Intracranial pressure: to monitor or not to monitor?

Abstract

✓ The authors have analyzed their experience with intracranial pressure (ICP) monitoring in 207 patients over a 4-year period. Patients with either high-density or low-density lesions on computerized tomography (CT) at admission had a high incidence (53% to 63%) of intracranial hypertension (ICP persistently over 20 mm Hg). In contrast, patients with normal CT scans at admission had a relatively low incidence of ICP elevation (13%). Among these patients, three features were found to be strongly associated with the development of intracranial hypertension: 1) age over 40 years; 2) systolic blood pressure under 90 mm Hg; and 3) motor posturing — unilateral or bilateral. When two or more of these features were noted at admission, the incidence of intracranial hypertension was 60%, as compared to 4% when only one, or none, of these features were present. Thus, the patients at high risk for developing intracranial hypertension after severe head injury are those with abnormal CT scans at admission, and those with normal CT scans who demonstrate two or more of the above-mentioned adverse features. Based on these criteria, only 16% of this series of patients with normal CT scans would have qualified for monitoring. In addition to the three clinical features noted above, multimodality evoked potential (MEP) studies were also found to be strong predictors of ICP elevation in the normal CT scan group, with a 75% incidence of intracranial hypertension in patients with disseminated deficits. There was no statistically significant correlation between the Glasgow Coma Scale score, eye movements, pupillary reaction, hypoxia, or anemia at admission and subsequent ICP elevation in the group with normal CT scans. In this series, an intraventricular catheter was used as the sole monitoring device in 91% of the cases. In the remaining 9%, subarachnoid screws were employed, either alone, or upon failure of the ventriculostomy. While no mortality was directly ascribed to the monitoring process, there was a 7.7% complication rate (infection 6.3% + hemorrhage 1.4%). Eighty-five percent of the infections occurred in patients who had been monitored for 5 days or more, while no infections were noted in those monitored for less than 3 days. Used judiciously, this technique can be valuable in the monitoring and treatment of the brain-injured patient.

Depth of Intraparenchymal Brain Monitoring Devices in Neurosurgical Intensive Care

“…9 In three publications involving over 200 patients with ICP monitoring, 0.5% of patients required surgical evacuation of an ICP monitor-related haemorrhage. [12][13][14] Similarly malfunction of ICP monitoring devices has been widely reported, between 0% and 16% for microstrain gauges and subarachnoid bolts respectively. 10,15,16 It is not current practice in our unit to confirm the location of the ICP catheter on CT scan immediately after insertion, therefore we could only measure the depth of insertion in those patients who had undergone a repeat CT scan for another reason at some point following ICP catheter insertion.…”

Intracranial pressure monitoring in patients with severe traumatic brain injury

“…Пðè âèêîðèñòàíí³ ñóбäóðàëüíèх òà ñóбàðàхíî¿äàëüíèх äàòчèê³â ãåмî-ðàã³чíèх óñêëàäíåíü íå бóëî [35].  îïóбë³êîâàí³é ñå𳿠äîñë³äaeåíü [34,37,40], щî âêëючàëè ïîíàä 200 хâîðèх, яêèм ïðîâîäèëè мîí³òîðèíã ÂЧТ, зíàчí³ ãåмàòîмè, щî ïîòðåбóâàëè åâàêóàö³¿, âèяâëåí³ ó 0,5% хâîðèх.…”

Usos e abusos da hiperventilação nos traumatismo crânio-encefálicos graves

“…O FSC é tipicamente menor que 30 ml/100g/min durante as primeiras 8 horas após o trauma, e pode ser menor que 20 ml/100g/min durante as primeiras 4 horas após o TCE grave [4][5][6][7]12,13 . Ainda mais, nos TCE graves o FSC é baixo em pacientes com hematomas subdurais, lesões difusas e hipotensão arterial sistêmica, aumentado naqueles com hematomas epidurais e com tomografias computadorizadas de crânio (TCC) normais [24][25][26][27] . Existe correlação direta entre FSC, escala de coma de Glasgow (ECG) e prognóstico somente nas primeiras 48 horas após o TCE 4,9 .…”

“…Mesmo na ausência de HIC o FSC é baixo nos TCE graves 16 devido ao vasosespasmo pós-traumático, como documentado em 40% desses pacientes 36 . O FSC é aumentado naqueles com hematomas epidurais (evidências de herniações e HIC) e com TCC normais (sem evidências de herniações e HIC) [24][25][26][27] . c) A nova hipótese é que a queda do FSC é devida a lesão primária da barreira hematoencefálica (BHE) provocada pelo TCE grave e consequente perda do controle do volume cerebral (edema e inchaço) 37,38 .…”