7762 A Unique Case Of Sepsis-Driven Bilateral Adrenal Hemorrhages In A Patient With HIT

7762 一例由脓毒症引起的HIT患者双侧肾上腺出血的特殊病例

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Abstract

Disclosure: A. Siddiqui: None. B. Shalit: None. H. Nadeem: None. Z. Khan: None. D. Pinkhasova: None. Introduction: Bilateral adrenal hemorrhages, commonly seen in the setting of sepsis as Waterhouse Friderichsen syndrome, is a rare life-threatening condition. This process is driven by the release of bacterial endotoxins leading to the activation of coagulation, fibrinolysis, and proinflammatory pathways. It is by a similar process that now non-septic hypercoagulable states, including heparin-induced thrombocytopenia (HIT), factor V Leiden and protein C resistance are also being recognized as etiologic for bilateral adrenal hemorrhaging. The following case demonstrates a combination of the two etiologies leading to adrenal insufficiency from bilateral adrenal hemorrhages. Clinical Case: A 48-year-old male presented to the emergency department with right upper quadrant pain, dyspnea, and a low-grade fever. Laboratory results indicated leukocytosis with a predominance of neutrophils. Initial computed tomography imaging revealed a 4 x 3.5 cm right lower lobe multi-loculated lung abscess and multiple right lower lobe segmental/subsegmental pulmonary emboli. The patient was started on a heparin drip and empiric antibiotics. Infectious disease was consulted to help determine the etiology of the lung abscess. Extensive workup including sputum, blood, fungal cultures, and acid-fast bacillus smear testing were negative. The patient improved on routine broad-spectrum antibiotics and was planned to be transitioned to a direct oral anticoagulant until serial imaging revealed incidental bilateral 4 cm adrenal hemorrhages. Endocrinology was emergently consulted; a random cortisol level was drawn and found to be low at 2.7 (3-17 µg/dL) with an elevated Adrenocorticotropic hormone (ACTH) level of 114 (6 - 50 pg/mL) indicative of primary adrenal insufficiency. The patient subsequently became hypotensive and was started on stress-dose steroids. Upon further investigation, the patient was found to be thrombocytopenic, and hematology was involved. Based on his 4T score of 5, concern was raised for HIT and argatroban was initiated. Moreover, the patient was eventually stabilized for discharge with close follow-ups with endocrinology, infectious disease, and hematology as an outpatient. Conclusion: There have been 17 reported cases of bilateral adrenal hemorrhaging in the setting of HIT uniformly presenting with complete hemodynamic collapse. This case serves as even more unique given the added component of sepsis. Both sepsis and HIT respectively have been well established to pose individual risk for developing bilateral adrenal hemorrhages. Hence, we hope to highlight the importance of exploring all potential causes of adrenal insufficiency in the setting of bilateral adrenal hemorrhaging and emphasize the harms of anchoring to a single etiology. Presentation: 6/3/2024

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