8. Neurological Emergencies Flashcards

1
Q

What is RICP, its presentation, DDx and Mx?

A

S+S = seizures, lethargy, irritability, vomiting, neck stiffness, tinnitus, dizziness, paraesthesia, headache, sun setting sign, forehead veins, focal neurology

DDx = comp of neurological injury, hydrocephalus (impaired absorption), brain tumour, intracranial infections, hepatic encephalopathy, impaired CNS venous outflow

Mx = head positioned midline, head end tilted 20-30 degrees, isotonic fluid at 60% maintenance, intubation + ventilation if GCS >9, mannitol, maintain normothermia/BP

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2
Q

What is status epilepticus, its causes and presentation?

A

Seizures lasting more than 5 minutes or more than 3 seizures in one hour

S+S = tonic-clonic, tonic, clonic or myoclonic seizures, LOC

Causes =
- Intake of substance accidental/intentional, meds
- Infection = bacterial meningitis, encephalitis (travel - malaria)
- Hypoglycaemia = DM (insulin over use, illness), new-borns, metabolic disorders
- Febrile convulsion (common 6m-6y, generalised tonic-clonic short, swift recovery, complex/atypical) - usually triggered by the initial rise in temp
SOL = AV malformation, bleed, hypotensive encephalopathy, tumour
- Electrolyte abnormalities = hypoCa, hyperNa, hypoNa, hypoMg, hypoGly (SAIDH, fluid loss, Ca metabolism)
- Epilepsy = not associated with fever, but at higher risk of seizure when ill
- Vascular = stroke (MRI, MR angiogram)
- Cerebral hypoxia = significant resp/cardio failure
- Hepatic encephalopathy, renal encephalopathy, metabolic encephalopathy (mitochondrial)
- Congenital brain abnormalities
- Jaundice - kernicterus

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3
Q

Outline the Mx of status epilepticus

A

Acute = A-E (airway, oxygen, glucose), call for senior help, if airway compromised call ITU/anaesthetist

IV access - (if cant get consider rectal, buccal, IO)

  • Bloods (FBC, CRP, clotting, U+Es)
  • Cultures
  • VBG
  • Pabrinex = vitamins B1, B2, B3, B6, C (if alcoholism or malnutrition)

1) buccal midazolam

2) IV/IO lorazepam (1st line - quicker, less resp depression) after 10m repeat lorazepam
- IM midazolam 10mg

3) Phenytoin infusion over 20m (whilst waiting for the phenytoin to be prepared: can give rectal paraldehyde) even if the seizure has stopped continue entire dose
- consider airway: nasopharyngeal
3) Transfer to ICU - anaesthetist involvement (trial IV midazolam, RSI: rapid sequence induction, intubate and muscle relaxant)

Sepsis = start sepsis 6 (cefotaxime, ceftriaxone)
Meningitis = LP if can be performed quickly before Abx, if not then give Abx with no delay then LP later 
PICP = mannitol, furosemide

? cause = CT head, blood cultures, blood alcohol levels, examine for meningism, ?LP

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4
Q

Outline the aetiology of meningitis

A

0-3m = group B strep, e.coli, listeria

3m-6y = strep pneumonia, Neisseria meningitidis, H.influenza

6-60y = strep pneumonia, Neisseria meningitidis

> 60y = strep pneumonia, Neisseria meningitidis, listeria

Viral (2/3) = enterococcus, EBV, adenovirus, mumps

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5
Q

What are the signs and symptoms of meningitis?

A

Early:

  • Headache
  • Leg pains
  • Cold hands/feet
  • Abnormal skin colour
  • Fever

Later:

  • Meningism = stiff neck, photophobia
  • Kernigs sign (pain + resistance on passive knee extension with hip fully flexed)
  • Brudzinski’s sign = +ve when passive forward flexion of the neck causes involuntarily raising of knees or hips in flexion
  • Decreased conscious level, coma
  • Seizures
  • Petechial rash - non-blanching
  • Sepsis = slow cap refill, decreased BP, increased temp, increased pulse
  • Bulging fontanelle
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6
Q

How would you investigate meningitis?

A

Bloods = FBC, U+Es, LTF, glucose, coag (on LP don’t want the pt to bleed), BM

Blood cultures, throat swabs, rectal swabs

LP (do not perform in RICP) = CSF for microscopy, biochem, culture, PCR

CT head

CXR

VBG

Ophthalmoscopy

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7
Q

How would you manage meningitis?

A

A-E assessment

Dexamethasone 4-10mg/6h IV = reduced RICP/inflam

Start Abx

  • <3m = IV cefotaxime + oral amoxicillin
  • 3m-50y = IV cefotaxime
  • > 50y = IV cefotaxime + oral amoxicillin

Viral = 3w acyclovir

IV fluids

Isolate for 1st 24h

Careful monitoring

Household/close contacts = rifampicin or oral ciprofloxacin

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8
Q

Outline the pathophysiology of CES

A

Surgical emergency = compression of the corda equina (L2-5)

Peak onset between 40-50 years of age

Results in LMN signs and symptoms

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9
Q

Outline the aetiology of CES

A

Disc herniation = most common at L5/S1 and L4/L5 level

Trauma = vertebral fracture and subluxation

Neoplasm = either primary or metastatic (most common cancers that spread to spinal vertebrae are thyroid, breast, lung, renal and prostate)

Infection = discitis or Potts disease

Chronic spinal inflammation = ankylosing spondylitis

Iatrogenic = haematoma secondary to spinal anaesthesia

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10
Q

What are the symptoms of CES?

A

Reduced lower limb sensation (often bilateral)

Bladder or bowel dysfunction

Lower limb motor weakness

Severe back pain

Impotence

Perianal (the lower sacral dermatomes, termed “saddle” anaesthesia)

Lower limb anaesthesia

Loss of anal tone

Urinary retention

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11
Q

How would you investigate CES?

A

Whole spine MRI

Lower limb neurological exam

PR exam

Post-void bladder scan

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12
Q

How would you manage CES?

A

Urgent decompression

High-dose steroids (dexamethasone) = reduce any localised swelling

Malignancy = radiotherapy and/or chemotherapy can be used

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13
Q

What is GCA?

A

Chronic vasculitis of large/medium sized vessels - pts aged >50yrs

Most commonly causes inflam of arteries originating from the aortic arch

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14
Q

What are the signs and symptoms of GCA?

A

Headache - localised, unilateral, over the temple

Tongue/jaw claudication

Visual - amaurosis fugax, blindness, diplopia, blurring

Scalp tenderness - particularly over the temporal artery

POSSIBLE proximal weakness - GCA commonly presents alongside polymyalgia rheumatica (often affecting shoulders/hips)

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15
Q

How is a diagnosis of GCA made?

A

Presence of any 2 or more of the following in patients >50 years with:

  • Raised ESR, CRP or PV
  • New onset of localized headache
  • Tenderness or decreased pulsation of temporal artery
  • New visual symptoms
  • Temporal A biopsy: granulomatous inflam with skip lesions
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16
Q

How is GCA managed?

A

Prednisolone 60–100 mg PO per day for at least 2 weeks before considering tapering down slowly

For acute onset visual symptoms, consider 1g methylprednisolone IV pulse therapy for the 1–3 days

Low-dose aspirin therapy to reduce thrombotic risks

17
Q

What is subarachnoid haemorrhage?

A

Bleed between arachnoid and pia mater

Usually occur spontaneously – ruptured berry aneurysm (mainly found in the anterior cerebral circulation)

Middle aged group 40-60

Fills basal cisterns with blood

Ix =
- CT: focal areas, white basal cisterns

18
Q

How does a subarachnoid haemorrhage present?

A

Sudden onset ‘thunderclap’ headache

Meningism

N+V

Fever

Focal neurological deficits

LOC

19
Q

How are subarachnoid haemorrhages managed?

A

ITU

Prevent re-bleeding

Treat cerebral vasospasm

20
Q

Discuss a basilar skull fracture

A

Bony fracture within the base of skull (temporal, occipital, sphenoid, or ethmoid bone)

Pathophysiology = Trauma –> tears in the meninges –> CSF leakage.

Identify secondary injuries

Signs = raccoon eyes, CSF rhinorrhea, CSF otorrhea, battle sign, haemotympanum, bump

Management = elevation of depressed skull, CSF leak management, surgery, ICP control

21
Q

What indications warrant a CT head?

A

Consciousness <13

Seizure

Focal neurological deficit

Suspected skull fracture

2+ discrete episodes of vomiting

22
Q

Define diffuse axonal injury

A

Shearing of interface between grey and white matter following traumatic acceleration/deceleration or rotational injuries to the brain damaging the intra-cerebral axons and dendritic connections

Trauma –> shearing of grey and white matter interface –> axonal death –> cerebral oedema –> raised ICP –> Coma

23
Q

Outline the pathophysiology of concussion

A

Head injury with a temporary loss of brain function

Trauma –> Stretching and injury to axons –> impaired neurotransmission, loss of ion regulation, and a reduction in cerebral blood flow –> Temporary brain dysfunction

Damage to the reticular activating system = lose consciousness

24
Q

Outline acute respiratory distress

A

Ae = dementia, cerebrovascular disease, MND, myopathy, CNS disease (cervical myelopathy), lower brainstem injury, diffuse bihemispheric involvement, NMD

Path = direct brain injury, depressed level of consciousness and inability to protect the airway, disruption of natural defence barriers, decreased mobility, and secondary neurological insults

S+S = tachypnoea, SOB

Ix = CXR, O2 sats

Mx = oxygen

25
Q

Describe acute bulbar palsy

A

Range of different S+S linked to impairment of function of the CN 9, 10, 11, 12

Ae = medullary infarction, Guillain–Barré syndrome, poliomyelitis, Lyme disease, brain-stem glioma, malignant meningitis, botulism, myasthenia gravis

Path = LMN lesion in the medulla oblongata or from lesions of the lower CN outside the brainstem

S+S = dysphagia, diff chewing, nasal regurgitation, slurring of speech, diff handling secretions, aspiration, dysphonia, dysarthria

Ix = electromyography + Sx, CT/MRI

Mx = SALT, enteral feeding (aspiration), baclofen (spasticity), anticholinergics (drooling)