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CICM > Neuro > Flashcards

Neuro Flashcards

1
Q

SAH risk factors

A 
female
age >50
smoking
OCI
alcohol
HTN
Connective tissues disorders
PKD
FHx
previous SAH
coarctation of aorta
fibromuscular dysplasia
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2
Q

WFNS

A 
I – GCS 15, no motor deficit
II – GCS 13-14, no motor deficit
III – GCS 13-14, motor deficit
IV – GCS 7-12 +/- motor deficit
V – GCS 3-6, motor deficit present or absent
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3
Q

modified fisher scale

A

grade 0
no subarachnoid haemorrhage (SAH)
no intraventricular haemorrhage (IVH)
incidence of symptomatic vasospasm: 0% 3

grade 1
focal or diffuse, thin SAH
no IVH
incidence of symptomatic vasospasm: 24%

grade 2
thin focal or diffuse SAH
IVH present
incidence of symptomatic vasospasm: 33%

grade 3
thick focal or diffuse SAH
no IVH
incidence of symptomatic vasospasm: 33%

grade 4
thick focal or diffuse SAH
IVH present
incidence of symptomatic vasospasm: 40%

Note: thin SAH is < 1 mm thick and thick SAH is >1 mm in depth.

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4
Q

Poor prognositc signs with SAH

A 
pre-existing severe medical illness
clinically symptomatic vasospams
delayed cerebral infacrt
hyperglycaemia
fever
anaemia
medical complications including pneumonia and sepsis
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5
Q

Causes of neurological deterioration following SAH

A

metabolic causes - CO2, O2, ammonia, temp, pH ,electrolytes, glucose

Drugs

Seizures

intracranial hypertension

hydrocephalus

re-bleed

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6
Q

Complications following SAH

A

re-bleed - highest risk in first 6 hours

acute hydrocephalus - see drop in GCS, sluggish papillary response, bilateral downward deviation of eyes

Vasoospasm

Delayed cerebral ischamia

Parenchymal haematoma

Seizures

HypoNa

Medical complications - arrythmias, liver dysfunction, neurogenic pulmonary oedema, pneumonia, ARDS, renal dysfunctio

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7
Q

vasospasm definition

A

dynamic narrowing of vessels

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8
Q

delayed neurological deterioration

A

clinically detected neuro deterioration after stabilisation that is not due to rebleeding
may be due to multiple other causes

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9
Q

delayed cerebral ischamia

A

any neurological deterioration (focal deficit, GCS drop by 2 or more) for >1 hour
presumed due to ischaemia - all other causes exlcuded

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10
Q

risks for vasospasm

A

higher radiological grade - esp if blood in basal cisterns or lateral ventricles
age <50
hypertension
hyperglycaemia

no difference if aneurysm coiled or clipped

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11
Q

prevention of vasospasm

A

oral nimodipine - 60mg q4H for 21 days

reduces risk of ischamic stroke by 34%

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12
Q

risks for seizures post SAH

A 
MCA
clots
infarction
clipping
poor grade
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13
Q

VTE prophylaxis after SAH

A

all should have UFH unless unsecured and awaiting intervention
Should be started at least 24 hours after aneurysm secured

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14
Q

Modified Rankin score

A

used to show neuro/disability outcomes - used by ISAT trials

0 - 6

0 - no symptoms
3 - moderate disability - requires help, but can walk without assisstance
4 - moderate severe - unable to walk or attend own needs without assistance
6 - dead

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15
Q

Causes of aseptic meningitis

A 
viral - most common (often enterovirus or coxsackie)
partially treated bacterial meningitis
TB meningitis
fungal
lymphoma
sarcoidosis
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16
Q

causes of seizures with meningitis

A

raised ICP
cerebritis
cerebral abcess
septic venous thrombus

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17
Q

Main point on cryptococcal meningitis

- who it affects, how Dx, treatment

A

can cause a chronic meningitis
seen in immunocompromised
CSF should be stained with india ink
Treat with amphoteracin B

May need to aggressively Mx raised ICP (eg daily CSF drainage)

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18
Q

Encephalitis - definition and causes

A

viral infection of the brain
may be due to direct infection or by post-infectious immune medicated mechanisms

HSV 1 most common - affects frontal and temporal lobes; 25% mortality, even with treatment

Arboviruses - japenese enceph, west nile virus

Antibody medicated - NMDA receptor encephalitits

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19
Q

Clinical presentation of encephalitits

A

key - focal neurological signs indicating involvement of parenchyma
- esp speech disturbance, seizures, altered cognition, LOC

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20
Q

Clinical signs of cerebral venous thrombosis

A

headache
focal deficits - esp cranial nerves
seizures
papilloedema

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21
Q

third nerve palsy

A 
down and out
ptosis
mydriasis
Failure of light reflex (but consensual constriction of the opposite eye is intact)
Failure of accommodation

Can be injured due to trauma or ischaemia/infection
- the parasympathetic fibres often spared with non trauma so pupillary response is preserved

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22
Q

fourth nerve palsy

A

paralysis of superior oblique
vertrical diplopia
patient can’t look down and in

onlu cranial nerve to innervate opposite side - so lesion in contrlateral to eye affects

very small nerve - at risk of damage during trauma

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23
Q

sixth nerve palsy

A

paralysis of lateral rectus
unable to turn eye out - results in horizontal gaze palsy
diplopia

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24
Q

risks of cerebral venous/sagital sinus thrombus

A

infection - meningitis, epidural/subdural abcess, facial/dental infection
DKA
COCP
ecstasy use

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25
Q

GBS investigations

A

CSF - high protein, some have high WCC, may have oligoclonal banding

Bloods - high IgG, antiganglioside GM1 antibodies

Nerve conduction studies

  • reduced conduction velocity
  • multifocal conduction blocks

MRI - to exlcude high cervical lesion

Lung function

  • if FVC <20 - transfer to ICU
  • if <15 - intubation

Screen for infection -

  • viral PCR/antibodies
  • stool for campylobacter
  • mycoplasma antibodies
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26
Q

Clinical findings GBS

A

minor illness 2-8 weeks before
25% have motor weakness, 50% paraesthesia, 25% both

Flacid paralysis in ascending pattern
areflexia
cranial nerve in 45%
autonomic dysfunction
sensory loss is mild
pain may be a major feature
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27
Q

Miller fisher varient GBS

A

cranial nerves predominate
ataxia, areflexia and opthalmoplegia

stongly associated with campylobacter jejuni

may have GQ1b antibodies

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28
Q

Treatment of GBS

A

Plasmapheresis - most effective if carried out within 7 days of symptoms

IVIG - 2g/kg over 2-5 days

10% will replase with either- most will respond well to a second course

no point in doing both
no poing in crossing over

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29
Q

Indications for intubation in GBS

A

VC <15ml/kg
VC rapidly falls over 6 hours
respiratory failure
if secretions are difficult to manage

  • NB - may have severe bulbar involvement ( LMN CN 9, 10, 12)
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30
Q

Drugs that may cause CVS instability in GBS

A

Low BP - morphine, frusemide, thio

Increased BP - ephedrine, dopamine, isoprenaline,

arrhythmias - sux

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31
Q

Poor prognostic features of GBS

A

> 60yrs
rapid progression or quadrapersis in <7 days
need for ventilation
preceding diarrhoeal illness

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32
Q

Critical illness polyneuropathy

A

acute
diffuse
a motor neuropathy, due to axonal degeneration
presents in recover phase of illness

quadriparetic weakness
hyporeflexia
difficulty weaning

high mortality (likely related to underlying condition)

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33
Q

Critical illness myopathy

A

linked with asthma and some drugs (steroids, NMBDs, aminoglycosides)

reflexes and sensation usually normal
CK often raised
muscle necrosis is seen on histology

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34
Q

Intensive care acquired weakness (ICUAW)

A

occurs in upto 45% patients who need ventilation, have sepsis, have MOF

Usually associated with long period of immobilisation

CLinical signs

  • normal cognitiion
  • sparing of cranial nerves
  • symmetrical flaccid paralysis

subgroups -

  • polyneuropathy
  • myopathy
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35
Q

Treatment of MG

A

anticholinesterase drugs - pyridostigmine
steroids
IVIg - 5 days may have long term benefit
thymectomy

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36
Q

Triggers of MG crisis

A 
infection
pregnancy
surgery
drugs - 
 - Abx
 - Antiarrythmics
 - LAs
 - muslce relaxants
 - analgesia
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37
Q

Factors predicting need for ventilation post op in MG patient

A

long pre-op duration of MG
high anticholinesterase requirement
co-existant resp disease
pre-op viral capacity of <2.9L

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38
Q

Key points about motor neuron disease

A

no treatment, progressive group of related disorders
Affects both upper and lower motor neurons

Pathogeneisis -

  • cerbral cortex, anterior horns of spinal cord - shrinkage and degeneration
  • lateral sclerosis

Present -

  • asymmetrical insidious weakness and wasting
  • more symetrical with progression
  • have spactisity, hyperreflexia and muscle wasting

Dx made on clinical grouds and EMG showing denervation

Mx - riluzole (glutamate antagonist) may slow progression slightly

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39
Q

SHort notes on botulism

A

caused by endotoxins from clostridium botulinium
Irreversibly binds to cholinergic nerves at NMJ, postganglionic parasympathetic nerve endings and autonomic ganglia

may be food bourne or from food

Symptoms -

  • GI upset
  • dry eyes and mouth
  • general weakness - symmetrical, descending
  • early CN involvement

treatment is supportive
can use metronidazole for wound botulism

most patients improve in a week or so

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40
Q

tetanus clinical presentation

A

due to spores from clostridium tetani

muscle rigidity and spasms
autonomic instability - severe increase in sympathetic drive most significant (although parasympathetic surge may be [re-terminal)

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41
Q

management of tetanus

A

neutralise circulating toxin
- human anti-tetanus immune globulin - IM

source control and limitation of toxin production
- debridement and cleaning of wound; metronidazole

control of spasms

  • avoid stimulation
  • sedation, paralysis

Management of autonomic dysfunction

  • magnesium
  • labetelol
  • clonidine
  • sedatives

initiation of full active tetanus immunisation (different site from HIG)

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42
Q

Delirium definition

A

a disturbance of consciousness that develops over a short period of time, fluctuates and is associated with perceptual changes, such as hallucinations

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43
Q

Clinical subtypes of delirium

A

Hypoactive - most common
Hyperactive - only 5% of cases
Mixed

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44
Q

impact and relevance of delirium in ICU patients

A

seen in upto 70% ventilated patients
patients have a 3x higher 6/12 mortality
associated with long term cognitive decline and early dementia

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45
Q

Pathophysiology of delirium

A 
neuroinflammation 
impaired oxidative metabolism
altered cerebral blood flow
increased BBB permeability
neurotransmitter imbalance
 -> cholinergic hypoactivity
relative state of dopamine excess
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46
Q

Modifiable risk factors for delirium

A 
infection
use of opiates and sedative drugs
immobility
polypharmacy
low Na, O2, pH and raise CO2
use of physical restraints
used of IDC
pain
sensory impairment
sleep disturbance
anticholinergic drugs
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47
Q

non-modifiable risk factors for delirium

A 
>65
dementia
depression
cognitive impairment
liver impairment
institutionalised resident
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48
Q

Screening tools for delirium

A

Confusion assessment model for ICU (CAM-ICU)

  • assesses for fluctuating mental status, inattention, altered LOC and disorganised thinking
  • is a point in time assessment

Intensive care delirium screening checklist (ICDSC)
- assessed over a nursing shift

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49
Q

RASS score

A

Richmond agitation and sedation scale

+4 - combative
0 - alert and calm
-3 - movement or eye-opening to voice (no eye contact)
-5 - no response to voice or physical stimulation

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50
Q

dexmedetomidine MOA

A

alpha 2 agonist

  • sedative action mediated by post synaptic receptor agonism in locus ceruleus
  • analgesic action medicated by posy synaptic receptor agonism in the brain and spinal cord
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51
Q

dexmedatomidine side effects

A

transient HTN hypotension, brdycardia, nausea

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52
Q

dexmedatomidine dose

A

0.1 - 1mcg/kg/min infusion

can load with 1mcg/kg over 10mins

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53
Q

dexmedatomidine evidence

A

Lancet 2016 -

  • pts >65 in ICU after non-cardiac surgery
  • n =700
  • showed a marked decrease in delerium incidence (23 –> 9%)
  • also less tachycardia and HTN

DahLIA trial 2016
- included patients in whom extubation was delayed due to severe agitation
- found more ventilator free hours with use of dexmed
BUT - underpowered

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54
Q

pharmacological treatment for delerium

A

haloperidol - if QTc ok

  • 2.5mg doses, max 18mg in 24 hours
  • SEs - extrapyramidal effects, neuroleptic malignant syndrome, torsades, not for use in parkinsons

Olanzapine - 5mg, max4 doses
- use if CI to halp

risperidone

dexmedatomidine or clonidine

benzos

  • only to be used if safety is an issues
  • have been linked to 7x increase in delirium in burns patients
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55
Q

Preconditions for brain stem testing

A

cause for coma consistent with brain death

at least 4 hours with - GCS3, pupils non reactive, no cough, apnoea

nomothermia (>35)

normotension (MAP >60, SBP >90)

no sedation or analgesia

absence of severe electrolyte, metabolic and endocrine disturbance

intact neuromuscular function

ability to access one eye and one ear

ability to perform apnoea test (no high spinal injury, severe resp failure)

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56
Q

brain stem testing

A
  • preconditions met
  • TOF
  • GCS3 - no response to deep nail bed pain in all 4 limbs, no response to CN V and VII
  • pupils fixed, non responsive - 2 and 3
  • no corneal reflex - 5 and 7
  • no oculo-vestibular reflex - 3, 4, 6, 8
  • no gag bilaterally - 9 and 10
  • no cough - 10
  • positive apnoea test
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57
Q

testing oculo-vestibular reflex

A

inspect external auditory canal to ensure eardrum visible
head to 30
instil 50mls ice cold water into canal
watch eyes with eyelids held open, for 60 seconds

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58
Q

apnoea test

A

pre-oxygenated for 5 mins
disconnect from ventilator and supply oxygen (2l/min) down catheter into ETT
watch chest
no breath with PaCO2 >60, or increase by 20 from baseline if retainer
- would expect a rise by 3/min

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59
Q

Investigations for brainstem testing

A

4 vessel intraarterial angiography with digital subtraction
- injected into carotids (no flow above siphon) and vertebrals (no flow above foramen magnum)

Radionucleotide imaging -
- lack of perfusion accross BBB to be retained by brain parenchyma

CT angio - less experience, with no large studies done

  • absent enhancement at 60 seconds in different cerebral artery distributions
  • MCA, PCA, pericallosal arteries and internal cerebral arteries

MR - not recommended

Doppler -
- used to rule out, not in

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60
Q

Brain death testing with regards to children

A

if over 30 days - same as adults

Term newborn

  • minimum period of observation 48 hours
  • two examinations done, >24 hours apart

<36/40
- clinical determination can not be done with certainty

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61
Q

Responsibilities of ICU staff in organ and tissue donation

A

care of dying patient
care of their family
recognising the possibility of organ donation
determination of death
respectful treatment of the dead patient
discussing the option of organ donation with family
liason with donor coordination service
maintaining physiological stability
aftercare for the family (irrespective of if donation occurred)

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62
Q

Absolute contraindications to organ donation

A

HIV
CJD
metastatic or non curable malignant disease
history of malignancy that poses high risk of transmission (melanoma)

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63
Q

Relative contraindications to organ donation - need individual consideration

A

past malignancy with a long cancer free interval
treated bacterial infection
infection with hep B and C
risk factors for HIV and viral hepatitis

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64
Q

Common medical issues seen in potential donors

A

CVS -autonomic storm followed by loss of sympathetic flow

  • issues with arrhythmias common
  • fluid management difficult as varies depending on organs being donated
  • target MAP >70

DI

  • hyperNa associated with worse outcome for liver and kidney recipients
  • DDAVP early - 2-4mcg q2-6hrs prn

Hypothermia

  • due to;
  • reduced whole body heat production
  • inabiliy to conserve heat
  • loss of hypothalamic thermoregulation

Anterior pituitary function
- replacement is not routinely used

Anaemia and coagulopathy
- products as needed

Respiratory - ongoing routine cares

Nutrition - continue enteral feeds

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65
Q

warm ischaemia time

A

time from treatment withdrawal to start of cold perfusion

most important phase is when SBP <60

impacts on graft function

66
Q

WIT for

  • liver
  • kidney
  • pancreas
  • lungs
A

liver - 30mins
kidney and pancreas 60mins
lungs 90mins

67
Q

DCD vs brain death liver

A

DCD has lower graft and patient survival at 1 and 3 years

DCD also has a higher incidence of biliary strictures, hepatic artery stenosis, hepatic abscess and biloma formation

68
Q

DCD vs brain death kidney

A

DCD has higher incidence of delayed graft function

69
Q

DCD donor criteria

A

ventilated patient in whom treatment is to be withdrawn

when death is likely to occur in time frame

medical suitability

Meeting Maastricht criteria

70
Q

Maastricht criteria

A

only 3 and 4 suitable for DCD

3 - withdrawal of treatment in ICU - known and limited WIT - controlled

4 - cardiac arrest followong formal determination of brain death testing but before planned organ retrieval - known and potentially limited WIT - uncontrolled

71
Q

Important points for discussion with family re DCD

A

organ retrieval needs to occur without delay

organ donation may not be possible due to time issues

consenting to donation will delay withdrawl

assessment may mean that organ donation can not proceed

circumstances of death may need to be reported to the coroner and coronial post-mortem may occur, independent of donation process

family can change their minds at any time

72
Q

retrieval related procedures occurring before death -

- guidelines

A

supported by NHMRC ethical guidelines in the following circumstances -

  • evidence that individual wanted to be a donor
  • patient or family ahve had enough time to make an informed decsion
  • consent for the specific intervention has been obtained
  • interventions do not contribute to death
  • measures are taken to prevent pain or discomfort
73
Q

retrieval related procedures occurring before death include;

A

heparin to prevent small-vessel thrombosis - 20,000U

moving to OT before withdrawal

cannulation of femoral vessels to infuse preservation solutions once death has occured

bronchoscopy

74
Q

Determination of death - DCD

A

Immobility
Apnoea
absent skin perfusion
Absence of circulation and evidenced by absent arterial pulsatility for a minimum of 2 minutes as measured by feeling the pulse or monitoring IAP

MUST use one clock for all documentation

Don’t monitor ECG
Can reintubate with no ventilaiton to prevent aspiration

75
Q

VTE prophylaxis in neurosurgical patients

A

guidelines by Neurocritical care society - 2016

76
Q

VTE prophylaxis aneurysma; SAH

A

UFH in all, except those with unsecured ruptured aneurysms expected to undergo surgery

IPC (intermittent pneumatic compression) as soon as enter hospital

UFH at least 24 hours after aneurysm secured

77
Q

VTE prophylaxis TBI

A

IPC within 24 hours of presentation of TBI or within 24 hours of craniotomy

LMWH or UFH within 24-48 hours of presentation or 24 hours after craniotomy for TBI and ICH

78
Q

VTE prophylaxis SCI

A

Start as early as possible, within 72 hours of injury

recommend against use of mechanical measures alone

79
Q

Early post-trauma seizures - impact and Mx

A

Phenytoin recommended to decrease incidence of early seizures (<7 days) if benefit outweighs risk BUT early PTS have not been associated with worse outcomes

80
Q

DECRA trial

A

looked at secondary DC as a neuro-protective measure

n = 155
ICP >20mmHg for >15 mins within a 1 hour period pt randomised to bifrontal Decomressive craniectomy and medical Mx or medical Mx

Surgical - better ICP control, received fewer interventions for raised ICP, and had a reduced length of stay in the intensive care unit (ICU).

BUT- higher rate of unfavourable outcomes (death, vegetative state, severe disability) in surgical patients at 6 months

81
Q

RESCUE icp

A

examined secondary DC as a last-tier intervention

n=400, multicentre
DC vs barbituate coma if ICP >25mmHg for 1-12 hours, despite stage 1 and 2 medical Mx

DC group had improved survival but increased rates of vegetative state and severe disability

for every 100 DC done
- 22 more survivors; 6 VS, 8 fully dependent, 8 independent but only within the home

82
Q

What do the Brain trauma foundation guidelines outline

A

treatment, monitoring and threshold

83
Q

Complications of prolonged immobilisation (SCI)

A 
pressure ulcers
difficult intubation
potential venous obstruction -> increased ICP
less options for CVL
high risk VTE
higer risk resp infections
gastrostasis
inabilty to provide optimal oral care
84
Q

ASIA scoring

A

A - complete; no motor or sensory function, including S4/5

B-incomplete; preserved sensory but no motor including S4/5

C - incomplete; motor function preserved below level of injury -> <1/2 muscles muscle grade <3 (ie 2 - gravity eliminated or 1 - contraction only)

D - incomplete; motor function preserved below level of injury -> > 1/2 muscles have muscle grade of 3 or more

E - normal motor and sensation

85
Q

Muscle grading

A 
0 - no contraction
1 - palpable or visible contraction
2 - movement with gravity eliminated
3 - movement against gravity
4 - movement against gravity and some resistance
5 - against gravity and full resistance
86
Q

NEXUS guidelines

A

for imaging of C spine

Imaging is indicated for all trauma patients unless they meet all of the cirteria;

  • no posterior midline tenderness
  • no evidence of intoxication
  • normal level of alertness (three object recall at 5 mins)
  • no focal neurological deficit
  • no painful distracting injuries

very high senitivity (99.6% for significant injuries) but specificity is 12.9% ( ie lots more Ix than needed)

87
Q

what type of CT scan done from SCI

A

multi-detecot row CT (MDCT) - sensitivity of almost 100% (including ligamentous injury)

88
Q

ICU Mx principles for SCI

A

Prevention of secondary injury
Care of respiratory function; likely need for intubation
CVS - unopposed sympathetic tone; once ensured fluid filled give norad
- may need atropine/pacing

Attention to pressure areas, bowel care, VTE prophylaxis (within 72 hours), pain and psychological care

89
Q

Insults know to independently worsen outcome in secondary brain injury

A 
hypotension SBP <90
hypoxia sats <90%
hypoglycaemia
hyperpyrexia - temp >39
prolonged hyocapnia - CO2 <30
90
Q

Phases of cerebral blood flow alteration after TBI

A

1) Hypoperfusion - first 72 hours
- neuronal ischaemia can cause cytotoxic cerebral oedema

2) Hyperaemic phase
- once autoregulatory mechanisms have recovered
- ICP may increase due to intracranial inflammation and medical therapies that have been aimed at maintaining adequate perfusion
- can caue vasogenic cerebral oedema
- lasts 7-10days, sene in 25-50% patients

3) vasospastic phase (esp in those with severe primary or secondary injuries, esp in SAH)
- complex hypoperfusion due to vasospasm, post-traumatic hypometabolism and impaired autoregulation

91
Q

Indications for ICP monitoring

A

New BTF guidelines - all patients with severe TBI should be managed with monitor to reduce in hospital and 2 week post injury mortality

Classical - 
GCS = 8 AND any of the following;
 - abnormal CT OR
 - normal CT head and 2 or more of;
     - age >40
     - motor posturing
     - significant extracranial trauma with hypotension (SBP <90)
92
Q

Vessels that can be viewed using transcranial doppler

A

anterior, middle and posterior cerebral arteries

terminal internal carotid

anterior and posterior communicating arteries

93
Q

Complications of Decompressive craniotomy

A 
Herniation though the defect
Delayed paradoxical herniation
Subdural hygroma
Infection
Bleeding
Post-traumatic hydrocephalus
"Sinking Flap Syndrome"
Bone resorption
94
Q

Causes of coma with miosis

A 
Bilateral pontine lesions
Bilateral thalamic lesions
Metabolic encephalopathy
Cholinergic drugs
 - Organophosphates
 - Myasthenia gravis drugs (the 'stigmines, eg. pyridostigmine)
 - Alzheimers nootropics (the 'pezils, eg. donepezil)
 - Sarin gas
Non-cholinergic drugs:
 - Opiates
 -Barbiturates
 - Clonidine
 - Valproate
 - Atypical antipsychotics
95
Q

Causes of 6th nerve palsy

A

Head injury (most common) with BOSF
Raised intracranial pressure
Localising lesion…. at any number of levels:
- Damage to the frontal eye field of the frontal lobe, which occupies some of the middle frontal gyrus
- Damage to the posterior hemispheres, which would be accompanied by a hemianopia
- Brainstem (tumour, stroke)
- Petrous portion of temporal bone (otitis media-associated osteomyelitis, mastoiditis)
- Clivus (intraforaminal extension of nasopharyngeal carcinoma or similar)
- Cavernous sinus (thrombosis)
- Superior orbital fissue (base of skull fracture)
Any where (basal forms of meningitis, eg sarcoidosis, tuberculosis, cryptococcus)

96
Q

Advantages of invasive ICP monitoring

A

Prediction of outcome: average ICP in the first 48 hrs is a good independent predictor of both mortality and neuropsychological outcome

Response to ICP-lowering therapies (or lack thereof) is a useful predictor of poor outcome.

ICP monitoring did not appear to increase the length of stay or intensity of “brain-specific treatments”

The BTF recommends ICP monitoring (i.e. the weight of international authority is behind this practice, whatever that means in court)

An EVD is both a monitoring tool and a means of managing ICP.

ICP monitoring is continuous

97
Q

Risks of ICP monitoring

A

Risks of anaesthesia
Risks of craniotomy
Risks of haemorrhage, especially in view of brain injury associated coagulopathy
Risk of infection
Malposition and poor monitoring quality
Incorrect readings may stimulate incorrect management
EVDs may clog with debris; parenchymal monitors may “drift” from their zero calibration value, leading to errors in decisionmaking.

98
Q

The ICP waveform

A

The P1 wave = percussion wave
- correlates with the arterial pulse transmitted through the choroid plexus into the CSF,

The P2 wave = tidal wave
- represents cerebral compliance

The P3 wave = dicrotic wave
- correlates with the closure of the aortic valve

Increasing amplitude of the waveform suggests rising intracranial pressure

Decreasing amplitude of the P1 waveform suggests decreased cerebral perfusion

Increasing amplitude of the P2 waveform suggests decreased cerebral compliance

99
Q

Secondary brain injury definition

A

Secondary brain injury is the preventable negative effect of several associated physiological variables on the neurological outcome from a primary brain injury.

100
Q

Parameters to control to avoid secondary brain injury

A 
Increased ICP (aim <22)
Hypotension ( aim SBP >90)
Hypoxia (aim PaO2 >60)
Hypercapnea/hypocapnea
Hypoglycaemia and hyperglycaemia
Hyponatremia and hypernatremia
Hyperthermia
Seizures
101
Q

What are the advantages of saline over mannitol?

A

Its cheap
It does not cause massive diuresis and hypovolemia
It is easy to monitor therapy with blood gases (aiming for a Na+ level around 145-155)
It seems to have some sort of mysterious anti-inflmmatory properties which decreases the permeability of the injured blood-brain barrier

102
Q

Disadvantages of hypertonic saline

A

Need for central venous access
No standards for which concentration to use, or how to give it
Hypokalaemia
Hyperchloraemic acidosis
Should not be used if the patient is chronically hyponatremic
Possible seizures due to wild fluctuations in serum sodium
Increase in circulating volume with risk of fluid overload.
Coagulopathy (APTT and INR)
Altered platelet aggregation.
May affect normal brain more that injured brain which theoretically may worsen herniation

103
Q

risk factors for post-traumatic seizures

A 
Glasgow Coma Scale (GCS) Score < 10
Cortical contusion
Depressed skull fracture
Subdural hematoma
Epidural hematoma
Intracerebral hematoma
Penetrating head wound
Seizure within 24 h of injury
104
Q

major prognostic features of severe brain injury are

A

Age > 60 (poor outcome risk increases by 20-30%)

Pupillary abnormalities (70-90% mortality with bilaterally absent light reflex)

Presence of hypotension (doubles mortality)

Presence of hypoxia (doubles the likelihood of a poor neurological outcome)

Low GCS on presentation (65% mortality if the GCS is 3)

CT scan abnormalities (absence of abnormalities equates to a better prognosis)

Co-morbidities

105
Q

signs of poor prognosis with intracerebral bleed

A

Age over 80
A high NIH-SS score (National Institutes of Health stroke scale)
GCS (3-4)
Volume of blood exceeding 30ml (30cm2)
Infratentorial origin
Intraventricular extension of haemorrhage

106
Q

What counts as Progression of an MCA infarct to a “malignant” MCA infarct:

A

MCA territory stroke of >50% on CT
Perfusion deficit of >66% on CT
Infarct volume >82 mL within 6 hours of onset (on MRI)
Infarct volume of >145mL within 14 hours of onset (on MRI)

107
Q

Patient selection for decra with MMCAS

A

Age <60 years.
Within 48 hours of symptom onset.
It seems the benefit of craniectomy was lost after 96 hours; presumably all the salvageable penumbra has died, and mass effect is maximal.

108
Q

Absolute Contraindications to thrombolysis ]

A

History of head trauma in the last 3 months
History of stroke in the previous 3 months
Arterial puncture in a non-compressible site in the past 7 days
Platelet count less than 100
Any heparin within 48 hours of the stroke
Current anticoagulant therapy,
Hypoglycaemia
Multilobar infarction (more than one-third of a cerebral hemisphere) on CT scan

109
Q

relative contraindications to thrombolysis in stroke

A 
Minor or rapidly improving stroke
Seizure at time of stroke
Major trauma in the past 14 days
GI bleeding in the last 21 days
Haematuria in the last 21 days
110
Q

indications for thrombolysis in stroke

A

Age over 18 and less than 80

Onset of symptoms < 3 hours ago (some places now do upto 4.5 hours)

111
Q

tachniques to monitor for vasospasm

A

clinical
DSA - gold standard, can treat at same time
CTA
transcranial doppler -100% specific (poorly sensitive)
EEG - very sensitive and specific, can pick vasospasm up before clinical signs evident; but not practical

112
Q

gastrointestinal complications seen after spinal cord transection.

A

Ileus
acute gastric dilatation
stress ulcerations

113
Q

metabolic and endocrine complications seen after spinal cord transection.

A

Inappropriate antiduiretic hormone secretion (SIADH)
Hyperaldosteronism
Insulin resistance
Suxamethonium sensitivity
Hypercalcemia, osteoporosis and renal calculi
Hypothermia of spinal cord injury

114
Q

Respiratory consequences of spinal cord transection

A

Decreased maximum tidal volume
Rapid respiratory fatigue
Vital capacity increases in the supine position

115
Q

Cardiovascular consequences of spinal cord transection

A 
Decreased peripheral vascular resistance
Decreased preload
Increased α-adrenoceptor responsiveness
Autonomic dysreflexia
Loss of postural homeostatic reflexes
Bradycardia.
Fixed cardiac output
116
Q

Problems with c spine collar

A

Pressure areas under the collar
- Source of sepsis
- Need for skin grafts
- Increased hospital stay
Increased intracranial pressure
Airway is made more difficult by in-line stabilisation
Central venous access is made more difficult (IJ is out of bounds)
Oral care is made more difficult, increasing the risk of VAP
Nutrition is affected:
- Gastroparesis and ileus results from prolonged immobility
0 Aspiration risk is increased by supine position
Physiotherapy is delayed or impossible
A greater risk of DVT/PE results from prolonged immobility
A minimum of 4 nursing staff are required to turn the patient.

117
Q

Conus Medullaris vs. Cauda Equina Disease

A

Conus Medullaris

Mild motor deficits
Symmetrical deficits
Impaired pain and temperature sensation in a saddle distribution, with intact light touch sense
Achilles tendon reflex is present
Sphincters are impaired early and the impairment is severe
Onset is sudden and bilateral

Cauda Equina

Severe motor deficits
Asymmetrical deficits
Saddle sensory loss is complete; no dissociation of sensory loss
Absent reflexes
Sphincters are impaired late and the impairment is relatively mild
Onset is gradual and unilateral

118
Q

Jefferson fracture:

A

Burst fracture of the atlas (C1)
Usually combined anterior and posterior arch fractures
Results from axial compression of C1
Load of force must come from the vertex of the head, eg. diving into water head first or being thrown against the roof of a car or aircraft;
May also result from hyperextension
Unstable.

119
Q

Hangman’s fracture:

A

Bilateral fracture of the posterior arch of C2 and disruption of the C2-3 junction
The posterior longitudinal ligament may be severed
Due tot his, there may be significant anterior displacement of C2 on C3
This can sever the spinal cord at this level
Caused by C-spine hyperextension with vertical compression of the posterior column
One scanrio suggested by the cllege is “a car accident victim’s head striking the dashboard”.
Unstable.

120
Q

Clay-shoveller’s fracture:

A

Fracture of the spinous process only
An avulsion fracture by the supraspinous ligament of the spinous process caused hyperflexion.
Stable.

121
Q

Status epilepticus definition

A

5 minutes or more of continuous seizure activity, or two seizures with no intervening recovery of consciousness.

122
Q

“Refractory” status epilepticus definition

A

any sort of seizure activity which fails to respond to the usual bolus dose of benzodiazepines and first-line antiepileptics.

123
Q

“Super-refractory” status epilepticus definition

A

any seizure activity seen on EEG which continues despite general anaesthesia, i.e. sedation deep enough to permit major surgery.

124
Q

Management of statu epilepticus

A

First line agents
- Benzodiazepines: boluses every 2-5 minutes; should be given EARLY as gaba receptors decrease during a seizure
- Phenytoin: 20mg/kg loading dose
Must both be given

Second line agents
Midazolam infusion
Phenytoin
Phenobarbital and levetiracetam

Third line agents: for refractory status epilepticus
Propofol infusion, or midazolam infusion, or thiopentone infusion.
At this stage, continuous EEG monitoring becomes mandatory

Fourth line agents: for these, there is little evidence.
Volatile anaesthetic agents
Ketamine
Lignocaine
Magnesium
Pyridoxine
Fifth line therapies:
Hypothermia 
Ketogenic diet
Deep brain stimulation
Surgical management
125
Q

Requirements for the diagnosis of non-convulsive status epilepticus;

A

A change in behaviour or responsiveness
A duration of change for longer than 30 minutes
No obvious seizure activity
Epileptiform discharges on EEG

Not required by may indicate NCSE if there is paradoxical restoration of normal alertness following the administration of an IV benzodiazepine.

126
Q

Risk factors for non-convulsive status epilepticus

A

Structural brain disease:
- Stroke
- Space occupying lesion (blood, pus or tumour)
- Gliosis due to previous stroke, brain injury or neurosurgery
- Dementia
Metabolic
- Sepsis in a patient with known epilepsy

127
Q

Non-convulsive status epilepticus definition

A

Seizure activity seen on EEG without the clinical findings associated with convulsive status epilepticus

128
Q

Positive symptoms seen in NCSE

A 
agitation/aggression
automatisms
uncontrollable blinking
delirium, delusions, psychosis
echolalia
facial twitching (particularly, small periorbital muscles)
nystagmus/eye deviation
129
Q

Features associated with poor outcome in NCSE

A 
Severe mental status impairment
Longer seizure duration
Less than 10hrs: 10% mortality
More than 20hrs: 85% mortality
Unknown cause
130
Q

Drugs that cause status epileptius

A 
cocaine and amphetamines.
In overdose;
 - Phenothiazines
 - Tricyclic antidepressants
 - Olanzapine
 - Isoniazid 
 - Tranexamic acid (need very large doses)
 - Beta-lactam drugs – particularly cephalosporins and carbapenems, and esp in  renal failure

Drug withdrawal:

  • any sort of depressant, but classically from alcohol benzodiazepines and barbiturates.
  • abrupt cessation of (or noncompliance with) regular antiepileptic therapy in a known epileptic.
131
Q

Disadvantages of GCS

A

It was never meant as an assessment tool for trauma.
It is unreliable in patients in the middle range of 9-12
People dont know how to use it correctly.
It has high inter-observer variability
It is inadequate to assess higher cortical functions.
It is inadequate to assess brainstem reflexes.
- Therefore, it cannot be used as a trigger for intubation (GCS of 8)
The eye score is unreliable if the eyes are damaged.
The eye score may be meaningless (it is possible to score an E4 even if one is braindead)
The total score is meaningless:
- The components are more important individually
- Depending on the individual component score, the prognosis may be very different for patients with the same total score.
It is affected by drugs and alcohol.
It is affected by language barriers
Intubation makes a mockery of its verbal conponent
It needs to be modified for use in young children.

132
Q

Classification of brain injury by GCS

A

Severe, GCS < 8–9
Moderate, GCS 8 or 9–12
Minor, GCS ≥ 13.

133
Q

Poor prognostic signs after cardiac arrest

A

Non-CPR downtime of over 8 minutes
ROSC after more than 30 minutes
Absent pupillary responses after 72 hours
Poor motor response after 72 hours (anything worse than withdrawal)
Absent spontaneous eye movements after 24 hours

134
Q

severe hypoxic encephalopathy is associated with the following EEG features:

A

Presence of theta activity
Diffuse slowing
Burst suppression
Alpha coma

135
Q

Unilateral miosis

A

Bilateral mydriasis

Horners syndrome

Damaged sympathetics

136
Q

Bilateral miosis

A

Opiates

Organophosphates

Pontine lesions

Thalamic lesisons

137
Q

Unilateral mydriasis

A

Uncal herniation

Midbrain lesions

138
Q

Bilateral mydriasis

A

Hypoxic brain injury

Bilateral midbrain lesion

Sympathomimetic drugs

Anticholinergic drugs

139
Q

A List of Causes for Altered Swallowing Function in Critical Illness

A

Vascular causes:
Ischaemic stroke

Infectious causes:
Oral and pharyngeal candidiasis
Retropharyngeal abscess, pharyngitis, toncillitis
Meningitis or brain abscess compressing the cranial nerves
Botulism
Tetanus

Neoplastic causes:
Oropharyngeal or laryngeal neoplasm

Drug-induced swallowing dyfunction:
Neuroleptic drugs causing “swallowing ataxia” as an extrapyramidal side-effect
Sedatives

Idiopathic miscellaneous causes:
Head and neck radiotherapy
Critical illness neuromyopathy

Autoimmune causes
Dermatomyositis
Multiple sclerosis
Myasthenia gravis
Guillain-Barre syndrome

Traumatic causes:
Base of skull fracture severing the cranial nerves
Traumatic neck injury
Facial trauma
Surgical complications following head and neck surgery
Prolonged intubation or tracheostomy, desensitising the swallowing reflex
Nasogastric tube

Endocrine and metabolic causes:
Hypocalcemia
Goitre, or invasive thyroid carcinoma
Metabolic encephalopathy, eg. uraemia

140
Q

the swallowing defects due to tracheostomy are as follows:

A

It prevents the larynx from elevating normally

  • thus, hypopharyngeal sphincter fails to open
  • thus, food spills into the larynx

It desensitises the sensation of the larynx, preventing normal cough in response to aspiration. The effect is likened to stroke-related bulbar dysfunction

Long periods of being NG-fed result in the deconditioning of muscles involved in swallowing

141
Q

signs of cerebellar disease

A 
Nystagmus
Titubation (head bobbing)
Truncal ataxia
Staccato speech
Dysarthria
Hypotonia
Kinetic tremor
142
Q

Protein which is specific to CSF

A

β2 transferrin

143
Q

Uses of EEG in ICU

A 
Non-convulsive status epilepticus
Herpes encephalitis
Hepatic encephalopathy
Ischaemic encephalopathy
SAH-associated vasospasm
continuous monitoring
144
Q

EEG findings in Ischaemic encephalopathy

A

Presence of theta activity
Diffuse slowing
Burst suppression
Alpha coma

145
Q

EEG findings in Hepatic encephalopathy

A

Triphasic waves
Early - alpha-wave slowing
Late - high-amplitude irregular delta waves.

146
Q

Argyle-Robertson pupil

A

The pupil accomodates to near and far objects, but fails to react to light

Seen in 
Syphilis
Diabetes
Alcoholic midbrain degerenation
Parinaud syndrome
147
Q

Flow of csf

A 
lateral ventricle
foramina of munro
3rd vent
aqueduct of sylvius
4th ventricle (sits in posterior fossa)

The basal cisterns surround the brainstem

148
Q

grey vs white matter

A

White matter is located centrally and appears blacker than grey matter due to its relatively low density

White matter has a high content of myelinated axons.

Grey matter contains relatively few axons and a higher number of cell bodies

149
Q

Insula

A

The insula forms an inner surface of the cerebral cortex found deep to the Sylvian fissure

clinical significance
Loss of definition of the insular cortex may be an early sign of an acute infarct involving the middle cerebral artery territory = insular ribbon sign

150
Q

Basal ganglia =

A

lentiform nucleus + caudate nucleus

151
Q

Important grey matter structures visible on CT (appear white)

A

cortex, insula, basal ganglia, and thalamus.

152
Q

Internal capsules

A

narrow white matter tracts which contain a high number of axons connecting the corona radiata and cerebral hemisphere white matter superiorly to the brain stem inferiorly
Each internal capsule has an anterior limb and a posterior limb connected at the ‘genu’ (asterisks)

clinical significance
The internal capsules are supplied by perforating branches of the middle cerebral arteries
As these vessels are small they are susceptible to lacunar infarcts
Even a small insult to the internal capsule can have a profound affect on motor and sensory function

153
Q

Corpus callosum - clinical significance

A

Malignant lesions of the brain can grow from one brain hemisphere to the other via the corpus callosum
Elsewhere the falx acts as a relative barrier to direct invasion

154
Q

Posterior fossa contents and blood supply

A

The brain stem
cerebellum
4th ventricle

Blood supply - vertebrobasilar arteries.

155
Q

Brainstem components (top to bottom)

A

Medbrain
pons
medulla oblongata

156
Q

What may a fluid level in the sphenoid sinus indicate

A

can be a helpful sign of a basal skull fracture

157
Q

Vasogenic vs cytotoxic odema

A

vasogenic

  • distrupted BBB
  • affects white matter only (dark on CT)

Cytotoxic

  • in tact BBB
  • due to failure of APT dependent ion transport -> intracellular retention of Na and waer
  • seen as loss of grey-white matter
158
Q

Risj factors for Posterior Reversible Leukoencephalopathy Syndrome

A 
Hypertension                                                                                                         
Eclampsia / Pre-eclampsia
Immunosuppressive therapy
Auto-immune diseases
Porphyria
Acute or chronic renal diseases
TTP / HUS
Infection / sepsis / septic shock
Bone marrow transplant
159
Q

clinical features of increasing intracranial pressure:

A

Cardinal features:

  • Decreased level of consciousness
  • Bradycardia and hypertension
  • Papilloedema
  • Unilateral or bilateral pupil dilatation

Associated features:

  • Headache and vomiting
  • Seizures
  • ST segment changes, T wave inversion
  • QT prolongation
160
Q

Risk factors for NCSE

A

Structural brain disease:

  • Stroke
  • Space occupying lesion (blood, pus or tumour)
  • Gliosis due to previous stroke, brain injury or neurosurgery
  • Dementia

Metabolic
- Sepsis in a patient with known epilepsy

CICM (20 decks)

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