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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
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
26
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
27
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)
28
Scoring systems in SAH
WFNS - based on GCS and motor Fisher —> radiological Hunt and Hess scale
29
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 ```
30
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
31
BP management in SAH
MAP to maintain CPP BUT hypertension before securing increases rebleed Maintain below 140 syst Labetalol
32
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
33
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.
34
Risks for DCI
``` High Fisher grade Smoker Hypertension Female Coma on admission ```
35
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…
36
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
37
Pathogens and GBS
Campylobacter Mycoplasma CMV EBS HIV
38
RIsks for CIM
``` Sepsis Steroid use NMDB Hyperglycaemia Electrolyte disturbance Immobility ```
39
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
40
Types of delirium
Hyperactive Hypoactive Mixed
41
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 ```
42
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 ```
43
Reversible causes of delierium
``` Hypoxia Hypoglyc Uraemia Sepsis CNS infection Retention/constipation Withdrawel ```
44
Types of CNS infection
Meningitis Encephalitis Brain abscess Empyema
45
CI to LP
Infection skin Thrombocytopenia (<50) Coagulopathy (INR>1.5) and anticoag Suspicious of raised ICP —> CT or MRI first
46
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
47
Features of bacterial meningitis on LP
WCC - NEUTROPHIL high, normal lymph Glucose (CSF: blood ratio) <0.4 Protein >1g/L
48
Features of viral meningitis
WCC - neuts normal, lymp high CSF:blood glucose ration >0.6 (normal) Protein 0.4-1
49
TB or fungal LP
WCC neuts normal, Lymph raised Glucose CSF: blood <0.3 Protein 1 - 1.5g
50
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
51
Classify meningitis
By CIRCUMSTANCE or By organism CIRC Spontaneous Post trauma Post op Organism Bac, viral, TB, fungal, aseptic (autoimmune/cancer)
52
Risk for meningitis
Age, young Proximity - halls of residence/barracks - meningococcus Sub-Saharan Africa - Mecca Surgery or fracture - staph Otitis media/pneumonia/asplenic - pneumoccocal
53
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
54
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
55
Causes of encephalitis
``` Largely viral HSV - most common EBV HIV Entero Measles ``` Rarely bacterial TB Listeria Syphillis Autoimmune - NMDA

FFICM (59 decks)

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