A complex case of alcoholic : From withdrawal to multi-organ failure Sunil Dommaraju, Christopher Llerena, & Gina Qin ¹ Department of Medicine, University of Illinois at Chicago, Chicago IL, United States

Chief Complaint: Alcohol withdrawal, in vomit, request for detox Diagnosis with Assessment/Plan (On admission): Current Research and New Treatments 56 yo undomiciled male with history of ETOH use disorder and reported hx DTs, polysubstance abuse, and History of Present Illness: 56 yo undomiciled male with history of ETOH use disorder and reported hx multiple psychiatric comorbidities admitted for alcohol withdrawal symptoms with CIWA of 5 on admission and Current Research: UI Health employs the Maddrey discriminant withdrawal seizure/possible DTs, polysubstance abuse, cluster B traits w/ attempts, impulse concerning for variceal bleed. Patient with significant prior history for hospitalizations related to function[6]. Patient had DF = 8.2 on 1/19/2020. control disorder, bipolar disorder, and PTSD who presents with multiple complaints - alcohol . Problem list includes: 1) Alcohol withdrawal 2)Hematemesis 3) Hepatitis 2/2 chronic alcohol use withdrawal, hematemesis and request for admission for detox. Patient has relatively frequent DF = (4.6 x [prothrombin time (sec) - control prothrombin time admissions via ED with complaints of hematemesis, with 3 within the past month. Endorses plans to PLAN: (sec)]) + (serum ) enter Haymarket rehab after discharge. However, upon leaving VA after prior admission, was unable to 1. CIWA protocol q4-6H 3. Thiamine and glucose (prophy Wernicke’s encephalopathy) make it to Haymarket due to admission hours. Consequently, he resumed drinking; reports 18 beers 2. Benzos for withdrawal symptoms PRN 4. IV fluids (isotonic saline) Patients with a DF value >= 32 have high short-term mortality, and 1 pint of vodka daily. Reports last drink was 1am this morning. Reports that withdrawal symptoms, whereas those below 32 have low short-term mortality. Basic namely shakes, started shortly after discontinuation of alcohol use. Denies hallucinations, crawling. Clinical Course management traditionally consists of alcohol abstinence and Reports that he had of his beer this morning with some streaks of blood; nothing since then. Patient presented to the ED with symptoms related to alcohol withdrawal. Patient was admitted to General providing hemodynamic and nutritional support. When indicated Medicine and monitored on CIWA protocol (CIWA score 5). Three days after admission patient developed high for steroids (MDF >32), patients take 40mg/day Past Medical History: 1) ETOH use disorder, 2) Polysubstance abuse (cocaine, marijuana, heroin), 3) (active form) for 28 days; in patients with contraindications for fevers >102ºF and recurrent . CT suggested possible . Figure 4: Maddrey Discriminant Function Bipolar disorder, 4) Cluster B personality w/ suicide attempt, 5) PTSD, 6) GERD, 7) HTN, 8) T2DM steroids or sepsis risk, at 400mg 3x/day may be Patient transferred to MICU due to worsening lactic acidosis of unclear cause despite IV fluids and now concern administered [7]. Past Surgical History: No known previous . for mesenteric ischemia. Further concern for sepsis of unknown origin. Started on Vancomycin and Zyosin. New Treatments: New therapies proposed for AH involve several different classifications based on their Patient with worsening acute kidney injury, function tests, and altered mental status with hallucinations due mechanisms of action Medications: 1) Atorvastatin calcium tab (800 mg, PO, Qbedtime), 2) Ergocalciferol (Vit D) cap (50000 to suspected toxic-metabolic encephalopathy over course of week in MICU. unit, PO, TH@0900) 3) Folic acid tab (1 mg, PO, Qdaily), 4) Gabapentin cap (300 mg, PO, Qam / 600 Clinical trials include drugs targeting the gut-liver axis, inflammatory signaling, apoptosis/oxidative stress, and hepatic regeneration. These mechanisms aim to decrease proliferation of harmful bacteria and mg, PO, Qbedtime / 600 mg, PO, Qpm), 5) Gabapentin cap (300mg, PO, PRN for alcohol Patient intubated and no longer responsive to diuresis. Two weeks since admission, patient developed large pathways that propagate the rapid cell in AH. Furthermore, the measurement of extracellular vesicles dependency/anxiety, 6) Lisinopril tab (40mg, PO, Qdaily), 7) Propranolol Hcl tab (10mg, PO, BID for bloody bowel movements requiring multiple blood transfusions and vasopressors. Sister signed DNR. Patient in the plasma shows promise as a diagnostic measure for AH, as they propagate alcohol-related liver tremor), 8) Thiamine tab (100mg, PO, Qdaily) (At time of presentation, patient was not taking any of his became asystolic next day and was pronounced dead with wife and niece at bedside medications, active meds while inpatient) damage and are easily measurable. [8] Discussion of Disease Processes/Clinical Correlations Allergies: No known allergies ❖CONCLUSIONS ETOH Withdrawal: Chronic ETOH consumption desensitizes response to GABA and inhibits response to Patient initially presented to the ED for symptoms of alcohol withdrawal and was admitted for further glutamate. Thus, stopping ETOH consumption results in a massive net excitatory response, resulting in tremors Social History: Undomiciled, lives in his truck. Intermittently stays at Haymarket. Divorced. Served in monitoring. High fevers, recurrent abdominal pain, and worsening lactic acidosis prompted transfer to MICU. [1]. ETOH lactic acidosis results from an increased NADH/NAD+ ratio, shunting pyruvate metabolism towards Suspected sepsis with worsening acute kidney injury, , altered mental status with Navy, lived on aircraft carrier Norfolk, Middle East. ETOH: 1 pint of vodka + up to 30 cans beer daily. lactate. Patient presented to ED with ETOH withdrawal symptoms of shakes and recent hematemesis, along with : Smoker, patient unable to quantify amount. Illicits: Denies (per EMR, hx cocaine/MJ/heroin) hallucinations, lung function, and blood loss despite treatment led to a rapid deterioration of patient. In this lactic acidosis and elevated AST of 82. case, life-saving care needed to be balanced with the individual and family’s desire to make their end-of-life decisions. Ultimately, this patient succumbed to multi-organ failure with family at bedside. : : CTAP with IV and PO contrast was performed, with mild peripancreatic graying of the fat CONSTITUTIONAL: (-)fever (-)chills HEENT: (-)eye redness (-)eye pain (-)sore throat CV: (-)chest pain with peripancreatic lymph nodes observed. Traditionally, mild acute pancreatitis presents with upper right (-)DOE (-)orthopnea (-)PND (-)LE edema PULM: (-)cough (-) GI: (+)abdominal pain ❖REFERENCES abdominal pain that can be poorly localized in alcoholics. Elevated serum lipase is more sensitive to pancreatitis 1. Dopamine transporters increase in after alcohol withdrawal. Laine TP, Ahonen A, Torniainen P, HeikkiläJ, Pyhtinen J, (+) (+)vomiting (+)hematemesis GU: (-)dysuria (-)hematuria NEURO: (-)headache (-)focal as compared to amylase in alcoholics [2]. Mild acute pancreatitis was considered despite normal lipase levels. Räsänen P, NiemeläO, Hillbom M. Mol Psychiatry. 1999;4(2):189. weakness (-)paresthesia MUSC: (-)back pain (-)arthralgia 2. A critical evaluation of laboratory tests in acute pancreatitis. Yadav D, Agarwal N, Pitchumoni CS. Am J Gastroenterol. 2002;97(6):1309. 3. European Association for the Study of the Liver. EASL Clinical Practice Guidelines: Management of alcohol-related . J OBJECTIVE: Lab Values: : Alcoholic hepatitis can be characterized through a history of more than 100g per day of Hepatol. 2018;69(1):154. Vital Signs: alcohol use for 20+ years, AST:ALT ratio ≥2, elevated serum bilirubin and INR, and a fatty liver change in 4.Diehl AM, Potter J, Boitnott J, Van Duyn MA, Herlong HF, Mezey E. Relationship between pyridoxal 5'-phosphate deficiency and Temperature: 37.4 C, Pulse: 78, Respiration: imaging [3]. The patient met all criteria. Biochemically, there is lower elevation of serum ALT relative to AST aminotransferase levels in alcoholic hepatitis. . 1984;86(4):632. because of hepatic deficiency of pyridoxal 5’-phosphate in alcoholic [4]. Elevated INR results from impaired 5.Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M, Sepsis Definitions 18, Blood Pressure: 123/78 Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic : For the Third International Consensus production of coagulation factors by inflamed liver. Diagnosis was strengthened by a negative anti-hepatitis A Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb;315(8):775-87. Physical Exam: antibody, anti-hepatitis B core antibody, and anti-HCV antibody. 6.Maddrey WC, Boitnott JK, Bedine MS, Weber FL Jr, Mezey E, White RI. therapy of alcoholic hepatitis. Gastroenterology. GEN: Obese disheveled male, malodorous 1978;75(2):193. 7. Singal AK, Bataller R, Ahn J, Kamath PS, Shah VH. ACG Clinical Guideline: . Am J Gastroenterol. HEENT: NC/AT, EOMI, sclerae anicteric, dry Multi-organ Failure: Given fevers and lactic acidosis, concern for sepsis of unknown origin was at top of ddx. 2018;113(2):175. Epub 2018 Jan 16. MM CV: RRR PULM: CTAB anteriorly, Patient was started on Vancomycin/Zosyn, although no sources of infection were elucidated via PCR. Patient 8. Current trials and novel therapeutic targets for alcoholic hepatitis. Singal, Ashwani K. et al. Journal of , Volume 70, Issue 2, normal WOB ABD: Obese, soft, reducible was monitored for end-stage renal disease (ESRD) and septic shock before multiorgan failure (MOF). Septic 305 - 313 , +voluntary guarding EXT: Warm, 1+ shock can be identified vasopressor therapy and lactate levels > 2mmol/L [5]. Lactic acidosis results from pitting edema BLE NEURO: AOx3, appears Figures 1-3: AST, ALT, AST:ALT, INR, unchecked cellular hypoxia, causing cell membrane ion pump dysfunction, intracellular edema, and inadequate ❖ACKNOWLEDGEMENTS intoxicated, no focal deficits PSYCH: and Tbil values for patient over course intracellular pH regulation. MOF concluded in worsening lung function on ventilator, worsening kidney failure, Thank you to Dr. Kevin Lee and Dr. Ajit Ramadugu for all of their support and guidance through the Mentors Psychomotor slowing, denies SI from admission until time of death liver dysfunction, and asystole. Program. Special thanks to Dr. Kevin Lee for providing this patient case and relevant documentation.