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45 Cards in this Set
- Front
- Back
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Differentials for POVL |
1/ globe
o corneal damage • direct trauma • exposure keratopathy • chemical injury o acute angle glaucoma o expansion of intra-ocular vitrectomy bubble via use of N2O 2/ Optic nerve injury o Ischaemic optic nerve neuropathy 3/ Vasculature o Central retinal artery occlusion o Vertebral artery injury 4/ Brain o Cortical blindness • Stroke • haemorrhage |
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Risk factors for POVL
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1/ Patient
-male -obesity possibly: DM, smoking, atherosclerosis, HTN, polycythaemia 2/ surgical -prolonged procedure - prone - external eye compression - large blood loss - spinal fusion 3/ anaesthetic - obstructed venous return - prolonged position - large amount of crystalloid use - external eye compression |
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Blood supply to orbit
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-retina via retinal artery under auto-regulatory control until IOP >40mmHg
- optic nerve anterior: via posterior choriodal artery until IOP >60mmHg (autoregulated) posterior via ophthalmic artery not autoregulated |
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Spinal cord supply
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-anterior spinal artery from vertebral arteries at foramen magnum. Runs in median sulcus. Supplies anterior 2/3. Receives radicular artery collateral, largest from artery of Adamkiewicz (low thoracic, high lumbar), also others from intercostal and iliac
- posterior spinal arteries. 2 run down posterior aspect. some collateral supply. supplies posterior 1/3 - vasa corona between the anterior and posterior but not always complete - number of watershed areas at high risk of ischaemia |
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Grade of aneurysm (World federation of neurosurgeons WFNS)
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• Grade 1 – GCS 15 nil motor deficit
• Grade 2 – GCS 13-14 nil motor deficit • Grade 3 – GCS 13-14, motor deficit • Grade 4 – GCS 7-12, motor deficit present or absent • Grade 5 – GCS 3-6, motor deficit present or absent |
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Hunt-Hess
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Grade Criteria*
I Asymptomatic, or minimal headache and slight nuchal rigidity II Moderate to severe headache, nuchal rigidity, no deficit other than cranial nerve palsy III Drowsiness, confusion, or mild focal deficit IV Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances V Deep coma, decerebrate rigidity, moribund appearance * Serious systemic diseases, such as hypertension, diabetes, severe arteriosclerosis, chronic pulmonary disease, and severe vasospasm seen on arteriography, result in placement of the patient in the next less favorable category. |
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Fishers
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Fishers - based in CT scan and provides risk of vasospasm
• Group 1 – No blood detected • Group 2 – Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm • Group 3 – Localized clots and/or vertical layers of blood 1 mm or greater in thickness • Group 4 – Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present |
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vasospasm
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-highest risk day 4-10
- risk is ~30% -due to breakdown products of Hb -use nimodipine 60mg PO Q4H or 0.5-2mg/hr IV for 3/52 for treatment. Not great at prophylaxis. Improves clinical vasospasm but not radiological -tripe H therapy for prevention Hypertension MAP +20% Hypervolumia CVP 8-12mmHg Hct 0.3-0.35 continue until improvement for 3-7/7 - balloon angioplasty or injection of vasodilators eg nimodipine, papaverine - Mg infusion - statins |
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complications of HHH
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- hypertensive brain swelling
- pulmonary oedema - LV failure/myocardial ischaemia and infarction electrolyte abnormalities - invasive monitoring complications eg infection |
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medical complications of SAH
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- occur in 40%
1/ rebleeding 4% in 1st 24/24, then 1.5%/day for 4/52 has 50% mortality 2/ DND (delayed neurological deficit) assoc with vasospasm 3/ raised ICP from clot mass effect, ischaemia, hydrocephalus 4/ systemic HTN 5/ cardiac effects from catecholamine surge - myocardial stunning - ST changes and TWI - 10% get AMI 6/ pulmonary oedema 7/ hyponatraemia from SIADH (euvolumic) or CSWS (hypovolumic) 8/ seizures 9/ others relating to immobility: DVT, pneumonia |
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Diabetes insipidus
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-inadequate ADH release
-causes: TBI, SAH, pituitary surgery -features: polyuria, polydipsia (in awake patients) - diagnosis Na >145mmol/L serum osmolality >305mOsm/L urine osmolality <350mOsm/L urine volume >3L/day or >3mls/kg for 2 consecutive hours -management replace H20 (NG) or IV via 5% dextrose ADH replacement 0.4µg or nasal 100-220µg avoid over rapid correction |
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Hyponatramia
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-causes: SIADH, iatrogenic, CSWS
SIADH - inappropriate excessive release of ADH means concentrated urine and reabsorb H2O -diagnosis: serum osmolality <280mOsml/L serum Na <135mmol/L urine Na >18mmol/l urine osmolality >serum osmolality clinical euvolumia (key difference to CSWS - will be hypovolumic) -treatment with fluid restriction, may need 3% saline if symptomatic (60% of weight x2 = mls of 3% saline to increase serum Na by 1mmol/hr, no faster than 0.5mmol/hr of >48/24 normal thyroid, renal and adrenal fn |
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CPP
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= MAP - ICP/CVP (whichever is higher)
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ICP
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-normal 5-12mmHg. Increases reflect an increase in contents (blood, CSF or brain)
- venous: ensure no elevations in intrathoracic pressure eg PEEP, coughing or obstruction to venous return from ETT ties -arterial: PaO2, PaCO2, pH, CMRO2, hyperthermia -brain: Na >145mmol, mannitol 0.5-1g/kg, dexamethasone, -CSF - lumbar drain |
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CBF
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-autoregulated between 50-140mmHg. If chronic HTN, curve is right shifted
-autoregulation lost with acidosis, hypoxia, hypercarbia, brain injury -factors that effect CBF --CMRO2 - increases with seizures, pain, anxiety, reduced with coma, hypothermia, anaesthetic agents --PaCO2 - increases linearly with 1mmHg change CBF by 4% --PaO2 vasodilation below PaO2 of 60mmHg --temperature-- hypothermia reduces cerebral metabolsim -- uncoupling of metabolism and flow with volatile agents >1MAC. IV agents decrease ICP (except ketamine) - normal temperature and glucose |
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awake craniotomy
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- allows for intra-operative assessment of patients neurological status
- indications: epilepsy surgery, movement disorder surgery eg parkinsons, tumour in eloquent area eg speech pre-op: - patient selection crucial: motivated, well-informed, able to lie still, not anxious or confused and can communicate efffectively - relative CI: GORD, obesity, airway obstruction - analgesia from scalp block intra-op - clear drapes and quiet theatre - technique: sedation (propofol/dexmetotomidine) or asleep/awake/asleep technique with remi/prop and LMA - difficult access to head and remote airway - Cx: seizures, VAE, brain swelling, restlessness, respiratory obstruction |
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phenytoin
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15mg/kg loading dose then 2mg/kg
can give 50mg/hr incompatible with large number of drugs, best to run on seperate line, particularly if running TIVA. |
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craniotomy issues
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- limited access to head
- limited access to lines - avoiding SNS stimulation with intubation and extubation - VTE prophylaxis with non-pharmacological measures (high risk of bleeding) - treating elevated ICP - paralysis |
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CVC considerations
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- is there a risk of large bleeding eg AVM, emergency aneurysm
- do I need to give vasoactive drugs - risk of VAE and is tip in correct position - need for CVC post op eg SAH - will it be in the surgeons way |
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tight brain troubleshooting
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A and B
- is PaO2 >60mmHg, is PaCO2 low normal, send ABG - no increased intrathoracic pressure eg PEEP, coughing, gas trapping, bronchospasm C - arterial: hypo/hypertensive - no venous obstruction from ETT, high airway pressures as above D - well anaesthetised - paralysed - febrile - fitting |
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'tight brain' and anaesthetic agent
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- propofol TIVA shows a decrease in ICP and improved CPP when compared to volatile
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treatment tight brain
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- kellie monroe doctrine
1/ brain - dexamethasone - thiopentone - mannitol 20% (2.5ml/kg = 0.5g/kg) - Na 2/ blood - venous - airway pressures, ETT ties, elevate head - arterial - PaO2, PaCO2, CMRO2, temp 3/ CSF - drain |
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avoidance of chronic pain post craniotomy
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- acute and chronic pain common post craniotomy
- multimodal approach recommended - LA and nerve blocks not shown to significantly reduce acute pain but does dramatically reduce chronic pain incidence |
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scalp block
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Need to block 6 nerves
- supratrochlear and supraorbital at supraorbital notch - auriculotemporal (posterior to temporal artery at external auditory meatus) - zygomaticotemporal (latreal border of orbit) - lesser occipital (posterior border of SCM) - greater occipital (mid 1/3 of line between occipital protuberance and mastoid process) |
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cerebral mets
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- median survival ~1/2 year
- treatment mostly palliative - mets are most common posterior fossa tumour in adults |
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GCS
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- best score
- eyes 4 - open spontaneously 3 - open to voice 2 - open to pain 1 - none Verbal 5 - orientated 4 - disorientated 3 - inappropriate 2 - moaning 1 - none Motor 6 - follow command 5 - localise pain 4 - withdraw to pain 3 - abnormal flexion 2 - abnormal extension 1 - none |
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BP and SAH
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- in unsecured aneurysm 120-160mmHg
aim to balance maintaining CPP in setting raised ICP vs causing rebleed - in secured >160mmHg |
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issues with SAH clipping
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- fasting status of patient
- avoid hypotension (due to impaired autoregulation and risk of hypoperfusion) - avoid hypertensive surges at intubation, insertion of pins - dont want to increase the transmural pressure gradient across the aneurysmal wall |
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Aneurysm coiling issues
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- remote anaesthesia including transport, help
- poorly equipped - poor ergonomics eg C arm pulling out lines/ETT. Cramped - less assistance from technicians and nurses no PACU, have to transport at end of case |
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coiling complications
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- must have neurosurgical support |
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nimodipine
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- dihydropyridine Ca channel antagonist
- exact MOA in vasospasm unknown ? anti-platelet action ? preferential cerebral vasodilator ?prevention of Ca entry into ischaemic neurons - improves clinical outcome but no change to radiological vasospasm |
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nimodipine how to give
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- IV infusion 0.5-2mg/hr or PO 60mg PO Q4H
- give for 10/7 post-op problems 1/ hypotension 2/ raised ICP from cerebral vasodilation 3/ abnormal LFTs 4/ metabolised by liver, need to dose reduce in liver failure 5/ given centrally |
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hypothermia
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- CBF is decreased with hypothermia due to reduction in CMRO2
- CMRO2 decreases by 7% for each decrease in 1 degree - flow metabolism is maintained - ICP is decreased - ?inhibits the mediators of secondary injury |
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IHAST2
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- NEJM
- surgically clipped SAH within 2/52 of bleed - WFNS 1-3 - randomised to hypothermia (33) or normothermia (36.5) - outcomes hypothermia did not improve 3/12 neurological outcome increased risk of bacteraemia in hypothermic group |
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barbiturates for cerebral protection
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- reduce CMRO2, CBF and ICP
- max reduction with isoelectric EEG - need 5mg/kg and infusion titrated to burst suppression - limitations hypotension monitoring of EEG |
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temporary clip
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- decrease BP just prior to clip going on ?propofol
- clip used to achieve focal hypotension when giant aneurysm, big, ruptures or calcified - 15mins tolerated without issue, 30mins will have 100% ischaemic injury - once clip on increase BP to achieve collateral flow to distal areas |
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ruptured aneurysm
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- mortality from intraop rupture is 35%
- must have plan in place goals -lower BP quickly - use agents with rapid onset and easy to titrate eg esmolol, propofol, GTN - deal with massive transfusion - get help |
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ISAT trial
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- Lancet 2002
- compared coiling and clipping of SAH in ~2000 patients - RCT multicentre - primary outcome was death at 1 year - secondary outcome was rebleedign and risk of seizures - found that ruptured aneurysms suitable for either clipping or coiling, coiling resulted in less death ~25% and less neurological dependency at 1 year - balanced by higher risk of rebleeding and lower rate of complete occlusion in coiling group |
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ISAT trial controversy
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- large amount of patients excluded as low number suitable for coiling
- clip group had far worse outcomes that published by neurovascular centres |
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AVMs
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- issues similar to SAH
- take longer than SAH - need central access - bleeding can be insidious and difficult to stop - hypotension requested - more likely to keep patient tubed and ventilated for 24/24 even if surgery goes well |
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transphenoidal surgery
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patient
- disease and side effects eg acromegaly anaesthetic - shared airway - remote anaesthesia - prolonged case - use throat pack - prepare for hypertension with insertion of vasoconstrictors into nose - packed nose at end of case surgical - risk of bleeding - post op DI |
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volatiles and CBF
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at 1 MAC halothane> desflurane> isoflurane> sevoflurane
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VAE
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pre-op
- ensure no PFO or passage to allow L-R shunt -discuss with surgeons position which allows best mix of surgical access and head down - discuss with surgeons what to do in event of VAE - consideration of insertion of R heart catheter to allow aspiration of air if it occurs intra-op CVS - keep well filled with IV fluids and encourage venous return - compress jugular veins during high risk or in event of VAE - ensure no air in IV lines Resp - using IPPV and avoid SV to keep intrathoracic pressure positive other - vigilance for signs of VAE |
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signs of VAE
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- TOE has highest sensitivity
- praecordial doppler has good sensitivity and moderate specificity and non-invasive - ETCO2 has good sensitivity but poor specificity - others eg praecordial stethoscope, CVC, HR are poor markers unless massive |
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management of VAE
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- limit further entrainment of air by warning surgeons, increasing venous pressure by placing entry site below level of heart, bolus of fluid
- compress veins proximal to entry site - surgeons flood field, bone wax - increase intrathoracic +ve pressure - place in L lateral position if possible to avoid obstruction to RVOT |
