British Journal of Anaesthesia, 2000, Vol. 84, No. 5 661
© 2000 The Board of Management and Trustees of the British Journal of Anaesthesia
Abstract |
Indomethacin: its role in the management of intractable intracranial pressure (ICP) after severe head injury
1 The Intensive Care Unit, Frenchay Hospital, Frenchay Park Road, Bristol BS16 1LE, UK
Abstract
Intracranial hypertension that fails to respond to first line medical and surgical treatment after head injury is associated with a 92% mortality overall.1 The addition of barbiturates will result in a good or moderate neurological outcome in 35% of patients,2 but those with hyperaemia do significantly worse. However barbiturates may not be a logical choice for those patients whose intracranial hypertension is secondary to hyperaemia, and may be associated with significant complications. In these patients cerebral vasoconstrictors such as indomethacin may be more appropriate and possibly associated with fewer unwanted effects. In one study six out of 10 patients who received indomethacin for intracranial hypertension unresponsive to barbiturates survived.3 However it is unclear how many were hyperaemic since jugular venous saturation (SjO2) was not monitored. We report our experience with indomethacin in 10 severely head-injured patients.
Our protocol aims to maintain a target cerebral perfusion pressure (CPP) and ICP through the application of sedation, diuretics, CSF drainage, mild hypothermia, muscle relaxation and control of arterial carbon dioxide (PaCO2). If the ICP remains elevated then SjO2 is monitored. The combination of raised ICP and SjO2 is taken to indicate hyperaemia (absolute or relative). In these circumstances the patient is hyperventilated to a PaCO2 of 28 mmHg and if necessary an intravenous infusion of thiopentone commenced. We used indomethacin infusions in 10 patients fulfilling these criteria of hyperaemia. In seven patients the hyperaemia was confirmed as absolute by demonstrating a raised middle cerebral artery velocity (MCAV) with transcranial Doppler. The mean age of the patients was 21.2 yr (range 8–55). Indomethacin was infused for a mean of 3.8 days (1–11) at a rate of 3–11 mg h–1. The effect of indomethacin on mean (SD) ICP, CPP and SjO2 is shown in Table 4.
At 6-month follow up there were seven survivors (three good recovery, three moderate recovery, one severely disabled). Three patients died with intractable ICP and septic shock. Two of these patients had associated renal failure. There were no episodes of gastrointestinal bleeding. Two of the three patients who died did not have MCAV measured, and therefore indomethacin may not have been strictly indicated. These results achieved in this subgroup of head injured patients is much better than that expected, and matches the outcome achieved in the overall ICU head injury population. Indomethacin may have a role in the management of raised ICP associated with hyperaemia after severe head injury. We recommend however that it should only be used with monitoring of both SjO2 and MCAV.