Bupivacaine-Induced Hepatotoxicity in a Healthy Patient Without Chronic Liver Disease After Shoulder Arthroscopy

Introduction: Bupivacaine is a local anesthetic which has been increasingly used in the post-operative state for pain control. Hepatotoxicity is a rare complication, and few cases are reported in patients with chronic liver disease. We present a case of acute liver injury from bupivacaine use in a healthy patient without prior history of liver disease. Case Description/Methods: A 68-year-old female with a past medical history of primary hypertension and recent nontraumatic complete tear of the right rotator cuff, presents to the hospital with fatigue, loss of appetite, and nausea. She recently underwent an arthroscopy of the right shoulder with repair of the rotator cuff two weeks prior. Her surgery was uncomplicated, and patient was started on bupivacaine ONQ pump infusion at 5 ml/hr for three days for post-operative pain. Further history reveals patient is non-alcoholic without prior liver disease, including cirrhosis. Review of systems is concerning for associated generalized abdominal discomfort. Physical exam demonstrated jaundice with scleral icterus with mild periumbilical tenderness to palpation without hepatosplenomegaly or ascites. Labs demonstrated elevated total bilirubin of 10.2 mg/dL with Alkaline phosphatase, ALT, and AST being 924 U/L, 429 U/L, and 279 U/L, respectively. Imaging studies including CT abdomen and pelvis with contrast, abdominal ultrasound, MRCP, and portal vein doppler were negative. Additional work up for underlying liver disease including acetaminophen and ethanol levels, SARS-CoV2, Hepatitis panel, EBV antigen, and urine toxicology were negative. It was determined patient had bupivacaine induced hepatotoxicity. Patient's health improved with conservative management and she was discharged with instructions for close monitoring of her LFTs. Discussion(s): Bupivacaine is an amino-amide anesthetic which binds to the intracellular portion of voltage-gated sodium channels and prevents depolarization of pain signals. It is metabolized by the liver and thus reports of hepatotoxicity, although rare, occur in patients with underlying liver pathology. Our patient became symptomatic with acute rise in LFTs. An extensive workup for other etiologies of acute liver toxicity was negative. Rapid vascular uptake of the drug is the most common reason for bupivacaine toxicity;and this remains a possibility for the mechanism of toxicity in our patient. A prior case report of bupivacaine hepatotoxicity demonstrated a cholestatic pattern, which is consistent with our findings.

Splanchnic vein thrombosis and Budd-Chiari syndrome after SARS-CoV- 2 vaccination-Incidence of VITT

Background: Several studies have been published on a rare side effect of severe venous thrombosis at unusual sites and thrombocytopenia after vaccination against SARS-CoV- 2, referred to as vaccine-induced immune thrombocytopenia and thrombosis (VITT). Aim(s): To identify new cases of acute splanchnic vein thrombosis (SVT) or Budd-Chiari Syndrome (BCS) who presented following SARS-CoV- 2 vaccination in the Vascular Liver Disease Group (VALDIG) network, and to evaluate the incidence of VITT. Method(s): We conducted a prospective international cohort study between May 1st, 2021 and January 10th, 2022, on consecutive patients with acute SVT or BCS who presented within 6 weeks following any type or dose of SARS-CoV- 2 vaccination. Anonymous data were collected including baseline characteristics, risk factors, treatment and survival. Cases were identified as definite VITT, probable VITT or possible VITT or unlikely VITT as defined by Pavord et al (NEJM 2021). Result(s): 25 patients with acute (N = 24) or recurrent (N = 1) SVT or BCS were collected from 14 centers in 4 countries (after ChAdOx1 nCoV-19 N = 11, BNT162b2 N = 9, Ad26.COV2.S N = 1, mRNA-1273 N = 1). Median time after vaccination to symptoms was 10 days (2-40). Median age was 52.5 years (21-66), 52% were female. Three patients (12%) fulfilled criteria for definite VITT, 6 (24%) for probable VITT, 2 (8%) for possible VITT, 14 (56%) for unlikely VITT. Thrombosis was located in the portal vein (N = 20), hepatic vein(s) (N = 9), mesenteric vein (N = 18) or splenic vein (N = 9). Concomitant extra-abdominal thrombosis was seen in 5 patients (20%). Patients were treated with LMWH (60%), DOACs (24%) or VKA (40%). Six (2/3 with definite VITT) received IVIG. Thrombophilia was found in 5 patients and 3 had a myeloproliferative neoplasm. Conclusion(s): 25 cases of acute SVT or BCS following SARS-CoV- 2 vaccination were identified. Although definite VITT was rare (12%), no underlying disorder was identified in the majority of patients, contrary to 'typical' cases of SVT and BCS.

ACUTE HEPATIC SEQUESTRATION CRISIS: AN OFTEN UNDERDIAGNOSED AND FATAL SYNDROME

SESSION TITLE: Critical Renal and Endocrine Disorders Case Report Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/17/2022 12:15 pm - 01:15 pm INTRODUCTION: Sickle Cell Disease (SCD) is an autosomal recessive disease characterized by an abnormal beta-globin chain of hemoglobin (Hb) that leads to malformed sickled cells with a multitude of downstream microvascular occlusions and anemia. While splenic infarction is by far the most common gastrointestinal (GI) manifestation, vaso-occlusion may occur in the liver, leading to an acute hepatic crisis. Acute hepatic sequestration of sickled erythrocytes is an exceedingly rare manifestation. CASE PRESENTATION: A 43-year-old man with homozygous sickle cell disease complicated by End-Stage renal disease was admitted with generalized malaise, right upper quadrant (RUQ) abdominal pain, nausea and vomiting. He was febrile with a temperature of 38.1°C, hypotensive with a blood pressure of 93/61 mmHg and tachycardic with a heart rate of 120 bpm. He was lethargic and uncomfortable with diffuse abdominal tenderness without guarding. Due to concern for septic shock, blood cultures, COVID PCR and influenza were obtained, and the patient was rapidly transferred to the intensive care unit for closer monitoring. Empiric vancomycin and cefepime were started promptly. The initial hemoglobin level was 6.1mg/dL with a leukocytosis of 31.2 K/CUMM and absolute neutrophil count of 21.8 K/CUMM;total hyperbilirubinemia of 17.45 mg/dL, direct hyperbilirubinemia of 11.46mg/dL and elevated INR at 1.66. Computed tomography of the abdomen and pelvis without contrast showed a known 4 cm cystic lesion of the right hepatic lobe and atrophic kidneys. Duplex flow of the abdomen and pelvis showed no portal vein thrombosis and patent flow in the portal vein and artery. Over the course of several hours, the patient's hemoglobin dropped to 3.8mg/dL with a steep rise in LDH and total bilirubin to 632 U/L and 27.04 mg/dL, respectively consistent with hepatic sequestration crisis. Patient was transfused with two units of packed red blood cells, fluid hydration and initiation of erythrocyte exchange transfusion. Prior to receiving exchange transfusion, the patient experienced rapid clinical deterioration with subsequent pulseless electrical activity. Return of spontaneous circulation was achieved transiently however patient's family at this point opted for palliative measures and the patient passed away shortly thereafter. DISCUSSION: Complications of SCD manifest in multiple organ systems. One of the few acute manifestations, hepatic sequestration crisis, is often unfamiliar to many clinicians and left unrecognized, results in poor clinical outcomes. It is rarely encountered and treatment options with blood and, more importantly, exchange transfusion remains often underutilized. CONCLUSIONS: Acute hepatic sequestration crisis is an often-unrecognized manifestation of SCD in which delay in diagnosis and prompt treatment with exchange and blood transfusions may impart a significant risk of mortality in an already prone patient population. Reference #1: Shah R, Taborda C, Chawla S. Acute and chronic hepatobiliary manifestations of sickle cell disease: a review World J Gastrointestinal Pathophysiology 2017;8(3): 108-116 Reference #2: Norris W. Acute hepatic sequestration in sickle cell disease. J of the National Medical Association 2004;96: 1235-1239 Reference #3: Praharaj D, Anand A. Sickle Hepatopathy J of Clinical and Experimental Hepatology 2021;11: 82-96 DISCLOSURES: No relevant relationships by Karim Dirani No relevant relationships by Georgiana Marusca No relevant relationships by Aryan Shiari

ACUTE MESENTERIC ISCHEMIA IN COVID-19: A DEVASTATING SEQUELAE OF A DEVASTATING DISEASE

SESSION TITLE: Extraordinary Cardiovascular Reports SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 01:35 pm - 02:35 pm INTRODUCTION: The COVID-19 pandemic has reshaped modern history with an estimated death count over 6 million globally. Symptoms are primarily respiratory;however, COVID also confers an increased risk for hypercoagulability with the common presentations of venous and small vessel arterial thrombi (1). Acute mesenteric ischemia (AMI) is rare. We present a case of severe AMI with arterial and venous thrombi related to COVID. CASE PRESENTATION: A 50-year-old non-COVID-vaccinated male with a history of alcohol abuse presented with 1 day of emesis and abdominal pain and was found to be COVID-19 positive without respiratory symptoms. Computed tomography angiogram of the chest, abdomen and pelvis revealed normal lungs, extensive non-calcified thrombi in the abdominal aorta extending into the celiac artery causing severe stenosis, complete occlusion of the superior mesenteric, right portal, and splenic veins, partial occlusion of the extrahepatic portal vein, left lower pulmonary embolism, small bowel perfusion injury, and splenic and right hepatic lobe infarcts. He denied a personal or family history of hypercoagulability. The patient was placed on a heparin drip and underwent placement of a transjugular intrahepatic portosystemic shunt and an infusion catheter for administration of tissue plasminogen activator into the portal vein. He ultimately required a thrombectomy. Later imaging showed patency of previously occluded vessels and resolution of arterial thrombus. Over the course of his hospitalization, his respiratory status did decompensate, and he required 13 days of mechanical ventilation, after which he was extubated, transitioned to warfarin, and discharged. DISCUSSION: AMI in COVID has been identified as a rare but serious complication with a reported incidence of 3-4%, with a reported mortality of up to 47% in all-cause-related AMI(2,3). COVID causes a prothrombotic state due to its affinity to angiotensin-converting enzyme-2(ACE2) receptors on enterocytes and endothelium, allowing it to infect the cells and causing direct damage to bowel tissue and vessels. The binding of ACE2 also increases IL-6, inducing cytokine storm and hypercoagulability (1). While there are no clear guidelines, treatment mainly involves revascularization and removal of necrotic bowel. Anticoagulation generally has favorable results within 48 hours and invasive intervention is not required (1,4). Thus, early recognition of AMI as a potential complication of COVID is essential for early treatment and reduction of the staggering morbidity and mortality. CONCLUSIONS: While the incidence of AMI in COVID is low, it can have severe effects on patients and requires early recognition and treatment. Further studies are needed to develop awareness of the disease, therefore improving surveillance and standard of care to minimize the chances of these poor outcomes. Reference #1: Patel, Suyog et al. "Bowel ischemia in COVID-19: A systematic review.” International journal of clinical practice vol. 75,12 (2021): e14930. doi:10.1111/ijcp.14930 Reference #2: Kaafarani, Haytham M A et al. "Gastrointestinal Complications in Critically Ill Patients With COVID-19.” Annals of surgery vol. 272,2 (2020): e61-e62. doi:10.1097/SLA.0000000000004004 Reference #3: Cudnik, Michael T et al. "The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis.” Academic emergency medicine : official journal of the Society for Academic Emergency Medicine vol. 20,11 (2013): 1087-100. doi:10.1111/acem.12254 Chen, Can et al. "Acute Mesenteric Ischemia in Patients with COVID-19: Review of the literature.” Journal of the National Medical Association vol. 114,1 (2022): 47-55. doi:10.1016/j.jnma.2021.12.003 DISCLOSURES: No relevant relationships by Mohamed Abdelhabib No relevant relationships by Naomi Habib No relevant relationships by Daniel Rabulinski No relevant relationships by Suresh Uppalapu

Superior Mesenteric Vein and Portal Vein Thrombosis in a Patient With COVID-19: A Rare Case

A 68-year-old man was referred to the general surgeons on account of his abdominal pain of unknown cause. He had contracted COVID-19, 9 days prior. CT chest abdomen and pelvis revealed an extensive thrombus extending from the portal vein to the superior mesenteric vein. Further investigation ruled out haematological causes, and COVID-19 was determined to be the cause. He was treated with an extended course of therapeutic dose low molecular weight heparin under the guidance of the haematology team. He was discharged once he was clinically stable and pain-free, with a plan to be followed up by both the surgeons and haematologists. This case highlights the different ways in which COVID-19 presents, and the need for clearer guidance on the treatment and prevention of thromboembolism in COVID-19.

Modern a COVID-19 Vaccine-Induced Immune Thrombosis of Central Retinal Artery-Report of a Case

Objective: To report a rarely isolated central retinal artery occlusion (CRAO) following Coronavirus disease 2019 (COVID-19) Vaccine Moderna (mRNA-1273). Background: COVID-19 caused by severe acute respiratory syndrome coronavirus was firstly reported in Dec 2019 and became pandemic as of Mar 2020. Fortunately, novel rapidly developed COVID-19 vaccines are capable of lessening the pandemic effectively. As billions of people vaccinated, however, COVID-19 vaccine-induced thrombosis (VIT) are gradually emerging. Design/Methods: A previously healthy 70-year-old man presented with acute painless visual loss of the right eye five days after the first dose of Moderna vaccine. On examination of the right eye, visual acuity (VA) was counting finger at 15 cm. Fundoscopy revealed a diffuse whitened retina with cherry-red spot. Optical coherence tomography (OCT) showed hyperreflectivity. Screening tests for platelet and D-Dimer levels were unremarkable. CRAO was treated with clopidogrel and hyperbaric oxygen therapy. The serum level of anti-platelet factor-4 (PF4) antibody was 73.34 ng/ml (ref, 0-49.99 ng/ml).Two months later, VA was counting finger at 10 cm3 and OCT revealed hyperreflectivity and mild inner retina atrophy Results: COVID-19 vaccine-induced thrombosis and thrombocytopenia (VITT) based on the victims receiving AstraZeneca and Johnson & Johnson vaccines is through autoimmune antibody against PF4. VITT is typically manifested within 6-24 days post-vaccination;thrombotic sites are in the cerebral sinus, portal vein, splanchnic vein, and pulmonary emboli;as well as thrombocytopenia and increased level of D-Dimer. Our patient had isolated CRAO five days post-Moderna vaccination but normal platelet count and D-Dimer level. Moreover, VIT with isolated CRAO was not published on PubMed. Conclusions: VIT could occur in the unusual site such as CRAO in our case. Normal platelet and D-Dimer levels might not be sensitive tools to exclude VIT. Suspected patient with thrombotic event after COVID-19 vaccines should have anti-PF4 antibody test to assure an effective treatment.

LDLT-donor: Impact of complex bilio-vascular donor anatomy on donor and recipient morbidity in adult LDLT

Rationale: With increasing experience, and widespread application of LDLT worldwide, experienced LDLT centers now accept right or left lobe donors with complex bilio-vascular anatomy. Though there are a few reports from high volume centers that this may not have an impact on graft or recipient outcome, the true impact in terms of vascular and biliary complications in the recipient and the donor is not well studied. Moreover, accepting these donors may also have an impact on donor morbidity, with possible higher incidence of biliary, vascular complications, re-explorations etc. The true implication would probably be identified if we were to not only analyze the absolute incidence, but also the incidence compared to a cohort of donors and recipients with standard vascular and biliary anatomy. This can probably done only in a multicenter study, where there are different donor acceptance criteria, and probably slightly variant surgical techniques. Aims: Primary objective -This study aims to determine the differences in incidence of bilio-vascular complications and morbidity in recipients of LDLT receiving grafts from donors with complex bilio-vascular anatomy, compared to those receiving grafts with single artery, portal vein, bile duct. Secondary objectives -To determine whether presence of complex bilio-vascular anatomy has an impact on donor complications, and adds to donor morbidity. To determine whether number (of graft artery/PV/ducts), type (according to classification of bilio-vascular donor anatomy), or type of anastomoses (using loupes vs. microscope for artery and bile duct, plasty with straight extension vs. Y graft in PV, duct to duct vs. Roux for multiple ducts etc.) determine incidence of complications. To determine whether complications have an impact on long term graft and patient outcomes. Update: While the two centers Medanta-The Medicity, India, and Asan Medical Center, South Korea have already started accumulating data on the subject in the designed form, we are awaiting Ethical Committee approval for the multicenter study. This has been delayed given the COVID pandemic. We have already received applications from 4 other centers: Icahn School of Medicine at Mount Sinai, RMTI, NY, USA, National Medical Research Center of transplantology and Artificial Organs named after V.I. Shumakov/ Surgical Department #2 (Liver Transplantation), National Medical Research Center of transplantology and Artificial Organs named after V.I. Shumakov/ Surgical Department #2 (Liver Transplantation), and University of Unimore, Modena, Italy. We will accept these other centers for the study as soon as we have IRB Approval.

Correlation of Portal Vein Diameter as a Reflection of Portal Hypertension With Clinical and Laboratory Parameters in Chronic Liver Disease

Chronic liver disease (CLD) patients develop portal hypertension which lead to complications like splenomegaly, ascites and esophageal varices. Portal hypertension is defined as hepatic venous pressure gradient more than 5mmHg, being invasive it is difficult to measure. Some studies show that increased portal vein diameter (PVD) on ultrasonography correlate with oesophageal varices and can indicate portal hypertension. Studies correlating PVD with other complications of portal hypertension like ascites and spleen size are lacking. Aim of this study was to correlate portal vein diameter with ascites, spleen size, thrombocytopenia and prognostic markers like Child-Turcotte Pugh (CTP) score and Model for End stage Liver Disease (MELD) score in Chronic liver disease patients. MATERIAL: This was a cross-sectional observational study of patients with Chronic liver disease conducted at tertiary care teaching hospital. All patient underwent clinical history, examination, blood testing and ultrasonography. Data collected was analysed by using statistical tests. OBSERVATION: Out of 97 CLD patients taken in study, the mean age of patients was 47.39 ± 12.64 year and majority were male (75.3%). Most common etiological factor was alcohol (in 53.7%). On clinical examination, 55.7% patients had pallor, 54.6% had icterus. Chest radiograph shows pleural effusion in 14.4% patients. Mean portal vein diameter was found to be 12.31 ± 2.71mm. Correlation coefficient of portal vein diameter with spleen size was 0.3 with p value of 0.004 suggesting a positive correlation. Parameters like thrombocytopenia, CTP score and MELD score correlation coefficient was -0.2(p-value: 0.066), 0.1(p value: 0.463) and 0.0(p-value: 0.725) respectively. The mean of PVD(mm) in ascites group was 12.43 and non ascites group was 11.92. Strength of association was 0.08 (Point Biserial correlation) indicating no association. CONCLUSION: Portal vein diameter had positive correlation with spleen size which is statistically significant in our study. No significant correlation was observed between PVD with ascites, thrombocytopenia, CTP score and MELD score. © Journal of the Association of Physicians of India 2011.

Congenital Portosystemic Shunts in Children: A Case Series From Single Centre

Background: Congenital portosystemic venous shunts (CPSS) are uncommon foetal vascular developmental anomalies where splanchnic venous flow bypasses liver. Four cases of CPSS are reported at our centre. Case Summary (1) Eight years old female child presented with Dengue with no features of chronic liver disease and normal liver function test (LFT). Ultrasonography (UGS) abdomen reported an incidental finding of abnormal vascular shunt in liver. Further imaging revealed an anastomosis between portal vein and intrahepatic part of inferior vena cava (IVC), hypoplastic portal vein and multiple nodules in bilateral liver lobes. Interventional Radiologist closed the anastomosis using vascular plug. Child sustained the procedure well. (2) Two months old female patient presented with high GGTP cholestasis, dysmorphism and deranged LFT. On USG abdomen there was intrahepatic portosystemic shunt. MDCT abdomen revealed 2 vascular shunts between left portal vein to middle hepatic vein and left portal vein. Cholestasis responded with symptomatic treatment, hence being followed-up for observation till 1year of age for complications and possibility of spontaneous closure. (3) Twenty-two days old, full term female child presented with convulsions and high GGTP cholestasis with multiple hematomas in brain. LFTs were deranged. 2D-ECHO showed small PFO. USG abdomen suggested a channel between left portal vein and hepatic vein. Patient tested COVID positive hence quarantined now and further evaluation is awaited. (4) One day old, late preterm male baby presented with respiratory distress and pulmonary hypertension with antenatal scan suggesting ductus venous agenesis with hepatic vascular malformation. Patient developed cholestasis with deranged LFT. 2D-ECHO showed PDA and ASD. MDCT abdomen revealed connection between main portal vein and intrahepatic IVC. Conclusions: CPSS has heterogeneous presentation. It can be diagnosed antenatal or postnatal, may be asymptomatic or may present as neonatal cholestasis and may be associated with anomalies. Management may vary from case to case and mainly depends on complications and age of presentation.

Necrotizing pancreatitis secondary to COVID-19

Case Report A 29-year-old male with a past medical history significant for severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection presented with epigastric pain, vomiting, fever, and inability to tolerate oral intake for 1 day. The patient was diagnosed with COVID-19 six weeks prior to presentation and four weeks later was diagnosed with idiopathic acute pancreatitis. He reported initial resolution of pain, however symptoms recurred for one day prior to this admission. The patient denied a history of alcohol use disorder. He is a lifetime nonsmoker. He does not take any medications. Vital signs were stable and he was afebrile. Labs on presentation were remarkable for elevated lipase of 1,527 and leukocytosis (23,000). The patient was still positive for COVID-19. However, he maintained oxygen saturation >95% on room air with no apparent distress. On physical examination, he had severe tenderness to palpation at the epigastrium and left upper and lower quadrants. Abdominal ultrasound had no evidence of gallstones. Triglyceride levels were within normal limits. CT abdomen showed necrotizing pancreatitis. MRCP showed evidence of acute pancreatitis with peripancreatic acute necrotic collection in the pancreatic head measuring up to 8.8 cm. Intrinsic T1 signal within the peripancreatic collection compatible with hemorrhagic pancreatitis. There was about 30% pancreatic parenchymal necrosis in the pancreatic head. A nonocclusive thrombus involving the main portal vein was also seen. Autoimmune workup was negative. In the setting of hemorrhagic pancreatitis, treatment with anticoagulation was deferred. The patient was treated with supportive measures, including intravenous fluids and adequate pain control with eventual advancement of his diet. He was started on empiric antibiotics and discharged for outpatient follow-up. SARS-CoV2 is known to cause many extrapulmonary effects, including transaminitis, myocarditis and pericarditis. There have been rare cases of SARS-CoV2-induced acute pancreatitis reported in the literature. The exact mechanism behind pancreatic injury in the setting of SARS-CoV2 infection remains unclear, but it is hypothesized that it may occur secondary to the presence of SARS-CoV2 receptors on the pancreas. The main receptor used by SARS-CoV2 is angiotensin- converting enzyme 2, which is also expressed in the GI tract. The most common causes of acute pancreatitis, including alcohol abuse, gallstones, medications and autoimmune causes were ruled out in our patient. In a patient with no particular risk factors, it is likely that SARS-CoV2 precipitated his first episode of acute pancreatitis. Moreover, it is well known that acute pancreatitis can commonly lead to necrotizing pancreatitis as the initial injury and inflammation from the first attack can cause the pancreatic tissue to necrotize and later become infected. This case highlights that SARS-CoV2 can be a possible etiology of acute pancreatitis and its local complications.