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Poster Presentations: Wednesday, October 26, 2011 |

Pathophysiological Mechanisms of Acute Lung Injury in Patients With Leptospirosis FREE TO VIEW

Hsing I Chen, MD; Yung-Hsiang Hsu, MD
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Tzu Chi University, Hualien, Taiwan



Chest. 2011;140(4_MeetingAbstracts):789A. doi:10.1378/chest.1081690
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Abstract

PURPOSE: Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a serious clinical problem, we investigated the pathogenic mechanisms of ARDS caused by leptospirosis due to spirochetes infection.

METHODS: The study involved five cases of leptospirosis. We monitored the arterial pressure (AP) and heart rate (HR) and analyzed the AP and HR variabilities for the assessment of autonomic functions. Histopathological changes in the lung, brain, kidney, heart, and liver were examined. In addition, we identified the expression of inducible nitric oxide synthase (iNOS) using immunohistochemical stain.

RESULTS: Five patients associated with leptospirosis died of ARDS. Before death, severe hypotension and bradycardia occurred, spectral analysis of AP and HR variabilities indicated decreased sympathetic drive and increased parasympathetic activity. Pathological examinations revealed spirochetes in the lung, alveolar hemorrhage, myocarditis, portal inflammation, and interstitial nephritis. Immunohistochemical stain disclosed iNOS expression in the lung, heart, liver, and renal tubules. Biochemical determinations indicated hypoxia, hyperglycemia, increased nitrate/nitrite, methyl guanidine (an index for hydroxyl radical), creatinine, and glutamic oxaloacetic transaminase.

CONCLUSIONS: The changes suggest that leptospirosis causes severe hypotension and bradycardia accompanied by autonomic dysfunction. Finally, multiple organ damage and failure ensued. The pathogenesis of lung and organ injury may involve iNOS and NO production.

CLINICAL IMPLICATIONS: ARDS induced by leptospirosis may be not common. The study provides information to the pathophysiological mechanisms of ARDS in patients with spirochetes infection.

DISCLOSURE: The following authors have nothing to disclose: Hsing I Chen, Yung-Hsiang Hsu

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