Of all the injuries sustained in a traumatic event, head injury is frequently associated with the most devastating outcome. The patient often survives the accident only to end up with a major neurologic deficit. In addition to the stress this puts on the victims and their families, the economic costs are high because most of the injuries occur in the young during their working years.1

Better prehospital care, the institution of regional centres with new imaging techniques and the ready availability of multidisciplinary teams have improved the very poor outlook that was previously associated with head trauma. However, outcome continues to be affected by abnormal physiology in the immediate postinjury period.2

Anaesthetists are commonly involved in the management of patients who have suffered head injuries. Their role is in the emergency room protecting the airway and instituting resuscitation, in the operating theatre while treating the neurological injury (e.g. evacuating a haematoma) or other injuries (e.g. laparotomy for ruptured viscera) and in the intensive care unit. In this chapter, we review the pathophysiology of head injury and highlight new advances in the management of the severely head-injured patient.

Physiology of Cerebral Blood Flow

The human brain receives about 15% of the resting cardiac output but uses only 20% of the body's oxygen consumption. This translates into a mean cerebral blood flow (CBF) of about 50 ml/100 g/min and a mean cerebral metabolic rate for oxygen (CMRO2) of 3.2 ml/100 g/min, with glucose as the main substrate (60 mg/100 g/min). Under normal circumstances regional CBF and metabolism are tightly coupled, with an increase in cortical activity leading to a corresponding increase in CBF. When oxygen delivery falls, CMRO2 declines to basal levels (1.2-1.5 ml 02/min/100 g) and there is an increase in anaerobic metabolism.

Brain tissue is particularly vulnerable to reductions in oxygen delivery because it has a high metabolic rate and no capacity to store substrate. It has to ensure that oxygen delivery is maintained at a constant level despite changes in the vascular and cranial environment. In the healthy, awake, normotensive individual, CBF is maintained at a constant level within the range of cerebral perfusion pressures (CPP) between 60 and 160 mmHg. This autoregulation is effected through direct variation in cerebral vascular resistance in response to alterations in the CPP. Since the CPP depends on the difference between mean arterial pressure (MAP) and intracranial pressure (ICP), changes to either can initiate autoregulation, i.e. a decrease in arterial pressure has the same effect on autoregulation as an increase in ICP. Although the exact mechanisms responsible for this very efficient process are not completely understood, it is likely that both myogenic and metabolic factors are involved. The process has been classically thought to occur in minutes but recent evidence suggests that, at least during small changes in blood pressure, it is complete in seconds.3 The limits of autoregulation may be affected by disease processes and are modulated by sympathetic nervous system activity. a and p-blockade can change the lower limit of autoregulation (shift the curve to the left) and chronic hypertension increases the limits of autoregulation by shifting the curve to the right.4 Autoregulation is also affected by the level of PaC02. Hypocapnia restores autoregulation when impaired and accelerates the process when present, while hypercapnia abolishes autoregulation and renders the cerebral circulation pressure passive.56

Arterial carbon dioxide tension is one of the most potent regulators of CBF. Within the range 3-10 kPa, CBF increases linearly by about 25% per kPa increase in PaC02. The effect of PaC02 on cerebral blood volume (CBV), however, is less pronounced. cBv changes by about 10% per kPa change in PaCO2 in the healthy individual but recent evidence has suggested that the relationship between PaC02 and CBV is not predictable in the patient with brain injury. The cerebral blood volume constitutes only around 5% of the total intracranial volume but, since the brain is situated in an enclosed space, even a small change in CBV can have a profound effect on the ICP, particularly in those with reduced intracranial compliance.

Arterial oxygen tension has little effect on CBF in the physiologic range. However, high arterial oxygen tension (>100 kPa) can cause cerebral vasoconstriction, and Pa02 below 7 kPa will cause cerebral vasodilatation which overrides any vasoconstriction due to hypocapnia. There is some evidence to suggest that CBF increases even during modest reductions in oxygen saturation.7

Pathophysiology of Head Injury

When the head is struck, neurones and intracranial blood vessels are subjected to direct impact as well as flexion, extension and shearing forces as the brain moves inside the cranium. While most management issues focus on the treatment of raised intracranial pressure as a consequence of intracranial haematomas, contusions or brain swelling, it is important to realize that diffuse axonal damage may result in profound neurologic deficit without intracranial hypertension.

The primary injury, which is not treatable and can only be prevented, describes the damage that occurs at the time of initial impact. The amount of primary injury is dependent on the degree of force applied to the brain and is the principal factor that delineates a viable from a non-viable injury. Of the 1.1 million head injuries seen in hospital in Britain every year, 10,000 are severe.1 Severe head injury renders the patient comatose from impact; those able to talk at any stage following the injury are unlikely to have sustained a substantial primary injury.

Secondary injury is the additional insult imposed on the neural tissue following the primary impact. Treatment is aimed at preventing secondary cerebral ischaemia and thereby reducing the incidence of patients with head injury admitted to hospital in a conscious state only to die later89. The main contributors to secondary ischaemia in the head-injured patient are:


• systemic hypotension;

• intracranial masses;

• intracranial hypertension;

• posttraumatic cerebral arterial spasm

Regulation of Cerebral Blood Flow in the Head-Injured Patient

In the healthy brain, local control mechanisms act to ensure that areas of the brain with higher metabolism are supplied with increased blood flow. This flow/metabolism coupling is produced by a combination of various factors, including hypoxic vasodilatation, the effects of changes in CO2 concentration, the balance of autonomic nervous supply and the release of local metabolites, including prostaglandins, nitric oxide, calcium ions, potassium ions and adenosine. The effect of head trauma on CBF and cerebral metabolism is not entirely clear. Despite a reduction in absolute CBF, most patients who are comatose as a result of head injury (Glasgow Coma Scale (GCS) <9) have relative hyperaemia, with high CBF relative to metabolism.10 However, in up to 90% of patients who die from head injury, lesions compatible with ischaemia are found at postmortem.1112 This paradox is partly explained by the recent findings of a severe reduction in CBF occurring in the initial period (3-8 h) following injury. Over the next 24 h, this is followed by a gradual increase in CBF until eventually, cerebral metabolic needs are exceeded.131415 Furthermore, vasospasm, which occurs in 20-40% of patients with head injury,161718 may reduce CBF after this initial hyperaemic phase, with an increase in the incidence of non-contusion related cerebral infarction.19 Thus, the change in the CBF:CMRO2 ratio is by no means uniform in head-injured patients. The majority of the severely injured patients will suffer an initial decline in CBF, followed by a return to normal flow or relative hyperaemia and the flow may then decline again, particularly if vasospasm occurs. Both extremely low CBF and high CBF after head injury are associated with poor outcome.1420

Head trauma impairs the mechanisms controlling CBF. Pressure autoregulation is commonly abolished following a severe head injury but this is not always indicative of poor prognosis.21 In contrast, the complete absence of CO2 reactivity with lack of vasoconstrictor response to barbiturates is associated with a poor outcome.22 Cerebrovascular reactivity to CO2 is often preserved but the magnitude of response may be reduced.23

Mechanisms of Secondary Neuronal Injury

Ischaemia may cause secondary injury by several different processes that increase the extent of damage to the central nervous system.24 These include:

• accumulation of glutamate and aspartate, excitotoxic amino acids which interact with NMDA (N-methyl-D-aspartate) receptors and lead to intracellular accumulation of calcium ions;25

• activation of phospholipase;26

• breakdown of arachidonic acid;

• generation of free radicals;2728

• lipid peroxidation.

The above processes can all contribute to eventual neuronal death. An understanding of the mechanisms involved may permit the development of pharmacological strategies that might help to prevent secondary neuronal injury.29

In the presence of a fixed energy supply, cellular outcome may be markedly affected by factors that modify energy demand. Thus hyperthermia,30 coma, fits or excitotoxic neuronal activation can result in greater neuronal loss, while hypothermia and metabolic suppression may provide significant neuroprotection. Owing to the number of confounding factors present,31 the mechanisms responsible for secondary neuronal injury are not easily studied in man. Much of the information has been obtained from animal models of focal ischaemia or craniocerebral trauma and extrapolation from these results to clinical situations must be undertaken with care.32 The detection of an ischaemic penumbra with inactive but viable neurones and the use of reperfusion to rescue this tissue, which would otherwise have infarcted, suggests that these secondary mechanisms do exist.33

While ischaemic thresholds for cessation of electrical activity and cell death have long been recognized, it is increasingly obvious that other vital functions are inhibited at higher blood flow levels and may, over time, be responsible for cell death.

Intracranial Pressure

The normal intracranial contents can be divided into four compartments: tissue volume, interstitial waters, cerebrospinal fluid (CSF 75 ml) and blood volume (50 ml). Resting ICP represents the equilibrium pressure at which CSF production and absorption are in balance. The production of CSF remains constant as long as CPP remains adequate. CSF absorption is a passive process through the arachnoid granulations and increases with the increase in CSF pressure. In the resting adults the normal ICP is between 1 and 10 mmHg.

The 'four lump' concept describes most simply the causes of raised ICP inside the skull (which acts as a rigid box): cerebral oedema, CSF accumulation, vascular congestion or the presence of an intracranial mass. Any increase in volume in any of the four components will lead to a rise in ICP. This pressure-volume relationship is commonly referred to as the intracranial compliance curve. As cerebral perfusion pressure is determined by the difference between mean arterial blood pressure (MAP) and iCP, a high ICP will lead to cerebral ischaemia.

Small increases in mass may be compensated for, initially, by translocation of CSF into the spinal subarachnoid space and by compression of the venous blood volume. However, once this compensatory mechanism is exhausted, ICP rises steeply with further increases in intracranial content. As prolonged raised ICP is associated with a poor prognosis,34-37 vigorous treatment is essential and should be instituted if ICP exceeds 25 mmHg for more than 5 min.

Systemic Effects of Head Injury

Up to 65% of spontaneously breathing head-injured patients may be hypoxaemic, even though they may not appear to be in respiratory distress.38 Hypoxaemia is associated with poor neurological outcome and should be promptly corrected.35 The causes of the impairment in gas exchange may include:

• chest and abdominal injuries with flail segments, direct lung trauma, haemothorax and tracheobronchial disruption;

• aspiration of laryngeal and pharyngeal secretions due to impaired reflexes, with the adult respiratory distress syndrome developing 24-72 h later;

• fat embolism syndrome from long bone fractures;

• abnormal respiratory patterns as a result of cerebral hemispheric or basal ganglia damage;

• neurogenic alterations in residual functional capacity and ventilation/perfusion matching;

• acute neurogenic pulmonary oedema. This is rare, typically occurring 2-12 h after the injury, and usually resolves within a few hours.39

Brainstem compression, medullary ischaemia and raised ICP may cause severe elevations of blood pressure as a result of increased sympathetic activity following head injury.40 This hyperdynamic response is responsible for the cardiac dysrhythmias and ECG abnormalities commonly seen after severe head injury41 4243 and such changes are severe enough to produce myocardial necrosis in up to 62% of those who die from an intracranial lesion.43 The presence of these cardiovascular changes may complicate the management of the head-injured patient with cerebral hypoperfusion, as the use of inotropes may worsen the myocardial ischaemia. On the other hand, the presence of intracranial pathology may prohibit the use of venodilators because of their cerebral vasodilatatory effects.

With the exception of young children, in whom blood loss from scalp lacerations may lead to hypotension, low blood pressure in a patient with acute head injury is usually due to causes other than the head injury and requires prompt investigation and treatment.

Coagulation disturbances occur in up to 24% of patients with severe head injury and, when severe, are indicative of poor outcome.444546 The release of tissue thromboplastin may lead to widespread activation of the coagulation cascade and disseminated intravascular coagulation (DIC).47 Hypothermia and large blood transfusion further increase the incidence of clotting abnormalities.48 Therefore, coagulation studies should be performed routinely and replacement of clotting factors is advised.

Endocrine and electrolyte abnormalities often accompany severe head injury. Stress-induced p-adrenergic stimulation, respiratory alkalosis from hyperventilation and diuretic therapy may result in hypokalaemia.

Hyponatraemia is also common after head injury and may be associated with diminished, normal or increased extracellular fluid volume. It is important to diagnose which category the patient belongs to before treatment is initiated. Democlocycline, which impairs the effect of antidiuretic hormone (ADH) on the kidney, is used to treat the syndrome of inappropriate ADH secretion. The judicious administration of hypertonic saline may be necessary if the serum sodium concentration falls below 120 meq/l. In contrast, damage to the hypothalamic/pituitary axis my lead to a lack of ADH secretion and diabetes insipidus. Diabetes insipidus occurs in 1% of head-injured patients and can result in hypernatraemia due to the loss of large volumes of dilute urine (20 l/day). This hypernatraemia and polyuria is treated with the administration of DDAVP (desamino desarginine vasopressin) and 5% dextrose in water with careful monitoring of blood sugar levels. A more common cause of hypernatraemia, however, is the repeated administration of mannitol.

Severe head injury is accompanied by a significant stress response. The increase in the levels of circulating catecholamines and cortisol results in hyperglycaemia. If not treated, this will worsen neurological outcome.49 The stress response is also associated with an increased risk of gastric ulceration and gastrointestinal bleeding. H2 antagonists or sucralfate are commonly used for prophylaxis.

Management of Head Injuries

The anaesthetist is normally involved in the management of those patients with moderate or severe injury and this chapter concentrates on the management of this group of patients. It is important, however, that any doctor is able to adequately assess the severity of head injury according to the history of injury and clinical signs and symptoms. A practical protocol for the assessment and management of the head-injured patient was recently outlined by Arienta et al50 and is given in Box 20.1.

The management of the patient with moderate to severe head injury falls into three phases: initial resuscitation and transfer, intraoperative management, and intensive care and rehabilitation. This chapter concentrates on the initial resuscitation and intraoperative management of such a patient.

Initial Resuscitation

The importance of securing the airway and maintaining adequate oxygenation and blood pressure in the head-injured patient cannot be overemphasized. Secondary brain damage begins and continues to occur from the moment of impact and for every second that the patient is hypoxaemic or hypotensive. For this reason, it is essential that ambulance teams are trained properly, are aware of the need for aggressive treatment of hypoxia and hypotension in the head-injured patient and have the equipment and expertise to be able to start resuscitation at the scene of the accident. It has been shown that hypotension or hypoxia is present in the prehospital phase of care in approximately 30% of patients with head injuries.51 Severely head-injured patients (GCS <8) are unlikely to be able to protect their airway and often have impaired gas exchange52 and early use of endotracheal intubation may be necessary to maintain adequate oxygenation. An improvement in the incidence of mortality after severe head injury has been associated with 'in-field' intubation.53 Accident and emergency departments must be forewarned of the impending arrival of a comatose patient and an anaesthetist should be available to intubate the trachea as soon as possible after arrival, if the airway has not been secured already. It is important to remember that a significant proportion of severe head injuries are associated with injuries to the cervical spine54 and therefore, manual in-line stabilization of the neck during induction and tracheal intubation is essential.55 If there is any doubt about the ability to intubate the trachea, because of either a difficult airway or significant facial trauma, the airway must be secured by surgical means. Nasal intubation is best avoided in the patient with basal skull fracture because of the risk of passing the endotracheal tube into the brain through the skull defect and because of the added risk of infection.56

Severely head-injured patients must be assumed to have a full stomach. Therefore, a rapid-sequence induction with a small dose induction agent followed by suxamethonium 1 mg/kg is mandatory. Apart from ketamine, which is contraindicated because of concerns about its effects on ICP, the choice of induction agent is not important as long as it is administered with care and large variation in blood pressure or significant hypotension is avoided. Thiopentone, propofol and etomidate are the main induction agents used at our centre. Lignocaine 1 mg/kg may be given as a useful adjunct in attenuating the cerebrovascular response to laryngoscopy and tracheal intubation.5758 59 Suxamethonium may result in a transient rise in ICP from increased CO2 production and cerebral stimulation via afferent muscle activity.60-63 However, the potential risk of hypoxaemia and hypercapnia far outweighs the risk of this transient increase in ICP. Furthermore, in sedated and mechanically ventilated patients with moderate to severe brain

Group A (minimal head injury GCS = 15)

• Patient is awake, orientated and without neurologic deficits and relates accident

• No loss of consciousness

• Absent or minimal subgaleal swelling

The patient is released into the care of a family member with written instructions.

Group B (minor head injury GCS = 15)

• Patient is awake, orientated and without neurologic deficits

• Transitory loss of consciousness

• One episode of vomiting

• Significant subgaleal swelling

The patient who has at least one of these characteristics undergoes neurologic evaluation and CT scan which, if negative, shortens hospital observation. If CT scan is not available, the patient has skull X-rays and is held for an observation period of not less than 6 h. If the skull X-rays are negative and a subsequent neurologic control is normal, the patient can be released into the care of a family member with written instructions. If the X-rays reveal a fracture, the patient undergoes CT scan.

Group C (moderate head injury or mild head injury with complicating factors GCS = 9-15)

• Impaired consciousness

• Uncooperative for various reasons

• Repeated vomiting

• Neurologic deficits

• Otorrhagia/otorrhoea

• Rhinorrhoea

• Signs of basal fracture

• Penetrating or perforating wounds

• Patients in anticoagulant therapy or affected by coagulopathy

• Patients who have undergone previous intracranial operations

• Epileptic or alcoholic patients

The patient with at least one of these characteristics undergoes a neurologic evaluation and a CT scan. Hospitalization and repeated scan, if necessary, within 24 h or prior to discharge.

Group D (severe head injury GCS = 3-8)

Necessary resuscitation manoeuvres followed by neurological evaluation and immediate CT scan (prior to surgical intervention). Coma management.

Box 20.1 Practical Protocol for Management of Head-Injured Patients in the Emergency Department (modified from reference50)

injury, suxamethonium has no clinically significant effects on ICP or the cerebral blood flow velocity.64 The increase in serum potassium associated with the use of suxamethonium is an important consideration at later stages (>48 h after the initial injury), but not in the acute setting.65

Once the airway is secured, the lungs are mechanically ventilated to maintain mild hypocapnia (not less than 4 kPa) and adequate PaO2. Oxygenation and ventilation are optimized and should be regularly verified by arterial blood gas analysis. The patient is best sedated and paralysed. There is no excuse for having the patient coughing or straining on the endotracheal tube. Clearly, not all patients with head trauma require tracheal intubation and the protocol used in our unit is outlined in Box 20.2.

The importance of maintaining systemic perfusion has recently been confirmed by the results from the American National Traumatic Coma Data Bank which demonstrated that systolic blood pressure <80 mmHg is a significant independent contributing factor to poor outcome.66 67 The combination of an increased ICP and systemic hypotension leads to a reduction in CPP and cerebral ischaemia. Except for young children, in whom blood loss from a scalp wound is sufficient to cause hypotension, hypotension should prompt an investigation of sites of blood loss with immediate laparotomy or thoracotomy if necessary. Hypovolaemia may be masked by systemic hypertension secondary to intense sympathetic stimulation of the reflex response to intracranial hypertension.68

The increase in blood pressure is a compensatory response to maintain cerebral perfusion. Therefore, moderate levels of hypertension should not be treated but a blood pressure above the upper limit of autoregulation (mean arterial pressure > 130 mmHg) must be actively treated, as it will increase CBV and ICP.

Although the effect of systemic hypotension on cerebral perfusion will depend initially on whether autoregulation is impaired or not, the final result will be a reduction in CBF. Hypotension will worsen cerebral perfusion in patients with impaired autoregulation as CBF is pressure passive. In contrast, in patients with intact autoregulation, hypotension will lead to cerebral vasodilatation with a resultant increase in ICP, a reduction in CPP and eventually decreased CBF.69 Patients who are severely injured may exhibit 'false autoregulation', where the ICP changes by the same magnitude as systemic blood pressure, resulting in a constant cerebral perfusion pressure.70

The choice of fluid used for resuscitation is less important than the amount given. The use of glucose-containing solutions is discouraged unless hypoglycaemia is suspected, as hyperglycaemia (leading to lactic acidosis) has been shown to correlate with poor outcome after head injury.4971 72 Hyperglycaemia should be actively treated and blood glucose levels controlled with an infusion of insulin. Because the majority of head-injured patients receive mannitol, an adequate urine output is often a poor indicator of volume status in these patients. Central venous pressure monitoring is often very useful as an aid to


• Coma (not obeying commands, not speaking, not eye opening, i.e. GCS = <8)

• Loss of protective laryngeal reflexes

• Ventilatory insufficiency as judged by blood gases:

hypoxaemia (PaO2 < 13 kPa) hypercarbia (PaCO2 >6 kPa)

spontaneous hyperventilation causing PaCO2 <3.5 kPa respiratory arrhythmia

• Uncontrolled seizures

Before start of journey to the neurointensive care unit

• Deteriorating level of consciousness (decrease in GCS by > 2 points since admission and not due to drugs), even if not in coma

• Bilaterally fractured mandible

• Copious bleeding into mouth (e.g. from a basal skull fracture)

Box 20.2 Indications for intubation and ventilation after head injury* (modified from reference95)

*An intubated patient must also be ventilated, aiming for a PaO2 > 13 kPa and PaCO2 of 4.0-4.5 kPa.

assessing intravascular fluid volumes and effectiveness of resuscitation and should be combined with the use of a pulmonary artery flotation catheter in the elderly, patients with heart disease and in those patients requiring inotropic support.

Transfer of the Head-Injured Patient

Adequate resuscitation and a thorough reexamination of the patient must be completed before making decisions about further treatment priorities. Quality radiographs are taken of suspicious areas and CT scans arranged (Box 20.3). Blind burr hole exploration is rarely effective, can be harmful to the patient and delays the transfer of the patient and the initiation of definitive therapy. There is no longer any indication for this procedure in the modern accident and emergency department.

Once the patient has been stabilized, a decision can be made regarding transfer to a regional neurosurgical unit for further treatment (Box 20.4). Interhospital transfer of the head-injured patient is a potentially hazardous procedure and often poorly managed. Evidence suggests that the neurologically injured patient is at greater risk of cerebral ischaemia during transfer.73 As the main causes of secondary brain damage are hypoxia, hypercarbia and cardiovascular instability, it is of vital importance to avoid any of these during transfer. The key to a successful and safe transfer involves:

• adequate resuscitation and stabilization of the patient prior to transfer;

• adequate monitoring during transfer with appropriate resuscitative equipment and drugs;

• the presence of an accompanying doctor with suitable training, skills and experience of head injury transfer;

• good communication between referring and receiving centres and an adequate, efficient and stable handover to the receiving team.7475

• Confusion (GCS <14) persisting after the initial assessment and resuscitation

• Unstable systemic state precluding transfer to neurosurgical centre

• Diagnosis uncertain

• Fully conscious but with a skull fracture or following first fit (admit and consider CT scan)

Box 20.3 Indications for CT scanning in a general hospital

Without preliminary head CT

• Coma (not obeying commands) even after resuscitation and even without a skull fracture

• Deterioration in the level of consciousness of more than two GCS points or progressive neurological deficit

• Open injury, depressed skull fracture, penetrating injury or basal skull fracture

• Tense fontanelle in a child

• Patient fulfils criteria for CT but this cannot be performed within a reasonable time (3-4 h)

After CT scan in a general hospital

• Abnormal CT (preferably after neurosurgical opinion on electronically transferred images)

• CT normal but patient's progress unsatisfactory

Box 20.4 Criteria for neurosurgical referral of head-injured patients

The fundamental requirement during transfer is to ensure adequate tissue oxygen delivery and to maintain stable perfusion. The head-injured patient is at risk of respiratory compromise and this risk is increased during transfer. We would recommend that any patient with a significantly altered conscious level should be sedated, intubated and ventilated during transfer. There is no place for transferring unstable patients to neurosurgical units. A patient persistently hypotensive, despite resuscitation, must be investigated thoroughly and the cause of hypotension identified and treated prior to transfer. The transferring team must ensure that all lines and tubes are secured before transfer, that they have sufficient supply of drugs and portable gases and that there is enough power in battery-operated monitoring equipment for the duration of the journey.

Monitoring during transfer should be of a standard appropriate to a patient in intensive care and we would recommend that this should include invasive arterial blood pressure monitoring, central venous pressure monitoring, where indicated, and the use of capnography. The transferring doctor must have appropriate experience in the transfer of patients with head injuries, should be familiar with the pathophysiology and management of such a patient and with the drugs and equipment they will use. It is also of paramount importance to discuss the patient with the neurosurgical centre at an early stage, so that treatment priorities can be decided upon and that the receiving team is prepared for the arrival of the patient (Box 20.5). The

• Patient's age and past medical history (if known)

• History of injury

Time of injury

Cause and mechanism (height of fall, approximate impact velocity)

• Neurological state

Talked or not after injury

Consciousness level on arrival at A&E dept

Trends in consciousness level after arrival (sequential GCS)

Pupil and limb responses

• Cardiorespiratory state

Blood pressure and pulse rate

Arterial blood gases, respiratory rate and pattern

Skull fracture Extracranial injuries

• Imaging findings

Haematoma, swelling, other

• Management

Airway protection, ventilatory status Circulatory status and fluid therapy (mannitol) Treatment of associated injuries (? emergency surgery) Monitoring

Drug doses and times of administration Box 20.5 What the neurosurgical centre needs to know at time of referral care of the transferring doctor does not end at the door of the receiving hospital but continues until he or she ensures that the stability of the patient is maintained and a full and accurate handover to the receiving team is made. A copy of the neurosurgical transfer letter used in our region can be seen in Figure 20.1.

Intraoperative Management

Head-injured patients may require anaesthesia for treatment of the primary neurological pathology or for the treatment of a non-neurological injury (e.g. fixation of compound fractures). The optimal timing of such operations is debatable and the decision to operate must be made only after thorough consideration by trauma, neurosurgical and neurointensive care teams. Recent evidence suggests that early long bone fracture fixation may lead to a greater risk of intraoperative hypoxaemia and hypotension.76 Since these are the principal factors contributing to secondary brain injury, the benefits of operating at an early stage after major trauma must be qualified by the potential for further damage to the brain.

For any operation on the head-injured patient, management priorities remain the avoidance of cerebral ischaemia, optimization of CPP and the prevention of intracranial hypertension.

Intraoperative care of the head-injured patient does not begin with knife to skin but should be a direct continuation of the resuscitation and stabilization process in the neurointensive care unit or the accident and emergency department. Transfer of the patient to and from the operating table must be achieved without subjecting the patient to hypotension or hypoxaemia. As the patient's head is inaccessible during the operation, the anaesthetist must ensure, before the patient is prepared and draped, that all the pressure points are padded, the eyes are protected, the endotracheal tube is secured and ventilation is adequate for maintaining good gas exchange. Venous drainage must not be obstructed with excessive neck rotation, ties or high inflation pressures. There is no point in employing pharmacological methods of controlling ICP to treat intraoperative brain swelling until these simple measures have been undertaken.

Because of the dangers of even short periods of cerebral hypoperfusion or hypoxia, it is essential that the patient is continuously and adequately monitored throughout the operation and throughout the transfer to and from the operating environment. Monitoring should include ECG, temperature, urine output, pulse oximetry and invasive systemic blood pressure. Special emphasis should be placed on end-tidal CO2 monitoring as a means of continuously assessing the level of hyperventilation and a comparison with PaCO2 is advisable. Central venous and/or pulmonary artery pressure monitoring, particularly in the elderly and in those with cardiac disease, will allow a more rational approach to fluid replacement, particularly in those patients requiring inotropic support to maintain an adequate CPP. In patients with neurological injury who require non-neurological surgical intervention, iCp monitoring is recommended especially if large intraoperative fluid shifts are possible. Intracranial pressure, cerebral venous oxygen saturation

(SJO2) monitoring and the use of transcranial Doppler (TCD) are discussed in detail in the respective chapters. It is now accepted that head-injured patients do not have reduced anaesthetic requirements.77 78 Inadequate

Figure 20.1

A copy of the East Anglia neurosurgical transfer letter.

Figure 20.1

A copy of the East Anglia neurosurgical transfer letter.

anaesthesia will allow the surgical stimulus to increase CMRO2, CBF and ICP. The choice of anaesthetic agent and technique will depend on the patient's preoperative neurological status, his preoperative medical conditions and the presence of associated injuries. There is simply no evidence that a particular approach is better for anaesthetizing the patient with head injury. However, most commonly recommended methods have these goals in common:

• smooth induction without sudden or pronounced changes in blood pressure;

• maintenance of adequate CPP;

• preventing rises in CMRO2, CBF and ICP;

• a rapid postoperative emergence, if desired.

The choice of maintenance agent should reflect these goals. In general, nitrous oxide and the inhalational agents are best avoided because of their effect on autoregulation, CBF and ICP.7980 Although nitrous oxide maintains autoregulation and CO2 reactivity, it has been shown to stimulate cerebral metabolism, resulting in vasodilatation and increased CBF.81 For this reason, its use in the head-injured patient is discouraged.

The inhaled volatile anaesthetic agents affect both CBF and autoregulation. The net effect of inhalational agents is to increase the CBF but their action on CBF is twofold. As all the inhalational agents tend to reduce cerebral metabolism, we would expect a corresponding reduction in CBF. The decrease in CBF, however, is overridden by a direct cerebral vasodilatory effect, partly mediated by nitric oxide. This vasodilatory effect increases with the dose of anaesthetic agent. Thus, although the increase in CBF produced by isoflurane, halothane and desflurane may be small at low doses, it is dose dependent and CBF may markedly increase at higher doses. This increase is further exaggerated when CMRO2 is depressed, as may be the case in the head-injured patient.80 Sevoflurane appears to be the "least" cerebral vasodilatory inhalational agent available at present.82

As blood pressure and CPP fluctuate in response to surgical stimulus, anaesthetic agents that maintain autoregulation and CO2 reactivity will allow stable cerebral haemodynamics. Inhalational anaesthetics, with the exception of sevoflurane, impair both the ability to autoregulate (static autoregulation), and the rate of autoregulation (dynamic autoregulation) in a dose-dependent manner.79 In addition, the inhalational agents impair CO2 reactivity. In contrast, sevoflurane has been shown to maintain static autoregulation and preserves dynamic autoregulation and CO2 reactivity better than the other commonly used volatile anaesthetic agents.83 The reported epileptogenic side effects of enflurane prohibit its use in neuroanaesthesia.

Opioids have very little effect on CBF and metabolism but the newer synthetic opioids, fentanyl, sufentanil and alfentanil, have been shown to cause an increase in ICP in patients with head injury. This increase is thought to be secondary to respiratory depression and hypotension. These agents should therefore be used with great care to avoid systemic hypotension. Remifentanil, the recently introduced opioid agent with an ultra-short half-life, will probably affect ICP via its hypotensive effect.

We prefer to use a total intravenous anaesthetic technique of propofol and fentanyl infusions. Propofol reduces CMRO2, CBF and ICP. It does not impair autoregulation and CO2 reactivity, even at high enough doses to produce electroencephalographic isoelectricity.84 The reduction in CMRO2 with propofol anaesthesia may be neuroprotective. The patient's lungs are ventilated with O2/air mixture to maintain mild hypocapnia. Although prolonged excessive hyperventilation is associated with poor neurological outcome, acute hyperventilation may be essential to reduce ICP in the head-injured patient.85 Hypocapnia induces cerebral vasoconstriction and the resultant decrease in CBF and ICP may improve cerebral perfusion pressure. However, excessive cerebral vasoconstriction has been shown to cause cerebral ischaemia and hyperventilation must be used with great care. Should a PaCO2 lower than 4 kPa be required, monitoring cerebral oxygenation with a jugular venous bulb catheter is advisable. Jugular bulb oximetry, though unable to detect local ischaemia, is a good indicator of the adequacy of CBF and global cerebral oxygenation. Hyperoxia can be used as a temporary measure to improve cerebral oxygen delivery during marked hyperventilation.86 87

Neuromuscular blockade should be maintained intraoperatively in all head-injured patients to prevent coughing or straining and the extent of neuromuscular block monitored with a neuromuscular stimulator.

The use of neuroprotective treatment regimens in the patient with moderate or severe head injury is of secondary importance to the maintenance of cerebral oxygenation, the avoidance of hypotension and the control of intracranial pressure. Hyopthermia has theoretical advantages in that it reduces CMRO2, the production of cytokines, free radicals and glutamate and has been shown to be of benefit in animal studies.88 Although conclusive outcome data are still lacking, a recent study in humans suggested that moderate hypothermia for 24 h was beneficial in improving outcome of head-injured patients with admission GCS of 5-7.89 As hypothermia is not without its complications, mainly increased systemic vascular resistance and myocardial work and potential coagulation abnormalities, it cannot, therefore, be recommended as first-line treatment in head-injured patients. Hyperthermia, however, has been shown to adversely affect outcome and must be aggressively treated.90

As mentioned previously, the loss of pressure autoregulation in the damaged brain occurs frequently and results in the CBF varying directly with the patient's systemic blood pressure. Intraoperative hypotension can cause a marked reduction in the CBF and this reduction is reflected in significantly worse outcomes in those patients experiencing a prolonged fall (>5 min) in blood pressure during their operation. Pietrapaoli et al91 demonstrated an 82% mortality in patients experiencing intraoperative hypotension, compared with a 25% mortality in those who remained normotensive. In addition, the duration of intraoperative hypotension was related directly to worsening outcomes. We would advocate, therefore, the use of early and sufficient resuscitation with intravenous fluids and blood and a low threshold for the appropriate use of inotropic support to maintain CPP.

The statistics in children with head injury also serve to emphasize the importance of the avoidance of hypoxia and hypotension. Pigula et al92 showed a mortality of 22% in children with severe head injury with normal systemic blood pressures and PaO2 levels on admission. However, in children who were hypotensive on admission, the mortality increased to 61% and, if the child was also hypoxaemic, mortality was closer to 85%.

The maintenance of normotension in the head-injured patient undergoing surgery is made more difficult by some of the problems and physiological effects associated with intracranial mass lesions. An acute intracranial lesion (subdural or extradural haematoma) with mass effect is normally accompanied by intense sympathetic stimulation leading to an increase in systemic vascular resistance. Surgical evacuation of such a lesion is commonly associated with an abrupt decrease in the blood pressure at the time of decompression. It is important to make sure that hypovolaemia is not concealed by this increased systemic vascular resistance. Patients who are able to compensate for hypovolaemia by systemic vasoconstriction and tachycardia may have a precipitous fall in blood pressure with cardiovascular collapse at the time of surgical decompression. Therefore, a high index of suspicion is needed in the management of those patients who are tachycardic and normotensive, with early initiation of vigorous fluid therapy, meticulous attention to the blood pressure and prompt treatment of hypotension with intravenous fluids and, if necessary, vasopressors at the time of decompression.

Although haemodilution reduces blood viscosity and may theoretically improve blood flow through the microcirculation, haemodilution therapy in patients with cerebral ischaemia has failed to support this contention.93 Haemodilution does not produce an increase in tissue PO2 and therefore cannot be recommended as a therapeutic manoeuvre in those at risk of cerebral ischaemia.94 Blood transfusion is advocated for maintaining adequate cerebral oxygen delivery.


Patients with severe head injury requiring surgery generally need continuing postoperative care in the neurointensive care unit and they should remain paralysed and ventilated at the end of the procedure. In patients with mild to moderate head injury (GCS between 12 and 15) undergoing evacuation of an epidural or subdural haematoma, it is not unreasonable to allow the patient to wake up at the end of the procedure. A rapid return to consciousness permits early clinical assessment and the detection of unexpected neurological deficit. This emphasis on rapid emergence makes the maintenance of haemodynamic stability difficult. Care must be taken to avoid excessive coughing and bucking which may cause not only a transient increase in ICP but, more importantly, an increased risk of venous bleeding. Uncontrolled hypertension on emergence may be responsible for intracerebral haemorrhage following neurosurgical procedures. Intravenous lignocaine (up to 3 mg/kg in divided doses) can be given during emergence to suppress coughing without significant effect on ventilation. Rises in blood pressure can be controlled with p-blockers. Finally, it is important to make sure that the patient is awake, can protect his or her airway, is able to maintain oxygenation and is normocapnic before extubation in order to avoid increases in ICP.


The principal aim of managing the severely head-injured patient is the prevention of secondary neuronal injury. The greatest impact on outcome is made by the institution of adequate and early resuscitation, by the availability and involvement of multidisciplinary teams and by the maintenance of adequate oxygenation and cerebral perfusion pressure throughout the entire posttraumatic period.


1. Jennet B, McMillan R. Epidemiology of head injury. BMJ 1981; 282: 101-104.

2. Andrews PJD. What is the optimal cerebral perfusion pressure after brain injury? A review of the evidence with an emphasis on arterial pressure. Acta Anaesthesiol Scand 1995; 39(suppl): 112-114.

'3. Aaslid R, Lindegaard K-F, Sorteberg W et al. Cerebral autoregulation dynamics in humans. Stroke 1989; 20: 45-52.

4. Edvinsson L, Owman C, Seisjo B Physiological role of cerebrovascular nerves in the autoregulation of cerebral blood flow. Brain Res 1976; 117: 518.

■5. Paulson OB, Olesen J, Christensen MS Restoration of autoregulation of cerebral blood flow by hypocapnia. Neurology 1972; 22: 286-293.

6. Aaslid R, Newell DW, Stooss R et al. Simultaneous arterial and venous transcranial Doppler assessment of cerebral autoregulation dynamics. Stroke 1991; 22: 1148-1154.

7. Gupta AK, Menon DK, Czosnyka M, Jones GJ. Thresholds for hypoxic cerebral vasodilatation in volunteers. Anesth Analg 1997; 85(4): 817-20.

■8. Lobato RD, Rivas JJ, Gomez PA et al. Head injured patients who talk and deteriorate into coma. Analysis of 211 cases studied with computerised tomography. J Neurosurg 1991; 75: 256-261.

■9. Rockswold Gl, Leonard PR, Nagib MG Analysis of management in thirty-three closed head injury patients who 'talked and deteriorated'. Neurosurgery 1987; 21: 51-55.

10. Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA. Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg 1984; 61(2): 241-253.

11. Graham DI, Adams JH, Doyle D. Ischaemic brain damage in fatal non-missile head injuries J Neurol Sci 1978; 39(2-3): 213234.

12. Graham DI, Ford I, Adams JH et al. Ischaemic brain damage is still common in fatal non-missile head injury J Neurol Neurosurg Psychiatry 1989; 52(3): 346-350.

13. Bouma GJ, Muizelaar JP, Choi SC et al. Cerebral circulation and metabolism after severe traumatic brain injury: The elusive role of ischemia. J Neurosurg 1991; 75: 685-693.

14. Bouma GJ, Muizelaar JP. Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma 1992; 09: S333-S348.

■15. Marion DW, Darby J, Yonas H. Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg 1991; 74: 407-414.

16. Weber M, Grolimund P, Seiler RW Evaluation of posttraumatic cerebral blood flow velocities by transcranial Doppler ultrasonography Neurosurgery 1990; 27(1): 106-112.

17. Martin NA, Doberstein C, Zane C et al. Post-traumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings. J Neurosurg 1992; 77: 575-583.

18. Kakarieka A, Braakman R, Schakel EH. Clinical significance of the finding of subarachnoid blood on CT scan after head injury. Acta Neurochir (Wein) 1994; 129: 1-5.

19. Chan KH, Dearden NM, Miller JD. The significance of post-traumatic increase in cerebral blood flow velocity: a transcranial Doppler ultrasound study. Neurosurgery 1992; 30: 697-700.

■20. Robertson CS, Narayan RK, Gokaslan ZL et al. Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients. J Neurosurg 1989; 70: 222-230.

21. Newell DW, Aaslid R, Stoos R et al. Evaluation of closed head injury patients using transcranial Doppler monitoring. In: Avezaat CJJ, Van Eijndhoven JHM, Maas AIR, Tans JTJ (eds) ICP VIII International Symposium. Springer-Verlag, Heidelberg, 1993, pp 309-312.

■22. Schalen W, Messeter K, Nordstrom CH. Cerebral vasoreactivity and the prediction of outcome in severe traumatic brain lesions. Acta Anaesthesiol Scand 1991; 35: 113-122.

23. Cold GE. Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance for therapy. Acta Neurochir (Wien) 1990; 49: 1-64.

24. Siesjo BK. Pathophysiology and treatment of focal cerebral ischaemia. Part I: Pathophysiology. J Neurosurg 1992; 77: 169-184.

25. Mayer ML, Miller RJ Excitatory amino acid receptors, second messengers, and regulation of intracellular Ca2+ in mammalian neurones. Trends Pharmacol Sci 1990; 11: 254-260.

26. Smith WI, Borgeat P, Fitzpatrick FA. The ecosanoids: cyclooxygenase, lipoxygenase, and epoxygenase pathways. In: Vance DE and Vance J (eds) Biochemistry of lipids, lipoproteins and membranes. New comprehensive biochemistry. Elsevier Science Publishers, Amsterdam, 1991, pp 297-325.

■27. Traystman RJ, Kirsch JR, Koehler RC. Oxygen radical mechanisms of brain injury following ischaemia and reperfusion. J Appl Physiol 1991; 71: 1185-1195.

28. McCord JM. Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med 1985; 312: 159-163.

29. Faden AI, Salzman S. Pharmacological strategies in CNS trauma. Trends Pharmacol Sci 1992; 13: 29-35.

■30. Wass CT, Lanier WL, Hofer RE, Scheithauer BW, Andrews AG. Temperature increases of >1°C worsens functional neurologic outcome and histopathology in canine model of complete cerebral ischemia. J Neurosurg Anesthesiol 1994; 6: 305.

31. Molinari GF. Why model strokes? Stroke 1988; 19: 1195-1197.

32. Hsu CY. Criteria for valid preclinical trials using animal stroke models. Stroke 1993; 24: 633-636.

■33. Memezawa H, Smith M-L, Siesjo BK. Penumbral tissues salvaged by reperfusion following middle cerebral artery occlusion in rats. Stroke 1992; 23: 552-559.

■34. Miller JD, Becker DP, Ward JD et al. Significance of intracranial hypertension in severe head injury. J Neurosurg 1977; 47: 503516.

■35. Miller JD, Butterworth JF, Gudeman SK et al. Further experience in the management of severe head injury. J Neurosurg 1981; 54: 289-299.

■36. Saul TG, Ducker TB. Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982; 56: 498-503.

■37. Marshall LF, Smith RW, Shapiro HM. The outcome with aggressive treatment in severe head injuries. Part II: Acute and chronic barbiturate administration in the management of head injury. J Neurosurg 1979; 50: 26-30.

38. Frost EAM. The pathophysiology of respiration in neurosurgical patients. J Neurosurg 1979; 50: 699-714.

39. Baigelman W, O'Brien JC. Pulmonary effects of head trauma Neurosurgery 1981; 9: 729-740.

40. Schulte AM, Esch J, Murray H et al. Haemodynamic changes in patients with severe head injury. Acta Neurochir 1980; 54: 243246.

41. Hersch C. Electrocardiographic changes in head injury. Circulation 1961; 23: 853-860.

42. Miner ME. Cardiovascular effects of severe head injury. In: Frost EAM (ed) Clinical anesthesia for neurosurgery. Butterworth, Boston, 1991, pp 439-455.

43. Kolin A, Norris JW. Myocardial damage from acute cerebral lesions. Stroke 1984; 15: 990-995.

44. Piek J, Chestnut RM, Marshall LF et al. Extracranial complications of head injury. J Neurosurg 1992; 77: 901-907.

45. Kumura E, Sato M, Fukuda A et al. Coagulation disorders following acute head injury. Acta Neurochir (Wien) 1987; 85: 23-28.

46. Olson JD, Kaufman HH, Moake J et al. The incidence and significance of hemostatic abnormalities in patients with head injuries. Neurosurgery 1989; 24: 825-832.

47. Van Der Sande JJ, Veltkamp JJ, Boekhout-Mussert RJ et al. Head injury and coagulation disorders. J Neurosurg 1978; 49: 357365.

48. Ferrara A, MacArthur JD, Wright HK et al. Hypothermia and acidosis worsen coagulopathy in the patient requiring massive transfusion. Am J Surg 1990; 160: 515-518.

49. Lam AM, Winn HR, Cullen BF et al. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 1991; 75: 545-551.

■50. Arienta C, Caroli M, Balbi S. Management of head-injured patients in the emergency department: a practical protocol. Surg Neurol 1997; 48: 213-219.

■51. Wald S, Fenwick J, Shackford SR. The effect of secondary insults on mortality and long-term disability of severe head injury in a rural region without a trauma system. J Trauma 1991; 31: 104.

■52. Gildenberg PL, Maleka M. Effect of early intubation and ventilation on outcome following head trauma. In: Dacey RG Jr et al (eds) Trauma of the central nervous system. Raven Press, New York, 1985, pp 79-90.

■53. Pfenniger EG, Lindner KH. Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission. Acta Anaesthesiol Scand 1991; 35: 148-152.

54. Crosby ET, Lui A. The adult cervical spine: implications for airway management. Can J Anaesth 1990; 07: 77-93.

55. Lam AM. Spinal cord injury and management. Curr Opin Anesthesiol 1992; 5: 632-639.

56. Grande CM, Barton CR, Stene JK. Appropriate techniques for airway management of emergency patients with suspected spinal cord injury. Anesth Analg 1988; 67: 714-715.

■57. Bedford RF, Winn HR, Tyson G et al. Lidocaine prevents increased ICP after endotracheal intubation. In: Shulman K (ed) Intracranial pressure IV. Springer-Verlag, Berlin, 1980, pp 595-615.

■58. Hamill JF, Bedford RF, Weaver DC et al. Lidocaine before endotracheal intubation: intravenous or laryngotracheal? Anesthesiology 1981; 55: 578-581.

■59. Wojciechowski ZJ, Lam AM, Eng CC et al. Effect of intravenous lidocaine on cerebral blood flow velocity during endotracheal intubation. Anesthesiology 1992; 77: A194.

60. Lanier WL, Milde JH, Michenfelder JD. Cerebral stimulation following succinyl choline in dogs. Anaesthesiology 1986; 64(5): 551-559.

61. Lanier WL, Iaizzo PA, Milde JH. Cerebral function and muscle afferent activity following i.v. succinylcholine in dogs: the effect of pretreatment with defasciculating doses of pancuronium. Anesthesiology 1989; 71: 87-95.

62. Wright SW, Robinson GG, Wright MB. Cervical spine injuries in blunt trauma patients requiring emergent endotracheal intubation. Am J Emerg Med 1992; 10: 104-109.

63. Cottrell JE, Hartung J, Giffin JP et al. Intracranial and hemodynamic changes after succinylcholine administration in cats. Anesth Analg 1983; 62: 1006-1009.

64. Kovarik WD, Lam AM, Mayberg TS et al. Succinylcholine does not change intracranial pressure, cerebral blood flow velocity or the electroencephalogram in patients with neurologic injury. Anesth Analg 1994; 78: 469-473.

65. Frankville DD, Drummond JC. Hyperkalemia after succinylcholine administration in a patient with closed head injury without paresis. Anesthesiology 1987; 67: 264-266.

66. Chestnut RM. Secondary brain insults after head injury: clinical perspectives. New Horizons 1995; 3: 336.

67. Marmarou A, Anderson RL, Ward JD et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg 1991; 75: S59-S66.

68. Gushing H. Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression. Johns Hopkins Hosp Bull 1901; 126: 290-292.

69. Rosner MJ, Daughton S. Cerebral perfusion pressure management in head injury. J Trauma 1990; 30: 933-941.

■70. Enevoldsen EM, Jensen FT. Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury. J Neurosurg 1978; 48: 689-703.

■71. Young B, Ott L, Dempsey R et al. Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. Ann Surg 1989; 210: 466-473.

■72. Michaud LJ, Rivara FP, Longstreth WT Jr et al. Elevated initial blood glucose levels and poor outcome following severe brain injuries in children. J Trauma 1991; 31: 1356-1362.

■73. Andrews PJD, Piper IR, Dearden NM, Miller JD. Secondary insults during intrahospital transport of head-injured patients. Lancet 1990; 335: 327-330.

■74. Association of Anaesthetists of Great Britain and Ireland. Recommendations for the transfer of patients with acute head injuries to neurosurgical units. AAGBI, London, 1996.

■75. Royal College of Surgeons of England. Report of the working party on the management of patients with serious head injury. RCS, London, 1988.

76. Jaicks RR, Cohn SM, Moller BA. Early fracture fixation may be deleterious after head injury. J Trauma 1997; 42(1): 1-6.

■77. Todd MM, Weeks JB, Warner DS. A focal cryogenic brain lesion does not reduce the minimum alveolar concentration for halothane in rats. Anesthesiology 1993; 79: 139-143.

■78. Shapira Y, Paez A, Lam AM, Pavlin EG. Influence of traumatic head injury on halothane MAC in rats. Anesth Analg 1992; 74: S282.

■79. Strebel S, Lam AM, Matta BF et al. Dynamic and static cerebral autoregulation during isoflurane, desflurane and propofol anesthesia. Anesthesiology 1995; 83: 66-76.

■80. Matta BF, Mayberg TS, Lam AM. Direct cerebrovascular effects of halothane, isoflurane and desflurane during propofol-induced isoelectric electroencephalogram in humans. Anesthesiology 1995; 83(5): 980-985; discussion 27A.

■81. Matta BF, Lam AM. Nitrous oxide increases cerebral blood flow velocity during pharmacologically-induced EEG silence in humans. J Neurosurg Anesthesiol 1995; 7: 89-93.

■82. Matta BF, Heath K, Tipping K, Summors A. Direct cerebral vasodilatory effect of sevoflurane: a comparison with isoflurane. Anesthesiology 1999 (in press).

■83. Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation during sevoflurane anaesthesia: a comparison with isoflurane. Anesth Analg 1999; 88: 341-345.

■84. Matta BF, Lam AM, Strebel S, Mayberg TS. Cerebral pressure autoregulation and CO2-reactivity during propofol-induced EEG suppression. Br J Anaesth 1995; 4: 159-163.

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

■86. Matta BF, Lam AM, Mayberg TS. The influence of arterial hyperoxygenation on cerebral venous oxygen content during hyperventilation. Can J Anaesth 1994; 41: 1041-1046.

■87. Thiagarajan A, Goverdhan P, Chari P, Somasunderam K. The effect of hyperventilation and hyperoxia on cerebral venous oxygen saturation in patients with traumatic brain injury. Anesth Analg 1998; 87: 850-853.

■88. Xue D, Huang ZG, Smith KE et al. Immediate or delayed mild hypothermia prevents focal cerebral infarction. Brain Res 1992; 587: 66-72.

89. Marion DW, Penrod LE, Kelsey SF et al. Treatment of traumatic brain injury with moderate hypothermia. N Engl J Med 1997; 336: 540-546.

■90. Wass CT, Lanier WL, Hofer RE, Scheithauer BW, Andrews AG. Temperature increases of >1°C worsen functional neurologic outcome and histopathology in canine model of complete cerebral ischemia. J Neurosurg Anesthesiol 1994; 6: 305.

■91. Pietrapaoli JA, Rogers FB, Shackford SR, Wald SL, Schmoker JD, Zhuang J. The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries. J Trauma 1992; 33(3): 403-407.

■92. Pigula FA, Wald SL, Shackford SR, Vane DW. The effect of hypotension and hypoxia on children with severe head injuries. J Paediatr Surg 1993; 28: 310-316.

■93. Scandinavian Stroke Study Group Multicentre Trial of Haemodilution in Acute Stroke. Results in the total population. Stroke 1987; 18: 691.

■94. Chan R, Leniger-Follet E. Effects of isovolaemic hemodilution on oxygen supply and electrocorticogram in cat brain during focal ischemia and in normal tissue. Int J Microcirc 1983; 2: 297-333.

■95. Gentleman D, Dearden M, Midgley S, Maclean D. Guidelines for the resuscitation and transfer of patients with serious head injury BMJ 1993; 307: 547-552.

Intensive Care after Acute Head Injury

David K. Menon & Basil F. Matta

Introduction 301

Determinants of Outcome in Acute Head Injury: Primary vs Secondary Insults 301

Pathophysiology in Acute Head Injury 302

Monitoring in Acute Head Injury 303

Therapy 307

Novel Neuroprotective Interventions 311

Sequential Escalation Versus Targeted Therapy for the Intensive Care of Head 313 Injury

References 313


Approximately 1.4 million patients suffer a head injury in the United Kingdom each year1 and about 2500 of these suffer a severe head injury2 (defined as a postresusc

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