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COMMENTARY
Year : 2012  |  Volume : 4  |  Issue : 9  |  Page : 399-400

Infection with influenza a (H1N1) virus: Prediction of a bad outcome


Department of Internal Medicine, Little Rock Diagnostic Clinic and Baptist Health Medical Center, Division of Pulmonary and Critical Care Medicine: AR 72205, USA

Date of Web Publication14-Sep-2012

Correspondence Address:
Samer Homsi
Department of Internal Medicine, Little Rock Diagnostic Clinic and Baptist Health Medical Center, Division of Pulmonary and Critical Care Medicine: 10001 Little Drive, Little Rock AR 72205
USA
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Source of Support: None, Conflict of Interest: None


PMID: 23050249

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How to cite this article:
Homsi S. Infection with influenza a (H1N1) virus: Prediction of a bad outcome. North Am J Med Sci 2012;4:399-400

How to cite this URL:
Homsi S. Infection with influenza a (H1N1) virus: Prediction of a bad outcome. North Am J Med Sci [serial online] 2012 [cited 2020 Jan 26];4:399-400. Available from: http://www.najms.org/text.asp?2012/4/9/399/100985

The H1N1 virus causes a spectrum of diseases ranging from mild upper respiratory tract infections to severe lower respiratory tract infections that can lead to acute lung injury (ALI) or acute respiratory failure (ARDS). Severe lung injury from H1N1 viral infection carries a high mortality rate. Prior identification of potentially fatal (H1N1) cases and early and aggressive treatment in the intensive care unit (ICU) for such patients may affect their outcomes. In the study "H1N1-infected patients in ICU and their clinical outcome" by Talkad et al., [1] the authors addressed important goals in studying the clinical profile, risk factors, and laboratory parameters of H1N1 patients admitted to the ICU in relation to their outcomes (survivor vs. non-survivor). In this study, ARDS was observed to be the main cause of mortality and PaO2/FiO2 was important in determining the severity of lung injury and mode of ventilation.

Severe lung injury from the H1N1 virus is thought to be a result of direct infection of the alveolar lining cells (type I and type II) by the H1N1 virus, causing severe alveolar damage. [2] There is a long period of virus activity along with a high rate of virus replication, which is probably responsible for the virus virulence and the illness severity. [3] Further lung injury can occur from an aberrant pulmonary immune response triggered by the virus or from a superimposed bacterial infection. Major pathogens isolated from lung tissue of the lethal cases include Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes, Streptococcus mitis, and Haemophilus. [4]

Laboratory findings at presentation in patients with severe illness from the H1N1 virus typically include normal or low-normal leukocyte counts with lymphocytopenia. A poor prognosis is associated with increased levels of creatinine, creatine kinase, metabolic acidosis, thrombocytopenia, and elevated lactate dehydrogenase. [5] In this study, serum procalcitonin (PCT) was positive in nine fatal cases. Thus, the serum PCT level may be useful in determining the outcome.

Specific risk factors that can predict increased risk for developing critical illness from an influenza A (H1N1) viral infection are not completely understood. Young adults, pregnant women, and patients with pre-existing medical conditions, such as morbid obesity, chronic lung or liver disease, and diabetes mellitus, were reported to be at risk for severe illness from influenza A (H1N1) viral infection. [6] Recognizing early signs and symptoms of lower respiratory tract infection with the virus, especially in the high-risk groups, and understanding the pathophysiological profile of the illness are crucial for disease management.

 
  References Top

1.Kumar TC, Shivakumar NS, Deepak TS, Rashmi K, Goutam MS, Vivek G. H1N1-infected patients in ICU and their clinical outcome. North Am J Med Sci 2012;4:394-8.   Back to cited text no. 1
    
2.Childs RA, Palma AS, Wharton S, Matrosovich T, Liu Y, Chai W, et al. Receptor-binding specificity of pandemic influenza A (H1N1) 2009 virus determined by carbohydrate microarray. Nat Biotechnol 2009;27:797-9.  Back to cited text no. 2
    
3.Itoh Y, Shinya K, Kiso M, Watanabe T, Sakoda Y, Hatta M, et al. In vitro and in vivo characterization of new swine-origin H1N1 influenza viruses. Nature 2009;460:1021-5.  Back to cited text no. 3
[PUBMED]    
4.Morens DM, Taubenberger JK, Fauci AS. Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: Implications for pandemic influenza preparedness. J Infect Dis 2008;198:962-70.  Back to cited text no. 4
[PUBMED]    
5.Domínguez-Cherit G, Lapinsky SE, Macias AE, Pinto R, Espinosa-Perez L, de la Torre A, et al. Critically Ill patients with 2009 influenza A(H1N1) in Mexico. JAMA 2009;302:1880- 7.  Back to cited text no. 5
    
6.Bautista E, Chotpitayasunondh T, Gao Z, Harper SA, Shaw M, Uyeki TM, et al.; Writing Committee of the WHO Consultation on Clinical Aspects of Pandemic (H1N1) 2009 Influenza. Clinical aspects of pandemic 2009 influenza A (H1N1) virus infection. N Engl J Med 2010;362:1708-19.  Back to cited text no. 6
    




 

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