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Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

Michael G. O'Sullivan Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Patrick F. Statham Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Patricia A. Jones Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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J. Douglas Miller Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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N. Mark Dearden Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Ian R. Piper Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Shirley I. Anderson Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Alma Housley Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Peter J. Andrews Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Susan Midgley Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Jane Corrie Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Janice I. Tocher Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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Robin Sellar Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland

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✓ Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition.

Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP ≥ 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP ≥ 30 mm Hg) and duration. Reduced CPP (≤ 60 mm Hg lasting longer than 5 minutes) was recorded in five patients.

Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

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