COVID-19感染背景下双侧肾上腺梗死

S. Haider, F. Shaikh, V. Rayasam, Dilpat Kumar, N. Helmstetter
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引用次数: 2

摘要

1例71岁男性,既往有慢性肾脏疾病III期、高血压、高脂血症、口服抗凝治疗心房颤动(AF)和甲状腺功能减退,表现为急慢性肾脏疾病(AoCKD)、转氨酶升高和发育不良。新型冠状病毒聚合酶链反应(PCR)阳性。胸部x线显示双侧空域斑片状病变。胸部、腹部、骨盆CT及腹部磁共振成像(MRI)除双侧肺片状浸润外,未见明显病变。患者不需要类固醇和/或瑞德西韦,因为他没有缺氧。五天后,他服用利伐沙班出院。出院一周后,患者出现全身无力加重,下肢加重,最后摔倒。再入院时,实验室研究显示横纹肌溶解、AoCKD和转氨酶升高。此外,白细胞增多,无感染症状。重复进行COVID-19检测,结果呈阳性,其余的感染性检查包括血培养均无显著差异。胸部、腹部、骨盆的重复CT扫描显示,在COVID-19感染的情况下,脂肪滞留在双肾上腺周围,与梗死有关(图1)。随后,获得早晨皮质醇,与肾上腺功能不全有关。这一怀疑被共syntropin刺激试验证实,结果显示肾上腺功能不全。他开始使用氢化可的松和氟化可的松,在接下来的三天里症状有所改善。肾上腺梗死和出血的常见原因包括血栓栓塞性疾病、高凝状态、HIT、物理创伤、术后状态、败血症和任何严重生理应激的原因。我们仍在深入了解COVID-19的多系统疾病表现及其对房颤等其他疾病的预防性剂量慢性口服抗凝治疗。在排除其他原因的情况下,在COVID-19感染背景下出现非特异性症状(如虚弱、低血压、电解质异常、腹痛、恶心和/或呕吐)的患者,应考虑梗死引起的肾上腺功能不全。在COVID-19感染患者中有肾上腺梗死的报道,例如我们的患者。由于肾上腺血管丰富,容易发生梗塞和出血。据推测,SARS-CoV-2病毒血症造成的高凝状态对肾上腺微血管有特殊的风险。抗凝治疗和继发性肾上腺坏死可导致再灌注损伤和出血。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bilateral Adrenal Gland Infarction in the Setting of COVID-19 Infection
A 71-year-old man with past medical history pertinent for chronic kidney disease stage III, hypertension, hyperlipidemia, atrial fibrillation (AF) on oral anticoagulation, and hypothyroidism presented with acute on chronic kidney disease (AoCKD), elevated transaminases and failure to thrive. COVID-19 polymerase chain reaction (PCR) was positive. Chest x-ray showed patchy bilateral airspace disease. Computed tomography (CT) of chest, abdomen, pelvis and magnetic resonance imaging (MRI) abdomen were unremarkable apart from Bilateral patchy infiltrates in the lungs. The patient did not require steroids and/or remdesivir as he was not hypoxic. He was discharged five days later on rivaroxaban. A week after discharge, he presented with worsening generalized weakness, worse in the lower extremities, culminating in a fall. On readmission, laboratory studies revealed rhabdomyolysis, AoCKD, and elevated transaminases. Additionally, a leukocytosis was present without symptoms concerning for infection. COVID-19 testing was repeated and was positive, with the remainder of the infectious workup including blood cultures being unremarkable. A repeat CT scan of chest, abdomen, pelvis with contrast demonstrated fat stranding around both adrenals concerning for infarction in the setting of COVID-19 infection (image 1). Subsequently, a morning cortisol was obtained, which was low concerning for adrenal insufficiency. This suspicion was confirmed with cosyntropin stimulation testing, which demonstrated adrenal insufficiency. He was started on hydrocortisone and fludrocortisone with improvement in symptoms over the next three days. Common causes of adrenal infarction and hemorrhage include thromboembolic disease, hypercoagulable states, HIT, physical trauma, the postoperative state, sepsis, and any cause of severe physiologic stress. We are still gaining insight into the multisystem disease manifestations of COVID-19 and its prothrombotic effects despite chronic oral anticoagulation therapy at prophylactic doses for other maladies like AF. Adrenal insufficiency due to infarction should be considered in patients who present with non-specific symptoms such as weakness, hypotension, electrolyte abnormalities, abdominal pain, nausea and/or vomiting in the setting of COVID-19 infection when other causes have been ruled out. Adrenal infarction has been reported in patients with COVID-19 infection, such as our patient. The adrenal glands are susceptible to infarction and hemorrhage due to their vascularity. It has been hypothesized that the hypercoagulable state wrought by SARS-CoV-2 viremia poses a particular risk to the adrenal microvasculature. In turn, reperfusion injury and hemorrhage can ensue due to anticoagulant therapy and secondary adrenal necrosis.
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