Neuro Flashcards by Peter latham

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

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Adverse effects of sedation

Prolong MV and ICU stay
Can’t assess neurological function
Benzos worsen delirium
Propofol causes hypotension
Awareness

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Benefit of a sedation hold

Reduce MV and LOS
Reduces PTSD and psychological issues
Decreased vasopressors
Less mortality in hospita
lIncrease likelihood of extubation
Less need for a trachy
Assess neurology

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Sedation scoring systems

RASS - Richmond Agitation Sedation ScoreNegative score - sedatedPositive score - hyperroused0 - calmTarget -1

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Target receptors of sedation

Agonist of inhibitory neuroreceptors —> GABA A, glycine (Propofol)Antagonise excitably receptors —> NMDAAgonist at alpha 2. —> reduces central sympathetic outflow

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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.

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Classify TBI

Mild GCS 13-15Mod 8-12Severe <8

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Describe primary TBI

At the time of injuryAXIAL LOADING and SHEARING FORCES —> DIFFUSE AXONAL INJURYCT - diffuse swelling, loss of grey white, and contusions (contracoup)Vascular injury —> sub/extradural, parenchymal

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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)

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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)

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Normal autoregulation of CPP

Over a range of MAP 50-150mmHg —> shifts right in chronic hypertensionAutoregulation dysrupted by TBICO2 - rise, dilates, increased ICP Low - constricts, lower ICP initially, but compromise supplyO2 - no effect except when <8 when flow rises

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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

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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

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Other circumstances to use ICP monitor in non trauma

Spontaneous ICH complicated by comaAnoxic brain injury (drowning, arrest)Hepatic enceph and cerebral oedema from fulminant failureMeningitis/Enceph

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ICP waves

P1, 2, 31 - Percussion wave = arterial pressure transmit from choroid plexus to ventricle2 - Tidal wave = affected by brain compliance3 - Dicrotic wave - aortic valve closureWhen P2>P1, elevated ICP, loss of compliance

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Lindberg Waves

Measures ICP over time, not morphology of one waveA - 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 COMPLIANCEB - 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 signC - 4-8 minute cycles,. not clinically important

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Other forms of Neuro monitor

TCD —> flow through MCA good for vasospasm in SAHSjVO2 —> 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 onlyBrain tissue oxygenation —> adapted bolt, oxygen tissue sensor, normal oxygen tension in that tissueMicro dialysis catheter - into parenchyma via bolt. Diasylate into catheter, low molecular weight moleculres (lactate, pyruvate, glucose diffuse out) rising lactate to pyruvate ratio —> bad

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Poor outcomes in TBI

Increasing agePoor motor score post resusLack of pupil reactionCT —> worsening Marshall grade			oedema, midline shift, extra axial blood		presence of Sub arachnid bloodHypoxia/hypotensionCo-morbids

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Causes of polyuria in TBIHow to investigate

AlcoholMannitolCold diureticsHigh BMDI ?CSWS

BM, temperature, alcohol level (or from Hx)Plasma and urine sodium and osmols.

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Define status epilepticus

Seizure activity of more than 30 minutes
OR Recurrent seizures without return of consciousness between events

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Causes of seizure

Intracranial or systemic

CranialInfection - men/encephalitisAbscessTumourStrokeEpilepsyHaemorrhage

SystemicDrugs - TCA, aminophylineAlcohol withdrawalHypoglycHyponatraemiaHypoxia

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Principles of management of seizures

ABCDECheck a BM earlyFirst line - loraz 4mg (0.1mg/kg children) DiazepamSecond - Phenytoin/keppraThird - Thio/propofol/anaesthesia

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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 suppressionThen taper anaesthetic agent.

What’s the role of EEG in general in ICU

Diagnose, monitor and prognosticateDiagnose Patterns associated with conditions - seizures, enceph, CJD, Monitor Look for ongoing seizure activity Depth of sedation/awarenessPrognosticate 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, arrhythmiaOther - after an op, glycaemic control, complications (sepsis/pneumonia)

Scoring systems in SAH

WFNS - based on GCS and motorFisher —> radiologicalHunt and Hess scale

WFNS SYSTEM

GRADES 1-5```1 - GCS 15 - no motor2 - 13-14 no motor3 - 13-14 with motor4 - 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 CPPBUT hypertension before securing increases rebleedMaintain below 140 systLabetalol

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 FIRSTHydration to euvolaemia (HHH is out)NimodipineIntra-arterial nimodBallon angioOther - Mg, statins, intra the cal thrombolysis…

Differential diagnosis of weakness

By anotomy —> Brain to muscleCortex - vascular event, encephalopathyStem - Pontine infarct/haemorrhage```Cord - Transvese myelitis Compression Ischaemia Infection, CMV, legionella MND Poliomyeltiits```Nerves - GBS, CIP, Eaton Lambert, Ureamia. MononeuroNMJ - MG, botulism, NMBDFibre - steroid myopathy, electrolytes, CIM, disuse atrophy

Pathogens and GBS

CampylobacterMycoplasmaCMVEBSHIV

RIsks for CIM

```SepsisSteroid useNMDBHyperglycaemiaElectrolyte disturbanceImmobility```

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

HyperactiveHypoactiveMixed

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 hygieneMaintenance of sleep wake cycleRemove lines/monitorsRe-orienate, clocks, dates etcFAMILYEARLY MOBILISATION```

Reversible causes of delierium

```Hypoxia Hypoglyc Uraemia Sepsis CNS infection Retention/constipation Withdrawel```

Types of CNS infection

MeningitisEncephalitisBrain abscessEmpyema

CI to LP

Infection skinThrombocytopenia (<50)Coagulopathy (INR>1.5) and anticoagSuspicious of raised ICP —> CT or MRI first

Tests for an LP

Microscopy : cell count and gram stainMC&S Biochemi - protein, glucose (paired) Viral PCRAntigens - pneumococcus, meningococcus, GBS, H.infl Tuberculous analysis

Features of bacterial meningitis on LP

WCC - NEUTROPHIL high, normal lymphGlucose (CSF: blood ratio) <0.4Protein >1g/L

Features of viral meningitis

WCC - neuts normal, lymp highCSF:blood glucose ration >0.6 (normal)Protein 0.4-1

TB or fungal LP

WCC neuts normal, Lymph raisedGlucose CSF: blood <0.3Protein 1 - 1.5g

Red cells in the CSF

Presence of blood —> SAH OR traumatic tapProblem is working out how many WCC are from blood, and how many from inflammationPredicted 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 opOrganism Bac, viral, TB, fungal, aseptic (autoimmune/cancer)

Risk for meningitis

Age, youngProximity - halls of residence/barracks - meningococcus Sub-Saharan Africa - Mecca Surgery or fracture - staphOtitis media/pneumonia/asplenic - pneumoccocal

Organisms by age

Neonates - E.coli, listeria, GBSChildren - neiserria, strep pneum, h.infAdults- neiserrie and strepElderly - strep, neiserira, listeriaVIRAL Entero, mumps, HSV, CMV, EBV, Variccela

Abx in meningitis

High dose ceftriaxoneAdd 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 TBListeriaSyphillisAutoimmune - NMDA