Head Injuries And Sport

Chapte r5   - Injuries  ­ Head  

 

 

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Introduction

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Mechanisms of brain injury 

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Forces producing brain injury 

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Pathophysiology of primary brain injury 

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Pathophysiology of secondary brain injury 

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Intracranial complications 

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Extracranial complications

Non­traumatic sports related brain injury  ○

Cerebral air embolism 

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High altitude cerebral oedema

Clinical features of brain injury  ○

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Concussion

On site assessment and management of head injury  ○

Assessment and management of the unconscious athlete 

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Assessment and management of the head injured conscious athlete

Gradings of concussion and return to competition 

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Post concussion monitoring if not hospitalised 

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On going management of mild head injury 

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Clinical assessment of recovery 

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Post concussion symptoms 

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Cumulative effects of concussion 

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Chronic traumatic encephalopathy 

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Psychometric indices of impairment and recovery

Prevention of sporting head injuries  ○

Devices reducing the severity of the initial injury 

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Mouthguards 

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Helmets

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Selection and conditioning of individual athletes 

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Rules regulating play and individual participation 

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Education of athletes and officials ­ structured interview

Introduction Head injury is one of the most common forms of acquired neurological damage, particularly in young males. Head injuries are especially prevalent in contact sports that produce collisions, in sports where participants move or fall at high velocity and in sports that involve the use of force imparting implements (1). The incidence is highest in combat sports, such as boxing, where the head is a legitimate target. However, head injury is also common in contact sports such as the various codes of football, especially gridiron, where the annual incidence may be as high as 10 20% of participants, and rugby, which has up to twice the risk of other (non gridiron) football codes (2, 3). Other non-contact sports with a higher risk of head injury include motor racing, equestrian and gymnastic events, snow, board and blade sports, and cycling. Sports where head injury is rare but potentially severe include golf, shooting, cricket, baseball, and field hockey. The focus in this chapter is on brain injury. However, head injuries often involve significant damage to scalp, skull, meninges and blood vessels as well as the face, jaws, eyes, ears and neck. While the initial assessment and management of head injury described in this chapter includes injuries to these other tissues and sites, the subsequent management of extra-cranial head injuries is dealt with in Chapters 6 and 7. The most common form of head injury in sport is an episode of concussion (Latin: concutere, to shake violently), from which a full recovery is usual. However, any head injury can have immediate or delayed life threatening consequences and serious long-term sequelae. As such, all head injuries require thorough systematic assessment by the sports physician (a) to recognise and manage the acute consequences, including the prevention of secondary brain damage (b) to arrange the safe transfer of the injured athlete to an appropriate treatment facility when necessary or (c) to ensure that the athlete is closely monitored for at least 24 hours and returns to participation only when fully recovered. Finally, (d) prevention also needs to be addressed by the sports physician. •

This chapter has five main sections:

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Mechanisms of brain injury, which provides a summary of the anatomical, physiological, and pathological issues that influence management and prevention.

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Clinical features of brain injury, including symptoms and signs of concussion.

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On site assessment and management of head injuries.

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Post acute assessment and management of concussion, which includes clinical and

 

psychometric assessment of recovery and guidelines for the return to participation in sport. •

Prevention measures including athlete preparation, protective devices and rule modifications.

Mechanisms of brain injury Head injuries in sport usually result from direct impact of the head but can occur when the head is subjected to forces translated from elsewhere on the body. Brain injury may be primary, due to the direct application of physical forces damaging brain and associated vascular tissue, or secondary, arising from intracranial and extracranial complications of injuries to the head and other parts of the body (4, 5, 6). Forces producing brain injury

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Forces acting on the brain produce three types of tissue stress: compressive, tensile, and shearing. Compressor forces tend to produce focal contusions and if relieved promptly produce the least long-term consequences. Tensile (stretching) forces act mainly on long fibre pathways and damage tends to be more diffuse (diffuse axonal injury). Shearing forces operate parallel to surfaces and can produce serious consequences by tearing brain and vascular tissue.

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Most forces are dynamic and result in propulsion and rotation of the brain within the cranium following impacts to either the head or body. Cerebro spinal fluid (CSF) dissipates focally applied forces and permits gliding of the hemispheres within the cranium.

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A forceful blow to the head usually produces maximal brain injury at the site of impact (coup injury) particularly if the head is stationary before impact. A moving head striking a non-moveable surface, as in falls or collisions, may also produce brain injury at the opposite pole of the cranium (contra coup injury). This is because the brain lags behind in the moving cranium, thereby squeezing protective CSF away from the trailing pole (Fig 1).

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The magnitude of any force is the product of mass and acceleration (Newton’s Law). If the neck muscles are tensed at impact, the mass of the head approximates that of the whole body and acceleration (or deceleration) of the head is greatly reduced for any given force. Conversely, when the head is not braced, as in unanticipated blows or further blows in an already stunned state, a given force produces much greater acceleration of the head.

Pathophysiology of primary brain injury

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Gliding of the brain within the cranium is impeded at three main sites (a) dura mater -

brain attachments e.g. midline falx cerebri and tentorium cerebelli (b) irregular and protuberant surfaces of the frontal and middle fossa of the base of the skull (c) wherever CSF is dissipated by acceleration, especially at the poles of the frontal and temporal lobes.

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Focal contusions occur mainly at or opposite sites of impact and comprise local petechial haemorrhages and necrotic damage, which are often accompanied by surrounding oedema and subarachnoid haemorrhage.

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Propulsion and rotation of the hemispheres on the relatively fixed brainstem may cause damage to ascending brain stem pathways, ranging from stretching with transient impairment of consciousness to tearing of subcortical fibre tracts with immediate unconsciousness and coma.

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General cerebral oedema due to a combination of local metabolic derangement, breakdown of the blood-brain barrier and obstructions to venous outflow, leads to a rise in intracranial pressure (see below).

Pathophysiology of secondary brain injury Head injuries may result in complications that are life threatening and can have serious longterm consequences. Because they are often remediable in their early stages, they require immediate attention. Intracranial complications Intracranial complications include skull fracture, intracranial haemorrhage, raised intracranial pressure, cerebral hypoxia, and infection.

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Skull fractures may result in direct brain compression, intracranial bleeding, CSF leaks and infection. Brain injury may occur without a skull fracture; however the presence of a skull fracture greatly increases the risk of intracranial bleeding and infection. The site of a fracture is also critical in anticipating complications e.g., temporo-parietal damage to meningeal vessels, frontal damage to sinuses. Fractures may be either of the vault or the base of the skull.

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Vault fractures, which may be linear or depressed, are usually associated with scalp haematomas or a localised area of swelling and tenderness.

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Basal fractures are harder to detect and usually involve intracranial bleeding. Periorbital haematomas, subconjunctival haemorrhage and CSF rhinorrhoea are signs of an anterior fossa fracture; CSF otorrhoea, haemotympanum and retromastoid bruising (Battle’s sign) are signs of a petrous bone fracture.

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Close observation and radiological investigation are required for all suspected skull fractures. Opinions differ on the value of routine CT scan for all mild head injuries. Early CT scan and early discharge of patients with normal radiological and neurological

findings has been advocated as being as safe and more cost effective than hospitalization for observation with CT scan performed only after clinical deterioration (7).

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Intracranial haemorrhage may result in local compression, raised intracranial pressure, and ischaemia to the area of supply of the damaged vessel. All intracranial haematomas constitute a priority in the management of head injury because of their immediate threat to life and eventual recovery of function and because they may be surgically remediable. Haematomas may develop immediately or some time after the initial injury preceded by a lucid interval. Delay in recognising and treating intracranial bleeding is the most common cause of avoidable mortality and morbidity due to head injury. Vigilance needs to be maintained for at least 24 hours. The four types of intracranial haemorrhage are:

(a)

Extradural haematomas result from shearing forces or skull fractures that tear blood

vessels supplying the dura and skull. Haematomas may form rapidly (high pressure bleeding between dura and skull) and compress the brain leading to early loss of consciousness and localising neurological signs or they may occur up to several hours following the initial injury. (b)

Subdural haematomas are the most common form of sports related intracranial bleeding.

Shearing and direct impact forces tear small veins resulting in low pressure bleeding between the brain and dura matter. Signs and symptoms may be subtle and develop insidiously over days or even weeks. (c)

Subarachnoid haemorrhage may result from any head injury, however mild. Severe

headache and localising signs usually develop rapidly. (d)

Intracerebral haemorrhage occurs with major brain injury. Intraventricular haemorrhage

may lead to subsequent blockade of CSF outflow. Brainstem haematomas are life threatening.

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Raised intracranial pressure is a serious consequence of brain injury that may result from several causes including depressed fractures, hypoxia, hypercapnia, hyperperfusion, hypoperfusion, intracranial haemorrhage, and intracranial infection. Raised intracranial pressure leads to cerebral compression, which may be followed by herniation around the brainstem with venous obstruction and infarction. Signs include fluctuations in consciousness, fits and focal neurological deficits.

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Two rare conditions are associated with life threatening rises in intracranial pressure after even minor head injuries (4).

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Malignant brain oedema syndrome occurs in children and adolescents as diffuse brain swelling with extreme hyperaemia. It may be due to loss of autoregulation but the mechanism is unknown. After even relatively minor head injury, there is a deterioration of consciousness resembling, in its rapidity, extradural bleeds in adults. Prompt

intubation and measures to reduce intracranial pressure such as hyperventilation and osmotic diuretics are required. The mortality rate is high.

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Second impact syndrome is a variant of malignant brain oedema syndrome that is seen in adults following even minor head trauma when still suffering symptoms of a previous head injury. Loss of autoregulation precipitated by an unknown mechanism leads to massive and diffuse hyperaemia and oedema of the brain. Intracranial pressure rises within minutes and may lead to herniation and coma. Prompt measures to maintain respiration and reduce intracranial pressure as above are indicated. The mortality rate approaches 50% and morbidity is near to 100%.

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Hypoxia due to loss of CNS control of airway patency and breathing may occur following either serious primary injury to the brain stem or may be secondary to raised intracranial pressure with brain herniation. Brain hypoxia may also result from extracranial complications (see below).

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Infection (meningitis or brain abscess) may occur when the dura is penetrated. Direct contamination of the intracranial cavity may occur in compound depressed fractures of the vault, whereas contact with middle ear cavity and nasal sinuses may introduce infection in basal fractures.

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Concussive convulsions seen within seconds of insult are to be distinguished from later epileptic seizures. Such concussive convulsions are rare, transient and do not necessarily lead to the development of epilepsy (8).

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Post-traumatic epilepsy may develop within days to months. It usually follows traumatic brain injury with prolonged periods of unconsciousness, and occurs in about 23% of hospital admissions of sports-related head injury (9).

Extracranial complications

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Extracranial complications of head or associated injuries may interfere with brain metabolism and perfusion. Given the immediate dependency of brain tissue on its oxygen supply and the potential for remediation of many of the complications, recognition and management of extracranial causes of secondary brain damage constitutes a clinical priority. Causes include injuries interfering with ventilation, such as chest, neck or facial injuries that obstruct airways and affect chest movement, and injuries interfering with brain circulation by producing haemodynamic instability and hypovolaemia.

Non-traumatic sports related brain injury There are two main causes of non-traumatic sports related brain injury (10). Cerebral air embolism •

unique to underwater diving, second most common cause of death after drowning

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occurs in rapid ascents from > 10 metres

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symptoms may occur within moments to hours of surfacing

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signs include: seizure, hemiplegia, diplopia, tunnel vision, vertigo, or dysarthria

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if diver surfaces unconscious, diagnosis is strong presumption

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seek to recompress subject as soon as possible

High-altitude cerebral oedema

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accounts for up to 5% of deaths above 4000 metres

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symptoms develop within 72 hours and include ataxia, vertigo, confusion, and hallucinations

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immediate treatment is return to lower elevation and oxygenate

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monitor for signs of raised intracranial pressure and treat accordingly

Clinical features of brain injury •

The primary clinical features of brain injury are loss or alteration in consciousness, orientation and responsiveness, followed by a period of post-traumatic amnesia. Other clinical features will depend on the nature and severity of the injury and any supervening complications (4, 5, 6, 11)

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Head injuries may be open or closed. Open head injuries may arise from skull fractures or as a result of a penetrating missile or implement, whereas closed head injuries usually result from blunt impacts or translation of dynamic forces to the head. There are no universally agreed clinical criteria for classifying the severity of closed head injury (12, 13, 14). Gradings into mild, moderate and severe categories based on the duration of loss of consciousness, the period of post traumatic amnesia and the initial Glasgow Coma Scale score are shown in Table 1.

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About 80% of head injuries are defined as mild as they result in post traumatic amnesia of less than 24 hours duration (15). Approximately 2/3 of these mild head injuries occur as the result of a sporting injury (16).

Concussion •

The commonest consequence of a sports head injury in concussion.

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Concussion is a trauma induced transient alteration in mental status that may or may not involve loss of consciousness. Confusion and amnesia are the hallmarks of concussion and may be immediate or delayed by several minutes. Other neurological features may include temporary disturbances of balance and vision (17).

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Depending on severity and recency of the trauma, athletes may display some or all of the clinical features of concussion listed in Table 2 (18).

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Signs and symptoms may occur immediately or take several minutes to evolve. Concussed athletes may be able to continue to play automatically with sensorimotor functions intact.

On site assessment and management of head injury The sports physician may be required to triage and respond on site to four main categories of head injury:

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Injuries requiring resuscitation of the unconscious athlete, stabilisation and transport to an appropriate clinical facility.

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Injuries requiring withdrawal from contest and transport to an appropriate clinical facility.

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Injuries requiring withdrawal from contest and monitoring on site and at home.

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Injuries sufficiently minor to permit resumption but with monitoring.

The following description refers to injuries sustained in a team game and needs to be modified for the circumstances prevailing in individual sports. Assessment and management of the unconscious athlete This is an emergency that supersedes all other event considerations. •

Take charge of the situation and direct others in accordance with their training and the situation.

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Institute resuscitation (DR ABC) procedure (see Table 3). Airway protection and maintenance takes precedence over possible spinal injury.

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If airway is clear, strong rhythmical breathing is present and pulse is normal, then ‘log roll’ into coma position, manually controlling head and neck, and check for other injuries using primary survey protocol (see Tables 4 and 5).

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If the athlete has required resuscitation or has not recovered consciousness or has a GCS <14 within 3 minutes, arrange immediate transport to hospital (see Table 6).

Assessment and management of the head injured conscious athlete The following is based on recent recommendations for best practice on site (17, 18, 20, 21). •

If an athlete has had no loss of consciousness and is free from all symptoms and signs of concussion. They may be deemed to be fit to continue but should be rechecked in 10-15 minutes to determine whether any symptoms have developed, including a gap in memory or somatic complaints and should be monitored closely for the rest of the event.

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If athlete has lost consciousness, however briefly, or has any symptoms or signs of concussion, remove to sideline and conduct a neurological screen (see Table 7) and

mental status examination (see Table 8 and Appendix A). If neurological and mental status examinations are clear and there are no apparent signs or symptoms, conduct physical tests if return to participation is contemplated. Physical provocation tests should include two 20 metre shuttle runs out of play, 10 sit-ups, 10 push-ups, and 10 squats. Then check for complaints and assess capability to perform sport specific tasks.

Gradings of concussion and return to competition

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Gradings of concussion shown in Table 9 (not to be confused with gradings of severity of closed head injury, Table 1) are used to facilitate clinical decisions about mild head injuries, which constitute an overwhelming majority of sports head injuries.

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After a Grade 1 concussion athletes may return to play, providing mental status is normal and they are symptom and sign free, after physical exertion testing.

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If symptoms persist longer than 15 minutes (Grade 2), or if there was a brief loss of consciousness (Grade 3), or if a second Grade 1 concussion has been sustained, return to participation should be prohibited that day.

Post concussion monitoring if not hospitalized •

Athletes with Grade 2 or 3 concussions should have their mental status rechecked every 15 minutes, until they respond to all items appropriately on three consecutive occasions, indicating a continually lucid period of 30 minutes.

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Record duration of post traumatic amnesia, which is defined as the period of time following trauma when the athlete is disoriented, confused, and unable to lay down new memories reliably.

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If there is no further deterioration, and signs and symptoms are resolving, concussed athletes may be allowed to return home in the company of a responsible adult. If supervision is not available referral to hospital is advisable.

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Provide written instructions for monitoring in the next 24 hours (see Table 10).

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Any of the criteria listed in Table 11 are an indication for referral to hospital. Negative changes in mental status (other than minor expansion of retrograde amnesia in the first few hours) or any deterioration in physical condition necessitates immediate transport to a hospital.

On going management of mild head injury This is a contentious area because there are no agreed objective measures of individual recovery from concussion. New guidelines for return to competitive sport (Table 12) that have been designed to assist the decision about duration of absence from sport are based on the severity of the presenting injury, recent history of other concussions and extent of recovery (17). Clinical assessment of recovery

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Milder injuries commonly cause headaches, fatigue, dizziness, loss of concentration and impaired higher mental function for up to several weeks before recovery.

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More severe nonfatal injuries lead to long term changes in cognitive and emotional function including loss of intellectual capacity, memory, motivation and personality as well as more specific cognitive and behavioural deficits related to the location and depth and of lesions. Physical sequelae may include localized neurological deficits and post-traumatic epilepsy.

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CT or MRI scans (even if obtained earlier) may be required if symptoms persist longer than 1 week or worsen.

Post concussion symptoms

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Symptoms may be classified as acute (minutes to hours), prolonged (days to weeks), or chronic (months to years). Acute symptoms are presented in Table 2. Prolonged symptoms include persistent low-grade headache, concentration and memory deficits, sleep disturbance, reduced alcohol tolerance, irritability and lowered frustration tolerance, sensitivity to light and noise, tinnitus, easily fatigued, anxiety and/or depressed mood, specific cognitive dysfunction. Chronic symptoms include those listed for prolonged symptoms, but are usually accompanied by changes to behaviour, secondary changes in mood/affect, and family and/or social problems (18).

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Acute and prolonged symptoms require monitoring to determine when an athlete may return to participation. In the absence of any generally accepted clinical measures that assess extent of recovery the protocol detailed in Table 13 is recommended.

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Chronic post concussive sequelae may be minimized through counselling player, coach, and parents of the likely course of recovery and likely negative effects of early return to high-risk activities.

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The unrealistic expectations of athlete, family, peers, or work colleagues have been linked to the onset and persistence of post concussive complaints. Graded return to work or school activity minimizes the effects of symptoms and maximizes opportunity for recovery.

Cumulative effects of concussion Successive episodes of concussion may have cumulative effects.

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Post-concussive symptoms, such as poor co-ordination or balance, impaired concentration, judgement and fatigue may predispose the player to further head or other injuries. An athlete with a history of concussion is up to four times more likely to receive a further concussion (or injuries) than an athlete with a clear history (3). Appendix B provides a structured interview covering previous sports head injuries.

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Psychometric tests indicate greater initial impairment and extended recovery of mental functions in individuals with previous episodes of concussion (22).

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A second, even lesser, insult may have a disproportionately large effect. Repeated concussion predisposes athletes to a catastrophic outcome (Second impact syndrome) if the brain has not sufficiently recovered (23).

Chronic traumatic encephalopathy Repeated concussion, which is most common in professional boxers, may lead to the permanent structural changes of chronic traumatic encephalopathy (estimates vary from 1755%) (24). •

MRI and/or CT scans providing evidence of atrophy or structural abnormality are an indication for cessation of all high-risk sports or activities.

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Signs and symptoms range from mild neurologic dysfunction to dementia, and evolve slowly but may emerge more rapidly following a significant incident.

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The full Dementia Pugilistica syndrome occurs over several years in a minority of boxers and is more closely related to the number of bouts rather than knockouts.

Psychometric indices of impairment & recovery of function ○

Delayed onset of retrograde amnesia may occur within 10-15 minutes, and the amnesia may initially extend to a period of several hours before reducing (25).

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Various post traumatic amnesia scales are available to measure the severity of head injury but they were designed for hospital rather than on site testing (26, 27, 28, 29), and for amnesia lasting longer than 24 hours. Since the duration of post traumatic amnesia is rarely more than a few hours in most sports head injuries, a more suitable instrument for measuring severity of sports concussion is repeated administrations of the mental status examination (see Table 8 and Appendix A) (20, 25).

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Psychometric measures of attention, psychomotor speed, judgement and decision making, and memory have been extensively studied as a means of providing objective measures of subsequent recovery of function after the period of post traumatic amnesia resolves. Currently the most widely used are the Digit Symbol test (30) and the Paced Auditory Serial Addition Task (31). However, the Digit Symbol test has proved relatively insensitive compared to a more recent test, which involves judging whether sentences are true or false (32). It is recommended that the following three psychometric tests are used to monitor recovery of mentation from concussion: Digit Symbol subtest of the WAIS-R (30), Symbol Digit Modalities Test (33), and the Speed of Comprehension subtest of the Speed and Capacity of Language Processing Test (32) at weekly intervals until performance returns to normal levels.

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Performance levels of elite athletes on most tests of speed of information processing are often better than comparable population norms. Since

reference to regular norms could thus result in premature return to participation, it is desirable for professional athletes in high risk sports to have at least two baseline preseason measures on alternate forms of the three tests (34).

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Detailed psychometric testings (35, 36, 37), brain electrophysiological measures (38) and computerized dynamic posturography (39) have demonstrated recovery of cerebral function from concussion usually resolves within 1 week to 3 months. However reliable correlations between measures of severity of concussion and rate of recovery have yet to be established. Until then, the exclusion guidelines listed in Table 13 should be considered in conjunction with the results of individual based testing.

Prevention of sporting head injuries Given the potentially irreversible effects of head injury, even after apparently minor trauma, the sports physician has particular obligations to institute and advocate preventative measures aimed reducing the severity of head trauma, minimizing secondary brain damage arising from the initial incident and lowering the incidence of recurrent head injures (40). Devices reducing the severity of initial injury The use of protective devices such as mouthguards and helmets can reduce the degree of brain injury sustained for a given force and also afford protection against associated injuries of the skull, face, scalp and jaws(see chapter 24). Mouthguards

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Mouthguards protect teeth, facial bones and mandibles. Further, they open the temporomandibular joint (double type more so than single) and thereby decrease the force transmitted to the base of the skull by a mandibular blow.

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Fitted mouthguards moulded by taking a cast are superior to the heat and mould variety.

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Fitted single upper are recommended for contact sport, whereas fitted double (upper and lower) are necessary for combat sports.

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Non fitted mouthguards are probably better than nothing

Helmets There are two basic types, soft and rigid (often with soft inner). Soft helmets have been shown to reduce scalp and eyebrow injuries, but their efficacy in preventing brain injury is unproven. There are many types of rigid helmets can provide substantial protection to the head and face. As a general principle, the use of rigid helmets is recommended (and in some sports mandatory) unless there are compelling reasons for their avoidance, such as injuries to other athletes. While helmets provide protection against direct blows, they have at least three disadvantages:

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Helmets increase size of the head, thereby permitting a blow which would otherwise have missed to connect. The increase in diameter of the head can also increase the rotational component of a blow.

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Helmets can obstruct vision (especially if not correctly fitted) thereby hindering avoidance manoeuvres.

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Helmets may give a false sense of security, encouraging the athlete to perform more recklessly.

Selection and conditioning of individual athletes •

Selection and conditioning of athletes for particular sports and for roles within them is best directed at selecting appropriate physiques for particular sports and roles within them and at improving general physical fitness.

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It is not possible to condition the brain to resist external force; on the contrary, damage from repeated trauma, however minor, tends to be cumulative.

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In certain sports and roles within them that have a higher risk of head injury, neck strengthening exercises may have a protective effect by reducing acceleration of the head following blows to the head or body and by protecting against cervical spine injury.

Rules regulating play and individual participation It is one of the sports physician’s roles to advocate for rule changes that reduce the chance of head injury. Such rules can be designed to reduce initial injury and prevent recurrence, by regulating both the contest and individual athlete participation. •

Hard objects in the arena of play should be padded wherever possible.

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Rules requiring the use of protective devices are desirable.

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Rules that require the presence of trained personnel with first aid qualifications are highly desirable in high risk sports.

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Rules that permit immediate assistance to injured athletes are essential.

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Rules that prevent head injured athletes from resuming immediately without appropriate screening are essential.

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Rules that provide for mandatory exclusion periods following documented head injuries are desirable.

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Rules making the head an illegitimate target in contact sports are highly desirable. Combat sports that encourage blows to the head such as boxing and martial arts, provide a moral dilemma. Do sports physicians that attend such sports in order to assess and manage head trauma, nevertheless lend sanction to them?

Education of athletes and officials The sports physician not only has a clinical and an advocacy role as described above but also

has a responsibility to educate those involved with the sport about its risks, the recognition of head injury and its consequences, and the procedures for its assessment and management.

Bibliography 1. Lehman, L. B. and Ravich, S. J. (1990). Closed head injury in athletes. Clinics in Sports Medicine, 9, 247-261. 2. Seward, H., Orchard, J., Hazard, H., and Collinson, D. (1993). Football injuries in Australia at the elite level. The Medical Journal of Australia, 159, 298-301. 3. Gerberich, S. G., Priest, J.D., Boen, J. R., Staub, C. P., and Maxwell, R. E. (1983). Concussion incidences and severity in secondary school and varsity football players. American Journal of Public Health, 73, 1370-1375. 4. Cantu, R. C. (1992). Cerebral concussion in sport: Management and prevention . Sports Medicine, 14, 64-74. 5. Bruno, L. A., Gennarelli, T A., and Torg, J. S. (1987). Management guidelines for head injuries in athletics. Clinics in Sports Medicine, 6, 17-29. 6. McLatchie, G. and Jennett, B. (1994). Head injury in sport. British Journal of Medicine, 308, 1620-1624. 7. Ingebrigtsen, T. and Romner, B. (1996). Routine early CT-scan is cost saving after minor head injury. Acta Neurologica Scandanavica, 93, 207-210. 8. McCrory, P. R., Bladin, P. F., and Berkovic, S. F. (1997). Retrospective study of concussive convulsions in elite Australian rules and rugby league footballers: phenomenology, aetiology, and outcome. British Medical Journal, 314, 171-174. 9. Ryan, A. J. (1991). Protecting the sportsman’s brain (concussion in sport). British Journal of Sports Medicine, 25, 81-86. 10. Moriarty, J. M. and Simons, S. M. (1994). Sports Neurology. In Current Review of Sports Medicine (eds. R. J. Johnson, and J. Lombardo), pp. 176-189. Current Medicine: Philadelphia. 11. Maroon, J. C., Bailes, J. E., Yates, A., and Norwig, J. (1992). Assessing closed head injuries. The Physician and Sports Medicine, 20, 37-44. 12. Bigler, E. D. (1990). Neuropathology of traumatic brain injury. Traumatic Brain Injury (ed. E. D. Bigler). Pro-ed: Austin, Texas 13. Jennet, B. and Teasdale, G. (1981). Management of head injury. F. A. Davis: Philadephia. 14. Rimel, R. W., Giordani, B., Barth, J. T., and Jane, J. A. (1982). Moderate head injury: completing the clincial spectrum of brain trauma. Neurosurgery, 11, 344-351. 15. Levin, H. S., Eisenberg, H. M., and Benton, A. L. (1989). Mild Head Injury. Oxford University Press: New York. 16. Wrightson, P. and Gronwall, D. (1980). Time off work and symptoms after minor head injury. Injury, 12, 445-454. 17. Quality Standards Subcommittee, American Academy of Neurology. (1997). Practice parameter: The management of concussion in sport. Neurology, 48, 581-585. 18. Kelly, J. P. and Rosenberg, J. H. (1997). Diagnosis and management of concussion in sports. Neurology, 48, 575-580.

19. Teasdale, G. and Jennet, B. (1974). Assessment of coma and impaired consciousness, a practical scale. Lancet, ii, 81-84. 20. McCrea, M., Kelly, J. P., Kluge, J., Ackley, B., and Randolph, C. (1997). Standardized assessment of concussion in football players. Neurology, 48, 586-588. 21. Roos, R. (1996). Guidelines for managing concussion in sport: A persistent headache. The Physician and Sportsmedicine, 24, 67-74. 22. Gronwall, D. and Wrightson, P.(1975). Cumulative effects of concussion. Lancet, 2, 995-997. 23. Cantu, R. C. and Voy, R. (1995). Second impact syndrome: A risk in any contact sport. The Physician and Sports Medicine, 23, 27-34. 24. Shores, E. A., Marosszeky, J. E., Sandanam, J. et al. (1986). Preliminary validation of a clinical scale for measuring the duration of post-traumatic amnesia. The Medical Journal of Australia, 144, 569-572. 25. Maddocks, D., Dicker, G., and Saling M. (1995). The assessment of orientation in following concussion athletes. Clinical Journal of Sports Medicine, 5, 32-35. 26. Levin, H. S., O’Donnell, V. M., and Grossman, R. G. (1979). The Galveston Orientation and Amnesia Test: a practical scale to assess cognition after head injury. Journal of Nervous and Mental Disorders, 167, 675-684.. 27. Mendez, M. F. (1995). The neuropsychiatric aspects of boxing. International Journal of Psychiatry in Medicine, 25, 249-262. 28. Forrester, G. and Geffen, G. (1995). Julia Farr Centre - Post Traumatic Amnesia Scales Manual. Glenelg Press: Adelaide. 29. Forrester, G., Encel, J., and Geffen, G. (1994). Measuring post-traumatic amnesia (PTA): An historical review. Brain Injury, 8, 175-184. 30. Wechsler, D. (1981). Wechsler Adult Intelligence Scale - Revised. Psychological Corporation: New York. 31. Gronwall, D. (1977). Paced auditory serial-addition task: A measure of recovery from concussion. Perceptual and Motor Skills, 44, 367-373. 32. Baddeley, A., Emslie, H., and Nimmo-Smith, I. (1992). The Speed and Capacity of Language Processing Test. Thames Valley Test Company: Bury St Edmunds, Suffolk. 33. Smith, A. (1982). The Symbol Digit Modalities Test. Western Psychological Services: Los Angeles. 34. Hinton-Bayre, A. D., Geffen, G., and McFarland, K. (1997). Mild head injury and speed of information processing: A prospective study of professional rugby league players. Journal of Clinical and Experimental Neuropsychology, 19, 275-289. 35. Hinton-Bayre, A.D, Geffen, G.M., & McFarland, K. (1997) Impairment and recovery of speed of information processing after mild head injury: A prospective study of rugby league players. International Perspectives in Traumatic Brain Injury. (in press) 36. Maddocks, D. and Saling, M. (1996). Neuropsychological deficits following concussion. Brain Injury, 10, 99-103. 37. Macciocchi, S. N., Barth, J. T., Alves, W., Rimel, R. W., and Jane, J. (1996). Neuropsychological functioning and recovery after mild head injury in collegiate athletes.

Neurosurgery, 39, 510-514. 38. Montgomery, E. A., Fenton, G. W., McClelland, R.J., MacFlynn, G., and Rutherford, W. H. (1991). The psychobiology of minor head injury. Psychological Medicine, 21, 375-384. 39. Guskiewicz, K. M., Perrin, D. H., and Gansneder, B. M. (1996). Effects of mild head injury on postural stability in athletes. Journal of Athletic Training, 31, 300. 40. Garnham, A. P. (1992). Injuries to the head, eye and ear. In Textbook of Science and Medicine in Sport (ed. J. Bloomfield, P. A. Fricker, and K. D. Fitch), pp. 279-296. Blackwell Scientific Publications: Melbourne. Additional references on measurement of severity and recovery from head injury 41. Clark, C. R., O'Hanlon, A., Wright, M. J., and Geffen, G. M. (1992). Event-related potential measurement of deficits in information processing following moderate to severe closed head injury. Brain Injury, 6, 509-520. 42. Cremona-Meteyard, S. L., Clark, C. R., Wright, M. J., and Geffen, G. .M. (1992). Covert orientation of visual attention after closed head injury. Neuropsychologia, 30, 123-132. 43. Cremona-Meteyard, S. L., and Geffen, G. M. (1994a). Event-related potential indices of visual attention following moderate to severe closed head injury. Brain Injury, 8, 541-558. 44. Cremona-Meteyard, S .L. and Geffen, G. M. (1994b). Persistent visuospatial attention deficits following mild head injury in Australian Rules Football players. Neuropsychologia, 32, 649-662. 45. Cremona-Meteyard, S. L. and Geffen, G. M. (1995). Persistent visuospatial attention deficits following mild head injury in Australian Rules Football players.In Year Book of Sports Medicine. (ed. R Sheperd), pp.312 - 319. Mosby - Year Book Inc: New York. 46. Geffen, G. M., Encel, J. S., and Forrester, G. M. (1991). Stages of recovery during posttraumatic amnesia and subsequent everyday memory deficits. Neuroreport, 2, 105-108. 47. Geffen, G. M., Butterworth, P., Forrester, G. M., and Geffen, L. B. (1994). Auditory Verbal Learning Test components as measures of severity of closed head injury. Brain Injury, 8, 405411.

Appendix A

Mental status examination test form

Name: ------------------------------------------------------------ Date: ............................................................ Age:...............................................Sex: ..............................Years of education:.................................... Loss of consciousness..........................minutes Examiner’s name:...................................Time of assessment:.........................................................

1. IMMEDIATE MEMORY: Say to the athlete ‘I will say some words. Try to remember them’.  

Read the words aloud at one per second to the athlete. Then ask him/her to say all the words in any order. Write the words as they are spoken. Read them again for Trial 2. Again ask for recall

 

including words they said before. Repeat for Trial 3. TOTAL

/15

 

 

LIST Baby Monkey Perfume Sunset Iron No. of words

 

TRIAL 1

TRIAL 2

TRIAL 3

 

 

NOT tell the athlete that memory for the words will be tested later

 

 

 

 

 

2. PROCESSING SPEED: (no. sentences correctly judged in 2 min - see Table 9)

 

I am going to read you sentences which could be true or false. As I read each sentence please say ‘true’ if the sentence is sensible or ‘false’ if it is silly. We will have a practice at these three sentences at your own speed. 1. Rats have teeth. 2. Nuns are made in factories. 3. Ants are living creatures. Are there any questions? Read each sentence aloud in a clear voice. Read sentences at a natural rate - between 1.5-2.5 seconds per sentence. Allow 2 seconds after the sentence is read for the answer. As soon as the person responds place a T or F on the line for each block of 10 sentences. Immediately read the next sentence aloud. We are going to work quickly. Let us see how many you can do in 2mins. Are you ready? I will start now. Begin stopwatch recording. Read sentences from the Speed of Comprehension subtest of the Speed and Capacity of Language Processing Test.(32). After exactly two minutes stop testing. Record the number of correct judgements made within the 2 minutes 1 - 10

11 - 20 21 - 30 31 - 40 41 - 50 Number correct in 2 mins = ________________ Scores below 38 indicate impaired comprehension  

 

 

3. ORIENTATION:

eg.,

time - What is the time? the day? the month?

/3 place - Where are we?  

/1

 

situation - What happened to you? /1 TOTAL

 

/5

 

 

4. RETROGRADE AMNESIA: Ask the athlete up to 5 questions concerning events occurring before the incident. Ensure that  

responses required are readily verifiable, and avoid questions using a true/false response

 

format. TOTAL /5

 

 

 

5. DELAYED RECALL: (approx. 5 minutes after completing List Learning - 1 point each)  

 

DO NOT READ WORDS. Say ‘Can you tell me any those words I asked you to remember earlier’.

 

 

 

DELAYED RECALL

 

 

TOTAL

/5

SUMMARY 1. IMMEDIATE MEMORY /15  

2. PROCESSING SPEED (>38)

Y/N  

3. ORIENTATION

/5

4. RETROGRADE AMNESIA

/5

5. DELAYED RECALL

/5

All items must be passed to be considered clear of mental status abnormalities  

USE A DIFFERENT FORM ON RETESTING

 

 

 

 

 

Appendix B

 

Previous sports head injuries - structured interview

Explain the nature of concussion A concussion can result from a direct blow to the head or even from the heavy contact of bodies, without actual head contact. You may have been concussed if you were knocked unconscious or if you were unable to remember part of a game clearly (that is, you had a gap in your memory). You may have just been confused or disoriented for a period of time. After a concussion you may have experienced headaches, blurred vision, nausea, dizziness, tiredness, irritability, loss of co-ordination, or difficulty concentrating or remembering things. Over your sporting career have you ever been concussed during an evrent? If NO

If YES

go to (1)

go to (14)

(1)

How many times have you been concussed?

(2)

How long ago was your most recent concussion (weeks, months, years)?

(3)

Were you knocked unconscious? If YES How long?

(4)

Was there a period of time where you were confused or disoriented or you could not

remember the incident or you had a gap in your memory? If YES how long? (5)

How many times have you been actually been knocked unconscious?

Ask (6) to (10) only if a player has had more than one concussion. (6)

When was the last time you were knocked unconscious?

(7)

What was the longest period of time you have been knocked unconscious?

(8)

How many times have you had a memory gap after a concussion?

(9)

What was the longest gap in your memory after a concussion?

(10)

In which years did each of your concussions occur?

Re-start here if only one concussion (11)

Have you missed any games due to concussion? If YES how many?

(12)

Have you ever been off work or other activities because of a concussion? If YES how

long? (13)

Do you believe you have changed in any of the following ways as a result of your head

injuries? Rate each 0 ‘no’ to 4 ‘greatly’. mental - attention, memory, decision making, follow conversation, detailed instructions, fatigue easily physical - fatigue more easily, increased sleep, emotional - depressed, anxious, irritable more easily social - enjoy leisure activities, relationships, friends, family commitments work - maintaining workload, increasing productivity playing ability - fatigue, decision speed, reaction time, skills under pressure Begin here if no previous sports-related concussion (14)

Over your career how many non-head injuries have you had that required you to miss a

game (15)

How many games have you missed due to non-head injuries?

(16)

Have you ever received a head injury outside of competitive contact sport?

If the subject says YES...record length of unconsciousness, post traumatic amnesia, and other

clinical symptoms.

Table 1

A classification of severity of head injury

Mild

loss of consciousness

post traumatic amnesia

<1 hour

Glasgow coma score

13-14

Moderate

0-5 min

loss of consciousness

post traumatic amnesia

1 - 24 hours

Glasgow coma score

9-12

Severe

loss of consciousness

post traumatic amnesia

>24 hours

Glasgow coma score

<9

Table 2

5 min - 6 hours

>6 hours

Acute clinical features of concussion

•

Transient loss of consciousness (not obligatory)

•

Confusion, including:

reduced vigilance; heightened distractibility; inability to think coherently; inability to sequence goal directed moments; disorientation for person, time or place; dazed facial expression. •

Amnesia, including: anterograde amnesia for events after the injury; retrograde amnesia for events before the injury; inability to acquire new memories.

•

Other neurological features including: blurred vision or diplopia; slurred speech; dizziness; impaired balance or incoordination; nausea or vomiting; emotional lability; convulsions.

Table 3

DR ABC procedure for resuscitation of unconscious athlete

Danger •

Remove athlete and self from dangerous environment. Response

•

Loudly say ‘Hello, can I help you?’ If athlete responds verbally then airway must be patent

and some cognition is present. Airway •

to clear - insert gloved finger into oral cavity and remove mouthguard, loose teeth, vomit etc.

•

to open - place athlete on back then move mandible anteriorly (jaw thrust).

•

if airway obstructed (full or partial) then slight cervical extension may help.

•

if available oropharangeal airway (Gaddell), supplemental oxygen and oral suctioning may

be necessary. Breathing •

check colour

•

listen to breathing rate and character

•

check chest for movement and air entry

•

if not breathing start expired air resuscitation Circulation

•

Check carotid pulse (if palpable systolic BP is > 60 mmHg)

•

If absent commence cardiopulmonary resuscitation.

•

Check for torrential arterial bleeding and treat.

Table 4

Primary Survey

When resuscitated and in coma position:

 

•

Inspect and palpate scalp (for wounds or skull fractures)

•

Inspect and palpate face and anterior neck

•

Check cervical spine alignment (run fingers along supraspinatus processes)

•

Glasgow coma score (see Table 5)

•

Pupillary size, symmetry and reaction to light

•

Check nose and ears for bleeding or CSF leak

•

Inspect and palpate abdomen, pelvis and limbs

 

 

  Table 5

Glasgow Coma Scale (19)

Eye Opening Spontaneous

4

To speech

3

To pain

2

None

1

Best verbal response Oriented

5

Confused

4

Inappropriate words

3

Incomprehensible sounds Nil

2

1

Best motor response Obeys commands Localizes to pain

6 5

Withdraws from pain Abnormal flexion Extension Nil

3 2

1

Total Score Table 6

4

3-15

Transport of head injured athlete to hospital

•

complete resuscitation and primary survey;

•

protect airway and cervical spine with sandbags or neck brace;

•

treat and stabilize other injuries;

•

arrange others to carry the injured athlete;

•

travel with patient if paramedics unavailable. Table 7

•

eyes:

Neurological screening examination visual acuity and fields, pupil size and reflexes, nystagmus

 

•

ears:

haemotympanum

•

nose:

rhinorrhea

•

power:

all limbs

•

coordination:

finger-nose touching, heel-toe walking, balance on one leg with eyes

closed Table 8

Mental status examination for concussion (test form in Appendix A)

Immediate memory: Five words read to athlete and recalled on three successive trials, scored out of 15. Processing speed: Sentences read aloud for two minutes, number correctly identified as true or false. Scores less than 38 indicate impairment. Orientation: Query orientation for time, place, situation, scored out of 5. Retrograde amnesia: Query event recall prior to trauma (may vary with time post trauma), scored out of 5. Delayed recall Free recall of five items presented at immediate recall, scored out of 5. Table 9

Grading concussion

Grade 1 •

transient confusion

•

no loss of consciousness

•

concussive symptoms and/or mental status abnormalities fully resolve within 15 minutes. Grade 2

•

as for Grade 1 except symptoms and abnormalities persist for longer than 15 minutes Grade 3

•

any loss of consciousness whether it be brief (seconds, Grade 3a) or prolonged (minutes,

Grade 3b) Table 10

Sports Head Injury Card

Name: Time of concussion:

Date:

Watch closely for the next 24 hours. Take to hospital immediately if •

they vomit

•

severe headache develops or increases

•

they become restless or irritable

•

they become dizzy, drowsy, or can not be aroused

•

they have a fit (convulsion)

•

anything else unusual occurs For 24 hours after injury they should:

•

rest quietly

•

not drive a vehicle or operate machinery

•

not consume alcohol or non prescribed drugs Medical advice should be sought before returning to sport

 

 

  Table 11

 

Criteria for referral to hospital

•

Loss of consciousness greater than 3 minutes

•

Post traumatic convulsion

•

Focal neurological signs

•

Symptoms of marked cerebral irritation persisting longer than 1 hour

•

Any deterioration of mental status, particularly the development of drowsiness following a

 

lucid period •

More than one episode of concussion in any one playing session

•

Non-availability of responsible adult to monitor for next 24 hours. Table 12

Guidelines for return to competitive sport

Grade of Concussion

Grade 1

Number of concussions (within a calender Initial concussion same day if

year) Repeat concussions 1 week or longer*

asymptomatic within  

Grade 2 Grade 3a 3b

15 mins 1 week asymptomatic 2 weeks or longer* 1 week asymptomatic 1 month or longer* 2 weeks 1 month or longer*

 

asymptomatic  

* Period may be prolonged depending on frequency and severity of previous concussions.

Table 13

 

Recommendations for progressive return to activity

•

Training should not commence when symptomatic at rest

•

Training should cease upon development or recurrence of symptoms (requires systematic

questioning). •

First day asymptomatic, allow brisk walk for at least 20 minutes. If still asymptomatic, allow

light exercise (20 minutes), then check for symptoms.

 

•

Second to seventh days, continue to monitor graded increases in training.

•

No full exertion until asymptomatic for at least one week with progressive loading

•

If symptoms persist or develop, a full medical examination is required