Endotracheal lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics in patients with severe head trauma.

ABSTRACT

INTRODUCTION: In patients with severe head trauma, endotracheal suctioning can result in adverse reactions including cough, systemic hypertension, increased intracranial pressure, and reduced cerebral perfusion pressure. The aim of this prospective, blinded clinical trial in mechanically ventilated patients with severe head trauma whose cough reflexes were still intact was to assess the effectiveness of endotracheally instilled lidocaine in preventing endotracheal suctioning-induced changes in cerebral hemodynamics (increase in intracranial pressure and reduced cerebral perfusion pressure) after a single endotracheal suctioning. METHODS AND RESULTS: Ten minutes after lidocaine instillation into the endotracheal tube, secretions were suctioned for <30 s through a standard closed endotracheal suctioning circuit. Heart rate, arterial pressure, intracranial pressure, and cerebral perfusion pressure were continuously monitored. The first patient studied received an endotracheal lidocaine dose of 2.0 mg/kg. The dose for the next study patient was titrated upwards or downwards in 0.5 mg/kg steps according to, whether the intracranial pressure reached the predefined threshold of > or =20 mmHg. A total of 41 patients were studied. Lidocaine instillation into the endotracheal tube had no effect on hemodynamic and ventilatory variables. In 21 patients lidocaine dose instilled into the endotracheal tube effectively prevented the endotracheal suctioning-induced intracranial pressure increase behind the predefined threshold of > or =20 mmHg and cerebral perfusion pressure remained unchanged. In the remaining 20, although intracranial pressure rose significantly cerebral perfusion pressure remained constant. CONCLUSIONS: In mechanically ventilated patients with severe head trauma endotracheal lidocaine instillation effectively and dose-dependently prevents the endotracheal suctioning-induced intracranial pressure increase and cerebral perfusion pressure reduction.