Successful treatment of adults with severe Hantavirus pulmonary syndrome with extracorporeal membrane oxygenation

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Abstract
Objective: To describe our experience with the use of extracorporeal membrane oxygenation (ECMO) as a rescue therapy in adult patients with severe cardiopulmonary failure from Hantavirus pulmonary syndrome. Design: Case series. Setting: Tertiary referral center. Patients: Patients with confirmed Hantavirus infection, who developed severe cardiopulmonary failure in which conventional therapy was assessed as being unsuccessful. Interventions: Records of previous patients treated for Hantavirus pulmonary syndrome were reviewed and findings consistent with 100% mortality were found. Measurements and Main Results: Findings associated with a 100% mortality rate were a) cardiac index of 4.0 mmol/L (normal range 0.0 to 2.2); c) pulseless electrical activity or ventricular fibrillation or ventricular tachycardia; and d) refractory shock despite fluid resuscitation, and vasoactive medications. From 1994 to 1996, seven patients were admitted with confirmed Hantavirus pulmonary syndrome and severe cardiopulmonary failure. Three of the seven patients had at least two of the four criteria for a 100% morality rate listed above, and appeared to be failing optimal conventional therapy. These three patients received support with venoarterial ECMO. The first patient was placed on ECMO during cardiac arrest and died. The next two patients who received ECMO for Hantavirus pulmonary syndrome survived after relatively short, uncomplicated ECMO runs, and were discharged without complications. Conclusions: ECMO successfully provided cardiopulmonary support in two patients with severe Hantavirus pulmonary syndrome who survived with a good outcome. Our experience suggests that ECMO is a beneficial therapy for patients critically ill with Hantavirus [ulmonary syndrome. (Crit Care Med 1998; 26:409-414) In 1993, an outbreak of an acute illness with a high mortality rate affecting previously healthy young adults occurred in the southwestern United States. This illness, called Hantavirus pulmonary syndrome (HPS), is caused by Sin Nombre Virus, a Hantavirus genus, and is characterized by fulminant cardiopulmonary failure in adults with a history of rodent or rodent dropping contact. Cases of HPS have now been reported nationwide and in Canada and South America. Nationally, 48 patients were diagnosed with HPS in 1993. Of these, 29 patients died, resulting in a 60% mortality rate [1-5]. At our institution, the University of New Mexico Hospital (UNMH), we have the largest experience with patients with HPS. In 1993, 14 patients with HPS were treated at UNMH and five died, with a resultant mortality rate of 36% [6]. As of October 1996, 143 patients nationally have been identified with HPS, with a still unacceptably high mortality rate of 48%. The continued high mortality rate, despite greater awareness and recognition of HPS, and improvement in critical care treatment of HPS, led us to consider the use of extracorporeal membrane oxygenation (ECMO) as a rescue therapy for these patients. ECMO has been demonstrated [7] to be effective for cardiopulmonary support in some adult patients with severe respiratory and cardiac failure. We will describe our experience from 1994 to 1995 with the use of ECMO for patients with HPS. Patients who become critically ill with HPS present with a history of a mild flu-like illness, then deteriorate rapidly over several hours. A common scenario for patients with HPS is to be stable on admission, requiring only supplemental oxygen and intravenous fluids. Within 24 hrs, however, certain patients with HPS require endotracheal intubation, mechanical ventilation, and a high level of respiratory and circulatory support. Clinical deterioration is associated with diffuse pulmonary infiltrates on chest radiograph, copious amounts of nonpurulent pulmonary secretions, and severe hypoxemia (PaO2/FIO2 <100 torr [<13.3 kPa]) [6,8]. The typical “early” hemodynamic profile for patients with HPS is a low pulmonary artery occlusion pressure (PAOP) and a low cardiac index [6]. Patients who went on to have a poor outcome then developed a picture consistent with cardiogenic shock with a low cardiac index, and an increased systemic vascular resistance index (SVRI). Echocardiograms showed that left ventricular function was severely depressed in those patients who died, and was normal in survivors [6,9]. Treatment for cardiopulmonary failure of patients critically ill with HPS includes conventional critical care interventions such as vasoactive drug infusions, and various ventilator strategies, including the use of high mean airway pressure, inverse inspiration/expiration (I/E) ratio, and pressure-limited ventilation. Investigational therapies, intravenous ribavirin, and a bradykinin antagonist were employed in 1993 without apparent benefit. Most critically ill patients with HPS who survived required aggressive intensive care for only a few days, after which they made a full recovery, without residual deficits. The recovery was often as remarkably rapid as the clinical deterioration had been on presentation. Autopsy findings showed a structurally normal heart and lung parenchyma with intra-alveolar edema, scant to moderate interstitial infiltrates, and hyaline membrane formation. The lungs lack severe inflammatory or irreversible changes [10]. Since HPS occurred in previously healthy adults and did not cause structural damage to the heart and lungs, and since survivors recovered quickly, we speculated that the severe cardiopulmonary failure seen in nonsurvivors of HPS could be reversible if the patient could be supported more effectively during the acute period after presentation. We believed that venoarterial ECMO could provide this support and possibly improve the outcome of patients with cardiopulmonary failure from HPS not responding to conventional intensive care treatment modalities.