Neuro Flashcards
SAH risk factors
female age >50 smoking OCI alcohol HTN Connective tissues disorders PKD FHx previous SAH coarctation of aorta fibromuscular dysplasia
WFNS
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
modified fisher scale
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.
Poor prognositc signs with SAH
pre-existing severe medical illness clinically symptomatic vasospams delayed cerebral infacrt hyperglycaemia fever anaemia medical complications including pneumonia and sepsis
Causes of neurological deterioration following SAH
metabolic causes - CO2, O2, ammonia, temp, pH ,electrolytes, glucose
Drugs
Seizures
intracranial hypertension
hydrocephalus
re-bleed
Complications following SAH
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
vasospasm definition
dynamic narrowing of vessels
delayed neurological deterioration
clinically detected neuro deterioration after stabilisation that is not due to rebleeding
may be due to multiple other causes
delayed cerebral ischamia
any neurological deterioration (focal deficit, GCS drop by 2 or more) for >1 hour
presumed due to ischaemia - all other causes exlcuded
risks for vasospasm
higher radiological grade - esp if blood in basal cisterns or lateral ventricles
age <50
hypertension
hyperglycaemia
no difference if aneurysm coiled or clipped
prevention of vasospasm
oral nimodipine - 60mg q4H for 21 days
reduces risk of ischamic stroke by 34%
risks for seizures post SAH
MCA clots infarction clipping poor grade
VTE prophylaxis after SAH
all should have UFH unless unsecured and awaiting intervention
Should be started at least 24 hours after aneurysm secured
Modified Rankin score
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
Causes of aseptic meningitis
viral - most common (often enterovirus or coxsackie) partially treated bacterial meningitis TB meningitis fungal lymphoma sarcoidosis
causes of seizures with meningitis
raised ICP
cerebritis
cerebral abcess
septic venous thrombus
Main point on cryptococcal meningitis
- who it affects, how Dx, treatment
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)
Encephalitis - definition and causes
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
Clinical presentation of encephalitits
key - focal neurological signs indicating involvement of parenchyma
- esp speech disturbance, seizures, altered cognition, LOC
Clinical signs of cerebral venous thrombosis
headache
focal deficits - esp cranial nerves
seizures
papilloedema
third nerve palsy
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
fourth nerve palsy
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
sixth nerve palsy
paralysis of lateral rectus
unable to turn eye out - results in horizontal gaze palsy
diplopia
risks of cerebral venous/sagital sinus thrombus
infection - meningitis, epidural/subdural abcess, facial/dental infection
DKA
COCP
ecstasy use
GBS investigations
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
Clinical findings GBS
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
Miller fisher varient GBS
cranial nerves predominate
ataxia, areflexia and opthalmoplegia
stongly associated with campylobacter jejuni
may have GQ1b antibodies
Treatment of GBS
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
Indications for intubation in GBS
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)
Drugs that may cause CVS instability in GBS
Low BP - morphine, frusemide, thio
Increased BP - ephedrine, dopamine, isoprenaline,
arrhythmias - sux
Poor prognostic features of GBS
> 60yrs
rapid progression or quadrapersis in <7 days
need for ventilation
preceding diarrhoeal illness
Critical illness polyneuropathy
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)
Critical illness myopathy
linked with asthma and some drugs (steroids, NMBDs, aminoglycosides)
reflexes and sensation usually normal
CK often raised
muscle necrosis is seen on histology
Intensive care acquired weakness (ICUAW)
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
Treatment of MG
anticholinesterase drugs - pyridostigmine
steroids
IVIg - 5 days may have long term benefit
thymectomy
Triggers of MG crisis
infection pregnancy surgery drugs - - Abx - Antiarrythmics - LAs - muslce relaxants - analgesia
Factors predicting need for ventilation post op in MG patient
long pre-op duration of MG
high anticholinesterase requirement
co-existant resp disease
pre-op viral capacity of <2.9L
Key points about motor neuron disease
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
SHort notes on botulism
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
tetanus clinical presentation
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)
management of tetanus
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)
Delirium definition
a disturbance of consciousness that develops over a short period of time, fluctuates and is associated with perceptual changes, such as hallucinations
Clinical subtypes of delirium
Hypoactive - most common
Hyperactive - only 5% of cases
Mixed
impact and relevance of delirium in ICU patients
seen in upto 70% ventilated patients
patients have a 3x higher 6/12 mortality
associated with long term cognitive decline and early dementia
Pathophysiology of delirium
neuroinflammation impaired oxidative metabolism altered cerebral blood flow increased BBB permeability neurotransmitter imbalance -> cholinergic hypoactivity relative state of dopamine excess
Modifiable risk factors for delirium
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
non-modifiable risk factors for delirium
>65 dementia depression cognitive impairment liver impairment institutionalised resident
Screening tools for delirium
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
RASS score
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
dexmedetomidine MOA
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
dexmedatomidine side effects
transient HTN hypotension, brdycardia, nausea
dexmedatomidine dose
0.1 - 1mcg/kg/min infusion
can load with 1mcg/kg over 10mins
dexmedatomidine evidence
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
pharmacological treatment for delerium
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
Preconditions for brain stem testing
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)
brain stem testing
- 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
testing oculo-vestibular reflex
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
apnoea test
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
Investigations for brainstem testing
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
Brain death testing with regards to children
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
Responsibilities of ICU staff in organ and tissue donation
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)
Absolute contraindications to organ donation
HIV
CJD
metastatic or non curable malignant disease
history of malignancy that poses high risk of transmission (melanoma)
Relative contraindications to organ donation - need individual consideration
past malignancy with a long cancer free interval
treated bacterial infection
infection with hep B and C
risk factors for HIV and viral hepatitis
Common medical issues seen in potential donors
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
warm ischaemia time
time from treatment withdrawal to start of cold perfusion
most important phase is when SBP <60
impacts on graft function
WIT for
- liver
- kidney
- pancreas
- lungs
liver - 30mins
kidney and pancreas 60mins
lungs 90mins
DCD vs brain death liver
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
DCD vs brain death kidney
DCD has higher incidence of delayed graft function
DCD donor criteria
ventilated patient in whom treatment is to be withdrawn
when death is likely to occur in time frame
medical suitability
Meeting Maastricht criteria
Maastricht criteria
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
Important points for discussion with family re DCD
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
retrieval related procedures occurring before death -
- guidelines
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
retrieval related procedures occurring before death include;
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
Determination of death - DCD
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
VTE prophylaxis in neurosurgical patients
guidelines by Neurocritical care society - 2016
VTE prophylaxis aneurysma; SAH
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
VTE prophylaxis TBI
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
VTE prophylaxis SCI
Start as early as possible, within 72 hours of injury
recommend against use of mechanical measures alone
Early post-trauma seizures - impact and Mx
Phenytoin recommended to decrease incidence of early seizures (<7 days) if benefit outweighs risk BUT early PTS have not been associated with worse outcomes
DECRA trial
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
RESCUE icp
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
What do the Brain trauma foundation guidelines outline
treatment, monitoring and threshold
Complications of prolonged immobilisation (SCI)
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
ASIA scoring
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
Muscle grading
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
NEXUS guidelines
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)
what type of CT scan done from SCI
multi-detecot row CT (MDCT) - sensitivity of almost 100% (including ligamentous injury)
ICU Mx principles for SCI
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
Insults know to independently worsen outcome in secondary brain injury
hypotension SBP <90 hypoxia sats <90% hypoglycaemia hyperpyrexia - temp >39 prolonged hyocapnia - CO2 <30
Phases of cerebral blood flow alteration after TBI
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
Indications for ICP monitoring
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)
Vessels that can be viewed using transcranial doppler
anterior, middle and posterior cerebral arteries
terminal internal carotid
anterior and posterior communicating arteries
Complications of Decompressive craniotomy
Herniation though the defect Delayed paradoxical herniation Subdural hygroma Infection Bleeding Post-traumatic hydrocephalus "Sinking Flap Syndrome" Bone resorption
Causes of coma with miosis
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
Causes of 6th nerve palsy
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)
Advantages of invasive ICP monitoring
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
Risks of ICP monitoring
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.
The ICP waveform
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
Secondary brain injury definition
Secondary brain injury is the preventable negative effect of several associated physiological variables on the neurological outcome from a primary brain injury.
Parameters to control to avoid secondary brain injury
Increased ICP (aim <22) Hypotension ( aim SBP >90) Hypoxia (aim PaO2 >60) Hypercapnea/hypocapnea Hypoglycaemia and hyperglycaemia Hyponatremia and hypernatremia Hyperthermia Seizures
What are the advantages of saline over mannitol?
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
Disadvantages of hypertonic saline
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
risk factors for post-traumatic seizures
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
major prognostic features of severe brain injury are
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
signs of poor prognosis with intracerebral bleed
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
What counts as Progression of an MCA infarct to a “malignant” MCA infarct:
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)
Patient selection for decra with MMCAS
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.
Absolute Contraindications to thrombolysis ]
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
relative contraindications to thrombolysis in stroke
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
indications for thrombolysis in stroke
Age over 18 and less than 80
Onset of symptoms < 3 hours ago (some places now do upto 4.5 hours)
tachniques to monitor for vasospasm
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
gastrointestinal complications seen after spinal cord transection.
Ileus
acute gastric dilatation
stress ulcerations
metabolic and endocrine complications seen after spinal cord transection.
Inappropriate antiduiretic hormone secretion (SIADH)
Hyperaldosteronism
Insulin resistance
Suxamethonium sensitivity
Hypercalcemia, osteoporosis and renal calculi
Hypothermia of spinal cord injury
Respiratory consequences of spinal cord transection
Decreased maximum tidal volume
Rapid respiratory fatigue
Vital capacity increases in the supine position
Cardiovascular consequences of spinal cord transection
Decreased peripheral vascular resistance Decreased preload Increased α-adrenoceptor responsiveness Autonomic dysreflexia Loss of postural homeostatic reflexes Bradycardia. Fixed cardiac output
Problems with c spine collar
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.
Conus Medullaris vs. Cauda Equina Disease
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
Jefferson fracture:
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.
Hangman’s fracture:
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.
Clay-shoveller’s fracture:
Fracture of the spinous process only
An avulsion fracture by the supraspinous ligament of the spinous process caused hyperflexion.
Stable.
Status epilepticus definition
5 minutes or more of continuous seizure activity, or two seizures with no intervening recovery of consciousness.
“Refractory” status epilepticus definition
any sort of seizure activity which fails to respond to the usual bolus dose of benzodiazepines and first-line antiepileptics.
“Super-refractory” status epilepticus definition
any seizure activity seen on EEG which continues despite general anaesthesia, i.e. sedation deep enough to permit major surgery.
Management of statu epilepticus
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
Requirements for the diagnosis of non-convulsive status epilepticus;
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.
Risk factors for non-convulsive status epilepticus
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
Non-convulsive status epilepticus definition
Seizure activity seen on EEG without the clinical findings associated with convulsive status epilepticus
Positive symptoms seen in NCSE
agitation/aggression automatisms uncontrollable blinking delirium, delusions, psychosis echolalia facial twitching (particularly, small periorbital muscles) nystagmus/eye deviation
Features associated with poor outcome in NCSE
Severe mental status impairment Longer seizure duration Less than 10hrs: 10% mortality More than 20hrs: 85% mortality Unknown cause
Drugs that cause status epileptius
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.
Disadvantages of GCS
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.
Classification of brain injury by GCS
Severe, GCS < 8–9
Moderate, GCS 8 or 9–12
Minor, GCS ≥ 13.
Poor prognostic signs after cardiac arrest
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
severe hypoxic encephalopathy is associated with the following EEG features:
Presence of theta activity
Diffuse slowing
Burst suppression
Alpha coma
Unilateral miosis
Bilateral mydriasis
Horners syndrome
Damaged sympathetics
Bilateral miosis
Opiates
Organophosphates
Pontine lesions
Thalamic lesisons
Unilateral mydriasis
Uncal herniation
Midbrain lesions
Bilateral mydriasis
Hypoxic brain injury
Bilateral midbrain lesion
Sympathomimetic drugs
Anticholinergic drugs
A List of Causes for Altered Swallowing Function in Critical Illness
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
the swallowing defects due to tracheostomy are as follows:
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
signs of cerebellar disease
Nystagmus Titubation (head bobbing) Truncal ataxia Staccato speech Dysarthria Hypotonia Kinetic tremor
Protein which is specific to CSF
β2 transferrin
Uses of EEG in ICU
Non-convulsive status epilepticus Herpes encephalitis Hepatic encephalopathy Ischaemic encephalopathy SAH-associated vasospasm continuous monitoring
EEG findings in Ischaemic encephalopathy
Presence of theta activity
Diffuse slowing
Burst suppression
Alpha coma
EEG findings in Hepatic encephalopathy
Triphasic waves
Early - alpha-wave slowing
Late - high-amplitude irregular delta waves.
Argyle-Robertson pupil
The pupil accomodates to near and far objects, but fails to react to light
Seen in Syphilis Diabetes Alcoholic midbrain degerenation Parinaud syndrome
Flow of csf
lateral ventricle foramina of munro 3rd vent aqueduct of sylvius 4th ventricle (sits in posterior fossa)
The basal cisterns surround the brainstem
grey vs white matter
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
Insula
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
Basal ganglia =
lentiform nucleus + caudate nucleus
Important grey matter structures visible on CT (appear white)
cortex, insula, basal ganglia, and thalamus.
Internal capsules
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
Corpus callosum - clinical significance
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
Posterior fossa contents and blood supply
The brain stem
cerebellum
4th ventricle
Blood supply - vertebrobasilar arteries.
Brainstem components (top to bottom)
Medbrain
pons
medulla oblongata
What may a fluid level in the sphenoid sinus indicate
can be a helpful sign of a basal skull fracture
Vasogenic vs cytotoxic odema
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
Risj factors for Posterior Reversible Leukoencephalopathy Syndrome
Hypertension Eclampsia / Pre-eclampsia Immunosuppressive therapy Auto-immune diseases Porphyria Acute or chronic renal diseases TTP / HUS Infection / sepsis / septic shock Bone marrow transplant
clinical features of increasing intracranial pressure:
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
Risk factors for NCSE
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
