Krishnaveni Janarthanan

Pancreatico-Pleural and Bronchial Fistulae and Associated Pseudocysts: Case Series

CONTEXT Pancreatico-pleural fistula is rare complication of chronic or acute pancreatitis. Previous studies have reported imaging features and various management options of this condition including conservative/medical management, endoscopic treatments and surgery.This article reviews the myriad of imaging appearances of this condition in multimodality imaging and different strategies for the successful management in a short case series. METHODS After obtaining the institutional ethics committee approval, retrospective review of the medical records of five patients of pancreatico-pleural fistulae who were diagnosed and successfully managed in our hospital in 2012 and 2013 was done. Follow up with out patient records of these patients was also included.Findings were compared with the current available literature on this entity. RESULTS AND DISCUSSION Pancreatico-pleural fistulae presents with massive pleural effusion.A high index of suspicion is essential for accurate diagnosis. Demonstration of the fistulous tracts requires cross sectional imaging with contrast enhanced CT being most commonly used and affords accurate diagnosis. MRI demonstrates the tracts and ductal disruptions with greater detail and are helpful in confirming the CT findings. Endoscopic ultrasound and ERCP also offer potential of diagnosis, although being technically demanding and invasive is reserved for interventions. Management of these conditions should be initially conservative with endoscopic stenting being offered in selected cases with favourable anatomy and not responding to conservative management. Surgery is reserved for cases not responding to conservative and endoscopic management. CONCLUSION In conclusion this case series highlights the clinical and imaging spectrum of pancreatico-pleural fistulae and provides insight into the different management strategies that can be adopted for this condition.

Chronic Pancreatitis Presenting with Pseudocyst of Pancreas and Pseudo-aneurysm of Hepatic Artery

A 2-y-old girl presented with recurrent abdominal pain and hematemesis. The patient was diagnosed to have chronic calcific pancreatitis complicated by pseudocyst of the head of pancreas and pseudo-aneurysm of the common hepatic artery. Diagnosis was made using abdominal ultrasonography and CT angiography. The rarity of the presentation of pseudocyst with pseudo-aneurysm formation in a pediatric patient is noted. The pseudo-aneurysm was treated by embolization of the artery and the pain being refractory to analgesics was managed by celiac plexus blockade.

Role of noninvasive markers to predict the presence of esophageal varices in cirrhosis: Pilot study

Cirrhosis of liver leads to portal hypertension and development of esophageal varices (EV), rupture of which results in spontaneous hematemesis. Upper gastrointestinal (UGI) bleeding is a catastrophic presentation of EV. Endoscopy remains the standard procedure for diagnosis [1] and esophageal variceal ligation as treatment of varices for decades; but with each passing day, the demand to develop noninvasive methods to diagnose varices is increasing. This pilot study aimed to find the association between esophageal varices, liver stiffness, spleen stiffness, and platelet counts and also to assess whether these indicators can be used to establish benchmarks in the future as noninvasive predictors of portal hypertension. A cross-sectional observational study was done at a tertiary health center from February 2014, to January 2015. Adult patients of ages ≥ 18 years of either sex with newly diagnosed chronic liver disease (CLD) and portal hypertension were included. The patients underwent routine biochemical and radiological investigations. Patients underwent an UGI and esophageal varices were graded as per Baveno V consensus. Liver stiffness (LS) and spleen stiffness (SS) values were assessed in patients with Acoustic Radiation Force Impulse (ARFI) (Siemens Acuson S2000TM). Individual readings were taken for the liver and spleen, the mean of which was taken as a final value expressed in meters per second. For LS, the METAVIR scoring system was used. Toshiba SSA-70 was used to carry out ultrasound examination. Fifty patients (with mean age of 50.44 ± 13.11 years were taken. OnUGI endoscopy, the presence of EVwas noted in 39 (78%) patients. Thirty-two (94.12%) patients had platelet count < 150,000/mm and 7 (5.88%) patients had platelet count ≥ 150,000/mm (p < 0.001). Sixteen patients (41.03%) had liver size ≥ 14.6 cm and 23 patients (58.97%) had liver size < 14.60 cm. However, this difference was statistically not significant. The diagnostic accuracy of liver size in predicting EV was 38% with 41.03% sensitivity, 27.27% specificity, and 0.56 positive likelihood ratio. Twenty-six had LS ≥ 2.09 while 11 patients (had LS < 2.09 [p = 0.104]. LS had an accuracy of 68% in predicting EV with 71.79% sensitivity and 54.55% specificity and positive likelihood ratio was 1.58. SS was ≥ 2.87 in a significantly higher number of patients (26 patients; 89.66%) compared to those who had < 2.87 (13 patients; 61.9%) (p = 0.023). SS had an accuracy of 68% for EV, with sensitivity of 66.67%. Among the 39 patients with EVs, a majority of the patients had LS of ≥ 2.09, that is 28 (71.8%) patients and 11 patients (28.2%) who did not have EV, but the difference was statistically not significant (p = 0.104). However, the sensitivity of LS in predicting EV was slightly high, that is 71.79% but less specific 54.55% resulting in diagnostic accuracy of 68% and positive likelihood ratio of 1.58. There is a wide variation of LS values in the literature that ranges from 2.5 to 75 kPa. These values are altered by gender, BMI, etiology, and necroinflammatory change [2, 3]. Normal TE values are 3.8 to 8 kPa in men and 3.3 to 7.8 kPa in women while in fibrosis (METAVIR fibrosis stage ≥ 2) the values are 7 to 8 kPa and in cases with cirrhosis, the values are 13 to 17 kPa [4]. Platelet count has been reported as the most sensitive and specific noninvasive parameter for predicting * Shiran Shetty drshiran@gmail.com

Endoscopic ultrasound of duodenal heterotopic gastric mucosa

A 50-year-old woman presented with dyspepsia but no history of weight loss or gastrointestinal bleeding. Esophagogastroduodenoscopy (EGD) showed a sessile polypoidal submucosal lesion in the second part of the duodenum close to the ampulla with a central opening (fish-mouth appearance) (▶Fig. 1). The contour of this lesion was smooth and there was no disruption of the surrounding folds, nor ulceration or bleeding. Linear endoscopic ultrasound (EUS) was performed for evaluation of the lesion. This revealed that the lesion was arising from the mucosa/submucosa of the duodenum and had a cystic anechoic central core in the submucosa with no solid component and well-demarcated margins (▶Fig. 2; ▶Video1). On the basis of the EUS images, it was suspected that this was heterotopic gastric mucosa (HGM) and therefore the decision was made to resect the lesion endoscopically. The patient underwent polypectomy and the submucosal lesion was sent for histopathology. The histopathological examination confirmed the presence of HGM revealing fundal and pyloric glands covered by duodenal epithelium (▶Fig. 3). HGM is common in all organs of the gastrointestinal tract, particularly in the esophagus and duodenum [1]. A recent study found duodenal HGM appearing as solitary or multiple small nodules in 1.9% of 28210 patients who underwent EGD with duodenal biopsy [2]. EUS for the evaluation of submucosal lesions is a well-established entity, but literature with regard to the EUS description of duodenal HGM is rare. Hizawa et al. [3] described duodenal HGM presenting as a simple anechoic mass within the submucosa. In a recent series of six patients with duodenal HGM, the lesions appeared as solitary, sessile submucosal lesions with a depression at the top [1]. On EUS, these lesions had a heterogeneous pattern with or without an anechoic area and were located within the mucosa/submucosa. Although HGM is a benign entity, it may require laparoscopic or endoscopic resection if the lesion is large in size.

An unusual cause of obstructive jaundice in a 2-year-old child

Background and Objectives: Pancreaticobiliary ascariasis is common problem in tropical countries. The roundworm in the bile duct can cause biliary colic, obstructive jaundice, or pancreatitis. Live Ascaris worms are usually diagnosed on ultrasonography (USG) or endoscopic ultrasonographic (EUS) showing characteristic features of linear mobile echogenic structure with central anechoic lumen. However, the worm can die inside the common bile duct (CBD) and create a foreign body acting as a nidus for stone or sludge formation. Obstructive jaundice due to dead Ascaris is a rare but important cause in the developing World. As the worm shrivels up after death, accurate identification requires a high index of suspicion. The features of dead worm on EUS include hyperechoic structure without any acoustic shadow. Methods: We present a case of a 2-year-old Indian female child referred with biliary colic and jaundice for the last 3 weeks. Abdominal USG revealed multiple ill-defined, oval, hyperechoic shadows near the lower end of dilated CBD. MRCP showed multiple intraluminal curvilinear, hypointense areas in lower CBD. Results: Linear EUS from the duodenal bulb revealed dilated CBD with multiple hyperechoic structures without acoustic shadowing. It showed 2–6 mm sized curvilinear, disc-shaped, short-segment echogenic structures with central anechoic core parallel and equidistant from each other, suggestive of recently broken down parallel fragments of round worms. The central anechoic core represents the digestive tract of Ascaris. After multiple balloon sweeps on ERCP, creamy white structures and yellow-colored material were removed suggestive of recently fragmented Ascaris. Conclusions: Biliary ascariasis should be considered in any child presenting with obstructive jaundice in endemic regions.

Abdominal catastrophe in infective endocarditis

A 49-year-old male with Type II diabetes mellitus presented with fever for 3 months and on evaluation was found to have infective endocarditis involving the aortic valve. Blood culture grew Streptococcus viridans. He was treated with intravenous antibiotics and improved clinically. He developed severe abdominal pain with vomiting and minimal clinical signs on the tenth day of hospitalization. CT abdomen showed a 3.3 cm × 1.6 cm lobulated aneurysm of the distal superior mesenteric artery (SMA) along with early ischemic changes of the small bowel (Figs. 1 and 2).

Diffuse intestinal polypoid angiodysplasia

This 6-year-old boy presented with bleeding per rectum for two days. He was pale but hemodynamically stable. There were no mucocutaneous lesions. He had two similar episodes in the past treated conservatively elsewhere. Hemoglobin was 6 g/dL and other blood investigations were normal. Esophagogastroduodenoscopy, ultrasound abdomen and colonoscopy did not reveal any abnormal findings. Meckel’s isotope scan was negative. Laparoscopy assisted enteroscopy revealed diffuse bluish polypoid lesions in the jejunum with ooze in one particular segment (Fig. 1a). The oozing segment was surgically resected and end-to-end anastomosis was done (Fig. 1b). Histopathological examination showed foci of dilated, tortuous, thin-walled vascular channels and few arterial channels in the submucosa with focal

Onset of Type 1 Diabetes Mellitus During Pegylated-interferon Alfa and Ribavirin Therapy for Chronic Hepatitis C Virus Infection

A 16-year-old female was treated with pegylated-interferon (PEG-IFN) alfa (a)-2b and ribavirin combination therapy for chronic hepatitis C virus (HCV) infection. She attained rapid virological response. She presented with diabetic ketoacidosis after 41 weeks of therapy. Anti-glutamic acid decarboxylase antibodies and islet cell antibodies were negative. Her fasting serum C-peptide level was <0.1 ng/mL, and the treatment course was completed. This case underlines the importance of periodic plasma glucose monitoring in patients during and after PEG-IFN and ribavirin therapy.

Esophageal lipoma presenting as a long tongue

A 42-year-old man presented with history of non progressive dysphagia both for solids and liquids for the past 2 years. He used to bring out a fleshy mass from mouth during retching, followed by choking. Upper gastrointestinal endoscopy revealed a soft, long, smooth, bulging lesion in the upper esophagus, extending for a length of 20 cm. Pillow-sign was positive. Patient coughed immediately after the procedure, and brought out a fleshy pink tubular mass with a blind end from the mouth (Fig. 1), which caused sudden choking. The mass was maneuvered back by the patient himself. Endoscopic ultrasound showed hyperchoic lesion arising from the third layer of esophageal wall suggestive of lipoma. His CT thorax showed submucosal elongated polypoidal lesion with feeding blood vessels, and luminal narrowing in the upper part of the esophagus (Fig. 2). Surgical excision of the