Farshad Aduli

Hiccups : A Subtle Sign in the Clinical Diagnosis of Gastric Volvulus and a Review of the Literature

Hiccups are defined as sudden, involuntary, spasmodic contractions of the diaphragm and external intercostal muscles that result in inspiration abruptly ending with the closure of the glottis [1]. The innervation of the hiccup reflex includes an afferent pathway via the vagus, phrenic, and sympathetic branches of T6–T12 and the efferent pathway via the phrenic nerve to the diaphragm, glottis, and external intercostal muscles [1]. The etiologies of hiccups are many, and over 100 have been reported in past reviews [2]. Some of the more common causes include luminal distention of the esophagus and stomach, irritative stimuli such as gastroesophageal reflux disease (GERD), pathologic conditions of the central nervous system (CNS), and metabolic abnormalities such as uremia [3]. We report on two cases where patients with gastric volvulus had hiccups as their presenting symptom. Volvulus is defined as an abnormal twisting of bowel upon itself, resulting in luminal obstruction [4]. A volvulus can occur anywhere in the gastrointestinal tract where there is redundant bowel around a fixed mesentery. This often occurs in the small intestine of children with malrotation, leading to obstruction. It is also seen in the large intestine, most commonly causing obstruction in the cecal and sigmoid regions. Another less common, often overlooked condition is the gastric volvulus. The incidence and prevalence of gastric volvulus is unknown at this time, as many cases are chronic and intermittent and often go undiagnosed [5]. However, acute gastric volvulus is an emergency, and an accurate, timely diagnosis is critical. Two patients recently presented to our facility with similar complaints and were found to have gastric volvulus. A major complaint of both our patients was hiccups. Review of the literature does not mention this as a related finding in patients with gastric volvulus. We believe that, in the right clinical setting, persistent hiccups are an important clinical finding and can lead to a timely diagnosis, thus preventing strangulation and ischemia.

Strongyloides Duodenitis: Case Report and Review of Literature

Strongyloides stercoralis affects 30 to 100 million people worldwide and is a common cause of abdominal pain and diarrhea. Strongyloidiasis is a chronic and limited disease; however, in immunocompromised patients, hyperinfection syndrome can occur. Diagnosing strongyloidiasis early is important, as almost all deaths due to helminths in the United States are due to S stercoralis hyperinfection. Patients infected with human immunodeficiency virus (HIV) do not appear to be at an increased risk for S stercoralis hyperinfection. We report a case of an HIV-infected Hispanic woman presenting with dyspepsia, emesis, abdominal pain, and diarrhea diagnosed with S stercoralis on an esophagogastroduodenoscopy biopsy of the duodenum. The diagnostic workup had been inconclusive and deciding to biopsy the small bowel based on the nonerythematous boggy appearance of the duodenal folds was the key step in making the correct diagnosis. Early diagnosis and treatment thwarted the developing hyperinfection syndrome and likely prevented further morbidity and probably saved her life.

Ischemic duodenal ulcer, an unusual presentation of sickle cell disease

Sickle cell disease is caused by molecular abnormalities in the formation of hemoglobin, leading to pain crisis from recurrent vascular occlusion by sickled hemoglobin. Impaired flow in the microvasculature can lead to ischemia, tissue infarction and ulceration. Abdominal pain, a common complaint in sickle cell disease, can be due to an uncommon etiology, ischemic duodenal ulceration. This is due to primary mucosal infarction caused by sickling, leading to poor healing of infarcted areas. Prompt endoscopic and/or urgent surgical intervention should be considered, particularly if anticoagulation is an issue, as proton pump inhibitor use is ineffective in healing this type of ulcer.

Recurrent Spontaneous Gastrointestinal Graft-Versus-Host Disease in Autologous Hematopoietic Stem Cell Transplantation

Acute graft-versus-host disease (GVHD) is a major complication after allogeneic stem cell transplantation (SCT). A similar manifestation involving skin, gastrointestinal (GI) mucosa, and liver can occur after autologous hematopoietic SCT (autoHSCT), either spontaneously or after treatment with cyclosporine or interferon. Severity of spontaneous GI GVHD among patients treated with autoHSCT is variable. Recurrent spontaneous GI GVHD induced by succeeding cycles of chemotherapy has rarely been reported and is poorly understood. Enteric-coated budesonide has been studied extensively in Crohns disease, and beclomethasone has been studied in GI GVHD. There are no comparative studies between these drugs for GI GVHD. Furthermore, GI GVHD has to be considered when microbiologic workup remains negative during the workup of persistent diarrhea in autoHSCT. Endoscopic appearances can be normal, and pathologic diagnosis is essential. Further research into risk factors involving type of chemotherapy, interval between chemotherapies, and gene polymorphisms have to be considered for better understanding of autologous GVHD. We report for the first time a patient with spontaneous recurrent GI GVHD after autoHSCT for multiple myeloma with predominant lower GI symptoms and excellent response to enteric-coated budesonide therapy.

Endoscopic management of post-liver transplant biliary complications.

Biliary complications are being increasingly encountered in post liver transplant patients because of increased volume of transplants and longer survival of these recipients. Overall management of these complications may be challenging, but with advances in endoscopic techniques, majority of such patients are being dealt with by endoscopists rather than the surgeons. Our review article discusses the recent advances in endoscopic tools and techniques that have proved endoscopic retrograde cholangiography with various interventions, like sphincterotomy, bile duct dilatation, and stent placement, to be the mainstay for management of most of these complications. We also discuss the management dilemmas in patients with surgically altered anatomy, where accessing the bile duct is challenging, and the recent strides towards making this prospect a reality.

Cirrhosis of Liver and an Unusual Ectopic Site of Portosystemic Shunt: Left Adnexal Venous Varix Presenting With Hematuria

Cirrhosis of Liver and an Unusual Ectopic Site of Portosystemic Shunt: Left Adnexal Venous Varix Presenting With Hematuria

Hemobilia after Percutaneous Liver Biopsy Presenting as Hematochezia: A Rare Complication of a Commonly Performed Procedure

Background: Hemobilia is defined as hemorrhage into the biliary tract. With frequent use of invasive hepatobiliary procedures in current gastroenterology practice and promptly advancing imaging and endoscopic techniques, this disease process is increasingly being diagnosed. Clinically, this condition often presents as a classic triad of biliary colic, jaundice and upper gastrointestinal bleed (manifesting as hematemesis or melena). Case Report: A 35-year-old white woman with recent liver biopsy presented to the emergency department with 1 week’s history of right upper quadrant abdominal pain, nausea, vomiting, and multiple episodes of bleeding per rectum. X-ray abdomen and CT scan were unremarkable. Esophagogastroduodenoscopy was performed which showed ongoing blood flow through the ampulla of Vater. Diagnosis of hemobilia was made. Angiographic embolization of the segmental hepatic artery was done with resolution of bleeding. Conclusion: To conclude, hemobilia is a rare cause of upper gastrointestinal bleed. Trauma, predominantly iatrogenic and occasionally accidental, is the most common cause for this disease entity. Bleeding in these cases manifests predominantly as hematemesis or melena. In rare cases, as in our patient, bleeding may present as hematochezia. Diagnosis is predominantly made on upper gastrointestinal endoscopy. Angiographic embolization remains the cornerstone of management.

Idiopathic esophageal ulcers after autologous hemopoetic stem cell transplant: Possible role of IgA levels

Dear Editor, Idiopathic esophageal ulcers have been well described in immunocompromised individuals with acquired immunodeficiency syndrome [1–3]. There has been recent description of this disease in organ transplant recipients [4–6]. It is unknown if this is a consequence of immunosuppression or occurs as a result of host response to transplantation. We herein describe a case of autologous hemopoetic stem cell transplant recipient with idiopathic esophageal ulcers. To our knowledge, there has been no previous description of this entity in autologous hemopoetic stem cell transplant patients. A 55-year-old white gentleman with IgG kappa light chain multiple myeloma treated with autologous hemopoetic stem transplant was evaluated for complains of recent onset, gradually progressive dysphagia and odynophagia over a period of 2 weeks. Symptoms ensued within 4 weeks of the stem cell transplant and continued despite adequate acid suppression with proton pump inhibitor therapy and empiric antifungal and antiviral therapy with liposomal amphotericin-B and gancyclovir respectively. No history of nausea, vomiting, hemetemesis or melena was reported. The patient received high dose chemotherapy with melphalan 300 mg/m2 BSA, bortezomib (Velcade), thalidomide and dexamethasone followed by stem cell transplant in June, 2007. The dose of melphalan was higher than usual given high-risk disease features (cytogenetics and gene array profile) and the fact that the patient had relapsed after a total therapy of three regimens (two induction cycles followed by tandem transplants with melphalan 200 mg/m in 2005). Given history of CMV reactivation in past (PCR testing at that time being negative) and also given history of candidemia in past, patient was continued on ganciclovir and liposomal amphotericin-B therapy. However symptoms were persistent and later these were discontinued. Esophageoduodenoscopy revealed multiple ulcers in the mid esophagus within 30 cm of the gastroesophageal junction. Multiple biopsies were taken from the margins of the ulcers. Pathologic evaluation of the biopsy specimens indicated acute ulcerative esophagitis. Gomori methamine silver (GMS) stain and periodic acid Schiff (PAS) stain for fungal organisms was found to be negative. Immunohistochemical stains for cytomegalovirus (CMV) and herpes simplex virus (HSV) were also found to be negative. No evidence of neoplastic process was found. Histopathologic evaluation of random gastric biopsy specimens revealed mild gastritis with no evidence of Helicobacter pylori infection. All specimens were found to be negative for presence of amyloid deposition. In light of the clinical presentation, endoscopic evaluation and histopathologic findings, a diagnosis of idiopathic esophageal ulcers was made. Therapy with a proton pump inhibitor (pantoprazole 40 mg twice daily) and oral sucralfate was initiated with gradual and complete resolution of symptoms. These were started 1 month after Ann Hematol (2008) 87:1031–1032 DOI 10.1007/s00277-008-0533-5

Systemic Mastocytosis Causing Refractory Pruritus in a Liver Disease Patient

Systemic mastocytosis (SM) results from clonal, neoplastic proliferation of abnormal mast cells. Patients become susceptible to itching, urticaria, and anaphylactic shock, which occurs due to histamine release from mast cells. SM may coexist alongside other systemic diseases, thus confounding the overall clinical presentation. We discuss a 23-year-old woman with refractory pruritus, which was initially attributed to primary sclerosing cholangitis but had a nonresponse to antihistaminics, ursodiol, and cholestyramine. Concurrent evaluation for polyarthritis revealed increased uptake in the proximal femur on a bone scan, and subsequent bone marrow biopsy revealed indolent SM, and this was understood to be the cause of her intractable pruritus.

Leg Swelling and Mildly Deranged Liver Tests: An Unusual Presentation of a Usual Diagnosis

Gastroenterology 2015;149:e10–e11 Question: A 72year-old woman presented to the hospital with progressively worsening left lower extremity swelling and pain of 1 weeks’ duration. She also reported vague right upper abdominal discomfort, but did not complain of nausea, vomiting, shortness of breath, chest pain, fever, or jaundice.Her past history was significant for hypertension and Meniere disease. She had had no prior surgeries and was a lifetime nonsmoker. Her current medications were hydrochlorothiazide-triamtrene, aspirin, calcium-vitamin D, and amultivitamin. On examination, she had 2þ pitting pedal edema with mild tenderness of left lower extremity. Abdomen was soft and nontender with no palpable organomegaly or mass. The rest of the physical examination was unremarkable. Laboratory tests showed: hemoglobin, 11.8 g/dL; platelets, 277,000/mL; International Normalized Ratio, 1.3; total bilirubin, 1.4 mg/dL; alkaline phosphatase, 279 IU/L; alanine aminotransferase, 39 IU/L; and aspartate aminotransferase, 38 IU/L. Lower extremity ultrasound duplex examination was performed and showed deep venous thrombosis of left femoral vein. CT of the abdomen with oral and intravenous contrast was subsequently obtained (coronal sections; Figure A, B). What is the diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI.