bluuebunny/crossref_metadata_2025 huggingface dataset:
3109 A Rare Cause of Dysphagia—Epiphrenic Diverticulum
Authors: Lopez Michell , Then Eric O. , Gayam Vijay , Ofosu Andrew , Culliford Andrea , Gaduputi Vinaya
Published: October 2019

INTRODUCTION:

An epiphrenic diverticulum is a rare, benign disorder of the distal esophagus characterized by protrusion of the esophageal mucosa through the musclular layer, proximal to the gastroesophageal junction. They are false diverticula mainly associated with motility disorders. The most frequent symptoms experienced by patients are dysphagia, regurgitation, and aspiration, but most cases are usually asymptomatic. We present a rare case of epiphrenic diverticulum in a 71-year-old male.

CASE DESCRIPTION/METHODS:

The patient is a 71 year-old man with a medical history of cerebrovascular accident (with residual left sided weakness, and chronic encephalopathy), and hypertension who presented to our emergency department after family members noticed he was unable to tolerate oral intake and had multiple episodes of vomiting over the past two days. Notable imaging in the emergency department included a computed tomography (CT) of the chest which showed irregular wall thickening in the distal esophagus suggestive of a neoplasm. Laboratory workup including a complete blood count and comprehensive metabolic panel were within normal limits. Upon admission the gastroenterology service was consulted who recommended the patient undergo esophagogastroduodenoscopy (EGD) to rule out malignancy. Given the risks associated with EGD the patients family refused the procedure. They did however agree to a barium swallow to better evaluate the esophagus. This was done and showed an epiphrenic diverticulum in the distal esophagus (Figure 1). After this was discovered the patients family refused any intervention including EGD or surgery. During his admission the patient was able to tolerate a pureed diet and his medications were crushed which were also tolerated appropriately. He was then discharged home with follow up appointments scheduled.

DISCUSSION:

Esophageal diverticula are uncommon acquired disorders of the esophagus that have an estimated incidence of 1 in 500,000 people per year. As opposed to Zenkers diverticula which occur in the proximal esophagus, epiphrenic diverticula are rarer and occur in the distal esophagus. To put its rarity into context the estimated ratio of epiphrenic divertila to zenkers diverticula is 1:5. Although most cases are asymptomatic, some cases may present with dysphagia, regurgitation of undigested food, heartburn and aspiration pneumonia. Surgical resection is the treatment of choice, but endoscopic procedures such as per-oral endoscopic myotomy are challenging that concensus.
3112 Eosinophilic Esophagitis (EE) Presenting With Severe Dysphagia Showing Dramatic Response to Oral Steroid Therapy
Authors: Miah Ma Rahim , Hossain M. Shamiul , Ghosh C.K. , Kamal M.
Published: October 2019

INTRODUCTION:

During the last decade of clinical practice, a rapid increase of a “new” disease termed as “eosinophilic esophagitis (EE)” have been identified among patients who were thought to have gastroesophageal reflux disease (GERD) but did not respond to medical and/or surgical GERD treatment. Over the last decade eosinophilic esophagitis is increasingly being recognized in adults and children throughout the world. Population-based studies suggest the prevalence to be in excess of 1:1000 with a predilection for white males. The disease is very rare in Bangladesh.

CASE DESCRIPTION/METHODS:

A 40 years old house wife presented with one-year long history of severe dysphagia with significant weight loss; endoscopic evidence of a long linear ulcer with stricture involving almost the whole length of the esophagus; histopathologic evidences of eosinophilic esophagitis and a dramatic response to systemic steroid therapy.

DISCUSSION:

Diagnosis of Eosinophilic Esophagitis is based on (i) symptoms including but not limited to food impaction and dysphagia in adults and feeding intolerance and gastro-esophageal reflux symptoms in children; (ii) histological evidence of ≥15 eosinophils /HPF; (iii) exclusion of other disorders associated with similar clinical, histological, or endoscopic features, especially gastro-esophageal reflux disease. The overlapping symptoms of EE and GERD sometimes may delay or confuse the diagnosis of the disease in many cases. Most patients present with dysphagia and food impactions, atypical chest pain and heartburn that is refractory to PPI therapy. Fibrosis, narrowing of the lumen and stricture esophagus can occur with EE. Appropriate treatments include dietary approaches based upon eliminating exposure to food allergens, and topical/systemic corticosteroids. This patient presented with severe dysphagia with significant weight loss; endoscopic evidence of a long linear ulcer with stricture involving almost the whole length of the esophagus; histopathologic evidences of eosinophilic esophagitis and a dramatic response to systemic steroid therapy. In conclusion, although EE is a very uncommon disease in Bangladesh, the intent of this report is to grow awareness of the clinicians about this disorder to make early diagnosis and treatment of the disease with systemic steroid to prevent the development of complications like esophageal stricture or perforation.
3128 A Rare Case of a Gastroduodenal Ulcer Arising From Checkpoint Inhibitors
Authors: Raman Daya
Published: October 2019

INTRODUCTION:

Ipilimumab and Nivolimuab are in a class of immune checkpoint inhibitors that are widely used in the treatment of advanced malignancies.
1
Immunotherapy with monoclonal antibodies targeting cytotoxic T lymphocyte-associated antigen 4 (CTLA4) and the programmed death-1 receptor (PD-1) and its ligand PD-L1 has become the standard of care for cancer treatment today.
1
Gastrointestinal (GI) toxicity from cancer immunotherapy is well described for anti-CTLA4 Abs, but less well studied in combination of anti-CTLA4 and anti-PD-1Abs. GI effects of these immunotherapies range from enterocolitis, pancreatitis, diarrhea, and ulcerations involving the sigmoid colon and rectum.
1

CASE DESCRIPTION/METHODS:

Here, we present the case of an 80 year old male with past medical history of renal cell cancer (RCC) that was diagnosed 3 months prior to admission, who presented with melenic stool for one day. The patient had been initiated on a chemotherapy regimen of Ipilimumab and Nivolimuab of which he received three rounds, the last dose one week prior to hospitalization. He had not been on any anticoagulation nor had he endorsed NSAID use. Patient's hemoglobin was closely trended. One day into admission, patient had a large melenic bowel movement with Hb change from 9.0 to 8.7 mg/dL with significant hypotension and tachycardia. Patient was emergently intubated for airway protection for an EGD. EGD revealed a large 4-5 cm ulcer in the second portion of the duodenum and found to have a large artery protruding from the ulcer base, likely the gastroduodenal artery. Endoscopic intervention was performed by placing 5 clips at the ulcer base in an effort to further prevent bleeding. Hemoglobin was trended closely following the procedure, however post-EGD bleeding continued and patient became acutely hypotensive, requiring vasopressor support. As further EGD intervention was considered to be high risk, Interventional Radiology was consulted for embolization with empiric embolization of gastroduodenal artery using a microcoil, which was successful. Hemoglobin continued to trend downwards despite control of bleeding and vasopressor support increased at which point patient was transitioned to comfort measures.

DISCUSSION:

This case outlines a rare case of immune checkpoint inhibitors as a cause of a gastroduodenal ulcer and the adverse outcomes with checkpoint inhibitors as treatment for malignancies.
3133 Bleeding Peptic Ulcer Disease in Polycythaemia Vera Patient
Authors: Al Yassin Sarmed , Fatakhova Karina , Al-Naqeeb Ghadah , Haggerty Gregory , Tofano Michael
Published: October 2019

INTRODUCTION:

Polycythaemia vera (PV) is a myeloproliferative disease, characterized by hematopoietic proliferation, expressed as inappropriate increase in circulating RBCs. It affects middle-aged and elderly patients Gastrointestinal disorders are common in PV, mainly represented by peptic ulcers. Our case highlights a severe fatal presentation of GI bleeding in a patient with recent diagnosis of PV.

CASE DESCRIPTION/METHODS:

63 years old M presented with altered mental status. He was recently diagnosed with Jak2+ P. Vera & A. Fib, not on anticoagulation, he takes daily low dose Aspirin 81 mg. In ED, He went into hemorrhagic shock. Significant amount of coffee ground vomitus seen upon intubation. NGT drained a large volume of blood. Labs revealed leukocytosis (185.9 K/uL), thrombocytosis (606 K/uL), AKI (BUN/Cr 83/4.6). Hgb was 14.8 g/dL 2 weeks prior to presentation. On arrival Hgb was 10 g/dL and decreased to 8.5 g/dL within 2 hours. Resuscitation started with IV fluids, blood transfusions and PPI drip. Emergent EGD revealed a large bleeding pyloric channel ulcer, which was treated with epinephrine injections and three clips. Urgent hemodialysis was initiated for worsening acidosis. LFTs were elevated, AST/ALT of 2080/1167 U/L, Alk. Phos. 1510 U/L. CT abdomen revealed infarcted liver, kidneys and bowel. CT of the brain showed acute posterior circulation infarction involving bilateral occipital & emporal lobes Family decided to withdraw care and made patient comfort care.

DISCUSSION:

Peptic ulcer (PU) disease manifested in higher frequency in PV patients compared to population. Various pathogenetic mechanisms suggested for PU in PV, altered mucosal blood flow due to increased plasma viscosity, and/or increase histamine release, due to high basophil count, a study suggested high risk of H. pylori infection in PV patient compared with controls. Limited evidence regarding the prevalence of GI bleeding in PV due to the retrospective nature of studies. In the ECLAP trial, the rate of total & major bleeding were 2.9% and 0.8%/year. 4% of deaths were attributed to bleeding. GIB was the most common cause of major bleeding. hence both the thrombotic and hemorrhagic manifestations of myeloproliferative disorders depend on the platelet count. Typical pattern of GI bleeding has not been well reported in literature, but it's more evident in the setting of extreme thrombocythemia. It is important to underline that gastroduodenal lesions present in 77% of asymptomatic PV patients, suggesting the need for endoscopic examination in those patients.
3136 Complex Rebleeding Cameron Ulcer in a Young Male—A Case Report
Authors: Schieferdecker Nicola , Pasan Botheju Welathanthrige Savindu , Mehta Amit , Buffie Charlie , Wan David
Published: October 2019

INTRODUCTION:

A Cameron lesion is a gastric ulcer or erosion located in a diaphragmatic hernia that can be a rare source of occult GI bleeding. These types of lesions are commonly missed during EGD and are believed to be caused by mechanical damage to the mucosa in a sliding hiatal hernia. Here, we report the case of a young man without risk factors, with a complex rebleeding Cameron ulcer.

CASE DESCRIPTION/METHODS:

A 31-year-old male with no significant medical history presented with two episodes of syncope resulting in head and chin lacerations. He reported worsening headaches, nausea, and black stools for 3 days. He was alert, oriented, in no distress, hemodynamically stable and afebrile when brought in by EMS. He denied use of NSAIDs, reported normal bowel movements, and stated he never had an EGD or colonoscopy. He admitted to social alcohol and smoking for 10 years. Physical exam was remarkable for melena on rectal exam. Initial blood work was notable for hemoglobin 7.5, WBC of 13.0, BUN/Crea ratio of 39, with otherwise unremarkable CBC, CMP, troponin, coags, and urine analysis. UGI series showed no abnormalities. The patient was transfused 1 unit packed RBCs and was admitted to medicine. An EGD was performed and showed a large type III hiatal hernia and a Cameron ulcer with visible vessel in hernia (Figures 1 and 2) that was treated with two mechanical clips (Figure 3). Pathology of ulcer margins showed no diagnostic abnormality. Ten days after discharge he again presented with black stools, and repeat EGD showed bleeding under previously placed clips. Clips were removed and the lesion was cauterized with hemostasis.

DISCUSSION:

Cameron lesions are an uncommon cause of upper GI bleed that occur predominantly in women due to their higher incidence of diaphragmatic hernias. Patients usually present with anemia or occult GI bleeding. Diagnosis is made endoscopically, and first line treatment includes common hemostasis techniques including clipping. In this case, the patient presented without evidence for a hernia on UGI series, which could demonstrate a sliding hernia. However, he showed significant recurrent bleeding with hemodynamic instability that required multiple interventions. In summary, Cameron lesions or ulcers can be a rare cause of severe upper GI bleed and surgical hernia repair should be strongly considered in complex cases.
3151 Ustekinumab Administration Prior to Week Eight Following Induction Improves Symptoms and Maintains Remission of Severe Crohn's Disease: A Case Series
Authors: Azam Mohammad U. , Koehler Tara , Jackson Christian , Vega Kenneth J.
Published: October 2019

INTRODUCTION:

Ustekinumab is a recently approved immunosuppressive agent for management of moderate to severe Crohn's Disease (CD). In trials, dosing was determined at 6 mg/kg for induction with maintenance injection of 90 mg every 8 weeks. Approximately half of the patients in the UNITI Induction trials did not respond to ustekinumab treatment when assessed at 6-8 weeks, and were included in the Maintenance trial with ustekinumab provided at week 8 or 12. Only 30-40% of these patients continued to have remission at maintenance trial conclusion. We present a case series of two CD patients who were initiated on ustekinumab therapy but required a shortened maintenance dose interval to achieve/maintain remission.

CASE DESCRIPTION/METHODS:

Case 1: A 33 year old female presenting clinically with intermittent abdominal pain, diarrhea, occasional blood in stool & nocturnal symptoms was diagnosed with CD in 2017 via computed tomography of the abdomen combined with colonoscopy revealing terminal ileum aphthous ulceration. Previous therapies included budesonide, prednisone & adalimumab. Ustekinumab induction was initiated on 2/2/2018. However, on 3/20/2018, the patient developed severe abdominal pain consistent with a CD flare. Following, she has received ustekinumab injections every 4-6 weeks to maintain disease remission. Case 2: A 47 year old male initially diagnosed with CD at the age of 22, complicated by emergent colectomy with end ileostomy in 2014 presented with an acute flare consisting of abdominal pain, peristomal fistulas and increased ostomy output. Following evaluation, he underwent surgical correction of fistula, drainage of intraabdominal wall abscess & abdominal wall reconstruction in December 2018. Prior to this, he was treated with sulfasalazine, mercaptopurine, azathioprine along with immunomodulators including infliximab & certolizumab without adequate response. In January 2019, ustekinumab therapy was initiated with standard induction followed by injectable dosing every 4 weeks due to CD severity and physician recommendation. Following this schedule, the patient has had improved ostomy output and symptom control.

DISCUSSION:

In our experience, shortening the interval of injectable ustekinumab dosing to 4-6 weekly from 8 weeks has proven successful in maintaining remission for patients with severe CD. This subsegment of CD patients was excluded in trials and further investigation is needed to assess long term efficacy of shortened ustekinumab therapy intervals to maintain remission.
3152 Out of the Blue: Unexpected Urine Color After Colonoscopy
Authors: Pierre-Louis Marvah Hill , Wan David
Published: October 2019

INTRODUCTION:

Chromoendoscopy combines endoscopy and staining as a diagnostic technique to identify pre- and cancerous lesions. Methylene blue, one of many stains used, is sprayed directly in the lumen. Here we report the case of a man who experienced blue urine after undergoing chromoendoscopy.

CASE DESCRIPTION/METHODS:

71-year-old man with a history of UC on sulfasalazine and colon cancer presented to the endoscopy suite for colonoscopy. He was diagnosed with colon cancer 2 years ago and underwent resection and chemotherapy, with PET scan 1 year later showing no evidence of disease. On surveillance colonoscopy a few weeks prior to current presentation, a malignant polyp was found in the rectum along with significant inflammation. He presented to the endoscopy suite for chromoendoscopy to evaluate for dysplasia. It showed residual high-grade dysplasia. Shortly after, the patient's urine color turned blue. Initially, he feared he was having a stroke or seizure, but his wife confirmed indeed his urine was blue. The patient had been on the same two medications for years: atorvastatin and sulfasalazine. The only new agent was methylene blue for his endoscopy. This led us to conclude the blue dye used during chromoendoscopy is the source of the blue urine.

DISCUSSION:

Methylene blue has few indications, one of which is endoscopic dysplasia screening especially in cases of IBD and Barrett's esophagus. The absorption of methylene blue by the colonic lumen is a known but rare side effect. In fact, we have not found any case reports of blue urine in humans as result of chromoendoscopy. There are case reports of blue-green urine but primarily due to blue dye added to enteral feeds and intravenous administration. Many patients undergo chromoendoscopy however without any changes in their urine color. In our patient, the active inflammation could have led to enhanced absorption of methylene blue. There are a few reports to suggest that intestinal mucosa permeability is increased in IBD, possibly correlating to the degree of inflammation, which could have led to increased absorption of methylene blue and ultimately urine excretion. We conclude that our patient with active ulcerative colitis who underwent chromoendoscopy with methylene blue had increased intestinal absorption of methylene blue and urine excretion. This effect was possibly enhanced by active inflammation causing damage to the intestinal lumen leading to enhanced permeability.
3162 Through the Scope Retrieval of a Migrated AXIOS Stent
Authors: Gollol Raju Narasimha Swamy , Mudireddy Prashant
Published: October 2019

INTRODUCTION:

Endoscopic drainage of pancreatic fluid collections (PFC) is widely accepted modality of therapy due to its less invasive nature, shorter recovery time, lower cost and complication rates. Lumen apposing covered self-expandable metallic stents (LACSEMS) are increasingly utilized in the management of PFC. LACSEM have excellent safety profile and adverse effects are generally low. Rare migration of these LACSEMS has been described, noted at follow up, both in to the enteral lumen as well in to the cyst cavity. We here by present a case of AXIOS stent migration in to PFC that was successfully retrieved.

CASE DESCRIPTION/METHODS:

A 33 year-old Caucasian male with H/O ETOH related pancreatitis presented with 3 months of intermittent nausea and vomiting with nearly 100-pound weight loss. CT abdomen showed a 24 × 21 × 14 cms PFC causing GOO (Figure 1). Under EUS guidance, a 15 × 10 mm hot AXIOS stent (Xlumena Inc., Mountain view, CA, USA) was deployed by transgastric approach in to the cyst but the stent migrated in to the cavity. A second 15 × 10 mm hot AXIOS stent was successfully placed in to the cyst (Figure 2). The lumen of the AXIOS stent in good position was dilated to 15 mm using a wire guided CRE balloon. Large amount of necrotic material was visualized in the cyst cavity. Through the stent necrosectomy was performed. The migrated stent within the cyst was localized by fluoroscopy. Under endoscopic and fluoroscopic guidance, attempt at grabbing the migrated stent with forceps and removal through the stent in good position was unsuccessful. Few days later, migrated stent removal was attempted again. A therapeutic scope was advanced through the AXIOS in good position in to the WON cavity. The migrated stent was grabbed with a Rat-Tooth forceps and was pulled in to the working channel and successfully removed through the scope (Figure 3).

DISCUSSION:

In our case, the AXIOS stent migrated in to the WON cavity at the time of initial deployment necessitating a second AXIOS stent placement. Immediate removal of the migrated stent was not pursued due to risk of dislodging the second stent in good position. Subsequently, after endoscopic necrosectomies and improved WON size, the migrated stent was removed by intubating the WON with a therapeutic gastroscope through the AXIOS stent in good position and pulling the migrated stent in to the working channel of the gastroscope. To the best of our knowledge, retrieval of a migrated LACSEMS inside a WON through the scope via an AXIOS stent has not been previously described.
3165 The Great Masquerade
Authors: Balarajah Sharmili , Lin Valerie
Published: October 2019

INTRODUCTION:

Syphilis is a sexually transmitted infection caused by T. pallidum. It is often described as “the great imitator,” affecting multiple organ systems, and has a wide variation in its clinical presentation. Syphilitic hepatitis is a rare and occurs in 0.2-3% of cases of secondary syphilis. We present a case of mixed hepatocellular and cholestatic hepatitis that led to the diagnosis of syphilis in a patient who presented with non-specific symptoms.

CASE DESCRIPTION/METHODS:

A 39-year-old homosexual male was referred for evaluation of worsening jaundice following a course of acyclovir for genital herpes 3 months prior. He reported non-specific symptoms including acute diarrhea, abdominal pain, myalgia, rash and weight loss with no change in mental status. He had no pertinent past medical or family history and denied any exposure to IV drugs or blood transfusions. Clinical exam showed scleral icterus, a soft and non-tender abdomen and macular rash in the extremities. Laboratory evaluation showed AST 209, ALT 617 and ALP 1195 (peaked at 2170). INR was 1.0 and albumin was 3.1. Viral hepatitis A, B, C, EBV and HIV testing were negative. F-actin IgG was positive (36) and ANA negative. MRI abdomen showed hepatomegaly without evidence of biliary obstruction. Liver biopsy showed moderate portal/periportal edema; mixed acute and chronic inflammation and pericholangitis with cholestasis. Syphilis immunostaining and Warthin-Starry staining were negative. Our patient was initially treated as presumed autoimmune hepatitis with prednisone. He had significant clinical and LFT improvement over 3-4 weeks but developed new-onset arthralgia in the midst of treatment. Rheumatological workup revealed positive rapid plasma reagin with T. pallidumreactivity. He completed a course of benzathine penicillin, following which he had complete resolution of his symptoms and normalisation of his LFTs.

DISCUSSION:

SH presents a diagnostic challenge in view of its infrequency and there are currently no standardised diagnostic criteria. Liver chemistry typically demonstrates a cholestatic picture with a disproportionately elevated ALP, likely secondary to pericholangiolar inflammation. However, in our patient, there was also moderate lobular activity with plasma cells, corresponding to a moderately elevated ALT. It is imperative that clinicians have a high index of suspicion for syphilis in view of the morbidity and mortality associated with a missed or late diagnosis and the availability of an effective treatment.
3172 A Rare Complication of Hepatic Cirrhosis: Nephrotic Syndrome in IgA Nephropathy
Authors: Jiyani Rucha , Patel Saumil , Patel Parth , Ghosh Sudeshna , Desai Jiten , Jacob Bobby
Published: October 2019

INTRODUCTION:

There have been many documented cases of cirrhosis and associated Parenchymal renal disease (Ig-A nephropathy, glomerulonephritis). We discuss here rare case of hepatorenal syndrome type 2, in-patient with no clinically and imaging finding indicative of portal hypertension. Also, further interesting finding is to have nephrotic range proteinuria in nephritic syndrome.

CASE DESCRIPTION/METHODS:

56-Year-old Indian male with no past medical or surgical history presented with complaints of generalized weakness and occasional abdominal discomfort. He denied significant family history and alcohol, tobacco or illicit drug use. Ultrasonography (USG) abdomen showed cirrhotic changes. All work up including autoimmune panel negative, hence diagnosed with idiopathic liver cirrhosis. Patient managed with conservative approach, as there were no changes indicative of portal hypertension including Esophagogastroduodenoscopy. After about a year, on routine follow up he found to have his serum creatinine (Cr) progressed from 0.8 to 3.8 mg/dl. Repeat USG abdomen showed diffuse liver parenchymal disease with mild ascites and normal size of kidney with cortical thickness. Urine Microscopy revealed proteinuria and hematuria with 24 hour measured urinary protein 5 gm. Renal biopsy was performed and showed diffuse proliferative glomerulonephritis-Ig A Nephropathy (nephritic syndrome with nephrotic range proteinuria). Autoimmune profile was negative. Hospital course was complicated by septic shock and hemorrhagic cystitis. Patient was treated with inotropes, Pulse dose of intravenous methylprednisolone, albumin and other supportive approach. Decision was made not to continue cyclophosphamide due to hemorrhagic cystitis. Patient Cr later stabilized after peak of 4.3 mg/dl. Presently, is on diuretics and prednisone with Cr is stable around 1.3 mg/dl.

DISCUSSION:

Hepatorenal syndrome is divesting complication of liver cirrhosis, which can occur due to various mechanism one of which is described as in our case. Literature has focused mainly on mechanism of Ig-A nephropathy in portal hypertension. Our aim for this case report is to focus on monitoring renal function in cirrhotic patient even without no evidence of portal hypertension as there is no firm correlation between degree of portal hypertension and severity of IG A nephropathy. Thus, further studies can effect future era of hepatic transplant by more effectively understanding complex mechanism and managing complications.
3178 Augmentin-Induced Liver Injury in a Patient With Progressive Familial Intrahepatic Hepatic Cholestasis (PFIC)
Authors: Farooq Saba , Einstein Micheal
Published: October 2019

INTRODUCTION:

We are reporting a case of drug induced liver injury (DILI) within 48 hours of Augmentin administration in a patient with progressive familial intrahepatic cholestasis.

CASE DESCRIPTION/METHODS:

27-yo female with PMH of severe ATP8B1 protein deficiency, PFIC S/P hepatojejunostomy with external biliary diversion, not a transplant candidate due to psychosocial issues, presented with epigastric pain, vomiting and constipation. Home meds included hydroxyzine, questran and rifampin. On admission vitals were BP: 110/59, pulse: 107, temp: 98.3, O2 sat: 100% on RA. Physical exam was unremarkable except icteric sclera. Labs showed WBCs: 19.1, H&H: 14.1/41.4, PLT: 187, Total Billi: 17.9, AST/ALT/ALP of 566/398/172, normal BMP except Bicarb: 15. INR: 1.8, lipase 25, UA negative for infection. CT Abd/pelvis W/contrast did not show any acute hepatobiliary pathology, except endometrial prominence with some fluid. Rifampin was stopped, aggressive bowel regimen, IV hydration and IV antibiotics including Unasyn and doxycycline were started. Fuid from endometrial cavity was cultured. Pt's abdominal pain improved as constipation resolved. Antibiotics were switched to Augmentin for presumed endometrial infection. LFTs started rising within 48 hrs of augmentin administration. Peak LFTs were T.Billi/AST/ALT/ALP:21.5/762/528/132. Complete laboratory evaluation included negative serologies for hepatitis, A, B, C, EBV, CMV and negative assays for ANA, AMA, ASMA. Augmentin was stopped. Two weeks after discontinuation of Augmentin, patient's LFTs started to improve.

DISCUSSION:

DILI is a well-recognized complication of Augmentin use and multiple cases have been reported. Associated mortality can be as high as 10%, and thus prompt recognition and removal of the offending agent is of critical importance. In our patient, while systemic infection and rifampin use were other possibilities for liver injury however, worsening and improvement in LFTs correlated with Augmentin administration and discontinuation. Moreover, dose of rifampin was not changed for over a year. Several risk factors have been identified for DILI including older age, genetic determinants, preexisting liver disease and properties of certain medications. Our patient had PFIC and Augmentin use caused liver injury within 48 hrs of administration as compared to other case reports where latent period of Augmentin induced liver injury varied from days to weeks. In both DILI and PFIC, treatment options are very limited thus Augmentin should be avoided.
3186 Fatal Case of Acetaminophen Toxicity in a Young Female Patient
Authors: John Jaison , Al-Douri Abdul , Bhakta Meera , Kapadia Anupama
Published: October 2019

INTRODUCTION:

Acetaminophen is the most common cause of acute liver failure (ALF) in the United States. We report a fatal case of acetaminophen overdose after both delayed presentation for treatment and transplant evaluation in a non-liver transplant academic center.

CASE DESCRIPTION/METHODS:

An 18-year-old woman presented to the emergency department (ED) after attempting suicide by overdosing on acetaminophen. She ingested 48 of the 500 mg tablets (24-gram total dose) 18 hours prior to arrival to the ED. Her only symptom was back pain. Her medical history was significant for depression and three prior suicide attempts by acetaminophen overdose. Her mental status declined over the next few hours to the point of becoming non-verbal and mildly drowsy. On physical exam, patient was tachycardic and had self-inflicted scars to her forearms. Initial labs were significant for white blood cell count of 22,300 cells/mm3, bicarbonate of <5 mmol/L (21-31), glucose 59 mg/dL (70-110), alkaline phosphatase 91 units/L (42-121), aspartate aminotransferase 479 units/L (5-34), alanine aminotransferase acetaminophen 228 mcg/mL (<30), PT 27 seconds (9.4-12.5 sec), INR 2.5, and ammonia 147 mcmol/L (18-72). Venous blood gas revealed pH 6.819, pCO2 29 mmHg (39-51), pO2 51 mmHg (30-50), calculated bicarbonate of 4 mmol/L, and lactate of 14 mmol/L (0.5-2.20). Table 1 highlights changes in laboratory values during admission. The patient was admitted to the ICU, started on N-acetylcysteine (NAC) and bicarbonate infusions, and had urgent renal and general gastroenterology consultations. 48 hours after admission the patient was intubated due to deteriorating mental status and seizure activity. It was suspected that she was having cerebral edema and was emergently transferred to a liver transplant center. Ultimately, she did not undergo transplant and died from complications of ALF.

DISCUSSION:

Acetaminophen overdose carries a high risk of ALF and mortality. Survival depends on early treatment as high doses can overwhelm liver metabolism resulting in hepatotoxicity by N-acetyl-p-benzoquinoneimine (NAPQI). Treatment from time of ingestion was delayed in this case due to the patient's delay in seeking care. Transfer to transplant center was delayed due to lack of insurance, history of multiple attempts that affected her liver transplant candidacy, and under-appreciating risk of developing ALF. This case highlights the fatal complications of acetaminophen overdose, and underscores the importance of emergent transfer to transplant center.
3191 Two Cases of False Positive Hepatitis B Surface Antigen With Positive Hepatitis B E-Antigen
Authors: Shah Niraj J. , Paine Elizabeth , Burton Mary
Published: October 2019

INTRODUCTION:

Hepatitis B surface antigen (HBsAg), is a HBV surface protein particle that indicates current HBV infection. Hepatitis B e Ag (HBeAg) indicates active HBV replication. HBsAg, is a sensitive test, that utilizes anti-HBs to bind to and detect surface antigens to HBV. Any weakly positive HBsAg test needs to be further confirmed using a neutralization test to confirm infection. Below we have briefly described two cases of unusual hepatitis B serology.

CASE DESCRIPTION/METHODS:

Case 1- 78-year-old Caucasian male, with CKD, was worked up for hepatitis B as he was being considered for dialysis. Initially, on history he had provided positive risk factors (use of illicit drugs and multiple sexual partners) for hepatitis B infection. He denied any recent vaccinations. The transaminases were within normal limits. The hepatitis B surface antigen (HBsAg) was positive. However, the neutralization test was not confirmatory on two occasions. He had hepatitis B e Ag (HBeAg) positive as well. He was negative for Hepatitis B surface antibody (HBs Ab), hepatitis B core total antibody (AntiHBc-T), hepatitis B core IgM (AntiHBc- IgM) and HBV e antibody (anti-HBe). The hepatitis B viral DNA was also negative. The patient was negative for hepatitis C and HIV. The results were similar 6 months later. Case 2- 65-year-old Caucasian male, with psoriatic arthritis, was screened for hepatitis B as part of his management for psoriatic arthritis and was found to have a reactive HBsAg. He had no defined risk factors for HBV. His initial HBsAg was negative 7 years back. His hepatitis B serological profile was similar to the first patient.

DISCUSSION:

Heterophile antibodies could explain why the confirmatory test for HBsAg, after neutralization, was negative. Our patient had not received the HBV vaccination. Also, it does not explain why the HBeAg would be positive. HBsAg “escape” mutants are generally considered when the HBeAg and/or the HBV DNA is positive, in chronic HBV infection, which was not our case. Though we have come a long way in improving diagnostic laboratory capabilities, we still require better assays to accurately diagnose HBV. Present HBV guidelines do not define our case. We were unable to identify similar case reports. We continue to monitor our two patients, for if we decide to start them on hemodialysis (our first patient) or initiate immunosuppressive agents (for our second patient), the challenges of HBV reactivation are real.
3194 Sneaky Abscess-Ion: A Pyogenic Liver Abscess Masquerading as the Flu
Authors: Likhtshteyn Michelle , Arroyo-Mercado Fray , Iqbal Sadat , Ho Johnson , Botti Evan , Kim Joseph K. , Masub Natasha , Cobb Kaycie
Published: October 2019

INTRODUCTION:

Pyogenic liver abscess (PLA) is due to leakage of intra-abdominal contents with hepatic spread via the portal circulation. The incidence of PLA is estimated to be 2.3 cases per 100,000 people with higher rates among men than women [1]. We present a case of a 58-year-old male with no abdominal tenderness, risk factors, or recent travel history, who was found to have a 3 cm liver abscess growing Klebsiella Pneumoniae (K.pneumoniae).

CASE DESCRIPTION/METHODS:

The patient is a 58-year-old African American man with a medical history of HTN and HLD who presented with 3-day history of muscle aches, subjective fevers, and chills. Initially the patient was suspected to have a flu and was treated with fluids and antipyretics. He was noted to have transaminitis (AST/ALT: 202/139), however denied nausea or abdominal pain. An ultrasound demonstrated a complex cystic mass in the right lobe of the liver, and a CT Abd/Pelvis showed a 3.2 × 3.1 × 2.3 cm heterogeneous hypodense mass in segment V. The patient remained febrile with a Tmax of 102 and began to develop severe RUQ on day two of admission. The patient was maintained on Zosyn 3.375g q6h and initial blood cultures grew gram negative rods. Patient tolerated IR drainage of liver abscess yielding 10cc pustular fluid with subsequent resolution of fever. Both blood and liver cultures grew pan-sensitive K.pneumoniae.

DISCUSSION:

PLA commonly develops as a complication of biliary tract disease in 40% of cases [2]. In the United States, K. pneumoniae is the predominant pathogen causing PLA; isolated in greater than 60% of monomicrobial and polymicrobial PLA [3]. Groups who are susceptible to infection with K. pneumoniae include patients of Asian ethnicity, diabetics, and those with antibiotic use [2]. Our patient did not have any risk factors for PLA; he had minimal medical history and only took amlodipine on presentation. Common symptoms of PLA include fever, right upper quadrant abdominal pain, and rarely jaundice [1]. Our patients' initial presentation was consistent with a flu like prodrome; however, his transaminitis suggested an underlying hepatic process. While a PLA was unlikely on admission, worsening sepsis and new abdominal pain elucidated the diagnosis. K. pneumoniae PLA can lead to disseminated infections including meningitis; the identification and drainage of an abscess early in the hospital course can alter a patients' mortality. While PLA is rare, it should still remain on the differential diagnosis for septic patients.
3200 A Rare Case of Hepatitis B Association With Sarcoidosis and Treatment Challenge With Immunosuppressive as Resulting in Colonic Histoplasmosis
Authors: Jiyani Rucha , Patel Pinakin , Patel Saumil
Published: October 2019

INTRODUCTION:

There have been documented cases reflecting association between Hepatitis C virus (HCV) and sarcoidosis but it is very interesting as in this case that we discussed about association of Hepatitis B virus (HBV) and sarcoidosis, presenting with vague symptoms and confirmed with liver biopsy and immunologic markers. Further challenging is treatment with immunosuppressive medication leading to colonic histoplasmosis.

CASE DESCRIPTION/METHODS:

58 year old Indian female with past medical history of cirrhosis secondary to HBV diagnosed six months ago, hypertension and diabetes mellitus 2 presented with bilateral pedal edema, anorexia and mild epigastric discomfort. She has been started on Entecavir since diagnosis six months ago. Patient denied any significant surgical, social and family history. Ultrasonography Liver revealed hepatosplenomegaly and mesenteric lymphadenopathy. 21.3kPa liver stiffness on elastography and HBV level 83. Liver biopsy showed multiple non caseating granulomas consist of Langerhans cell in parenchyma and portal tract, associated with moderate inflammation. Chest CT scan showed upper and middle lobe fibrosis of lung, diagnosis further confirmed with elevated Angiotensin converting enzyme. She was started on prednisone; within 3 months she experienced weight loss, diarrhea and fever. Colonoscopy was done after CT abdomen showed mural thickening of ascending colon and terminal ileum, which on biopsy confirmed Histoplasmosis as described in Figure 1. Prednisone stopped and patient treated with Hydroxychloroquine, amphotericin followed by itraconazole. Patient improved symptomatically and repeated colonoscopy was normal.

DISCUSSION:

As in this report, studies are scarce to prove association. However; reasonably assumed that the alterations in the pool of cytokines and immune cells caused by HBV infection may have a vicious influence on the immune regulation and can be a trigger for granuloma. Further studies can impact future era for better understanding in pathophysiology of sarcoidosis and HBV correlation and treatment options.
3209 Mesenteric Vein Thrombosis: An Unusual Cause of Small Bowel Obstruction
Authors: Boppana Vaishnavi , Paleti Swathi
Published: October 2019

INTRODUCTION:

Mesenteric venous thrombosis (MVT) is an uncommon cause of acute to sub-acute abdominal pain. Early recognition and treatment have survival implications.

CASE DESCRIPTION/METHODS:

A 42 year-old male with past medical history of hypertension and obstructive sleep apnea presented with 3 weeks of worsening abdominal pain, nausea and vomiting. Physical exam revealed diffusely tender abdomen with mild guarding, no rebound tenderness and normoactive bowel sounds. Pertinent labs on admission included an elevated white count of 13.5 K/mm3 and lactate of 2 mmol/L. A non-contrast CT abdomen demonstrated small bowel loops with abnormal wall thickening and associated inflammatory changes. He was started on broad spectrum antibiotics for enteritis, however he had worsening abdominal pain and an abdominal x-ray revealed small bowel obstruction. Patient was made NPO and conservatively managed with IV fluids. His hospital course was complicated by fever of 100.8 F and leukocytosis of 26.3 K/mm3 Infectious work up was unremarkable and a CT abdomen with contrast revealed thrombosis of main portal, superior mesenteric and splenic vein. Hypercoagulable workup resulted in decreased Protein S activity (1779X) and Factor II heterozygosity (prothrombin G20210A mutation).

DISCUSSION:

MVT accounts for 6%–9% of all the cases of acute mesenteric ischemia. Most common presenting symptom is abdominal pain which occurs in 91–100% of the cases followed by nausea, vomiting and melena. Associated portal venous thrombosis can be seen if the disease originates in the major veins instead of the small vena rectae. Young patients without known risk factors for venous thromboembolic (VTE) and thrombosis in unusual sites such as portal, mesenteric and cerebral veins should be evaluated for thrombophilias. Approximately 20-40% of patients have previous history of deep vein thrombosis or may have a pre-existing hereditary hypercoagulable state such as protein C deficiency, protein S deficiency, anti thrombin III deficiency, factor V Leiden deficiency, or antiphospholipid syndrome. In general, outcomes in MVT are better when compared to arterial thrombosis with mortality of 44% as compared to 66–89% respectively. Studies have shown that early use of heparin has been associated with improved survival. Early recognition of MVT and treatment with anti coagulation has led to non-surgical treatment and improved outcomes.
3211 An Incidental Duodenal Lymphangioma Presenting as Diarrhea
Authors: Pagan Andrea , Mony Shruti , Gill Jeffrey , Arroyo Yadis , Bertran-Rodriguez Carlos E.
Published: October 2019

Introduction:

The small bowel is a rare site for neoplasia and only account for over 3% of the cases in the digestive tract. Lymphangiomas are benign tumors formed by dilated lymphatic channels that occur more commonly in the neck and axillary regions. Duodenal lymphangiomas are extremely rare in the adult population. It s thought to be a benign congenital malformation of the lymphatic vasculature that is able to grow to form a mass lesion. Their clinical presentation ranges from asymptomatic to obscure bleeding, small bowel obstruction, intussusception or even volvulus. We present a case of a duodenal lymphangioma presenting with chronic abdominal pain and diarrhea.

CASE DESCRIPTION/METHODS:

A 37-year-old male with no significant past medical history presented with chronic diarrhea, constipation and abdominal discomfort for 3 years. Physical examination and laboratory data were in the normal limits. Remainder of his infectious and inflammatory workup for diarrhea was negative. He underwent endoscopy which revealed a 1-cm polypoid submucosal lesion in the post-bulbar area. Multiple deep bites-on-bite biopsies were obtained from the lesion. Histological examination showed dilated lymphatics with reactive epithelial changes, consistent with Lymphangioma. During the follow up visit the patient referred improvement of the presenting symptoms.

DISCUSSION:

Lymphangiomas of the duodenum are a very rare lymphatic system tumor. The clinical presentations are usually variable and nonspecific and may mimic a variety of vague abdominal symptoms like abdominal discomfort, diarrhea, anorexia, nausea, and vomiting. These lesions typically exist as small incidental polyps; however, some of these tumors present as mass lesions capable of causing bowel obstruction, abdominal pain, and gastrointestinal bleeding. By endoscopic examination, they usually appear as a sessile or semi-pedunculated mass with smooth surface mucosa with lymphatic cystic dilatation with a whitish granular appearance. These benign tumors require treatment if they are accompanied by symptoms and complications such as infection, obstruction and hemorrhage. Endoscopic unroofing or polypectomy has become the treatment of choice for small to intermediate lymphangiomas. Physicians must thus be cognizant of the differentials for small bowel nodules in order to avoid unnecessary surgical interventions.
3217 Intussusception in a Patient With Marijuana Use: Coincidence or Possible Correlation?
Authors: Khan Zarak H. , Paul Jonathan R. , Singh Tejveer , Jarodiya Vijay , Khan Tahir , Alam Ariful , Korpole Pranay R. , Rai Raveen
Published: October 2019

INTRODUCTION:

“Intussusception” is a term initially used by the Scottish surgeon, Dr. John Hunter in 1789 which means invaginating or telescoping. It is caused by any condition that disrupts the normal physiological mechanism of intestinal peristalsis. Intussusception in adults is rare with incidence of 2-3 cases per population of 1000000 annually. The most common cause of intussusception in adults is neoplasms.

CASE DESCRIPTION/METHODS:

22-year-old female, with multiple past episodes of abdominal pain and vomiting, presented with one day duration of sudden onset worsening abdominal pain, vomiting and diarrhea. The stools were black but without tarry clots or frank blood. She also had four episodes of non-bilious and non-bloody emesis. Of note, she had more than one year history of extensive marijuana use. Upon presentation, her vitals were unremarkable. Physical exam was pertinent for diffuse abdominal tenderness without guarding or rebound. Initial labs were unremarkable except for an elevated lactic acid level (4.6 Mmol/L). Pregnancy test was negative. Patient received anti-emetics, proton pump inhibitor and IV fluids. She then underwent a CT scan of the abdomen and pelvis which revealed a small bowel intussusception in the left hemiabdomen. She was made NPO and subsequently underwent both upper endoscopy and colonoscopy which were normal. She was treated conservatively with bowel rest, anti-emetics and IV fluids. She gradually improved with resolution of symptoms on day four of hospital stay. Her intussusception had resolved on a follow up small bowel series. She was discharged home with outpatient Gastroenterology follow up.

DISCUSSION:

There is enough evidence to support that cannabis acts on several segments of the bowel. It has been demonstrated that interaction through inhibition of intrinsic cholinergic mechanisms can result in cannabis-induced inhibition of gastrointestinal motility. Fernández-Atutxa et al. and Olga et al. presented a 3 patient case series and a case report respectively with clinical presentation similar to our patient. These patients were diagnosed with intussusception with no apparent organic cause but had a history of extensive marijuana use. Our case presentation is intended to pay attention to adverse effects of cannabis in light of increasing legalization and increasing therapeutic use of cannabis and its derivatives.