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Head Injury

Article  in  Scottish Medical Journal · May 2010

DOI: 10.1258/rsmsmj.55.2.12 · Source: PubMed

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 ORIGINAL ARTICLE
Head Injury
KA Hureibi1, GR McLatchie2
1
Specialist Registrar, Department of Surgery, Crosshouse Hospital, Kilmarnock, KA2 0BE
2
Professor and Consultant Surgeon, University Hospital of Hartlepool, Hartlepool, TS24 9AH
This article is taken from a Tribute Lecture given at Edge Hill University in February 2009 in memory of Professor Bryan Jennett.
Correspondence to
Mr KA Hureibi MB BS, MRCS, Specialist Registrar, Department of Surgery, Crosshouse Hospital, Kilmarnock, KA2 0BE
E-mail: alhureibi@gmail.com
Abstract
Head injury is one of the commonest injuries in sport.
Most are mild but some can have serious outcomes.
Sports medicine doctors should be able to recognise the
clinical features and evaluate athletes with head injury. It
is necessary during field assessment to recognise signs
and symptoms that help in assessing the severity of injury
and making a decision to return-to-play. Prevention of
primary head injury should be the aim. This includes
protective equipment like helmets and possible rule
changes.
Key words
Head injury, Concussion, Sports.
Introduction
Head injuries in sport have become increasingly important and
doctors in sports medicine should be capable of recognizing
and managing them. Although most head injuries are mild,
some can have deleterious effects. The long-held belief
regarding the benign nature of minor head injuries (concussion)
are thought now to be misleading and there is evidence that the
potential seriousness of concussion might be more common
than previously thought.1 75% of brain injuries in sport are mild2
and this group represents the greatest management challenge.
Unlike other patients with head injury, athletes pose a problem
especially where the treating doctor has to make a decision
when they can resume play.
Incidence
Sports Injuries represent about 11% of all cases of head
injuries.3 A study of data gathered in Scotland in 1978 revealed
that the sports most frequently causing serious head injuries
were golf, horse-riding and football.4
Nature of Brain Damage
Brain damage is either primary (impact) or secondary.
12
Impact (or primary) damage can take two forms:
Cerebral contusion. This is the most common form of impact
damage. It involves bruising on the brain surface due to impact
with the overlying skull. Diffuse contusion results when the head
decelerates, usually by hitting the ground, resulting in
movement of the brain as a whole against the interior of the
skull.5 Contusions can lead to secondary brain damage such as
local brain swelling or an intradural hematoma.6,7
Diffuse axonal injury. This is characterized by a widespread
tearing of the white matter fibres producing characteristic
radiological features on CT scanning.8 It usually causes
immediate unconsciousness and in its most severe form can
be associated with significant cognitive, memory and motor
deficits. The mortality rate is more than 50%.9
Secondary brain damage
Secondary brain damage results from three main mechanisms
namely raised intracranial pressure, hypoxia and ischemia, and
infection.10
1- Raised intracranial pressure. This is due to either an
intracranial hematoma/haemorrhage or brain swelling.
Extradural Haematoma. This is a common brain injury in
athletes especially in sports where helmets are not used.
They result from bleeding from the middle meningeal
vessels. They are associated with the phenomenon of a
“lucid interval” and subsequent neurological
deterioration.11
Intradural Haematoma. They are either subdural or
intracerebral but are often a combination of both-
formatting the so called burst lobe, usually located
frontotemporally. Subdural hematomas are usually caused
by bleeding from superficial veins ruptured by shearing
forces or directly by impact.
Subarachnoid Haemorrhage. This results from a tear or
dissection of the vertebral artery. It presents typically with
meningeal irritation i.e. neck stiffness, headache and
photophobia. Such injuries have often a poor outcome.
Subdural hematomas and intracerebral haemorrhages
account for the majority of fatal brain injuries in sport.12
Brain Swelling. This can result from cerebral oedema or
vascular engorgement, or both, and it may be focal or
 SCOTTISH MEDICAL JOURNAL Volume 55 Issue 2 May 2010

diffuse. It is thought that trauma may cause loss of Box 1:

The Glasgow
autoregulation of the blood supply to the brain and this in
Coma Scale
turn causes vascular engorgement and hence intracranial
hypertension.13 Respiratory inadequacy also can
aggravate cerebral oedema by causing vasodilatation in
cerebral vessels secondary to hypercapnia.

2- Hypoxia and ischemia. These result from raised

intracranial pressure which reduces cerebral blood flow.
An aggravating factor is low blood pressure secondary to
bleeding from other injuries in the body.

3- Intracranial infection. Meningitis and abscesses can

complicate head injury if the dura is breached and
contamination ensues as sometimes happens with
compound depressed fractures.

Concussion
There has been an increasing interest in concussion in athletes
in recent years. Concussion represents the most common form
of athletic head injury.14
Concussion originated from the Latin word concussus, which
means “a shaking”. There is no universal definition of
concussion; however the most widely accepted definition is the
one proposed by the Head Injury Nomenclature of Neurologic
Surgeons in 1966. They defined concussion as ‘‘a clinical
syndrome characterized by the immediate and transient
posttraumatic impairment of neural function such as alteration of Field Assessment of Level of Consciousness and
consciousness, disturbance of vision or equilibrium, etc., due to
Mental Status
brain stem dysfunction.’’15 The clinical symptoms of concussion
reflect a functional disturbance rather than structural injury.
After evaluating the ABC and ruling out serious injuries, the level
Following concussion, cells show metabolic dysfunction as a
of consciousness should be assessed. Any loss of
result of the subtle changes in both extracellular and intracellular
consciousness (LOC) should be established. LOC only
environments. This leads to a state of “hyperglycolysis” that is
happens in 10% of concussion injuries in sport and it is
accompanied by a decrease in blood flow due to cerebral
infrequent in sport related injury to last more than one to two
neurovascular constriction. As a result of that a metabolic
minutes.19 Players who lose consciousness should be removed
mismatch ensues and causes the concussed cells to be
from the field.
vulnerable.16 This was further supported by functional MRI of
athletes with concussion.17 Confusion and amnesia are more common than LOC in
concussion. The doctor should ask the player certain questions
Clinical Features to assess if he is confused or suffering from amnesia such as
“what happened to you?”, “what is the score?”, “where are
Altered consciousness is the hallmark of diffuse brain damage. you?”....etc. Answering the questions slowly or inappropriately
It is evidenced by immediate change in responsiveness and in indicates confusion.
subsequent loss of memory for an interval after the injury- post- Amnesia needs to be evaluated carefully when assessing
traumatic amnesia (PTA). The Glasgow coma scale (Box 1) is players with head injury. Its duration correlates with the severity
the most widely accepted means of assessing patients with of injury. Amnesia is retrograde where the player forgets events
head injuries, both initially and with continued observations, for before the event. Posttraumatic amnesia occurs when there is
signs of deterioration that would indicate complications that call loss of memory associated with events following the injury. It
for immediate action. Based on the GCS score, brain injuries has been found that posttraumatic amnesia, even for seconds,
are graded into mild (13-15), moderate (8-12) and severe (<8). can be highly predictive of post injury neurocognitive deficits
and persistent symptoms.19 A summary of neurological
Most head injuries are mild, resulting in only a minute or so of examination is shown in Box 2.
eyes closed coma with no speech and not obeying commands.
As a player regains consciousness the important observation
is whether there is a rapid return to full orientation (in person, Box 2:
time and place). Some athletes might only present with • Glasgow Coma Scale Neurological
Examination
headache after head injury which is the most common symptom • Pupil sizes and responses to light
following concussion.18 Others might present with primary • Examination of ears and nose for blood,
cognitive difficulties such as memory or concentration losses. cerebrospinal fluid, haemotympanum
Headache per se doesn’t represent a medical emergency, but
• Sensation (including perianal area)
a severe progressive headache - especially if accompanied by
vomiting or worsening mental status- may signal a serious injury • Deep tendon reflexes (including plantar
responses)
and an urgent CT scan of the brain is indicated.

13
 Scalp wounds often lead to brisk bleeding and players should
be removed for careful inspection of the wound and control of
haemorrhage.
A more difficult decision to make is what further management
players or contestants with head injury need. They should be
referred to hospital if they are still confused or worse after 10
minutes or so. That would also apply to those in whom an open
injury is suspected because of a scalp laceration or blood and
fluid coming from the nose or ears. The accident and
emergency department can then decide whether a skull X-ray is
required to exclude a skull fracture. If a vault fracture is found
then the patient will need to be kept in for observation, and
computed tomography, because the risk of an acute intracranial
heamtomas is considerably increased if there is a vault fracture.
Accident and emergency departments sending home patients
with head injuries now usually give the family or accompanying
people a head injury card (Box 3) with specific instructions.
Sports organizations might make use of such a card, which will
include the telephone number of the local hospital. Players who
have sustained head injury should avoid alcohol for at least the
next 24 hours because its effects may lead to confusion in
interpreting symptoms which could indicate complications.
Box 3:
This patient has received an injury to the head. Head Injury Card
A careful examination has been made and no
sign of any serious complications have been
made.
It is expected that recovery will be rapid, but in
such cases it is not possible to be quite
certain.
If you notice any change in your behaviour,
vomiting, dizziness, headache, double vision,
excessive drowsiness, please telephone the
hospital at once.
Table I: Zurich Concussion Conference: Graduated return to play protocol
14
Sequelae of Head Injury
Injuries that were severe, either initially or because of
complications are often associated with persisting and even
permanent effects. The post-concussion syndrome is not
uncommon especially among athletes with successive
concussions.20 This includes a host of symptoms like persistent
headache, lack of concentration, irritability, dizziness, general
fatigue, loss of intellectual capacity and personality change.
Most of these symptoms are self limiting in minor head injury
and take a benign course. They usually resolve by six to eight
weeks.21 It is important to notice that these effects are more
pronounced after the second concussion22 and any athlete still
symptomatic should not be allowed to go back to sport as the
brain is still vulnerable to cumulative injury and to the rare, but
lethal syndrome, the ‘second-impact syndrome’.23
Return to Sport
It is a challenging decision for the doctor to decide when it is
safe for the athlete to return to play (RTP). There have been
several guidelines published in the literature to help the sport-
medicine practitioner to make the decision as when the players
can RTP.24 The first consensus guidelines came in 2002 when
the Concussion in Sport (CIS) group met in Vienna and
published a document on the diagnosis and management of
sport related concussion.25 A third series of recommendations
was issued recently based on the meeting of the group in Zurich
in 2008.26 They recommended a stepwise RTP protocol where
the player progresses from one step to the next if asymptomatic.
Generally each step should take 24 hours and it would take the
athlete a week to complete the rehabilitation protocol (Table I).
If any post concussion symptoms develop while on the
programme, the athlete should drop back to the previous
asymptomatic level.
Prevention of Head Injury
Prevention of primary head injury should be the aim, but in some
sports like boxing this would be extremely difficult unless there
were radical changes in the rules. In non-combative sports,
however, most injuries are accidental.
Much effort has been made to
lessen the incidence of serious
head injury. The emphasis on
wearing helmets has become
commonplace and has been
implemented in a wide range of
sports like equestrian sports,
bicycling etc. The aim of the
helmet is to spread the force of
impact and the inner lining helps
to dissipate the kinetic energy of
the acceleration forces.27
Biomechanical research has
proven a reduction in impact
forces with the use of head gear
and helmets, evidenced by
studies that have demonstrated
the protection helmets provide
against head injury such as in
skiing,28 football,29 rugby,30
bicycling31 and horse riding.32
 SCOTTISH MEDICAL JOURNAL
Conclusions
Head injury is one of the most common injuries in sport. Most
injuries are mild but some can be potentially catastrophic. Initial
management should involve careful evaluation and neurological
assessment. Sport-medicine doctors should be familiar with the
signs and symptoms and initial management. The post-
concussion syndrome can complicate head injury and
cumulative injuries should be avoided by refraining from sport
until a full recovery has occurred. Return to sport should be
governed by a graduated return to play protocol. Protective
equipment and revision of rules can help to prevent head
injuries and decrease their severity.
Summary of clinical features and action required
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