We report a case of intestinal perforation after ERCP and endoscopic sphincterotomy (ES), highlighting the location and mechanism of injury.
A 78-year-old male with a history of chronic obstructive pulmonary disease and severe heart disease was admitted to the emergency room for vomiting and epigastric pain.
Physical examination revealed cutaneous mucocutaneous jaundice and epigastric tenderness without signs of peritoneal irritation.
Analytically, leukocytosis (16.870*109 leukocytes/l); bilirubin 9.1 mg/dl; AST 230 U/l and amylase in blood and urine 10972 U/l, respectively stand out.
Abdominal ultrasound revealed a distended gallbladder, non-lithiasis and a common bile duct caliber.
She was admitted to the Digestive Service with a diagnosis of acute pancreatitis.
After an asymptomatic period of five days, the patient developed epigastric pain and vomiting.
Computed tomography (CT) reports contrast in the small intestine and colon, pancreas of normal characteristics and a distended gallbladder with probable gallstones at cystic level.
With conservative treatment the patient remains asymptomatic with 2.4 mg/dl bilirubinemia and 154 U/l amylasemia.
On the twelfth day of admission, the abdomen was distended and nasogastric aspirated (600 cc).
A simple abdominal X-ray showed a stomach of retention and first bowel loops and rectum and contrast.
Under these conditions, the Digestive Service performs ERCP and ES due to the presence of two microcalciums in the main bile duct.
After performing the procedure, the patient has a marked bronchoperitoneum.
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With the suspicion of perforation, gallstones were found in the gallbladder, as well as a groove that partially obstructed the duodenal angle and caused a 40 cm internal herniation, as well as an antimesenteric margin and Treal.
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The bridle section, jejunal resection with primary anastomosis, cholecystectomy and intraoperative cholangiography were performed, which was normal.
In a prospective study on the experience in nine hospitals with ERCP in 2,769 patients over a two-year period, Loperfido et al.
(1) reported 4% major complications, a statistically significant difference between diagnostic (1.38%) and therapeutic use (5.4%) of the procedure.
The incidence of perforation secondary to EE ranges between 0.3 and 1.8%, is usually retroperitoneal and although its therapeutic management is controversial, it will depend on the mechanism of the lesion and the time elapsed until its conservative diagnosis (8) can be conservative.
The incidence of duodenal wall perforation attributable to neoplasms oscillates between 0.08 and 0.56% (6.7), usually occurs within a multifactorial pathology (7.8) usually in the absence or presence of pathological intestinal or inflammatory conditions.
The perforation mechanism in our patient could be due to hyperpressure on a closed loop since, as seen in the surgical intervention, the perforation level was located at the proximal level of the intestinal stenosis caused by a jejunal hernia.
While ductal perforation by metal guidewire or periampullary perforation is usually diagnosed during ERCP, distal perforation of the ampulla may go unnoticed, so the diagnosis can be delayed until signs or symptoms are present (8).
In our patient, symptoms began immediately after ERCP manifested pain and abdominal distension with a significant CAT proven pneumoperitoneum. For this reason, duodenal obstruction was diagnosed 2h-3a.
Perforations due to ERCP are usually larger than those secondary to ES and require immediate surgery (6), achieving a postoperative mortality of up to 25% (8).
Our patient, after intestinal resection and primary anastomosis, was discharged 12 days after surgery and remains asymptomatic 2 years after hospital discharge.
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M. T. García Martínez, A. Ruano Poblador, L. Galán Raposo, A. M. Gay Fernández and J. E. Casal Núñez
General and Digestive Surgery Department.
Hospital do Meixoeiro.
Vigo, Pontevedra
