Definitions, Tables, facts - Neuro Flashcards
Why sedate
A - facilitate ETT and tolerance B - comply with the vent C - reduce oxygen consumption D - comfort, augment analgesia, manage anxiety, agitation, delierium, safety control ICP
Adverse effects of sedation
Prolong MV and ICU stay Can’t assess neurological function Benzos worsen delirium Propofol causes hypotension Awareness
Benefit of a sedation hold
Reduce MV and LOS Reduces PTSD and psychological issues Decreased vasopressors Less mortality in hospital Increase likelihood of extubation Less need for a trachy Assess neurology
Sedation scoring systems
RASS - Richmond Agitation Sedation Score
Negative score - sedated
Positive score - hyperroused
0 - calm
Target -1
Target receptors of sedation
Agonist of inhibitory neuroreceptors —> GABA A, glycine (Propofol)
Antagonise excitably receptors —> NMDA
Agonist at alpha 2. —> reduces central sympathetic outflow
Dexmed
A2 agonist
Sedation and anxiolytics
Analgesic
Antihypertensive (good and bad)
No effect on resp function
Dose dependent brady and hypotension
Non inferior to propofol and midaz (PRODEX MIDEX trials)
Reduces MV and less delirium than midaz.
Classify TBI
Mild GCS 13-15
Mod 8-12
Severe <8
Describe primary TBI
At the time of injury
AXIAL LOADING and SHEARING FORCES —> DIFFUSE AXONAL INJURY
CT - diffuse swelling, loss of grey white, and contusions (contracoup)
Vascular injury —> sub/extradural, parenchymal
Secondary TBI
When cerebral oxygen consumption exceeds delivery
Due to increased CMRO2 —> seizures, pyre is
Poor delivery, low BP, hypoxia
Rising ICP impedes flow, (CPP)
Causes if secondary TBI
Cranial - seizures, rise CMRO2
Haematoma, rise ICP
Hydrocephalus, rise ICP
Infection, rise ICP and CMRO2
Systemic - hypoxia hypercapnia —> rise ICP Pryexia Low Na Low glucose (impaired metabolism)
Normal autoregulation of CPP
Over a range of MAP 50-150mmHg —> shifts right in chronic hypertension
Autoregulation dysrupted by TBI
CO2 - rise, dilates, increased ICP
Low - constricts, lower ICP initially, but compromise supply
O2 - no effect except when <8 when flow rises
Methods of ICP monitoring
GCS - non invasive, cheap, quick, no expertise needed.
BUT - fall in GCS is non-specific and multi factorial
CT head - loss of CSF filled spaces, loss of grey white
BUT - intermittent, transfer, needs interpretation
Intraperenchymal bolt - non dominant hemisphere.
Easy to insert, low risk of bleed or infection
Drift - cannot be recalibrated
EVD - surgically placed in ventricle - greater risk of infection and haemorrhage Drain CSF (diagnostic or therapeutic), can be recalibrated
BTF guidelines on invasive ICP
Severe TBI (GCS <8) with abnormal CT
OR
Severe TBI with normal CT brain, but 2 out of 3 of: >40
Sys BP <90
Abnormal motor score
Other circumstances to use ICP monitor in non trauma
Spontaneous ICH complicated by coma
Anoxic brain injury (drowning, arrest)
Hepatic enceph and cerebral oedema from fulminant failure
Meningitis/Enceph
ICP waves
P1, 2, 3
1 - Percussion wave = arterial pressure transmit from choroid plexus to ventricle
2 - Tidal wave = affected by brain compliance
3 - Dicrotic wave - aortic valve closure
When P2>P1, elevated ICP, loss of compliance
Lindberg Waves
Measures ICP over time, not morphology of one wave
A - slow vasogenic waves in critical perfusion
Mean ICP 50-100 lasts for 5-10 minutes.
reflex dilation to a low map. Terminates with increasing MAP
ALWAYS PATHOLOGICAL - SUGGEST LOW COMPLIANCE
B - cycles of 30 seconds to 2 minutes. Transient increases to 20-30 above base
Evidence of normal autoregulation
Absence AFTER head injury is a bad sign
C - 4-8 minute cycles,. not clinically important
Other forms of Neuro monitor
TCD —> flow through MCA
good for vasospasm in SAH
SjVO2 —> reduced CBF —> increased tissue extraction —> SjVO2 falls.
marker of global but not local perfusion
50% false positive for raised ICP
Fibre optic catheter in IJV into jugular bulb (mastoid air cells level)
NIRS local conditions only
Brain tissue oxygenation —> adapted bolt, oxygen tissue sensor, normal oxygen tension in that tissue
Micro dialysis catheter - into parenchyma via bolt. Diasylate into catheter, low molecular weight moleculres (lactate, pyruvate, glucose diffuse out)
rising lactate to pyruvate ratio —> bad
Poor outcomes in TBI
Increasing age Poor motor score post resus Lack of pupil reaction CT —> worsening Marshall grade oedema, midline shift, extra axial blood presence of Sub arachnid blood Hypoxia/hypotension Co-morbids
Causes of polyuria in TBI
How to investigate
Alcohol Mannitol Cold diuretics High BM DI ?CSWS
BM, temperature, alcohol level (or from Hx)
Plasma and urine sodium and osmols.
Define status epilepticus
Seizure activity of more than 30 minutes
OR
Recurrent seizures without return of consciousness between events
Causes of seizure
Intracranial or systemic
Cranial Infection - men/encephalitis Abscess Tumour Stroke Epilepsy Haemorrhage
Systemic Drugs - TCA, aminophyline Alcohol withdrawal Hypoglyc Hyponatraemia Hypoxia
Principles of management of seizures
ABCDE
Check a BM early
First line - loraz 4mg (0.1mg/kg children)
Diazepam
Second - Phenytoin/keppra
Third - Thio/propofol/anaesthesia
Complications of prolonged seizures
CVS - tachy, hypertension —> myocardial ischaemia
Resp - Aspiration pneumonia, ARDS, pulmonary oedema
Met - High lactate, raised CK, Rhabdo, hyperthermia
Neuro - hypoxia brain injury
Effects of drugs - resp depression, arrhythmia, hypotension
Why do an EEG in status
Status needs continuous EEG, check for ongoing activity
Titration drugs until BURST suppression
Then taper anaesthetic agent.
What’s the role of EEG in general in ICU
Diagnose, monitor and prognosticate
Diagnose
Patterns associated with conditions - seizures, enceph, CJD,
Monitor
Look for ongoing seizure activity
Depth of sedation/awareness
Prognosticate
Burst suppression, low voltage —> anoxic
Types of EEG waves
Alpha - 9-12 Hz - occipital, presents when awake, eye closed. Hypoxia if generalised
Beta - 13-20 Hz - Primary frequency ins drug induced coma
Delta - 0-4 Hz - high voltage —> metabolic enceph
Theta 4-8 children
Why admit a stroke to ICU
Airway due to low GCS
Monitoring - post thrombolysis Risk of deterioration Seizures Raised ICP Low GCS
Haemodynamics - uncontrolled hypertension, arrhythmia
Other - after an op, glycaemic control, complications (sepsis/pneumonia)
Scoring systems in SAH
WFNS - based on GCS and motor
Fisher —> radiological
Hunt and Hess scale
WFNS SYSTEM
GRADES 1-5
1 - GCS 15 - no motor 2 - 13-14 no motor 3 - 13-14 with motor 4 - 7-12 5 3-6
Fisher Scale
Grades 1 - 4
1 - no blood
2 - diffuse deposition without clots or layers>1mm
3 - localised clots, or blood >1mm
4 -Diffuse, or no sub arachn blood, but inter cerebral /ventricular clots
BP management in SAH
MAP to maintain CPP
BUT hypertension before securing increases rebleed
Maintain below 140 syst
Labetalol
Risks after SAH
Early rebleeding - repair
Hydrocephalus - fall in GCS, change in pupils. Insert EVD (lumbar if communicating)
Vasospasm/DCI Days 4-14, prophylactic nimod 60mg 4 hourly
How to monitor for DCI
Clinical - low GCS, focal Neuro (quick, free but subjective, ?sedation)
DSA - gold standard, can intervene if vasospasm seen. Needs specialist centre, risk of arterial injury and stroke
CT angio - can explain brain parenchyma, does not need arterial access. No as sensitive as DSA.
TCD - quick, Velocity MCA>200cm/S
Lindegaard index (MCA:ECA >3)
EEG - expertise.
Risks for DCI
High Fisher grade Smoker Hypertension Female Coma on admission
Management of DCI
Induce hypertension —> SECURE ANEURYSM FIRST
Hydration to euvolaemia (HHH is out)
Nimodipine
Intra-arterial nimod
Ballon angio
Other - Mg, statins, intra the cal thrombolysis…
Differential diagnosis of weakness
By anotomy —> Brain to muscle
Cortex - vascular event, encephalopathy
Stem - Pontine infarct/haemorrhage
Cord - Transvese myelitis Compression Ischaemia Infection, CMV, legionella MND Poliomyeltiits
Nerves - GBS, CIP, Eaton Lambert, Ureamia. Mononeuro
NMJ - MG, botulism, NMBD
Fibre - steroid myopathy, electrolytes, CIM, disuse atrophy
Pathogens and GBS
Campylobacter
Mycoplasma
CMV
EBS
HIV
RIsks for CIM
Sepsis Steroid use NMDB Hyperglycaemia Electrolyte disturbance Immobility
Key features of delirium
Disturbance in consciousness, fluctuating, reduced ability to focus
Change in cognition/perception
Onset over of short period of time and fluctuating
Evidence (Hx/OE/Ix) of a physical precipitant
Types of delirium
Hyperactive
Hypoactive
Mixed
Risk factors for delirium
Pre-existing and those from ICU
Pre: Increasing age known cognitive impairment Alcohol/drug/nicotine addiction Hypertension Emergency surgery or trauma
ICU High APACHE II score MV Metabolic acidosis Coma Steroids Sepsis Use of benzos
Prevent delirium
Avoid drugs that make it worse
Good sleep hygiene Maintenance of sleep wake cycle Remove lines/monitors Re-orienate, clocks, dates etc FAMILY EARLY MOBILISATION
Reversible causes of delierium
Hypoxia Hypoglyc Uraemia Sepsis CNS infection Retention/constipation Withdrawel
Types of CNS infection
Meningitis
Encephalitis
Brain abscess
Empyema
CI to LP
Infection skin
Thrombocytopenia (<50)
Coagulopathy (INR>1.5) and anticoag
Suspicious of raised ICP —> CT or MRI first
Tests for an LP
Microscopy : cell count and gram stain
MC&S
Biochemi - protein, glucose (paired)
Viral PCR
Antigens - pneumococcus, meningococcus, GBS, H.infl
Tuberculous analysis
Features of bacterial meningitis on LP
WCC - NEUTROPHIL high, normal lymph
Glucose (CSF: blood ratio) <0.4
Protein >1g/L
Features of viral meningitis
WCC - neuts normal, lymp high
CSF:blood glucose ration >0.6 (normal)
Protein 0.4-1
TB or fungal LP
WCC neuts normal, Lymph raised
Glucose CSF: blood <0.3
Protein 1 - 1.5g
Red cells in the CSF
Presence of blood —> SAH OR traumatic tap
Problem is working out how many WCC are from blood, and how many from inflammation
Predicted CSF WCC = CSF RCC x (FBC WCC/FBC RCC)
Then Actual WCC - Predicted WCC
expect 1 additional white cell for 1000 RCC per mm3
Classify meningitis
By CIRCUMSTANCE or By organism
CIRC
Spontaneous
Post trauma
Post op
Organism
Bac, viral, TB, fungal, aseptic (autoimmune/cancer)
Risk for meningitis
Age, young
Proximity - halls of residence/barracks - meningococcus
Sub-Saharan Africa - Mecca
Surgery or fracture - staph
Otitis media/pneumonia/asplenic - pneumoccocal
Organisms by age
Neonates - E.coli, listeria, GBS
Children - neiserria, strep pneum, h.inf
Adults- neiserrie and strep
Elderly - strep, neiserira, listeria
VIRAL
Entero, mumps, HSV, CMV, EBV, Variccela
Abx in meningitis
High dose ceftriaxone
Add amoxicillin if risk of listeria (elder)
STEROID - Dec 0.15mg/kg - reduced risk of hearing loss in ALL types. Mortality ben in pneumococcal
Causes of encephalitis
Largely viral HSV - most common EBV HIV Entero Measles
Rarely bacterial
TB
Listeria
Syphillis
Autoimmune - NMDA
