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FFICM > Definitions, Tables, facts - Neuro > Flashcards

Definitions, Tables, facts - 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 hospital
Increase likelihood of extubation
Less need for a trachy
Assess neurology
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4
Q

Sedation scoring systems

A

RASS - Richmond Agitation Sedation Score

Negative score - sedated
Positive score - hyperroused
0 - calm
Target -1

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5
Q

Target receptors of sedation

A

Agonist of inhibitory neuroreceptors —> GABA A, glycine (Propofol)

Antagonise excitably receptors —> NMDA

Agonist 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 13-15
Mod 8-12
Severe <8

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8
Q

Describe primary TBI

A

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

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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 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

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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 coma

Anoxic brain injury (drowning, arrest)

Hepatic enceph and cerebral oedema from fulminant failure

Meningitis/Enceph

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15
Q

ICP waves

A

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

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16
Q

Lindberg Waves

A

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

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17
Q

Other forms of Neuro monitor

A

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

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18
Q

Poor outcomes in TBI

A 
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
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19
Q

Causes of polyuria in TBI

How to investigate

A 
Alcohol
Mannitol
Cold diuretics
High BM
DI 
?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

Cranial
Infection - men/encephalitis
Abscess
Tumour
Stroke
Epilepsy
Haemorrhage
Systemic
Drugs - TCA, aminophyline
Alcohol withdrawal
Hypoglyc
Hyponatraemia
Hypoxia
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22
Q

Principles of management of seizures

A

ABCDE
Check a BM early

First line - loraz 4mg (0.1mg/kg children)
Diazepam

Second - Phenytoin/keppra

Third - 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 suppression
Then taper anaesthetic agent.

25
Q

What’s the role of EEG in general in ICU

A

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

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, arrhythmia

Other - after an op, glycaemic control, complications (sepsis/pneumonia)

28
Q

Scoring systems in SAH

A

WFNS - based on GCS and motor

Fisher —> radiological

Hunt and Hess scale

29
Q

WFNS SYSTEM

A

GRADES 1-5

1 - GCS 15 - no motor
2 - 13-14 no motor
3 - 13-14 with motor
4 - 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 CPP
BUT hypertension before securing increases rebleed

Maintain below 140 syst

Labetalol

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 FIRST

Hydration to euvolaemia (HHH is out)

Nimodipine

Intra-arterial nimod

Ballon angio

Other - Mg, statins, intra the cal thrombolysis…

36
Q

Differential diagnosis of weakness

A

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

37
Q

Pathogens and GBS

A

Campylobacter

Mycoplasma

CMV

EBS

HIV

38
Q

RIsks for CIM

A 
Sepsis
Steroid use
NMDB
Hyperglycaemia
Electrolyte disturbance
Immobility
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

Hyperactive

Hypoactive

Mixed

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 hygiene
Maintenance of sleep wake cycle
Remove lines/monitors
Re-orienate, clocks, dates etc
FAMILY
EARLY MOBILISATION
43
Q

Reversible causes of delierium

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

Types of CNS infection

A

Meningitis
Encephalitis
Brain abscess
Empyema

45
Q

CI to LP

A

Infection skin
Thrombocytopenia (<50)
Coagulopathy (INR>1.5) and anticoag

Suspicious of raised ICP —> CT or MRI first

46
Q

Tests for an LP

A

Microscopy : cell count and gram stain

MC&S

Biochemi - protein, glucose (paired)

Viral PCR

Antigens - pneumococcus, meningococcus, GBS, H.infl

Tuberculous analysis

47
Q

Features of bacterial meningitis on LP

A

WCC - NEUTROPHIL high, normal lymph

Glucose (CSF: blood ratio) <0.4

Protein >1g/L

48
Q

Features of viral meningitis

A

WCC - neuts normal, lymp high

CSF:blood glucose ration >0.6 (normal)

Protein 0.4-1

49
Q

TB or fungal LP

A

WCC neuts normal, Lymph raised
Glucose CSF: blood <0.3

Protein 1 - 1.5g

50
Q

Red cells in the CSF

A

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

51
Q

Classify meningitis

A

By CIRCUMSTANCE or By organism

CIRC
Spontaneous
Post trauma
Post op

Organism
Bac, viral, TB, fungal, aseptic (autoimmune/cancer)

52
Q

Risk for meningitis

A

Age, young

Proximity - halls of residence/barracks - meningococcus

Sub-Saharan Africa - Mecca

Surgery or fracture - staph

Otitis media/pneumonia/asplenic - pneumoccocal

53
Q

Organisms by age

A

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

54
Q

Abx in meningitis

A

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

55
Q

Causes of encephalitis

A 
Largely viral
	HSV - most common
	EBV
	HIV
	Entero
	Measles

Rarely bacterial
TB
Listeria
Syphillis

Autoimmune - NMDA

FFICM (59 decks)

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