Neurology: Emergencies Flashcards
State some examples of neurological emergencies
- Raised ICP
- SAH
- Meningitis
- Encephalitis
- Status epilepticus
- Acute stroke
- Spinal cord compression or cauda equina
- Head trauma
- Temporal arteritis
- Acute bulbar palsy
Remind yourself of the GCS
GCS is a universal assessment tool for assessing level of consciousness. Looks at 3 components; eye, verbal and motor response. Minimum score of 3, maximum score of 15.
Eyes
- Spontaneous = 4
- Speech = 3
- Pain = 2
- None = 1
Verbal response
- Orientated = 5
- Confused conversation = 4
- Inappropriate words = 3
- Incomprehensible sounds = 2
- None = 1
Motor response
- Obeys commands = 6
- Localises pain = 5
- Normal flexion = 4
- Abnormal flexion = 3
- Extends = 2
- None = 1
At what GCS score, would you need to consider securing someone’s airway because they are not able to maintain it on their won
8 or below
State some potential causes of raised ICP
- idiopathic intracranial hypertension
- traumatic head injuries
- infection
- meningitis
- tumours
- hydrocephalus
Describe typical presentation of raised ICP
- headache
- vomiting
- reduced levels of consciousness
- papilloedema
- Cushing’s triad
- widening pulse pressure
- bradycardia
- irregular breathing
Describe the pathophysiology behind Cushing’s triad
- Increased ICP activates the Cushing reflex, a nervous system response resulting in Cushing’s triad.
- As the ICP begins to increase, it eventually becomes greater than the mean arterial pressure, which typically must be greater than the ICP in order for the brain tissue to be adequately oxygenated.
- The difference in pressure causes a decrease in the cerebral perfusion pressure (CPP), or the amount of blood and oxygen the brain is receiving, therefore leading to the brain not receiving enough oxygen (also known as a brain ischemia).
- To compensate for the lack of oxygen, the sympathetic nervous system is activated, causing an increase in systemic blood pressure and an initial increase in heart rate.
- The increased blood pressure then signals the carotid and aortic baroreceptors to activate the parasympathetic nervous system, causing the heart rate to decrease.
- As the pressure in the brain continues to rise, the brain stem may start to dysfunction, resulting in irregular respirations followed by periods where breathing ceases completely. This progression is indicative of a worsening prognosis.
What investigations & monitoring may be done if you suspect raised ICP?
- CT/MRI head: investigation underlying cause
- Invasive ICP monitoring (catheter placed in lateral ventricles to monitor pressure. Can also use to take CSF samples and to drain small amounts of CSF to reduce pressure)
Discuss the management of raised ICP
- Investigate and treat the underlying cause
- Nurse with 30º head elevation
- IV mannitol may be used as an osmotic diuretic
-
Controlled hyperventilation
- aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
- leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain
-
Removal of CSF, techniques include:
- drain from intraventricular monitor
- repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
- ventriculoperitoneal shunt (for hydrocephalus)
State some risk factors, generally, for intracranial haemorrhages
- Head injury
- Hypertension
- Aneurysms
- Ischaemic stroke can progress to haemorrhage
- Brain tumours
- Anticoagulants such as warfarin
How may intracranial haemorrhages present?
- Sudden onset headache
- Seizures
- Weakness
- Vomiting
- Reduced consciousness
- Other sudden onset neurological symptoms
Remind yourself of the following for subdural haemorrhages:
- Pathophysiology
- Who common in
- Appearance on CT head
- Management of acute subdurals
- Management of chronic subdurals (symptomatic and asymptomatic)
- Rupture of bridging veins- blood accumulates between dura and arachnoid matter. *Bridging veins allow cerebral veins in SA space to drain into dural venous sinuses by traversing the subdural space
- Elderly (atrophy of brains puts tension on vessels so more likely to rupture)
- Crescent/banana shape on CT (falx cerebri stops it spreading to other hemisphere)
- Mx acute:
- Small or incidental finding → observed
- Surgical options → decompressive craniectomy
- Mx chronic:
- Small or incidental finding with no neurological deficit → observation
- Large or associated neurological deficit → surgical decompression with burr holes
**Image shows acute haemorrhage (blood is white), in chronic blood will be black
Remind yourself of the following for extradural haemorrhages:
- Pathophysiology
- Typical presentation
- Appearance on CT head
- Usually due to rupture of middle meningeal artery in pterion region (temporo-parietal region) causing accumulation of blood between skull and periosteal dura
- Presentation:
- Hx of traumatic head injury
- Headache
- Lucid interval (period of improved consciousness & neurological symptoms followed by rapid decline)
- Bi-convex, lemon shaped haematoma (as limited by sutures)
**Pterion region where the frontal, parietal, temporal, and sphenoid bones join. It is located on the side of the skull, just behind the temple.
How would intracerebral haemorrhages present?
Potential causes?
- Present similarly to ischaemic stroke
- Cause:
- Spontaneous
- Tumour
- Bleeding into ischaemic infarct
- Rupture of aneurysm
NOTE: intracerebral haemorrhagescan be anywhere in the brain tissue:
- Lobar intracerebral haemorrhage
- Deep intracerebral haemorrhage
- Intraventricular haemorrhage
- Basal ganglia haemorrhage
- Cerebellar haemorrhage
Outline general principles of management of intracranial haemorrhages
*NOTE: separate FC for management of SAH
- Immediate CT head to establish the diagnosis
- Check FBC and clotting
- Admit to a specialist stroke unit
- Discuss with a specialist neurosurgical centre to consider surgical treatment (craniotomy & evacuation of haematoma)
- Consider intubation, ventilation and ICU care if they have reduced consciousness
- Correct any clotting abnormality
- Correct severe hypertension but avoid hypotension
**NOTE: in pts with extradural haemorrhage and no neurological deficit cautious clinical and radiological observation is appropriate
Remind yourself of pathophysiology of subarachnoid haemorrhage- include the most common cause
- Bleeding into the subarachnoid space, between pia mater and arachnoid
- Most common cause is head injury (termed traumatic SAH)
- In absence of trauma (termed spontaneous SAH) may be due rupture of saccular ‘berry’ aneurysm (~80%), AV malformation, arterial dissection etc…
State some risk factors for subarachnoid haemorrhages
- Hypertension
- Smoking
- Excessive alcohol consumption
- Cocaine use
- Sickle cell anaemia
- ADPKD
- Connective tissue disorders e.g. Marfan’s, Ehlers-Danlos
- Neurofibromatosis
- Family history
- Black ethnicity
- Female aged 55yrs and over
Describe typical presentation of subarachnoid haemorrhage
- Thunderclap headache (sudden onset of very severe headache that rapidly reaches maximum intensity)
- Neck stiffness
- Photophobia
- Vision changes
- Neurological symptoms such as speech changes, weakness, seizures and loss of consciousness
What investigations would you do if you suspect subarachnoid haemorrhage?
- First line: non-contrast CT head
- Lumbar puncture (generally used if CT head negative)
- Angiography (CT or MRI) can be used once SAH is confirmed to locate source of bleeding
What might you find on CT head of subarachnoid haemorrhage?
- Blood in basal cisterns (star-like pattern), sulci & potentially ventricular system
- See as hyper attenuation/hyperdense/bright
*NOTE: CT may be negative in 7% cases
What might you find on LP of someone with subarachnoid haemorrhage?
- Xanthochromia (**yellowish discoloration of the supernatant of a centrifuged CSF that contains bilirubin)
- Raised red cell count (if cell count decreasing over number of samples may be due to traumatic LP)
- Normal or raised opening pressure
Explain why giant cell arteritis can cause visual loss
If vasculitis is severe it can occlude the vessel (occlusive arteritis) and cause anterior ischaemic optic neuropathy and acute visual loss
State what you might find on clinical examination of someone with giant cell arteritis
*Might not necessarily be any examination findings
- Superficial temporal artery tenderness, thickening or nodularity
- Absent temporal artery pulse
- Tenderness over temporal area
- Abnormal fundoscopy
What sign do you see on duplex ultrasound of temporal artery in giant cell arteritis?
Hypoechoic halo sign
State the red flags for:
- Cauda equina
- Infection
- Fracture
- Malignancy/metastatic disease
Cauda Equina
- Back pain
- Bilateral sciatica
- Neurological deficit of legs e.g. motor weakness
- Saddle anaesthesia
- Painless urinary retention
- Erectile dysfunction
- Faecal & urinary incontinence (decreased anal tone)
Infection
- Immunsupression
- IV drug use
- Unexplained fever
- Diabetes
- TB or recent UTI
Fracture
- Significant trauma
- Osteoporosis or metabolic bone disease
- Chronic steroid use (oral steroids =/3 months)
Malignancy/metastatic disease
- History of malignancy
- New onset over 50yrs
- Night pain that disturbs sleep (suggest pain not mechanical/not due to axial loading as pain occuring when supine and spine is not loaded)
*NOTE: be concerned about age <18yrs and >55yrs. Be concerned about thoracic pain as thoracic spine is least mobile so unlikely to be mechanical.
What scale is used for neurologic classification of spinal cord injury?
ASIA impairment scale (American Spinal Injury Association Impairment Scale). Divides spinal cord injuries into 5 categories:
- Complete
- Incomplete sensory
- Incomplete motor (muscle grade below 3)
- Incomplete motor (muscle grade 3 or above)
- Normal
For Brown-Sequard syndrome, discuss:
- What it is
- Tracts affected
- Presentation
- Injury to half of spine (hemi section of spinal cord)
- Tracts affected on one side:
- Lateral corticospinal tract
- Dorsal columns
- Lateral spinothalamic tract
- Presentation:
- Ipsilateral motor loss at and below lesion
- Ipsilateral segmental anaesthesia
- Ipsilateral loss of DC modalities (proprioception, vibration, fine touch, two point discrimination) below lesion
- Contralateral loss of ST modalities (crude touch, pain, temperature) below lesion
For subacute combined degeneration of the spinal cord, discuss:
- What it is
- Tracts affected
- Presentation/clinical features
- A neurological complication of vitamin B12 deficiency. It is characterized by degeneration of the posterior and lateral spinal cord due to demyelination
-
Tracts affected:
- Dorsal columns
- Lateral corticospinal tracts
- Spinocerebellar tracts
- Presentation/features:
- Bilateral paralysis
- Bilateral loss of DC modalities (proprioception, vibration, fine touch, two point discrimination)
- Bilateral limb ataxia
What is acute bulbar palsy?
State some causes of bulbar palsy
State some symptoms & signs of bulbar palsy
What is the focus of management?
- Bulbar palsy is a set of signs and symptoms due to impaired function of lower cranial nerves (CNIX, CNX, CNXI, CNXII); hence acute bulbar palsy is short duration of these symptoms
- Causes:
- Brainstem strokes
- Brainstem tumours
- Motor neurone disease
- Gillian-Barre
- See image for symptoms
- Focus of management is treating symptoms
*NOTE: pseudobulbar palsy is due to damage to UMNs. Similar symptoms but pseudobulbar palsy characterised by atypical expression of emotion (usually unusual outbursts of laughing or crying)
What would you see on CT head if there was a brain abscess?
Ring enhancing lesion
