Neurosciences Flashcards
Clipping vs coiling aneurysmal SAH
ISAT 2005
coiling better short term outcomes, less invasive
coiling may require repeat procedures
less dependency and death at 1 year with coiling but higher rebleeding
surgical clipping - wide neck
improving coiling techniques
ICU management SAH
- allow HTN first 21 days once porected
- MAP > 90
- ICP < 20 CPP > 60
- treat seizures (avoid prophylaxis - worse outcomes)
- repeat CT if change
- feed
- thromboprphylaxis
DCI vs vasospasm
vasospasm = narrowing of blood vessels
DCI = new neurological deterioration, may be due to basospasm
DCI management
- nimodipine
- euvolaemia, avoid anaemia
- end-vascular - coiling, angioplasty, IR vasodilator
HHH - hypertension, hypervolaemia, haemodilution - no longer recommended
Primary brain injury
neuronal dammage occurring immediately as a direct result of initial trauma. it is irreversible
impact - head striking object
inertial loading - he’d moving rapidly back / forward
penetrating
blast
Types of TBI
Fracture
- simple skull fracture
- depressed skull fracture - more likely to tear dura
Haematoma
- EDH
- SDH
- intraparenchymal
Other
- SAH
- Intraventricular haemorrhage
- contusion - coup / contrecoup
- diffuse axonal injury - shearing o axons
Secondary brain injury
neuronal damage due to sequelae of primary injury. hours - days after primary injury and main determent of outcome
causes
intracranial
- haematoma
- hydrocephalus
- vasopsasm
- infection
-seizures
extracrnial
- hypotension
- hyoxia
- hypo.hypercapnia
- hyponatraemia
- hypo/hyperglycaemia
- hyperthermia
Indications for CT head in head injury
- GCS < 13 on initial assessment
- GCS < 15 at 2 hrs
- Seizures
- Suspected open or depressed skull fracture
- signs of BOS fracture
- focal deficit
- > 1 vomit
ICP monitoring indications
GCS 3-8 and abnormal CT head scan
GCS 3-8 and normal CT head scan if 2 of:
- Age > 40
- SBP < 90
- Abnormal motor posturing
(GCS < 12 and sedated)
Physiological principles of preventing secondary brain injury
Maintain cerebral oxygenation
- PO2 > 10
- CPP 60-70
- treat anaemia
Reduce CMRO2
- treat seizure
- normoglycaemia
- normothermia
- deep sedation
- NMB
- barbiturate infusion
Manage increased ICP
- ICP monitoring
- Blood
- CO2 4.5 - 5
- hyperventilate if extreme
- Head up 30 degrees
- avoid tube ties
- Brain - osmotherapy
- CSF - EVD
- Decompressive craniectomy - DECRA 2011 - significant more GOSE 1-4, no difference in death
ICU management = tiers
TBI outcomes
Extended glasgow outcome scale GOSE
1 - 8
8 = upper good recovery
1 = death
CRASH 1
steroids in head injury GCS < 14
significanty higher mortality with methyprednisolone
Cooling in TBI
Eurotherm / Polar - trend to poorter outcomes, increased short term morbidity. not recommended
Intracerebral haemorrhage
Bleeding into the brain parenchyma
15% of strokes
Arterial / venous disease, vascular malformations, haemostatic disorders
precipitated by hypertension, CVST, drugs
usually deep sites - cerebellum, pions, thalamus
correction of coagulopathy
intensive BP reduction to 140 systolic (jay prevent haematoma enlargement, end organ dysfunction from hypertension however may reduce cerebral blood flow
BAMFORD classification ischaemic stroke
TACS - all 3
- unilateral motor / sensory / both deficit
- homonymous hemianopia
- higher cerebral dysfunction
PACS - 2 out of 3
LACS
- pure motor / sensory face/arm/leg
- sensorimotor deficit
- dysarthria
- acute movement disorder
POCS
- isolate hemianopia
- brainstem signs
- cerebellar ataxia
Investigation of ischaemic stroke
validated tool for diagnosis e.g. rosier
exclude hypoglycaemia
history - onset, anticoagulation
NIHSS
Non-contrast CT
CTA if thrombectomy indicated
Perfusion scan if thrombectomy > 6hrs
risk factors - HBA1c, lipid profile, ECG
Management priorities ischaemic stroke
supportive care - O2
BP < 185/110 if thrombolysis
consider reduction if > 220/120 or organ dysfunction
aspirin 300mg 2 weeks
thrombolysis < 4.5hr
stroke ward
contraindications to thrombolysis
- active bleeding
- BP > 185/110
- recent surgery
- DOAC last 48hr, INR > 1.7, platelet < 100
- ischemic stroke < 3 mo
- intracranial malignancy
- previous ICH
Malignant MCA syndrome
rapid neurological deterioration due to cerebral oedema following MCA territory stroke
inconclusive evidence of decompressive craniectomy
NICE
- MCA infarction NIHSS > 15
- reduced consciousness
- CT infarct > 50% MCA territory
CVST
Superior saggital, transverse, internal jugular, cortical veins
Risk factors
- those for thrombotic disorders plus
- head injury
- LP
- IJV CVCC
CVST pathophysiology
venous congestion upstream of occlusion
fluid extravasation into parenchyma
if venous pressure > arterial pressure ischaemia
CSF obstruction from swelling
CVST features
Headache - new, diffuse, severe, progressive
- seizures, paresis, papilloedema, altered mental state
- signs and symptoms of raised ICP
- focal neurology - visual disturbance
Consciousness
state of wakefulness and awareness
- wakefulness = eyes open, degree of motor arousal
- awareness - the ability to have experience of any kind
Disorders of consciousness
Confusional state - confusion, disorientation
Minimally conscious state
- plus - higher level responses e.g. following commands
- minus - lower level responses e.g. localising
vegetative state - reflexive and spontaneous movements only
- coma
Disorders of consciousness vs BSD
BSD = no wakefulness, no awareness, no consciousness. irreversible
coma = no wakefulness, no awareness, no consciousness. no response to environment or stimulation
VS = wakefulness but no consciousness or awareness
MCS = wakefulness, awareness and consciousness
Locked in syndrome
upper motor neurone quadriplegia affected cranial nerves
brain stem pathology
consciousness maintained
usually preserves eye movements in 1 or 2 axes
Prolonged disorders of consciousness
> 4 weeks
permanent if no change in trajectory for 6 months
- cause established
- not related to medictions
- reversible causes of loss of awareness treated
- exclusion of other potentially reversible causes
- coma recovery scale
longer someone in APDOC, lesss likely to regain consciousness
Long term management of PDOC
- clinically assisted nutrition and hydration
- pressure area relief
- physiotherapy - prevent joint stiffnes
- washing
- bladder / bowel management
Usually fully dependent
MDT / court involvement in withdrawing nutrition and hydration
Convilsive status epilepticus
- seizure > 5 mins
- recurrent seizures without complete recovery between
- refractory = failure to respond to first line treatments
- super-refractory = 24hrs
Complications of status epilepticus
- airway obstruction
- aspiration
- hypoxic ischaemic injury
- dysrhythmias
- lasting neurological dysfunction
- trauma
- rhabdomyolysis
Specific management principles in status epilepticus
- airway protection
- rapid termination of seizures with AEDs
- treat underling cause
- treat complications
Specific therapies - eclampsia - magnesium
- toxicity - as indicated e.g. intralipid for LAs
- Infection - abx, antivirals
- alcohol withdrawal - glucose, thiamine
Investigations
- collateral history
- bloods
- glucose
- U+E, Mg, TFTs
- toxicology
- bHCG
- serum AED levels
- TFTs
- CT
- EEG
- LP
- MRI
CSE manage,ent
0-5 mins
- protect airway
- oxygen
- IV access
- BM - treat if low
- alcohol history - glucose, thiamine
5-15mins
- Benzo
- no response after 5 min - 2nd dose
15 mins
- 2nd line
- phenytoin 20mg/kg (max 2g)
- valproate 40mg/kg (max 3g)
- keprra 60mg/kg (max 4.5g)
If ongoing seizures after infusion - consider 2nd
or phenobarbital 15mg/kg
30 mins
- GA
- propofol / thio / ketamine / midazolam
- propofol/midazolam maintenance
- EEG monitoring
24hr (super-refractory)
- thio coma
- ketogenic, magnesium, IVIG
- 24-48hr eeg control before waking
Meningitis definition
pathological inflammation of meninges
Causes of meningitis
bacteria
- pneumococcus over 50s
- meningococcus (n.meningitidis)
- listeria over 60s
- mycobacteria - TB
Viral
- HSV, enterovirus, VZV, HIV, influenza
Fungal
- crypto coccus
parasitic
- malaria, schistomsomiasis
non-infectious
- malignancy
- inflammatory - SLE, sarcoid
- medications
risk factors
- incomplete vaccination history
- mmunocompromise
- splenectomy (encapsulated bacteria)
- malignancy
- travel
- shared accomonidation
clinical features
fever, meningism, altered mental state
neuro
- headache
- seizures
- cranial nerve palsy
non-neuro
- sepsis
- rash
- dic
Management priorties meningitis
supportive care
- intubation if low gcs, seizure, agitation
- seizure management
LP ASAP but hold if severe spies,s DIC, rash
Sepsis management - abx, cultures, cvs support
10mg dexamethasone with 1st dose abx, continue for 4 days. don’t start after 12 hours
infection prevention and control
CT prior to LP
- GCS < 12
- papilloedema
- focal neurology
- seizures
Specific investigations in meningitis
Laboratory - standard
Micro
- HIV, meningococcal PCR, pneumococcal PCR
- urine pneumococcal angtigen
Radiological
- CT exclude differentials, complications
LP
- opening pressure
- cell count
- protein, glucose
- gram stain
- gram +ve diplococci - pneumococcal
- gram -ve diplococci - meningococcal
- gram +ve bacilli - listeria
- culture
- viral PCR - HSV, VZV
- Autoimmune encephalitis panel
- storage
Encephalitis
Inflammation of the brain parenchyma associated with neurological dysfunction
Causes of encephalitis
Viral
- HSV, VZV, EBV, CMV
- Measles
- Rubella
- Arboviruses - Japanese Encephalitis
Bactierla
- listeria
- mycoplasma
- TB
Fungal
- cryptococcal
Protozoal
- malaria
Post-infectious autoiumme ADEM
Non-infectious
- Anti NMDA
- Anti VGKC
- Paraneoplastic limbic encephalitis
Encephalitis presentation
Neuro
- altered mental state
- seizures
- headache
- cranial nerve abnormalities
Psychiatric
- altered behaviour
- altered personality
Systemic
- fever
- rashes
Diagnosis of encepahalitis
Major
- altered mental state for > 24hr with no alternative
Minor (2 = possible, 3 = probable)
- temperature > 38
- seizures - generalised, partial
- new focal neurologicy
- CSF WCC > 5
- abnormal brain parenchyma on imaging
- EEG abnormality
Investigations for encephalitis
LP - viral PCR
HIV serology
MR - HSV encephalitis - hyper intensity of frontal temporal areas on T2 flair
EEG - lateral periodic discharges
Tetanus
clostridium tetani
tetanospasmin toxin irreversible binding to NMJ
prevents inhibitory GABA release
Stimulation of motor neurones
spasm and autonomic instability
Airway - trismus, laryngospasm
Breathing - respiratory muscle rigidity
CVS - autonomic instability
Rhabdo, AKI, VTE
Treatment
- minimise toxin exposure - washout
- bacterial eradication - metronidazol
- neutralise toxin - human tetanus Ig
- supportive care 4-6 weeks
botulism
clostridium botulinum
wound / ingesttion / intestinal colonisation
toxin cleaves SNARE proteins - - allowing Ach to fuse with presynaptic membrane
ACH not release, flaccid paralysis, anticholinergic
afebrile, descending, symmetrical flaccid paralysis
loss of airway muscle tone, neck weakness
T2RF
postural hypotension
diplopia, nystagmus
ileus, urinary incontinence / retention
supportive treatment
wound debridement
trivalent antitoxin
Guillain barre syndrome
Acute demyelinating polyneuropathy
within 1 month of GI or resp infection
Subtyprd
- acute demyelinating polyradiculopathy (AIDP) - myelin sheaths
- Acute motor axonal neuropathy (AMAN)
- Acute motor sensory axonal neuropathy (AMSAN)
Diagnosis GBS
NINDS criteria
- progressive bilateral weakness of arms and legs
- absent / decreased tendon reflexes
supportive features
- < 2 weeks
- symmetry
- autonomic involvement
- pain
- CSF PROTEIN
- Abnormal neurophysioology
DDX GBS
CNS - brain stem inflammation egg, sarcoid, spinal cord e.g. transverse myelitis
anterior horn- myelitis e.g. polio
nerve roots - compression, infection
peripheral nerves - vitamin deficiencies, electrolytes
NMJ - MG, neurotoxins
Muscle - metabolic, myositis
Other - functional
Critical care admission for GBS
rapidly progressing
severe autonomic or bulbar features
respiratory insufficiency (EGRIS > 4)
- SOB at rest
- Abnormal PO2, PCO2
- Vital capacity < 1L
Myasthenia gravis clinical features
- weakness and fatiguability of skeletal msucles
- worse later in day
- ocular weakness on presentation
- craniocaudal progressioon
Diagnosis
- Serum ACHR antibodies
- neurophysiological
- tension test (cholingerigc crisis)
- Thymus - CXR , CT
- Resp function
Classification of myasthenia
- Occular
- Generalised
- mild
- moderate
- Severe generalised
- Crisis - worsening of respiratory muscle weakness requiring intubation or NIV (infection, pregnancy)
Indications for sedation in critical care
- facilitate tracheal intubation
- maintain tube tolerance
- facilitate synchrony with ventilator
- severe hyperactive delirium
- reduce oxygen demand and prevent secondary injury - TBI, seizures
- tolerance of invasive procedures
Why is depth of sedation important?
oversedation
- worse delirium
- increases LOS
- Increased ventilator days
Undersedation
- hyper catabolism
- increased sympathetic activity
- risk of patient harm e.g. self extubation
Muscle relaxants in critical care
- facilitation of intubation
- severe hypoxaemic respiratory failure
- suppress high ventilatory drive
- facilitate high pressure ventilation
- suppress ICP
- abdominal compartment syndrome
- transfers
sedation hold
temporatory cessation of sedative infusions
allow patient to wake, facilitate washout of drugs
thought to reduce LOS and mechanical ventilation
Withdrawal syndromes in critical care
prexisting alcohol / opiate / benzo - can anticipate
iatrogenic - cessation of prolonged sedation. 1/3 of over 7 days critical care
opiod - adrenergic excitation and exaggerated nociception. prevention - titrate analgesia, use adjuncts, perform sedationn holds. clonidine and weaning (10-20% per day)
Multimodal cerebral monitoring
- clinical
- ICP / CPP
- CBF
- Cerebral oxygenation
- cerebral electrophysiological
ICP monitoring
- bolt - transduce sensed pressure in specific region (ipsilateral to pathology). allows coninous monitoring but local impression only and can’t be recalibrated
- EVD - intraventricular catheter connected to transducer via continual fluid column. diagnostic, therapeutic, medication, can recalibrate. infection more common and more invasive
- optic nerve sheath diameter - intermittent and operator dependent
- pupillometry - intermittent and operator dependent
CBF monitoring
- transcranial doppler - intracranial arteries, evaluate velocities - identify emboli, stenosis, vasospasm . pulsatilla index correlates with ICP > 20
- in SAH / vasospasm - increased velocity with narrower vessels or increased blood volume
- lindegaard ratio. vasopsaspm LR > 3
- non-invasive, operator dependent, intermittent
Cerebral oxygenation monitoring
- NIRS - regional cerebral oxygen saturation - near IR high source and receiver - amount of light attenuation between the 2 measured. light spectra absorption between oxyHb and deoxyHb. non-invasive.
- jugular bulb venous oxygen saturation - fibre optic catheter into IJ and thread superiorly. global measure of O2 supply-demand. 55-75% normal. < 55% may be poor supply or increased demand. >75% may be increased supply or poor demand. continuous monitoring, CVC related complications
cerebral metabolic monitoring
cerebral micro dialysis - catheter with semi permeable membrane in white mater, perfused with dialyse. small molecules diffuse in. measure
- glucose
- lactate and pyruvate
- glutamate
= glycerol
electrophysiology
continue EEG used in coma and target sedation e.g. burst suppression
SSEP evoked response
Sleep
Normal physiological state of rest where level of consciousness and reaction to stimuli is reduced, but which is rapidly reversed.
Stages of sleep
Non-REM
N1- lightest, easy to rouse
N2 - 50% normal sleep
N3 - slow wave sleep - difficult to rouse
REM - 20% sleep, rapid eye movement and minimal muscle tone
Physiological effects of sleep
Resp
- partial airway obstruction due to reduced tone and increased resistance
- reduced TV, reduced MV, increased CO2
- decreased response to hypoxia and hypercapnia
CVS
- bradycardia, reduced SVR, reduced BP
- redistribution of blood to splanchnic organs
- reduced CBF (inc during REM)
Others
- increased pituitary outflow
- reduced oesophageal motility
EEG in sleep
N1 - loss of alpha, presence of theta
N2 - spindles and k complexes, theta
N3 - delta waves
REM - sawtooth, theta, flattening
Sedation and sleep
sleep - effect of hypothalamic GABA-ergic inhibition of arousal pathways
sedation - reduced GABA neurotransmission
critically ill sedated patient - N1 sleep, microarousal every 10 seconds
Normal EEG waveforms
- ISO - infra slow oscillations 0 preterm neonates
- delta - 0.5-4Hz - deep sleep, may be pathological in encephalopathy, dysfunction
- theta 4-7hz - drowsiness and early N1/N2 sleep. focal activity may be focal cerebral dysfunction
- alpha 8-12hz - normal awake EEG in occipital region
sigma waves - sleep spindles - beta - beta rhythm in health
