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SESSION TITLE: Issues After COVID-19 Vaccination Case Posters SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Immune mediated vaccine related pericarditis reports have been well documented;albeit rare and generally well tolerated, it remains a real complication with possible devastating impacts. The incidence has increased even more with the covid vaccine.3 Here we describe a 72 year old female that received her 4th BNT162b2 dose, 5 months after the 3rd dose, and subsequently developed pericarditis. CASE PRESENTATION: 72 year old female, previously well, who presented with a 3 day history of central, sticking chest pain associated with exertional dyspnea, cough, palpitations and malaise. She denied any coryzal symptoms. On presentation she was hemodynamically stable but hypoxic and tachycardic. Laboratory investigations revealed leucocytosis and troponinemia of 0.13ng/ml. ECG showed diffuse ST elevations. A transthoracic echo showed a small pericardial effusion with normal LV and RV function, EF 60-65% and a CT Pulmonary Angiogram revealed a small sub-segmental pulmonary embolism with atelectasis and trace effusions. On further questioning she revealed that the symptoms started 3 days after she received her 2nd booster dose of the Pfizer covid vaccine. She was started on colchicine and apixaban and was discharged home with follow-up. Two days after discharge the patient represented to the hospital with worsening chest pain. Investigations revealed worsening leucocytosis and increased inflammatory markers (CRP 303mg/L, ESR 62mm/h). A new finding of a small pericardial effusion and bilateral pleural effusions with consolidations were noted on a repeat CT scan. Decision was made to continue colchicine and commence prednisone. Other infectious and inflammatory causes of pericarditis were ruled out. The COVID spike IgG was negative and the NAAT Cov 2 IgG showed titres >250 (<50). DISCUSSION: The exact pathogenesis of the COVID-19 vaccine-induced pericarditis remains unknown. It is thought that mRNA vaccines produce a large number of antibodies which elicit a multi-system inflammatory response1;despite this, steroid therapy remains controversial given the risk of recurrent pericarditis.2 A shorter vaccine interval has been associated with adverse outcomes. CDC extended the dosing interval in young persons to reduce the risk of severe myocarditis;however the interval for persons 65 years or more and immunocompromised remained unchanged. Our case and the identical case described by Singh et al1 reinforces the need to determine the best time interval for administration of the covid booster vaccines;especially in patients more than 65 years. CONCLUSIONS: More research needs to be done as to the most appropriate interval between booster doses to reduce the inflammatory complications related to the vaccine. A consideration should also be made to determine if the measurement of SARS COV-2 IgG spike titres have any role in determining the timing of subsequent booster doses. Reference #1: Singh A, Nguyen L, Everest S, et al. (February 12, 2022) Acute Pericarditis Post mRNA-1273 COVID Vaccine Booster. Cureus 14(2): e22148. DOI 10.7759/cureus.22148 Reference #2: Hajjo R., Sabbah D.A., Bardaweel S.K., Tropsha A. Shedding the Light on Post-Vaccine Myocarditis and Pericarditis in COVID-19 and Non-COVID-19 Vaccine Recipients. Vaccines. 2021;9:1186. doi: 10.3390/vaccines9101186. Reference #3: Diaz GA, Parsons GT, Gering SK, Meier AR, Hutchinson IV, Robicsek A. Myocarditis and Pericarditis After Vaccination for COVID-19. JAMA. 2021 Sep 28;326(12):1210-1212. doi: 10.1001/jama.2021.13443. PMID: 34347001;PMCID: PMC8340007. DISCLOSURES: No relevant relationships by Zachary Banbury No relevant relationships by Michael Basir No relevant relationships by Alexandra Gottdiener No relevant relationships by Janeen Grant-Sittol No relevant relationships by Srikant Kondapaneni No relevant relationships by Ross Lavine No relevant relationships by Anesha White
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SESSION TITLE: Drug-Induced and Associated Critical Care Cases Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Drug-induced hepatotoxicity is a well-known occurrence from a variety of different medications. However, phenobarbital (PHB) induced hepatotoxicity has not been well studied, and acute liver injury from PHB even less so. In this case, although our patient had many reasons to develop acute liver failure, including alcohol and toluene exposure, timing and investigations seem to point to PHB being responsible. CASE PRESENTATION: Patient is a 39 y.o male with past medical history significant for hepatitis A and B, hyperlipidemia and alcohol abuse who was found unresponsive by EMS after friends reported witnessing patient drinking alcohol and sniffing paint thinner. Patient remained unresponsive on arrival and was intubated and transferred to the MICU. Patient was afebrile with BP 100/55 and otherwise normal vital signs. Significant labs on presentation included a WBC of 8.15, CO2 of 16, lactic acid of 3.6 and mildly elevated transaminases (ALT: 59, AST: 48). Urine toxicology was positive for marijuana. EKG, chest x-ray and CT Head without contrast unremarkable. COVID negative. Video EEG was negative except for generalized slowing. On hospital day 3, patient was increasingly agitated, at which point phenobarbital was started due to concerns for alcohol withdrawal. Hepatic function panel the following mornings showed significant increases in transaminases (ALT: 972 and 5,746, AST: 790 and 4,805) and total bilirubin (6.8 and 11.4), and mild increase in alkaline phosphatase (112 and 125), respectively. Hepatitis panel, acetaminophen level and salicylate level were unremarkable. RUQ ultrasound was also negative for pathology. Gastroenterology was consulted, who recommended starting NAC protocol. Phenobarbital was discontinued. Hepatic function panel the following morning showed significant improvement. Liver transplant was considered, however LFTs continued to downtrend and remainder of hospital course was unremarkable. DISCUSSION: PHB is an anticonvulsant developed primarily for seizure management. However its use has expanded to alcohol withdrawal and even sedative withdrawal. Studies have demonstrated in vitro liver toxicity as well as idiosyncratic reactions and acute liver failure in children (1) (2), with minimal documentation in adults. And while there has even been histological analysis with linkage of chronic phenobarbital use to hepatic necrosis and granulomatous formation (3), there has been minimal documentation regarding acute liver failure in an adults taking phenobarbital. CONCLUSIONS: In conclusion, it is clear that phenobarbital played a significant role in this patient's liver injury and may need to be considered in future episodes of acute liver injury with unclear etiology. Reference #1: Li AM, Nelson EA, Hon EK, Cheng FW, Chan DF, Sin NC, Ma KC, Cheung KL, Fok TF. Hepatic failure in a child with anti-epileptic hypersensitivity syndrome. J Paediatr Child Health. 2005 Apr;41(4):218-20. doi: 10.1111/j.1440-1754.2005.00591.x. PMID: 15813878;PMCID: PMC7166358. Reference #2: Roberts EA, Spielberg SP, Goldbach M, Phillips MJ. Phenobarbital hepatotoxicity in an 8-month-old infant. J Hepatol. 1990 Mar;10(2):235-9. doi: 10.1016/0168-8278(90)90058-y. PMID: 2332596. Reference #3: Di Mizio Di Mizio, G., Gambardella, A., Labate, A., Perna, A., Ricci, P., & Quattrone, (2007). Hepatonecrosis and cholangitis related to long-term phenobarbital therapy: An autopsy report of two patients. Seizure, 16(7), 653–656. https://doi.org/10.1016/j.seizure.2007.05.008 DISCLOSURES: No relevant relationships by Zachary Banbury No relevant relationships by Michael Basir No relevant relationships by Inessa Bronshteyn No relevant relationships by Kyle Foster No relevant relationships by Anna-Belle Robertson