Neurological Emergencies Flashcards
What is the normal intracranial pressure?
5-15mmHg
What is the intracranial volume composed of?
What is the Monro-Kellie Hypothesis?
Brain tissue
CSF
Blood
*if the volume of any of these increase, the volume of the others must decreased to maintain normal pressure
Demonstrate the assessment on the nervous system
- 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
Stages of increased ICP
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
Management of raised ICP
= 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
Define vial meningitis.
What is its management?
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
Define bacterial meningitis.
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
Pathogenesis of bacterial meningitis
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
Clinical manifestations of Bacterial Meningitis
(inc pathophysiology of why)
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
Investigations for Bacterial Meningitis
- Physical exam/Hx
- LP - CSF analysis
- CT (pre LP if signs of raised ICP)
- Routine path including BC
- PCR if BC -ve
Management of Bacterial Meningitis
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
Complications of Bacterial Meningitis
- Cranal nerve palsies
- Hydrocephalus
- Seizures
- Raised ICP (cerebral oedema/herniation)
- DIC
- Ischemic/haemorrhagic stroke (hempplegia/hemiparesis)
Define Encephalitis
What are its symptoms?
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
Investigations and management for Encephalitis
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
Difference between ischemic and haemorrhagic stroke on CT
Investigations for Stroke (once clinical diagnosis made)
- 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
Stroke management
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
Describe ‘Reperfusion Therapy’
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)
Guidelines for Endovascular Clot Retrieval
- 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.
Define TIA.
What is its management?
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)
Presentation of Subarachnoid Haemorrhage
- Sudden severe headache
*usually occipital, reaches maximal intensity instantly - Nausea and vomiting (75%)
- Brief/continuing LOC and neck stiffness
Investigations and management of Subarachnoid Heamorrhage
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
Define a seizure.
What types of seizures are there?
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*
Pathophysiology of seizures
- 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)
Causes of seizures
- Immunological disorders
- Low antiepileptic drug levels
- Stroke
- HTN
- Metabolic disorders
- CNS tumor
- Head trauma
- Alcohol withdrawal / intoxication
- CNS infection
- Organ failure
Management of seizures
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
Medical management of seizures
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
Define febrile convultion on children
- 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*
What to council parents on when discharging febrile convultion
- 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
Define Guillain-Barré syndrome
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.
Pathophysiology of Guillain-Barré syndrome
? 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
Signs and symptoms of Guillain-Barré syndrome
- 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
Management of Guillain-Barré syndrome
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*
Describe the difference between an epidural, subdural and intracerebral bleed
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
