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An unimmunised 5-week-old, term male infant presented to the intensive care unit with cardiorespiratory failure and peripheral lymphocytosis. The infant deteriorated despite intubation, ventilation, vasoactive drug infusions and exchange transfusion. Venoarterial extracorporeal membrane oxygenation (ECMO) was started. Infection with Bordetella pertussis was subsequently confirmed. The lungs remained radiologically opacified and tidal volumes were poor despite lung recruitment manoeuvres, resulting in a prolonged ECMO run. A speckled density consistent with calcification became visible within the left lung field by day 29. These changes progressed to involve both lungs over the subsequent week (figure 1). Serum calcium, phosphate and alkaline phosphatase were normal. The infant was separated from ECMO on day 34 and died shortly afterwards.
Calcification has been described in a limited number of respiratory infections but is not a recognised feature of pertussis1 or ECMO for other reasons. The deposition of calcium salts following tissue necrosis is known as dystrophic calcification and occurs despite normal serum levels of calcium and in the absence of derangements of calcium metabolism.1 Widespread pulmonary infarction has been demonstrated in lung biopsies performed in infants with pertussis that led to withdrawal of intensive care.2 Similar findings have been replicated in postmortem studies of those infants who did not receive ECMO.3 It is likely that the poor outcome of infants with severe pertussis requiring ECMO is because the underlying process is irreversible due to pulmonary infarction. We suggest that, by prolonging survival with ECMO in the presence of pulmonary infarction, dystrophic calcification occurred.
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.