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Wednesday, 26 January 2011 00:49

Traumatic Head Injuries

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Aetiological Factors

Head trauma consists of skull injury, focal brain injury and diffuse brain tissue injury (Gennarelli and Kotapa 1992). In work-related head trauma falls account for the majority of the causes (Kraus and Fife 1985). Other job-related causes include being struck by equipment, machinery or related items, and by on-road motor vehicles. The rates of work-related brain injury are markedly higher among young workers than older ones (Kraus and Fife 1985).

Occupations at Risk

Workers involved in mining, construction, driving motor vehicles and agriculture are at higher risk. Head trauma is common in sportsmen such as boxers and soccer players.

Neuropathophysiology

Skull fracture can occur with or without damage to the brain. All forms of brain injury, whether resulting from penetrating or closed head trauma, can lead to the development of swelling of the cerebral tissue. Vasogenic and cytogenic pathophysiologic processes active at the cellular level result in cerebral oedema, increased intracranial pressure and cerebral ischaemia.

Focal brain injuries (epidural, subdural or intracranial haematomas) may cause not only local brain damage, but a mass effect within the cranium, leading to midline shift, herniation and ultimately brain stem (mid-brain, pons and medulla oblongata) compression, causing, first a declining level of consciousness, then respiratory arrest and death (Gennarelli and Kotapa 1992).

Diffuse brain injuries represent shearing trauma to innumerable axons of the brain, and may be manifested as anything from subtle cognitive dysfunction to severe disability.

Epidemiological Data

There are few reliable statistics on the incidence of head injury from work-related activities.

In the United States, estimates of the incidence of head injury indicate that at least 2 million people incur such injuries each year, with nearly 500,000 resultant hospital admissions (Gennarelli and Kotapa 1992). Approximately half of these patients were involved in motor accidents.

A study of brain injury in residents of San Diego County, California in 1981 showed that the overall work-related injury rate for males was 19.8 per 100,000 workers (45.9 per 100 million work hours). The incidence rates of work-related brain injuries for male civilian and military personnel were 15.2 and 37.0 per 100,000 workers, respectively. In addition, the annual incidence of such injuries was 9.9 per 100 million work hours for males in the work force (18.5 per 100 million hours for military personnel and 7.6 per 100 million hours for civilians) (Kraus and Fife 1985). In the same study, about 54% of the civilian work-related brain injuries resulted from falls, and 8% involved on-road motor vehicle accidents (Kraus and Fife 1985).

Signs and Symptoms

The signs and symptoms vary among different forms of head trauma (table 1) (Gennarelli and Kotapa 1992) and different locations of traumatic brain lesion (Gennarelli and Kotapa 1992; Gorden 1991). On some occasions, multiple forms of head trauma may occur in the same patient.

Table 1. Classification of traumatic head injuries.

Skull injuries

                      Brain tissue injuries


Focal

Diffuse

Vault fracture

Haematoma

Concussion

Linear

Epidural

Mild

Depressed

Subdural
Intracranial

Classical

Basilar fracture

Contusion

Prolonged coma

(diffuse axonal injury)

 

Skull injuries

Fractures of cerebral vault, either linear or depressed, can be detected by radiological examinations, in which the location and depth of the fracture are clinically most important.

Fractures of the skull base, in which the fractures are usually not visible on conventional skull radiographs, can best be found by computed tomography (CT scan). It can also be diagnosed by clinical findings such as the leakage of cerebropinal fluid from the nose (CSF rhinorrhea) or ear (CSF otorrhea), or subcutaneous bleeding at the periorbital or mastoid areas, though these may take 24 hours to appear.

Focal brain tissue injuries (Gennarelli and Kotapa 1992;Gorden 1991)

Haematoma:

Epidural haematoma is usually due to arterial bleeding and may be associated with a skull fracture. The bleeding is seen distinctly as a biconvex density on the CT scan. It is characterized clinically by transient loss of consciousness immediately after injury, followed by a lucid period. Consciousness may deteriorate rapidly due to increasing intracranial pressure.

Subdural haematoma is the result of venous bleeding beneath the dura. Subdural haemorrhage may be classified as acute, subacute or chronic, based on the time course of the development of symptoms. Symptoms result from direct pressure to the cortex under the bleed. The CT scan of the head often shows a crescent-shaped deficit.

Intracerebral haematoma results from bleeding within the parenchyma of the cerebral hemispheres. It may occur at the time of trauma or may appear a few days later (Cooper 1992). Symptoms are usually dramatic and include an acutely depressed level of consciousness and signs of increased intracranial pressure, such as headache, vomiting, convulsions and coma. Subarachnoid haemorrhage may occur spontaneously as the result of a ruptured berry aneurysm, or it may be caused by head trauma.

In patients with any form of haematoma, deterioration of consciousness, ipsilateral dilated pupil and contralateral haemiparesis suggests an expanding haematoma and the need for immediate neurosurgical evaluation. Brain stem compression accounts for approximately 66% of deaths from head injuries (Gennarelli and Kotapa 1992).

Cerebral contusion:

This presents as temporary loss of consciousness or neurologic deficits. Memory loss may be retrograde—loss of memory a time period before the injury, or antegrade—loss of current memory. CT scans shows multiple small isolated haemorrhages in the cerebral cortex. Patients are at higher risk of subsequent intracranial bleeding.

Diffuse brain tissue injuries (Gennarelli and Kotapa 1992;Gorden 1991)

Concussion:

Mild concussion is defined as a rapidly resolving (less than 24 hours) interruption of function (such as memory), secondary to trauma. This includes symptoms as subtle as memory loss and as obvious as unconsciousness.

Classic cerebral concussion manifests as slowly resolving, temporary, reversible neurologic dysfunction such as memory loss, often accompanied by a significant loss of consciousness (more than 5 minutes, less than 6 hours). The CT scan is normal.

Diffuse axonal injury: 

This results in a prolonged comatose state (more than 6 hours). In the milder form, the coma is of 6 to 24 hours duration, and may be associated with long-standing or permanent neurologic or cognitive deficits. A coma of moderate form lasts for more than 24 hours and is associated with a mortality of 20%. The severe form shows brain stem dysfunction with the coma lasting for more than 24 hours or even months, because of the involvement of the reticular activating system.

Diagnosis and Differential Diagnosis

Apart from the history and serial neurologic examinations and a standard  assessment  tool  such  as  the  Glasgow  Coma  Scale (table 2), the radiological examinations are helpful in making a definitive diagnosis. A CT scan of the head is the most important diagnostic test to be performed in patients with neurologic findings after head trauma (Gennarelli and Kotapa 1992; Gorden 1991; Johnson and Lee 1992), and allows rapid and accurate assessment of surgical and nonsurgical lesions in the critically injured patients (Johnson and Lee 1992). Magnetic resonance (MR) imaging is complementary to the evaluation of cerebral head trauma. Many lesions are identified by MR imaging such as cortical contusions, small subdural haematomas and diffuse axonal injuries that may not be seen on CT examinations (Sklar et al. 1992).

Table 2. Glasgow Coma Scale.

Eyes

Verbal

Motor

Does not open eyes

Opens eyes to painful
stimuli

Opens eyes upon
loud verbal command

Opens eyes
spontaneously

Makes no noise

Moans, makes unintelligible
noises

Talks but nonsensical


Seems confused and
disoriented

Alert and oriented

(1) No motor response to pain

(2) Extensor response (decerebrate)


(3) Flexor response (decorticate)


(4) Moves parts of body but does not
remove noxious stimuli

(5) Moves away from noxious stimuli

(6) Follows simple motor commands

 

Treatment and Prognosis

Patients with head trauma need to be referred to an emergency department, and a neurosurgical consultation is important. All patients known to be unconscious for more than 10 to 15 minutes, or with a skull fracture or a neurologic abnormality, require hospital admission and observation, because the possibility exists of delayed deterioration from expanding mass lesions (Gennarelli and Kotapa 1992).

Depending on the type and severity of head trauma, provision of supplemental oxygen, adequate ventilation, decrease of brain water by intravenous administration of faster-acting hyperosmolar agents (e.g., mannitol), corticosteroids or diuretics, and surgical decompression may be necessary. Appropriate rehabilitation is advisable at a later stage.

A multicentre study revealed that 26% of patients with severe head injury had good recovery, 16% were moderately disabled, and 17% were either severely disabled or vegetative (Gennarelli and Kotapa 1992). A follow-up study also found persistent headache in 79% of the milder cases of head injury, and memory difficulties in 59% (Gennarelli and Kotapa 1992).

Prevention

Safety and health education programmes for the prevention of work-related accidents should be instituted at the enterprise level for workers and management. Preventive measures should be applied to mitigate the occurrence and severity of head injuries due to work-related causes such as falls and transport accidents.

 

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First Aid and Emergency Medical Services References

Cooper, PR. 1992. Delayed traumatic intracerebral haemorrhage. Neurosurg Clin N Am 3(3): 659-665.

Gennarelli, TA and MJ Kotapa. 1992. Trauma to the head—general considerations. In Principles and Practice of Emergency Medicine, 3rd edition, Vol. 1., edited by GR Schwartz, CG Cayten, MA Mangelsen, TA Mayer and BK Hanke. Philadelphia/London: Lea and Febiger.

Gorden, K. 1991. Head and neck trauma. In Emergency Medicine. An Approach to Clinical Problem-solving, edited by GC Hamilton, AB Sanders, GR Strange and AT Trott. Philadelphia: WB Saunders Company.

Jennett, B. 1992. Head trauma. In Diseases of the Nervous System—Clinical Neurobiology, 2nd edition, Vol. 2, edited by AK Asbury, GM Mckhann and WI McDonald. Philadelphia: WB Saunders Company.

Johnson, MH and SH Lee. 1992. Computed tomography of acute cerebral trauma. Radiol Clin N Am 30(2): 325-352.

Kraus, JF and D Fife. 1985. Incidence, external causes, and outcomes of work-related brain injuries in males. J Occup Med 27(10):757-760.

Sklar, EM, RM Quencer, BC Bowen, N Altman, PA Villanueva. 1992. Magnetic resonance applications in cerebral injury. Radiol Clin N Am. 30(2): 353-366.