弥漫性肺泡出血(DAH)可由各种条件引起,分为自身免疫和非自身免疫。免疫因子介导的血管炎,比如韦格纳肉芽肿病,显微镜下多血管炎,Goodpasture综合征,结缔组织疾病,和抗磷脂抗体综合征,是常见的自身免疫原因。非自身免疫因素包括感染性或毒性暴露和肿瘤状况。DAH的诊断,由于肾上腺嗜铬细胞瘤或肾上腺外副神经节瘤释放过多的儿茶酚胺,可以提出诊断挑战,需要及时治疗。在这份报告中,我们介绍一例嗜铬细胞瘤,表现为肾上腺偶发瘤(在胆囊切除术后突发性DAH治疗期间诊断).病例报告:一名39岁女性肾上腺偶发瘤患者在胆囊切除术后发展为DAH,表现为突发性咯血和呼吸困难。糖皮质激素的给药,已知会导致嗜铬细胞瘤危机(PCC),在确定原因之前需要。由于持续的低氧性呼吸衰竭和急性呼吸窘迫综合征(ARDS),必须进行插管和机械通气。在这种情况下,患者在进行机械通气时经历了两次PCC的水肿。随后的检查显示有26×25mm的左肾上腺腺瘤,激素证实儿茶酚胺分泌过多。八个月后进行了腹腔镜肾上腺切除术,以切除左肾上腺。随后的组织检查显示嗜铬细胞瘤,从而验证初步诊断。结论:肾上腺偶发瘤可能是嗜铬细胞瘤(肾上腺偶发瘤可表现为嗜铬细胞瘤),即使没有肾上腺素能症状.建议在进行侵入性手术或接受皮质类固醇治疗之前,对肾上腺偶发瘤进行嗜铬细胞瘤的评估。在不进一步阐明的情况下考虑DAH的潜在原因时,包括嗜铬细胞瘤或副神经节瘤(PPGL)在鉴别诊断中具有重要意义。
Diffuse alveolar hemorrhage (DAH) can be caused by various conditions, categorized as autoimmune and non-autoimmune. Immunofactor-mediated vasculitis, such as Wegener granulomatosis, microscopic polyangiitis, Goodpasture syndrome, connective tissue disorders, and antiphospholipid antibody syndrome, are common autoimmune causes. Non-autoimmune factors include infectious or toxic exposures and neoplastic conditions. The diagnosis of DAH, resulting from excessive catecholamine release from an adrenal
pheochromocytoma or extra-adrenal paraganglioma, can present diagnostic challenges and necessitate prompt treatment. In this report, we present a case of pheochromocytoma that manifested as an adrenal incidentaloma (diagnosed during the management of sudden-onset DAH after cholecystectomy). Case report: A 39-year-old female patient with adrenal incidentaloma developed DAH following a cholecystectomy procedure, presenting with sudden-onset hemoptysis and dyspnea. Administration of glucocorticoids, known to precipitate
pheochromocytoma crisis (PCC), was required before the cause was determined. Intubation and mechanical ventilation were necessary due to persistent hypoxemic respiratory failure and acute respiratory distress syndrome (ARDS). The patient in this case experienced two epidoses of PCC while she was on mechanical ventilation. Subsequent work-up revealed a 26 × 25 mm left adrenal adenoma with hormonal confirmation of catecholamine hypersecretion. A laparoscopic adrenalectomy was done eight months later to excise the left adrenal gland. Subsequent examination of the tissue revealed
pheochromocytoma, thereby validating the initial diagnosis. Conclusion: Adrenal incidentalomas may be pheochromocytomas (adrenal incidentalomas can manifest as pheochromocytomas), even without adrenergic symptoms. It is recommended that adrenal incidentalomas undergo evaluation for
pheochromocytoma before undergoing invasive surgery or receiving corticosteroid treatment. When considering potential causes of DAH without further elucidation, including a
pheochromocytoma or paraganglioma (PPGLs) in the differential diagnosis is important.