Neurosurgery - Sah, Post Fossa, Spine, Na Balance, Seizures

Front 1

SAH:

what are the scoring systems for SAH? Why use one over the other?

Back 1

there are dozens of scoring systems for SAH, the most commonly used ones are Hunt and Hess (HH), World federation Neuro Surgery (WFNS), PAASH (purely GCS scale) and fischer.

• The first 3 (HH, WFNS, PAASH) are purely clinical grading
  

GCS scale is best indicator of outcomes.

• Fischer is based on CT findings and the amount of blood seen.
  

Best predictor of vasospasm risk.

Front 2

SAH:

outline the WFNS grading scale.

Back 2

primarily based on GCS, motor deficit is only used to distinguish b/w 2-3 that are both GCS 13-14.

once GCS below 12, motor involvement doesn't matter.

Front 3

SAH:

what is the mortality rate of SAH?

how does it relate to the grade on admission?

What is the rebreeding rate and the risk of a re-bleed?

Back 3

overall mortality rate of 50%

this includes 15% who die pre hospital arrival.

% survival per grade is roughly 70%, 60%, 50%, 20%, 10% for grade 1 - 5

re bleeding rate:

highest risk in 1st 24 hours (4%). then 1% per day ongoing.

60% risk of death with any rebleed.

Front 4

SAH:

what investigations are used in the diagnosis of SAH? what is the indication for each test?

Back 4

• CT - first line investigation. 95% sensitivity
  
• If CT negative - LP performed 12 hours post headache, looking for bilirubin xanthachromium.
  
• MRI has greater sensitivity than CT but logistically hard to arrange.
  

Once SAH diagnosed:

angiography to show aneurysm.

- CTA, MRA, angiography (gold standard).

Vasospasm:

• CTA - non invasive, able to detect areas of ischiemia as well.
  
• angiography - gold standard. invasive but can be therapeutic. doesn't detect brain ischaemia like a CT.
  
• transcranial doppler - non invasive test. measures flow velocity in basal cerebral arteries. good to assess changes in flow over time rather than absolute numbers.
  

Front 5

SAH:

outline the issues in SAH management?

Back 5

1 - initial resus, stabilisiation and management with unsecured aneurysm.

2 - securing the aneurysm.

3 - delayed cerebral ischaemia (vasospasm)

4 - hydrocephalus

5 - seizures

6 - systemic complications.

Front 6

SAH:

outline the initial management of SAH until the time of securing the aneurysm?

Back 6

ABC's.

intubate as appropriate for GCS.

aim for "normal" PaO2, PCO2, BSL, temp.

CVS

aim for "normal" BP. hypertension (SBP >160) risks rebleeding. hypotension (SBP < 100) risks cerebral ischaemia.

ECG - frequent arrythmia's, ECG changes. treat conservatively

Fluid:

euvolemia, frequently get electrolyte abnormalities.

Front 7

SAH:

outline the methods for securing the aneurysm?

what is the evidence for which technique to use?

when should the aneurysm be secured??

Back 7

aneurysm can be either clipped (under GA with craniotomy in theatre) or coiled (under GA in lab).

ISAT = largest trail comparing the 2 methods, primary outcome was death and disability/dependence.

Coiling was better= 24% vs 31% death/dependence. only side note was that coiling gives slightly greater rate of delayed re-bleeding but still over all better.

Therefore: now all aneurysm are coiled unless anatomically to difficult (<10%).

When: earlier the better. <72 hours. used to wait till about 7 days, studies now show earlier the better.

Front 8

SAH:

what is delayed neurological decline (DND)?

is it the same thing as vasospasm?

Back 8

DND is the major cause of death and disability after a SAH.

DND is any decline in neurological function after the bleed has been stabilised.

vasospasm is one cause of this, also sezires, hydrocephalus, cerebral odema, electrolytes, sepsis.

Front 9

SAH:

when does vasospasm occur?

what are the signs?

how is it diagnosed?

if they have new symptoms, do they need to be scanned?

Back 9

• about 60% of SAH get some vasospasm, peak occurring day 4-10.
  
• vasospasm is symptoms and clinical signs, as can have radiographic vasospasm with out the clinical signs of altered GCS or focal neurology.
  
• if any new symptoms than they must be scanned as change could be due to other cause then vasospasm (re bleed, oedema, hydrocephalus)
  
• tests include CTA, MRA, angiography (DSA) and transcranial doppler.
  

Front 10

SAH:

What are the treatment options for vasospasm?

Back 10

1 - Nimidopine

2 - Triple H therapy.

3 - endovascular treatments.

4 - NOT considered at this time:

anti coagulant, anti platelet, Mg, statins, temp.

Front 11

SAH:

how should nimodipine be used?

is there evidence for it?

Back 11

should be commenced on diagnosis of SAH and continued for 21 days.

Level 1 evidence for reduction in DND and improved outcomes.

dose = 60mg/4 hourly. ideally O/NG. can be IV. dose can be halved and given 2 hourly if BP an issue.

Front 12

SAH:

triple H therapy - what is it and is there ay evidence?

what is the current guidelines?

Back 12

hypertension, hypervolemia and heamodilution.

• theory is to improve rheology and flow as cerebral auto regulation is impaired by the disease process.
  
• Some evidence for hypertension but not conclusive.
  
• No evidence for heamodilutin of hypervolemia as these INCREASE morbidity.
  
• aim for euvolemia.
  

Front 13

SAH:

why does hydrocephalus develop in SAH?

how is it treated?

are seizures an issue? should every SAH be on anti-epileptics?

Back 13

Hydrocephalus: develops when blood clots in the ventricles blocking CSF drainage. Mx is by EVD.

Seizures: occure in about 5% of SAH and cause neurological decline. routine prophylactic anti-epileptics cause > mortality.

Front 14

SAH:

What are the non neurological complications of SAH?

why do they occur?

Back 14

CVS (occur in > 50% of SAH):

ECG changes, arrythmia, myocardial stunning and CCF/APO.

intracerebral changes cause massive sympathetic surg and autonomic dysregulation.

norad is released in abundance from sympathetic terminals and can cause myocardial stunning.

Management: ventricular dysfunction is usually transient so is usually just supportive care with the focus on the cerebral injury. rarely it can go onto takotsubo type picture.

Fluid/electrolytes:

hypoNa is common along with hypovolemia due to excessive ANP release.

Front 15

SAH:

outline the issues involved in anaesthesia for SAH clipping or coiling?

what are the major physiological principals to discuss?

Back 15

divide into pre-op, intra-op post op.

Pre - Focus on:

assess GCS and impression of how bad ICP is as well as grade of SAH (affects post op plan of wake up vs leave intubated for ICU)

pre-op BP and what heamodynamics to defend intra-op.

Intra - op:

main principals to consider:

CPP - this determines the perfusion of the overall brain. = MAP - ICP (or venous pressure). want to aim for CPP 65-70.

Transmural pressure gradient (TMPG) - the pressure across the aneurysm wall = systolic pressure - ICP. Large TMPG = > risk of aneurysm rupture. so raised SBP or rapidly reduced ICP (e.g. rapid CSF drainage with EVD) can lead to greater pressure and rupture.

ICP - want a stabile ICP without major peaks and troughs as this will affect both the CPP and TMPG.

clearly the need to protect a high enough CPP with elevated BP while at the same time reducing TMPG to prevent rupture are opposite aims

the aim of anaesthesia is to provide a stable/controlled BP and ICP using short acting drugs (remi/propofol) during stimulating times and supporting BP with vasopressors.

key times:

- induction and intubation.

- pinning the head ring.

- raising the bone flap.

- clipping of the aneurysm

Post op:

major decision is if to wake or leave asleep.

if waking aim is rapid wake up for neuro assessment with short acting drugs.

Front 16

SAH:

what drugs are used in SAH operation?

what drugs should be avoided?

Back 16

most commonly would use relaxant induction with remi and propofol.

maintenance: can be TIVA or sevo. theory with sevo is that it reduces auto regulation, increasing blood flow and ICP - this is NOT seen < 1 mac. so if combining sevo with remi, shouldn't be an issues.

Other drugs used:

mannitol 20% - 0.5-1g/kg.

Thio - if aiming for isoelectric EEG. this is used if clamping of artery required to clip it or if get rupture to aneurysm before its clipped.

anti emetics - if going to wake up pt at the end. vomiting would be bad.

Drugs to avoid:

ketamine - increases ICP.

Front 17

SAH:

outline the management of rupture of the aneurysm intra-operatively:

Back 17

surgical emergency = get help:

can get massive blood loss, hard for surgeon to see surgical field.

options to reduce bleeding:

• clamp proximal to the rupture
  
• induce controlled hypotension to reduce bleeding with anaesthetic agent/beta blocker,
  

cerebral protection:

• thiopental bolus for isoelectric EEG.
  
• hypothermia: may be used if surgeon expecting difficult clipping or if going to electively clamp proximal artery.
  

Front 18

Posterior fossa surgery:

what structures are in the posterior fossa and what relevance does this have to the surgery?

Back 18

all the structures that are below the tentorium.

cerebellum:

Brainstem (pons, medulla, lower CN nuclei):

- may have bulbar palsy and aspiration risk.

- cardiovascular nuclei are here, surgical manipulation can cause profound CVS changes.

aquaducts (CSF drainage):

- blockage causes hydrocephalus.

Foramen Magnum:

- sudden changes in ICP in this area can lead to conning and cushing response.

Front 19

Posterior Fossa Surgery:

outline the pre-op issues to be addressed with posterior fossa surgery?

Back 19

CVS:

- due to vomiting or bulbar palsy (and not drinking) may be dehydrated...this is particular issue if going to be beach chair/VAE risk.

- exclude PFO - dangerous for VAE and stroke risk.

RESP:

- bulbar palsy = aspiration pneumonia.

Neuro:

- as there any evidence of raised ICP

- neuro exam and deficits.

Front 20

Posterior Fossa Surgery:

outline the intra op issues?

Back 20

Position:

• can be supine with head rotation, lateral, prone, sitting
  
• prone and sitting especially come with their own complications (VAE, CPP etc)

CVS:

• due to surgical manipulation of CVS nuclei
  
• due to sitting position
  

neuro monitoring:

• due to delicate structures in brainstem often use motor evoked potentials, SSEVP, auditory evoked potential.
  
• can't use NDMR for the case
  
• often run remi.

Front 21

Posterior Fossa Surgery:

Outline the issues for post op / recovery?

Back 21

Pneumocephalus:

• Often the brain is shrunk during operation (head up, mannitol etc).
  
• when its closed can get trapped air inside skull.
  
• this can raise ICP when supine.
  
• particular issue if used N2O - DONT USE N2O in neurosurg (increases ICP, cerebral metabolic rate)
  

PONV:

PONV issue for raised ICP post op.

Pain:

pain from post fossa much more than normal crani as need to cut through a lot of muscle. uncontrolled pain = Increased ICP

Aspiration:

bulbar palsy. if an issue should have NGT

Front 22

Posterior Fossa Surgery:

outline the issues with the sitting position for this surgery?

Back 22

CVS:

• CPP affected as head above heart - therefore need to drive up MAP
  
• legs below heart so venous return decreased.
  
• hypovolemia is particularly bad for this position.
  

Venous Air embolism:

Airway swelling:

head is flexed forward, this can impair venous drainage from the airway - macroglossia is seen.

Spinal injury:

prolonged flexion of the neck can cause ischaimic injury to the cervical spine.

Front 23

Posterior Fossa Surgery:

outline the prevention / detection and management of venous air embolism in the sitting position?

Back 23

VAE results when veins are open to atmosphere above the level of the heart. as these veins are elevated, they can have -ve pressure and entrain air.

Sx/Sgs of VAE:

small amounts of air causes profound pulmonary vasoconstriction leading to elevated right heart pressure, decreased RV ejection and cardiogenic shock.

large air embolus can cause mechanical obstruction in the RV and profound/acute shock/arrest.

Signs:

• hypotension, tachycardia, shock
  
• arrythmia and ECG changes
  
• decreased ETCO2
  
• elevated JVP
  
• mill wheel murmur.
  

Monitors used:

• TOE is the most sensitive but is invasive and need technician.
  
• precordial doppler is most sensitive non invasive.
  
• ET CO2 fall or ET nitrogen rise are good markers
  

Prevention:

• elevation of CVP by volume, raising the legs, limiting the amount of head up.
  
• offset of this is if CVP to high get > surgical bleeding.
  

Management:

INFORM THE SURG TEAM...

• soak the surgical field to limit more air.. can use saline soaked gauze of flood the field with water.
  
• can put pressure on veins in surgical field to close them.
  
• can put pressure on the IJ to prevent further air coming down...risk is it also occludes the carotid which isn't ideal if pt in shock in the sitting position.
• If CVC in position can try to aspirate air out...
• mainstay is supportive care of CVS:
  

- vasopressor/inotrope.

- fluid.

- CPR and change position in profound shock.

- left side down, trendelenburg.

• N2O will make VAE worse - again don't use N2O in neurosurg.
  

Front 24

Spinal Surg:

outline the major pre-op issues that should be addressed for spinal surg?

Back 24

this depends on the indication for spinal surg and the subsequent diseases associated with it.

in general it can be high blood loss area so should be fully CVS / haematology optimised.

Scoliosis:

RESP:

- RFT. can have severe restrictive disease. if <40% predicted may require HDU/ventilation post op.

CVS:

- about 25% have mitral valve prolapse

- can have other congenital abnormalities.

- can have pulmonary hypertension and RV hypertrophy due to resp disease.

Muscle:

association with dystrophy diseases that need to be excluded.

Cervical spine:

assess ROM and risk of unstable cervical spine for induction (e.g. trauma)

Rheumatoid arthritis often require cervical spine fixation and have multiple systems comorbidities that need to be investigated

Front 25

Spinal Surg:

outline the major intra-operative risks associated with spinal surgery?

Back 25

Blood loss:

- epidural veins can bleed a lot.

- worse if pressure on the abdomen (prone) or bladder (no IDC) as these distend epidural veins.

- consider cell saviour.

- must have X match/GH

Prone position has major complications:

Airway:

- ETT must be secured well.

- loss of ETT in prone position is disaster (LMA only bail out)

Eye injury:

- spinal surgery is the most common cause of post operative vision loss (outside of opthalmology)

Abdominal pressure:

- abdo should be allowed to hang free.

- support across chest and pelvis.

- pressure can increase bleeding and cause oat operative organ failure (esp liver).

Sitting position:

not commonly used but can be for cervical spine.

- risks same as for post fossa (macroglossia, CPP, VAE)

Front 26

Spinal Surg:

outline the rate, causes and types of visual loss post spinal surg?

Back 26

Post op Visual Loss (POVL) occurs in 1:100 000 operations (all types of operations)

outside of opthal surgery, >70% of POVL occurs in spinal surg.

80% of these = Ischaemic optic atrophy:

- this is ischaemia of the optic nerve causing unilateral or bilateral vision loss.

- risk are duration, hypotension, blood loss, anaemia, male, obesity.

- however can occur when no risks were present.

- this is NOT due to direct pressure on the eye.

20% = Central retinal artery occlusion:

- due to direct pressure on the orbit in the prone position.

- increase IOP, < perfusion and infarction of the retina.

- associated with pressure injuries to the cornea, eye lid, abrasions, ptosis.

Rare causes:

- central causes, eg CVA/bleed to occipital lobe.

Front 27

Spinal Surg:

outline the risks specific to anterior cervical spine surgery (e.g. ACDF)?

Back 27

Intubation:

unstable C spine (trauma/ RA etc) or immobile C spine may require advanced airway manoeuvres, AFOI etc.

Intra op;

- the surgical plane retracts the carotids and thyroid vessels out of the way

- can get catastrophic bleeding.

Post op:

- delayed airway obstruction due to swelling / bleeding.

- peaks 6-36 hours post op.

- management similar to thyroid bleeding

- if severe cut stitches to relieve pressure, this may not help if its not a heamatoma.

- theatre for emergency airway - may need emergency surgical airway

Front 28

Spinal Surg:

outline you anaesthetic plan for spinal surg?

Back 28

will depend on what the operation is:

Montioring:

low threshold for art line +/- CVC

big IVC

temp prob

BIS (as TIVA common)

Extra:

cell saver if large operation (scoli etc)

neuro physiologist for SSEP/MEPs

Induction:

whatever you deem appropriate to secure the airway

may require DLT for anterior thoracic levels.

secure tube very well

Maintenance:

• If straight for laminectomy etc can use what ever maintenance you want. inhalation/TIVA/NDMR
  
• use TIVA with remi/propofol/vasopressor if SSEP/MEP required.
  
• SSEP CAN HAVE inhalation AND NDMR, in fact SSEP often need NDMR to block out the background noise of small muscle movements.
  
• MEP - CAN NOT HAVE inhalational or NDMR.
  

Extubation:

extubate awake spent breathing.

make sure cuff leak if prone or anterior cervical approach.

Post op:

anterior cervical spine may reqire HDU for airway monitoring.

Pain - opioids, ketamine, gabapentins.

Front 29

Na Balance:

outline the disorders of Na balance that can be seen post brain injury/neurosurg?

outline the physiological characteristics of these?

Back 29

the main ones are:

SIADH

DI

cerebral salt wasting syndrome

Dehydration.

Front 30

Na Balance:

what is the MOA of ADH?

Back 30

ADH is synthesised in the hypothalamus and secreted from the post pit.

secretion is in response to osmoreceptors and high and low pressure receptors.

acts on V1 (vessels) and V2 (renal) receptors.

V2 receptors are on basal membrane in distal tubule.

they cause aquaproins to be inserted in to the apical membrane, dramatically increasing water permeability across the distal tubule and therefore water reabsorption.

NO ADH = 12% of GFR is excreted = >20L/day

100% active ADH = 1% of GFR is excreted = 500ml/day.

Front 31

Na Balance:

SIADH - cause, diagnosis and management?

Back 31

the exact reason why ADH is released in excess is unclear, but get inappropriately high ADH for serum osmolality and volume status.

results in:

- large reabsorption of water in distal tubule/collecting ducts.

- hypervolaemic circulation

- hyponatraemia (<135)

- Hypoosmolar (<185)

- small urine volume with > osmolality than the serum (that is inappropriate for hypoosmolar state)

Diagnosis is as above:

hypoNa, HypoOsmo, hypervolemic with urine osmo > then serum.

Management:

• most cases are treated by simple fluid restriction +/- diuretics (e.g. lasix).
  
• if severe hypoNa can use hypertonic saline to get up to 120-125/stop seizures etc.
  
• rarely use ADH inhibitors (names never heard of)
  

Front 32

Na Balance:

what is central salt wasting syndrome?

how is it different to SIADH?

Back 32

CSWS is another cause of hypoNa occurring in brain injuries.

issue is inability to reabsorb Na in tubule so get hyper excretion of Na, Increased urine output.

This causes hypoNa with normal or Hyper osmo and reduced fluid status.

- so fluid status and osmo are different to SIADH

Front 33

Na Balance:

what is the MOA of DI?

what are the clinical features, dx and mx?

What are the differentials for hypernatraemia post head injury?

Back 33

DI is inadequate ADH so get huge volumes of urine as water is not reabsorbed in the collecting systems.

Sx/Sg:

• polyuria with low urine osmo
  
• hypovolaemic state with hyperNa and hyper osmo
  
• classic sx are polyuria, polydypsia, thirst.
  

Management of DI:

• replace free water: 5% dext IV or NGT.
  
• DDAVP IV or intranasal.
  

Differntials for hyperNa:

• DI
  
• hyperglycemia: gives same combination of urine, serum osmo/Na
  
• dehydration from inadequate fluid: would have small volume, concentrated urine, not high volume dilute like DI.
  
• drugs - esp diuretics (mannitol/lasix)
  

Front 34

Seizure prophylaxis:

outline the evidence for giving seizure prophylaxis in neurosurgical patients?

Back 34

The three Major groups to discuss are:

- SAH

- TBI

- craniotomy for tumor/abscess etc.

SAH:

- seizure is a rare cause of delayed neurological decline - about 5% of cases.

- routine prophylaxis not recommended

- routine prophylaxis increased mortality.

TBI:

- depends on the grade.

- mild (GCS 13-15) and mod (GCS 9-12) do not require prophylaxis.

- Severe TBI (GCS <9) usually get prophylaxis and has been shown to reduce acute sezires (<1 week) but not long term seizures.

Craniotomy:

- cochrane r/v 2015 of non traumatic craniotomy in non epileptics.

- seizure rate = 15-20% post op

- 8 RCTs looking at either phenytoin vs placebo, phenytoin vs keppra, phenytoin vs phenobarbitol.

- only one study showed any benefit of phenytoin vs placebo. several showed no benefit.

Front 35

Seizure prophylaxis:

if giving prophyaxis, what drugs can be used?

at what doses?

what is the benefit/disadvantage of them?

Back 35

the 2 main ones are phenytoin and the newer leveteracitam (keppra).

Key points:

- no major difference in efficacy

- keppra is simpler to use with less side effects

- keppra is more expensive.

phenytoin:

- traditional one used.

- 15mg/kg load then 100mg TDS

- side effects:

main one is induces CYP 450 so alters drug levels.

requires serum measuring.

steven johnson syndrome

platelets

Keppra:

- 20mg/kg load (2g for 100kg)

- 1g BD maintenance

Benefits:

- no enzyme induction

- don't need serum levels

- no effect on platelets, skin.

disadvantage:

- money. about 3x cost.