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Guo L, Yang X, Yang B, Tang G, Li C. Prevalence, in-hospital mortality, and factors related to neurogenic pulmonary edema after spontaneous subarachnoid hemorrhage: a systematic review and meta-analysis. Neurosurg Rev 2023; 46:169. [PMID: 37432487 PMCID: PMC10335949 DOI: 10.1007/s10143-023-02081-6] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/16/2023] [Revised: 06/29/2023] [Accepted: 07/04/2023] [Indexed: 07/12/2023]
Abstract
Neurogenic pulmonary edema (NPE) is a life-threatening and severe complication in patients with spontaneous subarachnoid hemorrhage (SAH). The prevalence of NPE varies significantly across studies due to differences in case definitions, study populations, and methodologies. Therefore, a precise estimation of the prevalence and risk factors related to NPE in patients with spontaneous SAH is important for clinical decision-makers, policy providers, and researchers. We conducted a systematic search of the PubMed/Medline, Embase, Web of Science, Scopus, and Cochrane Library databases from their inception to January 2023. Thirteen studies were included in the meta-analysis, with a total of 3,429 SAH patients. The pooled global prevalence of NPE was estimated to be 13%. Out of the eight studies (n = 1095, 56%) that reported the number of in-hospital mortalities of NPE among patients with SAH, the pooled proportion of in-hospital deaths was 47%. Risk factors associated with NPE after spontaneous SAH included female gender, WFNS class, APACHE II score ≥ 20, IL-6 > 40 pg/mL, Hunt and Hess grade ≥ 3, elevated troponin I, elevated white blood cell count, and electrocardiographic abnormalities. Multiple studies showed a strong positive correlation between the WFNS class and NPE. In conclusion, NPE has a moderate prevalence but a high in-hospital mortality rate in patients with SAH. We identified multiple risk factors that can help identify high-risk groups of NPE in individuals with SAH. Early prediction of the onset of NPE is crucial for timely prevention and early intervention.
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Affiliation(s)
- Lei Guo
- Department of Neurosurgery, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China
| | - Xu Yang
- Department of Neurology, The Tradional Chinese Medicine Hospital of Leshan, Leshan, 614000, China
| | - Bo Yang
- Department of Neurology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China
| | - Guo Tang
- Department of Emergency, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
| | - Chunling Li
- Department of Neurosurgery, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
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Venkatesan AM, Karmpaliotis D, Silverman ES. Neurogenic Pulmonary Edema Following Catastrophic Subarachnoid Hemorrhage: A Case Report and Pathophysiologic Review. J Intensive Care Med 2016. [DOI: 10.1177/088506660101600505] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
Neurogenic pulmonary edema (NPE) is an increase in interstitial and alveolar lung fluid that occurs as a direct consequence of acute or subacute central nervous system (CNS) injury. In this review we describe a patient who developed hypoxemic respiratory failure as a result of NPE following catastrophic subarachnoid hemorrhage (SAH). The patient displayed many of the characteristic symptoms, signs, and physiologic aberrations associated with NPE, including an altered level of consciousness, dyspnea, cyanosis, crackles, hypoxemia, and diffuse pulmonary infiltrates. These clinical features can be mistaken for other causes of pulmonary edema and may lead to confusion in the diagnosis and therapeutic approach of hypoxemic respiratory failure in the setting of CNS injury. Although NPE is thought to be due to a combination of pulmonary capillary leakage and elevated intravascular pressures, many questions about its pathophysiology remain unanswered. Data from animal models using therapeutic trials of antiadrenergic agents suggest a significant role for sympathetic nervous system activation and massive catecholamine release in the pathogenesis of this disorder. The most common causes of NPE include head trauma, seizures, cerebral hemorrhages, subarachnoid bleeds, and increased intracranial pressure of any etiology. As is generally observed with this disorder, conservative and supportive management of our patient's respiratory failure led to complete resolution of the NPE within 96 hours. Although NPE is an infrequent phenomenon, it should be considered in the differential diagnosis of all patients who develop respiratory complications soon after CNS injury.
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Affiliation(s)
- Aradhana M. Venkatesan
- Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
| | - Dimitri Karmpaliotis
- Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA
| | - Eric S. Silverman
- Pulmonary and Critical Care Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
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Zhang L, Qi S. Electrocardiographic Abnormalities Predict Adverse Clinical Outcomes in Patients with Subarachnoid Hemorrhage. J Stroke Cerebrovasc Dis 2016; 25:2653-2659. [PMID: 27476337 DOI: 10.1016/j.jstrokecerebrovasdis.2016.07.011] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2016] [Revised: 06/13/2016] [Accepted: 07/02/2016] [Indexed: 11/30/2022] Open
Abstract
BACKGROUND We conducted a retrospective cohort study of a large sample to assess whether electrocardiographic (ECG) abnormalities are independently associated with the occurrence of neurogenic pulmonary edema (NPE), delayed cerebral ischemia (DCI), and in-hospital death after nontraumatic subarachnoid hemorrhage (SAH). METHODS In this retrospective observational study, patients who were admitted within 72 hours of SAH symptom onset between 2013 and 2015 were enrolled. Twelve-lead ECG findings obtained within 72 hours after SAH and the presence of NPE, DCI, and in-hospital death were collected based on the results reported in the medical records. RESULTS We included 834 patients. NPE occurred in 192 patients (23%). The median delay from SAH onset to NPE was 3 days (interquartile range [IQR]: 5 days). DCI occurred in 223 patients (27%; median delay to DCI, 4 days; IQR: 5 days). In total, 141 patients (17%) died in the hospital (median time to death, 12 days; IQR: 18 days). The frequency of ECG abnormalities for all enrolled patients was 65%. Corrected QT prolongation had an adjusted risk ratio (RR) of 1.5 (1.1-2.2) for NPE and 1.8 (1.3-2.4) for DCI. ST depression had an adjusted RR of 3.0 (1.2-7.5) for in-hospital death. NSSTTCs (nonspecific ST- or T-wave changes) had an adjusted RR of 2.7 (1.8-4.2) for NPE, 2.8 (1.9-4.3) for DCI, and 2.2 (1.3-3.5) for in-hospital death. All RRs were adjusted for age and Hunt-Hess scores. CONCLUSIONS ECG abnormalities assessed within 72 hours after SAH using a standard 12-lead ECG are independently associated with an increased risk of adverse clinical outcomes in patients with nontraumatic SAH.
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Affiliation(s)
- Limin Zhang
- Department of Anaesthesiology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, China
| | - Sihua Qi
- Department of Anaesthesiology, The Fourth Affiliated Hospital, Harbin Medical University, Harbin, China.
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Heart Rate Variability Predicts Neurogenic Pulmonary Edema in Patients with Subarachnoid Hemorrhage. Neurocrit Care 2015; 25:71-8. [DOI: 10.1007/s12028-015-0237-3] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/22/2022]
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Mrozek S, Constantin JM, Geeraerts T. Brain-lung crosstalk: Implications for neurocritical care patients. World J Crit Care Med 2015; 4:163-178. [PMID: 26261769 PMCID: PMC4524814 DOI: 10.5492/wjccm.v4.i3.163] [Citation(s) in RCA: 58] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/08/2015] [Revised: 04/29/2015] [Accepted: 05/28/2015] [Indexed: 02/06/2023] Open
Abstract
Major pulmonary disorders may occur after brain injuries as ventilator-associated pneumonia, acute respiratory distress syndrome or neurogenic pulmonary edema. They are key points for the management of brain-injured patients because respiratory failure and mechanical ventilation seem to be a risk factor for increased mortality, poor neurological outcome and longer intensive care unit or hospital length of stay. Brain and lung strongly interact via complex pathways from the brain to the lung but also from the lung to the brain. Several hypotheses have been proposed with a particular interest for the recently described “double hit” model. Ventilator setting in brain-injured patients with lung injuries has been poorly studied and intensivists are often fearful to use some parts of protective ventilation in patients with brain injury. This review aims to describe the epidemiology and pathophysiology of lung injuries in brain-injured patients, but also the impact of different modalities of mechanical ventilation on the brain in the context of acute brain injury.
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Junttila E, Ala-Kokko T, Ohtonen P, Vaarala A, Karttunen A, Vuolteenaho O, Salo T, Sutinen M, Karhu T, Herzig KH, Koskenkari J. Neurogenic Pulmonary Edema in Patients with Nontraumatic Intracerebral Hemorrhage. Anesth Analg 2013; 116:855-61. [DOI: 10.1213/ane.0b013e3182811cc7] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/05/2022]
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Lakkireddigari SKR, Durga P, Nayak M, Ramchandran G. Preoperative neurogenic pulmonary edema: A dilemma for decision making. J Anaesthesiol Clin Pharmacol 2012; 28:232-4. [PMID: 22557750 PMCID: PMC3339732 DOI: 10.4103/0970-9185.94905] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/05/2022] Open
Abstract
Neurogenic pulmonary edema may be a less-recognized consequence of obstructive hydrocephalus. The authors report a patient with acute obstructive hydrocephalus due to cerebellar metastatic lesion, who presented with neurogenic pulmonary edema. The edema resolved on placement of the ventriculoperitonial shunt. This report addresses the importance of recognition of neurogenic pulmonary edema as a possible perioperative complication resulting from an increase in intracranial pressure and the issues involved with anesthetic management of co-existing neurogenic pulmonary edema and intracranial hypertension.
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McLaughlin N, Bojanowski MW, Girard F, Denault A. Pulmonary edema and cardiac dysfunction following subarachnoid hemorrhage. Can J Neurol Sci 2005; 32:178-85. [PMID: 16018152 DOI: 10.1017/s0317167100003942] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/07/2022]
Abstract
BACKGROUND Pulmonary edema (PE) can occur in the early or late period following subarachnoid hemorrhage (SAH). The incidence of each type of PE is unknown and the association with ventricular dysfunction, both systolic and diastolic, has not been described. METHODS Retrospective chart review of 178 consecutive patients with SAH surgically treated over a three-year period. Patients with pulmonary edema diagnosed by a radiologist were included. Early onset SAH was defined as occurring within 12 hours. Cardiac function at the time of the PE was analyzed using hemodynamic and echocardiographic criteria of systolic and diastolic dysfunction. Pulmonary edema was observed in 42 patients (28.8%) and was more often delayed (89.4%). Evidence of cardiac involvement during PE varied between 40 to 100%. RESULTS AND CONCLUSIONS Pulmonary edema occurs in 28.8% of patients after SAH, and is most commonly delayed. Cardiac dysfunction, both systolic and diastolic, is commonly observed during SAH and could contribute to the genesis of PE after SAH.
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Affiliation(s)
- Nancy McLaughlin
- Department of Neurosurgery, Centre Hospitalier de l'Université de Montréal-Hôpital Notre-Dame, QC, Canada
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Avlonitis VS, Fisher AJ, Kirby JA, Dark JH. Pulmonary transplantation: the role of brain death in donor lung injury. Transplantation 2003; 75:1928-33. [PMID: 12829889 DOI: 10.1097/01.tp.0000066351.87480.9e] [Citation(s) in RCA: 161] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]
Abstract
The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of brain death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of brain death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.
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Affiliation(s)
- Vassilios S Avlonitis
- School of Surgical and Reproductive Sciences (Surgery), Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, United Kingdom.
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Wu JM, Wang JN, Tsai YC, Liu CC, Huang CC, Chen YJ, Yeh TF. Cardiopulmonary manifestations of fulminant enterovirus 71 infection. Pediatrics 2002; 109:E26-. [PMID: 11826236 DOI: 10.1542/peds.109.2.e26] [Citation(s) in RCA: 54] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/24/2022] Open
Abstract
BACKGROUND The pathogenesis of acute pulmonary edema and cardiac collapse after enterovirus 71 (EV71) infection are not completely understood. OBJECTIVE To determine the hemodynamic features and the mechanism of pulmonary edema (PE) after EV71 infection by direct intracardiac monitoring. DESIGN Prospective clinical and laboratory study at a tertiary medical center. PARTICIPANTS Five consecutive infants, ages 2 to 13 months, with EV71 infection-proved by viral isolation in 4 and antibody in 1-with PE were enrolled. The clinical characteristics were systemically assessed. Hemodynamic profiles were determined every 4 hours by simultaneously implanted pulmonary arterial and central venous catheters during the acute stage. RESULTS Magnetic resonance imaging revealed that all 5 infants had brainstem lesions. All patients had tachycardia and hyperthermia. Transient systolic hypertension was noted in 1 patient, and 1 presented with hypotension. Pulmonary artery pressure in all 5 infants was normal or mildly elevated (26-31 mm Hg), and central venous pressure ranged from 10 to 22 mm Hg. Pulmonary artery occlusion pressures were normal or slightly elevated (13-16 mm Hg). Systemic and pulmonary vascular resistances were transiently increased in only 1 patient. The stroke volume index decreased to 15.3 to 35.7 mL/M2 (normal: 30-60 mL/M2), but because of the elevated heart rate, the cardiac index did not decrease. All hemodynamics normalized within days. CONCLUSION Fulminant EV71 infection may lead to severe neurologic complications and acute PE. The acute PE and cardiopulmonary decompensation in EV71 infection are not directly caused by viral myocarditis. The mechanism of PE may be related to increased pulmonary vascular permeability caused by brainstem lesions and/or systemic inflammatory response instead of increased pulmonary capillary hydrostatic pressure.
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Affiliation(s)
- Jing-Ming Wu
- Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan.
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Venkatesan AM, Karmpaliotis D, Silverman ES. Neurogenic Pulmonary Edema Following Catastrophic Subarachnoid Hemorrhage: A Case Report and Pathophysiologic Review. J Intensive Care Med 2001. [DOI: 10.1046/j.1525-1489.2001.00236.x] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
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Dragosavac D, Falcão AL, Araújo S, Terzi RG. [Neurogenic pulmonary edema. Report of 2 cases]. ARQUIVOS DE NEURO-PSIQUIATRIA 1997; 55:305-9. [PMID: 9629392 DOI: 10.1590/s0004-282x1997000200020] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal aspiration or any other risk factor for development of adult respiratory distress syndrome. In the first case, with severe head trauma, neurogenic pulmonary edema was diagnosed at admission one hour after trauma, associated with severe systemic inflammatory reaction, and good outcome in three days. The second case, with hemorrhagic vascular insult, developed neurogenic pulmonary edema the fourth day after drainage of intracerebral hematoma and died.
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Affiliation(s)
- D Dragosavac
- Unidade de Tratamento Intensivo, Hospital das Clínicas Universidade Estadual de Campinas (UTI-HC-UNICAMP), SP, Brasil
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Shibamoto T, Wang HG, Tanaka S, Koyama S. No effects of large doses of catecholamines on vascular permeability in isolated blood-perfused dog lungs. ACTA PHYSIOLOGICA SCANDINAVICA 1995; 155:127-35. [PMID: 8669285 DOI: 10.1111/j.1748-1716.1995.tb09957.x] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
Neurogenic pulmonary oedema (NPO) is believed to be induced by intense activation of the sympathetic nervous system, characterized by massive secretion of catecholamines into the blood stream. There is a possibility that NPO is partly the result of increased vascular permeability. However, the mechanism for an increase in pulmonary vascular permeability is not known. The present study was designed to test the hypothesis that large doses of catecholamines increase pulmonary microvascular permeability directly. Adrenaline or noradrenaline (100 and 300 micrograms) was injected as a bolus into isolated dog lungs perfused with heparinized autologous blood at constant pressure. Adrenaline or noradrenaline produced sustained lung weight loss although both catecholamines increased pulmonary capillary pressure, assessed by double occlusion pressure, by 2-5 mmHG above baseline. Vascular permeability, as measured by the capillary filtration coefficient and the isogravimetric capillary pressure, did not change significantly from baseline at 30 and 60 min after catecholamine. Finally, the final-to-initial wet lung weight ratio of the catecholamine-treated lungs did not differ from that of saline-injected control lungs. Thus, we conclude that circulating catecholamines, even at supraphysiological doses, do not increase permeability in isolated blood-perfused dog lungs.
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Affiliation(s)
- T Shibamoto
- Department of Physiology, Shinshu University School of Medicine, Nagano, Japan
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Brito JC, Diniz MC, Rosas RR, da Silva JA. [Acute neurogenic pulmonary edema: a case report]. ARQUIVOS DE NEURO-PSIQUIATRIA 1995; 53:288-93. [PMID: 7487541 DOI: 10.1590/s0004-282x1995000200020] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
The authors report a case of acute neurogenic pulmonary edema in a 28-year-old woman who presented rupture of an internal carotid artery aneurysm and subarachnoid hemorrhage. The respiratory disorders started at the same time the patient's symptomatology aggravated. Some etiological and pathophysiological aspects on neurogenic pulmonary edema are revised.
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Affiliation(s)
- J C Brito
- Serviço de Neurologia e Neurocirurgia, Hospital Santa Isabel, João Pessoa, Paraíba, Brasil
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Vuong TK, Dautheribes C, Laaban JP. [Respiratory distress syndrome in adults: current data]. Rev Med Interne 1990; 11:42-8, 51-2. [PMID: 2183323 DOI: 10.1016/s0248-8663(05)80607-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Affiliation(s)
- T K Vuong
- Service de Pneumologie et Réanimation, Hôtel Dieu de Paris
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