Bronchoscopic Balloon Dilatation in the Combined Management of Postintubation Stenosis of the Trachea in Adults (original) (raw)
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Pulmonary hantavirus syndrome: case report and brief review
Southwest Journal of Pulmonary and Critical Care, 2015
A 31-year-old white man presented to the emergency department complaining of fever, headache, mild confusion, and muscle aches. Approximately three days earlier he had developed non-quantified fever and diffuse muscle aches and pains. He was employed as a feedlot worker. He had visited an urgent care center one day earlier and had been advised to increase his oral fluid intake and to use non-steroidal anti-inflammatory agents as needed. Upon arrival to the emergency department he was found to have a temperature of 103.6º Fahrenheit, blood pressure of 125/72 mm Hg, respiratory rate of 40 breaths per minute, and room-air oxygen saturation of 84% by pulse oximetry. Auscultation of the chest disclosed diffuse rales. Heart sounds were rapid and regular. Abdominal exam was benign. There was no skin rash. Central nervous exam demonstrated agitation and confusion, but was otherwise non-focal. Laboratory examination revealed a white blood count of 11.7 K/uL, hemoglobin of 21.5 g/DL, hematocrit of 66.8%, platelet count of 73 K/uL, partial thromboplastin time of 36 seconds, lactic acid of 2.4 mm/L, and procalcitonin of 43 ng/mL. Chest radiograph disclosed extensive bilateral infiltrates (Figure 1). Figure 1. Chest x-ray showing bilateral infiltrates
journal of applied pharmaceutical science, 2014
In the spring of 1993, an unknown group of hantaviruses emerged in the United States as the cause of an acute respiratory disease currently termed as Hantavirus pulmonary symdrome (HPS), also referred to as hantavirus cardiopulmonary syndrome (HCPS). HPS, a pan-American viral zoonosis, is a deadly viral hemorrhagic disease caused by sin nombre virus (SNV) and the extreme manifestations include increased capillary permeability (causing vascular leakage), circulatory instability, diffuse hemorrhage and thrombocytopenia. Virus infects the endothelial cells but does not disrupt the endothelium but leads to dramatic changes in both the function of infected endothelial cells and barrier function of endothelium. It has also been observed that capillary leakage is triggered by cytotoxic CD8+T cells (CTLs) and that cytokines contribute to the increased capillary permeability. Vascular permeability can also be increased by terminal soluble complement complex and this complement activation is ...
Lung, 2010
The objective of this study was to document persistent pulmonary symptoms and pulmonary function abnormalities in adults surviving hantavirus pulmonary syndrome (HPS). Acute infection by most hantaviruses result in mortality rates of 25-35%, while in Panama the mortality rate of 10% is contrasted by an unusually high incidence. In all types of HPS, the viral prodrome, cardiopulmonary phase due to massive pulmonary capillary leak syndrome, and spontaneous diuresis are followed by a convalescent phase with exertional dyspnea for 3-4 weeks, but the frequency of persistent symptoms is not known. In this observational study of a convenience sample, 14 survivors of HPS caused by Choclo virus infection in Panama and 9 survivors of HPS caused by Sin Nombre virus infection in New Mexico completed a questionnaire and pulmonary function tests up to 8 years after infection. In both groups, exertional dyspnea persisted for 1-2 years after acute infection in 43% (Panama) and 77% (New Mexico) of survivors surveyed. Reduction in midexpiratory flows (FEF(25-75%)), increased residual volume (RV), and reduced diffusion capacity (D(L)CO/VA) also were common in both populations; but the severity of reduced expiratory flow did not correlate with exertional dyspnea. Symptoms referable to previous hantavirus infection had resolved within 3 years of acute infection in most but not all patients in the Panama group. Temporary exertional dyspnea and reduced expiratory flow are common in early convalescence after HPS but resolves in almost all patients.
Hantavirus pulmonary syndrome. Pathogenesis of an emerging infectious disease
The American journal of pathology, 1995
A recent outbreak of a severe pulmonary disease in the southwestern United States was etiologically linked to a previously unrecognized hantavirus. The virus has been isolated from its major reservoir, the deer mouse, Peromyscus maniculatus, and recently named Sin Nombre virus. Clinically, the disease has become known as the hantavirus pulmonary syndrome (HPS). Since May 1993, 44 fatal cases of HPS have been identified through clinicopathological review and immunohistochemical (IHC) testing of tissues from 273 patients who died of an unexplained noncardiogenic pulmonary edema. In 158 cases for which suitable specimens were available, serological testing and/or reverse transcription-polymerase chain reaction (RT-PCR) amplification of extracted RNA was also performed. IHC, serological, and PCR results were concordant for virtually all HPS and non-HPS patients when more than one assay was performed. The prodromal illness of HPS is similar to that of many other viral diseases. Consisten...
Hantavirus Cardiopulmonary Syndrome and Diffuse Alveolar Hemorrhage in the Era of COVID-19
Case Reports in Infectious Diseases, 2021
Hantavirus Cardiopulmonary Syndrome (HCPS) can occur after infection with Hantavirus which can occur by inhaling aerosolized rodent urine, feces, and saliva contaminated with the virus. It presents with the rapid development of pulmonary edema, respiratory failure, and cardiogenic shock with the hallmark being microvascular leakage. We report a patient with a history of alcohol abuse and recent exposure to mice and sick kittens who presented with cough with sputum production, shortness of breath, orthopnea, and new-onset lower extremity edema. Imaging revealed bilateral infiltrates more common on the left with an unremarkable echocardiogram. Testing for COVID-19, Human Immunodeficiency Virus (HIV), influenza, bacterial pneumonia including tuberculosis and methicillin-resistant Staphylococcus aureus (MRSA), aspergillosis, histoplasmosis, Blastomyces, and Coccidiodes was negative. Bronchoscopy and bronchoalveolar lavage revealed diffuse alveolar hemorrhage (DAH) and were negative for ...
A Severe Case of Hantavirus Cardiopulmonary Syndrome in a Patient Presenting as STEMI
Journal of Cardiovascular Emergencies, 2023
Hantavirus cardiopulmonary syndrome (HCPS) is a rare disease caused by Hantaviruses, that are transmitted from rodents to humans through aerosols. In some patients, HCPS can have a severe evolution, with rapid progression to respiratory distress and cardiogenic shock. We present the case of a 56-year-old female patient who was transferred to our hospital with ST-segment elevation myocardial infarction (STEMI) and acute respiratory distress syndrome (ARDS). The coronary angiography showed normal epicardial coronary arteries and the lung computed tomography (CT) raised the suspicion of tracheoesophageal fistula, which was soon refuted by an upper digestive endoscopy. Initially, the evolution was very severe, requiring mechanical ventilation, hemodynamic support, and broad-spectrum antibiotics. Later, serological testing revealed an acute infection with Hantavirus Dobrava type. The patient lives in a rural environment, working in a wheat mill. Despite the severe presentation, the evolution was favorable, with complete remission of the pulmonary and myocardial damage after 2 weeks. We emphasize the importance of HCPS suspicion and specific testing in the early phase of the disease, as well as early admission to an intensive care unit, which is crucial in severe cases and can improve survival in a patient without any specific symptoms or a clear diagnosis.
Hantavirus Cardiopulmonary Syndrome: Implications for Transport Management and Care
Air Medical Journal, 2008
Introduction: A 14-year-old boy with cardiorespiratory failure was referred for air medical transport. The complexity of care during air medical transport and subsequent diagnosis of hantavirus warranted a post hoc review of the literature to establish optimal transport management criteria. Methods: This is a case report and literature review, defining epidemiology, presentation, cause of pulmonary edema and cardiac failure, management, and outcome. Results: Hantavirus cardiopulmonary syndrome is rare in children. Severe cases have manifestations similar to those seen in adults: atypical pneumonia progresses to respiratory failure with severe pulmonary edema and associated circulatory compromise. Mechanical ventilation, judicious fluid replacement, and early inotropic therapy are central to transport management. Critical care may require extracorporeal membrane oxygenation (ECMO). Mortality remains high, although it appears to be lower in children younger than 14 years. Conclusion: Hantavirus infection commonly progresses to a cardiopulmonary syndrome, in which mortality is high. Optimal management includes: early suspicion/recognition based on characteristic clinical course and history; provision of oxygen and comprehensive ventilatory support; judicious fluid replacement; early and intensive inotropic therapy; prompt referral to an appropriate level of care; skillful interfacility transport. Definitive care can involve ECMO.
High Levels of Viremia in Patients with the Hantavirus Pulmonary Syndrome
The Journal of Infectious Diseases, 1999
Hantavirus pulmonary syndrome (HPS) is a rare but acute fulminant disease caused by Sin Nombre virus (SNV). To understand the role of the viral load in the pathogenesis of HPS, the load of virus in the blood of patients with HPS was measured. A quantitative reverse transcription-polymerase chain reaction assay was developed for SNV, because SNV is difficult to grow in cell culture. Thirty-eight samples from 26 patients with HPS were analyzed. Twenty of the 26 initial samples were positive for viral RNA (7 of 9 samples were obtained from patients with fatal cases, and 13 of 17 were obtained from survivors). Mean viral RNA copy numbers were 10 4.1ע1.6 /mL in positive cases (10 4.1ע7.6 /mL in fatal cases, 10 3.1ע8.5 /mL in survivors) and were correlated with peak hematocrit () and with the lowest platelet count (P ! .05 P =). In 8 survivors who had serial samples obtained, viral RNA copy numbers decreased .05 promptly after resolution of fever.