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Bordetella pertussis infection causing pulmonary hypertension
  1. P Casano,
  2. M Pons Odena,
  3. F J Cambra,
  4. J M Martín,
  5. A Palomeque
  1. Hospital Sant Joan de Déu, Unidad de Cuidados Intensivos Pediátricos, Passeig de Sant Joan de Déu, 2 080950, Esplugues de Llobregat, Barcelona, Spain; mpons{at}hsjdbcn.org

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In Spain the incidence of whooping cough is less than five cases per 100 000 inhabitants.1 Mortality rate is 0.4% in the United States, heart failure being one of the most frequent causes.2 Although cases of death due to Bordetella pertussis infection as a consequence of lung hypertension have been described previously,3–5 this complication is not very well known. Here we report a recent case and review the literature.

A 23 day old girl, who had had a pertussive cough for several days, was admitted with breathing difficulty of 12 hours duration. On admission she had tachycardia (heart rate 180 beats/min), tachypnoea (70 breaths/min), pyrexia (38°C), and haemoglobin saturation 90% without oxygen. A chest x ray revealed right superior and half lobe infiltrates. Blood analysis showed 53 × 109 leucocytes with left deviation and 33 mg/dl C reactive protein. Testing for respiratory syncitial virus was negative; direct immunofluorescence and culture for B pertussis were both positive.

The patient was admitted and treated with oxygen and erythromycin. After 12 hours she developed respiratory failure (respiratory rate 100 breaths/min, pH 7.16, pco2 74 mm Hg, po2 37 mm Hg, HCO3 26, base excess −5) and was transfered to the paediatric intensive care unit with intubation and pressure control (peak inspiratory pressure 22, peak end expiratory pressure 3, Fio2 0.35, respiratory rate 40). Twenty four hours later, hypoxaemia necessitated increasing Fio2 to 1, and refractory hypotension required volume load and inotropics (TAM 38). Echocardiography diagnosed severe lung hypertension (pulmonary artery pressure 65 mm Hg) and decreased heart contractibility. Nitric oxide 8 ppm and milrinone 0.37 μg/kg/min temporarily improved po2, but this subsequently deteriorated (po2 40 mm Hg). High frequency ventilotherapy was initiated; nitric oxide up to 20 ppm was given, and inotropic support enhanced, but with no response. She suffered a fatal cardiac arrest 98 hours later. The family did not authorise necropsy.

Fatal myocardial failure secondary to lung hypertension has been reported in four infants under 2 months with verified B pertussis infection.3,5 All presented with initial tachycardia (160–230 beats/min) refractory to treatment with volume load, and developed posterior persistent hypotension that did not respond to inotropic support.

Lung vasodilators such as nitric oxide, milrinone, or prostacycline may be useful in management of these patients, although they did not prove beneficial in our patient.

Because of the rapid deterioration of all these cases, we recommend early echocardiography diagnosis, enabling vasodilator therapy to be initiated in the early phase of lung hypertension in order to improve prognosis.

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