Uncovering Cocaine Induced Eosinophilic Pneumonia

L. Ramdhanie, A. Daya, F. Nitol, K. Cervellione
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Abstract

Cocaine use has a significant public health impact, causing over 1.2 million ER visits annually. Cocaine can cause a wide range of pulmonary pathology, including diffuse alveolar hemorrhage (“Crack Lung”), barotrauma, bronchiectasis, granulomatous disease, and pulmonary vascular disease. Acute eosinophilic pneumonia (AEP) is a rare and potentially life-threatening complication of cocaine use that can be successfully treated if identified. We describe a case of persistent fevers, hypoxemia, and air space opacities due to AEP related to cocaine use.A 34-year-old male with a history of polysubstance abuse was found unresponsive, apneic, and surrounded by vomitus at a party, where he had smoked marijuana and cocaine and injected heroin. Upon hospital arrival, he was hypotensive and severely hypoxic and was intubated. He had severe rhabdomyolysis, lactic acidosis, acute kidney injury, and acute liver injury. His chest radiograph demonstrated diffuse bilateral alveolar infiltrates. COVID-19 was ruled out. Sputum cultures grew Klebsiella and E. Coli;Streptococcus Pneumoniae urine antigen was positive. He received IV fluids, vasopressors, and broad spectrum antibiotics for septic shock and aspiration pneumonia in the setting of drug overdose. His septic shock and hypoxemia improved, allowing tracheostomy and gastrostomy to be performed. Despite prolonged courses of antibiotics, he had persistent fevers, worsening infiltrates on chest radiograph, and persistent hypoxemia. CT imaging demonstrated diffuse, bilateral ground glass opacities and consolidations, with reticulation and interlobular septal thickening. Viral, bacterial, and fungal cultures collected via bronchoscopy were negative, however, cell count revealed 315 WBC / mm3, with 27% eosinophils. He was started on methylprednisolone 80mg IV every eight hours and had resolution of fevers and improvement in oxygenation and infiltrates. 1 month after discharge, he was decannulated and did not require supplemental oxygen. DiscussionThis case highlights an important aspect of assessing fever in the ICU despite broad spectrum antibiotics in patient with drug overdose. In the above , bronchoscopy unmasked an eosinophilic pneumonia allowing a rapid transition to trach collar and prevention of progression to pulmonary fibrosis. (Figure Presented).
揭示可卡因引起的嗜酸性肺炎
可卡因的使用对公共卫生有重大影响,每年造成120多万急诊室就诊。可卡因可引起广泛的肺部病理,包括弥漫性肺泡出血(裂肺)、气压损伤、支气管扩张、肉芽肿性疾病和肺血管疾病。急性嗜酸性粒细胞性肺炎(AEP)是一种罕见且可能危及生命的可卡因使用并发症,如果发现可以成功治疗。我们描述了一个病例的持续发烧,低氧血症,和空气空间混浊由于AEP与可卡因的使用。一名34岁男性,有多种药物滥用史,在一次聚会上被发现反应迟钝,呼吸暂停,周围有呕吐物,在那里他吸食大麻和可卡因并注射海洛因。到达医院后,他出现低血压和严重缺氧,并插管。他有严重的横纹肌溶解、乳酸酸中毒、急性肾损伤和急性肝损伤。胸片显示双侧肺泡弥漫性浸润。排除了新冠肺炎的可能性。痰培养培养克雷伯氏菌和大肠杆菌;肺炎链球菌尿抗原阳性。在药物过量的情况下,他接受静脉输液、血管加压药和广谱抗生素治疗感染性休克和吸入性肺炎。他的感染性休克和低氧血症得到改善,允许进行气管造口术和胃造口术。尽管延长了抗生素疗程,他仍持续发烧,胸片上浸润恶化,持续低氧血症。CT表现为弥漫性双侧磨玻璃混浊及实变,伴网状及小叶间隔增厚。然而,通过支气管镜收集的病毒、细菌和真菌培养呈阴性,细胞计数显示315 WBC / mm3,其中27%为嗜酸性粒细胞。患者开始服用甲强的松龙80mg IV,每8小时一次,发热消退,氧合和浸润改善。出院1个月后,患者停用体外循环,无需补充氧气。本病例强调了在药物过量患者使用广谱抗生素的情况下评估ICU发热的一个重要方面。在上图中,支气管镜检查发现嗜酸性粒细胞性肺炎,允许快速过渡到气管环和防止进展为肺纤维化。(图)。
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