Originally published in MedPage Today
by Michael Smith, MedPage Today North American Correspondent
Brazilian researchers have found three distinct patterns of lung damage in patients who died of the H1N1 pandemic flu.
They also found evidence of a so-called “cytokine storm,” a runaway immune response associated with the lung damage, according to Thais Mauad, MD, PhD, of Sao Paulo University Medical School, and colleagues.
The findings come from the first autopsy series of patients who succumbed to the pandemic influenza strain, Mauad and colleagues wrote in the Jan. 1 issue of the American Journal of Respiratory and Critical Care Medicine.
The researchers reported on autopsies of 21 patients performed during July and August of 2009, the winter flu season in the Southern Hemisphere.
Most patients with an H1N1 infection have standard flu-like symptoms that include fever, cough, and myalgia and a “benign course,” the researchers said.
But 86% of the patients in this series presented with shortness of breath, as well as cough, fever, and muscle aches, they found.
In addition, they said, 16 of the 21 had preexisting medical conditions, including chronic cardiovascular diseases and cancer. Relatively few had chronic respiratory disease, diabetes, or obesity — about 10% for all conditions.
All patients had respiratory failure and needed mechanical ventilation, while 15 had acute respiratory distress syndrome (ARDS). The remaining six had acute lung damage that did not meet all the criteria for ARDS, the researchers reported.
But not all cases of lung damage were the same:
* Nine patients had classic exudative diffuse alveolar damage (DAD), characterized by alveolar and interstitial edema, alveolar fibrinous exudate with hyaline membranes, and reactive pneumocytes.
* Six patients had DAD along with severe necrotizing bronchiolitis, characterized by extensive necrosis of the bronchiolar wall and a bronchiolar lumen densely infiltrated by neutrophils.
* And five patients had exudative DAD with an intense hemorrhagic component.
* The remaining patient had no interstitial changes induced by the virus. Death in that case — a patient with laryngeal cancer — was caused by pulmonary thromboembolism and bacterial pneumonia.
A large fraction of the patients (38%) had evidence of bacterial coinfection, the researchers found, suggesting that antibiotic therapy might have clinical value.
In addition, there were high circulating levels of toll-like receptor-3 and interferon-gamma, as well as a large number of CD8-positive T cells and granzyme B-positive cells in the lung tissue.
The researchers said in the journal that the results imply that “viral overload leads to altered innate immune responses” that lead to inflammation in the lung tissue.
Indeed, the study “suggests that an overly vigorous host inflammatory response triggered by the viral infection may spill over to and damage lung tissue,” according to John Heffner, MD, of Providence Health and Services in Portland, Ore.
That process could lead to “acute lung injury and fatal respiratory failure,” Heffner said in a statement. Heffner, a former president of the American Thoracic Society, was not part of the research team.
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