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68
CHAP TER3 Thehead
Peripheral neurological examination
This should also be under taken routinely as part of the evaluation of the
centr al nervous system (CNS). Decits in the limb may also occur with
spinal cord and peripheral nerve injur ies (see also E Chapter 4).
• Limb function:
•
Appearance (deformity, wasting, abnormal movement, fasciculations)
•
Muscletone
•
Power in each musclegroup
•
Limb reexes
•
Sensation in each dermatome (touch, pain, vibration, temperature,
proprioception).
• Coordination:
•
Romberg’s test for equilibrium
•
Gait
•
Finger-nose/heel shin test
•
Cerebellar signs (dysdiadochokinesia).
Higher functions
• Language ability:expressive, receptive, and nominal dysphasia
• Reading ability:dyslexia
• Writing ability:dysgraphia
• Calculation ability:dyscalculia
• Object recognition:agnosia
• Ability to perform specic tasks:dressing, geographical (follow
route), and constructional (copy drawing) apraxia.
• Memory test:immediate, short- term, long- term, verbal and visual
memory (cannot be tested if confused or dysphasic).
• Reasoning and problem- solving ability.
• Mental state:degree of anxiety, mood, emotional behaviour,
inhibition, speed of thought and response.
External examination ofthehead
Be methodical. Your examination will be guided by the suspected problem (trauma, sinusitis, headache, subarachnoid haemorrhage (SAH)):
• Inspection. Standing at a distance from the patient, take a general
look at the head and neck. Note any asymmetry, lumps, trauma,
scars, discolouration, and obvious neurological decit.
• Function. Check eye movements, vision, and the cranial ner ves.
• Palpation of the head. Depending on the presenting complaint, a
thorough palpation of any visual ndings is performed:
•
Scalp
•
Forehead. Percussion over the frontal sinus may elicit tenderness if
there is sinusitis
•
Supraorbitalridges
•
Nasalbridge
•
Occiput
•
Neck.
Feel for tenderness, uctuation, steps in bony continuity, and enlarged
lymph nodes or swellings in the neck. If there is an obvious exposed skull
fracture do not manipulate it. Cover with a sterile dressing
EXAMIN ATION OF THEHEAD
• Auscultation. Can be considered for vascularized lumps (e.g.
haemangioma, arteriovenous malformation (AVM)) or following
trauma (surgical emphysema/ carotid bruit). Acarotid cavernous
stula can cause an orbital bruit along with proptosis, chemosis,
ophthalmoplegia and loss ofvision
• Don’t forget to check for papilloedema.
Some usefulsigns
Facial nervepalsy
Following a head injury this can indicate a fractured base of skull. Often
with associated hearingloss.
Intercanthal distance
If greater than 30 – 32mm (female) or 32– 34mm (male) the patient may
have detached canthi secondary to an underlying NOE fracture. Check
for CSF leakage
Anosmia
Loss of smell can occur due to tearing or inltration of the olfactory
nerves (anterior cranial fossa fracture or tumour). It is common af ter
head injur y as the olfactor y nerves are vulnerable to injury as they run
across the skull base anteriorly.
Racoon (panda)eyes
Bilateral, well- dened ‘black eyes’— fractured base of skull (anter ior cranial fossa), Le For t II/ III, or NOE fracture.
Third nervepalsy
Dilated pupil, the eye look s down and out, and there is ptosis. In severe
head injuries this represents third nerve compression from an expanding
intracranial lesion. The patient may have a reduced GCS.
Superior orbital ssure (SOF) syndrome
Ophthalmoplegia, xed dilated pupil and ipsilateral forehead numbness—
fracture extending into the SOF, or possible carotid aneur ysm. This is
usually part of a signicant injury.
Orbital apex syndrome
As in the SOF syndrome but here the patient also has reduced visual acuit y.
Haemotympanum
Blood visualized behind the ear drum. Indicative of a fracture of the
middle cranialfossa.
Battle’ssign
Bruising around the mastoid region— fractured base of skull (Figure3.1).
CSF rhinorrhoea/ otorrhoea
‘Tramlining’— fractured base of skull (Figures 3.2 and3.3).
Bleeding fromtheear
May indicate a fractured base of skull or mandibular condyle.
69
70
CHAP TER3 Thehead
Figure3.1 Battle’ssign.
Repro duced with p ermi ssion from J ohnso n, C., A nder son S. R., Da llimo re J., eta l., Oxford
Handbook of Expedition and Wilderness Medicine, Second Ed ition, Plat e 22, Copyr ight © 20 15
with p ermi ssion from O xfor d Unive rsityPre ss.
Figure3. 2 CSF rhinorrhoea.
USEFUL INVESTIGATIONS
Figure3. 3 CSF otorrhoea.
Useful investigations
Laborator ytests
• Awhite cell count ( WCC) should be taken in all suspected infections
and patients presenting with severe headaches (for under lying
infections).
• C- reactive protein (CRP) or erythrocyte sedimentation rate (ESR)
are usually very high in temporal ar teritis and should prompt
administration of steroids and urgent referral.
• Lumbar puncture (LP) may be required for CSF analysis.
• Blood cultures in suspected meningitis/ encephalitis.
CT/ MRI scanning
These are now the investigation of choice in the assessment of most
head- related problems, especially trauma and suspected space occupying lesions. CT scanning is the mainst ay of imaging in head trauma.
Often the cervical spine is imaged simultaneously as there is a 5% r isk of
cervical spine fracture with a serious head injur y.
Fresh blood can be seen on CT and therefore it is often a preliminar y
investigation in the assessment of suspectedSAH.
CT angiography may be considered in carotid dissection or penetrat-
ing injury and CT venogr aphy for suspected cerebral venous thrombosis.
71
72
CHAP TER3 Thehead
Head trauma:introduction
Head injuries are a common reason for attendance at the emergency
department, particularly at night and weekends. A wide spectr um of
severity is seen and it is important not to over look the patient with a
potentially serious intracranial injury. However, there are also other
causes of an altered conscious level, in addition to head injuries. Alcohol
excess, drugs, hypoxia, hypotension, hypoglycaemia, and other metabolic disturbances should always be considered. Asystematic approach to tr auma
patients should be followed with airway, breathing, and circulation
remaining the priority, even in patients with an apparently isolated head
in ju r y.
Terminology
‘Primary’ brain injury occurs at the time of the trauma. As clinicians there
is nothing we can do about this. Prevention is the only way to reduce this.
‘Secondar y’ brain injur y occurs after the initial event and is due to complications such as hypoxia , hypercar bia, hypotension, raised ICP (haematomas or cerebral oedema), cerebral herniation, or infection. One
way or another, these all result in either hypoxia or inadequate cerebr al
perfusion.
The aim of head injury management is to prevent secondary brain injur y
by regular observation and rapid correction if any deterioration occurs. This
helps promote a physiological milieu that encourages natural recovery from
the primary injury.
Primary braininjury
Primary brain injury can take the formof:
Cortical lacerations (burstlobe)
This also usually results in an acute subdural haematoma together with
a cerebral haematoma and surrounding contusions. The aected brain
usually swells markedly. Acraniotomy is often necessary for evacuation
of the subdur al haematoma and debridement of the damaged brain.
Prognosis is usually poor due to the extent of the primary brain damage.
Cerebral contusions
This is discussed under ‘Intracranial haematomas’ in ‘Classication and
common types of head (brain) injuries’ topic later in this chapter, and
occurs when the brain strikes the inner table of theskull.
Diuse axonalinjury
This consists of widespread disruption and shearing of axon sheaths following a high- energy impact. It is particularly associated with a rot ational
or deceleration element to theforce. Concussion is a tr ansient impairment of consciousness following a minor or moder ate head injury is
probably a mild form of diuse axonal injury. The CT scan in diuse axonal injuries can be normal, but more of ten shows a tight, swollen brain,
with or without petechial haemorrhages. The degree of brain swelling
usually increases over the rst 48 hours post injury. The prognosis for
diuse axonal injury is poor and surgical options are limited.
=−
HEAD INJU RIE S:PATHOPHYSIOLOGY
Head injuries:pathophysiology
The brain is the most sensitive organ in the body to hypoxia and ischaemia.
Therefore it is essential to maintain an adequate supply of well- oxygenated
blood to the injuredbrain.
Autoregulation
This maintains a constant supply of blood to the brain between a mean
arterial pressure of 50 and 160mmHg. However, this mechanism can be
impaired following head injur y. The cerebral per fusion pressure (CPP) is
the force driving blood through the br ain and is normally over 70mmHg.
It is related to the mean ar terial pressure (MAP) and intracr anial pressure (ICP)by:
CPPMAP ICP
The eects ofintracranial swelling and bleeding
Any developing intracranial mass lesion will initially be compensated for
by displacement of venous blood and CSF, so the ICP will not rise. When
this compensator y mechanism has been exhausted, the ICP will rise and
the CPP will fall. The Cushing reex then comes into play, increasing the
systemic BP to maintain cerebral blood ow. The pulse rate falls due to
a vagal reex. When this compensatory reex fails, progressive cerebral ischaemia will occur leading to cerebral infarction and brain death.
Avicious circle becomes established with hypoxia, hypotension, and cell
breakdown products, which worsen the cerebral oedema, contributing
to further deterioration (Figure3.4).
Hypoxia
73
Toxins
Reduced
CPP
Low BP
Figure3.4 P athophysiolog y of rai sedIC P.
Cerebral
ischaemia
Raised ICP
Cerebral
oedema
Mass
lesions
74
CHAP TER3 Thehead
Brain herniation
Three main t ypes of herniation are commonly seen when a mass lesion
develops intracranially (Figure3.5).
Subfalcine herniation
One hemisphere is displaced beneath the falx, which is seen as midline shif t
on a CT scan. This can obstruct the foramen of Monro anteriorly, causing
unilateral ventricular dilatation. It can also compress the posterior cerebral
artery against the falx posteriorly, causing a posterior cerebral infarction.
Transtentorial herniation
The uncus of the medial temporal lobe herniates through the tentor ial
notch. This compresses the oculomotor nerve (dilated pupil), and the
midbrain.
Tonsillar herniation
The cerebellar tonsils herniate through the foremen magnum causing
brainstem compression (coning).
Criteria for admission (may vary with dierent units— check local policy)
• Skull fr acture (proven or suspected)
• GCS score<15
• Focal neurological decit
• Infants/ elderly
• Suspected non- accidentalinjury
• Alcohol intoxication
• High- risk mechanism ofinjury
• Social (e.g. livesalone)
• Risk factors (e.g. warfarin/anticoagulants).
1
2
3
Figure3. 5 Br ain he rniation . (1)Subfa lcine ‘midli ne’ her niat ion. (2)Tentoria l
herniation. (3)Tonsillar herniation.
Repro duced wit h perm ission from S mith J., Gr eaves I.and Po rter K., Oxford Desk Reference: Major
Trau ma, Figu re8.11, p.132, Cop yrig ht © 2010 with pe rmission f rom Oxfor d Univers ityPress .
ASSESSM ENT OF HEAD INJURIES
Assessment ofhead injuries
History
The following are important and should be determined in allcases:
• When it occurred.
• Mechanism of injury— suddenly stopping (a deceleration injury) will
transfer more energ y to the brain than a stationar y person struck by
a moving object (an acceleration injury).
• Loss of consciousness or seizure— any delayed loss of consciousness
implies complications are developing. With children, was a cry heard
immediately? This reduces the likelihood that there was loss of
consciousness.
• Progression of symptoms since injury.
• Alcohol or druguse.
• PMH.
• Medications, especially anticoagulants.
• Preceding headache or other symptoms such as collapse leading to
afall.
• Period of retrograde or antegrade post- traumatic amnesia.
• Other injuries.
Examination
• Airway, breathing, and circulation status.
• Always consider cervical spine injur y with airway assessment.
• Glasgow ComaScale.
• Pupil responses:unequal but reactive pupils occur in 20% of normal
individuals. Adilated unreactive pupil is usually on the side of a mass
lesion (a true localizing sign). The usual sequence is initial pupillary
constriction as CN III is irritated followed by dilatation as a palsy
occurs.
• Focal neurology:cranial ner ve and limbs. Ahemiparesis can be
caused by a mass lesion pressing on the opposite motor cor tex, or a
mass on the same side compressing the opposite cerebral peduncle
against the edge of the tentorium (Kernohan’s notch). Thus, a
hemiparesis does not help in determining the side of a mass lesion
and is considered a false localizingsign.
• Local signs of injury:
•
CSF rhinorrhoea or otorrhoea, bleeding from the ear:an open
(compound) skull base fracture.
•
Battle’s sign (bruising over the mastoid):a fractured petrousbone.
•
Panda eyes or periorbital haematoma (well- circumscribed
periorbital bruising):an anterior fossa skull base fracture.
•
Scalp lacerations, abrasions, swelling.
• Examination for other injuries:this should be repeated when the
patient has been st abilized (not ably neck/ scalp/ facial/ ocular).
Investigations
CT scanning is the mainstay of imaging in head trauma. Of ten the cer vical spine is imaged simultaneously a s there is a 5% risk of cer vical spine
fracture with a serious head injur y. Today, skull X- rays have little role in
current investigation of head injuries.
75
76
CHAP TER3 Thehead
Classification and common types
ofhead (brain) injuries
Head injuries are usually classied for management, epidemiological, and
research purposes into minor, moderate, and severe, based upon the
GCSscore.
cConcussion
This is a temporary disturbance in brain function following relatively
minor head injuries. Macroscopically, the brain structure remains undamaged. Typic ally the pat ient is ‘kno cked out’ for several minutes. Prolonged
episodes of unconsciousness are rare. In any event, the patient rapidly
wakes up and makes a full recovery. So long as there are no other complicating medical or social factor s such patients can go home providing they
can be carefully observed. They should avoid a second concussion/ head
injury (if due to sports). Documented advice should be provided, including risks of complications and when they might need to return. ‘Return to
play’ protocols are now widely used in contact sports.
fIntracranial haematomas
The risk of harbouring an intracranial haematoma is related to the
patient’s level of consciousness and the presence of a skull frac ture. One
of sever al dierent types of haematoma might develop.
fCerebral contusions and haematomas
In cerebral contusions, blood is interspersed between the neurons and
glia, whereas with cerebral haematomas, the bleeding forms a cavity
within the brain. However, cerebral contusions can enlarge and result in
a haematoma (Figure3.6).
Contusions often occur at the poles of the brain due to a contrecoup
injury, i.e. the contusion is in an area of the brain opposite the site of
impact. These can be associated with marked oedema and a greatly
raised ICP. Contusions are usually treated conservatively, but a lobectomy (or evacuation of an intracerebr al haematoma) can be performed if
the ICP cannot be controlled.
fExtradural haematomas
Extradural haematomas are usually associated with a skull fracture or
suture diastasis. The commonest site is temporal, due to a tear of the
middle meningeal artery, but they can also occur in the frontal and occipital regions. They are rare in young children, as the skull fractures are
not sharp enough to damage the ar ter y, and in the elderly, as the dura
is usually adherent to the skull. They classically present with delayed
deterioration due to the dura being only slowly stripped from the skull.
However, only a minority of patients are completely asymptomatic during this ‘lucid interval’.
Extradural haematomas are biconvex (lens) shaped on CT scans and
are mostly high density (Figure 3.7). Low- density areas within them are
due to active bleeding.
CLA SSIFICATION AND TYPES OF HEAD INJU RIES
Figure3.6 Intracerebral haematoma.
77
Figure3.7 Extradural haematoma.