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Y4 NSS > Neuro emergencies > Flashcards

Neuro emergencies Flashcards

1
Q

Why is raised ICP so damaging in neuro?

A

brain and ventricles enclosed by rigid skull - limited ability to accommodate additional volume → raised ICP

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2
Q

What is the normal ICP?

A

7-15 mmHg in supine position

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3
Q

What is the calculation for cerebral perfusion pressure?

A

*net pressure gradient causing cerebral blood flow to the brain

CPP = mean arterial pressure - ICP

  • hence when ICP rises CPP drops
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4
Q

What are some causes of raised ICP?

A
  • idiopathic intracranial hypertension
  • traumatic head injuries
  • infection - meningitis
  • tumours
  • hydrocephalus
  • Reye’s syndrome
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5
Q

How might raised ICP present?

A
  • headache - worse on bending forwards, coughing etc
  • vomiting
  • reduced levels of conciousness
  • papilloedema

*Cushing’s triad

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6
Q

What is the Cushing’s triad?

A
  • widening pulse pressure
  • bradycardia
  • irregular breathing
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7
Q

How might suspected raised ICP be investigated?

A
  • neuroimaging: CT, MRI
  • invasive ICP monitoring: catheter into lateral ventricles
  • blood glucose, renal function, electrolytes and osmolality
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8
Q

What are the indications and contraindications for ICP monitoring?

A

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

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9
Q

How would you manage raised ICP?

A

investigate cause
head elevation to 30 degrees
IV mannitol as osmotic diuretic
controlled hyperventilation
remove CSF - ventriculoperitoneal shunt

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10
Q

How does controlled hyperventilation help with raised ICP ?

A
  • 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
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11
Q

Where does subarachnoid haemorrhages occur?

A

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

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12
Q

What are some risk factors for an SAH?

A
  • 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
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13
Q

How would an SAH present?

A

“thunderclap headache” - sudden onset, occipital during strenuous activity
- meningism
- neuro sx - visual changes, dysphasia, focal weakness, seizures, reduced consciousness

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14
Q

How would you investigate a SAH?

A

CT head - hyperattenuation around circle of willis
LP - at least 12h after onset, bilirubin, RBC in CSF
CT angiography

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15
Q

Would a normal CT exclude a SAH?

A

normal CT doesn’t exclude as less reliable more than 6h after onset

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16
Q

How is a SAH managed?

A

*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

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17
Q

What are some complications of SAH?

A

re-bleeding, hydrocephalus, vasospasms, electrolyte disturbances, hyponatraemia

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18
Q

What is status epilepticus?

A

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
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19
Q

How would you manage status epilepticus?

A
  • 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
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20
Q

What is a stroke?

A

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

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21
Q

What is a TIA?

A

🧠 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
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22
Q

What are risk factors of stroke?

A
  • 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
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23
Q

What is the presentation of stroke?

A
  • sudden onset - vascular causes
  • asymmetrical
  • limb weakness
  • dysphasia
  • visual field defects
  • sensory loss
  • ataxia and vertigo - posterior circulation infarction
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24
Q

What are the investigations done in suspected stroke?

A
  • FAST
    • face, arm, speech, time (999)
  • Rosier tool
  • exclude hypoglycaemia
  • immediate CT brain to exclude haemorrhage
    underlying cause
  • ECG or ambulatory ECG
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25
Q

What is the initial management for stroke?

A
  • 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
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26
Q

What is the guidance for managing BP in ischaemic stroke?

A

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

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27
Q

What is the longterm managements of strokes?

A

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
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28
Q

What is the aetiology of spinal cord compression?

A
  • trauma
  • prolapsed intervertebral disc
  • atlantoaxial subluxation (RA complication)
  • infection - TB spine infiltration POTTS, ischitis (bacteraemia in IVDU)
  • bony metastases
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29
Q

What is the presentation of SCC? (excluding caudal equina)

A
  • 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)
30
Q

What causes caudal equina?

A
  • 2% of herniated lumbar discs
  • commonly prolapse of L4/5 or L5/S1
  • or other cord compressions like tumours, abscess, trauma
31
Q

How does caudal equina present?

A

b/L sciatica
leg weakness
urinary retention painless
urinary and faecal incontinence
decreased anal tone

32
Q

What are the metastatic diseases most likely to present with back pain and risk of SCC?

A

5B : breast, bronchus, byroid, bidney, brostate

33
Q

What investigates spinal cord compression investigations?

A

examine
emergency spinal MRI + CT pyelogram in contraindicated

34
Q

How would you manage SCC?

A
  • surgical decompression within 48h of onset as BASS
  • some non-surgical
    • mets → radiotherapy
    • ank. spond → steroids
    • infective discitis → antibiotics long term
35
Q

What is temporal arteritis?

A

systemic vasculitis affecting the medium and large arteries which can complicate into vision loss

36
Q

How does temporal arteritis lead to vision loss?

A

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

37
Q

How does temporal arteritis present?

A
  • 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
38
Q

What are some associated features of temporal arteritis?

A
  • PMR - shoulder and pelvic girdle stiffness and pain
  • systemic - WL, fatigue, low grade fever
  • muscle tenderness
  • carpal tunnel
  • peripheral oedema
39
Q

How is temporal arteritis diagnosed?

A
  • clinical presentation
  • raised inflammatory markers - ESR (>50)
  • temporal artery biopsy - multinucleated giant cells
  • duplex ultrasound - hypoechoic “halo” sign and stenosis of temporal artery
40
Q

How is GCA managed?

A

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

41
Q

What are some complications of GCA?

A
  • steroid related complications - weight gain, DM, osteoporosis
  • visual loss
  • cerebrovascular accident - stroke
42
Q

What is the Monro-kellie hypothesis?

A
  • 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
43
Q

What is the Cushing’s reflex?

A

🧠 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)
44
Q

What are the two types of brain injury?

A
  • 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
45
Q

How might head injuries present?

A
  • 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 #
46
Q

How might head injuries be investigated?

A
  • 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
47
Q

How might head injuries be managed?

A
  • 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
48
Q

What are some complications of head injuries?

A
  • 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’
49
Q

What is the pathophysiology of meningitis?

A
  • 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
50
Q

What are some late signs of meningitis?

A
  • 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
51
Q

What are some common signs of meningitis?

A
  • fever, neck stiffness and altered mental state
  • early - vague headache, N+V, lethargy, joint pains, ‘flu-like’
52
Q

How is meningitis investigated?

A
  • 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
53
Q

How would you manage meningitis?

A
  • 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)
54
Q

What is acute bulbar palsy?

A

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

55
Q

What is the pathophysiology of bulbar palsy?

A

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

56
Q

What is pseudo-bulbar palsy?

A

*UMN damage
atypical outbursts of emotions, absent facial emotions, exaggerated jaw jerk

57
Q

How does acute bulbar palsy present?

A
  • 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
58
Q

How is bulbar palsy managed?

A
  • analyse CSF - rule out MS
  • MRI - stroke or tumour

*no treatment, supportive
- medications for secretions, feeding support, SALT
- condition specific mx

59
Q

How would you differentiate between encephalitis and meningitis?

A

inflammation of brain parenchyma in encephalitis and preserved brain function in meningitis

60
Q

What are the common causative organisms of encephalitis?

A
  • HSV
  • arbovirus, rabies, TB and varicella zoster
  • non infectious - immune mediated in cancer, following infection
61
Q

How does encephalitis present?

A
  • non specific - irritability, altered personality, drowsiness, confusion
  • fever and headache
  • rapid neuro deficit
  • seizures
  • meningism

signs

  • focal neurology, cranial nerve palsies
  • disrupted breathing
62
Q

How does rabies present?

A
  • aching pain at infection site
  • facial spasms initiated by deep breaths or drinking - hydrophobia
  • myocarditis
  • ascending paralysis
63
Q

How is encephalitis investigated?

A
  • LP and CSF - viral PCR, RBC, WBC
  • CT head - lesions in temporal lobe
  • electroencephalogram
  • brain biopsy
64
Q

How is encephalitis managed?

A
  • HSV - acyclovir
  • rabies - no cure, protective vaccine, wound care and immunisation effective
  • manage sx
65
Q

What is ARDS?

A

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

66
Q

How does ARDS present?

A
  • 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
67
Q

How is ARDS investigated?

A
  • resp exam
  • bloods - infection
  • oxygen levels
  • ABG
  • CXR
  • CT
  • ECG or echo
  • bronchoscopy
68
Q

How is ARDS managed?

A

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

69
Q

How would you examine depressed consciousness?

A
  • general survey
  • neuro exam
  • GCS
  • brain stem reflexes
  • meningeal signs
  • motor response to pain
  • tendon reflexes
  • plantar response
  • pupil response
  • fundoscopy
70
Q

How is depressed consciousness investigated?

A
  • 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

Y4 NSS (11 decks)

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