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Trauma is the leading cause of death in the first four decades of life, with head injury being implicated in at least half the number of cases. In the UK, 1500 per 100 000 of the population (total one million) attend accident and emergency departments with a head injury, 300 per 100 000 per year are admitted to hospital, 15 per 100 000 per year are admitted to neurosurgical units, and 9 per 100 000 per year die from head injury. Recent advances in the management of head injury have occurred at several levels including prevention, pre-hospital care, immediate hospital care, acute hospital care, and rehabilitation. This synopsis aims to outline the principles of the treatment of head injury in the acute phase.
Fundamental processes occur at a cellular level following brain injury, which culminate in cell death.1 These processes include the release of excitotoxic quantities of the amino acids, glutamate and aspartate, production of free radicals, and increased production of lactate and hydrogen ions. One of the final common pathways of these processes is the entry of calcium ions into cells, which results in cell swelling. This swelling, within the confines of the rigid cranium, results in an increase in intracranial pressure (ICP) and reduction in cerebral perfusion pressure (CPP, defined as mean arterial blood pressure − intracranial pressure), with cerebral ischaemia and reduced delivery of oxygen to the tissues, provoking further acidosis, and glutamate and free radical release to potentiate the above cycle. The goal of treatment in these patients is to intervene in this cycle by reducing intracranial pressure and increasing cerebral perfusion pressure.2
The structural changes following head injury can be divided into two main groups:
diffuse injury—this ranges from mild injury with concussion to major injury with diffuse axonal injury characterised by histological changes, including axon retraction balls
mass lesions—these include either haematomas (extradural, subdural, intracerebral) or intracerebral contusions, which predominantly affect the frontal and temporal lobes and may be at the site of (coup) or opposite (contrecoup) the injury.
PRIMARY MANAGEMENT PHASE: ACCIDENT AND EMERGENCY
The recognition that the combination of hypoxia (oxygen saturation < 90%) and hypotension (systolic blood pressure < 90 mm Hg) is universally associated with unfavourable outcome underlies the importance of immediate action with airway protection, adequate ventilation, and intravenous access and fluid replacement. From the ictus all treatment needs to be directed at minimising further insults.
The implementation of pre-hospital and hospital advanced trauma life support protocols3 has standardised and streamlined the approach to the treatment of head injury. In addition to general management principles of the trauma patient, patients suspected of head injury require an assessment of the Glasgow coma score,4 a neurological examination including pupillary responses, and examination of the head and neck for signs of bruising, lacerations, and open fractures (fig 1). Bruising associated with skull base fractures (Battle’s sign and racoon eyes) often takes several hours to develop. Following initial assessment, repeated neurological observations are required to detect deterioration. Patients in coma (Glasgow coma score < 9) require the urgent placement of a definitive airway (endotracheal tube). Confused or agitated patients may also require controlled sedation, intubation, and ventilation before computed tomographic (CT) scanning. Mannitol (1 g/kg—200 ml 20% for an average adult) is a useful adjunct to the management of the severely head injured patient, both in the acute phase and on the neuro-critical care unit. In the acute phase, mannitol will lower intracranial pressure before the instigation of definitive treatment such as evacuation of a mass lesion.
The introduction of guidelines addressing indications for hospital admission, skull x ray, CT scanning, and neurosurgical referral has assisted in the decision making process.5 The detection of a skull fracture in combination with an impaired level of consciousness greatly increases the risk of intracranial haematoma formation, and a fracture demonstrated on skull x ray is now a definite indication for a CT scan. With increased access to CT scanners, however, there is now a move away from initial screening for fractures with skull x rays towards CT.
Historically, head injured patients have been managed under the care of general and orthopaedic surgeons, with the most severely injured—often only those with mass lesions requiring evacuation—being transferred to neurosurgical units. There is now recognition that all patients with moderate and severe head injury should be managed in neuroscience units.6 Those with minor injuries are best managed on observation wards in the accident and emergency department. Children represent special cases and should be managed jointly with paediatricians.
SECONDARY MANAGEMENT PHASE: NEUROSCIENCES
In addition to guidelines for the initial management of patients with head injury, guidelines have also been formulated for continuing care.7 The implementation of protocol driven therapy in the neuroscience critical care unit (NCCU) at Addenbrooke’s Hospital has been shown to improve outcome following severe head injury.8 The cornerstone of management is ventilation with sedation and paralysis, and invasive monitoring of arterial blood pressure and central venous pressure. In addition to routine monitoring, specific monitors are also employed. These include intracranial pressure transducers, jugular venous oxygen saturation catheters as a guide to oxygen extraction by the brain globally, intraparenchymal brain tissue oxygen sensors to measure regional oxygen concentrations, microdialysis catheters to monitor brain extracellular chemistry (for example, glucose, lactate, pyruvate, and glutamate concentrations), and transcranial Doppler to measure blood flow velocity. Some of these techniques are employed to assist in the management of individual patients, while others are research techniques which may translate into clinical practice in the future.9
NCCU treatment is directed at reducing the incidence of secondary insults. There is a relation between such events and outcome. Secondary events can be classified as respiratory (hypoxia, hypercapnia), haemodynamic (systemic hypotension, intracranial hypertension), space occupying lesions, seizures, and infection.
1. Respiratory events
Patients with severe head injury require intubation and ventilation to provide airway protection, maintenance of adequate arterial oxygen pressure, and avoidance of hyper- or hypocapnia. In the NCCU at Addenbrooke’s Hospital, propofol (switching to midazolam after two days) and fentanyl is used for sedation with atracurium induced muscle paralysis. The practice of aggressive hyperventilation to induce vasoconstriction, reduction in blood volume, and therefore reduction in intracranial pressure has been abandoned because of the vasoconstriction provoking ischaemia with inadequate oxygen supply to satisfy the demands of the injured brain. Positron emission tomography studies have shown that reducing the arterial carbon dioxide pressure to below 4.0 kPa significantly increases the volume of the ischaemic brain. In the NCCU we aim for a target arterial carbon dioxide of 4.0–4.5 kPa. Patients needing prolonged ventilation (longer than 10 days) for the management of intracranial hypertension or for respiratory complications require a tracheostomy.
2. Haemodynamic events
The monitoring and treatment of raised ICP is paramount for maintaining blood supply and oxygen delivery. Targets for CPP (70 mm Hg) and ICP (25 mm Hg) have been defined. In order to maintain the CPP, patients are kept well hydrated (central venous pressure 10 cm H20) and if necessary inotropes—for example, dopamine or noradrenaline—are applied with monitoring of pulmonary artery wedge pressure and cardiac output using Swan Ganz catheters. Protocols, comprising a number of stages, have been defined to manage patients with increased ICP and reduced CPP (table 1).8 Such stages include:
stage I—10–15° head up, maintaining arterial oxygen saturation (Sao2) > 97%, maintaining arterial oxygen pressure (Pao2) > 11 kPa, maintaining arterial carbon dioxide pressure (Paco2) at 4.5 kPa, maintaining jugular venous oxygen saturation (Sjvo2) > 55%, maintaining temperature < 37°C
stage II—commencing mannitol, inotropes, reducing Paco2 to 4.0 kPa, maintaining Sjvo2 > 55%, temperature 35–36°C
stage III—temperature 33°C
stage IV—application of thiopentone.
The use of hypothermia is controversial. Preliminary studies indicated a beneficial role, but the results of a multicentre trial indicated poorer outcome in patients treated with hypothermia.
In addition two surgical manoeuvres are employed to reduce ICP (table 1). These are the application of external ventricular drains to drain cerebrospinal fluid, and decompressive craniectomy (removal of a large area of skull with opening of the dura to increase the volume of the cranial cavity) (fig 2). External ventricular drains, which can be inserted using twist drills on the NCCU, can both monitor ICP and drain cerebrospinal fluid.
The role of decompressive craniectomy to reduce ICP following head injury is unclear. Some studies support the use of the operation, others do not, with the mortality ranging from 13–90%. Within the last 10 years representing the era of modern neuroscience critical care, only five studies involving more than 10 patients have been published, again with contradictory results. In order to clarify the role of this operation, two randomised controlled trials have been proposed: a US study randomising patients to either standardised craniectomy with duraplasty (bone off) or “traditional” craniotomy (bone on); and a European trial, to be conducted under the auspices of the European Brain Injury Consortium (EBIC), randomising patients to best medical treatment versus decompressive craniectomy.
3. Space occupying lesions
Space occupying lesions can be classified into extradural haematomas, subdural haematomas, and intracerebral haematomas/contusions (fig 3). The decision to evacuate mass lesions depends on the clinical condition of the patient, monitored parameters, particularly ICP, and the CT findings (size and location of lesion). It is important to recognise that mass lesions may evolve subsequent to an early CT and there should be a low threshold for repeat CT scanning. Following evacuation of a haematoma, in the presence of brain swelling or with the potential of brain swelling, consideration should be given to not replacing the bone flap. A cranioplasty (autologous bone, acrylic or titanium plate) can be inserted following recovery at a later date.
Seizures are a common complication following head injury. They result in raised ICP and may induce pupillary changes. Patients with depressed skull fractures are particularly at risk. We advocate the use of short term phenytoin during the acute phase with no role for prolonged prophylactic therapy.
Patients with head injury are prone to an increased risk of infection. The role of antibiotics has been defined with their application reserved for the presence of infection. Aspiration pneumonia and methicillin resistant Staphylococcus aureus infection are common complications in this group of patients. A base of skull fracture is no longer an indication for routine antibiotics.
Depressed skull fractures are associated with both infection and seizures. The indications for exploring depressed fractures are: if the fracture involves a skull sinus; if there is an overlying scalp laceration; and if a tear in the dura is suspected. A depressed fracture of the calvarium less than the thickness of the skull does not require elevation.
Defining the mechanisms underlying the pathophysiology of head injury raised high hopes for the application of drugs—for example, glutamate antagonists as neuroprotectants. Successful studies of neuroprotective drugs in the laboratory have not translated into benefit in man, with the possible exception of the use of nimodipine in traumatic subarachnoid haemorrhage. The reasons for these failures are thought to be multifactorial.10
Further trials are currently in progress, including the CRASH trial (re-examining the potential role of steroids in head injury), the dexarabinol trial (a combined glutamate antagonist and free radical scavenger in severe head injury), and a trial assessing the efficacy of magnesium as a calcium antagonist.
There are numerous delayed complications of head injury (table 2) which may present to the neurologist and can be divided into vascular, infective, epileptic, cranial nerve palsies, and psychological. Carotid–cavernous sinus fistulae and cranial nerve palsies warrant special mention. Carotid–cavernous sinus fistulae present with retro-orbital pain, chemosis, pulsatile proptosis, bruit, and deterioration in visual acuity. They are usually treated with endovascular embolisation. Cranial nerve palsies may be transient or permanent and are usually caused by fractures involving the skull base. The olfactory nerves, trigeminal nerves (facial pain), facial nerve (risk of corneal ulceration), and vestibulocochlear nerves (vertigo and deafness) are particularly at risk.
TERTIARY PHASE: REHABILITATION
Rehabilitation has been hampered by the practice of transferring patients back from neuroscience units to general wards in district hospitals. The importance of expert continuing care with dedicated multidisciplinary neurorehabilitation units is paramount to maximising recovery following head injury. Minor head injured patients are often neglected in this process, but there is now increasing recognition of the role of neuropsychologists. Late CT scans to detect hydrocephalus or chronic subdural haematomas should also be considered. In addition to the support for both patients and their families from within the hospital environment, charitable organisations such as Headway play a major role in integrating people back into the community.
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