bluuebunny/crossref_metadata_2025 huggingface dataset:
3176 Sickle Cell Intrahepatic Cholestasis Following Choledocholithiasis: A Case Report
Authors: Zafar Yousaf , Gondi Keerthi , Muthukumar Varsha
Published: October 2019

INTRODUCTION:

Sickle Cell Intrahepatic Cholestasis (SCIC) is an acute manifestation of Sickle Cell Disease (SCD) characterized by occlusive sickling in the liver, causing biliary obstruction. We present a case of a patient in vaso-occlusive crisis with SCIC following choledocholithiasis.

CASE DESCRIPTION/METHODS:

A 23-year-old male presented with severe abdominal pain after having a complicated stay for choledocholithiasis one week prior. Total bilirubin level was 42.2 mg/dL, and transaminases were elevated. Abdominal ultrasound did not demonstrate repeat biliary duct blockage. Magnetic Resonance Cholangiopancreatography revealed intrahepatic biliary duct dilation and scattered wedge-shaped enhancements peripherally. The patient underwent plasma exchange transfusion. Afterwards, patient rapidly recovered with reduction in bilirubin level and resolution of pain and jaundice. He was discharged without complication.

DISCUSSION:

SCIC is a rare and potentially fatal sequela of vaso-occlusive crisis in SCD. Our patient may have been predisposed to developing SCIC due to a prior complicated admission for choledocholithiasis which may have damaged the biliary system to induce SCIC. Plasma exchange transfusion results in rapid recovery and should be initiated quickly in these patients.
3177 Splenomegaly in an Adult Female With Sickle Cell Disease
Authors: Benjaram Sindhuri , Rahim Usman , Ehrinpreis Murray N.
Published: October 2019

INTRODUCTION:

A mutation in the beta globin chain of hemoglobin results in Sickle type of Red blood cells. To remove the sickle shaped red blood cells, the spleen becomes hyperactive and enlarged. These red cells have more affinity to the vascular endothelial membrane resulting in Vaso-occlusive phenomenon. Repeated episodes of this cause thrombosis, infarction leading to fibrosis and Autosplenectomy. This is generally complete by the age of 5 and for more than 80% in their first decade. Existence of spleen in adolescents and adults with sickle cell disease in uncommon. Here we present such a case.

CASE DESCRIPTION/METHODS:

A 22-year-old female with known history of homozygous sickle cell disease presents with abdominal pain. She started to have generalized body pains, later localized to all quadrants of the abdomen. She described it as achy type constant pain associated with nausea. She denies any emesis, changes with bowel or bladder habits and association with food intake. CT imaging done revealed an enlarged spleen with scattered densities and a 2 cm splenule in the inferior aspect. The enlarged spleen 14 × 5 × 15 cms was present in prior ultrasound imaging study done 4 years ago. Further laboratory work including complete blood counts with differential, reticulocyte count & index were consistent with sickle cell pain crisis.

DISCUSSION:

Although the presence of echogenic lesions increases the risk of sequestration crisis, increased Hemoglobin F levels and alpha thalassemia may cause splenomegaly, but the patient did not have either. Hemoglobin Electrophoresis showed Hb F 1% and Hb S of 70%. Some studies conclude splenic enlargement in adulthood may imply less severe form of the disease. With no other possible cause identified, this adult female with Sickle cell HbSS disease has Splenomegaly.
3184 A Case of Alcoholic Hepatitis With Unusual Leukamoid Reaction
Authors: Lakkasani Saraswathi , Barham Shaker , Depasqule Joseph , Abusalah Wala
Published: October 2019

INTRODUCTION:

Leukemoid reaction is defined by predominantly neutrophilic leukocytosis with a total leukocyte count >50,000 cells/µl, after excluding leukemia. Leukemoid reaction is seen in various conditions. It is very rare in alcoholic hepatitis (AH). Herein, we present a case of a young alcoholic male who was admitted with alcoholic hepatitis and leukemoid reaction. He underwent extensive workup to rule out other etiologies and subsequently improved after glucocorticoid therapy.

CASE DESCRIPTION/METHODS:

28-year-old male with history of alcohol abuse presented with a two-week history of abdominal pain, distention, jaundice and vomiting. On exam, the patient had a fever and tachycardia. He was also found to be icteric and had ascites. Investigations revealed a bilirubin of 9.4 mg/dl. WBC of 42,000 cells/µl with a left shift. Ultrasound showed enlarged fatty liver. MDF was 61 and MELD was 37. Septic workup was negative including ascitic fluid cell count and culture. He was started on prednisolone 40 mg. Hematologic workup including peripheral smear ruled out neoplasm. Leukocyte alkaline phosphatase was elevated at 249. The patient was discharged on prednisolone and was followed as an outpatient. He improved after four weeks and his WBC count normalized.

DISCUSSION:

Leukemoid reaction is a very rare event in AH and is a poor prognostic marker. The pathophysiology is likely due to the increased levels of granulocyte colony stimulating factor (G-CSF) released by the damaged hepatocytes. The release of excessive amounts of tumor necrosis factor-alpha has been postulated to be instrumental in the causation of leukemoid reaction in alcoholic patients as well. However, Arguelles-Grande et al. reported a patient in which the cytokine profile did not demonstrate increased amounts of TNF-a. In their patient, levels of IL-18 and IL-1b were increased. IL-1b stimulates the proliferation and maturation of neutrophils in the bone marrow both directly by the induction of granulocyte-macrophage colony-stimulating factor and G-CSF; thus the postulated pathogenic sequence for LR: increased IL-18 produces increased IL-1b, which along with increased IL-8 produces neutrophilia. In this setting, corticosteroids may play a role by their reported inhibition of IL-1b transcription. Hematologic evaluation in these cases is necessary to rule out underlying neoplasm. If patients with severe alcoholic hepatitis are found to have leukemoid reaction, treatment with steroids should be considered after excluding sepsis and neoplasm.
3189 Portal Vein Thrombosis Without Cirrhosis: A Case Report
Authors: Lopez Paola , Torres Victor , Morales Ahmed , Di Marco Anna , Ayala Alfredo
Published: October 2019

INTRODUCTION:

PVT is a rare entity in the absences of liver cirrhosis, malignancy, prothrombotic disorder or an intra-abdominal inflammatory state. In some cases, no clear etiology can be found and it can be triggered by a combination of factors. We report a case of non-cirrhotic woman with a symptomatic and progressive PVT in the setting of low antithrombin activity and liver lesions.

CASE DESCRIPTION/METHODS:

48 year old female without past medical or family medical history, was brought to the ED with diffuse abdominal pain. For the past ten weeks, she has experienced post-pandrial abdominal pain associated with nauseas and two episodes of non-bloody vomiting. She denied diarrhea, recent abdominal infections, drug use or OCP use. Patient has not undergone abdominal surgery. Her physical exam was unremarkable except for mild diffuse abdominal pain, no Murphy's sign, no guarding or rebound signs. CBC, BMP, lipase and liver function panel was unremarkable. Recent mammography, EGD and colonoscopy displayed no signs of malignancy or portal hypertension. MRA showed no stenosis or obstruction of arteries. CAT-scan of abdomen and pelvis with IV contrast showed extensive thrombosis of main portal vein, right portal vein, left portal vein and the portosplenic confluence. Also showed collateral vessels extending from the portosplenic confluence into the bilateral retroperitoneum, bilateral renal hilum and extending across the ovarian veins into the pelvis. There were multiple indeterminate hypodense liver lesions. Additional laboratory tests were ordered and samples collected before starting anticoagulation. Laboratory tests showed decrease antithrombin activity, which is a risk factor for PVT. She was admitted on low-molecular weight heparin (LMWH) until stabilization, and then discharged on oral anticoagulation. In this case, outpatient follow up evaluation by hemato-oncology was scheduled to rule out other coagulation disorders and malignancy.

DISCUSSION:

PVT in a healthy and young patient is not common. The prevalence of PVT is low in patients with cirrhosis; it is even lower in patients non-cirrhotic and without malignancy. It has been estimated that in non-cirrhotic PVT, hypercoagulable states account for 40%-60% of cases. The American Association for the Study of Liver Diseases (AASLD) guidelines recommend treatment with anticoagulation to prevent thrombi extension and to restore blood flow in occluded vessels. The outcome for non-cirrhotic, non-malignant PVT is good if the diagnosis and treatment occurs early.
3192 Sealing the Diagnosis of Celiac Disease in Pregnancy
Authors: Nahar Ritu , Amin Avani , Moleski Stephanie
Published: October 2019

INTRODUCTION:

Celiac disease (CD) is an immune-mediated disease that results from a reaction to dietary gluten and primarily affects the small intestine. The diagnosis of CD can be challenging in those that do not present with the classic gastrointestinal symptoms, and the diagnosis can further be complicated in pregnancy.

CASE DESCRIPTION/METHODS:

A 28-year-old G1P0 woman presented with hypertension and at 15 weeks gestation. Initial workup for the patient's transaminase elevation was remarkable only for hepatic steatosis on abdominal ultrasound, with normal liver size, echogenicity and echotexture. She was diagnosed with chronic hypertension with superimposed preeclampsia complicated by transaminase elevation. However, her transaminase elevation persisted postpartum prompting re-evaluation. Further testing revealed a weakly positive anti-tissue transglutaminase antibody (IgA tTG) of 6 units/mL. Biopsy at the time of esophagogastroduodenoscopy revealed duodenal mucosa with intraepithelial lymphocytosis and focal moderate villous blunting consistent with CD.

DISCUSSION:

While the prevalence of CD is approximated to be one percent of the American population, it can be as high as four percent in those with cryptogenic transaminase elevation.1,2 Untreated CD during pregnancy predisposes patients to increased rates of intrauterine growth restriction (IUGR), low birth weight, and preterm birth.3 Establishing a diagnosis of CD during pregnancy can be challenging. However, prenatal screening for CD in high risk populations can lead to more cost effective care as well as improved maternal and fetal outcomes.
3195 Autoimmune Hepatitis With Primary Biliary Cirrhosis: An Overlapping Syndrome of the Liver
Authors: Jobanputra Hardik , Shrimanker Isha
Published: October 2019

INTRODUCTION:

Autoimmune liver diseases consist of Primary Biliary Cirrhosis (PBC), Autoimmune Hepatitis (AIH) and Primary Sclerosing Cholangitis (PSC). Overlap syndromes are defined when there are characteristic features of AIH along with PBC and PSC. We report the presentation and management of an AIH-PBC overlap syndrome.

CASE DESCRIPTION/METHODS:

A 60-year-old Asian female with a past history of hypertension, presented with fatigue, myalgia, nausea, vomiting, and icterus for ten days. She denied the use of illicit drugs, alcohol consumption or family history of liver disease. On arrival, she had a temperature of 38.2°C, a pulse of 110 beats/minute, blood pressure of 100/70 mm Hg, and oxygen saturation of 97% on room air. Physical exam revealed icterus 1+, and mild tenderness in the right hypochondriac area. Laboratory investigations revealed leukocyte count of 15.2 K/ul, alanine transaminase of 1107 U/l, aspartate aminotransferase of 1010 U/l, alkaline phosphatase of 685 U/l, total bilirubin of 10 mg/dl with the direct component of 9 mg/dl, and gamma-glutamyl transferase of 666 U/l. Further workup revealed anti-nuclear antibody titer of 1:1000, antimitochondrial antibody (AMA) titer of 1:80 with negative peripheral antineutrophil cytoplasmic antibody and hepatitis serology. Ultrasound of the abdomen showed common-bile duct (CBD) stricture formation. The patient underwent endoscopic retrograde cholangiopancreatography with sphincterotomy and stenting. Liver biopsy showed interface hepatitis with portal tract inflammation. Brush border sampling from the CBD revealed lymphocytic and neutrophilic infiltrate. A diagnosis of AIH-PBC overlap syndrome was made. She was started on piperacillin/tazobactam 4.5 gm and metronidazole 400 mg along with with ursodeoxycholic acid (UDCA) 300 mg, thrice a day. After a month, the stent was removed and there was a resolution of symptoms with normalization of liver enzymes.

DISCUSSION:

The minimum criteria required for the diagnosis of AIH-PBC overlap syndrome include positive AMA and histology showing bile duct abnormality in an otherwise classical AIH (Table 1). Management is usually with UDCA, immunosuppressants, and corticosteroids. It is prudent to maintain a modest index of suspicion of overlap syndromes in patients such as ours. Early diagnosis and appropriate management are of paramount importance.
3196 A Rare Occurrence of Tricuspid Valve Histoplasma Endocarditis in a Patient With NASH Cirrhosis and No Intravenous Drug Use
Authors: Abraham Fiyinfoluwa , Subramanian Sruthi K. , Singh Khushboo , Machicao Victor
Published: October 2019

INTRODUCTION:

Bacterial endocarditis not commonly seen in patients with cirrhosis, while culture-negative endocarditis in the setting of cirrhosis is rarely seen at all. We present a case of Histoplasma endocarditis diagnosed in Nonalcoholic Steatohepatitis (NASH) cirrhosis.

CASE DESCRIPTION/METHODS:

A 66-year-old Caucasian female with a history of atrial fibrillation on rivaroxaban, diastolic heart failure, and decompensated NASH cirrhosis with controlled ascites presented with two weeks of weight gain, bilateral lower extremity swelling, and dyspnea. No history of intravenous drug use (IVDU). She had anasarca on physical examination and was admitted for diuresis. A transthoracic echocardiogram (TTE) five months before these symptoms described moderate tricuspid regurgitation. Due to acute anasarca, a repeat TTE was obtained which showed a left atrial thrombus, moderate to severe tricuspid regurgitation (Table 1) with anterior leaflet prolapse, and an echodensity (1.12 × 0.7 cm) seen on the tricuspid valve (Figure 1). A follow up transesophageal echocardiogram (TEE) was done 7 days later. It confirmed the tricuspid vegetation and severe tricuspid regurgitation (Table 1). Blood cultures returned negative. She was treated empirically with IV vancomycin, ceftriaxone, and doxycycline for infective endocarditis and switched to warfarin from rivaroxaban. The patient was later discharged; however, she had two more admissions for similar symptoms of dyspnea and anasarca. Repeat blood cultures remained negative; however, serology for Histoplasma antibody returned positive (1:8). The patient was started on Isavuconazonium and had improvement of symptoms upon outpatient follow up. She was not a surgical candidate for aortic/tricuspid valve replacement due to underlying liver disease; however, to re-evaluate surgical candidacy, she underwent a liver biopsy to confirm cirrhosis. A separate sample was sent for fungal culture in the setting of diagnosed Histoplasma endocarditis – currently pending.

DISCUSSION:

In the general population, fungal endocarditis is uncommon, but Histoplasma endocarditis is an infrequent manifestation of disseminated Histoplasmosis. It is frequently missed and usually involves prosthetic valves. The presence of Histoplasma endocarditis in a cirrhotic has been described in three other patients in a case series by Riddell et al. where two patients had hepatitis C-related cirrhosis. Our case describes an atypical occurrence Histoplasma endocarditis in NASH cirrhosis without prior IVDU.
3197 Pyogenic Liver Abscess in B-Thalassemia: A Case Report
Authors: Nnaoma Christopher , Ruberwa Joseph , Chika-Nwosuh Ogechukwu Z. , Pal Chitanya , Quintilliani Safiyya B.
Published: October 2019

INTRODUCTION:

Pyogenic liver abscess typically develops via systemic seeding of an infection or from biliary disease through direct spread or portal circulation. Invasive liver abscess though may occur in Beta-thalassemia major patients are a rarity in Beta-thalassemia minor.

CASE DESCRIPTION/METHODS:

36-year-old woman with a history of B-thalassemia minor presents to the ED with complaints of acute onset severe, non-radiating right upper quadrant pain. She endorses fevers, chills and night sweats but denied anorexia, nausea, vomiting, diarrhea or urinary symptoms. Never been transfused. Physical exam was pertinent for a temperature of 102.8 F, tachycardia of 138 bpm, and an upper quadrant abdominal tenderness with some guarding. Labs was notable for leukocytosis with neutrophil predominant, anemia with Hb of 5.3 g/dl. Elevated ESR and CRP. Lipase and amylase were normal. CT abdomen showed 10.3 cm thick-walled, complex fluid collection in the right hepatic lobe and splenic abscesses consistent with a pyogenic abscess. Blood cultures were negative. She was started on empiric antibiotic with vancomycin and piperacillin/ tazobactam and was subsequently taken to interventional radiology for drainage of the abscess, with a J-P drain left insitu. The patient received 2 units of packed red blood cells. Fluid culture from drain was positive for Klebsiella pneumoniae which was sensitive to Levaquin. The patient's condition improved while on antibiotics with subsequent removal of the J-P drain. She was successfully discharged on oral Flagyl and Levaquin for 14 days.

DISCUSSION:

Typically, thalassemia minor carriers are clinically asymptomatic with very little to no complications. Infections however, are a major complication, and constitute the second most common cause of mortality and a main cause of morbidity in patients with thalassemia. The major culprit bacterial infections in thalassemia patients are Klebsiella sppand Yersinia enterocolitica. K. pneumoniae is also associated with a community-acquired primary invasive liver abscess syndrome. Liver abscess occur more commonly in beta- thalassemia major as these group of patient have predisposing factors such as underlying hepatobiliary dysfunction and recurrent transfusions. This condition is rare in beta- thalassemia minor. Abscess rupture is a rare complication, while metastatic infection to other sites can occur. Diagnosis is usually made with CT scan of the abdomen while treatment is should be started with empiric broad-spectrum and drainage of the abscess.
3203 Atypical Presentation of Viral Gastroenteritis in a Three-Year-Old Child Due to a UNC80 Mutation
Authors: Stenehjem Kristen , Schweigert Jessica , Kumar Parag
Published: October 2019

INTRODUCTION:

We report on a three-year-old child with a rare genetic phenomenon, a UNC80 mutation, who had an unusual presentation of viral gastroenteritis. The UNC80 gene encodes for an important voltage-independent channel in neurons and a mutation in this protein can lead to severe hypotonia. The hypotonia manifests as delayed gastric emptying, impaired respiratory clearance, and/or delayed muscle coordination, which can predispose to infection susceptibility. UNC80 gene mutations have also been shown to cause global developmental delays, failure to thrive, and phenotypic dysmorphisms.

CASE DESCRIPTION/METHODS:

In our patient, we believe that his genetic defect precipitated a complicated hospital course. The patient's delayed gastric emptying caused difficulty in recovering from viral gastroenteritis while a concurrent pneumonia diagnosis required assistance in clearing respiratory contents.

DISCUSSION:

The UNC80 mutation is under-studied and more studies are necessary to understand the clinical implications of its phenotypes.
3206 Intestinal Motility: Not Part of Trihexyphenidyl's Job Description
Authors: Diaz Carolina , Fernández Carlos , Alegre-Boschetti Sergio M. , De Jesús Henry , Rodriguez Frances , Martinez-Souss Jaime , Martin-Ortiz Jose
Published: October 2019

INTRODUCTION:

Paralytic ileus presents similarly to mechanical obstruction; however, there is absence of a culprit anatomic lesion. It is commonly due to surgical intervention, peritonitis, trauma, medications, electrolyte disturbances, or intestinal ischemia.

CASE DESCRIPTION/METHODS:

This is the case of an 86-year- old male with past medical history of Parkinson's Disease and hypertension who was admitted at IM ward due to complicated UTI and bacteremia. During hospitalization, the patient developed abdominal distention and referred not having a bowel movement in 5 days. Physical exam was remarkable for a distended, tympanic, and non-tender abdomen. Labs displayed improving leukocytosis, normocytic-normochromic anemia, and absence of electrolyte disturbances. KUB was ordered, which revealed a very dilated stomach with gaseous distention in the stomach and small intestine as well as moderate amount of stool in the colon. As a result, Miralax, a sodium phosphate enema, and a nasogastric tube with intermittent suction were recommended. However, no bowel movements were reported as a result. Therefore, mineral oil was recommended the following day. Given lack of significant improvement, half a gallon of polyethylene glycol (golytely) was added to therapy. Two large bowel movements were achieved as a result. However, the patient's abdomen continued distended and tympanic for which CT abdomen with contrast was done. CT results showed no evidence of mechanical obstruction. Given lack of improvement despite interventions, trihexyphenidyl, which patient had recently started for Parkinson's Disease, was discontinued. Patient was not on opioid or other constipation inducing medications. Five bowel movements were reported in the 24-hours that followed removal of medication. The following day KUB displayed improvement and physical exam was remarkable for positive bowel sounds in all 4 quadrants and a non- tender, non-distended abdomen.

DISCUSSION:

Rapid resolution of symptoms suggests trihexyphenidyl as culprit. It is important to note that although anti-cholinergics are known to cause or precipitate paralytic ileus, few cases have been reported as a result of trihexyphenidyl use. Trihexyphenidyl is prescribed with frequency for the treatment of Parkinson's Disease, being aware of its side effects may lead to prompt diagnosis and better outcomes.
3214 Acute Extensive Jejunal Ulceration Following Single Balloon Enteroscopy
Authors: Maklad Muthena , Makar Ranjit , Lankarani Daisy S. , Aziz Hamza , Fayad Joseph
Published: October 2019

INTRODUCTION:

Small bowel ulceration can be difficult to diagnose and maybe confused with perforation or intestinal obstruction. The differential considerations for small bowel ulceration include inflammatory causes: PUD, isolated terminal ileal ulcers, drug induced, Crohn's disease. Vascular disorders: vasculitis, Behcet's, vascular dysplasia, microangiopathic ischemic ulcers, veno-occulsive. Other causes: ischemia, neoplasia and more. We are reporting a case of diffuse jejunal ulceration after episode of hypotension diagnosed by capsule endoscopy (CE).

CASE DESCRIPTION/METHODS:

75 yo male veteran with IBS-C, CAD, CHF, A fib on ApixabanPatient admitted for acute CHF exacerbation. Hgb was decreased to 8.1 g/dl (baseline 13 g/dl). Patient denied hematemesis, hematochezia, melena Due to patient cardiac issues, we used CE to evaluate for possible GI bleed. CE findings noted for AVM in early jejunum, distal jejunal polyp, bleeding ileal AVM. He was transferred to another facility for single balloon enteroscopy (SBE) with ablation of 4 areas of AVM's. A tattoo was placed to the most distal area of the jejunum reached. The jejunal polyp wasn't seen on SBE. Post procedure he developed hypotension, and started on pressor for blood pressure (BP) support. The patient was transferred back to our facility after 2 weeks. We were asked to evaluate if the jejunal polyp was missed on SBE. A repeat CE showed: multiple areas of severe, large circumferential ulceration throughout the jejunum. Jejunal polyp was noted distal to the tattoo, bleeding AVM in the ileum again. Anticoagulation was held and started iron supplement.

DISCUSSION:

Patients needing pressor support for BP control are at risk for CV events such as intestinal ischemia. Given the acute changes in the small bowel seen on the CE, likely due to either the hypotensive episode or use of vasoactive drugs to support the patient's BP. In our literature search, we didn't find any reports on acute extensive jejunal ulceration following a hypotensive episode or after use of vasoactive drugs. This entity may be under reported due to patients' hemodynamic instability preventing endoscopic eval. In general, unless targeted the small bowel is not routinely evaluated. We propose using CE, which requires minimal prep and no anesthesia, to help reveal the diagnosis of ileal ischemia in patients with pressor support or hypotension that aren't responding to supportive measures in order to alter the clinical intervention. This can be done as a future prospective study in ICU patients.
3218 Duodenal Adenocarcinoma Masquerading as Gastroenteritis: A Case Report
Authors: Marcuard Maurice , Samuel Gbeminiyi , Khalid Hamza
Published: October 2019

INTRODUCTION:

Small bowel cancers are rare only compromising 5% of gastrointestinal cancers and among those, 40% are small bowel adenocarcinomas.1 Duodenal adenocarcinomas in the 4th portion of the duodenum are even less frequent and are a diagnostic challenge as they typically at an advanced stage when they present.1,2 There are several risk factors associated with it including celiac disease, inflammatory bowel disease and smoking amongst others.1 Given the rarity we present a case of a young patient without any major risk factors that was thought to have gastroenteritis but was found to have something more sinister.

CASE DESCRIPTION/METHODS:

We present a 49 year old African American male with a medical history of hypertension who presented to the hospital with intermittent nausea, vomiting, and crampy abdominal pain over the last 4 months. He was seen in the emergency department (ED) early on, and was diagnosed with gastroenteritis and treated symptomatically. At this point his abdominal pain has worsened and recurrence of nausea and vomiting. He noted a 25 pound weight loss over this time. He denied blood in vomit or stools and any tobacco or alcohol use. He never had an endoscopy or colonoscopy. Physical exam showed decreased bowl sounds and tenderness in epigastrium, otherwise was unrevealing. In the ED the patient was evaluated during which a CT abdomen showed a severe bowel obstruction and bowel thickening suspected at the level of the third/fourth portion of the duodenum (Figure 1). With this a nasogastric tube was placed to decompress. On endoscopy there was a large circumferential fungating mass in the fourth portion of the duodenum causing a complete obstruction (Figure 2). Biopsies were taken which confirmed adenocarcinoma (Figure 3). He was returned to the floor and later underwent a resection of the 4th portion of his duodenum and first part of the jejunum.

DISCUSSION:

As seen here making a diagnosis can be a very challenging and might not always be correct the first time. We cannot perform endoscopies on all patients who arrive with nausea and vomiting, but with recurrent symptoms an endoscopy would be helpful in identifying these malignancies. In this case, even on endoscopy the lesion could have been missed since his malignancy was in the 4th portion which is rare and beyond the extent of the normal exam.2 In the end this case is a reminder to always keep the differential wide and be diligent to look further even when the patient does not fit perfectly with the description in the book.
3219 Intussusception Not Just a Pediatric Problem
Authors: Ali Sara , Capatina-Rata Ana M.
Published: October 2019

INTRODUCTION:

Intussusception is usually considered a pediatric condition, but it may also be present in adults, where it is more often associated with an underlying pathology. In adults, intussusception is found in only 1% of patients with bowel obstructions. Most cases have distinct lead points, this in comparison to the pediatric cases is contrasting where more 90% of the cases are idiopathic. Malignancy is the most common cause of pathologic lead point.

CASE DESCRIPTION/METHODS:

20 year old male with known history of Crohn's previously on Vedolizomab, presents with nausea, vomiting with melena. He was initially rehydrated intravenously along with IV steroids. On presentation his vitals indicated that he was slightly hypotensive and tachycardiac. Abdominal exam demonstrated a diffusely tender abdomen with no signs of guarding or rigidity. CT Abdomen revealed mucosal enhancement and wall thickening of the terminal ileum and cecum indicating Crohn's flare up along with Jejunu-jejunal intussusception in the left upper quadrant persistent on both arterial and delayed phases. Surgery was consulted however no surgical intervention was planned as no tumor, obstruction or lead point was identified. A small bowel follow through with gastrografin was planned which revealed resolution of the intussusception. The patient subsequently got better with appropriate management of his Crohn's flare. He was discharged with recommendations to follow up with his Gastroenterologist for Vedolizomab infusions.

DISCUSSION:

Adult onset intussusception presents with recurrent abdominal pain and due to the rarity of the condition the diagnosis is often missed or delayed. Abdominal CT is the most useful test in diagnosing intussusception. While most cases of adult onset intussusception require a surgical approach it is important for clinicians to be aware that it is not true for all cases. Transient intussusception has been observed occasionally on small bowel barium studies in patients with Crohn's and adult celiac disease. If no lead point is identified or in cases of transient small-bowel intussusceptions in the setting of celiac sprue or Crohn's disease surgery is not needed. Non surgical reduction in cases when no necrosis is identified has several advantages including avoidance of surgery, limiting the extent of bowel resection and decrease the risk of complications such as short gut syndrome. When dealing with adult onset intussusception it is important to consider the aforementioned factors.
3222 A Rare Presentation of a Sizable Asymptomatic Abdominal Aortic Aneurysm
Authors: Baseer Yaseen
Published: October 2019

INTRODUCTION:

An abdominal aortic aneurysm (AAA) occurs as plaque builds up in vessels due to long-standing atherosclerosis. AAA takes years to develop and has few if any noticeable symptoms during this time. The larger an aneurysm becomes, the more likely symptoms develop including abdominal pain, back pin, dizziness and nausea. Significant risk factors for the development of AAA include smoking, hypertension, old age and family history. Aneurysms are more likely to burst and rupture as its size increases. Symptoms generally develop when an AAA becomes larger than 3 cm and elective repair should be considered for aneurysms measuring greater than 5.5 cm in size. Here, we present a case of an asymptomatic patient presenting to the hospital with an incidental AAA measuring 14 × 11 cm.

CASE DESCRIPTION/METHODS:

A 100-year-old female with a history of dementia, emphysema secondary to 25 pack year smoking, and anemia presented to the hospital with right leg pain after a recent mechanical fall. She denied any complaints at the time of admission including chest pain, shortness of breath, dizziness, nausea, abdominal pain and back pain. CT of the pelvis revealed acute right subcapital femoral neck fracture as well as a large infrarenal AAA measuring 14 × 11 cm with high risk for rupture. Cardiology was consulted for preoperative risk assessment for hemiarthroplasty versus percutaneous pinning of the right femoral neck. Patient was deemed too high of a risk for hemiarthroplasty and decision was made by medical team to pursue percutaneous pinning although patient remained high risk for surgery due to large AAA. While patient was in the operative room immediately prior to surgery, the patient developed hypotension and hypoxia. After discussion with family and medical team, patient opted for palliative care.

DISCUSSION:

The case highlights an extreme clinical presentation of a massive AAA that was found incidentally on imaging after a recent mechanical fall. Current guidelines recommend that an AAA should be surgically evaluation when its size exceeds 5.5 cm due to the life threatening risk of rupture. This patient's unusual presentation of a large AAA despite not presenting with any of the classical symptoms is concerning because of the risk associated with spontaneous rupture and death. More research is needed for the evaluation and screening of AAA's to prevent potential catastrophic complications.
3225 A Rare Case of Ruptured Jejunal Diverticulitis
Authors: Gurala Dhineshreddy , Idiculla Pretty Sara , Philipose Jobin , Krzyzak Michael , Mukherjee Indraneil
Published: October 2019

INTRODUCTION:

Small intestinal diverticula are very rare, and the incidence ranges from 0.06 to 1.3%. Among these, duodenal diverticula are more frequent in 79% of patients followed by 18% in jejunum or ileum and 3% in all segments together. A jejunal diverticulum is usually asymptomatic, but only 10% develop complications. We report a unique case of a 70-year old female who presented with confusion, likely due to sepsis from perforated jejunal diverticulitis, that was successfully managed with initial resuscitation and definitive surgery.

CASE DESCRIPTION/METHODS:

A 76-year old female presented to the emergency room with confusion and epigastric pain for two days prior to presentation. Vital signs were stable. Physical examination was positive for mild epigastric tenderness. Laboratory results were normal except for leukocytosis of 15000, with left shift. Plain radiograph of the abdomen was negative for obstruction or perforation. Computed Tomography (CT) of the abdomen with oral and intravenous contrast showed the loop of thickened and edematous mid-jejunum and intraperitoneal free air consistent with perforated small bowel diverticulitis with abscess formation (Figure 1). She was initially resuscitated with intravenous fluids and was started on intravenous antibiotics. She underwent diagnostic laparoscopy with small bowel resection, primary anastomosis, drainage of the diverticular abscess. Pathology of resected jejunum was positive for diverticular disease with perforation. She did well postoperatively, tolerated diet, and discharged to home without any complications.

DISCUSSION:

Jejunal diverticula are usually multiple localized in proximal jejunum, develops as a result of herniation of mucosa, submucosa, serosa through muscular layer of bowel at the point of where vasa recta enter the muscular propria. Jejunal diverticulosis usually asymptomatic, only 10% develop complications. Perforation of jejunal diverticula is a severe complication that occurs in 2-6% of cases. A plain radiograph is the initial testing, but CT or Magnetic Resonance Imaging (MRI) is a gold standard for diagnosis. Acute uncomplicated jejunal diverticulitis is managed with intravenous fluids, bowel rest, and antibiotics. Acute Complicated diverticulitis needs surgical intervention such as laparotomy with segmental small bowel resection with primary anastomosis. Jejunal diverticulitis requires a high degree of clinical suspicion given the low incidence of the condition and increase in mortality after surgery up to 24%.
3233 Massive Gastric Distention… Aaand It's Gone!
Authors: Mulat Baruh , Boroda Konstantin , Hertan Hilary
Published: October 2019

INTRODUCTION:

Gastric outlet obstruction is usually a sequelae of malignancy or PUD. When these causes are ruled out, other etiologies like gastroparesis should be considered.

CASE DESCRIPTION/METHODS:

A 72 year old female nursing home resident with a history of schizophrenia, depression, dementia (on Mirtazapine, Trazodone, and Donepezil), hypothyroidism, and longstanding type 2 diabetes with a Hemoglobin A1c of 6.1% was admitted with abdominal pain, emesis, and increased agitation. CT of the abdomen and pelvis revealed marked fluid filled distention of the stomach and proximal duodenum with no clear gastric outlet obstruction (Figure 1). Nasogastric tube placement was not tolerated by the patient. She was then made NPO and gradually advanced to a clear liquid diet. EGD performed six days later revealed a normal duodenum with mild stomach distention and no evidence of gastric outlet obstruction (Figures 2 and 3). Her symptoms then resolved and she was discharged.

DISCUSSION:

Our patient presented with non-obstructive, massive gastric distention, which improved rapidly with dietary restriction. Gastroparesis was thought to be the primary diagnosis due to her risk factors of diabetes and psychotropic medication use. The cause of gastroparesis is most commonly idiopathic, but it is also linked to diabetes, certain medications, postsurgical injuries, hypothyroidism, and post viral syndromes. In diabetes oxidative stress and long-standing disease leading to autonomic dysfunction are postulated mechanisms for gastroparesis. A recent review demonstrated the following prevalence of gastroparesis over a 10 year time period: 5.2% in Type 1 Diabetes, 1.0% in Type 2 Diabetes, and 0.2% in controls. Additionally, antidepressants and antipsychotic medications (eg, anticholinergic, dopamine agonists, tricyclic antidepressants) have been suggested as possible triggers for gastroparesis. Commonly prescribed medications including calcium channel blockers, narcotics, glucagon-like peptide-1 agonists and amylin analogues have similar effects. Our case is interesting as it demonstrates how gastric distention can develop to a massive extent in the setting of offending drugs, despite well controlled diabetes. Patients with longstanding diabetes taking multiple psychiatric medications are at a particularly high risk of developing gastroparesis.
3235 Black Stomach: A Rare Clinical Entity in a Patient With Recurrent Primary Sclerosing Cholangitis With Cirrhosis
Authors: Stone Bryan , Real Mark , Hsu Christine
Published: October 2019

INTRODUCTION:

Acute gastric necrosis is rarely encountered given the stomach's rich vascular distribution and collateral circulation. Reported causes of gastric necrosis include gastric outlet obstruction, intrathoracic herniation, ingestion of caustic substances, anorexia nervosa and bulimia, and systemic hypotension. We present a case of “black stomach” secondary to persistent shock in the setting of end-stage liver disease.

CASE DESCRIPTION/METHODS:

A 33-year-old female with a history of primary sclerosing cholangitis status post orthotopic liver transplant in 2017 was initially hospitalized for pneumonia complicated by worsening graft function (MELD 38). Liver biopsy confirmed recurrent PSC with cirrhosis. Her course deteriorated after developing multiple episodes of coffee-ground emesis and melena requiring pressors. Initial EGD showed mild portal hypertensive gastropathy and two, 5 mm clean-based ulcers in the gastric antrum. No esophageal varices were visualized. Despite medical therapy, her melena and hypotension continued, leading to acute renal failure requiring CVVH. Repeat EGD two days later showed an adherent clot in the gastric fundus and severe portal hypertensive gastropathy with spontaneous oozing. Despite supportive measures, she continued to have melena. A third EGD showed a large blood clot in the fundus that was unable to be removed. Friable mucosa was noted throughout, as well as a non-healing, clean-based antral ulcer. Two days later, a fourth EGD revealed mucosa in the fundus and proximal body that appeared black and diffusely necrotic with sloughing of mucosa, with normal mucosa distally. The patient was not a candidate for IR embolization, TIPS procedure or surgery. One week later, she decompensated and died of septic shock from VRE bacteremia.

DISCUSSION:

Our case demonstrates that persistent gastric ischemia in the setting of shock and underlying end-stage liver disease results in gastric necrosis noted endoscopically over the course of a week. It is possible that the patient's underlying decompensated graft cirrhosis predisposed her to developing segmental gastric necrosis and “black stomach” in the area supplied and drained by the left gastric vessels, which can be affected by shock and portal congestion. Despite aggressive measures and supportive care, gastric necrosis carries a high morbidity and mortality. Therefore, a high index of clinical suspicion is required to make an early diagnosis in order to guide potential therapeutic interventions in such critically ill patients.
3244 Acute Massive Gastric Distention in an Adult Patient With Cerebral Palsy
Authors: Cezar Carensa , Ayoola Rotimi , Osho Azeez , Aduli Farshad
Published: October 2019

INTRODUCTION:

Cerebral Palsy (CP) is a motor impairment secondary to neurological abnormalities in the central and peripheral nervous systems. CP can affect the functioning of the gastrointestinal system. Common complications include dysphagia, constipation, regurgitation, vomiting and gastroesophageal reflux. Severe gastric distension is a very rare complication of CP with a high mortality risk. We present a case of severe gastric distension in a patient with CP.

CASE DESCRIPTION/METHODS:

A non-verbal 39-year-old man with history of CP, spastic quadriplegia, deep vein thrombosis, and obstipation status post colectomy and subtotal ileostomy presented with a 2-day history of poor oral intake, abdominal distention, and decreased ileostomy output. Patient had a similar presentation one-month prior. Vitals were within normal. Physical exam showed abdominal distension, abdominal tenderness, absent bowel sounds and tympany to percussion. Labs were normal except for hemoglobin of 8.3 g/dL, blood urea nitrogen of 42 mg/dL and a creatinine of 1.65 mg/dL. Computerized tomography showed markedly dilated stomach with air-fluid levels. Patient was placed on nothing by mouth. A nasogastric tube was placed to suction. An endoscopy was done that was negative for gastric outlet obstruction (GOO). Xrays showed resolution of the gastric distension. Patient tolerated liquids and then solids. He began to have stool output from the ileostomy and was discharged.

DISCUSSION:

Gastric distension in patients with CP is not fully understood. Gastric emptying and motility of the foregut are regulated by the vagus nerve. Predisposing factors include autonomic neuropathy, neuromuscular incoordination, air swallowing and malposition of the stomach. Death may be due to respiratory compromise by lung compression from a dilated stomach, or rupture of the stomach. Gastric distension can be seen in patients with GOO or diabetes mellitus with gastroparesis. Another cause is severe kyphoscoliosis of the vertebral columns causing malpositioning and posterior displacement resulting in mechanical obstruction preventing spontaneous decompression. In cases of recurrent or severe gastric distension, worsening of symptoms, or non-resolving distension after supportive management a venting gastrostomy may be needed. Severe gastric dilatation, with or without rupture, should be considered a potential cause of unexpected death in individuals with severe mental and physical disabilities.
3247 Don't Clean the Stomach With a Kitchen Sponge: Case of a Kitchen Sponge Presenting as a Gastric Bezoar
Authors: Mulat Baruh , Nawaz Waqas , Hertan Hilary
Published: October 2019

INTRODUCTION:

Gastric bezoars are rare and caused by ingestion of indigestible material. They are called polybezoars if resulted from the accumulation of ingested foreign bodies in the stomach. We present a rare case of a gastric polybezoar secondary to the ingestion of a kitchen sponge in a 53-year-old female which presented a significant endoscopic challenge during the removal.

CASE DESCRIPTION/METHODS:

A 53-year-old female with a history of major depressive disorder and multiple abdominal surgeries including gastric bypass was admitted for abdominal pain and vomiting for the last three days. Physical exam was remarkable for abdominal scars from prior surgeries. Initial laboratory data showed elevated blood urea nitrogen and creatinine. CT abdomen showed evidence of gastric bypass with a foreign body in the gastric remnant without any intestinal obstruction. On further questioning, she revealed that she had ingested the pieces of a kitchen sponge one week ago. An upper endoscopy was done which revealed an eight cm polybezoar made up of food material coating a sponge in the gastric pouch. The bezoar was fragmented using the biopsy forceps and removal was accomplished using Roth net and Trapezoid basket. An over tube was used to facilitate the repeated passages of the scope. The procedure lasted for two hours thus presenting a significant challenge.

DISCUSSION:

A gastric bezoar is defined as a foreign body resulting from the accumulation of ingested material in the stomach. It is a rare condition with the incidence of 0.4-4%. Depending on the type of the ingested material, it can be a phytobezoar (fibers), a trichobezoar (hair), a pharmacobezoar (medications), a polybezoar (foreign body) or a lactobezoar (milk product). Stomach is the most common site involved. Most bezoars are clinically asymptomatic due to large capacity of the stomach and are diagnosed incidentally on imaging or endoscopy done for other reasons. When symptomatic, they may present with epigastric pain, vomiting, hematemesis or small bowel obstruction. The major risk factors for the formation of the bezoars are conditions associated with gastric dysmotility, previous gastric surgery and psychiatric disorders. Complicated gastric bezoars impose a great challenge to an endoscopist. Several modalities have been suggested for the management of bezoar including chemical dissolution (sodium bicarbonate, Coca Cola lavage etc.) and endoscopic fragmentation with removal. Surgery is reserved for intestinal obstruction or a failed endoscopic treatment.