bluuebunny/crossref_metadata_2025 huggingface dataset:
1907 Methemoglobinemia: A Life-Threatening Complication of Topical Pharyngeal Anesthetics
Authors: Riaz Sana , Kudaravalli Pujitha , Saleem Sheikh A. , Heisig David
Published: October 2019

INTRODUCTION:

Topical pharyngeal anesthetics such as benzocaine are used in conjunction with moderate sedation to increase patient comfort during esophagogastroduodenoscopy (EGD). Topical pharyngeal anesthetics can cause methemoglobinemia, which is a rare and life-threatening complication. We want to highlight the potential complication with the use of topical pharyngeal benzocaine through this case presentation.

CASE DESCRIPTION/METHODS:

A 22-year-old female presented with odynophagia after swallowing a piece of meat. She underwent inpatient EGD and received topical pharyngeal benzocaine spray along with moderate sedation. EGD was unremarkable, but during recovery, the patient became dyspneic, cyanotic, and her oxygen saturation (SaO2) dropped to 85% on room air. On chest examination, she had no wheezing, rhonchi, or crackles. Arterial blood gas showed pH 7.50, partial pressure of carbon dioxide 21 mmHg, partial pressure of oxygen 409 mmHg, and SaO2 99%. Blood work showed a methemoglobin level of 27.8%. She was transferred to the Intensive Care Unit and was given supplemental oxygen through facemask and IV ascorbic acid, which resolved her cyanosis and hypoxemia. Repeat methemoglobin level was 8.3% with normal oxygen saturation on room air. Upon stabilization, she was discharged home 48 hours after her initial presentation.

DISCUSSION:

Methemoglobinemia is the oxidation of ferrous to ferric iron within hemoglobin, impairing its ability to transport oxygen, leading to tissue hypoxemia and death. The etiologies of methemoglobinemia are hemoglobinopathy (hemoglobin M), hereditary nicotinamide adenine dinucleotide reductase (NADH) enzyme deficiency and drug induced. Drug-induced methemoglobinemia should be considered in patients with cyanosis and hypoxemia following topical pharyngeal anesthetic use. Despite the rare incidence, most cases of topical-anesthesia-induced methemoglobinemia are secondary to benzocaine. If the use of topical pharyngeal anesthetics is deemed necessary during an EGD, topical viscous lidocaine should be preferred over benzocaine to avoid this potentially life-threatening complication. There is insufficient evidence for methemoglobinemia caused by topical pharyngeal lidocaine alone and reported cases of lidocaine associated methemoglobinemia occurred in patients with either cardiorespiratory diseases or with the use of other anesthetic agents.
1910 Listeriosis in an Immunocompetent Patient After Diagnostic Colonoscopy
Authors: Jacob Burch , Kandola Samanjit , Enofe Ikponmwosa
Published: October 2019

INTRODUCTION:

Although considered safe, colonoscopy, like all other procedures, involves inherent risks, including that of infection. Although rare, there are documented cases of patients with systemic infections caused by Listeria monocytogenes following mechanical disturbance of the GI tract. These systemic infections with Listeria are referred to as listeriosis. Previous cases describe patients with underlying risks for systemic infection, often patients with inflammatory bowel disease on chronic immunosuppressive medication. In this report, we examine the case of an immunocompetent patient with listeriosis following colonoscopy with biopsy.

CASE DESCRIPTION/METHODS:

An 80 year-old female with well controlled diabetes, who was sent to the ED for hemoglobin (Hgb) of 6.5 mg/dL. In the ED, her vitals were stable and physical exam was unremarkable. Labs revealed iron deficiency. Colonoscopy revealed three polyps along with a mass occupying 50% of the circumference of the descending colon. Snare cautery was performed to remove the smaller polyps. Polyp biopsies demonstrated tubular adenoma, with biopsies from the mass representing high-grade dysplasia. Thirty-six hours after colonoscopy she developed a fever of 38.3C (101oF). IV vancomycin and metronidazole were started for the empiric treatment of sepsis. Multiple blood cultures grew Listeria monocytogenes. Additional infectious workup ruled out other sources of infection. Following return of cultures and sensitivities, she was discharged home with three weeks of IV penicillin. Six weeks later, she underwent transverse colectomy with surgical pathology of the lesion showing intramucosal adenocarcinoma.

DISCUSSION:

Symptomatic infection following colonoscopy remains a rare occurrence and is most commonly found in immunocompromised patients. Prior reported cases of listeriosis following colonoscopy have been predisposed with underlying risks, including: cirrhosis, systemic malignancy, HIV, or chronic immunosuppression. In this case, the patient did not display convincing evidence of immunocompromise. The patient’s diabetes was well controlled and had been for over a year prior to her presentation based on two previous A1Cs of 5.9 and 6.5%. The patient’s colon mass found on colonoscopy was found to be intramucosal on surgical pathology and did not represent invasive malignancy. Considering this patient’s risk factors, this case represents a unique presentation of a patient with listeriosis following colonoscopy in an immunocompetent patient.
1911 Acquired Double Pylorus: The Road Less Traveled
Authors: Ali Hiba , Tasleem Syed , Prasad Sanjay , Jarbrink-Sehgal Maria
Published: October 2019

INTRODUCTION:

A double pylorus channel can be congenital or acquired. Acquired double pylorus is thought to be the result of a gastric or duodenal ulcer forming a fistula between the prepyloric antrum and the duodenal bulb. Although it is a rare endoscopic finding, seen in only 0.001%–0.4% of upper gastrointestinal endoscopies1, when acquired, it signifies peptic ulcer disease (PUD) which needs risk factor modification and treatment.

CASE DESCRIPTION/METHODS:

A 50-year-old man with alcohol use disorder, newly diagnosed alcoholic cirrhosis and recent NSAID use presented with confusion, melena and dark emesis. His physical exam was notable for hypotension (BP 86/55 mmHg), somnolence, confusion and positive asterixis. Laboratory values were remarkable for hemoglobin of 5 g/dL, BUN of 48 mmol/L, platelets of 271 × 109/L and INR of 2. Management included fluid resuscitation, blood transfusion, proton pump inhibitor and octreotide drip. Once hemodynamically stabilized, an upper endoscopy was performed revealing blood in the gastric body, two antral ulcers with visible vessels, but no endoscopic stigmata of liver disease. Adjacent to the pylorus, a slit-like channel connecting the prepyloric antrum to the duodenal bulb was noted and traversed with the endoscope. Helicobacter pylori work up revealed a positive serum antibody. Patient did well post-procedure and received Helicobacter pylori eradication treatment and counseling on alcohol cessation and NSAID avoidance.

DISCUSSION:

In contrast to congenital double pylorus which is an incidental finding, patients with acquired double pylorus often present with symptoms of PUD. In this case, likely culprits included NSAIDs and Helicobacter pylori. It should be distinguished from other similar appearing endoscopic findings such as gastric diverticulum, as risk factors for PUD need to be investigated in patients with an acquired double pylorus. While treatment with acid suppression and Helicobacter pylori eradication should be pursued, the fistula tract often persists despite treatment2. Endoscopic recognition and familiarity are key to ensure appropriate risk modification, treatment and prevention of endoscopic complications with side-viewing scopes.
1914 A Rare Complication of Interventional Radiology-Guided Arterial Embolization of Gastroduodenal Artery in the Setting of an Acute GI Bleed-Migrated Coils in the Duodenum
Authors: Kudaravalli Pujitha , Saleem Sheikh A. , Arif Muhammad Osman
Published: October 2019

INTRODUCTION:

Interventional radiology guided (IR) embolotherapy can be lifesaving when an acute gastrointestinal (GI) bleed cannot be controlled with endoscopic therapy. However, IR embolization can lead to various complications and herein we present a complication which has been published.

CASE DESCRIPTION/METHODS:

A 91-year-old male presented to the emergency room with hemodynamically significant upper gastrointestinal bleeding manifesting as hematemesis. After medical optimization, the patient underwent an upper GI endoscopy (EGD) which showed large amount of frank blood in the duodenum interfering with the visualization and treatment of the bleeding site. Hence, the patient underwent an urgent IR guided arteriogram and embolization of the gastroduodenal artery by placement of vascular coils. An EGD was done 48 hours later which showed a giant non-bleeding cratered duodenal ulcer with a visible vessel and vascular coils partially protruding into the duodenal bulb lumen. No active bleeding was noted from the ulcer. Patient had no further evidence of bleeding post embolization and was discharged. The patient presented 3 months later with abdominal pain. CT abdomen showed multiple liver abscesses. IR-guided drainage of abscesses was performed and the culture grew Streptococcus Intermedius. MRCP, ERCP and barium enema were unremarkable. The patient was treated with prolonged course of IV antibiotics and recovered without any further issues.

DISCUSSION:

IR guided arterial embolization can be life-saving in cases where GI bleeding cannot be controlled endoscopically, however it can lead to serious complications including endovascular coil migration into GI lumen. Endovascular coil migration can occur immediately or several years later which can result in fatal bleeding and infection. Endoscopic removal of the migrated coil with hot biopsy forceps has been reported however in most cases this complication has been conservatively followed by endoscopy. The best approach to prevent and manage migrated endovascular coils in GI lumen remains unclear.
1921 A Case of Ovarian Varices Bleeding Presenting as an Obscure GI Bleed and Abdominal Pain
Authors: Khan Adil , Panghal Ritvika , Naeem Raza
Published: October 2019

INTRODUCTION:

Upper GI bleed is one of the most common complications in cirrhotic patients with portal hypertension. However, when GI bleed cannot be found after performing endoscopy, one should consider an ectopic gastrointestinal variceal bleeding. Ectopic varices are portosystemic collaterals in locations other than the gastroesophageal region. We present you a case of 44 year old cirrhotic patient, who was seen for nausea, vomiting and abdominal pain with acute blood loss anemia. She was found to have an ectopic gastrointestinal variceal bleeding after a negative endoscopy.

CASE DESCRIPTION/METHODS:

44 years old female with past medical history of cirrhosis secondary to NASH presented to the ER with complaint of abdominal pain associated with nausea and vomiting while she was having sexual intercourse. Patient had CT Abdomen and Pelvis with IV contrast which was consistent with evidence of portal hypertension including large venous collaterals and splenomegaly. There was hyperdense ascitic fluid identified on the CT scan. On the left side of the hemiabdomen the fluid was hyperdense, suggestive of blood. But no site of bleeding could be identified on the study. Patient’s hemoglobin dropped by 2 grams in the ER. GI recommended to place NG tube and evaluate for blood contents. Gastric content via NG tube was non-bloody.IR was consulted who, after reviewing her CT scan images, noticed an unusual large IMV supplying large pelvic varices presumably as portal venous compression sites into systemic venous system. IR performed transhepatic portal access with pelvic variceal embolization. Interestingly, they did not find active bleed at the time of procedure. But, given recent history and CT findings, empiric embolization was performed of these varices. At completion, no residual pelvic varices was seen. Patient has successful sclerotherapy and coil embolization of the 2 pelvic-to-ovarian venous plexus varicosities for treatment of presumed source of variceal intraperitoneal bleeding. Patient was discharged home with stable hemoglobin.

DISCUSSION:

When GI bleed cannot be found after performing endoscopy, one should consider an ectopic gastrointestinal variceal bleeding. Out of all the variceal bleeding, 5% of them are ectopic variceal bleeds. As GI bleed with acute blood loss anemia can be fatal and outcome being time-sensitive, it is necessary to establish diagnosis early. Multi-slice computed tomography with contrast plays an important role in the early diagnosis of ectopic variceal bleed.
1929 Spots and Dots on the Skin and Stomach: Gastrointestinal Vasculitis
Authors: Viswanath Shilpa , Almouradi Tarek
Published: October 2019

INTRODUCTION:

Immunoglobulin A (IgA) vasculitis is often seen in the pediatric population but can also be seen in the adult cohort. The classic histopathological finding in IgA vasculitis is leukocytoclastic vasculitis (LCV), which is a neutrophilic inflammation in post-capillary venules. Classic signs of LCV include palpable purpura, small vessel involvement, and less likely but also extracutaneous manifestations. We present a unique case of a gastrointestinal (GI) manifestation of LCV with angiodysplasia in the stomach and duodenum.

CASE DESCRIPTION/METHODS:

This is a 66-year-old female with a history of hypertension, chronic kidney disease stage III, hypothyroidism, a recent diagnosis of LCV (Figure 1) two weeks prior that returns to the hospital with a complaint of watery diarrhea, bright red blood per rectum, lower abdominal cramping, and nausea. Her vitals were unremarkable and her laboratory studies revealed elevated blood urea nitrogen (BUN), acute kidney injury, mild anemia, and leukocytosis. A computed tomography (CT) scan of her abdomen demonstrated extensive wall thickening, multifocal periduodenal inflammation, and diffuse ileal wall thickening (Figure 2). An esophagogastroduodenoscopy (EGD) revealed ulcerative esophagitis, helicobacter pylori negative duodenal ulcers, and multiple non bleeding angiodysplasias in the stomach and duodenum that were cauterized (Figure 3). A colonoscopy revealed a tubular adenomatous polyp that was removed. The patient’s symptoms resolved and she did not demonstrate any further bleeding. Her hemoglobin stabilized and she was able to tolerate a regular diet on discharge.

DISCUSSION:

Abdominal pain and bloody diarrhea can have a milieu of differentials. This patient clearly demonstrated a vasculitic GI manifestations with bowel wall thickening and inflammation on imaging, elevated BUN, anemia, bloody diarrhea, and a history of LCV. Having a proper suspicion and confirming this with imaging, endoscopy, and biopsy is imperative for the diagnosis. Without a thorough history and physical, undiagnosed vasculitis can lead to fatal consequences such as gastrointestinal hemorrhage, perforation, or more rarely infarction.
1935 An Unusual Cause of Post-Polypectomy Bleeding
Authors: Kaila Vishal , Desai Amit P.
Published: October 2019

INTRODUCTION:

Myeloid sarcoma is a rare tumor characterized by a tissue mass of myeloid progenitor cells occurring outside of the bone marrow. Myeloid sarcoma can occur de novo or overlap with acute myeloid leukemia (AML). As with AML, myeloid sarcoma may also present as a blast transformation of myelodysplastic syndrome or neoplasm.

CASE DESCRIPTION/METHODS:

A 65-year-old male was transferred to our hospital for hematochezia after a cecal polypectomy. Two days prior to transfer, the patient underwent screening colonoscopy for colorectal cancer at an outside hospital. During the procedure, a large carpeted, sessile polyp was seen overlying the cecal fold. Endoscopic removal was attempted but was unsuccessful given the polyp’s location and size. Pathology from the partially removed polyp revealed a tubulovillous adenoma. His hemoglobin was 6.5 g/dL (13.0–17.0 g/dL) and white blood cell count was 70 M/μL (4.20–5.60 M/μL). Following blood transfusions and hemodynamic stabilization, repeat colonoscopy and bone marrow biopsy were performed. The polypectomy site revealed flat, polypoid ulcerated and friable tissue with multiple areas of bleeding and clot (Figure 1). Despite hemostatic clip placement and thermal therapy to treat areas of active oozing, the lesion continued to bleed. The surgical team was activated given known residual adenomatous tissue and the patient underwent a successful right hemicolectomy. Pathology of the surgical specimen showed a tubulovillous adenoma with focal high-grade dysplasia and central ulceration with fibrinous exudate and submucosal hemorrhage. In addition, there were immature myeloid cells infiltrating the submucosa underneath this polyp. Furthermore, sheets of myeloblasts, positive for CD34 and CD117, within the submucosa also formed a separate ulcerated, plaque-like, 1.0 cm mass distal to the polyp (Figure 2). Bone marrow biopsy showed a 70% cellular marrow with nearly 20% myeloblasts. The patient had both a tubulovillous adenoma with an infiltrating adjacent myeloid sarcoma.

DISCUSSION:

While myeloid sarcoma can affect any organ, they most commonly infiltrate the skin or gums. Colonic involvement is extremely rare. Treatment for myeloid sarcomas is identical to that of AML, even if there no evidence of bone marrow involvement.
1936 Levamisole Contaminated Cocaine Presenting as Gastrointestinal Ulcerations and Bleed
Authors: Williams Mary-Jane O. , Ayutyanont Napatkamon A. , Akhondi Hossein A.
Published: October 2019

INTRODUCTION:

Levamisole is a widely used cutting agent for cocaine and it also contributes to increased quantity of cocaine. Gastrointestinal (GI) ulcers and bleed is a rare presentation of levamisole intoxication. We report a case of GI ulcers and bleed suspected to be from levamisole contaminated cocaine.

CASE DESCRIPTION/METHODS:

A 58 year old female presented with sore throat, headache, oral ulcers and multiple necrotic skin lesions following a tooth extraction. On examination, she was noted to have oral ulcers, peri-anal necrotic ulcers, finger eschars and a left lower extremity open blister. Painful violaceous purpuric patches with well-delineated dusky necrotic centers and a bright erythematous rim were also observed peri-anally. Laboratory studies revealed neutropenia, hyponatremia, acute kidney injury, positive antineutrophilic antibody, Hepatitis C, HSV 1 and 2, D-dimers, antidouble-stranded DNA antibodies, anti-neutrophil cytoplasmic antibodies, lupus anticoagulant antibodies and decreased protein S levels. Urine toxicology screen was positive for cocaine and opiates. Patient admitted to cocaine use due to pain from the extracted tooth. Computed Tomography (CT) of abdomen revealed moderate ascites and body wall edema. She was managed with intravenous fluids, pressors, antibiotics, antiviral, antifungal therapy. She also received treatment with filgastrim. Over the course of her hospital stay, she developed lower GI bleed and required multiple units of blood transfused. Endoscopy revealed a clean based gastric ulcer and multiple cecal colon ulcers which was managed with epinephrine injections.

DISCUSSION:

Levamisole is mostly absorbed from the GI tract and metabolized by the liver. Our patient presented with immune derangements and GI bleed after the use of cocaine to help with her pain from tooth extraction. Laboratory results were compatible with levamisole contamination. CT of the abdomen showed moderate ascites and anasarca similar to MRI characteristics of levamisole-induced leukoencephalopathy which show peripheral ring-type enhancement and edema around lesions. The mechanism of levamisole in the formation of GI ulcers is presumed to be related to ischemia. To our knowledge, this is the first case of levamisole-contaminated cocaine induced gastrointestinal ulceration and bleed. This case illustrates the potential for severe gastrointestinal ulcers and bleed with the use of levamisole and the value of high index of suspicion.
1937 A Deadly Diagnosis: Aortic Stent Causing Aorto-Esophageal Fistula
Authors: Kailas Shilpa D. , Kulkarni Prasad
Published: October 2019

INTRODUCTION:

An aorto-esophageal fistula (AEF) is a rare but life-threatening cause of upper gastrointestinal bleeding caused by an abnormal communication between the esophagus and aorta. Etiologies include foreign body ingestion, malignancy, post-operative trauma, and ruptured TAA. We present the fatal case of a patient with profound anemia who suffered catastrophic consequences secondary to graft-esophageal fistula.

CASE DESCRIPTION/METHODS:

A 66-year-old male with history of percutaneous thoracic endovascular aortic repair 3 months prior presented with complaints of 2 weeks of dizziness, nausea, and intermittent dark stools. EGD/colonoscopy 2 months ago were negative for acute GI bleed. Upon evaluation, the patient was mildly tachycardic with positive orthostatic vital signs and fever of 100.4 F. Rectal exam did not demonstrate gross blood. Labs were remarkable for Hgb 6.8 with repeat 5.9, WBC 14, and BUN 14. CTA chest was done to investigate tachycardia and identified an enlarging distal aortic endoleak with stable short segment dissection. Vascular surgery was consulted but felt the endoleak was chronic. CT A/P ruled out retroperitoneal hematoma and he was treated with transfusions and beta blocker therapy. Following recurrent melena, our EGD revealed two areas concerning for aortic stent erosion into the esophagus at 34 and 36 cm from incisors with trace oozing, locating the source of hemorrhage. Vascular surgery reevaluated the patient with plan for graft removal and reconstruction of thoracic and abdominal aorta. Unfortunately, before advancing to surgery he decompensated after large volume hematemesis. Vasopressors were initiated for hemorrhagic shock but life-sustaining measures were eventually discontinued to respect family wishes. The etiology of his acute symptomatic anemia and massive hemorrhage was suspected to be graft-esophageal fistula.

DISCUSSION:

AEF is an unusual post-operative complication of prosthetic aortic repair. Secondary AEF can develop after open or endovascular repair of the aorta, occurring in 1.9% of patients post-endovascular aortic repair. Pathophysiology remains unclear but it is thought to arise from erosion of graft material into esophagus, graft infection with abscess rupture, or anastomotic pseudoaneurysm. Our case emphasizes the importance of raising clinical suspicion not only for hematemesis but for new onset fever with elevated inflammatory markers in the appropriate clinical setting as well as the need for emergent surgical intervention to avoid fatal outcomes.
1940 Acute Lower Gastrointestinal Bleeding Due to Multiple Colonic Polypoid Angiodysplasias in a Patient With Sickle Cell Disease
Authors: Mahpour Noah , Bhurwal Abhishek , Patel Anish V.
Published: October 2019

INTRODUCTION:

In patients with Sickle Cell Disease who present with hematochezia, ischemic colitis is often identified as the precipitating etiology. Angiodysplasia in sickle cell is infrequently described as the cause of hematochezia, especially in young patients. Our case illustrates the unusual finding of hematochezia due to multiple polypoid angiodysplasias distributed in the entire colon of a young patient with sickle cell disease.

CASE DESCRIPTION/METHODS:

A 26-year-old male with sickle cell disease leading to cirrhosis decompensated by ascites presented with multiple episodes of painless hematochezia for one day. On physical examination, he was noticed to have relative hypotension, with ascites and bright red blood on rectal exam.His initial lab work noted a hemoglobin level of 4.3 g/dL and an INR of 5.3. As he presented with hematochezia and hypotension, he underwent a computed tomography (CT) scan with intravenous contrast, which showed a blush of contrast at the splenic flexure, indicating an active luminal hemorrhage (Figure 1). However, emergent mesenteric angiography was unsuccessful in detecting active bleeding, thus, embolization could not be performed. A subsequent colonoscopy revealed 11 actively bleeding polypoid angiodysplasias distributed throughout the entire colon (Figures 2 and 3), each treated with argon plasma coagulation and clipping to prevent further bleeding. The patient did not have any recurrent episodes of bleeding throughout his hospital course, and was discharged.

DISCUSSION:

We present a case of acute lower gastrointestinal bleeding due to multiple colonic polypoid angiodysplasias in a young patient with sickle cell disease, successfully treated with argon plasma coagulation therapy. Colonic angiodysplasia is commonly found in individuals older than 40 years of age, generally appearing as a fern-like flat or elevated bright-red lesion on endoscopy. The polypoid form of angiodysplasia is extremely rare, reported primarily in the sigmoid and transverse colon, and is easily identified based on its striking appearance. Polypoid angiodysplasia has rarely been described in patients less than 50 years of age, and has no known association with sickle cell disease. CT angiography is a potentially crucial non-invasive initial test, as it can possibly detect extravasation from actively hemorrhaging angiodysplasias. Successful endoscopic eradication therapies include argon plasma coagulation, electrocoagulation, and snare polypectomy.
1948 Dominant Claw Control: Role of OTSC Clip as Salvage Hemostasis Therapy
Authors: Shapira Gilad , Kumar Manoj , Fahmawi Yazan , Mizrahi Meir
Published: October 2019

INTRODUCTION:

Upper Gastrointestinal Hemorrhage (UGIH) remains a common problem in modern day endoscopy. Etiologies of UGIH include variceal, nonvariceal, neoplastic, vascular malformation, and iatrogenic among others. Endoscopic hemostasis is typically achieved by through the scope (TTS) clips, epinephrine injections, ablation techniques, coils and glues and self-expandable stents. Despite having multiple tools for bleeding control, rebleeding risk remains high among single vessel ulcers and larger lesions. Here we present a case where traditional hemostasis methods failed, and an over-the-scope clip (OTSC) was used as salvage/rescue hemostasis therapy.

CASE DESCRIPTION/METHODS:

45-year-old asian Male with a history of cirrhosis secondary to alcohol presented with jaundice and melena with a hemoglobin of 5.9 gm/dl. EGD showed severe duodenitis. A side viewing duodenoscope showed a large, cratered duodenal bulb ulcer with a visible vessel. Epinephrine was injected and 5 hemoclips were placed. Despite this, there was still active oozing of blood. All the hemoclips were removed with snare. OTSC System was loaded onto a standard gastroscope and advanced to the lesion. Target tissue was sucked into the cap and OTSC® clip was released by turning the hand wheel. The clip closed itself and firmly anchored the tissue resulting in complete hemostasis. Proton pump inhibitors were continued and follow up endoscopy at 1 month showed healed ulcer site with clip in place.

DISCUSSION:

TTS clip can sometimes be not enough for UGI bleeding treatment especially during active bleeding, use in ulcers with a fibrotic base, or when the bleeding lesion is in a difficult-to-access anatomic location (e.g., gastric lesser curve or cardia, posterior duodenal wall). While OTSC have been well established in leaks, perforations, and fistulas, their role in UGIH is evolving. Several randomized trials comparing OTSC with conventional endoscopic hemostasis therapies are ongoing and results are awaiting, however our case reiterates that OTSC platform should be available and be part of endoscopic hemostasis armamentarium.
1949 Modern Coils and Glue: An Evolving EUS Application in the Management of Gastric Varices
Authors: Houston Jessica , Kumar Manoj , Fahmawi Yazan , Barker Michael , Mizrahi Meir
Published: October 2019

INTRODUCTION:

Ethylene vinyl alcohol (EVOH) is a liquid embolic agent approved for cerebrovascular lesions. DMSO solvent dissipates into the blood, causing the EVOH copolymer and suspended tantalum to precipitate in situ into a spongy, coherent embolus. Their role in the management of gastric varices is still unknown. We are presenting our experiences with this novel echoendoscope (EUS) guided use of EVOH to achieve gastric variceal obturation (GVO).

CASE DESCRIPTION/METHODS:

Case 1
: 44-year-old male with decompensated cirrhosis presented with melena. EGD showed large gastric varix (GOV-2). EUS- guided coiling and EVOH glue injection was planned. Gastric varices were identified using a linear echoendoscope at 7.5 MHz and 22G FNA needle was then advanced into varix with position confirmed by aspirating blood. Three embolization microcoils (5 mm/mm2, 8 mm/4mm, 7 mm/3mm; proximal end diameter/distal end diameter) were placed into the varix followed by needle flush with a 0.8 ml DMSO (dimethyl sulfoxide). Post DMSO flush, 5 mL EVOH glue was injected with excellent flow reduction on EUS doppler. 0.8 ml of DMSO was again used to flush the needle. Patient tolerated procedure well and had no signs of bleeding prior to discharge.
Case 2
: 39-year-old male with history of alcoholic and HCV cirrhosis and hepatocellular carcinoma, two prior banding procedures for bleeding esophageal varices, gastric varices, presented with signs and symptoms of decompensated cirrhosis, hematemesis and melena. EGD with banding was done for large esophageal varices with stigmata with successful hemostasis. Large gastric varix (GOV-1) was also discovered. Coiling and glue was injected with similar EUS guided technique as above (sixteen embolization microcoils of varying sizes (8 mm/4 mm, 7 mm/3 mm, 5 mm/2 mm); 3 mL EVOH glue injection). Post procedural EUS doppler imaging showed excellent flow reduction.

DISCUSSION:

EVOH is well-known as catheter based embolic therapy for neurovascular lesions. Its application under EUS image guidance for gastric varices has not been reported yet to our knowledge thus making our case as unique. However larger, prospective multicenter trials with EVOH will be required to study rebreeding rates and long-term outcomes in the management of gastric varices.
1950 An Unexpectedly Large Vascular Anomaly Causing Chronic Obscure GI Hemorrhage: A Case Report
Authors: Edwards Jade , Prabakaran Sabrina , Niknam Negar , Brady Patrick
Published: October 2019

INTRODUCTION:

Approximately 5–10% of patients who present with an acute gastrointestinal (GI) hemorrhage have a primary small bowel source. While small bowel angioectasias are one of the most common causes of small bowel hemorrhage, it is rare to find large vascular anomalies in the small bowel as a cause of chronic GI bleed.

CASE DESCRIPTION/METHODS:

We present a case of a 56-year-old woman referred to our institution for management of obscure GI bleeding, associated with severe iron deficiency anemia. She had intermittent melena and occasional dark red blood mixed with stool. Extensive work up in an outside facility including 2 endoscopies, 2 colonoscopies, and a capsule endoscopy were unrevealing. After referral to our institution; push enteroscopy, colonoscopy and retrograde single balloon enteroscopy were performed and were negative for source of bleeding. Capsule endoscopy revealed a small oozing angioectasia in proximal jejunum. The lesion was treated with heater probe via anterograde single-balloon enteroscopy. Due to persistent melena and anemia, antegrade balloon enteroscopy was repeated and demonstrated an abnormal cluster of vascular-appearing lesions in the proximal jejunum that were marked with two hemostatic clips. CT angiogram was consistent with a large arteriovenous malformation (AVM). Interventional radiology performed glue embolization of the high-flow jejunal arteriovenous malformation. The post procedure course was complicated by ischemic proximal jejunum which was confirmed on repeat enteroscopy. Fortunately, her symptoms completely resolved with conservative management without surgical intervention.

DISCUSSION:

AVMs are abnormal lesions with a direct connection between the arterial and venous blood supply without any true capillary bed connecting them. While extremely rare within the GI tract, they can cause significant amount of bleeding and must be considered in patients with obscure GI bleeding or chronic iron deficiency anemia. Studies have shown that AVMs typically only account for 1–2% of upper GI bleeds. More common sites for AVMs include the cecum and ascending colon, while other sites like the small bowel are much more rare. Diagnostic work up typically begins with upper endoscopy followed by colonoscopy. However, these tests are often unrevealing when dealing with small bowel AVMs. Patient’s typically undergo capsule endoscopy for further evaluation, as seen in our patient. If the source of bleeding is still un-identified, then angiography or bleeding scans may be required.
1956 Never Assume, Always Ask: Beyond Infectious and Inflammatory Proctocolitis
Authors: Pisipati Sailaja , Phoo Wut Yi , Hsieh Ting Hui , Fang Tom , Bronander Kirk
Published: October 2019

INTRODUCTION:

Chemical colitis can occur as a result of accidental or intentional exposure to various chemicals including alcohol. Ethanol enemas, practiced either to avoid hangovers and upper gastrointestinal (GI) symptoms or as klismaphilia appears to be dangerous practice. We report a rare case of alcohol-induced proctocolitis in association with sexual fetish.

CASE DESCRIPTION/METHODS:

38-year-old female with depression, bipolar disorder, polysubstance abuse, presented with lower abdominal and rectal pain, hematochezia, and tenesmus upon waking up. On questioning, she said that night prior to presentation, she was intoxicated (vodka, methamphetamine), participated in consensual intercourse when her partner “spit” vodka into rectum. She was mildly tachycardic. Examination revealed a distressed, tearful, dehydrated female with lower abdominal tenderness. Labs revealed leukocytosis, metabolic acidosis and hyperchloremia. Urine toxicology was positive for amphetamines, benzodiazepines, opiates, cannabinoids. Blood alcohol level was zero. CT demonstrated diffuse wall thickening of rectum and distal sigmoid colon. She was admitted for hydration, analgesia, systemic antibiotics and was placed nil per oral. Colonoscopy revealed longitudinal ulcers predominantly in the rectum with erythema and erosions extending up to 20 cms above the anus. Biopsies showed mild nonspecific inflammation. Hydrocortisone enemas, stool softeners and oral diet were commenced. Follow-up sigmoidoscopy in six weeks was advised, patient did not attend.

DISCUSSION:

Intentional administration of alcohol enemas has been implicated in sexual practices, suicidal attempts, bowel cleansing, hemorrhoidal pain relief. Symptoms of abdominal pain, diarrhea, hematochezia, tenesmus develop within 24 hours. Endoscopic evaluation reveals edema, friable, hemorrhagic or necrotic mucosa with ulcerations. Histologic features include mild erythema, extensive mucosal sloughing, necrosis. Diagnosis can be challenging if pertinent history is not obtained, given the non-specific nature of clinical, endoscopic and histological findings. Ischemic colitis, perforation and peritonitis, respiratory depression and CO2 narcosis causing noncardiogenic pulmonary edema and death are potential complications. Severity depends on the amount and speed of administration. GI symptoms usually resolve within 7–10 days. Careful history taking, particularly sexual practices, is crucial when evaluating young healthy individuals with lower abdominal pain and colitis of unclear etiology.
1964 Case of a Rare Coagulation Disorder: A Cause of Recurrent Upper GI Bleeding
Authors: Swaminathan Renugadevi , Pandit Sudha , Manas Kenneth J. , Morris James D.
Published: October 2019

INTRODUCTION:

The most common causes of acute upper gastrointestinal (GI) bleeding are peptic ulcer disease, variceal hemorrhage, Mallory-Weiss tear, and neoplasms. We report a rare case of an acquired hemophilia A diagnosed after recurrent GI bleeding.

CASE DESCRIPTION/METHODS:

A 63 years old male with a history of stroke, dementia, and anemia presented to the ED from clinic for low hemoglobin (Hb). On presentation, patient denied melena, hematemesis or hematochezia. Patient denied NSAIDs, antiplatelet, or anticoagulation therapy. Vital signs were stable. The examination was significant for pallor and right-sided hemiplegia. Admission labs showed Hb 3.9 g/dl and hematocrit 13.7%. Patient received 4 units of pRBC. and was initiated on PPI drip. Upper endoscopy showed active bleeding from duodenal bulb angioectasia, and hemostasis was achieved with 2 endoclips. During the admission, percutaneous endoscopic gastrostomy (PEG) tube was placed for dysphagia secondary to stroke. Subsequently, patient had continuous oozing of blood around the PEG tube insertion site. Aspiration from the PEG tube was negative for blood. Attempt to control the bleeding using external compression with pressure dressing and suture at the access site were unsuccessful. Patient had an episode of melena and required 3 more units of pRBC. Repeat EGD showed actively bleeding duodenal ulcer and non-bleeding gastric angioectasia. Hemostasis was achieved with thermal coagulation and epinephrine. Patient was worked up for coagulation disorder given persistent bleeding days after the PEG tube placement and secondary bleeding sites in the stomach. The lab results showed normal PT, elevated aPTT. and partial correction of the aPTT in the mixing studies. Subsequent labs revealed low Factor VIII activity of 2% and elevated factor VIII inhibitor of 23 Bethesda units/ml, which was consistent with acquired hemophilia A. Patient was initiated on Prednisone and Cyclophosphamide. After a week of initiating the therapy, patient did not have any GI or PEG tube site bleeding and the Hb remained stable.

DISCUSSION:

Acquired hemophilia A is a rare but life-threatening autoimmune condition and the treatment is immunosuppressive therapy to eliminate antibody production against Factor VIII. The risk for bleeding is increased with any invasive procedures including PEG tube placement. All GI bleeding patients in the absence of an obvious cause should have a coagulation work up. It is critical to recognize the underlying cause of GI bleeding for efficient management.
1965 A Case of Gastric Amyloidosis Manifested as Gastrointestinal Bleeding
Authors: Gupta Kamesh , Umar Jalaluddin , Chalhoub Jean , Budhraja Vikram
Published: October 2019

INTRODUCTION:

Gastrointestinal amyloidosis (GIA) ensues from the deposition of insoluble extracellular protein fragments. GIA is most frequently associated with chronic inflammatory disorders (AA amyloidosis), plasma cell dyscrasias like multiple myeloma (AL amyloidosis), and end-stage renal disease (Beta-2 amyloidosis).

CASE DESCRIPTION/METHODS:

A 60-year-old female with a history of diastolic heart failure, light-chain multiple myeloma complicated with systemic amyloidosis and CKD stage III presented with acute epigastric abdominal pain associated with vomiting and non-bloody diarrhea that started a week after she had chemotherapy with bortezomib and elotuzumab. She was on chronic steroid and PPi therapy. On exam, she was noted to have tachycardia, dry mucous membranes, macroglossia and epigastric tenderness with no rebound. Her labwork showed a drop in hemoglobin from 8 g/dL to 5.9 g/dL in a period of 2 days and a platelet count of 48000/mL. Coagulation profile, liver tests and kidney tests were all normal. In the ED, her stool was positive for occult blood. CECT abdomen showed diffuse small and large bowel wall thickening, including the stomach and duodenum. Gastroscopy showed diffuse discontinuous congestion, friability, and ulceration of the mucosa. Clots overlying ulcers were removed with forceps revealing mild oozing only. The gastric biopsy revealed mucosal cells with extracellular amorphous deposits, staining positive for congo red stain, consistent with amyloid. She was started on palliative chemotherapy given her multi-system involvement of malignancy.

DISCUSSION:

GIA involves the buildup of insoluble proteins, most commonly in the second part of duodenum which impedes the normal organ structure and function. Weight loss and GI bleeding are the most common presentations of GIA. Bleeding is a sequela of mucosal lesions, wall ischemia, or vascular friability. The endoscopic appearance of amyloidosis is nonspecific. The mucosa may have a finely granular appearance, polypoid protrusions, erosions, ulcerations, and thickening of the wall. Tissue biopsy is required to make the diagnosis of GI amyloidosis. Treatment depends on a sufficient suppression of the predisposing inflammatory disorder, or malignancy, along with supportive therapy. The prognosis of patients with AL amyloidosis is worse with GI involvement.
1971 Strongyloides Infection Presenting as a Massive GI Bleeding Without Eosinophilia
Authors: Lagos Samuel , Mehta Amit , Wan David
Published: October 2019

INTRODUCTION:

Nematode hyperinfection classically presents with eosinophilia. However, immunosuppressed patients on corticosteroid therapy or with chronic HTLV 1-2 infection do not necessarily express the eosinophilic pattern. This case of GI massive bleeding in a patient with T cell lymphoma and HTLV 1-2 infection illustrates this atypical scenario.

CASE DESCRIPTION/METHODS:

A 60 year-old male with a recent diagnosis of C. difficile colitiswas admitted to the ED with syncope and failure to thrive. His past medical history was notable for peripheral T cell lymphoma on azacitidine and CHOP, and chronic HLTV 1-2. The patient reported 6 days of nausea, vomiting, diarrhea, and chest pain. Patient was born in the Dominican Republic and moved to the US more than 10 years ago. On examination he was tachycardic and hypovolemic and responded to fluid resuscitation. The patient was in no acute distress. His labs were notable for hyponatremia, mild anemia without eosinophilia, cholestasis, hypoalbuminemia, increased PT and mild troponinemia. EKG was normal for acute coronary syndrome, and CT chest was significant for new small right and trace left pleural effusions with atelectasis. Abdominal US revealed gallbladder sludge and biliary duct dilatation. MRCP was normal. His course was complicated by melena and hematochezia. Given hemodynamic instability, he was managed with IV vancomycin and piperacillin/tazobactam in addition to vasopressors and blood products. EGD and flexible sigmoidoscopy showed diffuse mucosal oozing in the upper and lower GI tracts with targetoid, punched out duodenal lesions. Biopsy demonstrated worms suggestive of strongyloides on histopathologic evaluation. The patient was started on Ivermectin which was then switched to Praziquantel given concern of inadequate absorption due to ileus.

DISCUSSION:

Strongyloides infections usually present with variable grade of eosinophilia. However, eosinophilia may be suppressed or absent in disseminated disease because of concomitant pyogenic infection or steroid administration as we can see in this patient.3Additionally, patients with HTLV-1 infection express high levels of interferon-gamma production, which decreases the production of interleukin (IL)-4, IL-5, IL-13, and IgE, important molecules in host defense against Strongyloides.4 Strongyloides is typically diagnosed via serology, but was made after EGD was done for GI bleeding. Thus, Strongyloides infection should be on the differential for GI bleeding in an immunocompromised patient.
1972 Proton Pump Inhibitors Causing Severe Chronic GI Blood Loss Resulting in Severe Iron Deficiency Anemia
Authors: Hussain We'am , Musleh Mustafa
Published: October 2019

INTRODUCTION:

Proton pump inhibitors (PPI) are a commonly used medication for the treatment for gastroesophageal reflux disease (GERD), peptic and NSAIDs induced ulcers. We report a rare case of severe chronic GI bleeding leading to severe iron deficiency anemia, caused by extensive hemorrhagic fundic gland gastric polyps secondary to long term PPI therapy.

CASE DESCRIPTION/METHODS:

A 77-year-old woman with past medical history of GERD controlled with omeprazole 20 mg daily, who was referred to GI due to severe symptomatic iron deficiency anemia. For about a year, her hemoglobin was slowly trending down, when she was referred to GI, her hemoglobin was 8.2 g/dl, with MCV 69 FL. Her iron indices showed iron saturation of 8%, TIBC of 426 mg/dl, and ferritin level of 8. She was started on oral iron therapy, and underwent colonoscopy and esophagogastroduodenoscopy (EGD) which revealed left colon diverticulosis, and innumerable gastric polyps including numerous large hemorrhagic polyps involving the entire stomach but excluding the antrum. Polypectomy of multiple polyps was done, although due to the extensive polyps burden, could not practically remove all polyps in one session. Pathology evaluation confirmed fundic glands polyps, with focal adenomatous changes in one of the large polyps without dysplasia, and there was no evidence of H.Pylori. Patient was advised to stop omeprazole, and was given ranitidine 150 mg BID as needed for reflux symptom. She had a second EGD one month later which still revealed innumerable gastric polyps, further removal of multiple large polyps was done, pathology was consistent with fundic glands polyps. 6 months later on follow up, patient hemoglobin improved to 12.3 mg/dl, with normalization of ferritin level. She had a repeat EGD which revealed remarkable regression of the size and number of the gastric polyps.

DISCUSSION:

We report herein a case of extensive gastric polyposis consistent with stent fundic glands polyps leading to severe chronic blood loss causing severe iron deficiency anemia. Fundic glands polyps in our patient, are attributed to hypergastrenemia secondary to chronic long term PPI administration.Most polyps are sporadic, hypergastrenemia due to ZES or chronic PPI use is associated with increase in prevalence of FGPs. A study showed fourfold increased risk of FGPs in patients on long term PPI therapy (over 5 years). Case reports have showed regression in number and size of FGPs after cessation of PPI therapy, as seen in our patient case.