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Semester 2 > Neurological Emergencies > Flashcards

Neurological Emergencies Flashcards

1
Q

What is the normal intracranial pressure?

A

5-15mmHg

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2
Q

What is the intracranial volume composed of?

What is the Monro-Kellie Hypothesis?

A

Brain tissue

CSF

Blood

*if the volume of any of these increase, the volume of the others must decreased to maintain normal pressure

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3
Q

Demonstrate the assessment on the nervous system

A
  • Neurological history
  • (clinical manifestations, associated complaints, precipating factors, progression, familial history)*
  • Cognitive function
  • (apraxia, memory, amnesia, agnosia)*
  • GCS
  • Pupil response/size/shape/reflex
  • Motor response
  • Cranial nerve assessment
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4
Q

Stages of increased ICP

A

Stage 1 - Compensation
Awake and alert, PEARL, normal breathing, BP and temp

  • *Stage 2 - Compensation**
  • Episodes of confusion, restlessness, lethargy
  • *Stage 3 - Begining decompression**
  • Inability to stay awake continuing on to progressivly deeper coma
  • Small, reactive pupils, slowing of response to light
  • Normal breathing
  • Increasing SBP, decreasing DBP
  • Full, bounding pulse
  • *Stage 4 - Decompression**
  • Bilateral pupil dilation and fixation
  • Coma
  • Cheyne stokes/neurogenic hyperventilation/ataxic breathing
  • SBP/DBP decreasing
  • Slightly irregular pulse
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5
Q

Management of raised ICP

A

= Treat underlying cause

  • Maintain CPP - raise MAP
  • Lower ICP by:
    Elevate head of bed to at least 30º
    Ensure neck alignment/neutral position to facilitate venous drainage
    Promote hyperventilation to lower CO2
    Lumber puncture to drain CSF/diagnose
    EVD (external ventricular drain)
    Shunts
    Decompressive craniotomy

Medication management

  • Analgesia and sedation
  • Osmotic diuretics - Mannitol
  • Hypertonic saline solutions
  • Corticosteroids (if from vasogenic oedema)
  • Fever control
  • Seizure management
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6
Q

Define vial meningitis.

What is its management?

A

A viral infection of the meninges that line the CNS, the subarachnoid space and the CSF.

  • Leading cause of meningitis
  • S&S are similar to bacterial but less severe, slower onset and self limiting (symptoms last 7-10 days)
  • Infection limited to the meninges
  • Management = symptomatic +/- antiviral
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7
Q

Define bacterial meningitis.

A

Bacterial infection of the meninges, subarachnoid space and CSF.

  • Can have a high mortality rate
  • Most common organisms - N Meningitidis (meningococcus), S Pneumoniae
  • -* Can result in complications and ongoing neurological sequalae
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8
Q

Pathogenesis of bacterial meningitis

A

Bacteraemia/bacteria in CSF
→
Endothelial damage
→
Pro inflammatory cytokines
→
-increase permeability of blood/brain barrier (vasogenic oedema)
- Leukocyte attraction = meningeal inflammation (interstitial oedema)
- Cerebral vasculitis decreases cerebral blood flow (cytotoxic oedema)
→
Increased intracranial pressure
→
Decreased global perfusion
→
Neuronal injury - apoptosis

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9
Q

Clinical manifestations of Bacterial Meningitis

(inc pathophysiology of why)

A

Systemic inflammatory response

  • Fever
  • Tachycardia
  • Altered GCS → photophobia

Meningeal irritation - stimulates dural nociception
- Around the:
Brain - headache
Brainstem - stiff neck
Spinal cord - sore back

Meningeal irritation - irritates crnial nerves

  • Cranial nerve palsies
  • Photophobia

Irritation of lumbar/sacral meninges ‘excites’ nerves
Kernigs sign - pain on knee extention when supine
Brudzinski’s sign - hip/knee flexion on passive neck flexion

Meningococcus - immune response creates vasculitis causing clotting abnormalities

  • Petechial/pupuric rash
  • Can lead to limb ischemia
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10
Q

Investigations for Bacterial Meningitis

A
  • Physical exam/Hx
  • LP - CSF analysis
  • CT (pre LP if signs of raised ICP)
  • Routine path including BC
  • PCR if BC -ve
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11
Q

Management of Bacterial Meningitis

A

A

  • Assess LOC for signs of raised ICP
  • If GCS <8 - secure airway

B

  • RR, WOB, SpO2
  • O2/MV as required

C

  • HR, BP, cap refil, skin colour
  • x 2 IVC
  • Assess need for fluid - ?raised ICP
  • FBC

D
- Analgesia
- Position at 30º if signs of raised ICP
- Dark room
BSL

Meds:

  • ABx
  • Corticosteroids
  • Seizure management (prophylaxis not required)
  • Fever management for comfort
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12
Q

Complications of Bacterial Meningitis

A
  • Cranal nerve palsies
  • Hydrocephalus
  • Seizures
  • Raised ICP (cerebral oedema/herniation)
  • DIC
  • Ischemic/haemorrhagic stroke (hempplegia/hemiparesis)
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13
Q

Define Encephalitis

What are its symptoms?

A

Inflammation of the brain parenchyma with associated neurological dysfunction.

_Major criteria (required)_
- Altered mental state lasting \>24hours
_Minor criteria (2 for possible, \>3 for probable/confirmed encephalitis)_
- Fever \>38 within the 72 hours before/after presentation
  • Generalised/partial seizures
  • New onset of focal neurology
  • CSF WBC count >5/mm
  • Abnormality of brain parenchyma on neuroimaging
  • Abnormality on EEG

Exclusion of encephalopathy from non-infectious cause

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14
Q

Investigations and management for Encephalitis

A

Investigations:

Similar to bacterial meningitis
- may also include CXR, EEG and MRI to identify different source

Management:

  • Acyclovier +/- ABx (while awaiting results)
  • ICP management
  • Identify possible source for specific therapies
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15
Q

Difference between ischemic and haemorrhagic stroke on CT

A
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16
Q

Investigations for Stroke (once clinical diagnosis made)

A
  • Non-contrast CT
  • If not haemorrhage evident on plain CT → CTAP (provides more info on infarction size/location/vessel involvement)
  • Bloods → INR, APTT, FBE, UEC, trop, ck, g&h, bHCG (if relevant)
  • BGL
  • ECG
17
Q

Stroke management

A

A:

  • Consider airway adjuncts
  • Secure airway if required - consider signs of raised ICP
  • NBM, ?NGT

B:

  • WOB/RR/SpO2
  • Monitor for hypoventilation (hypercapnea = vasodilation)
  • Aim SPO2 94-96%

C:

  • Manula BP, HR, rhythm
  • Aggressively manage hypotension
  • Allow HTN
  • Ensure 2 x large bore IVC
  • CCM - AF/AMI

D:

  • Keep BSL <10mmol/L
  • Elevate head of bed to 30º
  • Monitor for signs of increased ICP

E:
- Manage hyperthermia >37.5ºC
​- Attend wounds

Reperfusion therapy / Clot retrieval

18
Q

Describe ‘Reperfusion Therapy’

A

Thrombolysis

  • If presented within 4.5 hours of symptom onset
  • If inclusion criteria is met
  • If no evidence of exclusion therapy

Current thrombolytics

  • Tenecteplase
  • Alteplase

Inclusion criteria

  • 18 years or older
  • clear onset of ischemic stroke within 4.5 hours
  • No alternative cause for presentation

Exclusion criteria

  • Acute intracranial haemorrhage
  • Symptom onset >4.5 hours
  • Significant bleeding risk (specific criteria for anticoagulated pt)
  • BP >185/100 refractory to treatment
  • Uncorrected significan hyper/hypoglycaemia
  • Clinical suspicion of septic embolism
  • Aortic dissection
  • Infective endocarditis (risk of symptomatic ICH)
19
Q

Guidelines for Endovascular Clot Retrieval

A
  • Large vessel occlusion (interior carotid artery/middle cerebral artery)
  • Should be undertaken in <6 hours of symptom onset
  • Can be 6-24 hours when CTPA/MRI indicates small infarct core and salvagable brain tissue with ongoing significant neurological deficit.
20
Q

Define TIA.

What is its management?

A

Transient neurological dysfunction with no area of acute infarction.

Management = prevention of stroke

  • Anticoagulant if cardioembolic cause
  • Antiplatelet therapy
  • Intervention for symptomatic carotid stenosis (stenting)
  • Treatment of risk factors (eg, statins)
21
Q

Presentation of Subarachnoid Haemorrhage

A
  • Sudden severe headache
    *usually occipital, reaches maximal intensity instantly
  • Nausea and vomiting (75%)
  • Brief/continuing LOC and neck stiffness
22
Q

Investigations and management of Subarachnoid Heamorrhage

A

Investigatios

  • Non contrast CT
  • *if -ve - for LP for RBC in CSF*
  • Once confirmed - CTA
  • ECG
  • Baselife bloods and coags

Management

  • Stablise ABCD
  • Fever, seizure, BP control
  • Analgesia
  • BGL monitoring/management
  • Surgical intervention - clipping and coiling
23
Q

Define a seizure.

What types of seizures are there?

A

Seizure: An episode of abnormal neurological function caused by abnormal discharge of brain neurons.
Convultion: Episode of excessive and abnormal motor function.

  • Partial seizure
    Focal motor signs, with/without LOC
    (seizure usually only limited to one half/lobe of the brain)
  • -* Generalised seizures
  • Tonic clonic and absence seizures*
  • Status epilepticus
  • 2 or more seizures without full recovery of consciousness / recurrent seizures for more than 30 minutes*
24
Q

Pathophysiology of seizures

A
  • Neuronal cell is in a hypersensitive state
  • Hyperexcited neuronal cell fires off impulse to adjacent normal neurons
  • Excitation of subcortical areas of basal ganglia, thalamus and brain stem
  • Tonic phase occurs (skeletal muscle contraction, LOC, apnoea, vocalisations)
  • Clonic phase occurs due to inhibitory neurons in the cortex, anterior thalamus and basal ganglia
    (alternating muscle contraction/relaxation, incontinance)
25
Q

Causes of seizures

A
  • Immunological disorders
  • Low antiepileptic drug levels
  • Stroke
  • HTN
  • Metabolic disorders
  • CNS tumor
  • Head trauma
  • Alcohol withdrawal / intoxication
  • CNS infection
  • Organ failure
26
Q

Management of seizures

A

A:
Protection, prevention of aspiration - lateral position, suction

B:
Restoration/preservation of O2 - supplemental O2

C:
Usually maintained without intervention - cyanosis due to reduced O2 rather than poor circulation

D:
Injury prevention

  • Cessation of seizure activity: note duration of seizure, use anticonvulsants
  • ID/treat precipating factors (neuroimaging, lumbar puncture, toxicity, EEG, anticonvulsant)
  • ID/treat complications
  • Provide seizure prevention / management plan to optimise seizure control
27
Q

Medical management of seizures

A

Benzodiazapines
Enhances the neuro inhibitory effect of GABA

Phenytoin/Dilatin

Blocks voltage sensative sodium channels

*If seizures do not resolve with benzo’s, start a phenytoin infusion

Sodium Valporate
Blockage of sodium channels, increases brain levels of GABA

*may interact with other drugs

Levitiracetam
Inhibits pre-synaptic calcium chanels

Barbituates
Influx of chloride ions into the neurons - decreases excitability

*can cause hypotension and LOC

Propofol
Potentiation of GABA activity, slowing channel closing time
Also acts as sodium chanel blocker

28
Q

Define febrile convultion on children

A
  • 6 months - 6 years
  • Fever during/after seizure
  • it is not the temp causing the seizure, it is the inflammatiory cytokines released in the brain*
  • Episode <15 minutes
  • Only one episode in 24 hours
  • Must be generalised
  • focal seizure is not febrile covultion

*atypical febrile seizure - violates one rule - needs workup*

29
Q

What to council parents on when discharging febrile convultion

A
  • antipyretics dont prevent them
  • can run in families
  • no negative cosequences

If it happens again:

  • make sure child is safe
  • check time
  • if > 5 minutes, call 000
  • if cyanotic, call 000
  • if resolved, have the child evaluated in the next few hours
30
Q

Define Guillain-Barré syndrome

A

A rare neurological disorder in which the bodies immune system mistakenly attacks part of it’s PNS.

Unknown cause - can be from resp/GI illness, recent surgery, vaccine, Zika virus.

Can range from mild, brief weakness to paralysis.

31
Q

Pathophysiology of Guillain-Barré syndrome

A

? immune response initiated to fight infection - some chemicals on infecting bacteria and virus resemble that of nerve cells

  • Antibodies or WBC attack the myelin sheath of nerves
  • Nerves inflame, slowing conduction to and from the brain
  • Eventually, the brain cannot effectively communicate with peripheral nerves, causing a state of paralysis
32
Q

Signs and symptoms of Guillain-Barré syndrome

A
  • Sudden bilateral weakness (over days/weeks)
  • SOB
  • Unable to perform previously effortless tasks such as swallowing
  • Cramps/body aches
  • Ascending paralysis
  • Areflexia
  • Absence of fever
  • Loss of vasomotor control:
  • fluctuating BP
  • Postural hypotension
  • Cardiac dysrhythmia
33
Q

Management of Guillain-Barré syndrome

A

Symptomatic management / supportive care

  • airway maintenance for secretions/choking
  • ventilation if resp failure
  • UDC
  • Pain relief

Medication management

*if started withing 2 weeks

  • Plasmaphoresis
  • Plasma exchange - plasma contains antibodies taht are attacking the myelin sheeths*
  • High dose immunoglobulin therapy (IVIg)
  • Reduces the immune attack on the NS, ‘dilutes’ the atacking antibodies with non-specific antibodies, antibodies also bind with attacking antibodies to take them out of commission*
34
Q

Describe the difference between an epidural, subdural and intracerebral bleed

A

Epidural bleed

A bleed between the dura and the scull

Subdural bleed

A bleed between the dura and the brain

Intracerebral bleed

A bleed inside the brain

Semester 2 (8 decks)

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