Treatment of raised ICP

The treatment of raised ICP allows adequate cerebral perfusion pressure and can prevent cerebral herniation. The aim of treating ICP and cerebral perfusion pressure is to minimize secondary insults and reduce the risk of cerebral ischemia.

A sustained ICP above 15 mmHg on the first day after injury demands investigation for cause. The accuracy of the transducer system should be verified, adequate cerebral venous drainage should be assured, hypoxemia and hypercapnia should be corrected, and adequate sedation to allow the patient to synchronize with the ventilator should be maintained. Ventilatory indices such as airway pressure and inspiratory-to-expiratory ratio should be reasonable, seizure activity must be excluded, core temperature must be in the range 35 to 37 °C, and serum biochemistry must be maintained (e.g. serum sodium concentration above 135 mmol/l). Once the ICP has risen to 20 to 25 mmHg treatment is mandatory, although after 48 to 72 h a level of 30 mmHg may be tolerated before treatment is necessary.

Failure of treatment or the onset of new neurological signs dictates an urgent CT scan to exclude newly developed lesions which may be amenable to surgery. Treatments for elevated ICP include drainage of cerebrospinal fluid, hyperventilation, osmotherapy, diuretics, hypnotics, and hypothermia.

Drainage of cerebrospinal fluid is continuous or intermittent via ventricular catheters against a back pressure of about 10 mmHg to avoid ventricular collapse, brain shifts, and loss of ICP monitoring capability. The Brain Trauma Foundation recommends this as a first-line maneuver in ICP control in those patients with ventricular catheters in situ. Potential problems include ventricular collapse, causing midline shift and obstructive hydrocephalus in the contralateral ventricle, and increased cerebral blood flow with formation of edema.

Hyperventilation is based on the sensitivity of the cerebral resistance vessels to CO 2. Hypocapnia to a PaCO2 of 3.5 kPa (26 mmHg) reduces the cerebral blood flow and volume by 30 per cent, thus reducing ICP. If ventilation is to be effective, CO 2 sensitivity must be retained. In normal volunteers the effect of hyperventilation on cerebral blood flow lasts for about 4 h, but in head-injured patients it may well last longer.

Hyperventilation may work best during the early post-resuscitation phase of head injury if there is cerebrovascular engorgement secondary to absolute hyperemia where reduction in cerebral blood volume and flow should not be associated with ischemia. Cerebral blood flows measured in the ischemic range of 15 to 20 ml/dg/min (normal flow is 50 ml/dg/min) may be produced by aggressive ventilation. Hypocapnia can cause autoregulation failure and ICP may even rise, and, if blood pressure falls with CO2 elimination, cerebral perfusion pressure may be further jeopardized, particularly during the early hypoperfusion phase of severe head injury during resuscitation. A worse outcome may be seen after prolonged aggressive hyperventilation to a PaCO2 of about 2 kPa (15 mmHg) when compared with a normocapnic group. The use of the acid-base buffer THAM (tromethamine) reduces the harmful ischemia-related effects of hypocapnia, presumably by correcting cerebral acidosis. Jugular venous oxygen saturation monitoring in the intensive care unit (ICU) has demonstrated episodes of severe jugular venous desaturation during excessive hyperventilation. Jugular desaturation episodes have been shown to affect head injury outcome adversely.

The present recommendations are that prophylactic hyperventilation should be avoided, although acute neurological deterioration or failure of other therapies are an indication for hyperventilation. Cerebral venous oxygen saturation monitoring or the more robust brain tissue pO2 measurement can be used to alert the clinician to impending cerebral ischemia (SjvO2 < 50 per cent and brain PO2 < 20 mmHg (2.7 kPa) respectively).

Intravenous 20 per cent mannitol solution works by two major mechanisms. Firstly, mannitol improves blood rheology, with its hemodilution leading to an increased cerebral blood flow and oxygen delivery. It works most rapidly at lower cerebral blood flows when given as a bolus of 0.5 to 1.0 g/kg over 20 min, repeated up to four times. Improved oxygen delivery in the presence of preserved cerebral autoregulation causes vasoconstriction, reduces cerebral blood volume, and leads to a fall in ICP. Secondly, there is delayed effect due to the osmotic gradient between plasma and cells which takes up to 30 min for onset and lasts for at least 8 h. Thus mannitol may be the first-line agent when raised ICP is associated with ischemic edema. Mannitol is also a free-radical scavenger and probably reduces production of cerebrospinal fluid.

Complications associated with mannitol infusions include the development of acute renal tubular necrosis, particularly in dehydrated hypotensive patients. The risk of serum hyperosmolality (> 320 mosmol/kg) can occur with doses above 3 g/kg/day; thus serum osmolalities should be monitored. To keep dosages to a minimum, it is recommended that mannitol be given as a bolus. Its use prior to ICP monitoring is restricted to patients with acute neurological deterioration.

Another hypertonic agent, 7.5 per cent saline, has been used as an alternative to mannitol to correct hypovolemia and improve ICP control. Loop diuretics may control ICP by reducing brain water and ion content irrespective of blood-brain barrier integrity, slowing the formation of cerebrospinal fluid and reducing central venous pressure. Some centers use diuretics and mannitol together and replace losses with colloid solutions, thus maintaining normovolemia but promoting intracellular dehydration.

Analgesics and sedatives decrease cerebral metabolism, which leads to vasoconstriction, reduces cerebral blood volume, and lowers ICP. Their effect can be monitored by recording cerebral electric activity. As a further prerequisite to their therapeutic efficacy, CO 2 vasoreactivity should be preserved.

Barbiturates may be long acting and remain in the body for several days. They can cause cardiovascular collapse in hypovolemic patients, thus worsening cerebral perfusion pressure. Monitoring cerebral oxygenation and systemic filling pressures may augment their safe use. Utilization is associated with reduced immune function and increased infection risk in diffuse head injury. The use of barbiturates may be associated with a higher mortality than that occurring with mannitol. Owing to their toxicity, the barbiturate drugs should probably be restricted to selected patients who retain electrical activity and CO 2 reactivity after severe head injury and who fail to respond to other therapies.

Hypothermia, or lowering brain temperature, reduces both the metabolic component affected by analgesics and sedatives and the basal cerebral metabolism. A controlled trial of the effect of induced hypothermia on outcome following severe head injury is currently in progress in the United States.

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