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Yr4 - Neuro + SS > Neurology Emergency > Flashcards

Neurology Emergency Flashcards

1
Q

Define Status Epilepticus

A

Recurrent seizures without recovering in between or a single seizure lasting more than 30 mins

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2
Q

Pathophysiology for status epilepticus

A

Mechanisms that abort seizure activity fail, either from excessive and abnormally persistent excitation, or ineffective inhibition
Accumulation of excitatory neurotransmitters (notably glutamate), hyperthermia, hypoxia, lactic acidosis and hypoglycaemia can cause cerebral injury

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3
Q

Presentation of status epilepticus

A

Types of seizures

  • generalised tonic-clonic or focal evolving tonic-clonic
  • focal aware motor
  • impaired awareness cognitive
  • absence
  • focal impaired awareness
  • focal aware
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4
Q

Ix for status eplipeticus

A

Anticonvulsant drug blood level
Toxicology screen
Comprehensive metabolic panel
FBC
- low platelets suggest intracranial bleed
- WCC indicates infection
ECG
- arrhythmias or cardiac ischaemia can occur after prolonged SE
EEG
- intermittent or continuous ictal discharges
ABG
- acidosis or alkalosis may be a complication
CT/MRI head
- rule out structural lesions
LP
- if meningitis or encephalitis suspected

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5
Q

Risk factors for status epilepticus

A 
Hx of epilepsy
Non-adherence to anticonvulsant drugs
Chronic alcoholism
Alcohol withdrawal
Refractory epilepsy
Electrolyte disturbances
Previous cortical structural damage
Drug use
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6
Q

Mx of status epilepticus

A

· 0 minutes – secure airway, give high flow oxygen
· 5 minutes – buccal midazolam (10mg)/IV lorazepam (4mg)
· 15 minutes – IV lorazepam (4mg) and call for a senior
· 25 minutes – Seek anaesthetic advice, rectal paraldehyde or IV phenytoin

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7
Q

Complications of status epilepticus

A

Focal neurological deficits
- may improve with time
Cognitive dysfunction
- most notably memory

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8
Q

DDx of status epilepticus

A

Psychogenic non-epileptic status epilepticus

  • differentiate with video-EEG
  • no epileptiform activity
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9
Q

Epidemiology of spinal cord compression

A 
Trauma is the main cord
Disc herniation
Bony fracture - osteoporotic, metastases
Spinal subluxation
Penetrating injuries
Tumour growth
Infection
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10
Q

Pathophysiology of spinal cord compression

A

Spinal cord extends from foramen magnum to L1/L2
Cord and surrounded CSF wrapped by dura mater
- CSF acts as buffer to slight compression
Corticospinal (control of trunk and limb movements) and spinocerebellar (unconscious proprioception) tracts most vulnerable

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11
Q

Presentation of spinal cord compression

A 
Back pain
Numbness/paraesthesia
Weakness/paralysis
Bladder/bowel dysfunction
Hyper-reflexia
Loss of tone below level 
Hypotension and bradycardia - neurogenic shock
Cauda equina syndrome
- saddle anaesthesia
- painless urinary retention
- bilateral sciatica and weakness
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12
Q

Onset of spinal cord compression

A 
Acute
- traumatic compression
- disc herniation
Chronic
- osteoporosis
- osteomyelitis
- malignancy
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13
Q

Ix for spinal cord compression

A

MRI spine - T2 weighted
- increased signal in disc compression and trauma
Gadolinium enhanced MRI spine
- assess for infection
Plain spine X-ray
- decreased disc space height - disc compression
- loss of bony detail - tumour, infection
- misalignment - trauma
- loss of end-plate definition - infection

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14
Q

Mx of spinal cord compression

A

Acute trauma
- immobilisation + decompression/stabilisation surgery
- IV dexamethasone
- supportive therapy - DVT prophylaxis, BP control, nutritional support
Epidural abscess
- vancomycin + metronidazole + cefotaxime
- consider decompression or CT-guided aspiration
- supportive
Cauda equina
- decompressive laminectomy
- supportive

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15
Q

Causes of brain damage in a head injury

A 
Primary damage
- focal cerebral contusions
- diffuse axonal injury
- extradural, subdural or subarachnoid haemorrhage
Secondary damage
- cerebral oedema
- hypotension
- hypoxia
- seizures
- hypoglycaemia
- infection
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16
Q

Immediate CT criteria

A

· Loss of consciousness lasting more than 5 minutes (witnessed)
· Amnesia (anterograde or retrograde) lasting more than 5 minutes
· Abnormal drowsiness
· Three or more discrete episodes of vomiting
· Clinical suspicion of non-accidental injury
· Post-traumatic seizure but no history of epilepsy
· GCS < 14, or for a baby under 1 year GCS (paediatric) > 15
· Suspicion of open or depressed skull injury or tense fontanelle
· Any sign of basal skull fracture – haemotympanum, periorbital ecchymosis, CSF leakage from the ear or nose, Battle’s sign
· Focal neurological deficit
· If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head
· Dangerous mechanism of injury – high-speed road traffic accident, fall from a height of greater than 3m

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17
Q

Clinical features of head injury

A 
Head signs
- haematoma
- laceration
- depressed fracture
- anterior fontanelle depression
CNS signs 
- decreased GCS
- abnormal fundi/pupillary reflexes 
- focal neurological signs
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18
Q

Pupil light response in head injury

A

Unilaterally dilated pupils with sluggish or fixed light response
- 3rd nerve compression secondary to tentorial herniation
Bilaterally dilated pupils with sluggish or fixed light response
- poor CNS perfusion
- bilateral 3rd nerve palsy
Unilaterally dilated or equal pupils with cross reactive light response
- optic nerve injury
Bilaterally constricted pupils with difficult to assess light reflex
- opiates
- pontine lesions
- metabolic encephalopathy
Unilaterally constricted pupil and preserved light reflex
- sympathetic pathway disruption

19
Q

Head injury mx

A 
Call for senior help and neurology
Nurse patient head up
Give O2
Maintain tight control over BP
Give adequate analgesia
Avoid hypoglycaemia
20
Q

Define acute respiratory distress

A

Non-cardiogenic pulmonary oedema and diffuse lung inflammation syndrome that often complicates critical illness

21
Q

Risk factors for ARDS

A

Critical illness - sepsis, aspiration, pneumonia, severe trauma, lung transplantation
Hx of alcohol abuse
Burns and smoke inhalation

22
Q

Pathophysiology of ARDS

A

Diffuse alveolar damage leads to injury of alveolar-capillary membrane
Flooding of alveolar air spaces with oedema, inflammatory cells and oxidants
Epithelial injury - necrosis, fibrin deposition on exposed basement membrane and surfactant dysfunction

23
Q

Presentation of ARDS

A

Low O2 sats - despite supplemental oxygen
Acute/progressively worsening resp failure
Critically ill patient
Dyspnoea/tachycardia
Pulmonary crepitations - diffuse
Low lung compliance
Fever, cough, pleuritic chest pain

24
Q

Diagnostic criteria for ARDS

A

Acute onset - within 1 week
Bilateral opacities on x-ray
PaO2/FiO2 ratio of < 300 on PEEP or CPAP > 5cm H2O

25
Q

Ix for ARDS

A

CXR - new onset bilateral opacities
ABG - low paO2
Blood/sputum/urine culture - sepsis most common cause of ARDS
Serum amylase/lipase - assess for pancreatitis as cause

26
Q

Mx of ARDS

A 
Oxygen and ventilation
Prone positioning
IV fluids
Targeted antimicrobial therapy
Supportive care 
- DVT prophylaxis
- glucose control
- beta-agonists to promote alveolar fluid clearance
27
Q

Complications of ARDS

A

Multiple-organ failure
Persistent dyspnoea
Abnormal lung function

28
Q

Define giant cell arteritis

A

Granulomatous vasculitis of large and medium sized arteries

- primarily affecting branches of external carotid

29
Q

Epidemiology of giant cell arteritis

A

Typically over 50s
Peak between 70 and 80
F:M = 2:1

30
Q

Pathophysiology of giant cell arteritis

A

Immune-mediated inflammation of walls of medium and large arteries
- presence of granulomas
Likely to be caused by environmental trigger (infection) in genetically predisposed individual

31
Q

Presentation of giant cell arteritis

A

Headache and scalp tenderness
- over temporal or occipital areas
Polymyalgia rheumatica symptoms
- aching and neck stiffness, shoulders, hips, worsens after inactivity
Jaw claudication
- pain on chewing
Loss of vision
Superficial temporal artery tenderness of thickening
Fundoscopy - pallor and oedema of optic disc (ischaemia of optic nerve)

32
Q

Ix for giant cell arteritis

A

ESR - raised
CRP - raised
FBC - normocytic, normochromic anaemia with normal WBC and elevated platelets
Temporal artery biopsy - granulomatous inflammation, multi-nucleated giant cells, focal and segmental inflammatory infiltrate
Temporal artery USS - wall thickening, stenosis or occlusion

33
Q

Mx of giant cell arteritis

A

Prednisolone - orally for 4 weeks then tape over 6-12 months

Aspirin

34
Q

Define Guillain-Barre Syndrome

A

Acute inflammatory neuropathy characterised by:

  • motor difficulty
  • absence of deep tendon reflexes
  • paraesthesia without objective sensory loss
  • increased CSF albumin with absence of cellular reaction
35
Q

Epidemiology of Guillain-Barre Sydnrome

A

1 per 100,000

Mean onset 40 years old

36
Q

Pathophysiology of Guillain-Barre Syndrome

A

Immune-mediated attack on Schwann cells of sensory and motor nerves
- usually triggered by preceding infection - CMV, EBV, hep B/C, HIV, campylobacter jejuni
Issues with propagation of nerve impulses
- conduction block and flaccid paralysis
When immune destruction stops, repair and remyelination occur

37
Q

Presentation of Guillain-Barre Syndrome

A 
Progressive symmetrical weakness
- lower extremities and proximal muscles first
Paraesthesia in feet and hands
Resp distress
Speech problems
Back/leg pain
Areflexia/hyporeflexia
Extra-occular muscle weakness
Facial droop
Dysautonomia
- sinus tachycardia
- hypertension
- postural hypotension
Fixed and dilated pupils
38
Q

Ix for Guillain-Barre Syndrome

A 
Nerve conduction studies - slowed
LP - elevated protein, normal/slightly raised lymphocytes
LFTs - elevated
Spirometry every 6 hours
- monitoring for resp signs
- reduced VC, mas inspiratory pressure
Antiganglioside antibody
39
Q

Mx of Guillain-Barre Syndrome

A 
IV immunoglobulin 
- contraindicated in IgA deficiency and renal failure
Plasma exchange
Supportive
 -DVT prophylaxis
- blood pressure control
- intubation and ventilation if needed
40
Q

Define acute bulbar palsy

A

Range of signs and symptoms linked to CN IX, X, XI and XII due to lower motor neurone lesion in medulla oblongata or lesions of lower cranial nerves outside brainstem

41
Q

Presentation of acute bulbar palsy

A 
Dysphagia
Difficulty chewing
Nasal regurgitation
Slurring of speech
Dysphonia
Atrophic tongue with fasciculations
Dribbling
Weakness of soft palate
Absent gag reflex
Sparing of ocular muscles differentiates from myasthenia gravis
42
Q

Causes of acute bulbar palsy

A 
Genetic
- Kennedy's disease
- acute intermittent polyphoria
Vascular
- lateral or medial infarction
Degenerative
- Guillain-Barre Syndrome
- poliomyelitis
- Lyme disease
Malignancy
- brainstem glioma
- malignant meningitis
Toxic
- botulism
- venom
Autoimmune
- myasthenia gravis
43
Q

DDx to acute bulbar palsy

A

Pseudobulbar palsy

  • damage located in UMNs
  • usually due to stroke
  • presents with brisk jaw jerk, stiff and spastic tongue and labile affect

Yr4 - Neuro + SS (9 decks)

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