Neuro emergencies Flashcards
Why is raised ICP so damaging in neuro?
brain and ventricles enclosed by rigid skull - limited ability to accommodate additional volume → raised ICP
What is the normal ICP?
7-15 mmHg in supine position
What is the calculation for cerebral perfusion pressure?
*net pressure gradient causing cerebral blood flow to the brain
CPP = mean arterial pressure - ICP
- hence when ICP rises CPP drops
What are some causes of raised ICP?
- idiopathic intracranial hypertension
- traumatic head injuries
- infection - meningitis
- tumours
- hydrocephalus
- Reye’s syndrome
How might raised ICP present?
- headache - worse on bending forwards, coughing etc
- vomiting
- reduced levels of conciousness
- papilloedema
*Cushing’s triad
What is the Cushing’s triad?
- widening pulse pressure
- bradycardia
- irregular breathing
How might suspected raised ICP be investigated?
- neuroimaging: CT, MRI
- invasive ICP monitoring: catheter into lateral ventricles
- blood glucose, renal function, electrolytes and osmolality
What are the indications and contraindications for ICP monitoring?
traumatic brain injury (TBI), hydrocephalus or conditions at high risk of developing hydrocephalus (e.g. space-occupying lesions or subarachnoid haemorrhage), idiopathic intracranial hypertension, or Reye’s syndrome
*contraindications - coagulopathies or anti-coagulation medication, scalp infections, or brain abscess
How would you manage raised ICP?
investigate cause
head elevation to 30 degrees
IV mannitol as osmotic diuretic
controlled hyperventilation
remove CSF - ventriculoperitoneal shunt
How does controlled hyperventilation help with raised ICP ?
- aim to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
- leads to rapid, temporary lowering of ICP so caution as may reduce blood flow to already ischaemic parts of brain
Where does subarachnoid haemorrhages occur?
bleeding in the subarachnoid space, where CSF is located between pia mater and arachnoid membrane - usually as a result of a ruptured cerebral aneurysm
*trauma, AVM, coagulopathies, tumour related
What are some risk factors for an SAH?
- aneurysmal - family history, cocaine use, sickle cell anaemia, connective tissue disorders like marfans and Ehlers-danlos, neurofibromatosis, ADPKD
- aged 45-70
- women
- black ethnic origin
- HTN
- smoking
- excessive alcohol intake
How would an SAH present?
“thunderclap headache” - sudden onset, occipital during strenuous activity
- meningism
- neuro sx - visual changes, dysphasia, focal weakness, seizures, reduced consciousness
How would you investigate a SAH?
CT head - hyperattenuation around circle of willis
LP - at least 12h after onset, bilirubin, RBC in CSF
CT angiography
Would a normal CT exclude a SAH?
normal CT doesn’t exclude as less reliable more than 6h after onset
How is a SAH managed?
*in specialist neuro unit
intubation and ventilation
surgical - repair vessel and prevent re-bleeding
- endovascular coiling, neurosurgical clipping
- Nimodipine - prevent vasospasm
- manage complications
- prophylactic levetiracetam to reduce seizure risk
What are some complications of SAH?
re-bleeding, hydrocephalus, vasospasms, electrolyte disturbances, hyponatraemia
What is status epilepticus?
medical emergency, with priority of seizure termination as otherwise lead to irreversible brain damage
- single seizure lasting >5 minutes
- ≥2 seizures within 5 min period without person returning to baseline
How would you manage status epilepticus?
- ABC
- IV lorazepam first line, PR diazepam or buccal midazolam
- repeat 5-10 min
- second line: levetiracetam, phenytoin, sodium valproate
- if refractory within 45 min GA or phenobarbital
What is a stroke?
clinical syndrome of presumed vascular origin characterised by rapidly developing signs of focal or global disturbance of cerebral functions which lasts longer than 24 hours or leads to death –> ischaemic or haemorrhagic
What is a TIA?
🧠 temporary neurological dysfunction, typically resolving symptoms within less than 1 hour, causing ischaemia without infarction
- rapid onset, may precede stroke
- crescendo TIAs are two or more TIAs within a week - indicate high risk of stroke
What are risk factors of stroke?
- previous TIA
- AF
- carotid artery stenosis
- hypertension
- diabetes
- raised cholesterol
- FHx
- smoking
- obesity
- vasculitis
- thrombophilia
- COCP - higher in patients for those with migraines with aura, smokers >34, Hx of stroke or TIA
What is the presentation of stroke?
- sudden onset - vascular causes
- asymmetrical
- limb weakness
- dysphasia
- visual field defects
- sensory loss
- ataxia and vertigo - posterior circulation infarction
What are the investigations done in suspected stroke?
- FAST
- face, arm, speech, time (999)
- Rosier tool
- exclude hypoglycaemia
- immediate CT brain to exclude haemorrhage
underlying cause - ECG or ambulatory ECG
What is the initial management for stroke?
- exclude hypoglycaemia
- immediate CT brain to exclude haemorrhage
- aspiring daily 300mg after exclusion of ^^
- admission to specialist stroke centre
- thrombolysis with alteplase
- tissue plasminogen activator to break clots after exclusion of bleed
- thrombectomy - confirmed blockage of proximal anterior circulation or proximal posterior circulation
- anticoagulation for AF after excluding bleed and finishing 2w of aspirin
- carotid stenosis - carotid endarterectomy, angioplasty and stenting
What is the guidance for managing BP in ischaemic stroke?
lowering BP can worsen ischaemia, so high BP only indicated in hypertensive emergency or to reduce risks when giving IV thrombolysis
*BP aggressively treated in pt with haemorrhagic stroke
What is the longterm managements of strokes?
secondary prevention
- clopidogrel, atorvastatin, BP and DM control, address modifiable RF
rehabilitation
- MDT - stroke physicians, nurses, SALT, dieticians, physio, OT, social services, optometry, ophthalmology, psychology, orthotics
What is the aetiology of spinal cord compression?
- trauma
- prolapsed intervertebral disc
- atlantoaxial subluxation (RA complication)
- infection - TB spine infiltration POTTS, ischitis (bacteraemia in IVDU)
- bony metastases
What is the presentation of SCC? (excluding caudal equina)
- above level of T1 or thoracic
- tetraplegia or quadraplegia
- below T1
- paraplegia
- significant
- can cause paralysis of affected limb
- partial
- paresis or parasthaesia (pain, numb, pins and needles)
What causes caudal equina?
- 2% of herniated lumbar discs
- commonly prolapse of L4/5 or L5/S1
- or other cord compressions like tumours, abscess, trauma
How does caudal equina present?
b/L sciatica
leg weakness
urinary retention painless
urinary and faecal incontinence
decreased anal tone
What are the metastatic diseases most likely to present with back pain and risk of SCC?
5B : breast, bronchus, byroid, bidney, brostate
What investigates spinal cord compression investigations?
examine
emergency spinal MRI + CT pyelogram in contraindicated
How would you manage SCC?
- surgical decompression within 48h of onset as BASS
- some non-surgical
- mets → radiotherapy
- ank. spond → steroids
- infective discitis → antibiotics long term
What is temporal arteritis?
systemic vasculitis affecting the medium and large arteries which can complicate into vision loss
How does temporal arteritis lead to vision loss?
vasculitic occlusion of medium-sized vessels supplying the optic nerve and the retina, profound and usually irreversible ischemia of the anterior optic nerve and the choroid
How does temporal arteritis present?
- unilateral headache - severe around the temple and forehead
- associated scalp tenderness - when brushing hair
- jaw claudication
- blurred or double vision
- loss of vision if untreated
- temporal artery - tender and thickened to palpation, reduced or absent pulsation
What are some associated features of temporal arteritis?
- PMR - shoulder and pelvic girdle stiffness and pain
- systemic - WL, fatigue, low grade fever
- muscle tenderness
- carpal tunnel
- peripheral oedema
How is temporal arteritis diagnosed?
- clinical presentation
- raised inflammatory markers - ESR (>50)
- temporal artery biopsy - multinucleated giant cells
- duplex ultrasound - hypoechoic “halo” sign and stenosis of temporal artery
How is GCA managed?
high dose prednisolone - weaned off 1-2 years
aspirin to decrease vision loss, stroke
PPI - gastro-protection with steroids
bisphosphnates and calcium and vitamin D
What are some complications of GCA?
- steroid related complications - weight gain, DM, osteoporosis
- visual loss
- cerebrovascular accident - stroke
What is the Monro-kellie hypothesis?
- skull is closed rigid box with fixed capacity holding brain tissue, CSF and blood
- when volume of one of these increases, to maintain constant ICP the volume of others must decrease → achieved through ‘compliance’
- once this compensatory mechanism is overwhelmed, a small increase in volume of any of the 3 can lead to dramatic increase in ICP
- leads to reduced cerebral perfusion, herniation of brainstem and death
What is the Cushing’s reflex?
🧠 physiological response to raised ICP which attempts to improve perfusion
- triad of hypertension (widened pulse pressure), bradycardia, irregular breathing pattern ‘Cheyne-stokes’ (as brainstem malfunctions)
What are the two types of brain injury?
- primary brain injury - initial injury to brain tissue, focal #, vessel injury, haematoma or diffuse contusion
- secondary - damage to tissue after primary, cerebral hypoxia, acidosis, hypoglycaemia, cerebral oedema → raised ICP
- other - expanding haematoma, increased metabolic demand eg: seizures
How might head injuries present?
- pain in area of trauma
- headache + raised ICP signs
- changes in hearing or vision
- memory loss
- dizziness
- raised ICP signs
- reduced GCS, focal neuro, eye signs
- basal #
How might head injuries be investigated?
- A-E, monitor
- GCS
- neuro exam - cranial nerves, power and sensation, cerebellar function
- blood glucose (4-5.8) - hypo <3
- CT head - intracranial bleeds, brain contusions, skull #, cerebral oedema
How might head injuries be managed?
- maintain airway
- opioid tox - reverse
- administer glucose
- reassess for shock etc
- bleeding management
- blood products
- large-bore IV access
- major haem protocol
- warm patient - hypothermia
- CPR if necessary
What are some complications of head injuries?
- increased ICP - herniation
- cerebellar tonsils through foramen magnum - compress brainstem and cause respiratory arrest - ‘coning’
- uncus of temporal lobe through tentorial notch - compress cranial nerve 3 leading to classical ‘blown pupil’
What is the pathophysiology of meningitis?
- viral more common - enteroviruses (echovirus, coxsackievirus), mumps, HSV, herpes zoster, HIV, measles, influenza
- neonates - group B strep, E.coli
- RF - low birth weight, prem, prem rupture of membranes
- anyone >3 - Neisseria meningitidis, streptococcus pneumoniae
What are some late signs of meningitis?
- bulging fontanelle
- neck stiffness or back rigidity
- Kernig’s sign - resistance on passive knee extension with hips fully flexed
- Brudzinski - knees and hips flex on bending the head forward
- non-blanching rash
- photophobia
- shock
- neuro - seizures, paresis, CN involvement
What are some common signs of meningitis?
- fever, neck stiffness and altered mental state
- early - vague headache, N+V, lethargy, joint pains, ‘flu-like’
How is meningitis investigated?
- U&E, CRP, FBC, Clotting, blood cultures, glucose, ABG, meningococcal PCR
- imaging - CT sometimes if mastoiditis suspected - cannot exclude raised ICP
- LP - within hour of arriving and before abx
- contraindicated in raised ICP signs, shock, extensive purpura, convulsions and coag abnormalities
- CSF check for glucose, protein, lactate and culture
How would you manage meningitis?
- bacterial - meningococcal suspected then IM benzylpenicillin ONLY if this will not delay transfer
- > 3m - IV ceftriaxone
- <3m - IV cefotaxime and amoxicillin (listeria cover)
- once organism confirmed - guidelines!
- IV dex in some
- prophylaxis - confirmed meningococcal give ciprofloxacin or rifampicin within 24h
- viral - no specific
- if encephalitis suspected IV aciclovir (HSV)
What is acute bulbar palsy?
set of signs and symptoms linked to the impaired function of the lower cranial nerves, damage to their lower motor neurons or the lower cranial nerve itself
What is the pathophysiology of bulbar palsy?
impacted nerves are those that arise straight from the brain stem - CN 9, 10, 11 and 12
*caused by brainstem strokes, tumours, amyotrophic lateral sclerosis, guillan-barre, Kennedy disease
What is pseudo-bulbar palsy?
*UMN damage
atypical outbursts of emotions, absent facial emotions, exaggerated jaw jerk
How does acute bulbar palsy present?
- glossopharyngeal
- dysphagia, reduced gag reflex
- others
- difficulty chewing, nasal regurgitation, slurred speech, aspiration of secretions, dysphonia, dysarthria
- nasal speech that lacks modulation
- difficulty with consonants, atrophic wasting tongue, drooling, weakness of jaw, facial muscles, normal or absent jaw jerk, absent gag reflex
How is bulbar palsy managed?
- analyse CSF - rule out MS
- MRI - stroke or tumour
*no treatment, supportive
- medications for secretions, feeding support, SALT
- condition specific mx
How would you differentiate between encephalitis and meningitis?
inflammation of brain parenchyma in encephalitis and preserved brain function in meningitis
What are the common causative organisms of encephalitis?
- HSV
- arbovirus, rabies, TB and varicella zoster
- non infectious - immune mediated in cancer, following infection
How does encephalitis present?
- non specific - irritability, altered personality, drowsiness, confusion
- fever and headache
- rapid neuro deficit
- seizures
- meningism
signs
- focal neurology, cranial nerve palsies
- disrupted breathing
How does rabies present?
- aching pain at infection site
- facial spasms initiated by deep breaths or drinking - hydrophobia
- myocarditis
- ascending paralysis
How is encephalitis investigated?
- LP and CSF - viral PCR, RBC, WBC
- CT head - lesions in temporal lobe
- electroencephalogram
- brain biopsy
How is encephalitis managed?
- HSV - acyclovir
- rabies - no cure, protective vaccine, wound care and immunisation effective
- manage sx
What is ARDS?
type of lung damage that can result from a variety of causes, including illness, trauma, or even as a complication that occurs following certain medical procedures
How does ARDS present?
- People typically experience extreme difficulty breathing and shortness of breath
- rapid, shallow breathing
- Low oxygen - confusion, dizziness, excessive sweating, low blood pressure, and rapid heart rate
- Some people may notice that their fingertips, lips, or skin take on a bluish hue
How is ARDS investigated?
- resp exam
- bloods - infection
- oxygen levels
- ABG
- CXR
- CT
- ECG or echo
- bronchoscopy
How is ARDS managed?
Oxygen and Ventilation
Medications to manage symptoms - diuretics to help clear away excess fluid buildup in the lungs, and pain medication to relieve discomfort
Treating underlying cause
Prone positioning
How would you examine depressed consciousness?
- general survey
- neuro exam
- GCS
- brain stem reflexes
- meningeal signs
- motor response to pain
- tendon reflexes
- plantar response
- pupil response
- fundoscopy
How is depressed consciousness investigated?
- biochem including glucose
- toxicology screen and alcohol
- known prescription drugs - epilepsy etc
- ammonia
- ABG
- imaging: non contrast CT for haemorrhage, infarctions or masses
- MRI if needed
- cerebrovascular imaging
- noninvasive angiogram for basilar artery
- venogram for venous thrombosis
- EEG
- lumbar puncture to exclude meningitis/ encephalitis
