Neurotrauma - Clinical Tree

Essentials

1
Neurotrauma is the most common cause of death in trauma.
2
A detailed history of the mechanics of the trauma experienced is invaluable.
3
Secondary brain injury is a major and potentially preventable cause of mortality and long-term morbidity.
4
Cerebral cellular dysfunction secondary to trauma is a result of both primary and secondary mechanisms and involves sodium, calcium and potassium shifts across the cell membrane; the development of oxygen free radicals; and lipid peroxidation.
5
There are two features of prime importance to resuscitation in patients suffering neurotrauma: maintenance of airway/ventilation and maintenance of cerebral perfusion pressure.
6
Rapid sequence orotracheal intubation, with in-line immobilization of the cervical spine is the preferred method for gaining definitive airway control in the head-injured patient.
7
Current adult emergency department and neurosurgical practice involves the use of computed tomography (CT) to investigate head injury.

Acknowledgements

The chapter’s authors for this edition would like to acknowledge the important contribution of authors for previous editions, including Professor Lee Wallis and Dr. Marcus Kennedy.

Introduction

Neurotrauma is a common feature in the presentation of multisystem trauma, particularly when it is associated with motor vehicle accidents and falls. Head injuries contribute to between 30% and 50% of all trauma deaths. The implications for the health system are enormous, with an annual rate of admission to hospital wards associated with head trauma approaching 300 per 100,000 population and twice this in the elderly. The long-term sequelae of moderate and severe neurotrauma constitute a major drain on health resources, and the morbidities associated with mild brain injury are becoming clearer.

Advances in preventative strategies, trauma systems, resuscitative therapies and rehabilitation management have improved outcomes. However, neurotrauma remains a serious health issue, with a huge impact from long-term disability on the quality of life and the productivity of society’s youth.

Pathogenesis

Primary brain injury occurs as a result of the forces and disruptive mechanics of the original incident: this can be avoided only through preventative measures such as the use of bicycle and motorcycle helmets.

Secondary brain injury is due to the complex interaction of factors and typically occurs within 2 to 24 hours of injury. A principal mechanism of secondary injury is cerebral hypoxia due to impaired oxygenation or impaired cerebral blood flow. Cerebral blood flow is dependent on cerebral perfusion pressure (CPP), mean arterial systemic blood pressure (MAP) and intracranial pressure (ICP).

CPP = MAP - ICP

$CPP = MAP - ICP$

ICP may be raised as a result of the mass effect of the haemorrhage or by generalized cerebral oedema. Cerebral vasospasm further reduces cerebral blood flow in patients in whom significant subarachnoid haemorrhage has occurred.

Cellular dysfunction is a result of both primary and secondary mechanisms and involves sodium, calcium, magnesium and potassium shifts across the cell membrane; the development of oxygen free radicals; lipid peroxidation; and glutamate hyperactivity. Excessive release of excitatory neurotransmitters and magnesium depletion also occur.

Classification of primary injury in neurotrauma

Primary injuries are classified as follows:

Skull fracture
Concussion
Contusion
Intracranial haematoma
Diffuse axonal injury
Penetrating injury

Skull fracture

The significance of skull fracture is not related to the specific bony injury but rather the associated neurotrauma. Fractures in the region of the middle meningeal artery in particular may be associated with acute extradural haemorrhage. Fractures involving the skull base and cribriform plate may be associated with cerebrospinal fluid (CSF) leak and the risk of secondary infection. Depressed skull fractures may compress underlying structures, cause secondary brain injury and require surgical elevation. Injury to underlying structures may result in secondary epilepsy.

Concussion

Concussion is a transient alteration in cerebral function, usually associated with loss of consciousness (LOC) and often followed by a rapid recovery. The proposed mechanism is a disturbance in the function of the reticular activating system. Post-concussive syndromes, including headache and mild cognitive disturbance, are common. Symptoms, particularly headache, are usually short-lived but may persist. ‘Second-impact syndrome’ describes a greater risk of significant re-injury following an initial injury causing a simple concussion. It is likely to be due to diffuse cerebral swelling. In animal models, concussion may be associated with modest short-term increases in ICP and disturbances in cerebral cellular function.

Contusion

Cerebral contusion is bruising of the brain substance associated with head trauma. Forces involved are less than those required to cause major shearing injuries and often occur in the absence of skull fracture. Morbidity is related to the size and site of the contusion and coexistent injury. Larger contusions may be associated with haematoma formation, secondary oedema or seizure activity. The most common sites for contusions are the frontal and temporal lobes.

Intracranial haematoma

Extradural

Extradural haematoma (EDH) is uncommon but classically associated with a fracture of the temporal bone and injury to the underlying middle meningeal artery. Haemorrhage subsequently occurs, stripping the dura from the skull and expanding to cause a rise in ICP and eventually uncal herniation and death. Haemorrhage may be from vessels other than the middle meningeal artery (e.g. brisk arteriolar or venous bleeding). Signs will depend on the site of the haematoma.

Subdural

Subdural haematomata (SDH) may have an acute, subacute or chronic course. They generally follow moderate head trauma with LOC. In the elderly, SDH may be associated with trivial injury and in children with shaking (abuse) injury. Haemorrhage occurs into the subdural space, slowly enlarging to cause a space-occupying collection whose functional implications will vary according to location. The mortality from acute SDH is high (approximately 30%) but this represents a decrease over recent decades. Subacute and chronic SDH may be associated with a degree of cerebral dysfunction, headache or other symptomatology and with a significantly lower mortality compared with acute SDH.

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