Duodenal Necrosis Research Articles

Duodenal Necrosis in the Setting of Acute Cholecystitis

Duodenal Necrosis in the Setting of Acute Cholecystitis

腹腔鏡補助下幽門側胃切除後の内ヘルニアにより十二指腸壊死を来した1例

腹腔鏡補助下幽門側胃切除後の内ヘルニアにより十二指腸壊死を来した1例

Black Duodenum and Black Esophagus

Purpose: Acute esophageal necrosis (AEN) or ‘black esophagus' is characteristically described as diffuse, circumferential, black appearance of the esophagus that stops abruptly at the gastroesophageal junction (GEJ). AEN commonly presents with symptoms of hematemesis, melena or coffee-ground emesis in about 90% of the cases. We describe the first case in the literature of AEN associated with duodenal necrosis (black duodenum) in a patient who presented with a pulmonary embolism without these classic characteristic symptoms. An 80-year-old male ex-smoker with a past medical history of hypertension was admitted to our hospital with symptoms of worsening shortness of breath, left sided back pain, nausea and non-bloody, non-bilious vomiting. He denied abdominal pain, chest pain, fever, chills, dysphagia, odynophagia, or history of caustic ingestion. The patient was tachycardiac, mildly hypoxic on room air and had normal abdominal and rectal examination. Pertinent laboratory results included a white blood cell count of 17.8/μl with 82% neutrophils and hemoglobin of 14.4 g/dl. Computed Tomography angiogram revealed bilateral pulmonary emboli, diffuse esophageal and proximal duodenal thickening. Esophagogastroduodenoscopy (EGD) revealed black discoloration with underlying friable hemorrhagic tissue from the mid-esophagus up to the distal esophagus and a normal appearing GEJ and stomach. The duodenal bulb and the proximal aspect of the second portion of duodenum had a black discoloration similar in appearance to the involved segment of the esophagus. Biopsies of the black mucosa from the esophagus and the duodenum revealed necrosis. The patient was discharged home on warfarin and proton pump inhibitor (PPI). A follow-up EGD one week later revealed a normal esophagus and a normal duodenum. Conclusion: This is the only case of AEN described in the literature associated with a pulmonary embolism (PE) and duodenal necrosis. AEN and duodenal necrosis may have been secondary to hypoxia from the PE, explaining the complete rapid improvement with anticoagulation therapy. Given our case, we suggest that a lower threshold for a diagnosis of pulmonary embolism should be considered in a patient with AEN in an appropriate clinical setting.Figure: [1331] Figure 1. Black esophagus and black duodenum.

Gastroduodeno-plasty performed by distal gastric transection.- A new technique for large duodenal defect closure

IntroductionDuodenal ulcer lesions can represent a surgical challenge, especially if the duodenal wall is chronically inflamed, the defect exceeds a diameter of 3 cm and the ulceration is located in the second part of the duodenum.Patient and methodWe present the case of a 70-year-old male, who suffered from a 3 x 4 cm duodenal defect caused by duodenal pressure necrosis due to a 12.5 x 5.5 x 5 cm gallstone. Additionally, this stone caused intestinal obstruction (Bouveret’s syndrome) and bleeding with signs of shock. Besides the gallstone extraction, the common bile duct was drained by a T-tube and the duodenal defect closure was performed by a gastroduodeno-plasty and Bilroth II gastroenterostomy. The postoperative phase was uneventful. The reconstructed duodenum was endoscopically accessible and showed no pathological findings on follow-up.ConclusionThe reconstruction of a large defect (> 3 cm) of the second part of the duodenum is safely feasible by a gastroduodeno-plasty. The critical gastroduodenal anastomosis can be protected by duodenal decompression, achieved by placing a T-tube in the common bile duct.

Duodenal necrosis secondary to a closed-loop bowel obstruction with novel reconstruction

Duodenal necrosis is rare in children and presents a significant surgical challenge. We describe a 12-year-old girl who presented with duodenal necrosis secondary to a closed-loop bowel obstruction. We describe the diagnostic images, operative findings, and a novel reconstruction technique. This case highlights an alternative strategy for reestablishing gastrointestinal and biliopancreatic continuity while avoiding more complex procedures.

Staged Enteric Conversion After Duodenal Necrosis in Simultaneous Kidney and Pancreas Transplant From a Donor After Cardiac Death: A Case Report

Simultaneous pancreas and kidney transplantation (SPK) is the treatment of choice for insulin-dependent diabetics with end-stage renal failure. The shortage of suitable pancreata has led to the use of donors after cardiac death (DCD). Although more than 20,000 pancreas transplants have been performed worldwide, the experience of pancreas transplantation from DCD remains limited. Factors during recovery, storage, and reperfusion may result in injury to the duodenal segment of the pancreas allograft. Here we have reported a case of duodenal necrosis after reperfusion in a patient who underwent SPK from a DCD. The pancreas was salvaged by excising the duodenum and performing a direct pancreas duct to bladder anastomosis. After recovery of function by the transplanted kidney, the patient developed recurrent urinary sepsis. The bladder-drained pancreas was converted to a direct enteric drainage, which resolved the recurrent urinary sepsis.

Local Toxicity of Hepatic Arterial Infusion of Hexokinase II Inhibitor, 3-Bromopyruvate: In Vivo Investigation in Normal Rabbit Model

3-Bromopyruvate (3-BrPA), an hexokinase II inhibitor, is known to have high necrotic rate in hyperglycolytic liver tumor models without apparent damage to the normal liver parenchyma. The toxicity of intra-arterial delivery of 3-BrPA in various concentrations has not been specifically investigated using a normal rabbit model. Twenty rabbits treated with intra-arterial 3-BrPA were divided into four groups according to its dose and infusion level: 1 mM at the left hepatic artery (group I), 5 mM at the left hepatic artery (group II), 25 mM at the left hepatic artery (group III), and 25 mM at the common hepatic artery (group IV). After selective catheterization, 30 ml of 3-BrPA was infused for 2 minutes. As a control group, five rabbits were treated with normal saline. During 1-week follow-up, toxicities were evaluated with blood laboratory results, mortality, and histopathologic examination. All 10 rabbits treated with 25 mM 3-BrPA and 2 rabbits treated with 5 mM 3-BrPA died within 3 days after treatment. In 10 of the 12 deaths, hemorrhagic pyloric or duodenal necrosis was noted. Hepatotoxicities on blood laboratory results were dose dependent but transient in the surviving rabbits. Selective intra-arterial administration of 25 mM 3-BrPA can cause considerable toxicities not only in the liver but also in the gastrointestinal system and are dose dependent and can cause death in high doses.

Traumatic duodenal necrosis with avulsion of Vater's papilla in a child

Blunt duodenal trauma with avulsion of the papilla of Vater is an extremely uncommon injury in children. The usual management of these injuries relies on complex reconstructive procedures and bypasses. We report the case of a 6-year-old girl with near total traumatic duodenal necrosis and avulsion of Vater's papilla managed by a simple physiological montage avoiding pancreatic resections and gastrointestinal bypasses.

Necrosis of the duodenum resulting from acute necrotising pancreatitis and treated with complete duodenopancreatectomy

Necrosis of the duodenum resulting from acute necrotising pancreatitis is a rare but potentially lethal complication. A small number of cases has been reported so far, the majority of which having, unfortunately, had a lethal outcome. We present the cases of two patients, a 21-year-old woman and a 54-year-old man, both suffering from extensive duodenal necrosis stemming from acute necrotising pancreatitis, and both cases involving the second and third sections of the duodenum, one of which was probably caused by the thrombosis of nutritive blood vessels, the other by an abscess of the head of the pancreas. Due to the extent of the necrosis of the duodenum, there was no option to close so large a hole or to employ any less drastic procedure, so that a complete duodenopancreatectomy had to be performed. One patient survived and has remained in good health for a period of almost ten years, to date. The other patient died six days after surgery due to infection, in spite of an abscence of any sort of anastomic complications.

Massive necrosis of the gastrointestinal tract after ingestion of hydrochloric acid.

To describe our experience of dealing with patients admitted as emergencies after massive ingestion of hydrochloric acid, and to find out the most important prognostic factors. Retrospective review. Teaching hospital, Spain. 21 patients with massive necrosis of the upper gastrointestinal tract after ingestion of acid who presented during the past 14 years (November 1984-March 1998). All patients were operated on immediately, 17 without an endoscopic examination. In all cases, the laparotomy showed various degrees of damage to the intra-abdominal oesophagus (from oedema to blackening) and gastric necrosis. Twelve patients also had necrosis of the entire duodenum. In the other nine, the necrosis did not affect more than the pylorus or duodenum. All these 12 patients were treated by a total oesophago-gastrectomy without thoracotomy. Of the 12 patients with total necrosis of the duodenum, 4 did not have resections and in 8, various massive resections of the necrotic structures were done. Mortality. Fourteen of the 21 patients died during the operation or in the early or late postoperative period. All 12 patients with total duodenal necrosis died, whereas only 2 patients in the other group. The ingestion of relatively small amounts of water-based solutions of hydrochloric acid of 24% or 32% concentration produces immediate and massive necrosis of the upper digestive tract, which results in high mortality. The poor prognosis might be improved by rapid responses to stop duodenal necrosis.

A CASE OF DUODENAL STENOSIS DUE TO ACUTE PANCREATITIS AFTER CONTINUOUS INTRA-ARTERIAL ADMINISTRATION

A 49-year-old man was admitted to the hospital because of severe epigastric pain. White blood cell count and serum CRP were high, the serum amylase, tripsin, phospholipase A2 and lipase were remarkably high on admission. The diagnosis of severe acute pancreatitis was made by CT scan of the abdomen. We performed continuous intra-arterial administration of FOY for 11 days, and pancreatitis improved. But he had nausea and vomiting, and the diagnosis of duodenal necrosis and stenosis was made by gastrofiberscope. The stenosis did not improve after 20 days, so PPPD was performed. Although leakage of duodenum-jejunum anastomosis was complicated, it was conservatively treated and he was discharged from the hospital 68 days after the operation. A duodenal stenosis due to pancreatitis is very rare. In a review of the Japanese literature, only 47 cases of duodenal stenosis due to pancreatitis including our case have been reported so far. We present a case of duodenal stenosis due to pancreatitis, together with some bibliographical comments.

Arterial embolization for bleeding pseudocysts complicating chronic pancreatitis.

To evaluate the efficacy of arterial embolization (EMB) in the management of bleeding pancreatic pseudocysts or pseudoaneurysms and to assess the possible indication for secondary surgery. Retrospective review with a mean follow-up of 60 months (range, 18-125 months). Tertiary care center, university hospital. The medical records of 14 patients who were referred to the hospital with bleeding pancreatic pseudocysts and/or pseudoaneurysms related to chronic pancreatitis, between 1983 and 1994, were reviewed. The clinical presentation was major bleeding in 10 patients (gastrointestinal or intraperitoneal) and chronic signs in 4. Celiac and superior mesenteric angiography with EMB attempt in all patients. The immediate effect on bleeding and the long-term safety of arterial EMB. Embolization failed in 3 patients and surgery was needed (1 patient died). Embolization was successful in 11 patients, but 2 complications occurred (duodenal necrosis and aortic thrombosis) (1 patient died). Among the 10 patients whose bleeding stopped, an intentional pancreatectomy was performed 4 times (all patients are alive). The 6 other patients did not undergo a further pancreatic operation due to unfavorable local or general condition. None of them had recurrent bleeding, 3 of them died later of extrapancreatic diseases. Overall, early mortality was 14%, with deaths occurring only in unsuccessful or complicated EMB cases. The immediate effectiveness of arterial EMB is undeniable but depends on the expertise of the radiologist. When EMB is successful, further surgery should be reserved for patients in good general condition who have other complications of chronic pancreatitis that are not amenable to minimally invasive techniques.

Synchronous Embolization of the Gastroduodenal Artery and the Inferior Pancreaticoduodenal Artery in Patients with Massive Duodenal Hemorrhage

To assess the efficacy and safety of synchronous embolization of the gastroduodenal artery (GDA) and inferior pancreaticoduodenal artery (IPDA) in patients with massive duodenal hemorrhage. All cases of synchronous embolization of the GDA and IPDA at the authors' hospital between 1980 and 1989 were retrospectively reviewed. Bleeding was successfully controlled acutely in all six patients who underwent synchronous embolization. Clinical evidence of recurrent hemorrhage was found in two patients, but repeat angiography showed no extravasation of contrast material. Three patients died within 30 days of embolotherapy. In one patient who also received an infusion of vasopressin, postmortem evidence of pancreatic necrosis was found. Synchronous embolization of the GDA and IPDA can be an effective treatment for continuing duodenal hemorrhage after failed endoscopic therapy in patients considered a poor surgical risk. The procedure should be undertaken only as a lifesaving measure due to the risk of pancreatic and duodenal necrosis.

Combined Duodenal and Colonic Necrosis

Two unusual cases of liquid caustic ingestion that resulted in gangrene of the duodenum and adjacent colon, and burns of the esophagus, stomach, and pancreas are presented. The routine evaluation of the oropharynx, esophagus, and stomach after liquid caustic ingestion can seriously underestimate the extent of injury to distal portions of the gastrointestinal (GI) tract, such as the colon and pancreas, that are not usually included in the initial evaluation of ingestion injuries. In stable patients managed nonoperatively, the entire upper GI tract, including the duodenum, must be visualized either by endoscopy or, less preferably, by barium series. Double-contrast computed tomography should be performed when significant duodenal injuries are present in order to inspect the colon, pancreas, and small bowel. With this approach, life-threatening, multi-organ, subdiaphragmatic ingestion injuries can be identified and treated early.

Hemorrhagic pancreatitis: A complication of transcatheter embolization treated successfully by total pancreatectomy

Since pancreatitis can be produced experimentally in dogs by embolization of microspheres into the pancreatic arterial circulation, there has been speculation that intentional or inadvertent embolization of the pancreas in human subjects could also produce pancreatitis. Although such therapeutic embolization has increased, no pathologically documented case of this complication has been recorded. We have reported the first such case occurring in a patient with a large, highly vascular, nonfunctioning islet cell carcinoma of the tail of the pancreas preoperatively embolized with Gianturco coils and Gelfoam particles suspended in sodium tetradecylsulfate solution to facilitate distal pancreatectomy. The resultant hemorrhagic pancreatitis and duodenal necrosis required a total pancreatectomy. We conclude that, by itself, occlusion of the origin of the splenic and gastroduodenal arteries with coils would have been effective and without complication; however, the addition of Gelfoam particles in a sclerosing solution reduced the microscopic pancreatic circulation to a critical point and resulted in hemorrhagic pancreatitis.

Choledochus ligature in the prevention of experimental thrombohemorrhagic duodenal necrosis.

Experiments on the rat indicate that a thrombohemorrhagic form of duodenal and upper jejunal necrosis can be produced by a single intravenous injection of agar. These lesions are prevented by complete, but not by incomplete, ligature of the common bile duct.

Effect of duodenal freezing on the secretin mechanism.

1. Experience with 17 dogs subjected to duodenal freezing for 10 minutes suggests that secretin release to acid stimulation of the duodenum is significantly impaired for at least 3 months. Average total response to HCl instillation in the post-freeze duodenum is 28.2% of control mean response. More prolonged periods of freezing do not result in greater depression. 2. No evidence of significant pancreatic derangement has been found to result from duodenal freezing. 3. If the duodenum is exposed to air during the freezing process, there is a significant incidence of duodenal necrosis, which was not observed with intraperitoneal freezing for 10 minutes.