Head injury



Head injury


In the UK, trauma is the leading cause of death in people under the age of 45, with head injury making a substantial contribution in more than 50% of cases. Approximately half of patients admitted to hospital with a serious head injury are under the age of 20, two-thirds are male and alcohol is frequently a contributing factor. Some head injuries are due to assaults, but the vast majority are accidental. Road traffic incidents are an important cause of more serious head injuries, accounting for 60% of fatal traumatic brain injury cases. Survivors are likely to be left with long-term physical and intellectual impairments and may require a prolonged period of neurological rehabilitation.



Clinical aspects


A distinction is made between primary and secondary brain damage. The term primary brain injury refers to direct (impact-related) damage which cannot be reversed. The main aim of medical treatment is to prevent or minimize secondary brain injury which is often due to hypoxia, ischaemia or infection. These complications develop in the hours or days after the initial injury and are usually associated with brain swelling and raised intracranial pressure.



Assessment and management


The best indicator of head injury severity is impairment of consciousness. This either reflects brain stem dysfunction or diffuse hemispheric damage. Level of consciousness is assessed using the Glasgow Coma Scale (GCS) which quantifies responses to verbal and painful stimuli in terms of eye opening, speech and movement (Fig. 9.1). The aggregate score ranges from a maximum of 15 (alert and orientated) to a minimum of 3 (comatose or dead).


image
Fig. 9.1 The Glasgow Coma Scale.
(A) Response to verbal and painful stimuli is assessed in terms of eye opening, verbal response and motor response. The minimum score is 3 (even in death) and the maximum score is 15 (alert and orientated); (B) Abnormal flexion to pain (an ‘M’ score of 3 out of 5) is also known as decorticate posturing, whereas abnormal extension to pain (an ‘M’ score of 2 out of 5) is called decerebrate posturing. From Teasdale, G and Jennett, B: LANCET (ii) 81-83: (1974) with permission.

A GCS score of 13–15 corresponds to mild head injury, accounting for the majority of cases. A total score of 9–12 represents moderate head injury, whilst a score of 3–8 signifies severe head injury. In addition to providing an initial assessment of severity, any reduction in the GCS score is a sensitive indicator that the clinical state has deteriorated. This may signify development of a secondary complication requiring urgent intervention. The role of imaging in the assessment of head injury is discussed in Clinical Box 9.1.



image Clinical Box 9.1:   Neuroimaging in head injury


Brain imaging is important in the assessment of moderate and severe head injury. The investigation of choice is computed tomography (CT), which is able to demonstrate lesions of the scalp, skull and brain. This can be supplemented by plain radiographs of the spine in cases with possible vertebral trauma. In severe head injury (GCS <9), significant focal lesions such as cerebral haemorrhages and contusions are identified in more than 50% of cases. The remainder often show small haemorrhages scattered throughout the white matter and at grey-white matter junctions. This is suggestive of diffuse axonal injury and is associated with increased morbidity and mortality.


The initial management of head injury is the same as for any other major trauma and begins with the ‘ABC’ of basic life support (airway, breathing, circulation). Attention is then directed to any potentially life-threatening pathologies in the chest, abdomen or pelvis. Once the patient has been stabilized they can be assessed for head and spinal injuries and any appropriate medical or surgical treatments initiated.



Outcome following head injury


The long-term outcome after moderate or severe head injury depends on the extent and severity of the damage, including any co-existing injuries. It also varies with the age and general health of the patient. Although the mortality rate is declining, around a third of patients with severe head trauma will ultimately die as a result of their injuries. Another third will eventually recover sufficiently to return to work, whilst the remainder will be left with at least moderate mental or physical disability.


A small proportion of people (less than 3%) enter a persistent vegetative state, in which there is partial arousal or apparent wakefulness without full conscious awareness; this is considered permanent if it lasts more than 12 months.


Factors that predict a less favourable outcome include increasing age (>60 years), an initial GCS score below 5, a fixed and dilated pupil, a prolonged period of hypotension/hypoxia or a haemorrhage requiring surgical decompression. Late complications may include hydrocephalus due to obstruction of CSF drainage pathways (see Ch. 2, Clinical Box 2.2) or seizures (Clinical Box 9.2).



image Clinical Box 9.2:   Post-traumatic epilepsy


Seizures occur in approximately 2–3% of patients with traumatic head injury (10–15% of those with severe injuries). Post-traumatic epilepsy is described as ‘early’ if it occurs within the first week or ‘late’ when the onset is beyond this point. Seizure risk is higher with penetrating trauma, depressed skull fractures and in the presence of an intracerebral haemorrhage. The focus may be an area of gliosis (glial ‘scarring’ ; see Ch. 8) resulting from a focal brain lesion. Individuals experiencing early post-traumatic seizures are at most risk of longer-term recurrent seizures.



Key Points





Pathology of head injury


Most traumatic brain damage is caused by blunt-force trauma. This usually results in a closed head injury. Penetrating (or missile) trauma such as stab wounds and gunshot injuries are less common and carry the additional risk of infection (e.g. meningitis or brain abscess).


Contact (or impact-related) damage occurs when the head collides with a hard surface or object. The energy from the impact is rapidly dissipated, causing direct mechanical injury such as cerebral contusion (bruising) and laceration (tearing; from the Latin lacerāre, to tear).


In addition, acceleration–deceleration (inertial) injury occurs when the head is suddenly set in motion – or is moving at high velocity and comes to an abrupt halt. The brain slides forwards or backwards within the cranial cavity and strikes the inside of the skull, which is most likely to damage the frontal, temporal or occipital poles. Complex rotational (‘swirling’) movements are also generated within the brain, which has a very soft, gelatinous consistency. This leads to widespread compressive, tensile and shearing forces, causing diffuse damage to axons and blood vessels.


Three main patterns of traumatic brain damage are found at post-mortem examination in people who died as a result of serious head injuries (due to a mixture of contact-related and acceleration–deceleration injury): cerebral contusions, intracranial haemorrhages and diffuse axonal injury.



Cerebral contusions


Cerebral contusions (bruising) and lacerations (tears) are common in traumatic brain injury, occurring in more than 90% of fatal cases. Contusions are most pronounced at the crests of gyri in the frontal and temporal lobes, particularly in places where the brain comes into contact with the irregular contours of the skull base (Fig. 9.2). Cerebral contusions may be associated with haemorrhage into the overlying subarachnoid or subdural spaces and if blood continues to accumulate it will begin to act as an intracranial mass lesion. The combination of a cerebral contusion with an overlying subdural haemorrhage is called a burst lobe. This most often occurs at the frontal and temporal poles.


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Fig. 9.2 Post-mortem photograph in a case of severe head injury showing widespread cerebral contusions.
They are particularly marked in the orbital cortex and frontal/temporal polar regions. From Prayson, R: Neuropathology 1e (Churchill Livingstone 2005) with permission.


Coup and contrecoup lesions (Fig. 9.3)


Contusions that occur at the point of impact are referred to as coup lesions (from the French, meaning shock or blow). These result from direct mechanical trauma, often from small, hard objects. Contusions may also be present on the opposite side of the brain, well away from the point of impact. These are contrecoup lesions which may be more severe and extensive than those at the impact site. This phenomenon is particularly common at the frontal and temporal poles in association with a blow to the back of the head. The mechanism is not fully understood. It is sometimes said that the contrecoup lesion is due to ‘rebound’ of the brain against the opposite side of the skull, but this does not explain why it is often more severe (as the kinetic energy of the second impact would be less). Experiments suggest that it may be due to a pocket of negative pressure (a ‘vacuum’) caused by rapid separation of the brain from the overlying skull.


image
Fig. 9.3 Coup and contrecoup lesions. The direct (coup) lesion is impact-related. The contrecoup lesion, which is often more severe, is probably due to extreme pressure changes which may damage thin-walled blood vessels as the brain is violently wrenched away from the overlying skull.


Key Points





Intracranial haemorrhage


Bleeding may occur at the moment of impact or as a secondary complication, leading to formation of a haematoma (blood clot) which acts as a mass lesion. If the haematoma becomes sufficiently large it may compress the underlying brain or cause a life-threatening rise in intracranial pressure. The three main types of intracranial haemorrhage are: extradural, subdural and intracerebral.

Related posts:

Sensory and motor pathways Epilepsy Sinonasal Olfactory Disorders Functional Anatomy of the Olfactory System I: From the Nasal Cavity to the Olfactory Bulb 1 Encephalopathy and Delirium 6 Cerebral Edema and Elevated Intracranial Pressure

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Jun 19, 2016 | Posted by in NEUROLOGY | Comments Off on Head injury

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