Abdominal Pain of Unknown Etiology

Unexplained abdominal pain may be due to mild pancreatic disease in up to 35% of patients. ERCP is often performed to establish or exclude a diagnosis of pancreatitis, however, ERCP is associated with a small but significant risk of pancreatitis, especially when sufficient contrast must be injected to delineate side-branches changes of pancreatitis. Endoscopic Ultrasound (EUS) provides detailed images of the main pancreatic duct and the surrounding parenchyma without contrast injection or fluoroscopy. Studies have validated the high sensitivity and specificity of EUS for the detection of early ductal and parenchymal changes of pancreatitis. 

Upper abdominal pain may also be due to sphincter of Oddi dysfunction (SOD). The sphincter is a smooth muscle that encompasses the confluence of the distal common bile duct and pancreatic duct as they penetrate the wall of the duodenum. Impedence in the flow of bile and pancreatic juice into the duodenum is postulated to be the cause of pain. SOD is diagnosed by sphincter of Oddi manometry using a special manometry catheter. 

Acute Recurrent Pancreatitis (ARP)

ARP is manifested by unrepredictable, intermittent episodes of abdominal pain. The attacks of pancreatitis often require hospitalization and may have significant morbidity and mortality. ARP may be due to pancreas divisum, sphincter of Oddi dysfunction, and biliary microlithiasis (sludge). These etiologies are evaluated according to the following algorithm:

1. Endoscopic ultrasonography is performed to evaluate the pancreatic parenchyma for changes of chronic pancreatitis, to rule out a pancreatic tumor, and to evaluate the pancreatic duct for dilatation and contour irregularities. Pancreas divisum can often be excluded on EUS. The CBD is evaluated for macro- and micro-lithiasis. The papilla is evaluated to rule out an ampullary neoplasm.
2. ERCP is performed when ductal dilatation is present, and may be indicated for the following: A) suspected pancreas divisum; B) suspected sphincter of Oddi dysfunction
3. If documented on manometry, sphincter of Oddi dysfunction is treated by pancreatic sphincterotomy. A 7-Fr stent is inserted for 5-7 days to prevent post-ERCP pancreatitis.
4. Pancreas divisum is treated by minor papilla sphincterotomy. A 7-Fr stent is inserted for 5-7 days to prevent post-ERCP pancreatitis.

Barrett’s Esophagus

We perform magnification (“zoom”) endoscopy combined with chromoscopy to maximize the detection of Barrett’s esophagus. Endoscopic treatment is indicated when dysplasia is present despite optimal control of reflux esophagitis. Treatment options include 1) thermal ablation 2) photochemical ablation (photodynamic therapy) and 3) endoscopic mucosal resection (EMR). EMR holds the greatest potential for cure in that the metaplastic epithelium is completely resected. In addition, the resected specimen is submitted for histopathological evaluation. We perform piecemeal EMR as the primary treatment for Barrett’s esophagus with high-grade dysplasia. Argon plasma coagulation is used as a complementary procedure to fulgurate residual areas of Barrett’s that are not amenable to EMR. 

Benign Dysphagia

Benign esophageal strictures are treated by standard over-the-wire esophageal dilation. Strictures that are refractory to dilation are treated with the following options:

1. Local four-quadrant injection of triaminolone acetonide followed by stricture dilation
2. Local argon plasma coagulation followed by stricture dilation
3. Diathermic stricture incision using a needle knife
4. Short-term placement of a plastic stent

Chronic (Painful) Pancreatitis

The goals of endoscopic therapy of chronic pancreatitis are to relieve pain and improve pancreatic duct drainage. The treatment varies according to the underlying structural pathology:

1. Pancreatic duct stricture. The stricture is dilated and a stent is placed. The stent is exchanged at 3-month intervals until the stricture is adequately stretched to provide drainage.
2. Sphincter of Oddi dysfunction. Sphincterotomy of the major papilla is performed. A pancreatic stent is inserted for 5-7 days to prevent post-procedure pancreatitis.
3. Pancreas divisum. Sphincterotomy of the minor papilla is performed, followed by short-term stenting to prevent restenosis and minimize the risk of post-procedure pancreatitis.
4. Pancreatic duct stones. Endoscopic stone extraction is performed after pancreatic sphincterotomy. Impacted stones are fragmented by extracorporeal shock wave lithotripsy.
5. Pseudocysts. Small pseudocysts that communicate with the pancreatic duct (“retention cysts”) are drained through the papilla with a stent. Large pseudocysts are drained transmurally with a stent through the stomach or duodenum.

Enteric Obstruction

Gastric outlet obstruction due to pyloric stenosis is treated by hydrostatic balloon dilatation. This is sometimes complemented by needle knife stricturoplasty. Duodenal and colo-rectal obstruction is treated with enteric expandable metal stents. 

Esophageal Variceal Bleeding

Esophageal varices are preferentially treated by band ligation. Sclerotherapy is used to treat varices that are refractory to band ligation (actively bleeding, previously treated, or recurrent varices). 

Gastric Variceal Bleeding

In contrast to esophageal varices, gastric varices are difficult to treat with sclerotherapy or band ligation because of their large size and volume. Endoscopic cyanoacrylate glue injection is used for gastric varices in the context of an investigative protocol (the treatment is not FDA approved, but well established outside the U.S.). When instilled into a varix using the standard method of intravariceal injection, the glue undergoes an instantaneous polymerization reaction and hardens, thereby occluding the varix lumen. This achieves rapid hemostasis of active bleeding and prevents rebleeding from the treated varix. 

Gastroesophageal Reflux Disease (GERD)If inadequately treated, GERD can result in serious complications including esophageal strictures, bleeding, and aspiration. Of greatest concern is the potential for malignant transformation (esophageal adenocarcinoma). While Barrett’s metaplasia has been linked with progression to adenocarcinoma, recent studies show that GERD itself predisposes to malignancy. These potential complications have prompted the development of endoscopic treatments for GERD. 

The goal of endoscopic therapy is to “tighten” the LES valve and reduce reflux. We are investigating a prosthesis that is endoscopically implanted in the submucosal space to augment the compromised lower esophageal sphincter (GatekeeperR reflux repair system). The method has been validated in animal studies and pilot clinical trials. The main advantages of this approach are simplicity and reversibility. 

Malignant Dysphagia

Malignant esophageal strictures are treated with covered expandable metal stents. Stents that cross the cardia are equipped with an anti-reflux “windsock” valve. Argon plasma coagulation complements stenting to treat a tumor in- or overgrowth. 

Nonvariceal Bleeding

Nonvariceal bleeding is treated with a spectrum of hemostatic modalities, including epinephrine injection, argon plasma coagulation (APC), and hemoclipping. Gastric antral vascular ectasia (GAVE) syndrome, tumor surface bleeding, and radiation proctitis are treated by APC. 

Zenker’s Diverticulum

The endoscopic treatment of Zenker’s diverticulum (pharyngoesophageal pulsion diverticula) consists of a gradual ablation of the septum between the diverticulum and the esophagus (septotomy) to allow the contents of the diverticulum to spill into the cervical esophagus. The septum is ablated using a needle knife.