Effects of respiratory physiotherapy on intracranial pressure and cerebral perfusion pressure in severe traumatic brain injury patients. 2008

Cassia Toledo, and Cinthia Garrido, and Eliane Troncoso, and Suzana Margareth Lobo
Programa de Aprimoramento, Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP, Brasil.

OBJECTIVE After brain injury intracranial hypertension is the major cause of mortality, in addition to the possibility of functional, behavioral and cognitive sequels. Scarcity of studies on the effects of respiratory physiotherapy on these patients may lead to contradictory performances. This study aimed to assess the effects of customary respiratory physiotherapy maneuvers on intracranial and cerebral perfusion pressures in patients with severe brain injury. METHODS Clinical, prospective trial with patients with severe traumatic brain injury, mechanically ventilated and with a continued measurement of intracranial pressure. The effects of manual vibrocompression maneuvers and intratracheal aspiration with or without saline infusion on the measurements of intracranial and cerebral perfusion pressures, between the first and third day after cerebral injury were evaluated. RESULTS Data were collected from 11 patients, 41 years of age (median) and APACHE II of 19.5 ± 5. The manual vibrocompression maneuver did not cause an increase of intracranial pressure on any of the days assessed. Intracranial pressure significantly increased after intratracheal aspiration maneuvers in relation to the basal measurement (day1, 9.5 ± 0.9 mm Hg vs 18.0 ± 3.2 mm Hg; day 2, 10.6 ± 1.7 mm Hg vs 21.4 ± 3.8 mm Hg; day 3, 14.4 ± 1.0 vs 24.9 ± 2.7 mm Hg; p<0.05 for all). However, these elevations were transient (about 27 seconds) and accompanied by compensatory increases of the cerebral perfusion pressure. CONCLUSIONS The manual vibrocompression maneuver did not increase intracranial pressure or cerebral perfusion pressure in patients with severe brain injury. Intratracheal aspiration induced a significant and transient increase of the intracranial and cerebral perfusion pressures.

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