Emergency Neuro Presentations Flashcards
As the brain and ventricles are enclosed by a rigid skull, they have a limited ability to accommodate additional volume. Additional volume (e.g. haematoma, tumour, excessive CSF) will therefore lead to a rise in intracranial pressure (ICP).
What is normal range for ICP?
7-15 mmHg in adults in the supine position
What is cerebral perfusion pressure?
cerebral perfusion pressure (CPP) is the net pressure gradient causing cerebral blood flow to the brain
CPP = mean arterial pressure - ICP
What causes raised intracranial pressure?
idiopathic intracranial hypertension
traumatic head injuries
infection e.g. meningitis
tumours
hydrocephalus
What features may raised ICP present with?
headache
vomiting
reduced levels of consciousness
papilloedema
Cushing’s triad
What is Cushing’s triad of raised ICP?
widening pulse pressure
bradycardia
irregular breathing
How can raised ICP be investigated?
neuroimaging : CT/MRI
invasive ICP monitoring:
catheter placed into the lateral ventricles of the brain to monitor the pressure
may also be used to take collect CSF samples / drain CSF
a cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP
What is the initial management of raised ICP?
investigate and treat the underlying cause
head elevation to 30º
IV mannitol may be used as an osmotic diuretic
controlled hyperventilation
removal of CSF
What is the purpose of controlled hyperventilation in the mx of raised ICP?
aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
leads to rapid, temporary lowering of ICP
caution needed as may reduce blood flow to already ischaemic parts of the brain
What are the methods for removing excess CSF?
drain from intraventricular monitor
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)
What are the 4 different types of intracranial haemorrhage?
Extradural haemorrhage (bleeding between the skull and dura mater)
Subdural haemorrhage (bleeding between the dura mater and arachnoid mater)
Subarachnoid haemorrhage (bleeding in the subarachnoid space)
Intracerebral haemorrhage (bleeding into brain tissue)
What is a subarachnoid haemorrhage?
bleeding in the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane
very high mortality (around 30%) and morbidity
may be traumatic or spontaneous
What are the causes of spontaneous subarachnoid haemorrhage?
intracranial aneurysm (saccular ‘berry’ aneurysms): 85% of cases
associated with hypertension, adult PCKD, Ehlers-Danlos and coarctation of the aorta
arteriovenous malformation
pituitary apoplexy
mycotic (infective) aneurysms
In which patient group are subarachnoid haemorrhages more common?
Aged 45 to 70
Women
Black ethnic origin
Give some risk factors for subarachnoid haemorrhage
Family Hx
Hypertension
Smoking and alcohol
Cocaine use
Sickle cell anaemia
Connective tissue disorders (e.g., Marfan syndrome or Ehlers-Danlos syndrome)
Neurofibromatosis
Autosomal dominant polycystic kidney disease
How does subarachnoid haemorrhage typically present?
sudden onset occipital ‘ thunderclap’ headache
often comes on during strenuous activity, such as heavy lifting or sex
nausea and vomiting
meningism (photophobia, neck stiffness)
seizures
coma
ECG changes including ST elevation may be seen
How should a suspected subarachnoid haemorrhage be investigated?
non-contrast CT head is the first-line investigation of choice : blood appears hyperdense/bright on CT
if CT head is done within 6 hours of symptom onset and is normal: do NOT do lumbar puncture
consider an alternative diagnosis
if CT head is done more than 6 hours after symptom onset and is normal: do a lumber puncture (LP) to confirm / exclude diagnosis
SAH seen on CT / confirmed on LP:
CT angiography is used after confirming the diagnosis to locate the source of the bleeding
What findings would you expect on an LP for a patient with SAH?
Raised red cell count (a decreasing red cell count on successive bottles may be due to a traumatic procedure)
Xanthochromia (a yellow colour to the CSF caused by bilirubin)
How can you manage subarachnoid haemorrhage?
bed rest, analgesia
oral nimodipine to prevent vasopasm
discontinuation of antithrombotics (reversal of anticoagulation if present)
intracranial aneurysms require prompt intervention (within 24 hours):
most treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
What are the complications of aneurysmal SAH?
re-bleeding
hydrocephalus
hyponatraemia
ventriculoperitoneal shunt
vasospasm (also termed delayed cerebral ischaemia)
seizures
What is the risk of rebleeding after aneurysmal SAH?
How should it be managed?
happens in 10% of cases
most common in the first 12 hours
if rebleeding is suspected then a repeat CT should be arranged
associated with a high mortality (up to 70%)
Hydrocephalus refers to increased cerebrospinal fluid, causing expansion of the ventricles.
Treatment options include:
Lumbar puncture
External ventricular drain (a drain inserted into the brain ventricles to drain CSF)
Ventriculoperitoneal (VP) shunt (a catheter connecting the ventricles with the peritoneal cavity)
When does vasopasm most commonly present post SAH?
How should it be managed?
also termed delayed cerebral ischaemia, typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist (e.g. vasopressin, adrenaline, noradrenaline)
Which are the most important prognostic factors in SAH?
conscious level on admission
age
amount of blood visible on CT head
Meningitis is defined as inflammation of the meninges (lining of the brain and spinal cord).
What are the common causative organisms?
How does it present?
Neisseria meningitidis and Streptococcus pneumoniae
GBS in neonates
Presentation:
fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures
meningococcal septicaemia = non-blanching rash
How may meningitis present differently in neonates?
Neonates and babies can present with very non-specific signs and symptoms
poor feeding, lethargy, hypotonia, hypothermia and a bulging fontanelle
What are the common causes of meningitis in the 0-3 month age group?
Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes
What are the common causes of meningitis in the 3 month - 6 year age group?
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
What are the common causes of meningitis in the 6 - 60 year age group?
Neisseria meningitidis
Streptococcus pneumoniae
> 60 age group are more at risk of meningitis caused by which organism?
Listeria monocytogenes
What are the 2 special tests that you can use to assess for meningeal irritation?
Both tests create a slight stretch in the meninges
Kernig’s test:
lying the patient on their back, flexing one hip to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees.
+ve = spinal pain or resistance to movement
Brudzinski’s test :
lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest
+ve = patient involuntarily flexes their hips and knees
How do bacterial v viral meningitis present on an LP?
(consider appearance, protein, glucose, WCC and culture)
Appearance
Cloudy V Clear
Protein
High V Normal
Glucose
Low V Normal
White Cell Count
Neutrophils V Lymphocytes
Culture
Bacteria Present V Negative
What is the pre-hospital mx of suspected bacterial meningitis?
IM benzylpenicillin urgently
How can meningitis be investigated?
Bloods:
FBC, CRP, U&Es
glucose
lactate
clotting profile
Additional tests that may be helpful include:
blood gases
throat swab for meningococcal culture
Consider LP + CSF analysis
When should a LP not be performed for suspected bacterial meningitis?
signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
How should patients with suspected bacterial meningitis and no contraindications to LP be managed?
IV access → take bloods and blood cultures
Lumbar puncture to confirm dx
IV antibiotics
3 months - 50 years: ceftriaxone (or cefotaxime)
> 50 years: ceftriaxone + amoxicillin
IV dexamethasone
avoid dexamethasone in septic shock, meningococcal septicaemia, or if immunocompromised
CT scan is not normally indicated
When an LP is taken for suspected bacterial meningitis, what should the CSF be tested for?
glucose, protein, microscopy and culture
lactate
meningococcal and pneumococcal PCR
enteroviral, herpes simplex and varicella-zoster PCR
consider investigations for TB meningitis
How should patients with suspected bacterial meningitis and signs of raised ICP be managed?
get critical care input
secure airway + high-flow oxygen
IV access → take bloods and blood cultures
IV dexamethasone alongside abx (cefotaxime +/- amoxicillin)
Arrange neuroimaging
How should patients with suspected bacterial meningitis and sepsis / rapidly evolving rash be managed?
get critical care input
secure airway + high-flow oxygen
IV access → take bloods and blood cultures
IV fluid resuscitation
IV antibiotics (cefotaxime +/- amoxicillin)
What should be offered to household members and close contacts of an individual with confirmed bacterial meningitis?
oral ciprofloxacin or rifampicin prophylaxis if they have have contact with the individual in the 7 days before sx onset
Viral meningitis is more benign condition than bacterial meningitis and is much more common.
What can cause it?
non-polio enteroviruses e.g. coxsackie virus, echovirus
mumps, measles
herpes simplex virus (HSV), cytomegalovirus (CMV), herpes zoster viruses
HIV
What are the risk factors for developing viral meningitis?
patients at the extremes of age (< 5 years and the elderly)
immunocompromised, e.g. patients with renal failure, with diabetes
intravenous drug users
How can viral meningitis be managed?
If there is any question of bacterial meningitis while waiting for LP results the patient should be commenced on broad-spectrum abx with CNS penetration e.g. ceftriaxone and aciclovir IV
viral meningitis is generally self-limiting, with symptoms improving over the course of 7 - 14 days and complications are rare in immunocompetent patients
aciclovir may be used if the patient is suspected of having meningitis secondary to HSV
What complications may arise as a result of meningitis?
sensorineural hearing loss (most common)
seizures
focal neurological deficit
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus
Patients with meningococcal meningitis are at risk of developing what condition?
Waterhouse-Friderichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage)
Encephalitis is inflammation of the brain tissue itself, that is primarily caused by HSV-1 in adults.
What features does it present with?
fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis
How can suspected encephalitis be investigated?
PCR for HSV, VZV and enteroviruses
CSF: high WCC and protein
MRI
medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
EEG
lateralised periodic discharges at 2 Hz
How can encephalitis be managed?
IV aciclovir
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral hemiparesis and sensory loss, lower extremity > upper
Anterior cerebral artery
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Middle cerebral artery
(MCA supplies Wernicke’s and Broca’s areas)
What is the likely site of the lesion for a stroke patient presenting with:
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Posterior cerebral artery
(PCA supplies area that contains visual cortex in the occipital lobe)
What is the likely site of the lesion for a stroke patient presenting with:
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
branches of the posterior cerebral artery that supply the midbrain - Weber’s syndrome
What is the likely site of the lesion for a stroke patient presenting with:
Ipsilateral: facial pain and temp loss
Contralateral: limb/torso pain and temp loss
Ataxia, nystagmus, double vision
Horner’s syndrome
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
What is shown here?
Extradural haematoma
Bleeding into the space between the dura mater and the skull
Most occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery
What is shown here?
What are the risk factors?
Subdural haematoma
Bleeding between the dura mater and the arachnoid mater
Risk factors include old age, alcoholism and anticoagulation
Slower onset of symptoms than a epidural haematoma, +/- fluctuating consciousness
What is shown here?
Subarachnoid haemorrhage
Give some signs of basal skull fracture
haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign
