Samer Homsi1. 1. Department of Internal Medicine, Little Rock Diagnostic Clinic and Baptist Health Medical Center, Division of Pulmonary and Critical Care Medicine: AR 72205, USA.
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 H1N1viral 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-infectedpatients 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 H1N1patients 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.
Authors: Edgar Bautista; Tawee Chotpitayasunondh; Zhancheng Gao; Scott A Harper; Michael Shaw; Timothy M Uyeki; Sherif R Zaki; Frederick G Hayden; David S Hui; Joel D Kettner; Anand Kumar; Matthew Lim; Nahoko Shindo; Charles Penn; Karl G Nicholson Journal: N Engl J Med Date: 2010-05-06 Impact factor: 91.245
Authors: Guillermo Domínguez-Cherit; Stephen E Lapinsky; Alejandro E Macias; Ruxandra Pinto; Lourdes Espinosa-Perez; Alethse de la Torre; Manuel Poblano-Morales; Jose A Baltazar-Torres; Edgar Bautista; Abril Martinez; Marco A Martinez; Eduardo Rivero; Rafael Valdez; Guillermo Ruiz-Palacios; Martín Hernández; Thomas E Stewart; Robert A Fowler Journal: JAMA Date: 2009-10-12 Impact factor: 56.272
Authors: Robert A Childs; Angelina S Palma; Steve Wharton; Tatyana Matrosovich; Yan Liu; Wengang Chai; Maria A Campanero-Rhodes; Yibing Zhang; Markus Eickmann; Makoto Kiso; Alan Hay; Mikhail Matrosovich; Ten Feizi Journal: Nat Biotechnol Date: 2009-09 Impact factor: 54.908