SESSION TITLE: Infectious Disease Student/Resident Cases
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 07:30 AM - 08:30 AM
INTRODUCTION: Leptospirosis is a potentially life-threatening zoonosis and may lead to multi-organ failure. Severe pulmonary hemorrhagic syndrome (SPHS) is emerging as a leading cause of death in many leptospirosis outbreaks with case-fatality rates quoted as high as 74%. We present a case of leptospirosis with SPHS presenting to an urban hospital successfully treated with high-dose corticosteroids.
CASE PRESENTATION: A 21-year-old male smoker presented with a two-day history of chest pain, fevers, vomiting, diarrhea, and mild hemoptysis. Of significance, he worked as a butcher in a poultry slaughterhouse. He was tachypneic, diaphoretic with fever of 103.3F and chest exam revealed diffuse expiratory wheezes. Laboratory studies showed a leukocytosis (11,100 /uL) and pre-renal azotemia (Cr 2.2mg/dL). Chest radiograph showed bilateral diffuse patchy infiltrates. Shortly after, the patient developed massive hemoptysis and became progressively hypoxic despite early empiric antibiotic therapy. His hemoglobin dropped from 11.5 to 5.7g/dl and he was transfused to a target of 7g/dl. He was intubated and ventilated (as per ARDSnet protocol) and tracheal lavage was consistent with diffuse alveolar hemorrhage (DAH). Common infectious pathogens and vasculitides were ruled out yet his clinical parameters deteriorated rapidly. His potential zoonotic exposure, an elevated ESR and widespread ground glass change on high-resolution CT led us to empirically pulsing him with high-dose methylprednisone. Significant clinical improvement was observed thereafter and a leptospira indirect hemagglutination test returned positive at a titer of >1:800 negating the need for an open lung biopsy. The patient was extubated 8 days later once his hemoptysis and oxygenation requirements had decreased.
DISCUSSION: Leptospirosis is typically a self-limiting disease, but SPHS is a rare and severe complication with a high mortality rate. The pathophysiology of SPHS is unclear, but leptospires appear to induce an acute lung injury affecting different components of the alveolocapillary membrane. Immunoglobulin and complement deposition in the microvascular circulation predisposes the lung to hemorrhage. These observed immune-mediated effects may explain the success of methylprednisolone in reducing mortality in a cohort of SPHS cases.
CONCLUSIONS: Systemic steroids are emerging as a crucial intervention in the treatment of leptospirosis associated SPHS. This case underlines the importance of detailed history taking, prudent supportive care and early immunosuppression to achieve favorable outcomes in sporadic cases, even in non-endemic urban centers. High-risk occupational exposures must lead providers to suspect this condition in the setting of DAH and consider immunosuppression at an early stage.
Reference #1: Shenoy, V.V., et al., Pulmonary leptospirosis: an excellent response to bolus methylprednisolone. Postgrad Med J, 2006. 82(971): p. 602-6.
DISCLOSURE: The following authors have nothing to disclose: Haider Ali, William Wong, Aanchal Gupta, Diane Maggiore, Christina Coyle, Virginia Chung, Amit Tibb, Irene Galperin
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