Intracranial Pressure and Cerebral Blood Flow (page 4)

Issue 8 (1998) Article 4: Page 4 of 4

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Intracranial Pressure and Cerebral Blood Flow (Continued)

Applied Physiology - Head Injury

Following acute head injury, the term "secondary injury" has been described. The primary injury is due to the actual trauma. The secondary brain injury is caused by ischaemia due to the combination of rapid brain swelling and hypotension. Any patient who is unconscious can easily develop an obstructed airway and become hypoxic, hypercapnic, possibly hypotensive and have a rise in intrathoracic pressure. Considering the physiological changes described already, the process that results in cerebral swelling and raised ICP is clear. In addition, pain from other injuries, despite the patient being unconscious, will cause an increase in CBF as a result of both the hypertensive response and local dilatation in the relevant sensory area of the brain. Thus in the initial management of the acutely head injured patient who is unable to maintain his airway, intubation and hyperventilation should be instituted following an intravenous anaesthetic agent, and an opiate, to attenuate the response to intubation. The dose must be carefully chosen to avoid hypotension in a patient who may also be hypovolaemic.

Teaching Point. In an article on the management and resuscitation of patients with serious head injuries Gentleman et al [9] noted that over an 11 year period there was significant reduction in mortality, (45% to 32%) and an increase in patients making a good recovery, (42%-58%) associated with a reduction in hypoxaemia and hypotension during treatment.

Hypotension must be treated aggressively with a rapid infusion of colloid or blood and if, necessary, intravenous (ephedrine 3-6 mg, methoxamine 1-3 mg).

References

Durward Q J et al. "Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension." J.Neurosurgery 1983; 59: 938-944.
McGraw C P. "A cerebral perfusion pressure greater than 80 mmHg is more beneficial." Intracranial Pressure VII. Edits. Hoff J T & Betz A L. 839-841. Springer-Verlag, Berlin. 1989
Rosner M J, Rosner S D & Johnson A H. "Cerebral perfusion: management protocol and clinical results." J.Neurosurgery 1985; 83: 949-962.
Chan K H, Miller J D, Dearden N M, Andrews P J D & Midgley S. "The effects of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain trauma." J.Neurosurgery 1992; 77: 55- 61.
Bouma G J, Muizelaar J P, Handoh K & Marmarou A. "Blood pressure and intracranial pressure - volume dynamics in severe head injury: relationship with cerebral blood flow." J Neurosurgery 1992; 77: 15-19.
Ruben B H. "Intracranial hypertension" in Advances in Anaesthesia. Edit. Gallagher T J. p.1, London Year Book Medical Publishers Inc. 1984.
Jones P W. "Hyperventilation in the management of cerebral oedema." Intensive Care Medicine. 1981; 7: 205-207.
Muizelaar J P et al. "Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomised clinical trial." J.Neurosurgery 1991; 75: 731-739.
Gentleman D., Dearden M., Midgeley S. & Maclearn D. "Guidelines for the transfer of patients with serious head injury." British Medical Journal 1993; 307: 547-552

This article contained links to the following additional information:

Table 1 - Non-pathological causes of raised ICP
Table 2 - Physiological causes of raised ICP
Issue 9 - Neuropharmacology - Intracranial pressure & cerebral blood flow