Vikram Kotwal

Should bowel preparation, antifoaming agents, or prokinetics be used before video capsule endoscopy? A systematic review and meta-analysis.

Objectives The ideal bowel preparation regime before small bowel video capsule endoscopy (VCE) is not known. We carried out a systematic review and meta-analysis to study the effect of purgatives, antifoaming agents, and prokinetics on the outcomes associated with VCE. Materials and methods We performed literature searches in MEDLINE and Cochrane Library and included randomized-controlled trials studying the effect of purgatives, antifoaming agents, and prokinetics in patients undergoing VCE. Our outcomes of interest were visualization quality, diagnostic yield, and completion rate. Meta-analyses were carried out using the RevMan software and heterogeneity was assessed using the I2 statistic. Results Fifteen studies fulfilled the inclusion criteria. As compared with no bowel preparation, bowel preparation with polyethylene glycol (PEG) led to adequate visualization in a significantly higher number of patients undergoing VCE [odds ratio (OR) 3.13; 95% confidence interval (CI) 1.70–5.75]. Both PEG and sodium phosphate significantly improved the diagnostic yield (OR 1.68; 95% CI 1.16–2.42 and OR 1.77; 95% CI 1.18–2.64, respectively) but did not affect the completion rate. All studies with simethicone showed significantly improved visualization quality with its use as compared with overnight fasting or purgatives alone. Prokinetics did not significantly improve the completion rate of VCE. Conclusion On the basis of the data available, a combination of PEG and simethicone appears to be the best approach for small bowel preparation before VCE. However, large multicenter randomized-controlled trials are needed to validate this recommendation and to evaluate the ideal dose of PEG and timing of bowel preparation before VCE. Prokinetics administered before VCE do not improve the completion rate and should not be used.

Chronic hepatitis E: A brief review

Hepatitis E viral infection has traditionally been considered an acute, self-limited, water borne disease similar to hepatitis A, endemic to developing countries. However, over the past decade, zoonotic transmission and progression to chronicity in human patients has been identified, resulting in persistently elevated transaminase levels, progressive liver injury and cirrhosis. In addition to liver injury, neurological, renal and rheumatological manifestations have also been reported. Chronic hepatitis E occurs mainly in immunosuppressed individuals such as transplant recipients, human immunodeficiency virus patients with low CD4 counts and in patients with hematological malignancies receiving chemotherapy. Diagnosis is established by persistent elevation of hepatitis E virus RNA in the stool or serum. This population often requires treatment with antiviral agents, particularly ribavirin, as spontaneous clearance with reduction in immunosuppression occurs only in about a third of the patients. The purpose of this review, is to further discuss the clinical presentation, and recent advances in diagnosis, treatment and prophylaxis of chronic hepatitis E.

Disconnected pancreatic duct syndrome endoscopic stent or surgeon's knife?

Disconnected pancreatic duct syndrome is a sequela of necrotizing pancreatitis or pancreatic trauma in which necrosis of a segment of the pancreas leads to lack of continuity between viable secreting pancreatic tissue (eg, body or tail) and the gastrointestinal tract. The endoscopic retrograde cholangiopancreatography showing total cutoff of the pancreatic duct along with an enhancing distal pancreas on contrast-enhanced computed tomography remains the criterion standard for diagnosis. Recently, the evolving literature supports a role for magnetic resonance cholangiopancreaticography, especially with secretin stimulation. A multidisciplinary approach is extremely important in the management of this condition. Conservative measures are usually not helpful, and interventional radiology, endoscopic, or surgical intervention is almost always needed for management of these patients. Recently, endoscopic ultrasonography-guided drainage procedures in conjunction with endoscopic retrograde cholangiopancreatography-assisted pancreatic duct stenting have emerged as a novel technique to manage this condition. The aim of this review was to give a detailed overview about the diagnosis and management of disconnected pancreatic duct syndrome with emphasis on the changing paradigm in endoscopic and surgical management.

Hematemesis in a patient with diabetic ketoacidosis and chronic HCV infection.

292 Question: A 55-year-old man with past medical history of poorly controlled diabetes mellitus, recurrent infective endocarditis (last episode 2 months ago), and chronic hepatitis C presented to the emergency department with 2 episodes of coffee ground emesis. He also complained of fatigue, polyuria and lightheadedness for 2 days before admission. He denied any abdominal pain, prior retching,melena, or hematochezia. He denied using any nonsteroidal anti-inflammatory drugs, smoking, and recent alcohol or illicit drug use. On admission he was afebrile, tachycardic at 116 bpm, with a blood pressure of 121/92 mmHg, was breathing 24 times a minute and saturating well on room air. On physical examination, his skin and oral mucosa were dry. He was alert and oriented, with lungs clear to auscultation, heart sounds normal, and abdomen soft, nondistended, and nontender. He had no stigmata of chronic liver disease. Laboratory examination revealed blood sugar of 331 g/dL, sodium of 127 mEq/L, potassium of 6.4 mEq/L, bicarbonate of 7 mEq/L, anion gap of 29, and pH of 7.023. His blood urea was 69 mg/dL and creatinine 2.6 mg/dL. His hemoglobin was 16.7 g/dL; white blood cell count and platelets were normal. He was treated for diabetic ketoacidosis with an insulin drip and his electrolytes were corrected as needed. Nasogastric lavage was done and was clear. He was started on pantoprazole drip and an upper gastrointestinal endoscopy was performed which revealed diffuse blackish discoloration of the mid and distal esophagus (Figure A), which abruptly ended at the gastroesophageal junction. There was also evidence of erosive gastritis and erosive duodenitis (Figure B) in the bulb and second portion of duodenum. What is the diagnosis? What is the appropriate management? Look on page 491 for the answer and see the GASTROENTEROLOGY web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.