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Delayed pulmonary dysfunction in head-injured patients

A J Popp, D M Shah, R A Berman

    Journal of Neurosurgery
    |December 1, 1982
    PubMed
    Summary
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    Serious head injury can lead to delayed pulmonary dysfunction. Increased pulmonary vascular resistance and altered lung perfusion, not intracranial pressure, were linked to these lung issues in patients with severe head trauma.

    Area of Science:

    • Neurology
    • Pulmonology
    • Critical Care Medicine

    Background:

    • Severe head injuries can result in significant intracranial pressure (ICP) and neurological deficits.
    • Delayed pulmonary dysfunction is a serious complication in patients with severe head trauma.
    • The relationship between intracranial pressure, neurological status, and pulmonary function requires further investigation.

    Purpose of the Study:

    • To investigate the link between intracranial pressure (ICP), cardiopulmonary function, and neurological dysfunction in patients with severe head injury.
    • To identify factors contributing to the development of delayed pulmonary dysfunction following head trauma.

    Main Methods:

    • Measured ICP, cardiopulmonary function, and neurological status in 13 patients with severe head injury (Glasgow Coma Scale ≤ 7).

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  • Utilized the multiple inert gas elimination technique to assess ventilation-perfusion matching.
  • Analyzed pulmonary vascular resistance (PVR), cardiac index, shunt fraction, and extravascular lung water.
  • Main Results:

    • Three patients developed hypoxemia (arterial pO2 ≤ 80 torr) despite ventilatory support.
    • Five patients with shunt fractions > 15% exhibited increased PVR and elevated cardiac index, suggesting impaired hypoxic pulmonary vasoconstriction.
    • Abnormalities in ICP and cerebral perfusion pressure did not correlate with observed cardiopulmonary changes.

    Conclusions:

    • Delayed pulmonary dysfunction in severe head injury appears related to altered pulmonary vascular resistance and ventilation-perfusion mismatching, rather than directly to intracranial pressure.
    • Impaired hypoxic pulmonary vasoconstriction may contribute to intrapulmonary shunting.
    • Further research is needed to elucidate the complex interplay between brain injury and lung function.