Neuromonitoring for Traumatic Brain Injury

The primary goal of management for traumatic brain injury is the prevention of secondary damage due to neuronal hypoxia and hypoperfusion. Monitoring modalities are aimed at identifying potential episodes of hypoxia and guiding therapy related to cerebral perfusion. Patients with severe brain injury are intubated to protect the airway and allow maximal oxygenation. Standard monitoring for all such patients is required including oxygen saturation (SaO2), ECG, mean arterial blood pressure (MAP) and urine output. These patients will require frequent determination of arterial blood gases and an intra-arterial catheter is helpful. Patients are maintained euvolaemic and central venous pressure measurements are used to guide therapy. Normocapnia is vital for maintenance of intracranial pressure (ICP), and patients should have continuous measurement of end-tidal CO2 (ETCO2) levels using a capnometer. These represent the baseline requirements for monitoring of these patients. Patients receiving inotropic agents to increase MAP and maintain cerebral perfusion pressure (CPP) may benefit from pulmonary artery occlusion catheters to guide therapy.

Key Recommendations The baseline requirements are SaO2, ECG, MAP, ETCO2, CVP and urine output.   ICP monitoring should be used in most patients with severe brain injury.   Multimodality monitoring including SjO2 and TCD should be employed where ICP and CPP cannot be maintained by standard methods.

Intracranial Pressure Monitoring

Cerebral perfusion pressure is maintained by supporting mean arterial pressure and/or reducing intracranial pressure. The principles of, and indications for ICP monitoring are discussed with the physiology of intracranial pressure. ICP transducers should measure the pressure range of 0 - 100mHg with an accurracy of 2mmHg in the range 0-20mmHg, and at least 10% accurracy for the rest of the measurable range. The most accurate and reliable method of monitoring intracranial pressure is with an intraventricular catheter connected to a pressure transducer. This system also allows intermittent drainage of cerebrospinal fluid from the ventricles to aid in control of ICP. Manometer type systems allow re-calibration whereas fibreoptic devices may suffer from baseline drift if used for several days. Catheters may also be placed in the cerebral parenchyma, or the subdural and subarachnoid spaces. While easier to insert in some cases these may not accurately measure the ICP when compared to an intraventricular catheter. Epidural devices are significantly less accurate.

In general complications related to ICP monitoring are rare. The greatest concern, ventriculitis, has never been demonstrated in prospective studies of clinically significant intracranial infections following ICP measurement. Bacterial colonisation does occur however (5% ventricular/subarachnoid, 15% parenchymal), and its incidence increases markedly after 5 days in situ. Irrigating ICP devices significantly increases the risk of colonisation. Treatment is removal of the ICP bolt.

It is difficult to assess the risk of haematoma formation associated with ICP monitors but the rate is around 1.4%, with 0.5% requiring surgical evacuation. Parenchymal catheters have a higher incidence of haematoma than other methods. Malfunction of the devices does occur, and readings over 50mmHg may be inaccurate with higher rates of obsturction and loss of signal.

Multimodality monitoring

While maintenance of cerebral perfusion pressure is important, it only measures one parameter affecting the delivery of oxygen to the neurons. Ultimately, the Cerebral Blood Flow (CBF) and oxygen content of the blood are the prime parameters. CPP provides a pressure gradient governing CBF, but flow is then affected by the resistance of the cerebral vessels. Neuronal demand for oxygen is governed by their metabolic rate. Neurons with high activity levels require greater amounts of oxygen than those which are quiescent. Globally this is described as the Cerebral Metabolic Rate for Oxygen (CMRO2).

CMRO2 = CBF x OEF x SaO2

OEF is the oxygen extraction fraction. How much oxygen is extracted can be measured by the Fick principle based on measurements of the arterial and venous oxygen content.

Thus monitoring only the ICP and CPP really gives very little idea of the overall state of the injured brain and no idea at all about oxygen delivery and usage. Multimodality monitoring allows using a combination of jugular venous bulb oximetry and transcranial doppler ultrasound allows a greater understanding of the state of the cerebral circulation and oxygen consumption. At present, methods to measure cerebral blood flow such as Positron Emission Tomography (PET), Xenon clearance or Single Positron Emission Computed Tomography (SPECT) remain too cumbersome for use in the ICU, but will no doubt play a greater role in the future.

Jugular Venous Bulb Oximetry

Jugular venous bulb oximetry involves placing a sampling catheter in the internal jugular vein, directed upwards, so that its tip rests in the jugular venous bulb at the base of the brain. Blood samples drawn from here measure the mixed venous oxygen saturation (SjO2) of blood leaving the brain. This is normally in the range 50-75%. Solving the Fick equation for SjO2 gives:

SjO2 = SaO2 - (Oxygen Consumption / Cardiac Output x Hb x 1.39)

The SjO2 will fall when there is an imbalance between oxygen consumption and delivery. If the SjO2 falls below 50% (without a fall in arterial oxygen saturation - SaO2), this implies either a fall in CBF or a rise in oxygen utilisation (higher CMRO2). If cerebral perfusion pressure is maintained, a fall in CBF is due to an increase in cerebrovascular resistance (CVR). Vascular spasm and a rise in CVR are very common after brain injury and are significantly worsened by hyperventilation. Jugular venous bulb oximetry should be employed whenever there is prolonged hyperventilation

Burst suppression to reduce CMRO2 may be used in patients who have presistent intracranial hypertension not responsive to standard therapy. Barbiturates are the most commonly used agents. Multimodality monitoring should probably be employed when such therapy is instituted.

An increase in SjO2 to 85%+ implies either a hyperaemia with a rise in cerebral blood flow, shunting of blood away from neurons or a decrease in CMRO2 (impending cell death / brain death).

Transcranial Doppler Ultrasound

Transcranial doppler is a non-invasive method of assessing the state of the intracranial circulation. The velocity of flow can be measured in the middle, anterior and posterior cerebral arteries, the opthalmic artery and internal carotid. Flow cannot be measured from velocity because the cross-sectional area of the arteries cannot be measured directly. . However the doppler shift measured is inversely proportional to the diameter of the vessel, so that, all other factors remaining constant, vascular spasm leads to an increase in flow velocity. Doppler waveform analysis can give further information about the state of blood flow, such as flow acceleration and pulsatility index (systolic velocity-diastolic velocity/mean velocity). However the value and utility of these measurements is as yet unknown.

Position of TCD probes and a sample tracing of normal Middle Cerebral Artery (MCA) waveform

There is an an inverse correlation between the severity of head injury and the middle cerebral artery velocity. Low velocities in the intracranial circulation after head injury is due to low cerebral blood flow and high ICP levels. Low velocities on admission are indicative of a poor prognosis. A reduction in CPP and rise in ICP are also reflected in a rise in the pulsatility index.

Vasospasm is common after head injury and can be an important cause of neurologic deterioration. Vasospasm usually occurs where there is traumatic subarachnoid haemorrhage. TCD is useful for monitoring at-risk patients for signs of vasospasm. Detection is made more difficult by the presence of cerebral hyperaemia in many patients, and the ratio of intracranial to extracranial velocities should be used to detect and correct for this. Concomittant jugular venous bulb oximetry may also provide valuable information in this setting.

Interestingly, during hyperventilation to PaCO2 of below 3.5 kPa (25 mmHg) the TCD signal can fall off almost to zero showing how profoundly detrimental hyperventilation can be. Again, TCD is indicated for patients whose intracranial hypertension and cerberal perfusion pressure cannot be maintained by standard therapy. 2 dimensional TCD is now becoming available.

Cerebral Function Monitoring

References

Intracranial pressure monitoring

Intracranial Pressure. trauma.org 5:1, 2000.

Ghajar J. Intracranial pressure monitoring techniques. New Horizons 3:395-399, 1995

Mayall CG, Archer NH, Lamb VA et al. Ventriculostomy-related infections. A prospective epidemiologic study. N Engl J Med 310:553-559, 1984

Aucoin PJ, Kotalainen HR, Gantz NM et al. Intracranial pressure monitors. Epidemiologic study of risk factors and infections. Am J Med 80:369-376, 1986

Winfield JA, Rosenthal P, Kanter RK et al. Duration of intracranial pressure monitoring does not predict daily risk of infectious complications.

Jugular venous bulb oximetry

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

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

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

Fortune JB, Feustel PJ, Weigle CGM et al. Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head injured patients. J neurosurg 80:461-468, 1994

Chan KH, Miller JD, Drearden NM et al. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular venous bulb oxygen saturation after severe brain injury. J Neurosurg 77:55-61, 1992

Transcranial Doppler Ultrasound

Aaslid R, Markwalder TM, Nornes H. Noninvasive transcranial doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 57:769-774, 1982

Weber M, Grolimund P, Seiler RW. Evaluation of post-traumatic cerebral blood flow velocities by transcranial doppler ultrasonography. Neurosurgery 27, 106-112, 1990

Martin N, Doverstein C, Zane C et al. Post traumatic vasospasm: transcranial doppler ultrasound, cerebral blood flow and angiographic findings. J Neurosurg 77:575-583, 1992

Seiler RW, Grolimund P, Aaslid R et al. Cerebral vasospasm evaluated by transcranial ultrasound correlated with clinical grade and CT-visualised subarachnoid hemorrhage. J Neurosurg 64,594-600, 1986

Chan KH, Miller JD, Drearden NM. Intracranial blood flow velocity after head injury: relationship to severity of injury, time neurological status and outcome. J neurol Neurosurg Psych 55:787-791, 1992

Chan KH, Miller JD, Drearden NM et al. The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular venous bulb oxygen saturation after severe brain injury. J Neurosurg 77:55-61, 1992