Sir,In H1N1 severe acute respiratory distress syndrome (ARDS) cases, native lung function is usually so compromised with resultant severe hypoxemia,[1-3] that the overall case fatality ratio has been estimated at <0.5%, with a short disease course and good prognosis.[23] The lung function in survivors of acute lung injury returns to normal over six to twelve months independently, on etiology.[4] We report a long-term respiratory functional exploration by a spirometer type Sensor Medics in six-survival patients among eighteen suffering from acute respiratory distress after the pandemic 2009 H1N1 influenza, requiring protective mechanical ventilation. They were strongly affected with a mean pulmonary compliance of 22.6 ± 3.9 ml/ cm H2O (range, 18 to 28), a PaO2/FiO2 of 109 ± 29 mmHg and a chest computed tomography (CT) showing ground glass opacities corresponding to areas of alveolar edema and necropsy, with pulmonary lesions in favor of fibrosis in one patient. No pulmonary co- or secondary infection was retained on admission and during ICU stay. The evolution was gradually favorable, which allowed mechanical weaning with a delay of 17 ± 9 days (range, 8 to 30). In the substantial proportion of mechanically ventilated patients with slow recovery, the chest CT realized between three and six months was normal in five patients, and showed a persistence of bilateral and diffuse interstitial infringement in the patient who developed early pulmonary fibrosis. The lung function testing realized between six months and a year was within normal limits in all patients, even in those developing pulmonary fibrosis [Figure 1]. According to literature data, all that we might know is the recuperation ad integrum of the respiratory function within a six- month- to- a- one year period, after an acute respiratory failure, independent from the virus AH1N1.[4] As a matter of fact, all the literature data published since April 2009 concerning secondary acute respiratory distress were interested in the predictable, clinical, and epidemiological aspects within the short-term.[56] No follow-up in the long term that includes a research study on the respiratory function has been subject for publication up to now. Our results match with the study of Suchyta,[4] with recuperation of a normal respiratory function, as witnessed in the forced results of the spirometer and in the movable volumes. This makes one believe that the evolution of ARDS due to the AH1N1 virus is always quite favorable if the patient manages to survive the initial phase of the disease; the patients’ respiratory functional follow-up being proof of the total recovery. As such, facing reduced numbers and surveillance on a larger scale would be desirable so as to justify these results.
Figure 1
Pulmonary function test in patient who developed early pulmonary fibrosis
Pulmonary function test in patient who developed early pulmonary fibrosis
Authors: Gerardo Chowell; Stefano M Bertozzi; M Arantxa Colchero; Hugo Lopez-Gatell; Celia Alpuche-Aranda; Mauricio Hernandez; Mark A Miller Journal: N Engl J Med Date: 2009-06-29 Impact factor: 91.245
Authors: Anand Kumar; Ryan Zarychanski; Ruxandra Pinto; Deborah J Cook; John Marshall; Jacques Lacroix; Tom Stelfox; Sean Bagshaw; Karen Choong; Francois Lamontagne; Alexis F Turgeon; Stephen Lapinsky; Stéphane P Ahern; Orla Smith; Faisal Siddiqui; Philippe Jouvet; Kosar Khwaja; Lauralyn McIntyre; Kusum Menon; Jamie Hutchison; David Hornstein; Ari Joffe; Francois Lauzier; Jeffrey Singh; Tim Karachi; Kim Wiebe; Kendiss Olafson; Clare Ramsey; Sat Sharma; Peter Dodek; Maureen Meade; Richard Hall; Robert A Fowler Journal: JAMA Date: 2009-10-12 Impact factor: 56.272
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