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Assessment of the Optimal Cerebral Perfusion Pressure in Head-Injured Patients

Nordström, Carl-Henrik MD, PhD

doi: 10.1213/01.ANE.0000156702.60474.2E
Letters to the Editor: Letters & Announcements

Department of Neurosurgery; Lund University Hospital; Lund, Sweden;

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To the Editor:

Cremer et al. (1) presented an interesting study regarding the effects of induced variation in cerebral perfusion pressure on intracranial pressure in head-injured patients. The pharmacologically induced increase in cerebral perfusion pressure was generally associated with a decrease of elevated intracranial pressure, and the authors came to the conclusion that daily trial manipulation of arterial blood pressure could provide information to optimize cerebral perfusion pressure management. This conclusion may be questioned.

From a physiological viewpoint, increased intracapillary hydrostatic pressure in patients with an impaired blood-brain barrier will obviously promote transcapillary water filtration and increase intracranial pressure (2–4). This effect is not momentary but proceeds over several hours. In the study by Cremer et al. (1) the changes in intracranial pressure were evaluated within 15 min (median) of the induced increase in cerebral perfusion pressure. These variations in intracranial pressure presumably reflect rapid changes in intracranial blood volume of limited significance for long-term treatment of brain edema. In a recent study in head-injured patients, pharmacologically induced hypertension almost invariably caused a further increase of intracranial pressure within 2–3 h (5).

Although a reduction of intracapillary hydrostatic pressure will promote transcapillary water reabsorption, there is a lower tolerable level for cerebral perfusion pressure that varies between different individuals (4). The logical approach to optimize cerebral perfusion pressure might be to adjust therapy according to changes in the cerebral biochemical pattern monitored online at the bedside (6) rather than daily trial manipulation of arterial blood pressure as suggested by Cremer et al. (1).

Carl-Henrik Nordström, MD, PhD

Department of Neurosurgery

Lund University Hospital

Lund, Sweden

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1. Cremer OL, van Dijk GW, Amelink GJ, et al. Cerebral hemodynamic response to blood pressure manipulation in severely head-injured patients in the presence or absence of intracranial hypertension. Anesth Analg 2004;99:1211–7.
2. Fenstermacher JD. Volume regulation of the central nervous system. In: Staub NC, Taylor AE, eds. Edema. New York: Raven Press, 1984:383–404.
3. Grände PO, Asgeirsson B, Nordström CH. Volume targeted therapy of increased intracranial pressure: The Lund concept unifies surgical and non-surgical treatments. Acta Anaesthesiol Scand 2002;46:929–41.
4. Nordström CH. Assessment of critical thresholds for cerebral perfusion pressure by bedside monitoring of regional energy metabolism. Neurosurg Focus 2003;15:5.
5. Oertel M, Kelly DF, Lee JH, et al. Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury. J Neurosurg 2002;97:1045–53.
6. Nordström CH, Reinstrup P, Xu W, et al. Assessment of the lower limit for cerebral perfusion pressure in severe head injuries by bedside monitoring of regional energy metabolism. Anesthesiology 2003;98:809–14.
© 2005 International Anesthesia Research Society