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Chest ; 162(4):A1047, 2022.
Article in English | EMBASE | ID: covidwho-2060760

ABSTRACT

SESSION TITLE: Critical Thinking SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Cephalosporins have been known to cause hypo-prothrombinemia and prothrombin prolongation (1). The proposed mechanism of this coagulopathy is secondary to a N-methylthiotetrazole side chain interfering with vitamin-k metabolism (1). Current literature supporting the association between cefazolin and hypo-prothombinemia have only been reported through case reports. As cefazolin is a commonly used antibiotic, it is important that healthcare professionals are aware of its potential bleeding risk. We present a case of a 72 year old female with cefazolin-induced hypo-prothrombinemia. CASE PRESENTATION: A malnourished 72-year old female with a past medical history of recent methicillin-susceptible Staphyloccocus aureus (MSSA) bacteremia and COVID-19 pneumonia presented to the emergency department from a skilled nursing facility (SNF) due to shortness of breath. The patient was previously discharged to SNF to complete a 14 day course of IV cefazolin due to her MSSA bacteremia. On admission, vital signs were significant for a respiratory rate of 22 and a pulse oximetry reading of 78% on room air. Laboratory findings were significant for an elevated prothrombin time of >100 seconds, an INR >15, and a D-dimer of 42,344 ng/mlL. A computed tomography angiography (CTA) of the chest revealed a small segmental pulmonary embolus in the right lower lobe of the lung. The patient was started on a heparin drip, placed on a non-rebreather mask, and admitted to the ICU for closer monitoring. Infectious disease was consulted and cefazolin was discontinued. Due to the patient's risk of bleeding her heparin drip was stopped. It was decided not to reverse the patient's coagulopathy with vitamin K as there were no signs of an acute bleed in the setting of an acute pulmonary embolus. The patient was started on nafcillin in place of cefazolin. Four days after discontinuation of cefazolin, the patient's INR had trended down from >15 to 1.6 and she was started on Lovenox 1mg/kg for the treatment of her acute PE. DISCUSSION: Due to the timing of the discontinuation of cefazolin and the correction of the hypo-prothrombinemia, a clear association between the two can be made. It has been proposed that cefazolin's side chain, heterocyclic thiol, 2-methyl-1,3,4-thiadiazole-5-thiol (MTD), causes a similar reaction that other cephalosporins have on the metabolism of Vitamin K (2). This altered Vitamin K metabolism was also likely exacerbated due to the patient's malnourishment and likely depleted vitamin k reserves (2). CONCLUSIONS: Although rare, this case demonstrates the need for clinicians to be aware of the potential bleeding risk associated with cephalosporins and cefazolin in particular. In the future, routine monitoring of PT/INR levels may be recommended when initiating cephalosporins. Reference #1: Park GH, Kim S, Kim MS, Yu YM, Kim GH, Lee JS, Lee E. The Association Between Cephalosporin and Hypoprothrombinemia: A Systematic Review and Meta-Analysis. Int J Environ Res Public Health. 2019 Oct 16;16(20):3937 Reference #2: Shearer, M. J., Bechtold, H., Andrassy, K., Koderisch, J., McCarthy, P. T., Trenk, D., Jähnchen, E., & Ritz, E. (1988). Mechanism of cephalosporin-induced hypoprothrombinemia: relation to cephalosporin side chain, vitamin K metabolism, and vitamin K status. Journal of clinical pharmacology, 28(1), 88–95 DISCLOSURES: no disclosure on file for John Abernathy;No relevant relationships by Ethan Goldberg No relevant relationships by Renee Miu No relevant relationships by Luis Osorio no disclosure on file for Satesh Saroop;no disclosure on file for Oliver Sevilla;no disclosure on file for Kristen Zubel;

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