Control of Intracranial Hypertension
Previously, hyperventilation was used routinely to maximally reduce PaCO2. No studies have shown this to improve outcome in these patients. Additionally, transcranial doppler (TCD) assessment and positron emission tomography (PET) shows this can induce significant constriction of cerebral vessels and this increase in cerebral vascular resistance may reduce cerebral blood flow to below the ischaemic threshold. One study has shown an improvement in long-term outcome when hyperventilation is not used routinely.
Consequently hyperventilation should be used only for short periods when immediate control of ICP is necessary. For example in the patient who has an acute neurological deterioration prior to CT scanning and surgical intervention. Hyperventilation should not take the PaCO2 level to below 3.5-4 kPa as there is minimal beneficial effect on ICP below this level.
Occasionally hyperventilation may be necessary for longer periods in patients with persistently high ICPs who have not responded to other treatment modalities. These patients may benefit from more intensive neuromonitoring such as jugular venous oxygen saturation and transcranial doppler assessments to ensure cerebral perfusion is not being compromised at the expense of ICP. Persistent hyperventilation should not be used in the first 24 hours and preferably not within the first 5 days following brain injury.
Intravenous fluid therapy
Patients with severe brain injury should be kept normovolaemic. Previous regimens recommending that patients be kept 'dry' have essentially been discarded as there is significant risk of both hypotensive episodes (leading to a fall in cerebral perfusion) and systemic inflammatory respinse syndrome (SIRS) or multiple organ failure (MOF) leading to failure of oxygenation and ventilation. Dehydration has little effect on cerebral oedema.
Free water (as dextrose solutions) should NOT be administered. This will decrease plasma osmolality and so increase the water content of brain tissue (the blood brain barrier acting as a semipermeable membrane). Elevated blood sugar levels are associated with a worsening of neurologic injury after episodes of global cerebral ischaemia. Ischaemic brain metabolises glucose to lactic acid, lowering tissue pH and potentially exacerbating ischaemic injury.
Hypertonic solutions and osmotic diuretics such as mannitol will have the opposite effect. This mechanism requires an intact blood brain barrier. If this is damaged, as may be the case following injury, low molecular weight, osmotically active particles may leak into the cerebral interstitium. In this case mannitol may have no effect in reducing brain water content, and maintenance of the colloid oncotic pressure in the vessels by administration of colloids, plasma proteins or other high molecular weight compounds may, theoretically, be of benefit. However in practice, colloids offer little benefit over crystalloid solutions.
There has been considerable interest in the use of hypertonic crystalloid solutions for the treatment of hypovolaemia in the presence of intracranial hypertension. Animal studies have proven the efficacy of hypertonic solutions in reversing shock, and sometimes in controlling ICP. Clinical trials suggest that survival after severe brain injury (GCS<9) may be improved with hypertonic solutions. However those injuries leading to a breakdown in the blood brain barrier show little or worsened response to hypertonic fluid administration.
There is no single best fluid for patients with traumatic brain injury, but isotonic crystalloids are widely used and have good scientific basis. Normal saline or lactated RInger's solution should be the standard resuscitation fluid until further studies show a clear benefit from other therapies. Regardless of the fluid type chosen, normovolemia must be maintained and episodes of hypotension avoided.
Mannitol, a 6-carbon sugar, is widely used in head injury management, though it has never been subjected to a randomised control trial against placebo and the methods and timing of administration vary widely. It is an osmotic diuretic and can have significant beneficial effects on ICP, cerebral blood flow and brain metabolism. Mannitol has two main mechanisms of action. Immediately after bolus administration it expands circulating volume, decreases blood viscosity and therefore increases cerebral blood flow and cerebral oxygen delivery.
Its osmotic properties take effect in 15-30 minutes when it sets up an osmotic gradient and draws water out of neurons. However after prolonged administration (continuous infusion) mannitol molecules move across into the cerebral interstitial space and may exacerbate cerebral oedema and raise ICP. Mannitol itself directly contributes to this breakdown of the blood brain barrier.
Mannitol is therefore best used by bolus administration where an acute reduction in ICP is necessary. For example the patient with signs of impending herniation (unilateral dilated pupil / extensor posturing) or with an expanding mass lesion may benfit from mannitol to acutely reduce ICP during the time necessary for CT scanning and/or operation.
Mannitol is wholly excreted in the urine and causes a rise in serum urine and osmolality. Patients with poor renal perfusion (shock), sepsis, receiving nephrotoxic drugs or with a serum osmolality over 320mOsm are at risk of acute tubular necrosis. Hypolaemia should be avoided with the infusion of isotonic fluids as necessary.
Sedation and anaesthesia
All but the most severely brain injured patients (GCS 3) will require anaesthesia for intubation. The cardiovascular responses to intubation induce a rise in ICP which is exaggerated in those patients on the cusp of the pressure-volume curve. Rapid sequence intubation is probably the safest method of establishing an airway in these patients.
Continuing sedation will be necessary in most patients to allow adequate ventilation and to prevent coughing or fighting the ventilator. Ensuing valsalva-type maneuvers cause sharp rises in intracranial pressure. Which agents are used to achieve sedation is probably less important. However short acting preparations will allow finer control of the depth of anaesthesia and faster recovery from sedation. Agents with a longer duration of action such as diazepam may be best administered by intravenous bolus as required rather than by constant infusion to avoid build-up of active metabolites.
Sedation is not analgesia, and pain requirements must be addressed to provide a quiet, comfortable patient. Adequate analgesia will also reduce the requirements for sedation and neuromuscular blockade.
The use of neuromuscular blocking agents is not routinely required for continued ventilation. However some patients whose high sedative requirements lead to adverse cardiovascular effects may benefit from pharmacologic paralysis.
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Cerebral blood flow following TBI
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Intravenous Fluid Therapy
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Sedation & paralysis
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