entity, and several authors, including my former professor Dr. Alfred Markowitz, reported on its clinical presentations and the need to have a high index of suspicion because immediate surgery could be life-saving.3-5
Just as there was a rapid increase and sustained prevalence of peptic ulcer disease in the decades before and after WWII,6 there was also an unexplained and dramatic decrease in the prevalence of this disease preceding the development, acceptance, and use of histamine receptor antagonists that began in 1977.3 With the addition of other nonsurgical therapies, such as proton pump inhibitors and antibiotics against , elective surgery for chronic peptic ulcer disease and its complications became uncommon. As a result, a whole generation of surgical residents has been trained with minimal exposure to resectional gastric surgery, methods of gastrointestinal reconstruction, and the resulting postoperative anatomy and complications.
Petersen’s hernia has recently made a resurgence due to the popularity of Roux-en-Y gastric bypass to treat morbid obesity. The single Roux limb forming the pouch gastrojejunostomy presents the same possibility for internal herniation as the loops of a standard gastrojejunostomy. The case that follows illustrates this problem in its most severe form.
A 51-year-old man came to the emergency department reporting abdominal pain, nausea, and vomiting 24 hours after arriving in New York City from California. He was hypotensive, tachycardic, dehydrated, and had a temperature of 96.2°F. His abdomen was not distended and no gross peritoneal signs were elicited, but there was diffuse tenderness upon palpation. The patient was hydrated and was able to produce urine after receiving 3 L of Ringer’s lactate solution. Laboratory examinations revealed a hematocrit of 51% (normal, 41%—50%), white blood cell count of 12,700/µL (normal, 4,500-10,000/µL), amylase of 83 U/L (normal 25-85 U/L), and pH of 7.26 (normal, 7.35-7.45). A plain abdominal radiograph revealed a diffusely gasless abdomen with one mildly distended air-filled small bowel loop in the left hypogastrium.
The patient’s surgical history included a successful laparoscopic Roux-en-Y gastric bypass 11/2 years earlier, which resulted in a 150-lb weight loss, as well as an abdominoplasty for excess skin laxity 6 months before his current presentation. Two weeks before his trip to New York City, the patient experienced mild intermittent abdominal cramping and occasional loss of appetite. A medical checkup found no abnormalities.
His initial evaluation at Roosevelt Hospital suggested the possibility of a compromised loop of small intestine incarcerated in a Petersen’s hernia. Within 1 hour of collecting the patient’s history and providing fluid resuscitation, he underwent emergency exploration. Because he was still mildly hypotensive, arterial and venous monitoring lines were placed. A generous midline incision was made, which revealed 1 L of nonodorous hemorrhagic ascites. The entire small intestine, from the jejunojejunostomy to the ileocecal valve, had herniated through a 4-cm Petersen’s hernia and was misplaced on the left side of the abdomen (Figure 1). All of the patient’s incarcerated small intestine was deep purple to black in color, and only the gastrojejunostomy limb and the proximal biliary pancreatic limb were pink (Figure 1). The compromised intestine could not be safely reduced because of the risks of creating an enterotomy and the possibility of spilling contents. The defect was instead enlarged by dividing part of the mesentery that formed the wall of the defect, and the severely compromised small intestine was then brought back to its normal anatomical position on the right side of the abdomen and pelvis, which resulted in a noticeable improvement in color (Figure 2).
After 7 minutes, the intestine was reexamined and was clearly less congested. Arterial pulsations were also observed in the distal mesenteric arcades. A 5-ft-long jejunostomy tube was fashioned and placed through the abdominal wall, and 2 L of hemorrhagic intestinal contents were removed. The hernia defect was closed with silk sutures. A large sheet of absorbable mesh was folded upon itself and quickly sewn to both sides of the divided linea alba, and the wide open subcutaneous and skin defects were filled with absorbent gauze and towels. Still intubated and hypotensive, the patient was brought to the intensive care unit for resuscitation and ventilator support until a second, planned laparotomy could be performed 24 hours later. Overnight, the patient underwent hemodynamic monitoring and continued fluid resuscitation and administration of broad-spectrum antibiotics. His acidosis, blood pressure, heart rate, and urine output normalized, and peritoneal fluid drainage remained clear and nonodorous. At reexploration, a long vertical slit was made in the mesh and the small intestine was observed to be grossly edematous and hemorrhagic but clearly viable. Cultures of peritoneal fluid were taken, the jejunostomy was checked for any sign of leakage, and copious peritoneal irrigation was performed. The mesh was then closed with a heavy running suture, and absorbent gauze and towels were applied as before.
After 3 days of intubation, sedation, and aggressive diuresis, the patient showed improvement in all areas. He returned to the operating room for further exploration, which revealed no sign of intestinal wall necrosis or leakage. Copious irrigation was performed, proper bowel position and closure of the Petersen’s defect were confirmed, the mesh was removed, and the linea alba, subcutaneous tissues, and skin were closed primarily. The patient had a slow but steady recovery and was discharged from the hospital 12 days later. For many months after the surgery, the patient had frequent loose bowel movements and excess flatus due to reduced small bowel absorption; however, this slowly improved, and when he recently returned to New York City, we shared a happy reunion and a hearty meal.
Although Petersen’s hernia involves the potential space posterior to a gastrojejunostomy, its presentation and physical, laboratory, and radiography findings are similar to those for other internal hernias. Treatment requires reduction of the incarcerated bowel and closure of the defect. Any nonviable bowel must be resected.
In the early postoperative period following Roux-en-Y gastric bypass, mild intermittent symptoms probably represent partial small bowel obstruction with spontaneous reduction. The resulting nausea, vomiting, abdominal cramping, and pain may be attributed to a host of postsurgical problems including edema, angulation, small leaks at the anastomoses, hematoma, or adhesive obstruction. In the late postoperative period, symptoms may be ascribed to anastomotic stricture or adhesions, gallbladder colic, pancreatitis, or failure to follow dietary restrictions. Investigative computed tomography (CT) scans and upper gastrointestinal and small bowel contrast studies may fail to reveal an internal hernia in 20% of cases, especially if the radiologist is unfamiliar with the anatomical changes following Roux-en-Y gastric bypass or is not advised of the patient’s surgical history and the suspicion of an internal hernia.7
Without an awareness of Petersen’s defect and other spaces produced by the Roux-en-Y reconstruction that have the potential for internal herniation, a patient’s condition may go undiagnosed until an acute attack results in complete small bowel obstruction and vascular compromise. Such patients must be resuscitated quickly and undergo urgent exploration because small bowel infarction and sepsis may be only hours away. While some surgeons may wish to have the more detailed information that a CT scan can provide, the time needed to obtain imaging might result in an unfortunate delay of surgery.
Bariatric surgeons must pay special attention to closing all potential hernia sites when performing the Roux-en-Y gastric bypass; however, it is to be expected that occasionally sutures may be too widely spaced or may pull through or that significant weight loss with its accompanying loss of mesenteric fat volume may result in a defect. Therefore, every patient having Roux-en-Y gastric bypass should be considered vulnerable to an internal hernia, and any abdominal symptoms in these patients should raise suspicion of this serious entity.
Petersen’s hernia occurs posterior to the limbs of a gastrojejunostomy, and although rare, this defect was well known during the first three quarters of the 20th century when elective surgery for chronic peptic ulcer disease was common. Although this internal hernia has been rarely encountered over the past 25 years, it is now being seen with increasing frequency due to the large number of Roux-en-Y gastric bypasses performed to treat morbid obesity.
An internal hernia should be suspected in any patient having undergone Roux-en-Y gastric bypass who develops abdominal symptoms. Acute presentations that include significant abdominal pain and vomiting suggest severe bowel obstruction and vascular compromise and require emergency laparotomy.
Arch Klin Chir.
1. Petersen W. Über Darmverschlinung nach der Gastroenterostomie. 1900;62:94-114.
2. Johnson JM, Wood M, Lawson J, et al. Retroanastomotic hernia. . 1974;108(3):363-365.
3. Fineberg HV, Pearlman LA. Surgical treatment of peptic ulcer in the United States. Trends before and after the introduction of cimetidine. 1981;1(8233):1305-1307.
Am J Surg
4. Sebesta DG, Robson MC. Petersen’s retroanastomotic hernia. . 1968;116(3):450-453.
5. Markowitz AM. Internal hernia after gastrojejunostomy. . 1961;49:185-194.
6. Mendeloff AI. What has been happening to duodenal ulcer? . 1974;67(5):1020-1022.
Am J Surg
7. Garza E Jr, Kuhn J, Arnold D, et al. Internal hernias after laparoscopic Roux-en-Y gastric bypass. . 2004;188(6):796-800.