bluuebunny/crossref_metadata_2025 huggingface dataset:
3125 CMV Infection Presented as Asymptomatic Inflammatory Polyp in Immunocompetent Patient
Authors: Shah Shashin , Hrad Valery , Nellis Eric
Published: October 2019

INTRODUCTION:

Colonic manifestations of the CMV infection are significantly more common in immunocompromised patients than immunocompetent individuals. Typical endoscopic findings include inflammatory changes of the colonic wall with ulcerations. Though extremely rare, mass lesions in colon due to CMV infection have been previously reported [1,2]. We report a case of a large inflammatory polyp secondary to CMV in immunocompetent patient during colonoscopy.

CASE DESCRIPTION/METHODS:

A 71-year old asymptomatic male patient presented for colonoscopy after positive Cologuard test. He denied any gastrointestinal symptoms and had no significant previous medical history. On exam patient had an inguinal hernia. Previous colonoscopy evaluation more than 10 years ago was normal. Colonoscopy revealed a sessile ascending colon 15 mm polyp and 10 mm semi-pedunculated polyp in sigmoid (Figure 1), both of which were removed with hot snare. Histopathology report showed positive immunostaining for CMV in sigmoid polyp.

DISCUSSION:

CMV related colonic lesion in immunocompetent patient is an unexpected finding. We found only 3 previous reports in the literature [3-5]. Given the potential infectious pathophysiology of this polyp infectious disease referral was made. In addition to the endoscopic removal via polypectomy, antiviral therapy was described as an effective treatment modality in the case of assumed superimposed CMV infection of suture line inflammatory polyps [3].
3126 Buried Bumper Syndrome
Authors: Jiyani Rucha , Jacob Bobby , Khan Nausheer
Published: October 2019

INTRODUCTION:

Feeding tube placement ensures appropriate delivery of enteral nutrition,however is associated with adverse effects which can occur at rate as high as 10%. Complications may be minor or fatal including death. Common complications include aspiration, wound infection, bleeding, perforation, necrotizing fasciitis and intestinal obstruction. Our case is a very rare early presentation of life threatening buried bumper syndrome.

CASE DESCRIPTION/METHODS:

56 year old Caucasian Male with history of benign esophageal stricture status post percutaneous gastrostomy tube (PEG) placement in 2016 and history of Bipolar disorder brought in by from nursing home to Emergency department for dislodgement of his PEG tube and complaint of abdominal pain and drainage from his gastric stoma. Interventional radiology attempted fluoroscopic guided PEG placement procedure, however procedure was aborted because an opacified contrast was noted in gastric lumen, which was suspicious for retained gastrostomy bumper. Further imaging was obtained with CT Abdomen/pelvis that revealed a metallic density projecting from the skin of the anterior abdominal wall to within the body of the stomach. Upper Endoscopy was subsequently performed but was limited due to a pinpoint stricture of esophagus was noted 30 cm from the incisors which could not betraversed by the upper endoscope. Laparoscopic removal of the buried bumper was performed with subsequent laparoscopic gastrostomy tube placement. Surgery and pathology report showed removed foreign body from stomach stated medical device consistent with gastric tube. Patient had successful removal of retained bumper with new placement of PEG tube. Patient tolerated procedure well without complication.

DISCUSSION:

Buried bumper syndrome is caused by migration of the internal bumper of the PEG into the gastric or abdominal wall. BBS presentation on average approximately is 18 months, depending on which kind of feeding tube has been used. Unfortunately, buried bumper syndrome presents with late stage and early presentation are usually rare. Implementation of post PEG placement follow up policies could have an impact in preventing these PEG tube related fatal complications. To our knowledge there are no guidelines, which recommend an interval of time for follow-up post PEG placement to assess for complications. We suggest that an optimal close follow up concord by each institution for status post PEG placement may prevent and minimize serious complication and provide better patient care.
3127 Blakemore? Wait More!
Authors: Voaklander Rebecca , Byrne Kathryn R.
Published: October 2019

INTRODUCTION:

This is a case of a decompensated cirrhotic patient with a non-variceal upper GI bleed that was nearly treated with placement of a Sengstaken-Blakemore tube, which would likely have perforated her acutely ischemic esophagus.

CASE DESCRIPTION/METHODS:

A 62-year-old woman with decompensated alcoholic cirrhosis and a history of esophageal varices was brought to the ED for “coffee ground” emesis and lethargy. She relapsed into drinking alcohol two weeks before presentation and shortly thereafter developed abdominal pain. Three days before admission, she developed non-bloody emesis. On the day of presentation she had at least 10 episodes of clear emesis that eventually turned black. She had a history of esophageal varices requiring banding, most recently 5 years prior to admission. Her most recent EGD was 3 years ago, which was significant for portal hypertensive gastropathy and small varices that did not require banding. Initial vital signs were significant for a HR of 110 and BP of 77/37. Abdominal exam demonstrated normoactive bowel sounds, diffuse tenderness to palpation, no guarding, and no rebound tenderness. In the ED, patient had at least 2000 cc of “coffee ground” emesis and she was intubated for airway protection. Placement of a Blakemore tube was considered but ultimately decided against given that observed emesis was not bright red and emergent endoscopy would soon be performed. Initial labs were significant for: Hgb 14.4 platelets 106 lactate 24 pH 6.9 INR 1.5 creatinine 3.4 total bilirubin 2.8 AST 281 ALT 168.

Emergent EGD in the MICU revealed no esophageal or gastric varices, however severe erosive esophagitis and acute esophageal necrosis with a “black esophagus.” Patient underwent a chest CT and cardiothoracic surgery consultation. After a brief stay in the MICU with supportive care, patient was ultimately extubated, her diet cautiously advanced and she was discharged to home.

DISCUSSION:

This case illustrates the need to think critically about the etiology of a brisk GI bleed, as not all significant GI bleeds in cirrhotic patients are related to varices. A clinical clue indicating that this may not have been an active variceal bleed was that the large-volume emesis was coagulated rather than fresh blood. Furthermore, the objective data reflected a state of severe hypovolemia and ischemia but no anemia in spite of recurrent hematemesis. Placement of a Blakemore tube in the setting of acute esophageal necrosis could have resulted in a catastrophic outcome of esophageal rupture.
3130 Unexplained Thrombocytopenia Associated to the Use of PPI in a Patient With a Bleeding Peptic Ulcer Disease
Authors: Arroyo Mercado Fray M. , Likhtshteyn Michelle , Chokshi Tanuj , Reka Safak
Published: October 2019

INTRODUCTION:

Proton pump inhibitors (PPIs) are used to suppress acid production and to promote hemostasis, which significantly reduces the risk of rebleeding in upper gastrointestinal bleeding [1]. Accumulating evidence indicates an association between PPIs and thrombocytopenia in patients treated for upper gastrointestinal bleeds [2-4].

CASE DESCRIPTION/METHODS:

A 38-year-old male with no significant past medical history presented to the hospital complaining of coffee ground emesis, hematochezia, dark stools and three episodes of syncope in the setting of daily naproxen use for one month. Vital signs revealed orthostasis without tachycardia or hypotension. Physical exam revealed a soft, non-tender, non-distended, abdomen with normoactive bowel sounds. Rectal exam was positive for melena but negative for hemorrhoids or any palpable masses. Initial laboratory workup was significant for a hemoglobin of 7.8, platelet count of 163, and BUN of 27. Intravenous (IV) PPI was administered for management of suspected bleeding PUD. The patient received packed red blood cells (PRBCs) with appropriate response to transfusion. Upper endoscopy revealed a pre-pyloric non-bleeding ulcer that was successfully treated. A significant drop in platelet count was noted on hospital day four which continued to decrease from 163 to 107. PPI route of administration was changed from IV to oral, resulting in an increase in platelet count to 116 by hospital day 7.

DISCUSSION:

PPIs are widely used for the treatment of PUD, GERD, Barrett esophagus, esophagitis, and gastritis. As the main medication used in the treatment of upper gastrointestinal bleeding, it is crucial to understand the effect of PPI therapy on platelets. Literature review suggests an association between thrombocytopenia and the use of PPIs [2-4]. However, further studies are needed to establish a direct association between PPIs and thrombocytopenia. In our case, thrombocytopenia was noted on hospital day 3 of PPI infusion. Route of administration of PPI was changed from IV to oral and thrombocytopenia improved steadily. Although the exact mechanism linking PPI therapy to thrombocytopenia remains unknown, it is important to be aware of this possibility. Close monitoring of platelet count is recommended upon initiation of PPI therapy.
3135 A Case of Epstein-Barr Virus (EBV) Mediated Acquired Hemophagocytic Lymphohistiocytosis (HLH) Presenting With Upper GI Bleed (UGIB)
Authors: Jariwala Ravi , Harris Patrick , Catron Tom , Shoreibah Mohamed
Published: October 2019

INTRODUCTION:

HLH often follows a fatal disease course with inflammation due to uncontrolled proliferation of macrophages causing multi-organ failure. Acquired HLH presents in adults secondary to infection (most commonly CMV or EBV) or malignancy. Several case reports have linked gastrointestinal bleed (GIB) to acquired HLH. We present a case of acquired HLH presenting with UGIB.

CASE DESCRIPTION/METHODS:

A 34 year old man with a history of chronic active EBV (CAEBV) presented from clinic for treatment of acquired HLH flare. He was diagnosed with HLH secondary to CAEBV infection 1.5 years prior and has been treated with steroids, rituximab, and etoposide with plans for stem cell transplant. Exam was notable for fever 102°F and hepatosplenomegaly. Labs were notable for EBV quant >1 million IU/mL, new CMV quant 7000 IU/mL, elevated ferritin, transaminitis, lactic acidosis, pancytopenia, and labs consistent with DIC (fibrinogen 155 mg/dL, D-dimer 1,082 ng/mL, platelets 41.6 × 103/cmm). He later developed episodes of hematemesis preceded by vomiting, requiring transfer to MICU due to hemodynamic instability. Abdominal ultrasound was without cirrhosis. EGD showed a 5 mm non-bleeding Mallory-Weiss tear (MWT) with stigmata of recent bleeding and clot extending down to GEJ; no intervention was conducted. The following day, he had more episodes of hematemesis. Emergent EGD showed large burden of clots in the esophagus extending to the GEJ; the clots were aspirated until mucosal defect could be visualized, revealing ulcerations with one actively oozing (Figure 1). Three hemostatic clips were placed followed by the application of hemospray with complete cessation of bleeding (Figure 2).

DISCUSSION:

HLH has been associated with GIB manifesting as diffuse or isolated ulceration anywhere in the GI tract. Here we present a patient with HLH who had a GIB that manifested as hematemesis and was found to have endoscopic evidence of MWT. About 80-90% of MWT heal spontaneously. However, this patient's coagulopathy manifesting as DIC resulting from his HLH prevented spontaneous healing leading to hemorrhagic complications. His GIB required clipping and the addition Hemospray aided in achieving hemostasis and hemodynamic stability. Hemospray's efficacy has been shown in peptic ulcer bleeds and cancer related GIB, however, there is minimal data on its use in acute esophageal bleed making this a unique case. Overall, this case highlights the GI complications of HLH and the importance of endoscopic management in controlling such a bleed.
3137 Metastatic Melanoma to the Stomach: A Rare Cause of Upper Gastrointestinal Bleeding
Authors: Buckshaw Ricky , Decker Robert , Shah Shashin
Published: October 2019

INTRODUCTION:

Upper gastrointestinal bleeding is a common diagnosis with annual incidence of hospitalization reported as 100 per 100,000 individuals. The most common causes are generally recognized to be esophageal varices or peptic ulcer disease. Neoplasm in the stomach is a less common cause, and is usually due to primary gastric adenocarcinoma. The gastrointestinal tract can also be a site of metastases, however malignant melanoma is a relatively rare cause of upper gastrointestinal bleeding, accounting for less than 3% of all severe cases of bleeding.

CASE DESCRIPTION/METHODS:

A 76-year-old male with a history of coronary artery disease status post drug-eluting stent, ischemic cardiomyopathy, hyperlipidemia and melanoma of the face treated thirty years prior, who presented to the emergency department (ED) with hematemesis and melena for 2-3 days along with progressively worsening dyspnea and fatigue. The patient had recently started aspirin and clopidogrel following cardiac stent placement. Upon evaluation in the ED, the patient's vitals were stable. A physical exam revealed pallor with poor capillary refill. There was no abdominal tenderness. Lab work revealed hemoglobin 5.6, which increased to 7.6 after two units of packed red blood cells, white blood cells 13.3, serum creatinine 1.35, troponin 0.37. The patient was evaluated by gastroenterology who recommended esophagogastroduodenoscopy. The patient was admitted to low level monitoring for continued blood transfusion requirement.

DISCUSSION:

The patient was initially managed with intravenous volume resuscitation. EGD showed large gastric ulcer with heaped margins along the greater curvature of the stomach with a visible vessel, for which an endo clip was placed for hemostasis. Biopsies were obtained which later revealed to be metastatic malignant melanoma (+S100 and +MART1). Next-generation sequencing was performed demonstrating negativity for BRAF, NRAS, and KIT mutations. Patients with metastatic melanoma to the GI tract have an overall poor prognosis with life expectancy as short as four months. With the rising incidence of melanoma and its subsequent GI metastasis, it is important to recognize metastatic disease early and potentially decrease the chance of life-threatening complications, which may lead to an early death. Approximately 4% of patients with gastrointestinal melanoma are diagnosed prior to death. Evaluation with endoscopy may be a powerful detection technique in patients diagnosed with melanoma and could detect early disease.
3138 Unusual Gastrointestinal Petechial Bleeding of the Small Bowel Associated With Newly Diagnosed Chronic Myeloid Leukemia
Authors: Dinh Brian , Triplett Drew , Agrawal Sangeeta
Published: October 2019

INTRODUCTION:

Chronic myeloid leukemia (CML) often is diagnosed in the chronic phase based off routine laboratory analysis in asymptomatic patients with findings include splenomegaly, anemia, leukocytosis, and thrombocytosis. Patients less commonly present with bleeding due to platelet dysfunction. In the case presented, a patient presented with unusual petechial bleeding of the small bowel found on video capsule endoscopy (VCE) as the initial symptom of undiagnosed CML which is highly atypical.

CASE DESCRIPTION/METHODS:

A 79-year-old Caucasian male with a past medical history significant for atrial flutter status-post ablation (not on anti-coagulation) presented to the emergency room with maroon colored stools for 2 days with no other complaints. He denied abdominal pain, nausea, vomiting, or weight loss. Physical exam was benign with vital signs within normal limits. Laboratory analysis revealed white blood cell count of 84.9 t/cmm with 89.9% segmented neutrophils and hemoglobin (HGB) of 10.2 g/dL (previous HGB 14.4 g/dL). The patient was admitted for gastrointestinal (GI) bleeding and malignancy work up. HGB down trended to 7.7 g/dL and an esophagogastroduodenoscopy (EGD) was performed showing no abnormalities. Due to the continued drop in HGB, a colonoscopy was performed which showed old blood in the colon with no identifiable source of bleeding. VCE, interestingly, showed multiple clustered pinpoint petechiae in the ileum. Concurrently, it was suspected that the patient had underlying CML given absence of infection and findings of 1% blasts, basophilia, and eosinophilia. Bone marrow biopsy showed hypercellular bone with myeloid hyperplasia with FISH positive for BCR/ABL confirming CML. It was unknown if the VCE findings may have been related to the patient's newly diagnosed CML.

DISCUSSION:

Anemia is observed in about a third of the patients with newly diagnosed CML depending on the degree of tumor burden. Due to platelet dysfunction, patients may present with bleeding. Because of the significant HGB drop and melena, GI bleeding work up was initiated and ultimately identified a highly unusual source of bleeding. The VCE yielded unexpected images of petechial hemorrhage within the small bowel which was most likely secondary to the underlying malignancy. The case highlights the importance of ruling out sources of GI bleeding in the setting of severe anemia rather than anchoring on the diagnosis of CML. To our knowledge, these VCE findings have not been documented in CML.
3139 Variceal Bleeding, Beyond the Liver Disease: Case Report
Authors: Badi Ahmed M. , Abuhamira Mohamed
Published: October 2019

INTRODUCTION:

Varices are dilated blood vessels in the esophagus or stomach caused by portal hypertension. They cause no symptoms unless they rupture and bleed, which can be life-threatening (1). We report unusual cause of variceal bleeding which is polycythemia rubra Vera causing splenic vein thrombosis. Splenic vein thrombosis (SVT) is known as one of the rare causes of upper gastrointestinal bleeding and is mostly seen in the fifth decade of life and male sex (2).

CASE DESCRIPTION/METHODS:

39 years old Lady presented to the emergency room with history of hematemesis and melena for 2 days. She had chronic headache for that she is advised to take paracetamol but did not work, so she took ibuprofen. She had more epigastric pain for which she took continuous ibuprofen too. She never had symptoms of dizziness, black out/syncope or palpitations with/without standing. Although she had active hematemesis and melena but her hemoglobin never dropped below 10 g/dl. She had no history of any chronic illness or surgical intervention. She was not smoker and denied alcohol intake. Gastroscopy revealed: Esophagus: normal, no varices Stomach: full of blood and there is large clot in the fundus. Large fundal varices (tortuous and complex). Isolated gastric varices IGV1: 2 large FIII ulcer seen in the fundus with one visible blood vessel seen on one gastric fold just near to gastroesophageal junction (Dieulafoy's lesion) which is typical for location. One rubber band was applied on the visible vessel. 1 mg histoacryl was injected in varices and hemostasis is maintained. Duodenum: normal.

DISCUSSION:

isolated obstruction (mainly due to thrombosis) of the splenic vein usually results in left-sided portal hypertension and isolated fundal varices formation. This syndrome is a rare cause of gastrointestinal bleeding. Pancreatic diseases are among the most common etiologies of splenic vein obstruction. Renal disorders are rarely reported as a cause of splenic vein thrombosis 3. We screen for most thrombophilia causes (Table 1). So, we deal with patient with Non cirrhotic liver. Isolated splenic vein thrombosis. Massive splenomegaly Negative hemophilia screen. No evidence of pancreatitis or pancreatic mass on cross sectional imaging. When we review her lab we noted that she had persistently high WBC, platelet and Hematocrit despite GI bleeding, so we screened for myeloproliferative Disorders, and we found mutation for JAK 2 exon 12 is positive. And this patient met the WHO criteria for polycythemia Vera. thrombophilia screen negative.
3140 An Unfortunate Triad: GI Bleed Due to Refractory DLBCL Complicated by Occlusive Thrombus of the Inferior Vena Cava
Authors: Cirac Ana , Niec Rachel , Crawford Carl V. , Wan David
Published: October 2019

INTRODUCTION:

Ileal ulcers are circumscribed, inflammatory and necrotic erosive lesions on the mucosal surface of the ileum and can have specific etiologies such as Crohn's disease, NSAID-intake, intestinal tuberculosis and eosinophilic enteritis. Here, we report a symptomatic terminal ileal ulcer caused by a diffuse large B-cell lymphoma (DLBCL).

CASE DESCRIPTION/METHODS:

A 71 year-old male with a history of gastrointestinal bleeds (GIB) due to ulcers presented with weight loss and small bowel obstruction due to a terminal ileum mass and was diagnosed with an EBV-negative DLBCL after a right hemicolectomy. In the setting of refractory disease (RCHOP, Ibrutinib and Lenalidomide on trial, salvage with DHAX) he presented again with an active GIB with hematemesis and dark stools, an EGD was normal but a colonoscopy showed a lymphoma of the terminal ileum (TI). Clinical examination showed no abnormalities. Initial work up showed mild anemia and elevated creatinine (1.68). A CT abdomen and pelvis showed a progressive disease with new circumferential thickening of the small bowel in the right abdomen. A PET showed a progressive lymphadenopathy throughout the abdomen and pelvis. The GIB was managed with IV pantoprazole and sucralfate. A biopsy of the terminal ileum mass showed a recurrent DLBCL. The patient was considered for a regeneron trial but developed nearly occlusive deep vein thrombosis (DVT) that extended into his inferior vena cava (IVC) and led to a DVT in his left subclavian vein, so that he no longer was a candidate for trial. Given the active GIB, he was planned for the placement of an IVC filter, however, the occlusive thrombus in the IVC prevented the procedure. The goals of best supportive care were discussed with the patient.

DISCUSSION:

The gastrointestinal (GI) tract is the most common extranodal site involved by lymphomas. While GI tract involvement is usually secondary during progression of the disease, primary GI tract lymphoma is relatively rare. Diffuse large B-cell lymphomas are the most common lymphomas affecting the GI tract. GI lymphomas present with unspecific clinical features and are therefore difficult to distinguish from other conditions. The diagnosis is made by pathology. In this case, a biopsy was obtained from the TI mass confirming the diagnosis of refractory DLBCL with GI involvement. This patient developed an unfortunate combination of multiple complications interacting with the respective treatments.
3144 Dieulafoy Lesions: A Rare Case of Recurrence
Authors: Martinez-Tapia Ana , Duarte-Chavez Rodrigo , Mehta Sagar V. , Chaput Kimberly J. , Wey Bryan
Published: October 2019

INTRODUCTION:

Dieulafoy lesions (DL) are thickened arteriole malformations commonly found in the stomach that account for less than 2% of acute gastrointestinal (GI) bleeds. Conventional treatment is endoscopic and rarely requires surgical intervention. The risk of recurrence is low, especially in previously treated patients.

CASE DESCRIPTION/METHODS:

A 59-year-old male with past medical significant for hypertension (HTN), previous DL treated with gastrectomy for recurrent bleeding and multiple packed red blood cell (pRBC) transfusion 18 years ago presented for evaluation of palpitations. Review of system was positive for melena and lightheadedness with unremarkable physical examination. The patient was not on anticoagulation or anti-platelet agents. Laboratory test resulted in a hemoglobin (Hgb) of 8 g/dL. Upper endoscopy revealed non-bleeding ulcers in the stomach and colonoscopy revealed three polyps with no obvious source of bleeding. Hgb continued to trend downward and patient required multiple pRBC transfusions. Capsule endoscopy was performed at discharged, but patient was readmitted for a repeat episode of melena. Result of the capsule endoscopy revealed a clot in stomach with active bleeding in duodenum. Repeat endoscopy showed a DL in the proximal stomach which required placement of three clips to control the hemorrhage. Patient was discharged on omeprazole with no recurrent symptoms.

DISCUSSION:

DL are arterioles with thickened caliber that can protrude through a defect in the submucosal base without signs of ulceration. The pathogenesis is not clear, but likely secondary to a congenital abnormality of the blood vessels or a thrombotic event of the arteriole causing necrosis. The distribution of DL is equal in all ages but has a male predominance. Risk factors include heart disease, use of anticoagulants or anti-platelet agents and alcohol exposure; However, the mechanism by which they exert their effect is controversial. Surgery was the preferred treatment for DL, but now is less common with more endoscopic techniques available. Our patient had certain risk factors that could have led to his original lesions, such as hypertension. The risk of recurrence following endoscopic treatment is less than 9% and less with surgical resection, which would suggest an underlying contributing factor. DL need to be included in the differential diagnosis for GI bleeding, even in previously treated patients, given there are underlying factors that have yet to be elicited contributing to recurrence.
3147 Acinar Cell Carcinoma—A Rare Cause of Gastrointestinal Bleed: A Case Report
Authors: Chaudhari Rahul B. , Shirodkar Manoj A. , Ho Immanuel K. , Kirkland Matt L.
Published: October 2019

INTRODUCTION:

Acinar cell carcinoma is a rare pancreatic exocrine tumor that comprises approximately 1-2% of adult pancreatic tumors. We present a case of this rare tumor in a patient who presented with recurrent GI bleed.

CASE DESCRIPTION/METHODS:

A 48 year female with history of brain AV Malformaation, Chiari malformation s/p brain surgery and platelet storage pool disease presented to our hospital with worsening fatigue and shortness of breath, and a question of melena, and was found to be anemic at Hgb of 6.5. She underwent an upper endoscopy which revealed bright red blood in the second part of duodenum with questionable AV Malformations that were treated with Argon Plasma Cauterization. She received blood and platelet transfusions and was discharged with Hb of 12.7. Several days later she had an outpatient colonoscopy which was normal. One month after that, she was readmitted with increasing fatigue, dyspnea and periumbilical abdominal pain and was found to have Hgb 8.7. She also noted to have recurrent melenas. A repeat upper endoscopy was performed with the addition of a side viewing duodenoscope. This revealed an ulcerated mass involving the ampulla with mild oozing of blood. Hemostasis was achieved with epinephrine injection after biopsies were taken. Biopsies revealed an epithelial neoplasm, but a specific diagnosis was elusive. Subsequent PET scan showed focal uptake in the second part of the duodenum. She underwent pylorus preserving Whipple without any complications. The pathology of the surgical specimen revealed the mass to be an acinar cell carcinoma. The pArient had a stable postoperative follow up and improved clinically with repeat Hgb three week later of 11.3.

DISCUSSION:

Acinar cell tumor is a rare pancreatic exocrine tumor that usually affects males more than female. Mean age at presentation is usually 60. The presenting symptoms are non-specific and include abdominal pain, nausea, vomiting and weight loss. As biliary tract involvement is rare, jaundice is uncommon. Lipase hypersecretory syndrome from elevated lipase secretion causing Schmid triad (subcutaneous fat necrosis, polyarthritis, eosinophilia) is also rare (<10%). In our case, the presentation with GI bleed is exceedingly unusual. The treatment of local disease is surgical. No clear treatment guideline exists for patients in whom complete surgical resection for curative intent is not possible.
3150 Deep Venous Thrombosis in Ulcerative Colitis
Authors: Baid Shreya , Gupta Kapil , Marcus Akiva , Bagatell Stuart
Published: October 2019

INTRODUCTION:

Inflammatory bowel disease (IBD) has a variety of both intestinal and extraintestinal manifestations. Among the range of extraintestinal manifestations of IBD, venous thromboembolism (VTE) is a rare complication with high morbidity and mortality. VTE can present in patients with both active disease, which is more prevalent, or in well-controlled disease, which suggests a prothrombotic risk in patients with IBD. The case below is a classic presentation of VTE in IBD, and raises questions involving lifelong anticoagulation.

CASE DESCRIPTION/METHODS:

A 62 year old male with ulcerative colitis presented to the office with a 2-week history of constant, achy pain in his right leg associated with swelling and stiffness of his right lower extremity. A right lower extremity venous duplex ultrasound revealed extensive thrombosis from the popliteal vein up to the common femoral vein. Despite a discussion about possible sequelae of untreated VTE such as further clot extension, acute pulmonary embolism, and death, the patient opted for outpatient treatment with lifelong apixaban. His swelling improved, and although he has had prior IBD exacerbations with significant bleeding, since the patient has been on apixaban, he has not had any significant bleeding.

DISCUSSION:

Patients with IBD have a threefold higher risk of VTE than the general population. Research suggests that it may be due to a complex interplay between inflammation and coagulation. Treatment of acute VTE in IBD patients has not been clearly defined and currently is similar to most patients. Consequently, the duration of anticoagulation is not established, and it is imperative to establish specific guidelines due to the risk of recurrent VTE in IBD. Currently, there are no data on the role of primary VTE prophylaxis for IBD patients in the outpatient setting and no specific biomarkers to identify IBD patients at risk. Future research should assess the prothrombotic risk in IBD to assist clinicians in preventive measures. Additional studies are needed to address the use of screening tests such as ultrasound or biomarkers. In this case, the patient was placed on lifelong apixaban due to his underlying risk factor of ulcerative colitis and showed clinical improvement with no significant bleeding. This case helps highlight the concern for major bleeding in a patient who has had previous significant major bleeding episodes during IBD exacerbations. In conclusion, VTE is a significant complication that should not be overlooked in patients with IBD.
3153 Occult Adenocarcinomas in Crohn's Disease Related Strictures: A Case Series
Authors: Singh Kevin N. , Singh Amandeep , Philpott Jessica
Published: October 2019

INTRODUCTION:

Small bowel tumors account for ∼2.3% of all gastrointestinal cancers. Strictures are frequent complications of Crohn's disease, but malignant ileal strictures are uncommon and their diagnosis is often challenging.

CASE DESCRIPTION/METHODS:

We retrospectively reviewed three cases of terminal ileum adenocarcinomas that developed in ileal strictures. In this case series, three patients with CD developed occult adenocarcinoma within an ileal stricture diagnosed only after surgery. In all of the patients, an underlying stricture was thought to have caused obstructive symptoms but there were no imaging or endoscopic findings suggestive of underlying malignancy. Subsequently, all patients underwent surgery and, unexpectedly, one patient was found to have a tumor within the ileal stricture intra-operatively and the remaining two were diagnosed post-operatively after histopathological examination. Though the findings of adenocarcinomas were unexpected, two of the three patients were over 60 years of age and had over 30 years of disease prior to their diagnosis.

DISCUSSION:

Conclusions: The diagnosis of adenocarcinomas arising within ileal strictures is uncommon and often challenging for clinicians. 2. Many cases are diagnosed only intra-operatively or post-operatively after histopathological examination in the absence of imaging studies or endoscopy that suggest the presence of underlying malignancy.
3154 Severe Shock as the Initial Presentation of Inflammatory Bowel Disease Unclassified
Authors: Rashed Laila Abu
Published: October 2019

INTRODUCTION:

Age dependent immune modulation plays a major role in the late uncovering of inflammatory bowel disease (IBD). 1/3 of IBD occurs in elderly, yet the diagnosis is delayed by 6 years on average when compared to younger peers who have a 2-year delay. Subtle and unconventional symptoms plus comorbidities play a major role in this.

CASE DESCRIPTION/METHODS:

A 61-year-old veterinarian female with a long-standing history of constipation presented with acute sharp abdominal pain associated with bloating, nausea and non-bilious vomiting. Vital signs were within the normal range. Physical examination showed a slender female in mild distress, with a soft but distended abdomen that was tender to palpation mainly in the left lower quadrant. Pertinent laboratory tests showed bands 24%, WBC 7 × 103/µL, platelets 47103/µL, lactic acid 4.6 mmol/L, and alkaline phosphatase 216 IU/L. A computed tomography (CT) of the abdomen showed segmental narrowing of the body of the stomach and stool impaction. She was admitted for observation for possible early sepsis; over the course of the next 6 hours she developed severe diarrhea and shock and required admission to the ICU where she was treated empirically for a gastrointestinal infection. She was worked up extensively, but the only significant finding was a positive serum Salmonella IgM. She improved with medical management and eventually antibiotics were deescalated, she completed a 10-day course; however, diarrhea persisted and eventually became bloody. Given her history of chronic constipation the possibility of Celiac disease was entertained but work up was negative. Sigmoidoscopy with biopsy was suggestive of ischemic colitis. The hematochezia resolved by itself and apart from the ongoing diarrhea she was doing well; she was discharged home. At follow up 2 months later she was back to her baseline constipation, her calprotectin level was found to be high and upper and lower endoscopy with biopsies showed minimal active chronic colitis concerning for idiopathic IBD.

DISCUSSION:

The products of genetic mutations related to IBD are involved in antigenic recognition and the modulation of humoral and cell-mediated immunity, at times this leads to loss of self-tolerance, normal flora tolerance or tolerance to antigens that are present at low concentrations or in immune privileged locations and this event is now considered the trigger that unleashes IBD.
3158 Sacral Osteomyelitis Secondary to Crohn's Disease
Authors: Khorsandi Pedram J. , Thaker Sarang , Carroll Robert
Published: October 2019

INTRODUCTION:

Increased ostomy output and abdominal pain can be concerning symptoms for patients with underlying gastrointestinal pathology such as Inflammatory Bowel Disease (IBD). While the acute etiology is often directly related to said underlying condition, alternative causes should remain on the differential diagnosis. The following is a case of sacral osteomyelitis as a result of direct extension from the gastrointestinal tract.

CASE DESCRIPTION/METHODS:

A 43 year old male with Crohn's disease complicated by recurrent fistula/abscess status post multiple colectomies with ileostomy and blind colostomy presented from a rehabilitation facility due to increased non-bloody watery ileostomy output and abdominal pain. He also presented with chronic rectal ulcers that appeared stable with scant purulent drainage. Vital signs were notable for hypotension and tachycardia that responded to fluids and empiric vancomycin and imipenem. Labs were notable for significantly elevated inflammatory markers, negative stool infectious panel, negative clostridium difficile, negative lactoferrin, white blood cell count of 23.9, and negative blood/urine cultures. Ileoscopy revealed colonization of the ileum and no source of high ostomy output was identified. Ileal biopsy revealed acute Crohn's enteritis. MRI pelvis fistula protocol revealed S5 osteomyelitis which was confirmed clinically by visualization in the OR. However, bone biopsy was negative in the setting of empiric antibiotic therapy. Patient was treated with approximately six weeks of vancomycin and ceftriaxone. He then followed up with Infectious Disease and had resolution of the infection and significant improvement in rectal ulcer drainage.

DISCUSSION:

Determination of the source of infection in patients with IBD can be challenging due to the inflammatory nature of the disease. Patients often present with systemic symptoms and non-specific complaints that could be mistakenly attributed to the underlying chronic disease. In any patient with fistulizing Crohn's presenting with sepsis, clinicians should have a high level of suspicion for osteomyelitis, especially in chronically debilitated patients with non-healing wounds. If routine infectious evaluation is unrevealing, clinicians should consider musculoskeletal infections due to direct extension from organic intra-abdominal processes. A broad differential diagnosis should be maintained for these Crohn's patients as multiple organ systems may be affected both directly and indirectly.
3160 The Medicaid Coverage Gap and IBD Care
Authors: Wade Francis , Srour Maria , Odufalu Florence-Damilola , Clarrett Danisa M. , Schroeder Katie S.
Published: October 2019

INTRODUCTION:

Medicaid expansion is a key provision of the 2010 Affordable Care Act (ACA) that bolsters healthcare access for Inflammatory Bowel Disease (IBD) patients. Prior to the ACA, Medicaid was guaranteed only to specific patient populations whose income falls within certain limits of the federal poverty level (FPL). Medicaid expansion ensures eligibility for all adults aged 18-65 years with incomes up to 138% of the FPL regardless of age, family, or health status. 17 states, including Missouri, have not expanded Medicaid which has created a coverage gap for low-income adults who do not qualify for Medicaid nor the ACA's Marketplace subsidies. We present a case of a young Missourian within the Medicaid coverage gap who was unable to gain healthcare access for severe fistulizing Crohn's disease until his incarceration.

CASE DESCRIPTION/METHODS:

A 27-year-old man with Crohn's disease presented from a correctional facility with enterocutaneous fistulae and abdominal wall abscesses. He was uninsured with limited healthcare access and unable to afford the recommended biologic therapy. Once incarcerated, he qualified for Department of Corrections healthcare coverage and sought care. Surgery with temporary colostomy was recommended due to his advanced disease. The patient did not want to have an ostomy in prison so instead opted for treatment with infliximab, complete bowel rest, and total parenteral nutrition. His hospital course was complicated by drug-induced liver injury from infliximab which extended his admission to 107 days. The correctional facility eventually enacted a compassionate release which paradoxically terminated his healthcare coverage and jeopardized further access to care. The patient was enrolled in Missouri Medicaid due to disability and underwent surgery but not before suffering significant morbidity from preventable complications of Crohn's disease.

DISCUSSION:

The Medicaid coverage gap in non-expansion states limits healthcare access for non-disabled, low-income IBD patients. Our patient's case exemplifies challenges to providing healthcare to IBD patients within the Medicaid coverage gap in non-expansion states. Healthcare costs for IBD patients are more expensive than for those without IBD, increasing the importance of maximizing healthcare coverage for this patient population. Policy change in non-expansion states would improve access to healthcare coverage which may reduce hospitalizations and improve outcomes for low-income IBD patients.
3166 Autoimmune Hepatitis: When You Cannot Blame the Gallbladder Anymore
Authors: Janssens Laurens , Penrice Daniel , Kashiwagi Deanne
Published: October 2019

INTRODUCTION:

Autoimmune hepatitis (AIH) is a chronic liver disease with varying degrees of onset severity often presenting with nonspecific symptoms such as abdominal pain, fatigue, jaundice and nausea. Although initial reports have suggested that AIH has a bimodal age distribution (with the second peak between 40 and 50 years), the condition has increasingly been recognized in all age groups, including the elderly.

CASE DESCRIPTION/METHODS:

A 70-year-old woman was admitted to our medical center with a 2-month history of abdominal discomfort, anorexia and fatigue. Past medical history was notable for hyperlipidemia. Five weeks prior to admission, the patient had presented to her primary provider with similar complaints and was found to have significantly elevated liver enzymes, as shown in Table 1. The patient denied alcohol use. At the time of admission, work-up showed similar transaminases with an increase in bilirubin (Table 1). Abdominal ultrasound revealed cholecystolithiasis and possible cholecystitis without intra- or extrahepatic ductal dilation. ERCP confirmed cholecystolithiasis without visualization of intraductal stones on cholangiogram or after sweeping of the biliary tree. Laparoscopic cholecystectomy was performed and pathology results revealed chronic cholecystitis. Despite these interventions, the patient was readmitted one week later for ongoing jaundice and malaise. She had no ascites on exam. Laboratory work-up showed persistently elevated liver tests (Table 1). Anti-smooth muscle antibodies (ASMA) were elevated at 1:80. Viral hepatitis panel was negative. Liver biopsy revealed marked panacinar hepatitis with cholestasis without hemosiderin deposition. The patient was diagnosed with autoimmune hepatitis and initiated on steroids with rapid resolution of symptoms. Transaminases and bilirubin decreased significantly one week after initiation of steroids and normalized after 6 weeks.

DISCUSSION:

The clinical presentation of AIH is often nonspecific and highly variable. Most patients present with insidious symptoms, but the spectrum of symptomatology can range from asymptomatic to severe acute disease. Acute AIH can mimic other conditions such as acute viral hepatitis and choledocholithiasis resulting in delayed diagnosis and sometimes unnecessary interventions such as ERCP and cholecystectomy. In the absence of an obvious alternative diagnosis, acute transaminitis warrants work-up that includes ASMA testing since AIH can present in virtually any age category, as highlighted in this case.
3169 Drugs! A New Mimicker of Primary Sclerosing Cholangitis
Authors: Kagihara Jaclyn E. , Kalathil Sumodh C. , Lopez Kristi T.
Published: October 2019

INTRODUCTION:

In the United States, drug-induced liver injury (DILI) is the most common cause of acute liver failure necessitating liver transplantation. DILI can be characterized biochemically based on specific patterns of injury - hepatocellular, cholestatic, or mixed. Detection of bile-duct strictures on magnetic resonance cholangiopancreatography (MRCP) is uncommon in DILI, and nearly pathognomonic for primary sclerosing cholangitis (PSC). Here we present two cases of “PSC-like DILI.”

CASE DESCRIPTION/METHODS:

Patient 1: A 68-year-old man with type 2 diabetes mellitus (T2DM) and hyperlipidemia was admitted for sepsis secondary to methicillin-sensitive staphylococcus aureus right wrist abscess, and subsequently started on cefazolin. He developed acute hepatitis with aspartate transaminase (AST) 665, alanine aminotransferase (ALT) 367, and alkaline phosphatase (ALP) 2317. Extensive work-up, including ferritin, anti-nuclear antibody (ANA), anti-mitochondrial antibody (AMA), anti-smooth muscle antibody (SMA), and viral serology, was unremarkable. MRCP showed multi-focal areas of intra-hepatic biliary ductal dilation and mild strictures without evidence of stones or malignancy, consistent with PSC. Liver biopsy was non-specific, demonstrating portal and lobular hepatitis with mild bile duct injury, and mild steatosis without steatohepatitis. Colonoscopy did not show inflammatory bowel disease. DILI with drug-induced PSC-phenomenon was suspected. The patient's liver function tests (LFTs) normalized within 24 hours of stopping cefazolin. Patient 2: A 63-year-old woman with T2DM was found to have AST 229, ALT 186, and ALP 652, 5 months after starting atorvastatin for stroke. MRCP revealed abnormal appearance of the central intrahepatic bile ducts (Figure 1). Ferritin, alpha-1 anti-trypsin, ceruloplasmin, and viral serology were unremarkable. ANA, SMA, and immunoglobulin G were elevated, suggestive of an immunologic process. Anti-liver-kidney-microsomal antibody and AMA, however, were negative. The patient was presumed to have a drug-induced autoimmune and cholestatic reaction with PSC-cholangiographic findings. LFTs normalized within 2-months after cessation of the statin.

DISCUSSION:

DILI with concurrent findings of bile-duct strictures on MRCP has yet to be described in the literature. The first case suggests cefazolin as the culprit, while the second points to atorvastatin as the suspected trigger for DILI and an “autoimmune-PSC overlap syndrome.” Clinicians should be aware that DILI can mimic PSC.
3171 Amoxicillin-Clavulanate Related Mixed Cholestatic-Hepatocellular Injury
Authors: Vaishnani Devin , Vekaria Pratikkumar , Patel Ravish , White Megan , Vaishnani Marvin , Raiyani Tejas
Published: October 2019

INTRODUCTION:

Recognition of Drug-induced Liver Injury (DILI) may be challenging as it is often diagnosis of exclusion, unavailability of diagnostic test and variability in presentation. Many antibiotics can cause DILI but Amoxicillin-Clavulanate has rare adverse reaction causing mixed cholestatic-hepatocellular injury. Since amoxicillin alone does not induce liver injury, combination of amoxicillin and clavulanic acid could be responsible for this adverse reaction. It can be due to metabolic idiosyncrasy or hypersensitivity mechanism.

CASE DESCRIPTION/METHODS:

64-year-old female with no pertinent PMH presented to ER with abdominal pain and jaundice. She had abdominal pain for 4-5 days. Abdominal pain was constant and located at right upper quandrant and epigastric region. She had associated complaint of nausea, vomiting, metallic taste and chills. Patient had been avoiding eating in fear of vomiting. She also had pale colored stool. Patient did not have any history of gall stones, hepatitis or alcohol use. On further inquiry, she reported being on Amoxicillin-Clavulanate for 4 days, for dental abscess, before onset of symptoms. She stopped taking antibiotic as soon as she started having above-mentioned symptoms. Patient was not on any other new medications during this time-period. On initial evaluation, patient was found to have elevated liver enzymes with T.bilirubin 6.4, AST 218, ALT 288, ALP 331. Due to broad differentials associated with elevated liver enzymes with abdominal pain, further workup was done. Abdominal CT scan and MRCP results were unremarkable. Hepatitis panel was also negative. Patient was provided with supportive care and hydration with IV fluids. Repeat labs done on 4th day after admission showed down trending LFTs – T.bill 3.8, AST 152, ALT 141, ALP 253.

DISCUSSION:

Amoxicillin-Clavulanate can cause hepatocellular, cholestasis or mix type of liver injuries depending upon genetic factors or pre-existing liver conditions. Early recognition and removal of offending medication is the initial mainstay of treatment along with supportive care. This case signifies proper history taking and review of medications could avoid unnecessary and expensive diagnostic tests for diagnosis. Our case emphasis importance of early recognition of this reversible condition due to Amoxicillin-Clavulanate or other medications to prevent worsening of liver faliure and its complication.