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Pete FFICM SOE/OSCE > Neuro > Flashcards

Neuro Flashcards

1
Q

Why sedate

A 
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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2
Q

Adverse effects of sedation

A 
Prolong MV and ICU stay
Can’t assess neurological function
Benzos worsen delirium
Propofol causes hypotension
Awareness
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3
Q

Benefit of a sedation hold

A 
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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4
Q

Sedation scoring systems

A

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

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5
Q

Target receptors of sedation

A

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

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6
Q

Dexmed

A

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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7
Q

Classify TBI

A

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

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8
Q

Describe primary TBI

A

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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9
Q

Secondary TBI

A

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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10
Q

Causes if secondary TBI

A

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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11
Q

Normal autoregulation of CPP

A

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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12
Q

Methods of ICP monitoring

A

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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13
Q

BTF guidelines on invasive ICP

A

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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14
Q

Other circumstances to use ICP monitor in non trauma

A

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

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15
Q

ICP waves

A

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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16
Q

Lindberg Waves

A

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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17
Q

Other forms of Neuro monitor

A

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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18
Q

Poor outcomes in TBI

A 
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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19
Q

Causes of polyuria in TBIHow to investigate

A 
AlcoholMannitolCold diureticsHigh BMDI ?CSWS
BM, temperature, alcohol level (or from Hx)Plasma and urine sodium and osmols.
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20
Q

Define status epilepticus

A

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

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21
Q

Causes of seizure

A

Intracranial or systemic

CranialInfection - men/encephalitisAbscessTumourStrokeEpilepsyHaemorrhage
SystemicDrugs - TCA, aminophylineAlcohol withdrawalHypoglycHyponatraemiaHypoxia
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22
Q

Principles of management of seizures

A

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

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23
Q

Complications of prolonged seizures

A

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

24
Q

Why do an EEG in status

A

Status needs continuous EEG, check for ongoing activity Titration drugs until BURST suppressionThen taper anaesthetic agent.

25
Q

What’s the role of EEG in general in ICU

A

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

26
Q

Types of EEG waves

A

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

27
Q

Why admit a stroke to ICU

A

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)
28
Q

Scoring systems in SAH

A

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

29
Q

WFNS SYSTEM

A

GRADES 1-5

1 - GCS 15 - no motor2 - 13-14 no motor3 - 13-14 with motor4 - 7-12 5 3-6
30
Q

Fisher Scale

A

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

31
Q

BP management in SAH

A

MAP to maintain CPPBUT hypertension before securing increases rebleedMaintain below 140 systLabetalol

32
Q

Risks after SAH

A

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

33
Q

How to monitor for DCI

A

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.
34
Q

Risks for DCI

A 
High Fisher grade
Smoker
Hypertension
Female
Coma on admission
35
Q

Management of DCI

A

Induce hypertension —> SECURE ANEURYSM FIRSTHydration to euvolaemia (HHH is out)NimodipineIntra-arterial nimodBallon angioOther - Mg, statins, intra the cal thrombolysis…

36
Q

Differential diagnosis of weakness

A

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
37
Q

Pathogens and GBS

A

CampylobacterMycoplasmaCMVEBSHIV

38
Q

RIsks for CIM

A 
SepsisSteroid useNMDBHyperglycaemiaElectrolyte disturbanceImmobility
39
Q

Key features of delirium

A

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

40
Q

Types of delirium

A

HyperactiveHypoactiveMixed

41
Q

Risk factors for delirium

A

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
42
Q

Prevent delirium

A

Avoid drugs that make it worse

Good sleep hygieneMaintenance of sleep wake cycleRemove lines/monitorsRe-orienate, clocks, dates etcFAMILYEARLY MOBILISATION
43
Q

Reversible causes of delierium

A 
Hypoxia
Hypoglyc
Uraemia
Sepsis
CNS infection
Retention/constipation
Withdrawel
44
Q

Types of CNS infection

A

MeningitisEncephalitisBrain abscessEmpyema

45
Q

CI to LP

A

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

46
Q

Tests for an LP

A

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

47
Q

Features of bacterial meningitis on LP

A

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

48
Q

Features of viral meningitis

A

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

49
Q

TB or fungal LP

A

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

50
Q

Red cells in the CSF

A

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

51
Q

Classify meningitis

A

By CIRCUMSTANCE or By organism
CIRC Spontaneous
Post trauma
Post opOrganism Bac, viral, TB, fungal, aseptic (autoimmune/cancer)

52
Q

Risk for meningitis

A

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

53
Q

Organisms by age

A

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

54
Q

Abx in meningitis

A

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

55
Q

Causes of encephalitis

A 
Largely viral	HSV - most common	EBV	HIV	Entero	Measles
Rarely bacterial TBListeriaSyphillisAutoimmune - NMDA

Pete FFICM SOE/OSCE (199 decks)

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