Fatal Asthma

1999 ◽  
pp. 296-311
Keyword(s):  
Fatal Asthma

Potentially (near) fatal asthma

2019 ◽  
Vol 40 (6) ◽  
pp. 403-405 ◽  
Author(s):  
Paul A. Greenberger
Keyword(s):  
Severe Asthma ◽  
Health Care Professionals ◽  
Rescue Therapy ◽  
Respiratory Acidosis ◽  
Acute Severe Asthma ◽  
Increased Risk ◽  
High Risk Type ◽  
Fatal Asthma ◽  
Long Acting ◽  
Near Fatal Asthma

Potentially (near) fatal asthma (PFA) defines a subset of patients with asthma who are at increased risk for death from their disease. The diagnosis of PFA should motivate treating physicians, health professionals, and patients to be more aggressive in the monitoring, treatment, and control of this high-risk type of asthma. A diagnosis of PFA is made when any one of the following are present: (1) a history of endotracheal intubation from asthma, (2) acute respiratory acidosis (pH < 7.35) or respiratory failure from acute severe asthma, (3) two or more episodes of acute pneumothorax or pneumomediastinum from asthma, (4) two or more episodes of acute severe asthma, despite the use of long-term oral corticosteroids and other antiasthma medications. There are two predominant phenotypes of near-fatal exacerbations: “subacute” exacerbation and “hyperacute” exacerbation. The best way to “treat” acute severe asthma is 3‐7 days before it occurs (i.e., at the onset of symptoms or change in respiratory function) and to optimize control of asthma by decreasing the number of symptomatic days and the days and/or nights that require rescue therapy and increasing baseline respiratory status in “poor perceivers.” PFA is treated with a multifaceted approach; physicians and health-care professionals should appreciate limitations of pharmacotherapy, including combination inhaled corticosteroid‐long-acting β-agonist products as well as addressing nonadherence, psychiatric, and socioeconomic issues that complicate care.

scholarly journals Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Renata Calciolari Rossi ◽  
Raquel Anonni ◽  
Diogenes Seraphim Ferreira ◽  
Luiz Fernando Ferraz da Silva ◽  
Thais Mauad
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Pulmonary Arteries ◽  
Endothelial Activation ◽  
Bronchial Arteries ◽  
Activation Markers ◽  
Asthma Attack ◽  
Collagen Iii ◽  
Asthma Patients ◽  
Fatal Asthma

Abstract Background There is interest in better understanding vessel pathology in asthma, given the findings of loss of peripheral vasculature associated with disease severity by imaging and altered markers of endothelial activation. To date, vascular changes in asthma have been described mainly at the submucosal capillary level of the bronchial microcirculation, with sparse information available on the pathology of bronchial and pulmonary arteries. The aim of this study was to describe structural and endothelial activation markers in bronchial arteries (BAs) and pulmonary arteries (PAs) of asthma patients who died during a fatal asthma attack. Methods Autopsy lung tissue was obtained from 21 smoking and non-smoking patients who died of an asthma attack and nine non-smoking control patients. Verhoeff–Masson trichrome staining was used to analyse the structure of arteries. Using immuno-histochemistry and image analyses, we quantified extracellular matrix (ECM) components (collagen I, collagen III, versican, tenascin, fibronectin, elastic fibres), adhesion molecules [vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1)] and markers of vascular tone/dysfunction [endothelin-1 (ET-1) and angiotensin II type 2 receptor (AT2)] in PAs and BAs. Results There were no significant differences in ECM components, ICAM-1, ET-1 or AT2 between asthma patients and controls. Smoking asthma patients presented with decreased content of collagen III in both BA (p = 0.046) and PA (p = 0.010) walls compared to non-smoking asthma patients. Asthma patients had increased VCAM-1 content in the BA wall (p = 0.026) but not in the PA wall. Conclusion Our data suggest that the mechanisms linking asthma and arterial functional abnormalities might involve systemic rather than local mediators. Loss of collagen III in the PA was observed in smoking asthma patients, and this was compatible with the degradative environment induced by cigarette smoking. Our data also reinforce the idea that the mechanisms of leukocyte efflux via adhesion molecules differ between bronchial and pulmonary circulation, which might be relevant to understanding and treating the distal lung in asthma.

scholarly journals Part 10.5: Near-Fatal Asthma

Circulation ◽  
2005 ◽  
Vol 112 (24_suppl) ◽  
pp. IV-139-IV-142
Keyword(s):  
Fatal Asthma ◽  
Near Fatal Asthma

Rhabdomyolysis after successful resuscitation of a patient with near-fatal asthma

2007 ◽  
Vol 25 (6) ◽  
pp. 736.e3-736.e4 ◽  
Author(s):  
Yi-Jung Chen ◽  
Shih-Heng Chang ◽  
Ang Yuan ◽  
Chien-Hua Huang ◽  
Chien-Chang Lee
Keyword(s):  
Successful Resuscitation ◽  
Fatal Asthma ◽  
Near Fatal Asthma

Identifying An At-Risk Population of Children With Recurrent Near-Fatal Asthma Exacerbations

2010 ◽  
Vol 47 (4) ◽  
pp. 460-464 ◽  
Author(s):  
Christopher L. Carroll ◽  
Burcin Uygungil ◽  
Aaron R. Zucker ◽  
Craig M. Schramm
Keyword(s):  
At Risk ◽  
Risk Population ◽  
Asthma Exacerbations ◽  
Fatal Asthma ◽  
Near Fatal Asthma

A community-based study of near-fatal asthma

2001 ◽  
Vol 86 (2) ◽  
pp. 190-195 ◽  
Author(s):  
Brad B. Moore ◽  
Robin Wagner ◽  
Kevin B. Weiss
Keyword(s):  
Community Based ◽  
Fatal Asthma ◽  
Near Fatal Asthma
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