bluuebunny/crossref_metadata_2025_split huggingface dataset:
2266 Simultaneous Coronary Artery Bypass Grafting and Orthotopic Liver Transplantation
Authors: Lourdusamy Vennis , Albers Christopher , Kemmer Nyingi , Syed Rashid , Malespin Miguel , Dhanireddy Kiran , Lu Amy , Porubsky Marian , Dunning John , Agrawal Saurabh 
Published: October 2019

INTRODUCTION:
Patients with Decompensated Cirrhosis requiring Coronary artery bypass grafting (CABG) before liver transplantation are at significant risk of liver failure and death. We discuss a simultaneous CABG and liver transplantation approach to offer the best therapeutic option in such cases.

CASE DESCRIPTION/METHODS:
Our patient is a 56-year-old male with decompensated cirrhosis related to Ethanol and Fatty liver. He had severe coronary artery disease of the proximal, mid and distal Right coronary artery (RCA) not amenable to PCI. Once a donor liver allograft was found to be suitable, simultaneous CABG with liver transplantation was performed. Initially after procuring the saphenous vein from the right leg, a median sternotomy incision was performed and the pericardium was opened. Single vessel CABG to RCA was performed using the Saphenous vein graft off cardiopulmonary bypass. Chest was left open for the liver transplantation surgery. A bilateral subcostal incision with midline extension was performed. After explantation of the native liver, donor liver implantation was performed in a piggyback fashion where the venocavoplasty formed using middle and left hepatic vein of the recipient was anastomosed with the donor IVC. Venovenous bypass was not used. A Choledochocholedochostomy was performed. There were no major perioperative complications. A month after surgery, he has normal liver function and is recovering at home.

DISCUSSION:
In advanced liver disease patients needing liver transplantation and with concurrent CAD not amenable to PCI, it is not always possible to perform staged surgeries. In our case the anticipated morbidity and mortality rate was high with either surgery performed alone. Our patient’s probability of post operative mortality one year after major surgery according to the Mayo Clinic risk calculator was 32%. Recipient hepatectomy during liver transplantation in the background of severe CAD and with already reduced systemic pressure could result in major hemodynamic instability and acute coronary ischemia. He underwent simultaneous CABG and liver transplantation successfully. Survival rates of 80% have been reported in case series from more than a decade ago (Table 1). All patients should have preserved ventricular function. Simultaneous CABG and liver transplantation can offer the best therapeutic option with good perioperative and long term survival rate for patients with advanced liver disease who have severe CAD not amenable to PCI.
2267 Drug-Induced Autoimmune Hepatitis From Valerian Root Tea
Authors: Lourdusamy Vennis , Albers Christopher , Malespin Miguel , Kemmer Nyingi , Agrawal Saurabh , Syed Rashid 
Published: October 2019

INTRODUCTION:
Differentiating drug induced liver injury from other causes of acute hepatitis, especially autoimmune hepatitis can be difficult secondary to overlapping histological features and confounding laboratory abnormalities. Stopping the offending drug should usually result in resolution of liver injury. We describe a rare case of drug induced liver injury secondary to valerian root tea with overlapping features of autoimmune hepatitis which resolved with limited duration steroid therapy.

CASE DESCRIPTION/METHODS:
Our patient is a 47-year-old female with hypothyroidism who presented with acute onset of generalized abdominal discomfort, jaundice and vomiting without fever or confusion. She denied prior similar episodes. She reported regular use of valerian tea for insomnia for a duration of 3 months prior to presentation. Physical examination revealed jaundice, mild diffuse abdominal tenderness and no features of chronic liver disease. Labs showed elevated alanine aminotransferase of 2741 U/L, aspartate aminotransferase of 1847 U/L, alkaline phosphatase of 199 U/L, total bilirubin of 9.2 mg/dL, albumin of 3.4 g/dL and International normalized ratio of 1.4. Autoimmune work up revealed positive smooth muscle antibody, mildly elevated Immunoglobulin G of 1980 mg/dL and negative antinuclear and mitochondrial antibodies. Viral hepatitis panel was negative. Imaging of the abdomen was unremarkable. Liver biopsy showed severe acute hepatitis with extensive necroinflammatory activity with plasma cells and bridging necrosis without significant fibrosis. With no significant improvement in liver enzymes after stopping valerian root tea and with concern for autoimmune hepatitis, she was started on prednisone 60 mg daily with improvement of transaminitis. Transaminases have remained normal for several months after stopping prednisone (Table 1, Figure 1).

DISCUSSION:
Diagnosing autoimmune like drug induced liver injury and differentiating it from autoimmune hepatitis can be difficult. Steroids should be considered in cases with severe or prolonged elevation of liver enzymes that do not resolve after stopping the offending drug. Valerian root can cause severe form of autoimmune like drug induced liver injury that responds to steroids. Complete recovery is possible with steroids for limited duration. Relapse following steroid cessation should prompt further evaluation for autoimmune hepatitis.
2269 An Unprovoked Crisis: Hemophagocytic Lymphohistiocytosis
Authors: Zghyer Fawzi , Buffie Charlie , Wan David 
Published: October 2019

INTRODUCTION:
Hemophagocytic Lymphohistiocytosis (HLH) is a syndrome of dysregulated immune response due to abnormal immune activation which can be life threatening and very aggressive. Here we report a woman with jaundice found to have hemophagocytosis on a bone marrow aspirate.

CASE DESCRIPTION/METHODS:
A 48-year-old woman with no past medical history presented with a diffuse erythematous morbilliform rash, fever, chills, and headache for one week. The headache is described as throbbing with associated photophobia. There was no history of travel, or hiking. On physical exam, the patient was afebrile but tachycardic, her BP was 85/64 mmHg, she was ill appearing, lethargic, and had scleral icterus. Her abdomen was tender to palpation with hepatosplenomegaly. She had a diffuse maculopapular rash. Labs were notable for hypoproliferative anemia, bandemia of 36%, thrombocytopenia, elevated AST/ALT, total bilirubin with predominance of direct bilirubin, alkaline phosphatase, and lactate. CT abdomen revealed moderate diffuse colonic wall thickening from the cecum to rectum. In the meantime, a very extensive infectious workup was sent. A bone marrow biopsy revealed a mildly hypercellular marrow with hemophagocytosis. Soluble CD-25 was found to be significantly elevated. The patient’s mental status continued to deteriorate and had to be transferred to MICU for airway protection. She received steroids, etoposide, and was eventually started on emapalumab due to progression in symptoms. The patient significantly improved, and was extubated. Over two weeks her mental status returned back to baseline.

DISCUSSION:
HLH results from the inability to downregulate active macrophages and lymphocytes. The primary tissue damage mechanism is thought to be due to cytokine release secondary to immune activation. The instigating factor for HLH is typically an infection or an altered immune homeostasis state. The typical presentation of HLH involves fevers, bicytopenia, splenomegaly, hemophagocytosis, elevated soluble CD25, hypertriglyceridema, hepatitis, and elevated ferritin. The dilemma in the case we present remains in the trigger for HLH; the extensive infectious workup was completely unrevealing, with the patient being negative to some of the very common viral pathogens. There is no family history of HLH or any immune related disorders, and she had no past medical history. With that being said, an episode of HLH of unknown etiology seems to have been the cause of her symptoms.
2270 The Path to Encephalopathy: A Case of Spontaneous Portosystemic Shunt Embolization
Authors: Jenkins Alexander , Skaret Michael M. , Hussell John J. , Kwok Ryan 
Published: October 2019

INTRODUCTION:
Hepatic encephalopathy (HE) is a debilitating complication of cirrhosis that can lead to alterations in consciousness, behavior, and overall functional decline. It has been suggested that up to 70% of patients with HE refractory to medical treatment have evidence of spontaneous portosystemic shunts (SPSS). While this is a relatively well-known sequela of longstanding cirrhosis, and current guidelines recommend at least consideration of closure of SPSS if found, the literature is limited regarding procedural occlusion of these potentially harmful vascular phenomena.

CASE DESCRIPTION/METHODS:
We present the case of a 70-year-old female with cirrhosis secondary to non-alcoholic steatohepatitis and progressive ascites requiring repeated therapeutic paracentesis. Over a short period, her need for paracentesis inexplicably declined and her HE simultaneously worsened, despite appropriately titrated lactulose. Imaging at this point revealed spontaneous splenosystemic and intrahepatic shunts. At the time of presentation, the patient’s Model for End-Stage Liver Disease (MELD) score was 14. Despite optimization of medical therapy and shunt embolization, the patient’s mental status did not improve. Upon further review of post-embolization imaging, there was evidence of shunt collateralization that still appeared to be patent. This patient’s lack of clinical improvement may have been due to several factors, but incomplete embolization of known shunts or presence of additional undiagnosed shunts seem most likely.

DISCUSSION:
As hepatic fibrosis progresses, portal hypertension rises steadily to the point where otherwise insignificant portosystemic microvasculature can engorge to sizes greater than 1 centimeter. This phenomenon can relieve portal hypertension at the expense of releasing higher levels of ammonia and other neurotoxins into systemic circulation, resulting in more pronounced HE. While the decision to pursue embolization should be individualized, the presence of SPSS should always be considered in the setting of refractory HE. A MELD score of 11 or less may be associated with more favorable outcomes following embolization of SPSS and a majority of patients show rapid clinical improvement of HE following successful shunt closure. Dedicated post-embolization imaging should be obtained, especially if a patient’s HE remains refractory after intervention.
2271 A Case of Portomesenteric Venous Thrombosis After Laparoscopic Sleeve Gastrectomy
Authors: Ramachandran Rajarajeshwari , Jani Niraj 
Published: October 2019

INTRODUCTION:
Portomesenteric venous thrombosis (PMVT) after laparoscopic sleeve gastrectomy (LSG) is exceedingly rare. We present the case of a 42-year-old woman who underwent an uncomplicated LSG and developed PMVT.

CASE DESCRIPTION/METHODS:
42-year-old woman with morbid obesity was admitted to the hospital with nausea, vomiting and epigastric pain on the 11th post-operative day after undergoing an uncomplicated LSG. Examination: Vital signs - BP 130/82 mmHg, pulse 100/min and temperature 36.9 °C. BMI – 45 kg/m2. Tenderness in the epigastric and umbilical area. No rebound or guarding. Bowel sounds were absent. Laboratory data: White blood cell count - 16.22 × 10³/microliter with neutrophil predominance, hemoglobin 12.3 g/deciliter, platelets 242 × 10³/microliter, lipase 15 IU/L, normal electrolyte levels/renal and hepatic function. Imaging studies: CT scan of the abdomen with contrast - portal and superior mesenteric thrombosis accompanied by peri-pancreatic edema and thickened small bowel loops. These findings were highly suggestive of venous ischemia. Anticoagulation with unfractionated heparin was initiated immediately and patient was aggressively volume resuscitated. Thrombophilia workup – negative factor V Leiden mutation, anti-cardiolipin antibodies and prothrombin/factor II gene mutation. Patient’s condition steadily improved and she was discharged home on oral anti-coagulation.

DISCUSSION:
PMVT is a rare complication of LSG with non-specific clinical presentation. Prompt diagnosis requires a high index of suspicion. Common clinical presentation includes abdominal pain, nausea, vomiting and low-grade fever. During LSG, there is increased intraabdominal pressure with carbon dioxide pneumoperitoneum. It is suspected that a decrease in the portal blood flow may contribute to the prothrombotic state in the portomesenteric circulation. The definitive diagnosis of PMVT is made with noninvasive imagining such as contrast-enhanced computed tomography (CT) or color Doppler ultrasonography. Therapeutic anticoagulation is recommended in stable patients with acute PMVT for 6-12 months. Acquired and inherited hypercoagulable conditions should be considered as predisposing factors for PMVT and require lifelong anticoagulation.
2272 A Case of Cryptococcal Hepatitis in HIV Patient With a Negative Serum Cryptococcal Antigen
Authors: Estifan Elias , Laxina Ian , Hlayhel Ahmad , Adib Sami , Baddoura Walid 
Published: October 2019

INTRODUCTION:
Infectious Cryptococcus neoformans occurs primarily in immunocompromised patients. The primary organ affected is the lungs, but CNS and skin involvement can also be seen. Disseminated Cryptococcosis can involve any organ in the body. However, hepatic involvement is rare. Here we offer a case of Cryptococcus hepatitis in a patient who presented with persistently elevated liver enzymes.

CASE DESCRIPTION/METHODS:
A 56-year-old Hispanic female with no known past medical history presented with fever, abdominal pain, nausea, unintentional weight loss, and diarrhea for two months. On physical examination, she was tachycardic with a heart rate of 110 bpm, and her abdomen was soft but tender to palpation in the right upper quadrant. Her liver function tests (LFTs) revealed elevated Aspartate Aminotransferase (AST) (415 U/L), elevated Alanine Aminotransferase (ALT) (201 U/L), elevated Alkaline Phosphatase (ALP) (763 U/L), normal total Bilirubin (0.9 mg/dl), and additional laboratory results in Table 1. Her HIV antigen screening was reactive, and absolute CD4 count was 22/ mcL. CT scan of the chest revealed two small calcified granulomas, for which she was started prophylactically on Azithromycin and TMP/SMZ. Over the course of her hospital stay, the patient's liver enzymes continued to trend upward while further workup ruled out hepatitis A, B, C, Wilson's disease, Hemochromatosis, AIH, PBC, PSC, other causes of viral hepatitis (CMV, EBV, HSV), with negative Histoplasma antibodies and negative serum Cryptococcal antigen titers. During the second week of hospitalization, her liver enzymes continued to rise with an ALP of 4046 U/L, AST of 407 U/L, and ALT of 276 U/L. With a persistent elevation of the liver enzymes without any definitive cause, an ultrasound-guided biopsy was warranted and performed. Pathology revealed Cryptococcal hepatitis (Figures 1 and 2), and the patient was started on a 15-day course of Amphotericin B with an 8-week course of Fluconazole 400 mg with LFTs nearly normalizing at 6 weeks.

DISCUSSION:
This case demonstrates an unusual manifestation of Cryptococcosis. Our patient did not present with the typical Cryptococcal pulmonary or central nervous system infection. As well, our patient's serum Cryptococcal antigen titers were negative, but biopsy results revealed Cryptococcal hepatitis, despite a very high sensitivity and specificity of the serum Cryptococcal antigen test. This case demonstrates the importance of maintaining a broad differential, specifically in immunocompromised patients.
2275 Anoxic Brain Injury From Hepatic Encephalopathy in Acute on Chronic Liver Failure: A Case Report
Authors: Aijazi Muaz , Noor Ahmed 
Published: October 2019

INTRODUCTION:
Hepatic encephalopathy (HE) is a complication seen in both acute liver failure and acute on chronic liver failure (ACLF). There is a paucity of data regarding IV HE resulting in global anoxic brain injury in those with ACLF. We present a case of anoxic brain injury from severe HE in a patient with ACLF.

CASE DESCRIPTION/METHODS:
74-year-old male with a past medical history of hypertension and CAD had recently been diagnosed with NASH cirrhosis when he presented to an outside hospital with ascites. Two months later he presented to our hospital with acute change in mental status. On presentation, the patient had normal vital signs. Physical examination revealed obtundation with response to noxious stimuli. There was no scleral icterus and labs were significant for WBC 5.1, platelet count 82, BUN/Cr 32/1.81, lactate 3.2, NH3 248, LFTs unremarkable, MELD Na 23. CT head and chest X-ray were negative for acute processes. On physical exam, patient was non-jaundiced with a mildly distended abdomen. He was started on lactulose every 6 hours. His mentation continuously deteriorated and he was intubated for airway protection and transferred to ICU 8 hours after admission, where he was started on rifaximin. Nephrology was consulted and CRRT was initiated after NH3 was noted to be >500 in the ICU. Repeat CT head now showed increased intracranial pressure, and subsequent MRI one day later showed global hypoxic ischemic injury. EEG with global slowing pattern signifying anoxic brain injury. Ammonia levels normalized on CRRT (although patient required dialysis for anuria after completion of 6 days of CRRT) and SSEP was done which did show evoked potentials, however no improvement was noted on neurological exam. Family eventually made the decision to transition care to comfort measures and the patient expired soon after.

DISCUSSION:
Overt cerebral edema leading to coma in HE and ACLF is rare given the chronicity of high ammonia and brain adaptation. The pathophysiologic mechanism for HE in ACLF is thought to be a combination of elevated serum ammonia and systemic inflammatory changes. Our attempts with hemodialysis did not change the clinical course suggesting irreversible tissue damage. Advanced therapies including embolization of portosystemic shunts was not pursued as none were identified on contrast enhanced imaging. Preventing decompensation and early recognition may be the modifiable factor in this high mortality disease.
2277 Multiple Liver Abscesses Caused by Streptococcus Intermedius Bacteremia in the Setting of a Routine Dental Cleaning
Authors: Hanna Angy , Odish Fadi , Imam Zaid , Dalal Bhavinkumar 
Published: October 2019

INTRODUCTION:
Streptococcus intermedius is a member of the Streptococcus anginosus group, also referred to as the “Streptococcus milleri” group. The S anginosus group is part of the oral cavity and GI tract normal flora. S intermedius has been known to cause abscesses in various locations in the body, most commonly in the liver and brain, however this is uncommon in healthy individuals. We report the clinical case of an immunocompetent 21-year-old male found to have multiple hepatic abscesses associated with streptococcus intermedius in the setting of a recent dental cleaning.

CASE DESCRIPTION/METHODS:
Patient is a 21-year-old immunocompetent male who presented to the hospital with complaint of right upper quadrant pain, fevers, and chills. He underwent a routine dental cleaning 3 months prior. On admission, his vitals were BP 88/53 mmHg, HR 142 beats/minute, RR 41 breaths/min and temperature 38.7C. His exam was remarkable for right upper quadrant tenderness and splenomegaly. The remainder of his diagnostic evaluation revealed (a) leukocytosis of 16,000 cells/mm3 with left shift, (b) elevated creatinine of 2.66 mg/dl, (c) elevated alkaline phosphatase of 573 U/L, aspartate aminotransferase of 102 U/L and alanine aminotransferase of 65 U/L with a bilirubin of 1.8 mg/dl. Computed-tomography (CT) of the abdomen and pelvis demonstrated multiple right lobe hepatic abscesses with the largest measuring 7.3 cm. Two sets of blood and fluid cultures from an ultrasound guided aspiration returned positive for S. Intermedius. The patient underwent 2 subsequent drainage procedures for the larger lesion. The patient demonstrated remarkable clinical recovery and was discharged with a 6-week course of PO ertapenem therapy. Follow-up laboratory values demonstrated resolution of his hematological abnormalities, acute kidney injury and transaminitis.

DISCUSSION:
Although S. intermedius has been been associated with pyogenic liver abscesses, it typically occurs in the setting of immunocompromised states. This case was particularly interesting in that it occurred in an immunocompetent young male in the setting of routine dental cleaning 3 months prior. While other case studies have reported liver abscesses from S. intermedius after dental cleaning, typical latency is 1 month from the dental cleaning while much longer latency is noted in the reported case. This raises the question of how long after a dental cleaning a patient may have an increased risk of developing abscesses, even if the patient is thought to be immunocompetent.
2278 Rapidly Progressive Hepatitis C After Liver Transplantation Treated With Glecaprevir/Pibrentasvir
Authors: Abdulla Hamza , Merwat Shehzad N. , Stevenson Heather , Kulkarni Rupak 
Published: October 2019

INTRODUCTION:
Hepatitis C recurrence following liver transplantation occurs in all patients with chronic HCV infection who have detectable serum HCV RNA levels prior to transplant. Less than 10% of these patients develop an acute and severe phenotype called fibrosing cholestatic hepatitis, which often involves fibrosis, rapid graft loss and decreased survival. The introduction of direct-acting antiviral agents (DAAs) have changed the paradigm of treatment of these patients.

CASE DESCRIPTION/METHODS:
A 62-year-old woman with a medical history of hepatitis C infection, hepatocellular carcinoma status post orthotropic liver transplantation, diabetes mellitus and hypertension who was hospitalized for fatigue and elevated liver chemistries following her liver transplantation. Laboratory tests showed a white cell count 6.67 × 103/μL, creatinine 1.1 mg/dL, aspartate aminotransferase 592 U/L, alanine aminotransferase 504U/L, alkaline phosphatase 312 U/L, bilirubin 3.5 mg/dL, albumin 2.9 g/dL. Acute hepatitis work up showed a positive hepatitis C virus antibodies with genotype 1B, with a viral load of 80 million IU/mL HCV RNA. HBsAg, HBc IgG, HBc IgM, and hepatitis A virus IgM were negative. Evaluation for Epstein-Barr virus, cytomegalovirus and herpes simplex virus were negative. Ultrasound of the abdomen revealed that the liver is normal in size, echotexture and contours. No focal hepatic lesions. Normal hepatic blood flow. The patient underwent liver biopsy that showed lymphocytic portal inflammation with frequent lobular apoptosis consistent with active chronic hepatitis C (MHAI: 5-6/18). Mild portal fibrosis (ISHAK FIBROSIS STAGE: 1/6) and minimal evidence of acute t cell-mediated rejection (rejection activity index: 1/9). During the patient hospitalization her liver chemistries significantly worsened and peaked to aspartate aminotransferase 740 U/L, alanine aminotransferase 511U/L, alkaline phosphatase 312 U/L, bilirubin 3.5 mg/dL. We decided to start the patient on Glecaprevir/Pibrentasvir for acute and severe hepatitis. Fourteen days after starting Glecaprevir/Pibrentasvir, the patient viral load decreased to 782 IU/mL HCV RNA and normalized liver chemistries with AST19 and ALT 27. The patient denied any adverse events due to the treatment.

DISCUSSION:
To our knowledge, this is the first case report of treating early and aggressive form of HCV recurrence with Glecaprevir/Pibrentasvir. The dramatic improvement of the patient suggest that DAA might be safe and effective in this situation.