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A Multi-Modal Approach to Life-Threatening Hemoptysis in a Patient with COVID-19 ARDS 多模式治疗COVID-19急性呼吸窘迫综合征患者危及生命的咯血
Pub Date : 2021-05-01 DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1995
G. Senyei, D. Nettlow, M. Nobari, R. Miller, G. Cheng
Introduction: Life-threatening hemoptysis is rare in patients diagnosed with COVID-19. Here, we describe a severe case of hemoptysis a patient with COVID-19 and the multi-modal approach to manage this condition. Case: A 57 year-old man with diabetes was admitted with hypoxemic respiratory failure due to COVID-19 pneumonia. Despite treatment with convalescent plasma, remdesivir and dexamethasone, he developed progressive respiratory failure eventually requiring VVECMO support on hospital day 8. He was started on heparin for therapeutic anticoagulation at this time. Anticoagulation was held on day 23 after large blood clots were suctioned via tracheostomy tube. CT revealed complete opacification of the bilateral lungs and major airways without evidence of acute arterial blushing (panel A). The patient underwent the first in a series of therapeutic bronchoscopies via a size 10 Shiley tracheostomy tube on day 28. Occlusive gelatinous blood clots were noted immediately upon entering the trachea. After failure of adequate clot evaluation with cryoprobe, a modified 24F chest tube was used as a suction catheter to achieve clot removal. After visualizing major airways, a bronchial blocker was positioned in the bronchus intermedius. Topical tranexamic acid was applied to sites of bleeding in the left upper lobe. Repeat bronchoscopy was performed on day 30, which showed new bleeding in the left lower lobe segments. An endobronchial blocker was repositioned in the left lower lobe and Surgicel was applied to ongoing bleeding sites within the right and left lung. Prior to repeat bronchoscopy, the patient was administered inhaled tranexamic acid three times daily due to findings of severely inflamed mucosa and diffused nature of bleed. On day 32, bronchoscopy revealed significantly improved bleeding. In-line suctioning was held in favor of daily diagnostic bronchoscopies to avoid suction trauma. Ultimately, the patient's bleeding resolved and he was eventually liberated from both ECMO and the ventilator with corresponding improvement on CT imaging (panel B). Discussion: We describe a case of a life-threatening hemoptysis in a patient with COVID-19 ARDS who was successfully managed using serial therapeutic bronchoscopies employing cryotherapy, mechanical tamponade, and pharamacologic coagulants to achieve hemostasis.
诊断为COVID-19的患者很少出现危及生命的咯血。在这里,我们描述了一名COVID-19患者的严重咯血病例以及治疗这种情况的多模式方法。病例:一名57岁男性糖尿病患者因COVID-19肺炎引起的低氧性呼吸衰竭入院。尽管给予恢复期血浆、瑞德西韦和地塞米松治疗,患者仍出现进行性呼吸衰竭,最终在住院第8天需要VVECMO支持。这时他开始使用肝素治疗抗凝。经气管造口管抽吸大血块后第23天进行抗凝治疗。CT显示双侧肺和主要气道完全混浊,未见急性动脉脸红(A组)。患者于第28天通过10号希利气管造口管接受了一系列支气管镜检查。闭塞的凝胶状血凝块在进入气管后立即被发现。在低温探针无法充分评估血块后,使用改良的24F胸管作为吸引导管以实现血块清除。在显像主要气道后,在支气管中间放置支气管阻滞剂。局部应用氨甲环酸于左上肺叶出血部位。第30天再次行支气管镜检查,发现左下肺叶段新出血。将支气管内阻滞剂重新放置于左肺下叶,并将surgical应用于左、右肺内持续出血的部位。在再次支气管镜检查之前,由于发现粘膜严重炎症和弥漫性出血,患者每天吸入氨甲环酸三次。第32天,支气管镜检查显示出血明显改善。为了避免吸入损伤,我们建议每日进行支气管镜检查。最终,患者的出血得到解决,并最终从ECMO和呼吸机中解放出来,CT成像也相应改善(B组)。讨论:我们描述了一个COVID-19 ARDS患者的危及生命的咯血病例,该患者成功地通过一系列治疗性支气管镜检查,采用冷冻疗法、机械压塞和药物凝血剂来实现止血。
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引用次数: 1
E-Cigarette or Vaping-Product Associated Lung Injury Complicated by Spontaneous Pneumothoraces in the Setting of COVID-19 Pandemic COVID-19大流行背景下电子烟或电子烟产品相关肺损伤并发自发性气胸
Pub Date : 2021-05-01 DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1993
S. Golob, L. Winston, D. Manson, S. Fedyna
Introduction: Electronic-cigarette or vaping-product associated lung injury (EVALI) was first identified in August 2019, when U.S. public health officials noted a clinical syndrome of acute respiratory failure and systemic inflammation associated with the use of aerosolized nicotine and cannabinoids. The presence of lipid-laden macrophages on bronchiolar lavage is a specific but not sensitive histological finding of EVALI, which is often a diagnosis of exclusion. In 2020, the first cases of COVID-19, caused by SARS-CoV2 virus, were seen in the U.S. Both COVID-19 and EVALI can affect previously healthy individuals, manifesting with severe hypoxemia and systemic inflammation, posing diagnostic challenges in distinguishing the two syndromes. Secondary spontaneous pneumothorax is a well-described complication of COVID-19 yet is only rarely associated with EVALI, with only one published case report of EVALI complicated by pneumothorax. Here, we report a case of a 34-year-old man presenting with hypoxemic respiratory failure complicated by pneumothorax, initially thought to be from COVID-19 pneumonia, found ultimately to have EVALI associated diffuse alveolar damage. Case: In April 2020, a 34-year-old man presented with one week of myalgia, shortness of breath, and a reduced exercise tolerance. Social history was notable for extensive vaping. His exam was notable for hypoxemia requiring nonrebreather. Testing showed elevated inflammatory markers and diffuse bilateral opacities on chest radiography. Nasopharyngeal PCR was negative for SARS-CoV2. CT chest revealed dense consolidation with ground grass opacities and air bronchograms. Rheumatologic and infectious workup was unremarkable. Despite six negative SARS-CoV2 tests, he was treated for COVID-19 with empiric steroids and antibiotics for community-acquired pneumonia. On hospital day 3, he developed a right-sided pneumothorax requiring chest tube. On hospital day 12, he developed a left-sided pneumothorax and a second chest tube was placed. A presumptive diagnosis of pneumonitis and diffuse alveolar damage secondary to EVALI was made. Given non-healing bilateral pneumothoraces, on hospital day 32, he underwent chemical pleurodesis with doxycycline which was complicated by ARDS. He was intubated, suffered a PEA arrest from refractory hypoxemia, and emergently cannulated to VV ECMO. A head CT demonstrated diffuse cerebral edema suggestive of anoxic brain injury. After extensive goals of care discussions, care was withdrawn and the patient passed away. Discussion: EVALI, similar to COVID-19, is syndrome of severe acute hypoxemia and systemic inflammation. Both conditions have similar radiographic findings with ground glass opacities indicative of alveolar damage, histological findings of tracheobronchitis and diffuse alveolar damage, and can lead to secondary spontaneous pneumothoraces.
电子烟或电子烟产品相关肺损伤(EVALI)于2019年8月首次被发现,当时美国公共卫生官员注意到与雾化尼古丁和大麻素使用相关的急性呼吸衰竭和全身性炎症的临床综合征。细支气管灌洗液中脂质巨噬细胞的存在是EVALI的特异性但不敏感的组织学发现,这通常是排除性诊断。2020年,美国出现了由SARS-CoV2病毒引起的第一例COVID-19病例。COVID-19和EVALI都可以影响先前健康的个体,表现为严重的低氧血症和全身性炎症,对区分这两种综合征提出了诊断挑战。继发性自发性气胸是COVID-19的一种常见并发症,但很少与EVALI相关,仅有1例EVALI合并气胸的报道。在这里,我们报告了一例34岁男性低氧性呼吸衰竭并发气胸,最初被认为是COVID-19肺炎,最终发现EVALI相关的弥漫性肺泡损伤。案例:2020年4月,一名34岁的男性出现了一周的肌痛、呼吸急促和运动耐受性降低。社会历史以广泛使用电子烟而闻名。他的检查显示低氧血症,需要非呼吸机。胸片检查显示炎症标记物升高和弥漫性双侧混浊。鼻咽PCR检测SARS-CoV2阴性。胸部CT示致密实变伴地草影及支气管充气征。风湿病学和感染性检查无显著差异。尽管六次SARS-CoV2检测呈阴性,但他仍接受了经验性类固醇和社区获得性肺炎抗生素治疗。住院第3天,他出现右侧气胸,需要胸腔插管。在医院的第12天,他出现了左侧气胸,并放置了第二根胸管。推测诊断为肺炎和弥漫性肺泡损伤继发于EVALI。由于双侧气胸未愈合,在住院第32天,他接受了强力霉素化学胸膜切除术,并发ARDS。他插管,因难治性低氧血症导致PEA骤停,并紧急插管至VV ECMO。头部CT显示弥漫性脑水肿提示缺氧脑损伤。经过广泛的护理目标讨论,护理被撤回,病人去世了。讨论:EVALI与COVID-19类似,是严重急性低氧血症和全身性炎症的综合征。这两种情况的影像学表现相似,均为磨玻璃影,提示肺泡损伤,组织学表现为气管支气管炎和弥漫性肺泡损伤,并可导致继发性自发性气胸。
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引用次数: 0
Clinical Features and Outcomes of Hospitalized Patients Co-Infected with COVID-19 and HIV: A Case Series COVID-19合并HIV住院患者临床特征及转归:一个病例系列
Pub Date : 2021-05-01 DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2009
J. Kirupakaran, D. Valentine, A. Idowu, M. Jiménez, M. Okaikoi, A. M. Thida, G. Bahtiyar, G. Aristide, G. Rodriguez
INTRODUCTION Coronavirus-19 disease (COVID-19) caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) continues to be a major cause of mortality worldwide. Advanced age and a number of chronic diseases have been investigated as risk factors for poor outcomes in patients with COVID-19. Likewise, Human Immunodeficiency Virus (HIV) has been proposed as a potential risk factor for COVID-19, however, the possible relationship between HIV and COVID-19 has remained difficult to fully elucidate due to a paucity of data. We describe a case series of 11 patients co-infected with HIV and SARS-CoV-2. CASE PRESENTATION Between March 20, 2020 and May 5, 2020, 11 patients with HIV were admitted for COVID-19at an underserved community hospital in Brooklyn, NY. . Patients ranged from 39 to 78 years of age. Seven patients were men and four patients were women. Seven patients were African American and four patients were Hispanic. All 11 patients possessed HIV RNA viral loads less than 40 copies/ml. The mean CD4 count was 556 cells/ml (range 171-1123 cells/ml). Nine patients were on antiretroviral therapy (ART). Six patients required invasive mechanical ventilation;five of the six patients died. Two of these five patients were not on ART, prior to admission and two of them developed acute respiratory distress syndrome during their hospital course. The mean length of stay was 10.9 days (range 2-21 days). Three of the six survivors were readmitted within 30 days for CHF exacerbation, bacterial pneumonia and COPD exacerbation. All three patients recovered without complications. At six-month follow-up, no mortalities were reported among the six surviving patients. DISCUSSION This case series presents a unique sample of African American and Hispanic patients co-infected with HIV and SARS-CoV-2. This is the first case series to report long term outcomes among minority population. The high mortality rate in this case series (45%) is also notable in comparison to prior research. This elevated mortality rate may reflect an increased burden of comorbidities in HIV patients. Further research is required to reveal if ART therapy reduces risk of poor outcomes, and if so, which regimen may confer protection against COVID-19.
由新型严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2)引起的冠状病毒19病(COVID-19)仍然是全球死亡的主要原因。研究表明,高龄和多种慢性疾病是导致COVID-19患者预后不良的危险因素。同样,人类免疫缺陷病毒(HIV)也被认为是COVID-19的潜在危险因素,然而,由于缺乏数据,HIV和COVID-19之间可能的关系仍然难以完全阐明。我们描述了11例HIV和SARS-CoV-2合并感染的病例系列。在2020年3月20日至2020年5月5日期间,11名艾滋病毒感染者在纽约布鲁克林一家服务不足的社区医院因covid -19入院。患者年龄从39岁到78岁不等。7名患者为男性,4名患者为女性。7名患者是非裔美国人,4名患者是西班牙裔。所有11例患者的HIV RNA病毒载量均小于40拷贝/ml。平均CD4计数为556个细胞/ml(范围171 ~ 1123个细胞/ml)。9名患者接受抗逆转录病毒治疗(ART)。6例患者需要有创机械通气,其中5例死亡。这5名患者中有2名在入院前未接受抗逆转录病毒治疗,其中2名在住院期间出现急性呼吸窘迫综合征。平均住院时间为10.9天(2-21天)。6名幸存者中有3人在30天内因慢性心力衰竭加重、细菌性肺炎和慢性阻塞性肺病加重而再次入院。3例患者均无并发症。6个月随访时,6例存活患者无死亡报告。本病例系列介绍了非洲裔美国人和西班牙裔患者合并感染艾滋病毒和SARS-CoV-2的独特样本。这是第一个报告少数民族人群长期结果的病例系列。与先前的研究相比,该病例系列的高死亡率(45%)也值得注意。这种高死亡率可能反映了艾滋病毒患者合并症负担的增加。需要进一步的研究来揭示抗逆转录病毒治疗是否能降低不良结果的风险,如果是这样,哪种治疗方案可以预防COVID-19。
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引用次数: 0
A Continuous Cough After COVID-19 COVID-19后持续咳嗽
Pub Date : 2021-05-01 DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1986
Lisa N Glass, Pulmonary Disease, Sandrine Hanna, John P Lichtenberger, Ivana Milojevic, J. Ahari
Organizing pneumonia is a process of lung parenchymal injury caused by multiple etiologies. Although organizing pneumonia may be an idiopathic process, it usually occurs secondary to infection, aspiration, autoimmune disease, and after organ transplantation or radiation. We present a case of organizing pneumona after confirmed SARS-CoV-2 (COVID-19) infection manifesting as chronic cough. Keywords: Organizing pneumonia; COVID-19; Post-viral syndrome; Chronic cough.
组织性肺炎是由多种病因引起的肺实质损伤过程。虽然组织性肺炎可能是一个特发性过程,但它通常继发于感染、误吸、自身免疫性疾病和器官移植或放疗后。我们报告一例确诊的SARS-CoV-2 (COVID-19)感染后的组织性肺炎,表现为慢性咳嗽。关键词:组织性肺炎;COVID-19;Post-viral综合症;慢性咳嗽。
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引用次数: 0
The Chicken or the Egg? Newly Diagnosed Interstitial Lung Disease (ILD) After Novel Coronavirus Pneumonia (COVID-19) 先有鸡还是先有蛋?新型冠状病毒肺炎(COVID-19)后新诊断间质性肺病(ILD)
Pub Date : 2021-05-01 DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2000
G. C. Chiang, T. Zaman, P. Noble
A 79-year-old male presented for evaluation of dyspnea and dry cough. Five months prior he was hospitalized with COVID-19 and a pulmonary embolus requiring 2L/min of supplemental oxygen, enoxaparin, hydroxychloroquine and remdesivir. He was discharged home with apixaban and supplemental oxygen. He had a 10 pack-per-year history of smoking and quit fifty years ago. He had no occupational or environmental exposures associated with pulmonary fibrosis. He had no family history of connective tissue disease or pulmonary fibrosis. On physical examination, he had normal vital signs and his saturation was 100% on room air. Pertinent positive exam findings were limited to bibasilar dry crackles. There were no skin, joint, or oral findings. Pulmonary function tests showed normal lung volumes with normal spirometry and a severely decreased diffusing capacity. A CT revealed improvement of ground glass opacities with persistent subpleural reticulations and honeycombing. Notably, lung images of the lower lobes from a CT scan of the abdomen six years prior to this evaluation showed bibasilar reticulations and ground glass infiltrates. Laboratory studies were notable for an elevated ANA titer in a speckled pattern, elevated CCP and elevated anti-SSA 52 kD. Additional autoimmune serologies were negative. Given the presence of interstitial lung abnormalities (ILAs) in prior imaging and elevated autoimmune markers, he was deemed to have had an exacerbation of previously subclinical ILD caused by COVID-19. The long-term effects of the inflammatory response from COVID-19 have not been characterized. Initial data of CT scans in patients show that up to 17% develop fibrotic changes during the course of the disease. It remains to be seen whether there will be a progressive fibrotic phenotype solely attributable COVID-19 itself. This has been described during the H1N1 and SARS-COV1 outbreaks in patients who developed ARDS but is not observed in post-ARDS pulmonary fibrosis caused by other etiologies. The key to differentiating between a primary ILD rather than post-COVID-19 hinges on antecedent history. The patient's prior radiographic findings meet the research construct of interstitial lung abnormalities (ILA) which refers to patterns of increased lung density in patients with no history of ILD. When post-COVID-19 pulmonary fibrosis is observed, due diligence must be taken to determine alternate etiologies of subclinical ILD that may have been unmasked by COVID-19, rather than caused by it. It remains unclear whether SARS-CoV-2 could activate a latent autoimmunity or potentially cause a de novo autoimmune lung disease as has been suggested.
79岁男性,因呼吸困难和干咳就诊。5个月前,他因COVID-19和肺栓塞住院,需要2L/min的补充氧、依诺肝素、羟氯喹和瑞德西韦。他出院回家时使用阿哌沙班并补充氧气。他有每年10包的吸烟史,50年前戒了烟。他没有与肺纤维化相关的职业或环境暴露。无结缔组织病或肺纤维化家族史。体检时,他的生命体征正常,室内空气饱和度为100%。相关阳性检查结果仅限于双基底干裂纹。没有皮肤、关节或口腔发现。肺功能检查显示肺容量正常,肺活量正常,弥散能力严重下降。CT显示磨玻璃影改善,持续胸膜下网状及蜂窝状影。值得注意的是,在此评估前6年腹部CT扫描的肺下叶图像显示双基底网和磨玻璃浸润。实验室研究显示,ANA滴度呈斑点状升高,CCP升高,抗ssa52kd升高。其他自身免疫血清学结果为阴性。鉴于先前影像学中存在间质性肺异常(ILAs)和自身免疫标志物升高,我们认为该患者先前由COVID-19引起的亚临床ILD加重。COVID-19炎症反应的长期影响尚未确定。患者CT扫描的初步数据显示,高达17%的患者在病程中发生纤维化改变。是否会出现仅由COVID-19本身引起的进行性纤维化表型还有待观察。在发生急性呼吸窘迫综合征(ARDS)的患者中发生H1N1和SARS-COV1暴发时曾描述过这种情况,但在其他病因引起的ARDS后肺纤维化中未观察到这种情况。区分原发ILD与covid -19后ILD的关键取决于既往病史。患者先前的x线表现符合肺间质性异常(ILA)的研究结构,即没有ILD病史的患者肺密度增加的模式。当观察到COVID-19后肺纤维化时,必须尽职调查确定亚临床ILD的其他病因,这些病因可能是由COVID-19揭示的,而不是由其引起的。目前尚不清楚SARS-CoV-2是否会激活潜在的自身免疫,还是可能像之前所建议的那样导致自身免疫性肺部疾病。
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引用次数: 0
期刊
TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION
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