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NEUROTRAUMA

 

 

Control of Intracranial Hypertension

As part of intensive treatment of traumatic brain injury, intracranial pressure (ICP) should be controlled when the cerebral perfusion pressure (CPP) falls below 70mmHg and/or the ICP is greater than 20mmHg. Intracranial hypertension occurs in approximately 40% of all patients with severe traumatic brain injury. Maintenance of an adequate cerebral perfusion pressure is more important than control of ICP per se. Measures to increase mean arterial pressure should be instituted prior to starting more complex methods of ICP control.

There are several methods for controlling ICP. These are usually applied in a stepwise fashion to achieve control, where possible. The absolute requirement for the potentially severely brain injured patient is tracheal intubation with a cuffed tube. This protects and maintains the airway and allows for maximal oxygenation and control of ventilation.

Ventilation

Carbon dioxide dilates the cerebral blood vessels, increasing the volume of blood in the intracranial vault and therefore increasing ICP. Patients should be ventilated to normocapnia (PaCO2 4.0 kPa / 30mmHg).

Key Recommendations

The baseline status for the severely brain injured patient is intubated, normovolaemic and normocapnic.

 

Hyperventilation should not be used routinely.

 

Mannitol should be reserved for acute control of ICP and administered in bolus form.

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

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.

trauma.org 5:1 2000


References

Cerebral blood flow following TBI

Muizelaar JP, Marmarou A, DeSalles AA et al. Cerebral blood flow and metabolism in severely head injured children. Part 1: Relationship with GCS score, outcome, ICP and PVI. J Neurosurg 71:63-71, 1989

Bouma GJ, Muizelaar JP, Stringer WA et al. Ultra early evaluation of regional cerebral blood flow in severely head injured patients using xenon enhanced computed tomography. J Neurosurg 77:360-368, 1992

Hyperventilation

Paul RL, Polanco O, Turney SZ et al. Intracranial pressure responses to alterations in arterial carbon dioxide pressure in patients with head injuries. J Neurosurg 36:714-720, 1972

Muizelaar JP, Marmarou A, Ward JD et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: A randomized clinical trial. J Neurosurg 75:731-739, 1991

Obrist WD, Langfitt TW, Jaggi JL et al. Cerebral blood flow and metabolism in comatose patients with acute head injury. J Neurosurg 61:241-253, 1984

Sheinberg M, Kanter MJ, Robertson CS et al. Continuous monitoring of jugular venous oxygen saturation in head injured patients. J Neurosurg 76:212-217, 1992

Gopinath SP, Robertson CS, Contant CF et al. Jugular venous desaturation and outcome after head injury. J Neurol Neurosurg Psych 57:717-723, 1994

Intravenous Fluid Therapy

Weed LH, McKibben PS. Experimental alteration of brain bulk. Am J Physiol 48:531-558, 1919

Shackford SR, Zhuang J, Schmoker J. Intravenous fluid tonicity: effect on intracranial pressure, cerebral blood flow and cerebral oxygen delivery in focal brain injury. J Neurosurg 76:91-98.1992

Zornow MH, Prough DS. Fluid management in patients with traumatic brain injury. New Horizons 3:488-498, 1995

Kaieda R, Todd MM, Warner DS. Prolonged reduction in colloid oncotic pressure does not increase brain edema following cryogenic injury in rabbits. Anesthesiology 71:554-560, 1989

Lanier WL, Stangland KJ, Scheithauer BW et al. The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischaemia in primates: examination of a model. Anesthesiology 66:39-48, 1987

Pulsinelli WA, Waldman S, Rawlinson D et al. Moderate hyperglycaemia augments ichaemic brain damage: a neuropathologic study in the rat. Neurology 32:1239-1246, 1982

Vassar MJ, Perry CA, Gannaway WL et al. 7.5% sodium chloride/dextran for resuscitation of trauma patients undergoing helicopter transport. Arch Surg 126:1065-1072, 1991

Mattox KL, Maningas PA, Moore EE et al. Prehospital hypertonic saline/dextran infusion for post-traumatic hypotension. Ann Surg 213:482-491, 1991

Schmoker JD, Zuang J, Shackford SR. Hypertonic fluid resuscitation improves cerebral oxygen delivery and reduces intracranial pressure after hemorrhagic shock. J Trauma 31:1607-1613, 1991

Wisner JD, Schuster L, Quinn C. Hypertonic saline resuscitation of head injury: effects on cerebral water content. J Trauma 30:75-78, 1990

Prough DS, DeWitt DS, Taylor CL et al. Hypertonic saline does not reduce intracranial pressure or improve cerebral blood flow after experimental head injury and hemorrhage in cats. Abstr Anesthesiology 75 (Suppl 3A):A544, 1991

Prough DS; Whitley JM; Taylor CL. Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion. J Neurosurg Anesthesiol 11: 102-11, 1999

Mannitol

Mendelow AD, Teasdale GM, Russell T et al. Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury. J Neurosurg 63:43-48, 1985

Muizelaar JP, Lutz HA, Becker DP et al. Effect of mannitol on ICP and CBF and correlation with pressure autoregulation in severely head injured patients. J Neurosurg 61:700-706, 1984

Rosner MJ, Coley I. Cerebral perfusion pressure: a hemodynamic mechanism of mannitol and the pre-mannitol hemogram. Neurosurg 21:147-156, 1987

Cruz J, Miner ME, Allen SJ et al. Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation. J Neurosurg 73:725-730, 1990

Cold GE. Cerebral blood flow in acute head injury. Acta Neurochir S49:18-21, 1990

Kaufmann AM, Cardozo E. Aggravation of vasogenic cerebral edema by multiple dose mannitol. J Neurosurg 77:574-589, 1992

Schwartz ML, Tator CH, Rowed DW. The University of Toronto head injury treatment study: A prospective randomised comparison of pentobarbital and mannitol. Can J Neurol Sci 11:434-440, 1984

Smith HP, Kelly DL, McWhorter JM et al. Comparison of mannitol regimens in patients with severe head injury undergoing intracranial monitoring. J Neurosurg 65:820-824, 1986

Sedation & paralysis

Prielipp RC, Coursin DB. Sedative and neuromuscular blocking drug use in critically ill patients with head injuries. New Horizons 3:456-468, 1995

Hsiang JK, Chesnut RM, Crisp CB et al. Early, routine paralysis for intracranial pressure control in severe head injury: is it necessary? Crit Care Med 22:1471-1476, 1994

Prough DS, Joshi S. Does neuromuscular blockade contribute to adverse outcome in head-injured patients? J Neurosurg Anes 5:135, 1994