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CHAP TER3 Thehead
The prognosis is ver y good if they are treated early enough. Very small
extradural haematomas with minimal symptoms can often be left alone
(although they should be discussed with the local neurosurgicalunit).
fAcute subdural haematomas
Acute subdur al haematomas may occur due to tearing of bridging veins
between the brain and skull. In such cases the prognosis is good with
prompt treatment. Alternatively a laceration of the brain surface (burst
lobe) may occur. This has a worse prognosis. There need not be a skull
fracture with subdur al haematomas. They are more common than extradural haematomas and can extend over a wide area of the lateral cortical
surface. They are crescent shaped on CT scans as the blood follows the
surface of the brain (Figure3.8).
Thin acute subdural haematomas can be treated conservatively with
close observation, but signicant ones need a craniotomy as the clotted
blood is too viscous to drain via burrholes.
cChronic subdural haematomas
Chronic subdural haematoma s are thought to be due to minor venous
bleeding following a minor head injur y several weeks previously. The
head injur y is often so trivial that it cannot be remembered in 50% of
cases. They usually occur in the elderly who have a degree of brain atrophy and stretching of the bridging cortical veins, but can also occur in
babies due to non- accidental injuries. They are of ten associated with
coagulopathies and alcohol excess.
Chronic subdural haematoma s can cause a wide variety of symp toms, including headaches, reduced consciousness, and focal neurology.
Therefore, consider this diagnosis in all elderly patients with intermittent
Figure3. 8 Acute subdural haematoma.
HEAD INJURIES:INITIAL MANAGEMENT
confusion or transient ischaemic attack (TIA)- like symptoms after trauma.
Chronic subdural haematoma s can be treated by bur r hole drainage as
the blood is liquid. They have a good prognosis but might recur, especially with a persistent coagulopathy.
fPenetrating headinjury
A penetrating head injury is an open injur y in which the dura mater has
been breached. These are often caused by high- velocity projectiles but
can also occur from objects such as knives, or bone fragments from an
overlying skull fracture. Penetr ating injuries are similar to closed head
injuries (such as contusion or ICH) but have an increased incidence of
infection. Haemorrhage may be harder to control. Initial management
is the same as closed injuries although antibiotics should also begiven.
Take care if exploring penetrating or open head wounds overlying a skull
fracture, especially those in the midline. This can result in massive blood loss
if a venous sinus has beentorn.
Head injuries:initial management
cScalp lacerations
Scalp lacerations should be thoroughly cleansed and closed urgently, in
two layers if possible. The use of tissue glue may be acceptable for small
lacerations. The possibility of foreign bodies or an underlying fracture
should be considered and imaging may be necessary to conrm this.
Also remember anti- tetanus prophyla xis. Scalp sutures can usually be
removed after 7 days. Haemorrhage can be signicant from these and
can result in haemodynamic instabilit y if neglected.
Potentially signicant head injuries
Observations should be performed hourly initially, and half- hourly in
higher- risk patients. Make sure the nur sing sta know when to call for
a medical review. Most patients can be discharged the following day if
asymptomatic. Stable patients who need longer admission can have their
observation frequency reduced to 2- hourly. Patients not admitted should
receive written guidelines of when to return to hospital and should only be
discharged with a responsible adult who can call for a ssistance if required.
Transferring patients
• Fully resuscitate in all patients before transfer— this may include
a laparotomy/ pelvic xation etc. to stop bleeding as per ATLS®
protocol.
• Intubate and ventilate comatose patients.
• If patients are being transferred for observation only, avoid intubation
and sedation if safe to do so (discuss with neurosurgeons). This allows
their conscious level to be assessed.
• Rapidly reverse anticoagulant medication to prevent further bleeding.
• IV mannitol can be given to buy time by reducing ICP. Maximum dose
is 1 g/ k g— in a 70kg adult, this is 350 mL of 20% mannitol.
• Hyper tonic saline is also increasingly used to reduce ICP, but always
seek advice from ICU/ neurosurgery before prescribing.
• Transfer promptly with an experienced anaesthetist.
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eHead injuries inchildren
These can be dicult to assess. Many of the clinical features which
would lead to concern in adults are often present, even following minor
injuries (vomiting, drowsy, headaches, etc.). An infant can become haemo dynamically unstable due to bleeding into a scalp haematoma. Consider
the mechanism of injury, other injuries present, and whether the parents
are capable of taking the child home for close observations. Interpretation
of skull X- rays can be dicult as large fractures may be confused with wide
sutures or vascular markings. If in doubt, refer or admit. Non- accidental
injury is the second most common cause of ICH in a child. This should be
considered if the history is inconsistent with the mechanism of injury, or
if the child has had multiple attendances with injuries at dierent hospitals. Retinal haemorrhages, multiple old fractures, and cigarette burns are
othersigns.
Otherissues
Post- concussion headache
This may have features of a tension- type headache but is often associated
with dizziness and loss of concentration.
Driving
A signicant head injur y will often result in a restriction from driving for
at least 6months.
CSFleaks
CSF can leak from the nose (rhinorrhoea) or from the ear (otorrhoea).
Clear CSF tends to mix with blood and presents as a heavily bloodstained, water y discharge. This trickles down the side of the face, where
peripher ally the blood tends to clot while the non- clotted blood in the
centre is washed away by CSF. This creates two parallel lines referred
to as ‘tramlining’. One bedside test for CS F is the ‘ring test’ (allow drops
to fall on blotting paper:blood clots centrally, and the CSF diuses outwards to form a t arget sign). Tell the patient not to blow their nose for
3 weeks. If they do, the increased pressure can force air intracranially
through the tear, which then cannot escape. This is the neurosurgical
equivalent of a tension pneumothorax and results in tension pneumocephalus. CSF should test positive for glucose. Bet a- 2 tr ansferrin is a
more specic test forCSF.
Post- traumatic seizures
Risk factors include intracerebral haematoma, open depressed fractures
with dural laceration, and focal neurologicalsigns.
cHeadache
Headache is a symptom, not a diagnosis. It can arise from a number of
dierent conditions involving the head, neck, and beyond. These include
the periosteum of the skull, muscles, ner ves, arteries and veins, subcutaneous tissues, eyes, ears, sinuses, and mucous membranes. There are
a number of dierent classication systems for headaches. Auseful one
is from the International Headache Society. Treatment of a headache
depends on the underlying cause. Take headaches seriously. Although
CLASSIFICATION OF HEADACHES
most cases are benign and self- limiting, a few are due to serious pathology. The key is awareness of important causes and eliminating them
from the dierential diagnosis clinically and by investigation.
Some useful facts indiagnosing headaches
• Headache may not necessarily be a symptom of head patholog y.
Consider also the eyes (glaucoma), TMJs (TMJ dysfunction
syndrome), sinuses (infection/ tumours), neck (degenerative
conditions), and systemic conditions such as hypertension and giant
cell arteritis.
• Pain in the cheek, orbit, or forehead can occur with migraine.
• Unilateral headache is characteristic of classic migraine or cluster
headache. The latter is usually frontotemporal, around the eye,
orcheek.
• Bilateral pain over the forehead or temples which can aect the
vertex, occiput, or eyes would be seen in tension headache.
Worrying features witha headache
• Associatedfever
• Sudden onset
• Late onset (new headache in over50s)
• Nausea or vomiting
• Sti neck/ photophobia
• Changes in personality or mental function/ neurological decit
• Change in usual pattern of headache/ present onwaking
• Pain that increases with coughing or movement
• Headaches becoming steadilyworse
• Associated painful red eye/ pain and tenderness near the temples
• Headaches in patient s with cancer or impaired immune systems.
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Headaches persisting for longer than 6 weeks with abnormal physical signs
should be thoroughly investigated, including:
• FBC with ESR (to exclude temporal ar teritis).
• CXR for bronchial carcinoma.
• CT or MRI brain to exclude space - occupying lesion.
Classification ofheadaches
The International Classication of Headache Disorders (ICHD) is a useful guide to the causes of headache and is accepted by the World Health
Organization. It contains diagnostic criteria. Several groups are listed.
Primary headaches
These are the most common types and include tension- type headache
and migraine. They have typical features. Rarer types include cluster
headache (severe pains that occur in bouts), and hemicrania continua
(a continuous headache on one side of thehead).
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Secondary headaches
These are classied based on their aetiolog y and not symptoms. There
are more than 200 types. Causes include:
• Head or necktrauma
• ICH:
•
SAH
• Post craniotomy
• Ischaemic strokeorTIA
• Vascular malformations
• Arteritis:
•
Temporal arteritis
• Cerebral venous thrombosis:
•
Cavernous sinus or sagittal sinus thrombosis
• Low or high pressures of the CSF pressure:
•
Hydrocephalus
•
Benign/ idiopathic intracranial hypertension
•
Post- LP headache
• Non- infectious inammatory disease
• Intracranial neoplasm
• Substance ingestion or it s withdrawal
• Intracranial infections:meningitis, brain abscess, subdural empyema
• Systemic infections
• Dialysis
• HighBP
• Fasting
• Injury to facial structures including teeth, jaws, orTMJ.
This list is not complete but illustrates the diverse nature and potential
seriousness of any patient you may encounter who has a headache. In the
absence of identiable pathology, management of headache is the treatment of its symptoms. Analgesia is often the initial treatment.
Assessing a patient witha headache
Ask about the following:
Character
• Severe, pulsatile headache is typical of common migr aine.
• Throbbing, sharp, headache is described in classic migraine.
• Stabbing or burning pain is described in cluster headache.
• Pressure, or a ‘band- like’ tightness that varies in intensit y, frequency,
and duration is consistent with tension headache.
Timing
Headaches that are worst on wakening are typical of r aised ICP. It can
also occur with caeine withdrawal.
Duration
Headaches at night for 1– 3 weeks are features of cluster headaches.
HEADACHES:ASSOCIATED SYMPTOMS
Exacerbating or precipitating factors
• Straining, coughing, or sneezing can worsen headaches associated with
raised ICP. Cough impulse headache is common in Chiar i malformation.
• Stress, diet (chocolate, cheese, red wine), hor monal state (pre-
menstrual, oral contraceptive pill), emotions, and barometric changes
are associated with migr aine. Caeine withdr awal can cause severe
symptoms, which are quickly relieved by ingestion of caeine.
Onset
Sudden- onset headache is often termed thunderclap headache. The
most concerning cause of this isaSAH.
Preceding symptoms
• Flu- like illness can precede temporal arteritis.
• Impending sense of ill health is a feature of classic migr aine.
• Visual aura can precede migraine.
Other associated factors
Family history
Often seen in migraine.
Age
Temporal arteritis is seen in patient s over 60. Migr aine is more often
seen in puberty.
Gender
Females are more likely to have SAH, migraine, venous sinus thrombosis,
and tension headache; men tend to get cluster headaches.
Associated medical problems
Depression and anxiet y often relate to tension headache; smoking and
hyper tension are risk factors for SAH and stroke. Pregnancy predisposes
to thrombosis or pre- eclampsia.
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Headaches:associated symptoms
Reduced level ofconsciousness
This is concer ning when it is associated with a headache. It may reect
raised ICP. Urgent investigation and treatment are required. SAH, ICH,
tumour, or intracranial infection are all possible diagnoses.
Visual disturbance
• Sudden irreversible loss of sight may occur within week s of the onset
of temporal arteritis. Often the presenting feature is of a visual
eld disturbance, which becomes progressively worse. Blindness
is thought to occur as a result of ischaemic optic neuritis caused by
arteritis of the ophthalmic arteries. Cavernous sinus thrombosis can
also cause loss of vision as can pituitar y apoplex y.
• Visual aura, such as ashing lights, are a feature of classic migraine.
• Loss of visual acuity or eld constriction can be a feature of raised
ICP and benign/ idiopathic intracranial hypertension.
• Ophthalmoplegia can occur in pituitary apoplexy, cavernous sinus
thrombosis, or in a cavernous carotid stula.
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Nausea and vomiting
These are often present in migraine but are seen with raisedICP.
Autonomic symptoms
Such as rhinorrhoea, unilateral nasal obstruction, a red eye (conjunctival
injection), and lacrimation. These are often seen in trigeminal autonomic
cephalalgias.
Photophobia
This is often seen in classic migraine but if seen with thunderclap headache, SAH must be considered. It also occurs in meningitis.
Neck stiness
This can be due to meningism in meningitis andSAH.
Focal neurological decit
Such as dysphasia , hemiparesis, or sensory disturbance, in association
with a headache is a concerning nding. Abrain tumour, SAH, or a stroke
could be the cause. However, some migraines can cause temporar y
hemiparesis or hemisensoryloss.
Jaw claudication
Pain on chewing due to temporal ar teritis of the facial artery (rare).
Seizures
May be seen in brain tumours, SAH, or intracranial infec tion.
Systemic symptoms
Weight loss, ar thr algia, and fever can occur in temporal arteritis.
eIntracranial infections
eMeningitis
Patients with meningitis can deteriorate extremely rapidly, so immediate attention is necessary. Consider this in any irritable child with a non-
blanching petechial rash. Meningitis is inammation of the linings of the
brain and spinal cord (the meninges) with infection of the CSF. Most frequently, the pathogen is vir al and may var y with age and social environment. Bacterial pathogens need urgent treatment.
Bacterial pathogens inmeningitis
Neonatal
• Streptococcus (groupB)
• Escherichiacoli
• Listeria monocytogenes.
Children (<14years ofage)
• Neisseria meningitidis
• Streptococcus pneumoniae
• Haemophilus inuenzae.
INTRACRANIAL INFECTIONS
Adults
• Neisseria meningitidis
• Streptococcus pneumoniae.
Clinical features
• Pyrexia
• Tachycardia/ tachypnoea/ shock
• Headache
• Photophobia
• Irritability
• Seizures
• Vomiting
• Neck stiness
• Positive Kernig’s sign (a strong sign of meningeal irritation)— pain
occurs with attempts at passive knee extension with the hips
fullyexed
• Maculopapular rash (meningococcal meningitis)
• Deteriorating conscious level in latecases.
Management
• Resuscitation, IV uids.
• Antibiotics should be given as soon as the diagnosis is suspected
and continued until the CSF WCC is nor mal. Discuss choice with
microbiologist/ neurologist.
• Take throat swabs and blood for polymerase chain reaction(PCR).
• Blood cultures.
• CT scan to determine safety of LP and rule out other pathology.
• LP for CSF analysis.
• Contact tracing (local public health department)— for single
cases treat close contacts only (‘kissing contacts’). Usual
regimens:r ifampicin 600 mg twice daily for 2days, ciprooxacin
500 mg singledose.
eSubdural empyema
Most cases of subdural empyema are secondar y to sinusitis or middle
ear infection. Patients initially present with an illness similar to meningitis, but can develop a hemiparesis due to cor tical venous thrombosis.
Seizures are common.
Investigations and management
This should follow the same pathway as for meningitis, but a LP should
be avoided due to the risk of coning. A CT scan will usually show a thin
subdural collection, and pus can accumulate along the falx. The size of
the collections is much less than with symptomatic chronic subdural
haematomas.
Patients should be resuscitated and referred for prompt neurosurgical
drainage of the pus, usually via a craniotomy. Eorts should be made to
look for a source of infection and to treat it accordingly. Investigations
such as an echocardiogram may be required.
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CHAP TER3 Thehead
eBrain abscess
Sinusitis and middle ear infec tions are com mon causes of b rain abscesses,
following direct spread intracranially. Haematogenous spread of infection
can also occur. Well- recognized causes include infective endocarditis and
dental caries. However, in some cases the cause is never determined.
Clinical features
• Headache
• Vomiting
• Focal neurology
• Epilepticts
• Deteriorating conscious level in latecases
• Pyrexia is of ten absent .
Investigations
• The WCC and CRP are of ten normal.
• CT scans show a ring- enhancing lesion with surrounding oedema.
In contrast to gliomas, abscesses are usually per fec tly circular with a
wall of unifor m thickness. Abscesses may be multiple.
• MRI—diusion-weighted sequence can help dierentiate from other
pathology, such as tumour.
• LP should not be performed due to the risk of coning.
The diagnosis is usually suspected on the basis of an enhancing circular
lesion on a CT scan of a patient with an infection elsewhere.
Management
Patients should be referred for prompt neurosurgical drainage. If their
consciousness is deteriorating, patients should be fully resuscitated and
consider administering steroids and mannitol prior to transfer.
eEncephalitis
This is an acute inammation of the brain and has both infective and
non- infective causes. Encephalitis which is associated with meningitis is
referred to as meningoencephalitis. Herpes simplex virus, poliovirus,
and measles virus are common pathogens. Others rare types of encephalitis include Japanese encephalitis and equine encephalitis. Bacterial
encephalitis may occur following spread of meningitis. Parasitic or protozoal infestations, such as toxoplasmosis, malaria, or amoebic infection, can also cause encephalitis. Cryptococcus neoformans causes fungal
encephalitis in immunocompromised patients.
Clinical features
Whatever the cause, common symptoms include:
• Headache
• Fever
• Confusion
• Drowsiness, and fatigue
• Seizures, tremors, hallucinations, and memory problems may
indicate advanced disease.
INTRACRANIAL BLEEDING (NON-TRAUMATIC)
Children or infants may present with non- specic symptoms such as irritability, drowsiness, andfever.
Always check for a sti neck— this indicates meningitis or meningoencephalitis.
Investigations
• CT scan is initially under taken to exclude brain swelling. If there is no
swelling a LP can be undertaken.
• CSF analysis usually shows increased amount s of protein and white
blood cells with normal glucose. Specic diagnosis is made with
detection of antibodies onPCR .
• Serological tests may show high antibody titres.
Management
• Patient s should be resuscitated and referred urgently. Supportive
treatment (IV uids/ sedation/ mechanical ventilation) may be
required.
• Antiviral agents (e.g. aciclovir for herpes simplex virus).
• Corticosteroids may be used to reduce brain swelling but this is
controversial in the presence of infection.
eIntracranial bleeding (non- traumatic)
eSubarachnoid haemorrhage
Aetiology ofspontaneousSAH
• 80% are from intracr anial saccular (Berr y) aneurysm. These
often remain asymptomatic and are found in 2– 3% of routine
post- mortems.
• 15% have no identiablecause
• 5% from other causes (e.g.AVM).
Up to 50% of aneurysmal SAH patients die within a month of the initial
bleed. Untreated, the re- bleed rate over the rst month approaches 50%
and 80% of these patients die or become dependent. It is therefore vital
not to delay the diagnosis, as patients are at risk of re- bleeding anddeath.
The risk of re- bleeding in AVMs is much less at around 6% in the rst
year and 3% for each subsequent year, so treatment can often be delayed.
Clinical features
• ‘Thunderclap’ headache— a sudden, severe occipital headache
radiating over the head and down theneck
• Impaired consciouslevel
• Neck stiness
• Photophobia
• Nausea or vomiting
• Seizure.
Unfor tunately ‘thunderclap’ is a non- specic symptom and less than 25%
of patients presenting with this symptom will actually have a SAH. The
dierential diagnosis is wide. All patients with a sudden- onset headache
should therefore be investigated for SAH, even if the headache has eased
within a fewhours.
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