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  • Meeting abstract
  • Open Access

Hantavirus Cardiopulmonary Syndrome: report of four cases

  • 1,
  • 1 and
  • 1
Critical Care20037 (Suppl 3) :P70

https://doi.org/10.1186/cc2266

  • Published:

Keywords

  • Pulmonary Edema
  • Acute Respiratory Distress Syndrome
  • Pulmonary Capillary Wedge Pressure
  • Pulmonary Artery Catheter
  • Fluid Replacement

Hantavirus Cardiopulmonary Syndrome was first described in southwestern USA as a condition that involves mainly the lungs, leading to a high mortality rate (over 50%), caused by a new Hantavirus species. The pathology of this disease involves the direct viral damage of lung endothelial vessel cells, leading to leaking and alveolar inundation. Huge fluid expansion may lead to deterioration of pulmonary function and increased mortality. Therefore, one has to be cautious about fluid reposition, and treatment must take into account the use of vasoactive drugs.

We report four cases of such a syndrome admitted to our intensive care unit from December 2000 to March 2002. All patients came from the same county. They were rural inhabitants, living near rice and soybean storehouses that allow rodents entrance. The patients' age ranged from 31 to 57 years (median 36.5 years), and two of them were female. The initial symptoms (coughing, muscular pain, fever and dyspnea) set in from 48 to 96 hours before admission. Two patients required mechanical ventilation (and one of them also required the use of a pulmonary artery catheter).

Three patients survived (intensive care unit discharge before 1 week after admission). One patient died due to pulmonary atelectasis on the seventh day after admission.

Chest X-rays demonstrated in all cases mainly alveolar compromise, both bilateral and symmetrical, reminiscent of acute respiratory distress syndrome patterns in the latter stages. Blood sample serology confirmed the suspected diagnosis. Treatment consisted of general support, cautious fluid replacement and vasoactive drugs for the treatment of shock. We did not use ribavirin (although its use is well described in the literature).

In conclusion, diagnosis is based on high clinical suspicion, taking into account the epidemiological aspects that are highly important in such cases. Clinical manifestation is mainly noncardiogenic pulmonary edema, due to the direct endothelial vessel cell damage, leading to leaking and alveolar inundation. Huge fluid expansion may increase mortality. Use of a pulmonary artery catheter plays an important role in selected cases, in which fluid replacement can be targeted according to the pulmonary capillary wedge pressure.

Authors’ Affiliations

(1)
Hospital Jardim Cuiabá, Brazil

Copyright

© BioMed Central Ltd 2003

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