Neurology: Emergencies Flashcards
(52 cards)
1
Q
State some examples of neurological emergencies
A
- Raised ICP
- SAH
- Meningitis
- Encephalitis
- Status epilepticus
- Acute stroke
- Spinal cord compression or cauda equina
- Head trauma
- Temporal arteritis
- Acute bulbar palsy
2
Q
Remind yourself of the GCS
A
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
3
Q
At what GCS score, would you need to consider securing someone’s airway because they are not able to maintain it on their won
A
8 or below
4
Q
State some potential causes of raised ICP
A
- idiopathic intracranial hypertension
- traumatic head injuries
- infection
- meningitis
- tumours
- hydrocephalus
5
Q
Describe typical presentation of raised ICP
A
- headache
- vomiting
- reduced levels of consciousness
- papilloedema
- Cushing’s triad
- widening pulse pressure
- bradycardia
- irregular breathing
6
Q
Describe the pathophysiology behind Cushing’s triad
A
- 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.
7
Q
What investigations & monitoring may be done if you suspect raised ICP?
A
- 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)
8
Q
Discuss the management of raised ICP
A
- 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)
9
Q
State some risk factors, generally, for intracranial haemorrhages
A
- Head injury
- Hypertension
- Aneurysms
- Ischaemic stroke can progress to haemorrhage
- Brain tumours
- Anticoagulants such as warfarin
10
Q
How may intracranial haemorrhages present?
A
- Sudden onset headache
- Seizures
- Weakness
- Vomiting
- Reduced consciousness
- Other sudden onset neurological symptoms
11
Q
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)
A
- 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
12
Q
Remind yourself of the following for extradural haemorrhages:
- Pathophysiology
- Typical presentation
- Appearance on CT head
A
- 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.
13
Q
How would intracerebral haemorrhages present?
Potential causes?
A
- 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
14
Q
Outline general principles of management of intracranial haemorrhages
*NOTE: separate FC for management of SAH
A
- 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
15
Q
Remind yourself of pathophysiology of subarachnoid haemorrhage- include the most common cause
A
- 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…
16
Q
State some risk factors for subarachnoid haemorrhages
A
- 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
17
Q
Describe typical presentation of subarachnoid haemorrhage
A
- 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
18
Q
What investigations would you do if you suspect subarachnoid haemorrhage?
A
- 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
19
Q
What might you find on CT head of subarachnoid haemorrhage?
A
- 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
20
Q
What might you find on LP of someone with subarachnoid haemorrhage?
A
- 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
21
Q
Discuss the management of subarachnoid haemorrhage, think about:
- Where should be managed and by who
- What care they need
- Pharmacological management
- Surgical management
A
Where should be managed and by who
- Need to be managed by specialist neurosurgical unit hence URGENT referral to neurosurgery once confirmed
- MDT management (SALT, dietician, physiotherapist, occupational therapy in both early stages and recovery)
Pharmacological management
- Nimodipine to prevent vasospasm (a common complication that can result in brain ischaemia following SAH)
- Antiepileptic medications to treat seizures
- Analgesia for pain
Surgical management
- Aneurysm can be treated with surgery, ideally within 24hrs due to risk of re-bleeding. Whilst waiting for surgery should be on strict bed rest with well-controlled BP and avoidance of straining. Surgical options include:
- Coil via endovascular approach- put platinum coils in aneurysm to seal it off from artery (most common)
- Clipping- requires craniotomy to clip aneurysm (stops blood flow to aneurysm)
- Hydrocephalus can be temporarily treated with external ventricular drain. Long term solution is ventriculo-peritoneal shunt
What care they may need
- May need intubation & ventilation
- Supportive care (e.g. fluids, catheters etc..)
22
Q
State some potential complications of SAH
A
-
Re-bleeding
- happens in around 10% of cases and most common in the first 12 hours
- if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
- associated with a high mortality (up to 70%)
- Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
- Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
- Seizures
- Hydrocephalus
- Death
23
Q
Discuss the prognosis of subarachnoid haemorrhages
A
High morbidity & mortality
“At 6 months after SAH, more than 25% of patients are dead and up to half of the survivors are moderately to severely disabled” BMJ best practice
24
Q
What is giant cell arteritis?
A
Systemic, chronic, granulomatous vasculitis of medium & large arteries; typically presents with symptoms affecting the temporal arteries (hence also known as temporal arteritis)
25
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
26
State some risk factors for giant cell arteritis
* **Age \>50yrs**
* Female
* Strong association with polymyagia rheumatica (~50%)
27
State some symptoms of giant cell arteritis
* Main presenting feature is **headache**:
* **Severe**
* **Unilateral**
* **Around temple & forehead**
* Scalp tenderness when brushing hair
* Jaw claudication
* Blurred or double vision *(potential complication is irreversible painless complete sight loss- amaurosis fugax)*
* Associated systemic symptoms
* Fever
* Fatigue
* Muscle aches
* Weight loss, loss of appetite
* Peripheral oedema
28
What is meant by jaw or tongue claudication?
Pain or weakness in the muscles of mastication that begins just after the onset of chewing and is relieved by rest
29
Explain why giant cell arteritis can cause jaw claudication
* Inflammation of arteries supply muscles of mastication
* Inflammation/vascualitis causes thickening of wall of artery and occludes lumen
* Ischaemia of muscles
30
Giant cell arteritis may present as a CVA; true or false?
True
31
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
32
What investigations would you do if you suspect giant cell arteritis, include:
* Bedside
* Bloods
* Imaging
* Other
*\*Where appropriate justify why we do each investigation/what it may show*
_Bedside_
_Bloods_
* **ESR:** *usually 50mm/hour*
* **CRP:** *elevated*
* **FBC:** *normocytic anaemia, thrombocytosis*
* **LFTs:** *raised ALP*
_Imaging_
* **Duplex ultrasound of temporal:** *may show thickening ("hypoechoic halo"), stenosis or occlusion*
_Other_
* **Biopsy:** *biopsy revealing necrotizing arteritis and in 50% there are multinucleated giant cells*
33
What do you find on/in the biopsy of giant cell arteritis?
* Necrotizing arteritis
* 50% show multinucleated giant cells
*\*NOTE: can be skip lesions hence biopsy can produce false negative result*
34
State some potential complications of giant cell arteritis, think about early & late complications
_Early_
* Visual loss
* Stroke
_Late_
* Relapse of condition
* Steroid related side effects & complications
* Stroke
* Aortitis leading to aortic aneurysm & dissection
35
What sign do you see on duplex ultrasound of temporal artery in giant cell arteritis?
Hypoechoic halo sign
36
What is a definitive diagnosis of giant cell arteritis based on? (3)
Presence of _2 or more in pt who are \>50yrs:_
* New onset of localised headache
* Raised ESR *(usuallyy 50mm/hour or more)*
* Tenderness or decreased pulsation of temporal artery
* New visual symptoms
* Temporal artery biopsy findings
*\*NOTE: **DO NOT delay** initiation of steroid therapy to await biopsy if strong clinical suspicion or visual changes are reported*
37
Discuss the management of giant cell arteritis
_Initial Management_
* **Steroids**
* ****60-100mg oral prednisolone daily *(for at least 2 weeks. This will be slowly tapered down over period of 12-18 months)*
* Or 1g IV methylprednisolone pulse therapy if visual symptoms
* **Consider aspirin oral 75mg daily** *(reduce thrombotic risk-visual loss & stroke.*
* For those at risk of gastric ulceration, **PPI** *(gastric protection)*
* For those at risk of osteoporosis, **bisphosphonates +/- calcium +/- vit D** *(dependent on if intake adequete)*
* **Refer to:**
* ****Vascular surgeons- biopsy
* Rheumatology- specialist diagnosis & management
* Ophthalmology review same day if they develop visual symptoms
38
If you are giving a pt steroids there are additional measures you must consider; these can be remembered by "**D**ON'T **STOP**"; state these measures
* Don't stop taking steroids abruptly
* Sick day rules
* Treatment card
* Osteoporosis prevention with bisphosphonates and supplemental calcium & vitamin D
* PPI for gastric protection? (not always needed)
39
If pt is \<55yrs what arteritis should you consider?
State a few facts about this arteritis (not one you need to know in detail- it is rare outside Japan)
* Takayasu's arteritits (aortic arch syndrome)
* Systemic vasculitis which affects aorta & its major branches
* Granulomatous inflammation
* Results in stenosis, thrombus & aneuryseums
* Women 20-40yrs
* Symptoms depend on arteries involve- but think about symptoms related to artery occlusion. Also have systemic symptoms as in GCA
* Diagnosis: raised ESR and CRP, MRI/PET scan
* Treat with steroids and vascular surgery if required
40
State some potential causes of radiculopathy
Most commonly a result of nerve compression which can be due to:
* **Intervertebral disc prolapse** *(lumbar spine most common)*
* **Degenerative diseases of spine which lead to neuroforaminal or spinal canal stenosis** *(cervical spine most common as it is most mobile)*
* **Fracture** *(trauma or pathological)*
* **Malignancy** *(most commonly metastatic)*
* **Infection** *(e.g. extradural abscesses, osteomyelitis, herpes zoster)*
41
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.*
42
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
43
# Define cauda equina syndrome
What age group is cauda equina syndrome common in?
What is most common cause of CES?
What investigation would you do?
What is the mangement?
* Compression of the lumbosacral nerve roots that extend below the spinal cord (cauda equina) are compressed
* 30-50yrs
* Most commonly caused by central disc prolapse (typically L4/L5 or L5/S1) but others include tumours, infection, trauma, haematoma
* Urgent MRI spine
* Emergency surgical decompression within 24-48hrs of onset of sphincter symptoms through laminectomy or discectomy
44
State some potential complications of cauda equina *(and suggest how we can help pts to manage these complications)*
* **Motor weakness dependent on which nerves affected- not necesarily paralysis!** E.g. if L4/L5: L3 and L4 intact
* **Bladder & bowel incontinence** *(Can't feel bladder filling so get pt to intermittently self-catheterise to empty bladder. Or indwelling suprapubic catheter. Empty bowels by clock, colonic lavage, colostomy)*
* **Sexual dysfunction**
45
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
46
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
47
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)*
48
State some potential sources of infection/causes of brain abscesses
* Middle ear
* Sinuses
* Trauma (to scalp/head)
* Surgery (to scalp/head)
* Penetrating brain injuries
* Embolic events from infective endocarditis
49
Describe presentation of brain abscesses
* headache (typical raised ICP headache)
* fever
* may be absent and usually not the swinging pyrexia seen with abscesses at other sites
* focal neurology
* e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure
* Will depend on site of abscess
* other features consistent with raised intracranial pressure
* nausea
* papilloedema
* seizures
50
What investigations would you do for suspected brain abscess?
**Main investigation is CT head**
FBC
CRP
?Blood cultures
Other usual bloods
51
What would you see on CT head if there was a brain abscess?
Ring enhancing lesion
52
Discuss the management of brain abscesses
Need urgent neurosurgical referral. In meantime:
* Treat ICP (e.g. nurse 30 tilt, controlled hyperventilation, dexamethasone, control BP etc…)
* IV abx (e.g. 3rd generation cephalosporin + metronidazole)
Definitive management is surgery for debridement of abscess
