PURPOSE: To describe the anatomic and physiologic sequels of I-H1N1 viral severe pneumonia at median term of discharge in hospitalized patients of UANL Universitary Hospital in Monterrey, Mexico.
METHODS: After discharge 6 patients with I-H1N1 severe pneumonia were followed up in the Pulmonary Clinic for, physiologic, clinic and radiologic evaluation with complete pulmonary function test (including DLCO) and chest HRCT.
RESULTS: Three patients were male. Age: 37.3±13.77 years. BMI showed obesity: 31.78±5.5. Previous duration of symptoms: 8.8±4.79 days. Days before antiviral treatment: 9. All patients had cough, dyspnoea, lymphopenia and elevated LDH and CPK. The PaO2/FiO2 ratio was 189±99. The A-aO2Dif was 181±161 mmHg. The APACHE II was 8±2.36 points. At entry all presented multiple consolidations, being the right inferior lobe the most affected. Four required ICU. The hospital stay was 9 days (median). During follow up pulmonary function test and chest HRCT were performed respectively 63.5 and 58.8 days after hospital admission, (medians). All HRCT showed traction bronchiectasis and reticulation. Ground glass was observed in 4 patients. Pulmonary damage extension was 62.5% (range 20-90). Physiologically, all patients showed a mild restrictive pattern. (TLC: 66.5±5.71, FVC: 63.67±8.01). The DLCO was 59.92±11.69 (% pred.). There was a significative correlation between DLCO and LDH levels (r = -0.823), PaO2/FiO2 ratio (r= 0.827) and A-aO2Dif (r= -0.818). The resting oxygen saturation was normal in all patients.
CONCLUSIONS: We observed a residual physiologic alteration and similar fibrosis as reported in postARDS patients despite low APACHE II. The residual diffusion was lower when there were more oxygenation disturbances during hospitalization. According to these findings, LDH could be a severity marker. It is necessary to explore deeper this point as well as the alterations during exercise in this patients.
CLINICAL IMPLICATIONS: The evolution of patients with ARDS secondary to I-H1N1 severe pneumonia is not different of that of patients with ARDS secondary to other causes. LDH can be a marker of gas exchange impairment.
DISCLOSURE: The following authors have nothing to disclose: Julio Gonzalez, Hector Gonzalez-Delgado, Ana Zamora, José Felipe Villegas-Elizondo, Roberto Mercado-Longoria, Uriel Chavarria
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