Neuro

Question 1

What are the goals of anaesthetising a patient w raised ICP?

Answer 1

CBF=(MAP-ICP (if ICP >CVP))/CVR
A: c-spine protection
intubate w adequate SNS blunting (pretreatment with lignocaine may attenuate ICP rise with intubation)
tape vs tie (limit impediment to venous drainage)
B: hyperventilate to eTCO2 30-32mmHg
Maintain SpO2>96% & PaO2>90mmHg
avoid coughing (sufficient sedation & m relaxation)
C:
avoid hypotension (biggest cause of secondary brain injury (& in conjunction with hypoxaemia, hypotension can cause reactive vasodilation & elevations in ICP))- treat aggressively
Maintain CPP 50-70mmHg (or >60mmHg, avoid CPP <50mmHg or normalisation of BP in pts w chronic HTN. Aim SBP at least 90) w fluid +/- vasopressors- intervene for hypertension if CPP >120mmHg & ICP >20mmHg
iAL
urinary catheter (esp if mannitol used)
Drugs:
adequate sedation, m. relaxation
mannitol 0.5g/kg
HTS (NaCl 3%) 1-2mL/kg
paracetamol for raised temp
E:
Maintain normothermia (esp avoid hyperthermia while excessive hypo may ex coagulopathy)
30 degrees head-up to improve venous drainage
Fluids:
Keep patients euvolemic & normo- to hyperosmolar (serum osmolality should be kept >280mOsm/L)
Keep serum Na+ above 130mmol/L
Avoid free water, Isotonic saline is preferred to glucose-containing solutions
Judicious use maintenance fluids to avoid cerebral oedema
Glucose:
Normo (insulin if necessary)
Haematology:
Ensure Hb adequate to optimise O2 content of blood, correct any coagulopathy in event of intracranial bleeding
Investigations:
CT, routine bloods incl clotting, U&Es, ABGs, X-match

Question 2

What’s the incidence of airway compromise requiring re-intubation after cervical spinal surgery?

Answer 2

up to 1.9%

Question 3

What’s the incidence of spinal cord damage & paralysis after corrective spinal deformity surgery?

Answer 3

1%

Question 4

What are some considerations with the use of throat packs?

Answer 4

Clearly justify the use of throat packs (risk/benefit)
Document it on the WHO safer surgery checklist.
Part of it must be left outside the mouth so easily visible.

Question 5

For which cases should an IDC be inserted? Why?

Answer 5

All cases lasting >2h & all major cases & all pts with spinal cord injury. An enlarging bladder may increase intra-op blood loss for spinal surgery as increased pressure may be transmitted to the valveless epidural veins.

Question 6

Considerations for spinal surgery?

Answer 6

PATIENT:
degenerative spine disease & herniated discs: pts under 60yrs of age
spine surgery for stenosis: pts aged >60yo

Airway management may be challenging for pts undergoing cervical or upper Tx spine surgery or with diseases impacting airway anatomy, neck or jaw movement (OA, RA, ank spond, NM disorders, prev head/neck radiation).
consider stability of cervical spine.

Pulm evaluation: may be restrictive lung physiology (decr VC & TLC), cor pulmonale & pulm HTN if significant spinal deformity.
PFTs with DLCO important for pts with lung disease undergoing thoracotomy for spine surgery to assist planning of ventilation.

Cardiac: consider that cardiac dysfunction may be a result of the pathology for the surgery (eg. pulm HTN if severe kyphoscoliosis)
pulm HTN & CCF sig risk periop adverse events
exercise tolerance estimation may be impaired by the pathology for which having spinal surgery
Spinal fusion & instrumentation= intermediate risk PACE. one or 2 level decompression sans fusion= low risk.
prone position: 12-24 % reduction cardiac index cf supine (reduced venous return, reduced LV compliance cf supine)

musculoskeletal: positioning may be challenging if restricted ROM- should position them in a position that’d be comfortable awake. could trial positioning pre sedation/induction.

Neuromuscular: evaluate & document existing motor & sensory deficits. existing motor deficits impact NMBDs & positioning of NMT.

Labs: usually unnecessary for single-level decompression if limited comorbidities. For multiple vertebral levels, fusion +/- instrumentation or procedures requiring osteotomies: Hb, plt, Cr, blood type & screen.

PATHOLOGY:

PROCEDURE:
May be emergency or elective
ERAS considerations to reduce LoS, complications, improve pt experience
multi D
pre: counselling, nutrition Ax Mx, optimise anaemia, cease smoking @ least 4/52, etoh @ least 4-8wks, limit fasting
intra: multimodal analg incl opioid sparing, antiemetics, normothermia, proph ABx, goal-directed fluid, VTE proph, surg technique/drain Mx
post: early mob’n, enteral intake, ongoing vte/ponv/pain prophylaxis
ongoing audit/QA of above outcomes
pre= optimise intra= stress minimisation post= protocolised normalisation

A: well-secured ETT (consideration of prone position, should have an action plan for intra-op ETT displacement), ensure access to the pilot tube & that it isn’t damaged during positioning.

B: lung protective (may be long)
If thoracotomy, may require lung isolation w DLT or BB

C: large-bore IV access x2 as spinal surgery= high bleeding risk, intra-op access to pt difficult. Have low threshold for art line depending on pt & surg factors.
Target MAP close to pts baseline to optimise perfusion of SC, optic nerve & other visual structures & other organs.
Reasons to avoid hypoT during spine surgery incl:
-severe stenosis–> high risk SC ischaemia
-spinal instrumentation & distraction may–> reduce SC perfusion & result in ischaemia
-risk POVL; defending MAP hasn’t been proven but is recommended to minimise the risk of ION
-sustained hypoT may be ass’d w incr 30 day mortality (even brief periods of hypoT may be ass’d w incr risk AKI, myocardial & neurol injury)
DON’T use hypotension to limit periop blood loss for spinal surgery; risks w hypoT, insignificant benefits (epidural venous plexus pressure & intraosseous pressure are important determinants of blood loss in spine surgery & are independent of arterial blood pressure)
All should have group & hold, consider X-match for anterior approach abdominal + vascular surgeon involvement.
Which spinal procedures are particularly prone to major haemorrhage?
Deformity surgery
Decompressive surgery for metastatic tumours

Those with EBL >1000mL: considered complex. They’ll be longer, likely more periop pain along with blood loss:
6-18 level instrumentation
>=3 level ant/post fusion
Pedicle subtraction osteotomy
Vertebral column resection
Tumour corpectomy or debulking

Major spinal surgery (EBL 100-1000mL):
Cranio-cervical fusion
3-4 level ACDF/PCDF
1-3 level ALIF (supine, involves laparotomy & vascular surgeons to move major vessels)/XLIF (pt lateral, lateral approach but only 1-2 levels can be done)/TLIF (prone but less muscle damage & pain vs PLIF)/PLIF
1-2 level ant/posterior
Degenerative corpectomy

Minor (EBL <100mL):
1-2 level ACDF
<=2 level decompression or microdiscectomy without instrumentation

Pt factors incr blood loss: age >50, obesity, tumour surgery
surg: incr IAP in prone position

Unless pt factors dictate otherwise of rapid ongoing blood loss, generally restrictive transfusion strategy (target Hb 70-80g/L)

PBM:
pre: optimise red cell mass, O2-carrying capacity, med Mx advice
intra: limit IAP back to valveless epidural veins, antifibrinolytics (TxA reduce blood loss, need for allogenic transfusion, volume transfused during spine surgery, side effects don’t incr morbidity or thromboembolic events although the risk in pts with high baseline risk of thromboembolism is uncertain), consider ICS for fusion (cost & labour intensive; becomes cost effective cf allogenic transfusion when >=2 units blood salvaged & re-infused), limit OT time meticulous technique ensure haemostasis
Post: ongoing optimisation of DO2, analgesia to limit SNS stimulation, VTE proph pharm once haemostasis assured

D: drugs
Analgesia-
pain severity depends on approach & duration;
multimodal opioid sparing; also pts undergoing spine OT may be opioid tolerant
pain after 1-2 level decompressive procedures may be controlled with non-opioid & prn po low dose opioid
multi-level intensive regimen
surgeons may infiltrate subarachnoid injection of 1mL 0.5% isobaric bupivacaine under direct vision.
consider avoiding NSAIDs due to risk of SC haematoma, some concern re: bone healing (evidence inconclusive, low-quality evidence overall, meta-analysis of case control & cohort studies found a sig incr risk of NSAIDs on poor bone healing which didn’t hold up when lower quality studies were excluded, D/W surgeons (may avoid if other risks for bone nonunion eg. smoking, LT NSAIDs).

Ketamine (1-2mg/kg/24hrs) useful.
May use unilateral PVB for thoracotomy pain but LA infusions may complicate neurological Ax.
Gabapentin & pregabalin have been shown to reduce the risk of chronic pain after spinal surgery- pregabalin has better bioavailability- 150-600mg pre-op then 50-300mg for up to 14 days.

intrathecal morphine may be safe & reduce pain scores/opioid use.

surgeons may place epidural under direct vision.
again, motor block may complicate post-op neurol Ax; if use epidural can place opioid only, then LA after post-op neuro Ax.

consider TAP or QL blocks for anterior Lx spine surgery

Documentation- of eye checks @ least 30-minutely
Disability- BIS
Neuromuscular monitoring for any surgery where the spinal cord is at risk, eg. deformity correction; SSEPs (amplitude <50% of baseline suggests SC @ risk) & MEPs (described as absent or present) are used

E: temp monitoring

F: fluids
Glucose

H:
I:
J:
K:
L:
M:
N:
O:
P: goals of positioning= avoid injury to eyes, peripheral nerves & bony prominences, reduce the risk of facial oedema, maintain low venous pressure @ the surgical site.
pressure points in prone: be able to regularly check eyes & face, use pillow which has no external pressure over the eyes
If neuro-monitoring used, place bilateral bite blocks between molars after intubation making sure tongue & lips won’t be injured w jaw clench. Tape in place, recheck once prone.
Thoracic spine surgery: anterior approach requires a thoracotomy w pt in lateral, DLT to allow deflation of one lung for surgical exposure
posterior: prone, ULs either tucked or on arm rests ant of body
Lumbar anterior approach: supine, laparotomy, vascular surgeons, risk blood loss, postop pain

Foam bolsters- one @ the level of chest under axillae & at level of ASIS
arms abducted no >90 deg, slight internal rotation & lie in front of the plane of the body to reduce the risk of brachial plexus injury. Particular attention to pressure @ ulnar nerve. If arms by pts side, thumbs down to avoid over-pronation.

Avoid pressure to the abdo which incr IAP (eg. Jackson table a good option)
-may incr bleeding risk as pressure distributed back via the valveless epidural venous plexus
-IVC obstruction worsens this, reduces VR & reduces CO, increasing risk of LL VTE
-incr IAP may impair ventilation

Post-op: disposition neuro-monitoring ward. visual Ax & early ophthalmologist R/V if concerns
generally extubate unless significant pt/surg/anaes factors; overall carefully Ax for evidence of facial oedema, position the pt w head up 30 deg to allow the oedema to recede. If significant oedema, extubate over tube exchanger
Generally keep intubated if was a prone case with EBL>2L, large volume fluid or blood resus, ant-post spine surgery.
ongoing multimodal analgesia/anti-emesis
Generally 10% of Lx spine fusion pts require post-op ICU.

Potential complications:

Bleeding
Postop pain
Spinal cord injury (surgical compression or vascular ischaemia): incidence of SC damage & paralysis after corrective spinal deformity surgery= 1%
If neuromonitoring changes, check dose of anaes agents, m relaxants; pt factors: temp (whole body/local), ventilation, perfusion (BP, CO, bleeding, local ischaemia), blood volume/rheology, raised CSF pressure, hypoglycaemia/electrolyte abnormalities
Surgical: stretch/pressure on plexus/nerves, surgical trauma/retractors, medications to surface (eg. Lignocaine, papaverine), electrode, recording, machine dysfunction)
Pressure injury
What’s a possible complication that may be occurring in a prone patient who develops metabolic acidosis & haemodynamic instability? What further tests done?
hepatic or pancreatic dysfunction from compromised blood flow with abdominal organ pressure. Check & relieve abdo pressure points (particularly look for pt migration), assess liver function & haematologic parameters.

Incidence of airway compromise requiring re-intubation after C-spine surgery?
1.9%
Usual time for evolution of post-op airway compromise after anterior C-spine surgery?
6-36hrs, due to haematoma or supraglottic oedema secondary to venous & lymphatic obstruction

Postop airway compromise risk factors with ACDF:
Pt: prev C-spine instrumentation
Surgical:
multilevel surgery
blood loss >300mL
operative duration >5hrs
anterior & posterior (combined) approach

POVL:
What is the rate of post-op visual loss after any operation?
1/60,000-1/125,000

What proportion of non-ophthalmic surgery postop visual loss occurs with spinal surgery?
70%

What’s a particular issue with consent for spinal procedures?
discussion of visual loss, particularly if prolonged (>4hr) & significant (>800mL) blood loss anticipated or if male/obese, HTN/PVD

What is the aetilogy of visual loss after spinal surgery?
ischemic optic neurophy (ass’d with PT: male gender, obesity, SURGICAL: procedure >6hrs, incr blood loss, ANAES: position of head in dependent position, use of Wilson frame (which has a relatively dependent position of the head incr risk ischaemic optic neuropoathy)
> central retinal artery occlusion (due to direct pressure on the globe causing raised IOP & compromising retinal perfusion, usually unilateral & accompanied by other signs of pressure (ophthalmoplegia, ptosis or altered sensation in supraorbital nerve territory)). What type of headrests have been implicated in cases of central retinal artery occlusion? Horseshoe-shaped
Have intra-op hypoT, PVD or DM been associated with intra-op visual loss?
No, despite the final common pathway being hypoperfusion of the optic nerve
What’s the best treatment for postop visual loss?
No Rx shown to be effective whether the cause be ischemic optic neuropathy or central retinal artery occlusion, so PREVENTION IS BEST:
-positioning without ocular pressure & with head level to heart
-meticulous haemostasis, ensure well-supported close to baseline MAP BP (fluids/blood, vasopressors) & Hb, Hct, oxygenation
-consider staging prolonged procedures
When a high-risk pt becomes alert, Ax vision. If potential loss, urgent ophthal consult, consider CT or MRI to r/o intracranial causes of VL & to visualise the optic nerves

Question 7

Which agents must be avoided for procedures with intro spinal cord monitoring?

Answer 7

Anaesthetic vapours, muscle relaxants

Question 8

Which agent is useful for intraoperative spinal cord monitoring?

Answer 8

remifentanil- short CSHT & negligible effect on intra-op evoked responses

Question 9

Should NSAIDs be used as part of multimodal analgesia for spinal cord surgery?

Answer 9

No, due to risks of SC haematoma

Question 10

Which medications have been shown to reduce chronic pain after SC surgery? which is better? which doses?

Answer 10

Gabapentin & pregabalin.
Pregab has better bioavailability.
150-600mg pre-op, 50-300mg for up to 14 days.

Question 11

Describe how SSEPs are measured? Are they influenced by volatiles?

Answer 11

Stimuli are applied to the posterior tibial nerves.
Low-amplitude potentials are carried via the posterior columns of the spinal cord, territory supplied by the posterior spinal arteries (which supply the posterior 3rd of the SC), and are measured over the sensory cortex or via epidural electrodes.
Since the signal-to-noise ratio of SSEPs is improved by increasing depth of muscle relaxation, SSEPs are not significantly affected by therapeutic concentrations of anaesthetic vapours.

Question 12

Describe how MEPs are measured? Are they influenced by NMBDs?

Answer 12

Short-duration constant current stimuli of 300-700V is applied to the motor cortex & measured via needle electrodes in the tib ant, abductor hallucis & vastus medialis. Other needle electrodes are placed in the small muscles of the hands for reference. MEPs rely on integrity of the corticospinal tract, which lies in the territory of the ASA. Since MEPs are large-amplitude & incompatible with profound muscle relaxation, caution w NMBDs.

Question 13

How do anaesthetic vapours influence MEPs?

Answer 13

Anaesthetic vapours reduce MEP amplitude in a dose-dependent manner & anaesthetic vapour concentrations >0.5MAC aren’t generally compatible with reliable monitoring.

Question 14

What’s the anaesthetic maintenance of choice when using MEPs? Is there any effect of propofol TIVA on cortically evoked responses?

Answer 14

propofol TIVA- it does cause a dose-dependent depression of cortically evoked responses of a smaller magnitude, influencing the reliability of neurophysiological monitoring, so intra-op BIS useful, avoid burst suppression to optimise neuromonitoring conditions

Question 15

Where might continual monitoring of muscles innervated by individual nerve roots be useful?

Answer 15

For procedures involving vertebral levels below the termination of the spinal cord

Question 16

What are PLIF & TLIF & particular considerations with each?

Answer 16

Posterior lumbar interbody fusion involves nerve root decompression by laminectomy performed via posterior approach. IV disc is removed & replaced with an implant. Fusion is done with pedicle screws & connecting rods. Modest blood loss but bleeding from epidural veins may be difficult to control.
Transforaminal lumbar interbody fusion utilises a more lateral approach, less muscle damage, less pain (ie. use PCA with PLIF but not TLIF)

Question 17

What are some particular considerations for anterior-approach spinal surgeries (eg. anterior lumbar disc replacement & anterior lumbar interbody fusion)?

Answer 17

Massive blood loss possible esp w risk of injury to iliac vessels- ensure group & hold, should be @ a centre with vascular surgery availability. In extremis, aortic X-clamp has been used.

Question 18

What are particular anaesthetic considerations for ACDF surgery?

Answer 18

anterior cervical decompression & fusion is commonly performed for Cx disc prolapse causing myelopathy.

risk factors for post-op airway compromise= multilevel surgery, blood loss >300mL, operative duration >5hrs, anterior & posterior (combined) approach, prev C-spine instrumentation; all these factors incr risk of airway oedema

A: reinforced TT often used
Risk of post-op haematoma as blood vessels to the thyroid gland may be sacrificed
Airway compromise requiring re-intubation after anterior C spine surgery relatively common (1.9% incidence). Symptoms of airway compromise related to haematoma or supraglottic (eg. retropharyngeal) oedema usually develop within 6hr & 36hr after surgery, include neck swelling, change in voice quality, agitation, signs of resp distress, may have tracheal deviation & bradycardia/hypoT due to compression of carotid sinus.
B:
C: arterial line, as cardiovascular instability may occur during retraction of the carotid sheath, which is necessary for access to the spine.
Access to the ULs is limited (arms by sides) so place IV in foot or have extensions on IV lines
D: Risk of post-op dysphagia with medial retraction of the oesophagus
positioning: slight extension (shoulder bolster) with limited traction via tape @ the chin
E: may be prolonged: normothermia
Fluids: not excessive (limit oedema)
P:
supine, arms tucked (may have limited access), padded head rest
if prone C-spine surgery, may have intra-op traction (eg. mayfield device w skull pins)

POST-OP:
SMOOTH emergence desirable, facilitate with low-dose remifentanil, targeting SBP 120-160mmHg (depending on pre-op arterial bp)
control ongoing HTN with agents such as labetalol, while excluding treatable causes

high-risk pts require monitoring in critical care, consider staged extubation using an AEC once leak confirmed around the TT

Question 19

What are the risk factors for airway compromise requiring reintubation after anterior c-spine surgery? What are some considerations for pts @ high risk?

Answer 19

Pt factors: previous C-spine surgery
Surg factors:
multi-level surgery
>300mL blood loss
duration >5hr
combined anterior & posterior operation

Consider staged extubation eg. with an airway exchange catheter once a leak around the ETT has been confirmed

Aim for a smooth emergence eg. w remi, aim SBP 120-160mmHg depending on pre-op BP, be ready to Dx & Rx any HTN

High-risk pts should be observed in critical care postop

Question 20

What’s the usual time for evolution of postop airway compromise after anterior C-spine surgery? what are some aetiologies? what are s&s?

Answer 20

-6-36hrs
-haematoma or supraglottic oedema secondary to venous & lymphatic obstruction
-neck swelling, change in voice quality, agitation, reaching for throat & signs of Resp distress (tracheal tug, use of accessory mm, noisy breathing, incr Resp effort, rate or decreased sats), tracheal deviation, compression of carotid sinus may cause Brady + hypoT

Question 21

What’s the algorithm for airway compromise following C-spine surgery?

Answer 21

-Send for help (surgeon, additional senior anaes, experienced anaes nurse), difficult airway trolley
-Immediate O2 15L/min via NRB or consider CPAP via mapleson C circuit
-Surgeons: remove clips/cut sutures- if oxygenation is maintained, urgent t/f, monitored, to OT
-Secure airway either with direct laryngoscopy, surg cricothyroidotomy, AFOI or LMA/aintree catheter
-If oxygen not maintained, immediate surgical cricothyroidotomy.
-Pt for crit care consult following surg exploration

Question 22

For propofol TCI, which of the following 3 models (schnider effect, marsh effect, marsh plasma) give:
a) the largest, middle & lowest bolus dose (mg)
b) the highest subsequent infusion rate

Answer 22

a) effect-target marsh, plasma marsh, schnider effect
b) plasma marsh, effect marsh, effect shcnider

Question 23

If I’m using Remi Minto effect & propofol effect site, do I start the infusions at the same time?

Answer 23

yes, synergy of action will be easier to achieve

Question 24

What should I be particularly mindful of if start remi first (at plasma target, aiming to get gradual effect-site equilibration then will require a lower propofol effect site [] for anaesthesia, speeding induction)?

Answer 24

pre-oxygenation since apnoea is a risk, reminding the pt to breathe deeply

Question 25

What are some clinical calibrations that I can use to ensure the pt ready for “knife to skin” when running prop/remi anaesthetic?

Answer 25

seek no response to shake/shout, vigorous jaw thrust, laryngoscopy- note the Ce for each at that point
BIS also useful

Question 26

What are the suggested minimum effect-site [] for a pt aged >50yo undergoing IPPV w prop/remi? and <50?
and spont breathing?
*of course for all seek clinical correlate + BIS for depth Ax

Answer 26

prop: 2-3microg/mL with remi 3-6ng/mL
<50: prop 3-4microg/mL, remi 5-8ng/mL

spont:
prop 2-4, remi 1-2
<50 prop 4-6, remi 1-3

Question 27

Which TCI models are best used for frail elderly? why?

Answer 27

-for either model, use gradual incremental approach assessing pts level of consciousness & cardiovascular status w each increment
-schnider since delivers overall lower amount of drug for any given target (despite the prediction of a higher plasma []) so haemodynamic side-effects are lessened for any given number, however the use of age (while it’s a modulating factor on initial bolus & subsequent infusion rate) has little adjustment so still need to program a gentle target.
-minto PLASMA since it delivers 3-4x smaller bolus than effect target so less risk chest wall rigidity or severe brady. reserve Minto effect targeting for young robust pts.

Question 28

At what point should remi & props be turned off at end of surg?

Answer 28

turn off the props when surgeons are finishing final skin sutures, keep the remi at 1-2ng/mL target to smooth extubation

Question 29

What’s normal ICP?

Answer 29

5-15mmHg

Question 30

What’s the proportion of components of the cranium as per the Monroe-Kellie doctrine?

Answer 30

brain 80%
CSF 10%
Blood 10%

Question 31

Outside of what MAP range does CBF become pressure-dependent (ie. outside of the normal autoregulation range)?

Answer 31

50-150mmHg

Question 32

For each mmHg reduction in PaCO2, what reduction in CBF occurs?

Answer 32

2%

Question 33

What’s the equation for cerebral vascular resistance?

Answer 33

CVR: 8nL/pir4

Question 34

What are some factors reducing cerebral vascular radius hence reducing CBF hence reducing cerebral blood volume & ICP?

Answer 34

reducing PaCO2 through hyperventilation (which reduces H+ in the CSF)
avoiding hypoxia (which promotes cerebral vasodilation)

Question 35

What’s the target PaCO2 to reduce ICP intra-op?

Answer 35

25+/-2mmHg

Question 36

What are the risks of extreme hypocapnia?

Answer 36

PaCO2 <20mmHg risks cerebral ischaemia through extreme cerebral vasoconstriction & L)-shift of OHDC reduces O2 delivery to brain

Question 37

What’s mannitol? uses? osmolality?

Answer 37

a six-carbon sugar alcohol, low MW (182Da)
used IV or PO as an osmotic diuretic & IV for acute raised ICP
10% solution is 596mOsm/kg & the 20% is 1192mOsm/kg

Question 38

What’s the dose of mannitol for acutely lowering ICP?

Answer 38

1g/kg bolus, then can repeat 0.25-0.5g/kg every 6-8hrs

Question 39

When do the effects of mannitol show, peak & how long do they last?

Answer 39

within minutes, peak @ 1hr, last 4-24hrs

Question 40

What are some concerns with mannitol?

Answer 40

-“rebound” raised ICP, probably when mannitol with repeated use enters the damaged BBB & increases intra-cerebral osmolality, reversing osmotic gradient- may also have rebound ICP if intact BBB due to production of idiopathic osmoles with cerebral dehydration

-may predicate acute congestive heart failure/APO due to the increase in circulating volume, increase MAP (incr preload, SV & CO via frank-starling but heart failure if impaired LV function)

-care with renal insufficiency (accumulates as relies on renal filtration- if it accumulates can cause volume expansion, hyponatremia, hyperkalemia & metabolic acidosis), also can cause REVERSIBLE AKI because of intra-renal vasoconstriction & intravascular volume depletion

-electrolyte imbalances:
hypernatremia from diuresis
increased Na+ delivery to DCT promotes kaliuresis (hypoK)
hypomagnesemia
hypocalcemia
hypochloremia
metabolic alkalosis (incr Cl- loss) or metabolic acidosis
concern if Na+ >150, if serum osmolality >320mOsm or if evidence fo evolving ATN

-may causes profound hypotension/dehydration following diuresis (particularly as mannitol ass’d w prostaglandins release which promotes vascular smooth muscle relaxation)- this may be ass’d with reduced CPP

-vascular irritant

-anaphylaxis & other allergic reactions

Question 41

What’s the Monroe kellie doctrine?

Answer 41

the skull is a rigid structure with of fixed internal volume of 1400-1700mL containing brain, blood & CSF
Increase in volume of any component (or presence of pathologic components) increases ICP if not compensated by a reduction in vol other components.
ICP is thus a function of volume & compliance of each component of the intracranial compartment.

Question 42

What acid/base disturbance is typically seen with mannitol?

Answer 42

hypokalemic hypochloraemic metabolic alkalosis

Question 43

What are some causes of intracranial hypertension?

Answer 43

Vascular malformation/anomalies
Intracranial haemorrhage (eg. subdural, epidural, intraparenchymal)
Cerebral oedema (eg. with ischaemic stroke, acute hypoxic-ischemic encephalopathy, diffuse axonal injury)
ruptured aneurysm
vasculitis
impaired cerebral venous outflow (eg. venous sinus thrombosis, jugular venous compression)
increased CSF production (eg. choroid plexus papilloma)
Decreased CSF absorption (eg. arachnoid granulation adhesions after bacterial meningitis)
obstructive hydrocephalus
hypertensive encephalopathy
idiopathic intracranial HTN
Infection of CNS (encephalitis, meningitis, abscess)
Trauma (eg. diffuse axonal injury, subdural haemorrhage)
Neoplasm

Question 44

What’s the ICP with pathologic intracranial HTN?

Answer 44

> =20mmHg

Question 45

What’s the rate of CSF production in the choroid plexus?

Answer 45

20mL/hr (500mL/day)

Question 46

What are the initial compensatory mechanisms allowing volume of intracranial components to increase with minimal ICP elevation?

Answer 46

displacement of CSF into thecae sac
decrease volume of cerebral venous blood Fia venoconstriction & extracranial drainage

Question 47

Whats the equation for cerebral blood flow (CBF)?

Answer 47

CBF = (CAP - JVP) / CVR

Question 48

What’s the equation for cerebral perfusion pressure?

Answer 48

CPP = MAP - ICP

Question 49

What’s normal cerebral blood flow?

Answer 49

50mL/100g/min

Question 50

What are some pathologic states where auto regulation of CVR may become dysfunctional, making CBF pressure-dependent?

Answer 50

stroke & trauma

Question 51

Why may acute reductions in BP, even within the normal range, promote ischemic symptoms in pts with chronic HTN?

Answer 51

They have altered (elevated) set-point of cerebral autoregulation

Question 52

What are some manifestations of raised ICP?

Answer 52

Global symptoms:
headache (mediated via pain fibres of CN V in the dura & blood vessels)
depressed consciousness (due to pressure on midbrain reticular formation)
vomiting

Signs:
CNVI palsies
papilloedema
spontaneous periorbital bruising
Cushing’s triad (bradycardia, respiratory depression, HTN)

focal symptoms/signs either due to local effects of lesions or herniation syndromes, eg. unilaterally or bilaterally fixed & dilated pupils, decorticate or decerebrate posturing)

Question 53

What are some problems with empiric therapy for presumed elevated ICP? What, therefore, should be an early goal of management of the patient with presumed elevated ICP?

Answer 53

Can’t monitor CPP reliably without measurement of ICP
Therapies have side effects
Therapies directed @ lowering ICP are effective for limited & variable periods of time

Placement of ICP monitoring device

Question 54

What’s the purpose of ICP monitoring?

Answer 54

Allow maintenance of adequate CPP & oxygenation (CPP = MAP - ICP)

Question 55

What goal CPP is recommended to improve survival & favours outcomes in TBI?

Answer 55

60-70mmHg

Question 56

What are some risks of ICP monitoring?

Answer 56

CNS infection
intracranial haemorrhage

Question 57

What are some radiographic findings suggestive of elevated ICP?

Answer 57

mass lesions, oedema, midline shift, effacement of cisterns & sulci

Question 58

What are some indications for ICP monitoring?

Answer 58

suspected @ risk for elevated ICP (up to 1/3 of pts with initially normal CTB can develop raised ICP in the first few days after closed head injury)
GCS <8
diagnosed with a process that merits aggressive medical care

Question 59

What are the 4 main anatomical sites used in clinical measurement of ICP?

Answer 59

intraventricular
intraparenchymal
subarachnoid
epidural

Question 60

What’s a big benefit of intraventricular ICP monitoring? and major disadvantages?

Answer 60

can treat some causes of elevated ICP via CSF drainage
infection in up to 20% of pts, 2% risk of haemorrhage during placement (greater risk in coagulopathic pts)

Question 61

Advantages & disadvantages of intraparenchymal ICP monitoring devices?

Answer 61

ease of placement, low risk of infection & haemorrhage (<1%) cf intraventricular devices
disadvantages= unable to drain CSF for diagnostic or therapeutic purposes, inaccuracy over several days (can’t recalibrate, greater risk mechanical failure)

Question 62

pros & cons of subarachnoid bolts (fluid-coupled systems)?

Answer 62

low risk infection or haemorrhage but often clog w debris & are unreliable/less accurate cf ventricular ICP devices

Question 63

For which patient group are epidurally-placed ICP monitors used?

Answer 63

coagulopathic patients with hepatic encephalopathy complicated by cerebral oedema
significantly lower risk intracerebral haemorrhage (4 vs 20-22% for intraparenchymal & intraventricular devices) in this setting.

Question 64

What are the waves represented in ICP waveform analysis?

Answer 64

C waves (related to cardiac cycle), B waves (related to respiration), pathologic waves are abrupt marked elevations in ICP of 50-100mmHg- these signify a loss of intracranial compliance & herald imminent decompensation of autoregulation- presence of A waves indicated need for urgent ICP control

A close-up of ICP waveform reveals initially the percussion wave (representation of arterial pulsation), tidal wave (proxy for intracranial compliance), dicrotic wave (pressure transmission of aortic valve closure). Raised tidal wave indicates raised ICP & reduced intracranial compliance,

Question 65

Are noninvasive systems for ICP monitoring useful?

Answer 65

Not generally.
transcranial doppler is a poor predictor of ICP but in trauma patients findings may correlate with 6/12 outcome.
tissue resonance analysis shows good correlation with invasive ICP measurements.

Question 66

What is the effect of hypotension on ICP?

Answer 66

may induce reactive vasodilation & elevate ICP.

Question 67

In which situations may hyperventilation be contraindicated? why?

Answer 67

traumatic brain injury
acute stroke

The vasoconstriction may critically decrease local cerebral perfusion & worsen neurologic injury, particularly in the first 24-48hrs. Carefully consider the need for hyperventilation & avoid prophylactic hyperventilation in the absence of elevated ICP.

Question 68

At what ICP level should intervention occur?

Answer 68

if >20mmHg for >5-10mins

Question 69

How should fluid management be approached for patients with raised ICP?

Answer 69

keep euvolemic and normo- to hyper-osmolar (avoid free water, use isotonic fluids, value of colloid vs crystalloid inconclusive. Keep serum osmolality >280mOsm/L)

Question 70

What is the sodium usually trending to in pts with elevated ICP?

Answer 70

hyponatremia is common with elevated ICP, particularly in conjunction with SAH

Question 71

What’s the dose of hypertonic saline for acute ICP elevations?

Answer 71

30mL (or 1-2mL/kg) 23.4% NaCl, over 10mins

Question 72

Why does the effect of hyperosmolar therapy diminish with time?

Answer 72

Compensatory increase in brain osmoles occurs within 24hrs so hyperosmolar agents should be weaned slowly after prolonged use to prevent a reversal in the osmotic gradient & rebound cerebral oedema

Question 73

Through what type of access should hypertonic saline be administered?

Answer 73

central, due to risk of extravasation injury when used with peripheral IV access, however short-term use via peripheral IV access is permissible if acute ICP elevation

Question 74

What are some theoretical advantages of hypertonic saline over mannitol in a trauma patient?

Answer 74

-volume depletion & hypovolemia don’t occur so it’s safer in pts with ongoing blood loss, hypovolemia or hypotension (mannitol higher UO)
-HTS has a reflection coefficient of 1.0 (cf 0.9 for mannitol) so is less likely to leak into brain tissue
-mannitol higher lactate (but HTS higher Na+ & Cl- burden)

Question 75

What are some potential disadvantages of using hypertonic saline over mannitol?

Answer 75

circulatory overload & pulmonary oedema
increased chloride burden, which may result in NAGMA
coagulation disturbance
thrombophlebitis (requires central access)

Question 76

What’s the role of glucocorticoids in patients with raised ICP?

Answer 76

Worsens outcome in pts with mod-severe head injury & aren’t useful for cerebral infarction or intracerebral haemorrhage BUT they have a role in intracranial hypertension caused by brain tumours & CNS infections (reduce vasogenic cerebral oedema)

Question 77

Is therapeutic hypothermia recommended as Rx for increased ICP?

Answer 77

No

Question 78

Why shouldn’t CSF be rapidly aspirated via an external ventricular drain (EVD)?

Answer 78

may lead to obstruction of the catheter opening by brain tissue
if an aneurysmal SAH, abrupt lowering of the pressure differential across the aneurysm may precipitate recurrent haemorrhage

Question 79

At what rate should CSF be removed via an EVD?

Answer 79

1-2mL/minute for 2-3 mins at a time, break for 2-3mins in between, until reach ICP <20mmHg

Question 80

Why is a lumbar drain generally contraindicated in the setting of raised ICP?

Answer 80

risk transtentorial herniation

Question 81

With decompressive craniectomy, by how much does craniotomy alone lower ICP? and with opening the dura?

Answer 81

15%
70%

Decompressive craniectomy also improves brain tissue oxygenation

Question 82

With decompressive craniectomy, by how much does craniotomy alone lower ICP? and with opening the dura?

Answer 82

15%
70%

Decompressive craniectomy also improves brain tissue oxygenation

Question 83

To what mechanisms is cerebral autoregulation (maintenance of CBF 50mL/100g/min across a broad range of MAP (50-150mmHg)) mainly attributed?

Answer 83

myogenic

Question 84

What is the KEY principle in the setting of raised ICP?

Answer 84

defend CPP (aim >60mmHg) via reducing ICP & maintaining MAP

Question 85

In which patient group may mild therapeutic hypothermia provide benefit?

Answer 85

TBI with raised ICP

Question 86

What proportion of severe TBI patients develop coagulopathy?

Answer 86

1/3 (release of tissue factor/brain phospholipid into circulation)

Question 87

What’s the CPP target for children?

Answer 87

40-65mmHg

Question 88

What did the BEST:TRIP trial (NEJM 2012) say about ICP guided management for severe TBI?

Answer 88

not superior to neuro exam/CT guided management

Question 89

What did the NICE-SUGAR trial show?

Answer 89

In TBI, no difference between tight (4.5-6) & conventional (<10) BGL control in terms of neurological outcome & mortality @ 2 yrs

Question 90

Should glucocorticoids be used in TBI?

Answer 90

No

Question 91

According to the Brain Trauma Foundation, which patients should have ICP monitoring?

Answer 91

All salvageable pts with a TBI (GCS 3-8 after resuscitation) & an abnormal CT scan of the head OR in patients with severe TBI & a normal CT scan but >= 2 of: >40yr, unilateral or bilateral motor posturing, SBP <90mmHg.

Question 92

According to the brain trauma foundation, what’s the SBP goal for pts aged 50-69, 15-49 & over 70?

Answer 92

> =100mmHg if aged 50-69, >=110mmHg for pts 15-49 or >70yo

Question 93

To which cranial nerves is the pituitary related? relevant palsies? any other structures?

Answer 93

III, IV, V & VI
oculomotor= ptosis, mydriasis, diplopia, eye down & out
trochlear= typically unilateral, ipsilateral hypertropia & excyclotorsion (CNIV= superior oblique which intortes & depresses eye), pt often has compensatory contralateral head tilt.
trigeminal: absent corneal reflex, loss of masseter/temporalis tone (scooped out face), trigeminal neuralgia
VI: diplopia with attempted abduction of effected eye- it sits adducted (medial strabismus) & is unable to abduct
internal carotid arteries

Question 94

What are some surgical complications of pituitary surgery?

Answer 94

cranial nerve palsies, visual field defects, major haemorrhage, CSF leaks

Question 95

SS_NS 1.2: How does the blood supply to the hypothalamus & pituitary differ? What’s unique about the hypothalamic-hypophyseal portal venous system? how does it function & how is the posterior pituitary connection different?

Answer 95

hypothalamus from circle of willis, pituitary from inferior & superior hypophyseal artery which are branches of the internal carotid.

The anterior pituitary doesn’t have a major direct arterial blood supply- it’s bathed in dense capillary network of pituitary portal blood (from sup hypophyseal artery). Venous blood empties into petrosal sinuses (high [] pit hormones, can sample) then via IJVs.
Post pituitary is supplied by inferior hypophyseal artery, drains into inferior hypopyseal veins & directly to the systemic circulation.

The hypothalamic-hypophyseal portal venous system is a specialised circulation allowing hypothalamic hormones to reach target cells in the pituitary in high concentrations.

Hormones from the PVN neurons have terminals in median eminence releasing hormones into primary capillary plexus, traverse long portal veins in pituitary stalk, enter secondary plexus in anterior pituitary gland. The primary plexus, long portal vv & secondary plexus= hypothalamic-hypophyseal portal venous system.

Axons of the SON travel down supraopticohypophyseal tract, releasing vasopressin & oxytocin directly to the posterior pituitary.

Question 96

SS_NS 1.11: What does ACTH ultimately cause in target organ (adrenals)?

Answer 96

production of glucocorticoids & aldosterone

Question 97

SS_NS 1.11: What does growth hormone do to target organs?

Answer 97

anabolic effects to bone & muscle, promotes lipolysis & increases free fatty acid levels, impairs glucose utilisation & cellular sensitivity to insulin

Question 98

SS_NS 1.11: How may pituitary adenomas present clinically? size of micro vs macroadenoma? What are the 3 most common clinical presentations of nonfunctioning pituitary adenomas?

Answer 98

MOST (65-70%) with signs & symptoms of hormone hypersecretion (eg. hyperprolactinemia, GH excess, hypercortisolism)

25-35% are clinically nonfunctioning/”silent”, most of which are gonadotroph adenomas (which are therefore the most common pituitary macro adenoma, they are generally clinically “silent” as poorly differentiated & secrete hormones inefficiently)- most of the symptoms in these pts are due to mass effects, manifest as hormone hyposecretion or other mass effects eg. cranial nerve signs

micro adenoma <1cm, macro adenoma >=1cm

1. neurologic symptoms- mainly visual symptoms, due to suprasellar extension of adenoma compressing optic chasm, most common symptom, usually visual field loss in temporal fields (superior temporal quadrantinopia or temporal hemianopsia). more rarely they may get diminished visual acuity with significant optic chaism compression, may get diplopia if oculomotor nerve is compressed due to lateral extension of adenoma. headaches
2. incidental finding
3. pituitary hypofunction- generally manifest with biochemical evidence, clinical symptoms are less common (eg. oligomenorrhoea, erectile dysfunction)

rarely: CSF rhinorrhoea (inf extension), pituitary apoplexy (sudden haemorrhage- excruciating headache, visual impairment)

Question 99

SS_NS 1.11: How big are macroadenomas? how present?

Answer 99

at least 10mm
often present with consequences of local mass effect; commonly headache & subtle visual field defects
larger tumours may cause hypopituitarism, cranial nerve palsies, hydrocephalus

Question 100

SS_NS 1.11: What are micro adenomas & how generally present?

Answer 100

<10mm, symptoms of hormonal excess, classically Cushing’s disease (excess ACTH)

Question 101

SS_NS 1.11: When does acromegaly generally present? what is it? diagnosis? anaesthetic considerations?

Answer 101

middle age- insidious disease, progressive multi system due to excess GH secretion after puberty.

secretion= from a functioning pituitary macro adenoma- pts present with local mass effect & excess GH.

Diagnosis= biochemical test. Serum IGF-1, doesn’t vary from hour to hour unlike GH. Unequivocally elevated in a pt with manifestations of acromegaly confirms the diagnosis. In pts with equivocal IGF-1, inadequate suppression of GH after a glucose load confirms the diagnosis. OGTT= the most specific dynamic test for a Dx of acromegaly, measure GH before glucose, have 75g glucose, 2hrs later >1ng/mL= acromegaly.

Anaesthetic considerations:
Neuroanaes
Coarse features (frontal & nose enlargement, macrognathia, large hands & feet)
Airway: laryngoscopy more challenging with upper incisors potentially spreading apart, macrognathia, prognathism & macroglossia & expansion of upper airway soft tissues
up to 70% have significant OSA

may have visual field defects

may have kyphoscoliosis & proximal myopathy (impairing respiratory function)

May have refractory HTN with eccentric LV hypertrophy, IHD, arrhythmias (tachyarrhythmias or HTN may be due to SNS stimulation), heart block, cardiomyopathy & bi-ventricular dysfunction, may develop high pulm pressures

venous cannulation may be difficult with excessive peripheral soft tissue deposition, increases risk of nerve entrapment syndromes eg. carpal tunnel syndrome (meticulous attention to OT positioning needed), care w radial art line (Allen’s test, may have soft tissues compressing ulnar artery, consider dorsalis pedis or femoral)

incr risk arthropathy
hyperhidrosis

Osteoporosis/joint deformities
colonic polyps/bowel Ca

T2DM may be present, along with other endocrine abnormalities

Question 102

SS_NS 1.11: What’s the blood supply of the adrenal glands?
What are the roles of glucocorticoids?
specifically, for the liver/CV, kidneys & immune system & substrate metabolism?
how does excessive glucocorticoid impact growth hormone?
impact of a lack of glucocorticoids on vasculature?
What controls ACTH release?
what are the roles of mineralocorticoids?

What’s Cushing’s disease & syndrome? how screened/diagnosed?
Anaesthetic considerations?

What’s Conn’s syndrome? What are some causes of secondary hyperaldosteronism?
Usual presenting signs of Conn’s?
Diagnosis of Conn’s? treatment of Conn’s?
Anaesthetic considerations for Conn’s?

Answer 102

arterial from branches of the renal & phrenic arteries of the aorta, venous drainage via a single adrenal vein into renal vein on L) & IVC on the R)

Globally: catabolic, cardiovascular, anti-inflammatory effects. Promote glycogen storage in the liver but promote glycolysis in skeletal muscle.
Liver: gluconeogenesis, promote glycogen storage, protein catabolism; antagonises role of insulin
Cardiovascular: maintenance of responsiveness to catecholamines
Kidneys: weak mineralocorticoid activity (significant in excess)- hyperNa, hypoK
Immune: immunosuppression & slowed healing
metabolism of carbs, fat & proteins

excess glucocorticoid–> depressed GH secretion by ant pit

vessels become unresponsive to catecholamines, vascular endothelium becomes more permeable

CRH, then cortisol exerts -ve feedback on CRH & ACTH.

Mineralocorticoids are essential for electrolyte & fluid balance; they promote sodium reabsorption from DCT & potassium & H+ excretion.

Excess glucocorticoid due to ACTH hyper secretion from pituitary corticotrophin adenoma (usually micro adenomas) which –> bilat adrenal hyperplasia (cf Cushing’s syndrome, non-specific chronic glucocorticoid excess regardless of cause eg. adrenal adenoma, exogenous glucocorticoid).

screening: 24hr urinary free cortisol, short dexamethasone suppression test (give 1mg PO nocte, should get suppression 9am cortisol if normal)
Then to differentiate: high-dose dex suppression test= suppression of cortisol if pit-dependent cushing’s (even corticotroph tumours generally retain some responsiveness to high-dose glucocorticoid -ve feedback inhibition), not adrenal cushing’s or ectopic ACTH.
get elevated ACTH in Addison’s disease, cushing’s disease ectopic ACTH but of course low in cushing’s syndrome due to adrenal tumour or exogenous GC.

Anaesthetic considerations Cushing’s:
Thorough pre-op assessment, optimisation of possible modifiable risk factors (eg. HTN) with multi-D input, plan (eg. centre, need HDU?), consent

Particularly consider:

higher incidence of obesity & osa may make airway more difficult- “buffalo hump” interfere with supine positioning.

Proximal muscle wasting may impair post-op respiratory function- may require ICU.

-more than 80% of pts with Cushing’s disease have systemic HTN, may be refractory to standard Rx. Longstanding disease associated with eccentric LVH & diastolic ventricular dysfunction. Ax pre-op ECG (may have ischaemic changes related to hypertrophy or due to Cushing’s disease itself) +/- ECHO.
Haemodynamic instability during induction common, art line.

Higher risk post-op VTE; ensure non-pharmacological prophylaxis.

Glucose intolerance in 2/3 of pts with Cushing’s, half of these have DM. Ax for end-organ effects & optimise control, liaise w endocrine, plan (first on list).

Increased risk of GORD (ensure well-fasted, consider RSI, pre-op acid suppression), peptic ulceration- NSAIDs used with caution.

Truncal obesity, moon facies & thin extremities. friable skin & thin peripheral veins= venous access difficult, high risk extravasation. atrophic skin easily damaged. CVC insertion difficult (cervical obesity, supraclavicular fat pads- US vital. Increased risk of blood-borne infections with central access).

pt handling & regional anaesthesia also more challenging with osteoporotic joints (fracture risk)

may get exophthalmos due to retro-orbital fat deposits seen in 1/3 of pts with Cushing’s- care ++ to avoid corneal injury.

Higher risk of post-op infections/slow wound healing; ensure prophylactic antibiotics given, meticulous asepsis for invasive procedures.

Consider need for stress steroids if iatrogenic Cushing’s. If status of HPA axis suppression is unknown, pre-op evaluation= measure morning (pre-8am) cortisol, if it’s <138mmol/L w 24hrs off glucocorticoids, suggests HPA axis suppression. Or, could do ACTH stimulation test; 250microg ACTH given, measure serum cortisol 30mins later, if it’s >497nmol/L, suggests adequate adrenal reserve.
may have hypokalaemia due to weak mineralocorticoid effect (Na+ retention, K+ loss)

CONN’S SYNDROME: primary hyperaldosteronism, excess aldosterone secretion, 60% from adrenal adenoma, 30% from bilat adrenal hyperplasia, rarely from a carcinoma.

Secondary hyperaldosteronism= where there’s high plasma [] renin & aldosterone. Causes incl CCF & liver cirrhosis.

Conn’s usually presents with HTN. This may be malignant & refractory, may be caused by aldosterone-induced VC.
Hypokalaemia (often severe, may be exac by Rx of HTN w diuretics)
may get met alkalosis due to H+ loss.

Conn’s diagnosed by an aldosterone:renin ratio of >400, MRI scan of adrenals may assist Dx.

Rx depends on cause; BAH Rx with spironolactone often w ACE-I. Adenoma often requires surgical Rx after medical optimisation.

Pre-op, aim to optimise HTN, hypokalaemia & metabolic alkalosis, may not be possible to normalise serum K+. Spironolactone may moderate the metabolic & electrolyte effects of Conn’s & assist normalising volume status, may also need ACE-I. Ax for end-organ effects of HTN (eg. LVH).

Art line (haemodynamic instability may occur on manipulation of the adrenal gland), useful to have short-acting alpha-blocker available (eg. phentolamine).

All pts having adrenelectomy require hydrocortisone (mineralocorticoid, glucocorticoid) from induction, continue until able to take PO steroid replacement.

HypoK may prol NDNMBA’s & suppress baroreceptor tone so Rx hypovolaemia.

Question 103

What’s the most common functioning pituitary adenoma? symptoms?

Answer 103

prolactinomas- 30% of pituitary tumours

hyperprolactinaemia= galactorrhea & menstrual dysfunction in women, secondary hypogonadism reduced libido & erectile dysfunction in men

First line= medical management (dopamine agonists eg. cabergoline)

pathophysiology of hyperprolactinaemia doesn’t impact periop care

Question 104

What are the endocrine hypo secretion syndromes associated with pituitary disease?

Answer 104

adrenocorticoid insufficiency, hypothyroidism, diabetes insipidus

Question 105

How does the severity of adrenocortical insufficiency due to pituitary disease compare with that due to Addison’s?

Answer 105

the renin-angiotensin-aldosterone axis is preserved, so fluid & electrolyte abnormalities are less severe
pts require IV hydrocortisone, saline resus & possibly glucose in the acute setting

Question 106

What are some considerations for periop management of hypothyroidism?

Answer 106

pituitary-related is less severe than primary thyroid failure

incr sensitivity & reduced metabolism of all anaesthetic drugs- reduce doses & titrate

emergence may be prolonged- post-op resp support may be needed

normal ventilatory responses to hypercapnia & hypoxia are obtunded

peri-op hypothermia is common

Question 107

What’s central DI? how treated?

Answer 107

failure of secretion of ADH. This can be a complication of pituitary surgery. May be delayed 24-48hrs. Up to 15% of cases permanent. May be triphasic; initial reduction in ADH & polyuria then uncontrolled ADH release then the DI recurs.

See serum sodium >145, urine osmolality inappropriately low cf plasma, serum osmolality high, urine volume increased (>3L/day or 4mL/kg/hr).

Rx with desmopressin, a synthetic analogue of ADH with a longer half life & lacking the vasoconstriction properties of endogenous ADH. Usually orally or intranasal, available subcut or IM. Can give fluid if symptomatic.

Question 108

SS_NS 1.27: What are the advantages & disadvantages of transsphenoidal approach vs conventional craniotomy? what use to minimise nasal bleeding?

Answer 108

minimal surgical trauma & blood loss
direct access to the gland
avoidance of generic hazards of craniotomy (postop pain, damage to other cerebral structures, infection)

complications= persistent rhinorrhoea (CSF leaks), postop meningitis, panhypopituitarism, transient DI, vascular damage/major haemorrhage (prox to internal carotids), cranial nerve injury, visual field defects, cerebral ischaemia, stroke due to vasospasm or thromboembolism.

administer mucosal vasoconstrictor (topical anaesthetic & vasoconstrictor eg. Adr or cocaine) to limit nasal bleeding with intentional nasal septum fracture; communication w surgeons, anticipate & Mx HTN

Question 109

SS_NS 1.27: Main considerations for transsphenoidal surgery

Answer 109

PATIENT/PATHOLOGY:
-consider pituitary function pre-operatively (hormone hyper or hypofunction & systemic manifestations)
-mass effects
-risk stratify/optimise comorbidities

PROCEDURE:
-art line required: monitor & anticipate haemodynamic swings with points of intense stimulation (laryngoscopy, vasoconstrictor administration, nasal septal fracture, extubation)
-head ring, slight head up for OT & surgeons may request relative hypotension
-SHARED AIRWAY endoscopic surgery; constant careful communication with ENT/NSx team.
either reinforced (if not going through MRI) or south-facing rae
manually check all connections before drape, BIS well-secured

Likely to go to intra-op MRI:
MRI safety checklist
change ecg dots to MRI-compatible
remove temp probe, NMT
all lines run downwards

Neuroanaesthetic:
remifentanil: consider starting (65yo) Ce 2, increase (hypotensive, bradycardia goals) with propofol TCI (eg. at 5 initially) with metaraminol running
Titrate remifentanil for most stimulating points: fracture nasal septum, breaching the dura

POTENTIAL COMPLICATIONS:
-monitor urine: consider diabetes insidious (differential= cerebral salt wasting)
-Surgical complications:
-bleeding in enclosed space: pt have a G&H. Damage control principles of: permissive hypotension (SBP 90mmHg), consider permissive hypoT/ temporarily suspending cardiac output eg. with adenosine, damage control surgery, damage control resuscitation (normothermia, avoid acidaemia & coagulopathy)
-cranial nerve palsy
-CSF leaks
-meningitis (ABx prophylaxis)
-panhypopituitarism; consider need for stress steroids (d/w surgeons)
-visual field defects
-cerebral ischaemia (hypoperfusion, vasospasm or thromboembolism)

Emergence:
smooth, with remifentanil (limit coughing- care re: rebound HTN w remifentanil)
CORONER’S CLOT risk (good suction under direct vision @ end, lift head), nasal bolster. discuss BP goals w surgeons.

CAN’T use CPAP postop due to transsphenoidal approach; may be an issue in the 70% of pts w acromegaly & OSA; postop HDU for OSA monitoring

Question 110

SS_NS 1.27: Main goals of anaesthesia for pituitary surgery?

Answer 110

optimise cerebral oxygenation
maintain haemodynamic stability- monitor w art line, titratable agents on-hand
optimise surgical exposure
rapid smooth emergence, short acting agents for neuro assessment & limit problems with post-op airway management
reinforced or south-facing tube tube (limited access to airway, use south-facing if intra-op MRI). care re: gauze to stabilise tube & protect lower airway, ?nasal packs post-op.
Remote anaesthesia w intra-op MRI.

prophylaxis vs infection & HPA axis suppression; consider Antibiotics & IV hydrocortisone on induction

Intense stimulation with nasal septal fracture & breeching the sphenoid for access to fossa.
Anticipate HTN w cocaine injection; consider GTN along w prop/remi/esmolol/Mg++

They may insert lumbar drain & inject saline or request controlled hypercapnia to promote descent of the tumour into operative field.

NSAIDs controversial.

PONV common- comprehensive multi-modal prophylaxis & options for Rx from different classes.

semi-recumbent position but venous air embolism still uncommon.

Post-op ICU (risk airway obstruction)- pts with OSA Hx at highest risk

nasal CPAP is contraindicated after trans-sphenoidal surgery (risk tension pneumocephalus)

Postop DI risk- usually develops in first 24hrs, resolves by 1/52. hyponatremia may occur with desmopressin.

Postop hormonal replacement therapy will be required- consult w endocrine.

Question 111

What are potential benefits & risks of prophylactic or therapeutic hypothermia for the CNS?

Answer 111

reduce tissue damage associated with CNS trauma by reducing metabolic rate & blood flow (reducing ICP)

risks= coagulopathy, immunosuppression, cardiac dysrhythmia, death

Question 112

How may mannitol and HTS reduce ICP?

Answer 112

combination of brain dehydration & reducing blood viscosity (improves microcirculatory flow)

Question 113

According to the BTF recommendations, at what doses is mannitol effective for control of raised ICP? what BPs should be avoided? in which pt groups should mannitol be restricted?

Answer 113

0.25-1g/kg body weight
avoid SBP <90mmHg
restrict mannitol use in pts with signs of transtentorial herniation or neurological deterioration not attributable to extracranial causes, prior to ICP monitoring

Question 114

At what level should an EVD system be zeroed?

Answer 114

midbrain
According to BTF, EVD zeroed at the midbrain with continuous drainage MAY be considered to lower ICP burden more effectively than intermittent. Use of CSF drainage to lower ICP in pts with initial GCS <6 during the first 12hrs after injury may be considered.

Question 115

Why do pts with severe TBI require definitive airway protection?

Answer 115

At risk of compromised respiratory drive & function
at risk of pulmonary aspiration
may require transient hyperventilation to treat cerebral herniation

Question 116

What is the PaCO2 goal for severe TBI pts in the absence of cerebral herniation?

Answer 116

35-45mmHg (normocapnia, given that we don’t know CMRO2 after TBI & there is risk of ischaemia as well as hyperaemia)

Question 117

What’s the most powerful determinant of CBF? at what ranges is CBF linearly responsive?

Answer 117

PaCO2

20-80mmHg

Question 118

When could hyperventilation be considered in pts with severe TBI?

Answer 118

As a temporising measure for the reduction of elevated ICP

Question 119

What’s the benefit of anaesthetics/analgesics/sedatives for TBI?

Answer 119

Barbiturates: control ICP, presumably by limiting movement, avoiding coughing & straining, suppressing metabolism, altering cerebral vascular tone. Barbiturates may improve regional flow:metabolism coupling, improving cerebral oxygenation with lower CBF & decreased ICP from decreased CBV.

Question 120

What’s the benefit of anaesthetics/analgesics/sedatives for TBI?

Answer 120

Barbiturates: control ICP, presumably by limiting movement, avoiding coughing & straining, suppressing metabolism, altering cerebral vascular tone. Barbiturates may improve regional flow:metabolism coupling, improving cerebral oxygenation with lower CBF & decreased ICP from decreased CBV.

Question 121

What’s the benefit of anaesthetics/analgesics/sedatives for TBI?

Answer 121

Barbiturates: control ICP, presumably by limiting movement, avoiding coughing & straining, suppressing metabolism, altering cerebral vascular tone. Barbiturates may improve regional flow:metabolism coupling, improving cerebral oxygenation with lower CBF & decreased ICP from decreased CBV.

Question 122

What’s the benefit of anaesthetics/analgesics/sedatives for TBI? What is the BTF recommendation on this topic?

Answer 122

Barbiturates: control ICP, presumably by limiting movement, avoiding coughing & straining, suppressing metabolism, altering cerebral vascular tone. Barbiturates may improve regional flow:metabolism coupling, improving cerebral oxygenation with lower CBF & decreased ICP from decreased CBV.

High-dose barbiturates are recommended to control elevated ICP refractory to maximum standard medical & surgical Rx- need to ensure haemodynamic stability before & during barbiturate therapy.
Propofol is recommended for the control of ICP but it doesn’t improve mortality or 6/12 outcomes. high doses can–> significant morbidity.

Question 123

What’s are the the BTF recommendations regarding steroids?

Answer 123

Level 1 recommendation: use of steroids NOT recommended for improving outcome or reducing ICP, high-dose pred associated with increased mortality in severe TBI

Question 124

What’s the BTF recommendation re: seizure prophylaxis?

Answer 124

Phenytoin recommended to decrease incidence of early PTS when overall benefit felt to outweigh complications ALTHOUGH early PTS haven’t been associated with worse outcomes

Question 125

What does the BTF recommend wrt ICP monitoring? and CPP?

Answer 125

the management of severe TBI patients should be undertaken using information from ICP monitoring (reduces in-hospital & 2/52 post-injury mortality)

using CPP monitoring for these pts decreases 2 wk mortality

Question 126

Where is MAP, by convention, calibrated to? and the JVP?

Answer 126

level of the R) atrium of the heart
RA

Question 127

What’s cerebral autoregulation?

Answer 127

maintenance of CBF over a wide range of CPPs (which is MAP-JVP or ICP whichever higher)- brought about by homeostatic change inCVR. no change in CBF is anticipated as long as CPP remains within upper & lower limits of autoregulation.

If cerebral autoregulation is not intact, dependent of SBP to prevent cerebral ischaemia & risk cerebral hyperaemia with excessive SBP

Question 128

What are some advanced cerebral monitoring techniques for blood flow & oxygen?

Answer 128

transcranial doppler/duplex sonography
arterio-jugular venous O2 (AVDO2 globally measures cerebral O2 extraction- measure at jugular bulb)- this MAY be considered to reduce mortality & improve outcomes @ 3 & 6/12 post-injury
measures of local tissue oxygen

Question 129

What are the thresholds recommended by the BTF for severe TBI pts?

Answer 129

BP:
Maintain SBP >=100mmHg for pts aged 50-69yo
>=110mmHg or above for pts 15-49 or over 70yo
These values may decrease mortality & improve outcomes
ICP: treating ICP above 22mmHg is recommended- values above this level associated with increased mortality (NORMAL ICP RANGE 0-10mmHg)
CPP: Recommended CPP target is 60-70mmHg (for survival & favourable outcomes)- which end of this CPP range is optimal minimal target needs to be tailored to the pt: when determining goal, consider the pts pressure auto regulatory status: pts with intact autoregulation are best served by higher CPP while pressure-passive pts do better with lower CPP. Avoid aggressive >70mmHg with fluids & pressors- may risk resp failure & poor outcomes.
ACM: jugular venous saturation of <50% MAY be a threshold to avoid to reduce mortality & improve outcomes- level III evidence

Question 130

In the RESCUE-ICP trial, what were stage 1 & 2 measures to maintain ICP <=25mmHg?

Answer 130

Stage 1:
Head elevation
sedation
analgesia
neuromuscular paralysis (optional)
CPP >60mmHg
normothermia, normoglycemia, mild hypocapnia, adequate oxygenation

Stage 2:
ventriculostomy (if EVD not already in situ for ICP monitoring)
pharmacologic BP augmentation
oxmotherapy
moderate hypocapnia
therapeutic hypothermia

Question 131

What are some causes of secondary brain injury? What may be the consequences of a single SBP <90mmHg?

Answer 131

haematoma, contusion, diffuse brain swelling, systemic shock, intracranial infection.

single SBP <90mmHg–> associated with a 150% incr mortality

Question 132

SS_NS 1.6 “outline the grading of SAH severity”
What’s the World Federation of Neurological Surgeons (WFNS) grading scale for subarachnoid haemorrhage?

Answer 132

WFNS: based on GCS & motor deficit

Grade 1= GCS 15, no motor deficit
Grade 2= GCS 13-14, no motor deficit
3= 13-14, motor deficit
4= 7-12, +/- motor deficit
5=3-6, +/- motor deficit

Question 133

SS_NS 1.6 “outline the grading of SAH severity”
What’s the Fisher scale? how modified fisher scale vary?

Answer 133

Devised as an index of vasospasm risk but not clinical outcome, based on haemorrhage pattern on initial CT head (Group 1-4, ranging from no blood (1), thin layer blood <1mm thick, diffuse (2), localised clots & SAH >=1mm thick (3), intraparynchymal or intraventricular extension with clots (4). Grade 3-4 almost always vasospasm, grades 1-2 almost never. Well-validated, relies on CT (convenient), has near-perfect inter-rater reliability with kappa of 0.9)

modified: index of risk of delayed cerebral ischemia due to vasospasm after SAH- doesn’t address clinical outcome
grade 0= no SAH or IVH
1= minimal SAH, no IVH
2= minimal SAH with bilateral IVH
3= thick SAH without bilateral IVH
4= Thick SAH with bilateral IVH

Question 134

SS_NS 1.6 “outline the grading of SAH severity”
What are the most important prognostic factors for SAH at presentation?

Answer 134

level of consciousness
age
amount of blood on initial CT head

Question 135

SS_NS 1.6 “outline the grading of SAH severity”
What clinical scales for sat have been developed to predict risk of delayed ischaemia or clinical outcome following SAH?

Answer 135

modified Fisher: predicting delayed cerebral ischaemia due to vasospasm- best predictors= thick SAH (completely filling any cistern or fissure) & bilateral IVH, ie. Grade 3 (just thick SAH) or 4 (thick SAH with bilateral IVH)

VASOGRADE: predict risk of delayed cerebral ischemia following SAH, based on WFNS scale & modified fisher scale at admission, green, yellow, red.
green= WFNS 1 or 2 and mFS 1 or 2
yellow= WFNS 1 to 3, mFS 3 or 4
red= WFNS 4 or 5 and any mFS
red higher risk delayed cerebral ischemia, yellow & green similar risk

Ogilvy & Carter predicts outcome for surgical management of SAH due to ruptured aneurysm. stratifies pt based on age, hunt & hess grade (clinical condition), fisher grade (SAH volume & vasospasm risk), aneurysm size. one point given for each of:
age >50
H&H 4-5 (in coma)
Fisher 3-4
aneurysm size >10mm
additional point for giant posterior circulation aneurysm >=25mm

Grades 0-2= good to excellent outcome in 78% pts, but only 25% of pts with grade 4 (out of max 5) had good outcome.

Question 136

SS_NS 1.6 “outline the grading of SAH severity”
What is the utility of the GCS?

Answer 136

Predicts outcome after SAH surgery (significant difference observed btwn GCS 14&15)
confounded by sedating meds & intubation
moderate interobserver variability

Question 137

SS_NS 1.6 “outline the grading of SAH severity”
Hunt & Hess scoring system? utility? WFNS? utility?

Answer 137

5 grades, related to symptoms (headache, nuchal rigidity, drowsiness- ambiguous/subjective.
can be collapsed into 3 grades: alert group (grades 1 & 2)- 71% good neurological outcome. drowsy (grade 3)- 14% good outcome. comatose grade 4&5 none had good outcome.

WFNS: ?survival. level of consciousness mortality predictor, motor deficit morbidity. what distinguishes G2 & 3 is motor deficit. grades 4 & 5 doesn’t matter whether or not motor deficit.
simple- doesn’t require imaging. Relies on GCS which is well-accepted & validated & predicts mortality in other intracranial catastrophes but it is confounded by sedation/ventilation- does have moderate inter observer variability. Rationale for division btwn categories unclear- there are very few grade 3 pts. significant gap in outcome btwn grade 2 & 3.

Question 138

SS_NS 1.27: In what situations may awake craniotomy be considered?
benefits?
During which parts is the pt completely awake vs sedated/anaesthetised?
important considerations & contraindications?

Answer 138

e/o lesions near eloquent cortex (area on surface of the brain necessary for language, motor & sensory functions; intra-op cortical stimulation to map resection margins), epilepsy surgery (electrocorticography map resection margin), DBS (eg. Parkinson’s pt, sub thalamic nuclei), Tourett’s, post-stroke thalamic pain

benefits= increased lesion removal, improved survival, minimising damage to eloquent cortex/post-op neuro dysfunction, shorter hospitalisation/cost, less PONV

mapping procedure while lesion resection takes place

Pt: selection critical- physical & psychological pre-requisites.
absolute contraindications= pt refusal, inability to lay still, inability to cooperate
relative contraindications= pt cough, learning difficulties, inability to lie flat, anxiety, language barriers, OSA, very young
type of lesion: low occipital tumours (eg. prone position), lesion s w significant dural involvement (painful resection, can’t cover w scalp block), complex tumours requiring protracted periods w pt awake. LBP, IDC, “head floating”
Preop consult involves:
Ax of suitability (co-morbidities eg. GORD, OSA, chronic cough, anxiety, parkinson’s, communication issues)
Consult:
Hx/Exam/Ix
Optimisation of comorbidities, be aware of how the pts PC & comorbidities affect them (eg. seizure type, pre-existing neurological deficits)
medication instructions:
-generally take usual steroid, anti-epileptic or anti-hypertensives. may be loaded with anti-convulsants or have plasma levels checked.
Explain/consent: providing detailed explanation of expectations- visiting the OT first may help psych prep, multi-D (may involve neuropsychologist if lesions involve speech & language), build rapport. PREADS VISIT(s) IMPORTANT ++ for PT PHYSICAL/PSYCH PREPARATION (eg. they’ll hear drilling etc, likely to be fatigued, consider if any back pain etc).

Procedure:
D/w surgeons postion, anticipated duration
Planning: multi-D incl OT setup (me be able to maintain visual & verbal communication w pt), consideration re: electrophysiological monitoring
issues with airway access
May need intra-op T/F to MRI (safety checklist w MRI radiographer- ensuring safety for pt/personnel (eg. ensure no MRI incompatible implants, the pre-theatre checklist should include MRI safety. COGNITIVE AIDS USEFUL- do checks pre induction, pre-drape, pre-transfer), change monitoring to be MRI compatible & ensure adequate battery (ensure I’m familiar with it), ensure pts bed will be MRI compatible (ie for awake crani, skull still technically open), pat self down (eg. no projectiles in pockets), emergency drugs, pt counselling & protection (noise, claustrophobia, earplugs), cognisant that MRI interferes w monitoring eg. ecg. consider long lines if any MRI incompatible devices, pt positioning (BURNS RISK), consider plan if needs resus (emergency drugs in MRI safe tray). Discuss our plan for MRI transfer w team before going into scanner.

Analgesia/anaesthesia:
scalp block for all techniques (or field infiltration where mayfield pins sit); block while sedated (dexmed/midaz), 50:50 2% lignocaine w Adr & 0.5% bupivacaine.
use sedation only or GA for induction (deepen for more stimulating points: application of Mayfield Pins, skin incision, removal of bone flap & dura mater, asleep when dura broached (stimulating ++), either stay awake or asleep again for closure)
awake for neurocognitive testing (need to allow enough time for the pt to adjust to the environment, calm/quiet- pt may have pain from pins or discomfort from prolonged immobility, agitation, nausea, vomiting- address all issues quickly as they impact surgical conditions), cortical mapping (localising eloquent areas of the brain through direct electrical stimulation of cerebral cortex by electrodes- stimulate areas involved in speech, language, motor function- any deficit noted with stimulation is communicated to the surgeon- seizures are most likely to occur during cortical mapping (occur in 3-16%) & are treated by irrigating the brain with ice-cold saline- occasionally BZD, anti-epileptics or re-sedation (props) with airway control are required, hence an emergency airway plan has to be in place which can be challenging as pt may be in pins remote from ventilator) & resection (only once functional mapping has occurred), can re-anaesthetise for closure (give the pt the option, see how they’re feeling under the drapes, could give low sedative to drift them to sleep), or could be “awake throughout”

*care ++ as sedation too deep–> hypoxia, hypercapnia, acidaemia which increase ICP & –> “tight brain”, while sedation too light= uncomfortable/anxious pt. advantages of sedation= avoid airway management & its risks. Advantages of GA= can control FiO2 & ventilation (EtCO2), can prevent airway obstruction- facilitates greater depth of anaesthesia during painful parts of OT.
Intra-op:
Thorough, continual anaesthetist & surgeon communication + other team-members vital; pre-op plan discussed in detail & verified pre-induction.
Ensure OT table as comfortable as possible, OT temperature comfortable for pt, limit staff numbers to limit unnecessary noise & pt anxiety. ensure drapes don’t cover pts face.
Careful consideration & execution of pt position: generally sitting for occipital lesions & testing visual cortex, lateral or supine for other lesions.
Pt must be positioned so they can see & communicate with the anaesthetist & neuropsychologist at all times when awake.
May use urinary convenes as IDC may be uncomfortable

Monitoring: art line (usually insert sedated or asleep), 12-lead ecg, SpO2, ecg, BIS may be useful to run lighter anaesthetic depth prior to wake-up, capnography or at least chest plethysmography while sedated

Assistant: limited ppl but skilled anaesthetic assistant

Drugs: generally avoid premed, consider GORD prophylaxis, aggressive antiemetic prophylaxis

Technique & drugs variable, principles:
-facilitate pt comfort; talk to them continually, have pre-planned topics to discuss, swab soaked with ice water for mouth, consider panadol/COX for back pain
-short-acting titratable agents to facilitate acute control of conscious level- generally dexmed (anxiolysis & analgesia with sedation WITHOUT resp depression, even @ high levels- also has anaesthetic sparing properties & no effect on ICP- pts are easily rousable despite sedation BUT it can cause dose-dependent hypotension & bradycardia), prop/remi TCI or BZD or droperidol & other short-acting opioids such as fentanyl
-analgesia: paracetamol, LOCAL ANAESTHETIC FOR SCALP BLOCK!!! *calculate dose with & sans epi- uptake of ropiv is rapid cf regional blocks @ other levels but low risk LAST if safe dose used- communicate w surgeon how much they can use for infiltration (skin/temporalis fascia/dura mater- brain not painful to stimuli)- better to use LA+1:200,000 Adr is preferable as higher amount can be used & less bleeding BUT care with systemic absorption, risk intra-arterial esp into superficial temporal artery when blocking the auriculotemporal nerve. Infiltrate LA to 7 nerves each side AND additional LA can be infiltrated locally @ the pin sites.
technique (see SAQ) 2016.2 06.
benefits of scalp block: haemodynamic stability, decreases stress response to painful stimuli, allows a stimulating procedure to be performed with “wake up” for neurocognitive testing/mapping/lesion resection- may be used for the sole anaesthetic.
Usually place bilateral scalp block prior to placing mayfield pins.
-prevention of PONV which increases ICP
-haemodynamic stability
-prophylactic antibiotics pre-incision
-ANTI-EMETICS +++++.
-remi can stay running on emergence for “smooth” wake-up with avoidance of coughing

Equipment:

Airway: own if sedation only, SGA (most common) or ETT (rare) if GA; have airway plan prospectively decided
Breathing: limit PEEP/Pit for optimising venous ouflow, avoid hypercapnia/hypoxia
C: large-bore IV, art line
D: consider BIS monitor
E:
F: judicious ++ fluids, idc or urinary convene

Postop to HDU or a neurosurgical ward.
neuromonitoring as postop haematoma can develop, esp 6hrs postop.
haemodynamic monitoring/Mx (discuss BP goals w surgeon)
consider postop agitation differentials (new pathology vs emergence agitation)
use systemic pain relief once scalp block worn off
Postop pain for craniotomy in general:
esp w supratentorial
Scalp blocks improve pain scores up to 12hrs & reduce opioid requirements up to 24hrs.
PCM alone ineffective!
NSAIDs more effective than PCM in reducing opioid requirement but no diff pain scores. morphine superior analgesic efficacy vs tramadol/codeine, w good safety profile.
if use remi, higher analgesic requirement post-op.

Possible complications uncommon, generally well-tolerated
-most issues related to pt intolerance (urinary catheter, prolonged positioning)/agitation/anxiety, tiredness/fatigue, revoking of consent, pain/discomfort, N&V
-LAST
-intra-op seizures (focal, generalised or both)
-hypoT/Brady/tachy
-inadequate or excessive sedation–> hypoV/hypoxia/hypercapnia
-failure of airway device, pulm aspiration
-VAE
-focal neuro deficit
-brain swelling

Question 139

how is SIADH treated in SAH (different from general asymptomatic SIADH)?

Answer 139

HTS, since fluid restriction may elevate risk of vasospasm-related ischaemic injury

Question 140

when does vasospasm typically occur after SAH? how does the risk of vasospasm impact our management of SAH pts?

Answer 140

day 3, peaks day 7&8 & continues up to 21 days

our goal is euvolaemia since hypovolaemia may incr risk cerebral ischemia in setting of vasospasm

Question 141

are venodilators generally used for cerebral aneurysm procedures?

Answer 141

no, due to risk venodilation & incr intracerebral venous volume & ICP

Question 142

BP goals for intracranial neurovascular procedures in adults?

Answer 142

unruptured aneurysm or ruptured with suspected normal ICP (ie. normal neuro exam): aim for BP <= the pts normal SBP, max 140mmHg, MAP >=60mmHg
ruptured aneurysm with suspected or known intracranial HTN: don’t treat passive HTN (may be normal haemodynamic response to maintain cerebral perfusion in setting of raised ICP) but avoid HTN due to noxious stimuli or iatrogenic from vasopressors. if ICP monitoring in place, CPP (= MAP - ICP) >=50-60mmHg should be maintained

Question 143

for which pts should adenosine be avoided?

Answer 143

severe reactive airways disease
severe coronary disease
cardiac conduction abnormalities

Question 144

considerations if adenosine is discussed with surgeons as part of the plan for circulatory arrest of flow through the aneurysm (as an alternative to clipping) or in the event of aneurysm rupture?

Answer 144

Discuss the possible need for adenosine in advance w the neurosurgeon, based on the risk of aneurysmal rupture.

Avoid in pts with severe reactive airways disease, severe coronary disease or cardiac conduction abnormalities

have transcut pacing pads in case need temporary pacing or cardioversion
incremental dosing- 6mg IV initially, further 6mg if tolerate- if no time (eg. rupture), 0.5mg/kg IV initially, expecting asystole for up to 60 secs. if repeat adenosine-induced flow arrest necessary, delay it until the pt returns to sinus & pre-adenosine BP.
may get self-limited post-adenosine arrhythmias & ST segment depressions.

Question 145

BGL goals for aneurysm surgery?

Answer 145

hyper & hypoglycaemia worsens outcomes
no consensus & tight control controversial
aim 8-18 & Rx if >18 with an insulin infusion

Question 146

temp goals for aneurysm surgery?

Answer 146

IHAST trial (intraop hypothermia for aneurysm surgery trial Anaesthesiology 2010) found no benefit from hypothermia cf normothermia for pts who had aneurysm clipping for SAH, so while fever should be avoided (worsens outcome after stroke, avoid & aggressively treat), I don’t apply induced hypothermia but I target temp to 36.5-37.5

Question 147

considerations with use of indocyanine green?

Answer 147

25mg rapid IV push to allow surgeons visualisation of brain perfusion after aneurysm clipped
may cause a brief, artifactual reduction in SpO2 (commonly low 90s)
rarely may cause anaphylaxis

Question 148

1.26 Anaesthetic considerations for intracranial vascular aneurysms (craniotomy for clipping, endovascular interventions)

Answer 148

PRE-OP:

Assessment:

in addition to usual pre-anaesthesia evaluation, assess

-neurologic status (aneurysm rupture usually–> SAH (accounts for 5% of all strokes. mortality 30-70% & 1/3 surviving dependent; M&M is usually due to the primary insult (neuronal damage @ initial bleed), rebleeding occurs in 2-4% untreated pts in the 1st 24hrs, 20% within 2/52, ischaemic damage from cerebral vasospasm, seizures, myocardial dysfunction; OUR JOB IS TO PREVENT SECONDARY BRAIN INJURY), should perform neuro Ax & grade severity of any haemorrhage, using WFNS/Fisher)

-physiologic effects of any SAH (acute hydrocephalus & incr ICP):
Multi-system effects:
-risk re-bleeding, raised ICP (may require EVD)
-GCS
-headache/nausea/vomit
-seizures (continue AEDs)

-cardiac abnormalities (ischaemia, arrhythmias, LV dysfunction, pulm oedema; characteristic ecg abnormalities with raised ICP= widespread giant TWI, QT prolongation & bradycardia (cushing reflex). may also get ST dep/elevation (catecholamine-induced cardiac injury, may mimic ischaemia (not hypoperfusion)or pericarditis), incr U wave amplitude), may get stress-induced CMO or Takotsubo. Ax cardiac biomarkers
-systemic HTN (AHA/ASA recommends SBP <160mmHg)

Neurogenic pulm oedema- 22% of cases & more commonly post circulation rupture
aspiration

Other:
-volume status (hypovolaemia may incr risk of cerebral ischaemia in setting of vasospasm; goal= euvolaemia)
-other ongoing Rx eg. nimodipine (a DHP CCB to prevent vasospasm) 60mg PO or NGT, 4hrly, continue intra-op (the issue is drop BP) & up to 21 days.

-consider pt factors that may incr risk of aneurysm rupture incl characteristics of the aneurysm, poorly controlled HTN, CAD, COPD (diseases ass’d w SAH incl HTN, smoking, AD PCKD- 8%, Ehler-Danlos Syndrome, NF-1, Marfan’s, CoA)

–> Hb; anaemia common after SAH & is ass’d w worse outcomes. Hb goal for transfusion hasn’t been defined for SAH but consensus is aim >=80g/L (outcomes optimal if Hb 80-115g/L); usually cross match & have blood available quickly

–>hyponatremia develops in up to 30% of pts with SAH, probably mediated by hypothalamic injury. H2O retention following SAH may result from SIADH (esp if vasospasm) or cerebral salt wasting, distinguished by the fact that SIADH= euvolemic, while asymptomatic hypoNa in SIADH usually Mx with H2O restriction, this is undesirable in SAH as it may–> intravasc vol contraction & vasospasm-related ischaemic injury, so hyponatremia in SAH is treated with HTS. Cerebral salt wasting characterised by vol depletion leading to release of ADH. Generally Rx with isotonic saline for volume repletion but may require HTS & fludrocortisone to counteract diuresis & natriuresis. Aim= restore euvolaemia which will suppress release of ADH. SIADH & CSW can be difficult to distinguish on labs, both have hyponatremia, low serum osmolality, high urine sodium, high urine osmolality; the main distinguishing feature= intravascular volume status (SIADH= euvolaemic or hypervolaemic, CSW= hypovolaemic)
–> glucose: both hyper- and hypoglycaemia are associated with worse outcome after SAH. optimal BGL goal is unclear, aim 8-18, treat >18 with insulin infusion.
-consider CXR if pt-specific factors eg. pulm oedema
-group & hold, blood product availability

CONSIDER LOCATION- if in angio suite, consider:
-layout of room
-expected movement of fluoroscopy machine (prior to draping, check movement of fluoroscopy machine through full range, ensuring lines are long enough & all lines/tubes out of the way)
-radiation lead apron protection & screen
-ensure monitors/breathing circuit away from the radiograph field (limit interference)
-consider that there’s a lack of pt access (pressure cares, lines secured)
-ensure emergency drugs available eg. protamine, metaraminol, NAdr, vasopressin; consider plts prepared if pt on DAPTs, (aneurysm: consider pads if risk pacing, consider adenosine if high risk rupture of an aneurysm)

DISCUSS with surgeons plan for:

-approach; ISAT trial showed disability-free survival @ 1yr greater if coil vs clip despite higher rebleed risk among coiling, survival benefits @ least 7 yrs. RRR 23.9% for death or dependency @ 1yr.
-BP goals, no strong evidence to support these nor the optimal therapy for HTN but generally if un-ruptured or ruptured with suspected normal ICP (normal neuro exam), goal SBP aim <= the pts normal, max 140mmHg & MAP >=60mmHg. if aneurysm ruptured, shouldn’t treat passive HTN (may be a normal haemodynamic response maintaining cerebral perfusion in setting of raised ICP) but should avoid HTN due to noxious stimuli or vasopressors. If an ICP monitor is in place, maintain CPP (MAP-ICP) >=50-60mmHg.
-management of ICP including CSF drainage if EVD in place
-location of aneurysm & pt position
-expected degree of difficulty
-plan for temporary aneurysm clipping
-plan for intra-procedural rupture
-use of neuromonitoring
-if endovascular, ?heparin, ACT goal?, intra-op antiplatelets (?OGT needed??- can give aspirin IV)
-brain relaxation- must be carefully considered with extra risks in setting of cerebral aneurysm; osmotic agents (mannitol, HTS) or aggressive CSF drainage prior to dural opening may acutely decr ICP, incr pressure gradient across aneurysm wall & risk rupture (transmural pressure = MAP - ICP). hyperventilation may result in cerebral ischaemia

PREPARE:
vasoactive medications immediately available:
-adenosine (temporary circulatory arrest to facilitate aneurysm clipping or to Mx intra-procedural aneurysm rupture, avoid if severe reactive airways disease, severe coronary disease, cardiac conduction abnormalities)- if this is part of plan, should have transcut pacing pads for possible temporary pacing or cardioversion. start with 6-12mg IV, add increments of 6mg (intraop rupture 0.3-0.4mg/kg IBW)
-esmolol
-labetolol
-nicardipine (another DHP CCB)
-phenylephrine infusion (esp pts within the vasospasm period 3-8 days)
-NAdr, vasopressin
-protamine (for heparin reversal in event of aneurysm rupture- for endovascular procedures the pt is frequently heparinised & the goal ACT should be established with the interventionist)
-?antiplatelets if endovascular
-consideration for endovascular: consider abciximab (GIIb/IIIa inhibitor) if thromboembolism occurs during coiling- bolus 0.25mg/kg IV then infusion). some advocate HTN after the aneurysm secured to limit thromboembolism & cerebral ischaemia.
-plts for pts on DAPTs in case of haemorrhage

Intra-op:

MONITORING:
-art line ideally pre-induction (continuous BP monitoring & blood sampling), if elective procedure consider deferring until post-induction if, in discussion with surgeons, risk aneurysmal rupture during induction & intubation is considered low
-SpO2, 12-lead ECG, 30-minutely NIBP, temp probe, BIS, NMT
-pt may have other monitors/devices (EVD, SjVO2 catheter, brain tissue O2 intra-parenchymal probe)

ACCESS:
-2x IVC, @ least 1 >=16g, consider CVC

MEDS:
-anxiolytic premedication usually appropriate for ELECTIVE aneurysm procedures

-IV induction to maintain haemodynamic stability, dose to avoid HTN & risk of aneurysm rupture while avoid hypotension- want to maintain stable CPP esp if high-grade SAH & lack of auto regulatory capacity- my choice premed glyco, prop/remi induction with metaraminol

Titrate agents for BP management which is dynamic during aneurysm surgery, must respond to the surgical conditions & requires close communication with the surgeon, OPEN key stages:
-skull pinning & skin incision: brief but highly painful (comparable w incision & laryngoscopy), attenuate HTN & tachycardia eg. w IV lig 1mg/kg, fent 100micorg, prop 20-50mg, esmolol 0.5-1mg/kg, consideration of LIA & scalp blocks
-dural opening (also stimulating)
-dissection: lighter plane of anaesthesia may be used as brain tissue has no pain receptors but need to avoid pt & iatrogenic movement during dissection of aneurysm & may request a lower BP (avoiding profound hypoT) during delicate dissection esp if SAH; induced hypoT has generally been replaced by use of temporary clips placed on feeding vessels, facilitating manipulation of the aneurysm.
-temporary clipping: on occasion surgeon may apply temporary clip on feeding artery prox to aneurysm to facilitate dissection. If the surgeon is going to do this, COMMUNICATION re: goal BP (decr BP may help surgeon manipulate artery but avoid profound HypoTN. Temporary clip does create an area of focal ischaemia, neurol outcomes are worse w prolonged occlusion times (TVO beyond 15-20mins risks ischaemia @ area distal to clip)
-Neuromonitoring (SSEPs, EEG esp for ICA or MCA aneurysms- NOT MEPs to allow for NMBDs) may be used to assess adequacy of blood flow when temporary clips are used (which create areas of focal ischaemia); if ischaemia is suggested or clip times are prolonged, incr MAP 10-20% may be appropriate. hypothermia & neuroprotective drugs aren’t beneficial during temporary clipping.
If the surgeon announces they’ll temporarily clip, I’d ensure the pt is physiologically optimal, that my pumps are full, pt paralysed, emergency drugs avail +/- blood.

-post the permanent clip placement, normal BP (SBP <140mmHg) is the goal. surgeon may request a brief period of induced HTN to ensure no flow distal to the clip with incr BP.

normothermia: IHAST found no benefit (neurol outcome & more bacteremia) of hypothermia cf normothermia so TTM goal is 36.5-37.5degC. Fever worsens outcome following stroke so should be aggressively avoided.

normoglycaemia: hypo- & hyperglycaemia both= worse outcome after SAH, optimal goal for BGL unclear.

immobility important: NMBAs with NMT (unless MEPs prohibit use)

Surgeon may ask for IV indocyanine green to visualise brain perfusion after aneurysm clipped; brief artefactual reduction in SpO2 to low 90s. rarely anaphylaxis. If the aneurysm was clipped in OT, ?go to II for post-clipping evaluation of circulation.

Prepare for risk of aneurysm rupture; may occur @ any time until the aneurysm is clipped but it’s most common during aneurysm dissection & clipping.

neurologic outcomes are worse for pts who sustain intra-op aneurysm rupture & they are particularly poor if the IAR occurs prior to aneurysm dissection.
Risks are anything that increases the TMP, eg. hypertensive episodes (laryngoscopy, pinning, extubation) or if sudden reduction in ICP (eg. mannitol rapidly administered, hyper V prior to dural opening, excessive CSF drainage via EVD) (CPP=MAP-ICP)

IAR= emergency requiring rapid, coordinated response. Useful to have a clear plan beforehand (48% occurs during dissection, 45% during application of clip).

MANAGEMENT DEPENDS ON WHETHER OR NOT THE ANEURYSM IS EXPOSED.
Continual communication with surgeons, call for skilled assistant
If exposed, goals are:
-create a BLOODLESS FIELD to facilitate clipping & to PROTECT THE BRAIN
–>induce hypoT- esmolol 10-20mg IV as needed to achieve MAP 50-60mmHg to reduce bleeding & facilitate clip placement (D/w surgeons re: OT conditions)
–>induce temporary flow arrest with adenosine 0.3-0.5mg/kg or 0.5mg/kg (to induce temporary bradycardia or cardiac arrest to reduce or suspend flow through the aneurysm; may be an alternative to temporary clipping in some pts or in the event of aneurysm rupture)
–>reduce CMR with propofol 20-60mg IV (if using prop for maintenance, incr rate to 125-200mcg/kg/min- aim to achieve burst suppression on BIS (I’d pref to bolus vs change my pumps as after hypoT/flow arrest will want to regain circulation),
*barbiturates theoretically useful to decr CMRO2, CBF & ICP but STP limited by CVS side effects, IHAST post hoc didn’t find pharmacological protection offered any favourable neurological outcomes
-VOLUME RESUS may be necessary once the clip placed; IVT & blood aiming for euvolaemia & Hb >=80g/L

-once clip in place, lighten anaesthesia to discontinue BS

If ruptures prior to exposure, may be difficult to detect (may be heralded but unexplained incr BP & ICP. rapid decision necessary re: Surg, imaging or angio). Support pt with:
–> optimising CPP by allowing permissive HTN, aim CPP 50-70mmHg if ICP monitor, if not, MAP >90mmHg. vasopressors as needed to incr BP (NAdr pref)
–> manage intracranial HTN (optimise cerebral venous drainage: elev head 15deg head-up, neutral position, tape vs tie of ETT, limit PEEP & Paw, treat any RV dysfunction; manage any cerebral VD: increase MV to reduce cerebral VD, TIVA, suppress CMRO2 (manage seizures, analgesia, depth of anaes); if EVD, drain CSF 5-10mL increments (*beware that opening of ventriculostomy abruptly may worsen bleeding (acutely elevates transmural pressure gradient)); osmotherapy?)
–> optimise O2 (aim PaO2 >80mmHg, PaCO2 32-38mmHg) & ventilation
–> osmotherapy, mannitol 0.25-1g/kg or HTS 100mL 3% NaCl, aim serum Na <=155mmol/L or serum osmolality <320mmol/L

–> neuro-protection with propofol 20-60mg IV or incr rate to >125mcg/kg/min, titrate EEG to burst suppression

IAR occurs with an endovascular procedure for an aneurysm (uncommon, if so it’s most likely with coil deployment), reverse heparinisation with protamine if requested by the radiologist. reduce BP to at or below pre-bleed level (care not to compromise CPP), reduce ICP (gentle hyperV, rev trendelenburg, osmotic agents), control seizures, cerebral protection (props/barbiturate), radiological control of leak should be obtained. if high load of extravasated blood, pt may need CT, EVD if imminent danger obstructive hydrocephalus. craniotomy may be required for evacuation intracranial haematoma & surgical clipping of aneurysm.

A complication of endovascular coiling= downstream thromboembolism; this is detected by angiography. abciximab (Gp IIb/IIIa inhibitor) may be given. May induce HTN after aneurysm secured as Rx for thromboembolism & resultant ischaemia.

Emergence:
-smooth, avoiding HTN/coughing/straining.
ideally a rapid emergence so can do neuro exam before leave OT.

POSTOP:
Always to ICU for serial neurologic examination, continuous BP monitoring & control, facilitate Rx of pain & PONV

Complications:
rebleeding
vasospasm
hydrocephalus
expanding haematoma
pyrexia
hyperglycaemia
seizures
electrolytes: typically hypoNa due to CSW (reduced aldosterone synthesis) or SIADH (more common with ant circn)

Question 149

1.26 What are some factors that may incr the risk of aneurysm rupture?

Answer 149

characteristics of the aneurysm
poorly controlled HTN
CAD
COPD

Question 150

1.26 Why is GA with paralysis always preferred for aneurysm procedures (both craniotomy & endovascular)?

Answer 150

such delicate procedures, any pt movement may –> vessel rupture or dissection, aneurysm rupture or displacement of coils.

Question 151

1.26 Anaesthetic considerations for pts having intravascular cerebral vasospasm Rx?

Answer 151

endovascular therapy (eg. angioplasty, intra-arterial vasodilators) may be used for symptomatic vasospasm after SAH

pts having intra-arterial Rx are critically ill & have cerebral ischaemia, often have advanced monitoring, high dose vasopressors & may have repeated procedures over days to weeks

-Ensure pt is resuscitated & comorbidities as stable as possible.

-This is remote anaesthesia; radiation hazards, pt access, risks w contrast; if in hours DA aware, experienced assistant w machine checked.

-these pts are I&V with art line, CVC +/- ICP monitoring; may have high-dose vasopressors
-transport considerations btwn ICU & interventional suite & monitoring for this transfer
-goal BP should be discussed with surgeon/interventionalist.

-interventionalist should communicate when about to administer intra-arterial vasodilator injection & I’ll anticipate hypotension after this & Rx it immediately; high-dose vasopressors may be required to support BP after intra-arterial VDs.

Question 152

1.27 What are some risks of brain arteriovenous malformations? how may they be treated? specific anaesthetic considerations?

Answer 152

intracranial haemorrhage
epilepsy

pts present for angiography +/- embolisation, surgical excision or stereotactic radio surgery (eg. gamma knife). may be treated with combined therapy, eg. endovascular procedure to occlude feeder arteries & reduce risk of haemorrhage, followed by surgical resection of the lesion.

discuss with surgeon beforehand expected degree of technical difficulty & potential for haemorrhage.

make preparations for possibility of significant, rapid haemorrhage:
-pre-op large-bore IVC x2, consider CVC, arterial line, blood type & cross, have blood in the OT for high-risk cases.

meticulously avoid HTN (while risk of rupture of AVM is less than aneurysm, 25% of AVMs include aneurysms)

Pts are at risk of NORMAL PERFUSION PRESSURE BREAKTHROUGH after removal of an AVM, phenomenon where cerebral oedema may rapidly develop & haemorrhage may result. may be due to penumbral sensitivity to increased perfusion pressures as the AVM is resected. Anaesthetic management= maintain normotension (volume restriction & diuresis & BP reduction NO LONGER recommended). In the event of postop haemorrhage, consider residual AVM before NPPB assumed as the mechanism.

For embolisation for a brain AVM:
-consider that the injection of ethylene vinyl alcohol polymer (onyx), a common embolising agent, may cause transient desaturation.
-there’s a low but present risk of the agent migrating through the AVM to distal venous circulation or R) heart & pulm circulation with resultant pulm HTN.
-interventionalist may request hypotension or adenosine-induced asystole during polymer injection to minimise passage into draining veins & the systemic circulation
-pts undergong onyx embolisation have a distinctive garlic smell persisting up to 24-48 hrs post procedure (metabolism of the solvent)

Question 153

Which pts may require extracranial-intracranial bypass? anaesthetic considerations?

Answer 153

it’s a direct anastamosis of either superficial temporal or middle meningeal artery to a branch of the MCA. considered for pts with ICA aneurysm requiring occlusion, pts with MoyaMoya disease.
Craniotomy
BP management to avoid cerebral ischaemia or infarction; maintain adequate CPP. MAP at or above awake level @ all times. need art line pre-induction to monitor for induction hypotension. AVOID hypovolaemia. Avoiding hypotension important as it may precipitate cerebral ischaemia.
NORMOCAPNIA: avoid hyperventilation (& hypoV); want to avoid cerebral VC & steal physiology, respectively.
neuromonitoring (eg. evoked potentials) to detect cerebral hypoperfusion. If ischaemia detected, surgeon & I should be notified. I’d ensure adequate MAP, normocapnia, Hb, adequate arterial O2 content.
surgeon may temporarily occlude an artery for vessel anastamosis & may ask for BP incr 10-20% to improve collateral flow while the vessels clamped.

Question 154

which patients should be managed with targeted temperature management to 32-36deg C?

Answer 154

comatose pts (not following commands) who’ve achieved ROSC following OOHCA & initial shockable rhythm, for @ least 24hrs

also suggested for non-shockable rhythms & in-hospital cardiac arrest, pregnant or haemodynamically unstable pts, pts undergoing coronary catheterisation or thrombolysis; only absolute CI is an AHD preventing aggressive care

Question 155

What’s the hypothalamus?

Answer 155

Coordinating centre of endocrine system.
Consolidates signals from upper cortex, ANS, environment (light & temp), peripheral endocrine.
Delivers precise signals to pituitary gland.
HPA axis directly affects function of thyroid gland, adrenal gland, gonads + influences growth, milk production & water balance.

Question 156

What are the 5 stimulatory hormones released by the hypothalamus & the 2 inhibitory hormones acting on hypothalamus?

Answer 156

Corticotrophin releasing hormon
Growth hormone releasing hormone
Thyrotropin-releasing hormone
Gonadotropin releasing hormone
Prolactin-releasing factors

inhibitory=
somatostatin
prolactin-inhibiting factors (incl dopamine)

Question 157

What are the 7 anterior pituitary hormones and what proportion of the anterior pituitary do they represent?

Answer 157

FLATPEG
FSH
LH (gonadotrophs = 15)
ACTH= 20%
TSH= 5%
Prolactin= 10-30%
Endorphins
Growth hormone = 50%

Question 158

Where’s the hypothalamus located?
Where’s the pituitary located?

Answer 158

Base of brain, below 3rd ventricle, above optic chasm & pituitary gland. Intersection btwn cortex/cerebellum/brainstem.
It lies in the sella turcica, below the optic chasm. It is connected via the pituitary stalk to the median eminence, the pituitary stalk passed through an opening in the dura so the pituitary lies outside the dura.

Question 159

What’s Sheehan syndrome?

Answer 159

infarction of the pituitary gland and hypopituitarism due to hypotension in the setting of PPH

Question 160

What are the clinical implications of destruction of pituitary stalk on anterior, posterior pituitary function & serum prolactin?

Answer 160

loss of post pituitary hormones as loss of neuronal function
anterior pituitary still receives some blood supply from inferior hypophyseal artery so if peripheral hypothalamic hormone [] are high enough the anterior pituitary will maintain viability
prolactin levels will increase due to loss of inhibitory signals from hypothalamus to lactotrophs

Question 161

How is pituitary adenoma evaluated?

Answer 161

Hx (focus= symptoms of hypopituitarism)
exam (esp visual fields & acuity)
MRI
biochemical testing:
-hypersecretion, test for excess of: serum LH, FSH & alpha subunit or FSH & alpha subunit response to TRH, prolactin, IGF-1 (for somatotroph adenomas), plasma ACTH & 24-hour urine free cortisol (corticotrophin adenomas)
-hyposecretion, test for deficiency of: 8am cortisol, T4 (if elevated, check TSH as it may be a thyrotroph adenoma), testosterone in men, E2 in premenopausal amenorrhoeic females
definitive diagnosis= pathologic evaluation of excised tissue.

Question 162

SS_NS 1.1 “Describe basic anatomy of skull”
“Describe the circle of willis”
“what does the middle cerebral artery supply? what are the signs & symptoms of occlusion?”
“what does the anterior cerebral artery supply? S&S of occlusion?”
“S&S of PCA occlusion?”
“What are the ventricles of the brain?”
“What are the 3 layers of meninges?”
“how many vertebrae are there? how many cervical nerves? name of C1?”
“where does the spinal cord end in adult? neonate?”

Answer 162

MCA:
Broca’s area of dominant hemisphere (usually in L) frontal lobe)- language production
Wernicke’s aphasia area of the dominant hemisphere (in 95% of R)-handed & 70% of L)-handed it’s in the L) hemisphere, superior temporal gyrus)- language comprehension
Motor cortex- frontal lobe in posterior pre-central gyrus- contralateral paralysis face/arm/leg
primary somatosensory cortex (anterior parietal lobes, behind motor cortex)- contralateral sensory impairment
Frontal eye fields (in BA8, prefrontal)- paralysis of conjugate gaze to opposite side
visual cortex/visual radiation- homonymous hemianopsia (often inf quadratic)

ACA:
Motor leg area- paralysis of opposite foot & leg, also gait apraxia
sensory area foot & leg- cortical sensory loss of toes/leg/foot
sensorimotor area in paracentral lobule- urinary incontinence
involvement of arm cortex- lesser degree of contralateral UL paresis, contralateral grasp reflex, paratonic rigidity
speech- slowness, lack spontaneity, whispering, distraction to sights & sounds

PCA:
peripheral territory:
homonymous hemianopsia- often upper quadratic
hemivisual neglect
cortical blindness
memory defect

central:
thalamic syndrome= sensory loss to all modalities
third nerve palsy
may get crossed cerebellar ataxia or contralateral hemiplegia

Communicating network of cavities filled with CSF, 2 lateral, third, cerebral aqueduct & 4th ventricle

What are the 3 layers of meninges?

33; 8 cervical, 12 thoracic, 5 lumbar, 5 sacral & 4 coccygeal
8; all but the first exit below corresponding vertebra
atlas

L1-2, upper border L3

Question 163

SS_NS 1.4 “outline changes to CBF control & CPP in pts with intracranial pathology”
-what’s monroe-kellie doctrine
-how increase or decrease cerebral blood volume?
-what’s normal CBF? how kept constant?
-what’s normal CPP & threshold for critical ischaemia?
-what does pathology eg. SAH do to autoregulation curve?
-what may happen to the BBB in intracranial pathology?
-what’s the normal rate of CSF formation?
-what are the compartments in the cranium & volumes?
-how may system compensate for raised ICP? decompensation?
-what are some conditions that may impair CBF autoregulation?

Answer 163

-brain is a rigid container of fixed volume, containing brain/blood/CSF. incr volume of any component incr ICP (normal is 5-15mmHg) if not compensated by reduction in vol of other components.
-cerebral blood volume may be increased by increasing flow (pressure/R: seizures (since metabolic rate coupled with CBF), some anaesthetics that vasodilate eg. volatiles), SNS activity has little role under normal conditions (aside from MAP increases) but may play a role in pathology where vasomotor/chemical/metabolic autoregulation overwhelmed, hypoxaemia (no change in physiological limits but CBF rises when PaO2 falls to 50mmHg), hypercapnia (2-4% change in CBF per mmHg, narrows autoregulation threshold), hyperthermia (CMR which is parallel to CBF, increases 7% per deg C), excessive MAP into cerebral circulation or reducing it’s outflow (eg. ties, head down)
-CBF normally kept constant 50mL/kg/min via autoregulation over range of MAPs 50-150mmHg (CPP best on X axis but since ICP usually constant, MAP used)
-CPP=MAP-JVP (or ICP) whichever is higher, normal CPP is 70-90mmHg & threshold for critical ishaemia 30-40mmHg
-In pathology such as subarachnoid haemorrhage, autoregulation curve altered eg. microvascular constriction may cause L)- and downward shift the upper threshold for CBF and in extreme cases this may be below critical perfusion threshold. larger upstream vessel constriction may cause right shift, with critical perfusion pressure being reached at a higher CPP. there may be a hybrid, narrowing the curve.
-altered permeability, eg. large polar charged substances may cross from systemic circulation to CNS which may raise ICP
-500mL/day, 60mL cranium & 60mL SC exchanged 4x/day
-1400mL brain tissue, 150mL cerebral blood vol, 150mL CSF
-Displacement of venous blood out of CNS, displacement of CSF brain–> SC, distension of meninges, increased CSF absorption (finite) via arachnoid granulations if ICP >7mmHg. If CPP falls below 70mmHg, reduction in CSF formation. Decompensates with oedema (from hydrostatic pressure)–>cerebral irritability. Intracranial compliance is poor, intracranial compliance curve is hyperbolic so even if small increases in volume occur, compensatory mechanisms are quickly overwhelmed.
-hypercapnia, TBI, ischaemic stroke, global hypoxic brain injury, regionally around a space-occupying lesion or haematoma, meningitis/encephalitis

Question 164

SS_NS 1.3 “Describe anatomy relevant to providing LA for awake craniotomy, including landmarks & complications, indications”.

Answer 164

Scalp block has potential to block 7 nerves, including branches from cervical spinal rami & from trigeminal divisions

*Supraorbital: branch of trigeminal (V1 division). forehead/ant scalp/top of head. palpate supraorbital notch, 2cm lat to midline (approx in line w pupil), needle perpendicular & inject 1mL.
*Supratrochlear: Branch of trigeminal (V1 division). forehead/ant scalp. Just medial to supraorbital n injection site, above eyebrow line at about angle of eyebrow. angle medially for medial spread.
use intradermic needle

zygomaticotemporal: branch of trigeminal V2 division. small area of forehead & temporal area. Passes through temporalis muscle to enter temporals fascia so infiltrate LA deep & superficial to temporals muscle- begin @ lateral edge of supraorbital margin, continue to distal aspect of zygomatic arch (concave)- 1-2mL.

Auriculotemporal: trigeminal V3. innervates temporal areas, lower lip, lower face, auricle & scalp over auricle. Inject LA 1.5cm anterior to auricle, above level of TMJ. Lies deep to superficial temporal artery- palpate this to avoid intra-arterial injection.

Greater auricular nerve: a branch of C2 & 3. emerges around posterior border of SCM, has ant & post branch, sensation over parotid, mastoid, auricle. LA 2cm posterior to auricle, @ level of tragus.

Lesser occipital nerve: branch of C2-3. ascends along posterior border of SCM, innervates lateral scalp & area of head posterior to auricle. Infiltrate LA subcut, behind auricle, top-down to auricular lobule, continue infiltration along superior nuchal line to greater occipital nerve

Greater occipital nerve: branch of C1-2, innervates posterior scalp, locate by palpating occipital artery 3-4cm lat to ext occipital protuberance along nuchal line. inject LA medial to occipital artery, 2-3mL after -ve asp, needle angled 90 deg to occiput.

Use total of 30mL LA with 1:200,0000 epinephrine. highly vascular so main risks= haematoma, LAST; aspirate frequently.
awake craniotomy, blunting haemodynamic responses to mayfield pins, incision, craniotomy, dural incision, postop analgesia, chronic pain, repairing lacerations, removing foreign body, exploring scalp wounds/drain abscesses or SDH.

Question 165

SS_NS 1.5 How do fluid and electrolyte disturbances alter brain function?

Answer 165

sodium perturbations most often lead to neurologic manifestations; serum [Na] is the primary determinant of serum tonicity (aka “effective serum osmolality”).

Fall in serum tonicity in hypotonic hyponatremia–> water movement into the brain. Manifestations depend on severity of over hydration, related to degree of hyponatremia, eg: nausea, malaise (125-130mmol/L), headache, lethargy, seizures, coma, resp arrest if <120mmol/L. pts with chronic generally are asymptomatic.

acute hyponatremic encephalopathy may be reversible but permanent neurological damage or death can occur esp premenopausal females. overly rapid correction may–> osmotic demyelination (severe neural symptoms usually delayed 2-6 days, may be irreversible).

chronic hyponatremia–> hydrostatic pressure gradient promoting fluid movement out of brain–> CSF & movement of solutes from brain (–> osmotic movement of water out of cells) decrease brain swelling. The process is reversed with correction but the movement of solutes back into brain slower than loss of solutes at onset of hyponatremia.

Acute sudden hypernatremia (eg. accidental infusion HTS) may–> rapid decrease in brain volume & rupture of cerebral veins, intracerebral & subarachnoid haemorrhages. may also get demyelinating brain lesions.
lethargy, weakness, irritability, twitching seizures, coma. Severe symptoms usually require acute Na >150mmol/L.

hypocalcaemia: tetany= hallmark (initial perioral & acral paraesthesia, stiffness, muscle spasms/cramps, Trosseau’s & Chvostek’s signs), diaphoresis, fatigue, hyperirritability, anx/depression.

hypercalcaemia: anxiety/depression/cognitive dysfunction

hypomagnesaemia-> tetany (incl Trosseau & Chvostek signs, muscle spasms/cramps), seizures, involuntary movements, apathy, delirium or coma, rarely vertical nystagmus (if severe), resp muscle weakness

hypermagnesaemia–> diminished deep tendon reflexes, somnolence, muscle paralysis incl resp function

hypophosphatemia: metabolic encephalopathy (paraesthesias, irritability, seizures, coma), weakness can–> respiratory muscle impairment

Question 166

SS_NS 1.7 Outline the radiological features of common acute neurosurgical conditions
what does T1 highlight? T2?

Answer 166

Subarachnoid haemorrhage: non contrast CT head, highest sensitivity in first 6hrs, declines thereafter. Blood generally in basal cisterns, sylvan fissures, interhemispheric fissure. Intracerebral extension in 30%, intraventricular blood in 20%, subdural blood in 5%.
Distribution of blood is a poor predictor of location of aneurysm except in pts with ruptured ACA or Acomm & if parenchymal haematoma. More likely traumatic if the blood is adj to bone in anterior or middle cranial fosse.

Subdural: crescent shaped, inner margin parallels the cortical margin of the brain. crosses sutures. look for mass effect/shift of midline structures (measure from septum pellucidum between L) & R) lateral ventricles). usually venous (eg tearing of cortical bridging veins).

extradural: lentiform. doesn’t cross sutures. generally arterial (eg. middle meningeal artery).

intracerebral haemorrhage: may be primary, no underlying lesion (eg. cerebral amyloid angiopathy, hypertensive haemorrhages). Secondary haemorrhages (other lesion complicated by haemorrhage).
typically hyperdense blood with surrounding hypodense oedema. There may be extension to other compartments, hydrocephalus, herniation.

Acute stroke: MRI more sensitive but less available & quicker/easier. non-con CT to exclude intracranial haemorrhage that would preclude thrombolysis, look for “early” features of ischaemia (eg. loss of grey-white differentiation, parenchymal swelling & gyrus effacement ) & exclude other intracranial pathologies eg. tumour that may mimic stroke. CT perfusion= useful to see core infarct + surrounding penumbra (may potentially be salvaged).

T1 fat
T2 fat AND water

Question 167

SS_NS 1.8: Discuss pharmacologic and non-pharmacologic methods to manipulate intracranial pressure

Answer 167

The methods directed @ lowering ICP have side effects & are effective for variable & limited periods of time.
BTF recommends that management of severe TBI should be undertaken with info from ICP monitoring (reduces in-hospital & 2/52 post-injury mortality).

Pharmacologic:

Hyperosmolar therapy may reduce ICP by combination of brain dehydration & reducing blood viscosity (improving microcirculatory flow):
0.2g/mL (20%) mannitol, 0.5g/kg- works within mins, peaks 1hr, lasts 4-24hrs, risks “rebound” raised ICP or precipitate acute congestive cardiac failure or incr MAP (incr circulating volume incr preload, SV, CO frank-starling but HF if impaired LV function), however ultimately may—> hypotension following diuresis; avoid if SBP <90mmHg. Accumulates in renal insufficiency, may cause AKI due to renal vasoconstriction & intra-vas volume depletion. hyper Na, hypokalaemia, hypoMg++, hypoCa++, hypoCl-, metabolic alkalosis or acidosis. Risk vascular irritation, anaphylaxis.
HTS (NaCl 3%, 1-2mL/kg ?3mL/kg on our CatA head guideline). Volume depletion & hypovolaemia don’t occur so HTS is safer in pts with ongoing blood loss, hypovolaemia or hypoT. Also it has reflection coefficient of 1 (cf mannitol 0.9) so less likely leak into brain tissue. There is however risk circulatory overload & pulmonary oedema, increased Cl burden which may —> NAGMA, risk coagulation disturbance & risks thrombophlebitis (requires central access ideally but peripheral acceptable in emergencies)
some guidelines recommend only use mannitol prior to ICP monitoring if imminent cerebral herniation or acute neurol deterioration not attributable to extra cranial causes

Seizure prophylaxis: phenytoin recommended by BTF to decrease incidence of early PTS if overall benefit felt to outweigh complications but early PTS haven’t been ass’d with worse outcomes. blocks V-D Na channels. Reduces effectiveness of hormonal contraception. renal failure impairs PB & may incr free [], pts with low serum alb or use of highly PB drugs also alter free levels. CYP2C9 polymorphisms affect metabolism. main adverse= gingival hypertrophy, rash, body hair, decreases BMD. neurotoxic: confusion, slurred speech, diplopia, ataxia, neuropathy (LT use). Has been ass’d with SJS or TEN.

To limit cough/strain/ventilator dyssynchrony & CMR: Adequate DOA/sedation (barbiturates are recommended by BTF for elevated ICP refractory to maximum medical & surgical Rx (thiopentone dose-dependent & marked reduced CMRO2, can get isoelectric EEG, raises seizure threshold), need to ensure haemodynamic stability before & during. Propofol is recommended for ICP control but doesn’t improve mortality or 6/12 outcomes & high doses may—> significant morbidity), analgesia, m relaxation & blunting of SNS (pre-Rx with lignocaine)

Glucocorticoids have a role in intracranial HTN caused by tumours or CNS infections (reduces vasogenic cerebral oedema) but WORSEN outcome in pts with mod-severe head injury, not useful for cerebral infarction or intracerebral haemorrhage. BTF have level 1 recommendation against pred to reduce ICP, high-dose ass’d w incr mortality in severe TBI. CRASH-1 halted early due to clear difference favouring placebo for mortality @ 2/52, recommended corticosteroids not routinely used to Rx head injury of any severity.

Non-pharmacologic:
Normothermia (36-37degC), as CBF increases 7% per degC. Therapeutic hypothermia not recommended as Rx for raised ICP; POLAR RCT, no improvement neurological outcomes @ 6/12.
Hyperventilate to eTCO2 30-32mmHg (PaCO2 35-40mmHg), CBF regulated by myogenic & vasodilator metabolites (eg. incr H+), hyperventilation promotes CO2 movement CNS—> blood—> alveoli, less CO2 to be hydrated via CA to H+ which precipitates VD (via NO). less of vasoactive metabolites= less vasodilation, reduces CBF & ICP. 2% reduction in CBF for every mmHg PaCO2. Hyperventilation initially reduces CBF within a minute, over 6-24hrs it’s attenuated by bicarb moving across BBB to normalise pH. PaCO2 <20mmHg risks cerebral ischaemia due to extreme cerebral VC & L)-shift OHDC reduces DO2 to brain tissue. aim to avoid in first 24hrs (reduced CBF)

Keep euvolaemic (judicious maintenance fluids) & normo- to hyperosmolar (serum osmolality >280mOsm/L), generally achieved w isotonic fluids. Avoid free water, value of colloid vs crystalloid inconclusive but one trial has found higher mortality ass’d w Alb vs N/S.
Serum Na+ above 130mmol/L
Normoglycaemia (BBL <10 but not hypo (incr risk brain injury); hyperglycaemia ass’d with pro-inflammatory cytokines, incr blood viscosity which may —> ischaemia & hypoxia in brain, exacerbates intracranial oedema, can induce BBB rupture, may accelerate cerebral vasospasm. NICE-SUGAR trial showed no difference btwn tight (4.5-6 & conventional (<10) control wrt neurol outcome & mortality@ 2yrs.

Maximise venous drainage: position 30 degrees head up/bed tilt, neutral head position & ensure tape vs tie & not too tight, limit pressure (eg. collar) on neck, PEEP<=5cmH2O & limit pIT

SpO2 >95% & PaO2 >90mmHg

Ensure MAP adequate for cerebral perfusion but not excessive to raise ICP, BTF goals SBP >=100mmHg 50-69, >=110mmHg 15-49 & >70.. Intervene for HTN if CPP >120mmHg & ICP >22mmHg. The target CPP is 60-70mmHg (survival & favourable outcomes)- the correct goal depends on pts pressure & auto regulatory status; pts with intact autoregulation better with higher CPP, pressure-passive better with low.

Question 168

SS_NS 1.9: Outline methods to reduce secondary injury and limit disability in traumatic brain injury and intracranial haemorrhage

Answer 168

What’s primary brain injury?

occurs @ the time of trauma.

direct impact, accel/decel, penetration, blast waves.

Shearing—>DAI, multiple small lesions in white matter tracts, severe DAI—> coma sans raised ICP, poor prognosis.

Cerebral contusions most frequently encountered, esp in basal frontal & temporal areas, susceptible to direct impact in accel/decel injuries. May get intraparenchymal haematoma w coalescing.

Extra-axial haematomas generally if forces distributed to cranial vault. eg. epidural haematomas- lentiform, generally no ass’d brain damage, torn dural vessels.

SDH from damaged bridging veins, crescentic & often underlying neuro injury, more common in older adults w minimal trauma (cerebral atrophy stretches & makes bridging vv more susceptible).

SAH: often w disruption small pial vessels.

intraventricular: may be from tearing subependymal vv or extension from intraparenchymmal or SAH.

What proportion of pts with severe TBI develop coagulopathy? 30%

What’s secondary brain injury in TBI?

A cascade of molecular injury mechanisms, initiated @ initial trauma, continue for hrs or days.
incl:
secondary ischaemia from vasospasm
electrolyte imbalances
inflammatory responses
mitochondrial dysfunction
NT-mediated excitotoxicity

lead to neuronal death & cerebral oedema & incr ICP—> further exacerbate brain injury.

What have clinical trials on neuroprotective treatments to prevent secondary brain injury from TBI found?

no clear benefit of any strategy.

what are the principles of ameliorating secondary brain injury?

avoiding hypotension & hypoxia (decr substrate delivery to injured brain); use isotonic fluid, N/S may be pref to Alb in post-hoc of pts with TBI in SAFE (alb may have incr 28-day mortality)- balanced crystalloids may decr AKI in other pts but N/S pref in TBI since balanced solutions relatively hypotonic & may worsen cerebral oedema. BTF BP goals SBP >=100mmHg 50-69yo, >=110mmHg 15-49 & >70yo

for severe TBI, keep sedated & artificially ventilated maintaining normocarbia & keeping PaO2>60mmHg

avoid episodes of raised in ICP/decreased CPP; cerebral autoregulation disrupted in approx 30% of pts with severe TBI.
Monitor: serial neuro exams every hour for 24-48hrs if mod TBI (since ICP monitoring typically not performed in these pts)- repeat imaging for any neurologic worsening or within 6 hrs if no deterioration but haematoma on initial scan. ICP monitoring should guide Mx in severe TBI or mod TBI sans reliable neurological exam. ICP goal <=22mmHg= threshold predicting survival & favourable outcome after TBI. To attain: CSF drain, sedation, analgesia.

avoid fever & seizures (incr metabolic demand)- levetiracetam may incr BP, vomiting, infection, drowsiness, psychotic symptoms, asthenia.
antipyretics, surface-cooling or endovasular temp management catheters to avoid fever.

avoid hyperglycaemia (exac ongoing injury mechanisms, exact glucose target unknown but avoid extremes)

Regularly monitor electrolytes

Monitor for & manage coagulopathy (ass’d w haemorrhage expansion/poor neurologic outcomes)

What’s the biggest cause of secondary brain injury (which in conjunction with hypoxaemia may cause reactive VD & elevations in ICP)?
hypotension.
Hypotension should be treat aggressively to maintain CPP 60-70mmHg to improve survival & favourable outcomes. Efforts to optimise CPP should first focus on Rx of elevated ICP (CSF drainage, analgosedation- fent infusions (greater efficacy cf morphine & they minimise haem instability), props preferred sedative given rapid onset/offset & neuroprotective but care w hypotension & prop infusion syndrome, osmotic therapy if icp not responsive to first 2 measures. infusion 3% NaCl for sodium 145-155mmol/L & supplemental boluses 30mL 23.4% NaCl over 10mins (ideally CVC). prior to raising MAP (as HTN more likely to worsen cerebral oedema when protective autoregulation is impaired). May hyperventilate to ETCO230mmHg as temporary intervention (best avoided in first 24-48hrs)
SBP at least 90mmHg (higher if chronic HTN) w fluid +/- vasopressors.

has any specific hyperosmolar therapy been shown to improve functional outcome or mortality?
no however there may be improved ICP control with HTS along with improved CPP & brain O2

What’s a limitation of hyperosmolar therapy?
effect diminishes with time due to compensatory increase in brain osmoles within 24hrs.

what’s the risk of targeting CPP >70mmHg?
acute hypoxic respiratory failure

What’s the risk of a single SBP <90?
Ass’d w 150% incr mortality

what are some other causes of secondary brain injury?
haematoma, contusion, diffuse brain swelling, systemic shock, intracranial infection.

Question 169

SS_NS 1.10: Describe the anaesthetic implications of spinal cord trauma

Answer 169

A trauma therefore may have MULTIPLE other traumatic injuries (eg. haemorrhage, cardiac tamponade, PTx).

What’s spinal shock?
altered physiologic state that can occur immediately after SCI, loss of spinal cord function caudal to the level of injury: flaccid paralysis, anaesthesia, absent bowel & bladder control, loss of reflex activity, impaired temperature control, can last days to weeks.

What’s neurogenic shock? part of spinal shock syndrome, occurs within 30mins of injury, lasts up to 6/52. Haemodynamic state (hypoT, bradycardia, hypothermia) due to disruption of descending SNS pathways after SCI. PSNS influence predominates: hypoT (lack of preload due to reduced SVR in splanchnic & skeletal vessels), bradycardia/bradyarrhythmias/heart block (unopposed vagal tone). Orthostatic hypoT may be profound early post-injury, even if SCI below T6.
Pt has: SBP 60-80mmHg
low CVP
pulse 40-50bpm
peripheral vasodilation (may feel warm despite low core temp)
heart sypathectomised–> risk pulm oedema (esp if aggressively resus aiming to normalise BP)
(looking @ XR, for C-spine injury consider soft tissue swelling (retropharyngeal space: pharyngeal air column to anterior inferior aspect of body of C2 >7mm abnormal. retrotracheal space: anterior inferior aspect of C6 to post-tracheal wall >14mm in chn & >22mm in adults is abnormal., oedema around laryngal area, potentially difficult airway. CXR: ?pulm oedema)

How may a pt with cord injury present?
potentially localised pain @ site of spinal # but may have associated brain/systemic injuries that limit ability to report localised pain (expect pain & manage it)
motor signs: weakness/paralysis
sensory signs: absence/alteration
laceration/deformity/bruising of spine
incontinence: bl/bowel

Initial management?
A: immobilising C-spine, secure airway if imminent threat (eg. hypoxaemia, flaccid chest wall)
B: ensuring supplemental O2
C: avoid hypotension MAP should be 85-90mmHg (may be due to other injuries or reduced preload due to neurogenic shock)-*for isolated SCI, avoid aggressive volume expansion which may –> pulm oedema. CVP monitoring useful ++.
*if the pt has a HR 70-80 this is relative tachycardia- high index suspicion coexisting hypovaloaemic shock. also monitor UO.
D: GCS, CN function, assess for life-threatening injuries
bl scan, IDC (their bladder doesn’t empty)
consider NGT (they all have an ileus)
Imaging, first full set Cx radiographs (AP, lat, open-mouthed odontoid views, oblique if suspect lat mass or facet injury), want to view all to top of T1.ideally MRI if pt & spine stabilised as this shows spinal cord better than CT. pts who are not clinically evaluable are assumed to have TSCI until proven otherwise.

Approx 1/3 of pts with Cx injuries need intubation within first 24hrs
What cardiovascular complications can occur with acute cervical and upper thoracic SCI?
Neurogenic shock- more common with complete C-spine injury (20-30%) cf T-L or incomplete.
Hypotension
Bradycardia (most common HR after SCI, almost all pts w complete Cx SCI have resting HR <60bpm, approx 70% have HR <45bpm, bradyarrhythmias peak day 4 after injury), other arrhythmias (eg. SVT, VT)
Early autonomic dysreflexia (more common in chronic phase, may occur in acute phase esp if severe cervical SCI)

Pulmonary complications: depend on level of lesion (diaphragm & accessory m of resp involvement) & pre-existing resp status
occur in 80% of pts w lesion above C4, 60% C5-8
Pts w complete lesions have flaccid chest wall w hypoxia, immediate ETT & mech vent
complete mid-lower Cx lesions may progress to resp failure, peak time 3-4.5 days

reduced vital capacity, impaired cough/sigh, diaphragm fatigue (or paralysis)
ventilatory failure
atelectasis
pneumonia
mucus plugging (ineffective cough)
pulmonary oedema
pulmonary embolism
Bronchospasm & incr pulm secretions due to sympathectomy w injuries above T6.
Tx SCI pts may have resp complications due to direct chest trauma (eg PTx, rib #, diaphragm or bronchus rupture).

GI complications: pts w SCI > mid-Tx have high risk aspiration due to gastric dilation & delayed emptying, paralytic ileus, acute gastroduodenal ulceration (risk of stress ulcers, should have prophylaxis with PPIs) & haemorrhage, acute acalculus cholecystitis

Urologic: risk for urinary retention, distension injury, AD triggering.

Haematologic complications: DVT

Electrolytes: may develop hyponatraemia related to disruption of renal SNS pathways regulating RAAS response.

Glucose: tolerance may be impaired due to stress response or glucocorticoid admin.

Temp regulation: impaired +++ due to VD & heat loss below level of injury, pts w C-spine injury can’t sweat below the lesion. *adjust the OT temperature.

Closed reduction & internal or external fixation: is to achieve normal alignment; doesn’t improve neurology but facilitates earlier mobn/rehab by 5-7 wks

GOALS:

Thorough airway assessment & plan (considering risk of other injuries eg. facial injuries, oedema, blood in the airway, head trauma/raised ICP, pts level of cooperation).

Assume C-spine unstable until radiologically cleared. spine protection devices (eg. halo, collar) may affect mask ventilation/airway instrumentation.

Plans A,B,C (likely plan A RSI with MILS (at pts shoulder, palms mastoid & fingertips occiput, enough pressure to counter laryngoscopy & keep head neutral but AVOID traction- don’t use MILS if HALO (it’s for C1-2 fractures, the pt can completely open their mouth but head & neck fixed- can’t align oral/pharyngeal/laryngeal axes so rely on fibreoptic or LMA+bougie/FO), if there’s a hard collar establish MILS & open collar if need space to open mouth) & D-blade or consider flexible scope intubation, limiting C-spine movement. consider awake depending on pt cooperation & anticipated degree of difficulty (benefits= can keep head/neck neutral with little/no movement, spont vent until airway secured safe if difficulty anticipated, neurologic eval can be performed after airway management. Disadvantages= awake takes longer, risk cough/gag, blood/secretions may prohibit, sedation may be required which impairs neurol assessment). Have difficult airway equipment & FONA setup).

If need mask vent, insert oral or nasal (if not CI) airway with outward jaw thrust.
(absolute CI= BOS #, facial trauma, disruption of midface/nasopharynx/roof of mouth, anticoagulants or coagulopathy)
Large-bore IV access (spine surgery may—> massive blood loss)

Consider CVC for access or vasoactive drugs

ART LINE for any GA.

Thorough pre-O2, consider nasal cannulae

RSI if intubate (however avoid cricoid to limit C-spine manipulation but use gentle BURP if need to improve view, use MILS) anti-emesis (aspiration risk). Avoid sux BEYOND 48hrs (risks life-threatening hyperkalaemia), consider roc with reversal prior to any neuromonitoring. pancuronium gives a tachy which is useful but with 0.1mg/kg, 3-5minute onset.

Consider risk of hypoT w induction- critical to maintain adequate MAP as hypoT may cause SC hypoperfusion & exac secondary SC injury. Autoregulation of SC blood flow may be lost after SCI.
Maintain MAP 85-90mmHg for 5-7 days after acute cervical SCI, avoid SBP <90mmHg. Reduced induction dose, vasopressor infusion prior to induction (ephedrine or glyco if also brady); also administer atropine or glyco for any pts with high Tx/Cx injuries as risk severe brady/cardiac arrest w airway manipulation (eg. atropine 1.2mg). titrate IV fluids, blood products, vasopressors, inotropes (dobutamine, dopamine) to BP targets. Injury above cardioaccelerator SNS innervation (T1-4) requires inotropic & chronotrophic properties as well as VC. Norepinephrine may be sl better for SC perfusion cf dopamine. Lower SC injuries often require a pure VC once euvolaemia is achieved, due to the peripheral sympathectomy & VD.
Want to limit secondary cord injury (possible ischaemia, hypoxia, inflammation, oedema, excitotoxicity, apoptosis which may manifest as neurological deterioration)

Consider if neuromonitoring used; if so, avoid m relaxant & volatile (in pts w normal neuromuscular transmission, SSEPs adequate up to 0.5-1MAC volatile but if any neurological impairment, even low level VA abolish SSEPs. TIVA is needed for MEPs as even low [] VA impair MEP responses. N2O has similar effects on neuromonitoring to VA but incr freq of EEG. IV agents have less effect than inhalation’s but very deep propofol can impair MEPs. SSEPs aren’t affected by barbiturates but MEPs are sensitive. Ketamine enhances SSEP & MEP amplitude, incr EEG amplitude & freq & can evoke seizures in epilepsy. BZDs don’t affect SSEP & MEP responses, slow EEG but no BS or electrical silence unlike most IV anaesthesics. Etomidate increases cortical SSEP amplitudes, doesn’t impact MEPs but it’s use is ass’d with adrenal suppression & worse outcome in sepsis. Also, low-dose etomidate can evoke seizure in epilepsy. Dexmed has conflicting literature re: impact on MEPs, effect on SSEPs is minimal. Opioids cause small, dose dependent SSEP & MEP depression but they can still be recorded, even @ high doses.
Manage brady/other arryhythmias with atropine/pacing.
low-threshold for intubation if resp m insufficiency

Ventilator management: TV 6-8mL/kg, I:E 1:3 to maximise VR, dopamine/dobutamine likely needed to keep BP up, use any atropine w suction (otherwise sig brady), early tracheostomy- useful w weaning from ventilation as often pts can’t cough effectively/unsuccessful extubation

Analgesia: adequate, limit SNS stimulation below level of injury, 25-95% of pts with SCI may develop chronic pain.

Fluids: avoid volume overload (pulmonary & SC oedema)- use acid-base, lactate levels, EBL & UO to guide fluid resuscitations. PPV >13% in supine ventilated pt suggests fluid responsive, prone the thresholds are higher so look @ trends.

IDC for surgery, monitor output & avoid kinking

TxA significantly reduces blood loss & rbc transfusion in spine surgery in healthy patients, impact on VTE risk in pts w acute trauma (high baseline risk of thromboembolic events) uncertain- often avoid as a precaution for pts where Hx unknown. dose-dependent risk of seizures. Reduce dose if significant renal dysfunction or low body weight, malnutrition.

VTE prophylaxis: pharmacologic & non-pharmacologic, DVT occurs in 50-100% of untreated patients & greatest incidence is 72hrs-14 days.

monitor electrolytes (esp. Na), glucose

Normothermia (monitor core temp, target with in-line fluid warmers (attach warm line to largest IV), FAWD)- avoid hyperthermia esp if ass’d TBI.

Care w positioning- risk POVL if prolonged surgery in prone. Strategies to limit haven’t been established to prevent ION: inform pts re: the risk. neutral head position @ or above level of heart, avoid Wilson frame. frequent eye checks to avoid pressure on globe (CRAO), avoid horseshoe headrest (risk CRAO). art line w MAP as close to prep baseline as possible to optimise perfusion to optic nerve/spine. Monitor Hb (determine pt-specific target), Hct (aim 30%), glucose, oxygenation. If evoked potentials deteriorate, incr MAP to baseline or slightly above & troubleshoot. If losing significant blood, give blood & colloids along w crystalloid to limit oedema.
Pressure injuries vital to avoid.

Disposition: often ICU intubated (if severe Cx SCI expectation of assisted vent +/- tracheostomy (generally 7-10 days unless extubation imminent), lower injuries depends on length of procedure, blood loss, associated injuries. Surgeon may want neurological exam straight after surgery despite ongoing intubation, may lighten until move all 4 limbs, allow Ax then re-deepen prior to ICU T/F.

Pts should have chest Physio asap, may need frequent airway suctioning.
OT, psychological counselling, enteral or parental feeding started within a few days.
Methylprednisolone has been suggested to improve neurological outcomes in acute, non-penetrating TSCI but evidence is limited.

Question 170

SS_NS1.10 cont’d: what’s the usual pattern of recovery from SCI? how may this impact respiratory function?
what pulmonary physiologic changes are seen following SCI?
innervation of external intercostals? scalene? SCM & traps innervation?
how can pts w high SCI sometimes breathe?
innervation of internal intercostals? RA, obliques, TA?
how are the intercostal & abdominal muscles important in pts with Cx or Tx SCI?
which level of injury produces near total ventilatory paralysis, requires immediate manual ventilation & assistance to cough?
How may pts with C6-8 resp function manage?
Thoracic?

What happens to lung compliance with tetraplegia?

PFT findings in tetraplegia? explanation?

Another resp risk in pts with SCI?

Answer 170

-initial flaccid paralysis of all muscles caudal to injury (spinal shock), over days to 6/52, spinal reflexes return & eventually become exaggerated as spasticity develops. For pts with injury C3-5, with variable diaphragm& accessory muscle of inspn impairment, they may require mech ventilation initially but reacquire sport vent as flaccidity transitions to spasticity & accessory muscles are recruited & strengthened. Still impaired cough, risk resp failure.

-impaired ventilatory muscle performance, changes in lung & chest wall compliance, changes in ventilatory control, airflow limitation & bronchial hyper-responsiveness.

-thoracic nerve roots, C4-8, C1-4 & cranial nerve 11.

-glossopharyngeal breathing

-thoracic nerve roots. RA=intercostal nerves T7-11 & subcostal nerve T12. obliques T7-12 & sensory iliohypogastric (L1). TA= T7-12 & L1 (iliohypogastric & ilioinguinal).

-stabilise rib cage, preventing inward collapse during diaphragm contraction for inspiration. act as a fulcrum for diaphragm contracion/efficiency. loss of abdominal tone makes abdo contents move caudad so diaphragm less dome-shaped & less efficient.

above C3

still have diaphragm & accessory insp muscles above level of injury, exhalation by passive recoil. with arms fixed the clavicular portion of pec man can contribute to exhalation. cough impaired.

Thoracic main issue is ineffective ought.

reduced. intercostal muscle spasticity, ankylosis of rib articulations with spine & sternum (may be due to inability to inspire to TLC)

main finding= restrictive ventilatory defect. they have reversible exp airflow limitation, usually only apparent with bronchodilator administration. may be due to unopposed vagal cholinergic activity–> bronchoconstriction/airway hyperresponsiveness.

sleep disordered breathing and blunted ventilatory response to hypercapnia.

Question 171

SS_NS 1.11: How may hypopituitarism present?
which pituitary hormones are more likely to be affected, as a general rule?

How does ACTH deficiency present? and what are 2 important clinical distinctions between cortisol deficiency due to ACTH deficiency vs due to primary adrenal disease (which is also associated with aldosterone deficiency, POMC & ACTH release)?
in which form of adrenal insufficiency may hyponatraemia occur?

How does TSH deficiency present?

How does gonadotropin deficiency present?

How does GH deficiency present?

How PRL deficiency present?

Answer 171

Depends on the rapidity with which the disease affected ant pituitary cells, severity of hormonal deficiency, number of ant pituitary cells affected (eg. impaired secretion of all= panhypopituitarism). if the hypopituitarism is due to a sellar mass, there may also be symptoms of mass effect.

gonadotropin & GH more likely to be affected than ACTH & TSH but many exceptions occur.

ACTH deficiency: may have few/no clinical findings so evaluate biochemically if pit or hypo disease. Mild (postural hypotension & tachycardia), severe= vascular collapse. mild chronic= fatigue, anorexia, weight loss, hypoglycaemia, eosinophilia.

acth deficiency= no salt wasting, volume contraction, hyperkalaemia as no clinically important deficiency in aldosterone.
Also no hyperpigmentation.

both cortisol deficiency due to ACTH deficiency & cortisol deficiency due to primary adrenal disease. it’s due to inappropriate ADH secretion with low cortisol (not aldosterone) deficiency.

Fatigue, cold intolerance, decreased appetite, constipation, facial puffiness, dry skin, brady, delayed relaxation of deep tendon reflexes, anaemia. Again may have few symptoms- screen biochemically.

hypogonadotropic hypogonadism; ovarian hypofunction (anovulation, hot flashes, decreased BMD), decreased testosterone secretion (decreased energy, libido, doesn’t cause decr m mass for many years. does decrease BMD).

in children: short stature. adults: incr fat mass & decreased lean body mass, in men decreased BMD. May also have dyslipidemia & increased inflammatory markers.

inability to lactate after delivery.

Question 172

SS_NS 1.13: Outline the criteria for the diagnosis of brainstem death
What’s death?
what’s brain death?
What are the clinical criteria for brain death?

Answer 172

an irreversible, biologic event that consists of permanent cessation of the critical functions of the organism as a whole

complete, irreversible cessation of brain functions (incl capacity for brainstem to regulate resp & vegetative activities)

Clinical prerequisites:
-clinical or neuroimaging evidence of acute CNS catastrophe compatible w Dx of brain death
-exclusion of complicating medical conditions that may confound clinical Ax (severe electrolyte, acid-base, endocrine or circulatory disturbance)
-no drug intoxication or poisoning (incl sedatives)
-core temp >36degC
-systolic BP >100mmHg (can use vasopressors)
-need minimum 4-hour observation prior to neurological determination of death using clinical examination alone

Neuro exam:
-coma (GCS 3)
-absent brain-originating motor response (eg. response to pain stimulus above the neck; test w noxious stimuli in CN distribution (trigeminal; supraorbital nerve) & all 4 limbs)
-absent pupillary light reflex & pupils midposition
-absent corneal reflexes
-absent oculocephalic (avoid if C-spine injury suspected, absent or asymmetric response implies brainstem death) & oculovestibular (caloric testing- ensure TM intact, 50mL ice cold water to irrigate ear canal w head elevated 30 deg, should show conjugate deviation to the irrigated side, absent or asymmetric indicates brainstem dysfunction, intact eye deviation with nystagmus suggests may not be in coma) reflexes, 5 mins apart
-absent gag reflex
-absent cough w tracheal suction
-apnoea w apnea test (have core temp >=36, SBP >=100, eucapnia, absence hypoxia, euvolemic. not valid if CO2 retainer or neuromuscular paralysis/high C-spine lesion. +ve apnoea test if no resp response to PaCO2 >60mmHg or 20mmHg greater than baseline values, standard observation 8-10mins; apnoeic oxygen (FiO2 100% to trachea (after pre-O2 for 5 mins), no ventilatory assistance). PaCO2 usually rises 3mmHg/minute.

Question 173

SS_NS 1.14: Evaluate the effects of anaesthetic agents on brain and spinal cord physiology *figure including metabolism, blood flow, intracranial and intra-spinal pressure

Answer 173

CMRO2: nitrous, ketamine & to a small extent opioids, INCREASE it. All others decrease CMRO2 by reducing CNS neuronal activity, ESPECIALLY propofol/thio/etomidate (thio particularly reduces CMRO2, can be up to 55% & can get flat EEG), iso reduces CMRO2 more than the other volatiles & incr CBF & ICP less than other volatiles).
CBF: nitrous & desflurane increase it to the greatest extent, sevofluorane somewhat & iso slightly (VD–> incr CBF from 1 MAC @ which point get flow-metabolism uncoupling & “luxury perfusion” in excess of metabolic demands. prop, thio & etomidate markedly reduce it, benzos, opioids & dexmed reduce it a bit, ketamine unknown (some report it incr CBF). Nitrous increases ICP &CBF substantially when used alone or with volatiles but the increases are blunted if it’s used with IV anaesthetics. Since autoregulation preserved, hyperventilation can prevent the incr in CBF during N2O anaesthesia.
ICP is increased by nitrous & des to a moderate extent but sevo & iso slightly (if >1MAC & incr CBF). prop/thio/etomidate reduce ICP. benzos & opioids both reduce ICP, ketamine unknown (some report incr ICP), dexmed no change.
none of the agents impact cerebral autoregulation apart from dexmedetomidine (& some report it impairs cerebral autoregulation).
Ketamine has conflicting evidence; some evidence that it incr CMRO2, CBF & ICP; others show no change or decr.
While etomidate doesn’t decrease BP or CO, it may cause cerebral vasoconstriction.
Opioids cause minimal effects on cerebral physiology so long as MAP is maintained. Morphine may cause histamine release which could increase CBF.
Overall, TIVA should be used for elective craniotiomy as slightly lower ICP & higher CPP with TIVA vs inhalational.
Dexmed is a cerebral vasoconstrictor.

Spinal cord perfusion pressure = MAP - intraspinal pressure (or vertebral venous plexus pressure, whichever is higher)
also, spinal cord blood flow = spinal cord PP/spinal vascular resistance

So, agents that reduce MAP (volatiles) may reduce intraspinal pressure

Question 174

SS_NS 1.15: Discuss the possible complications of sedative/hypnotic and analgesic agents in neurosurgical patients

Answer 174

stable haemodynamics important to limit drops in MAP which may reduce CPP & risk ischaemia
need to time & dose to adequately blunt SNS responses (eg. with laryngoscopy) to limit raises in MAP and ICP which may also reduce cerebral perfusion pressure
Ideally agents that reduce CMRO2 (ie. not N2O, ketamine), don’t incr CBF (prop/thio/etomidate) & don’t raise ICP (prop, thio) preferable to preserve CPP
shorter-acting sedative-hypnotics are important for rapid & smooth transition to the awake state for postoperative neuro assessment.
Agents that promote respiratory depression and hypoventilation risk hypercapnia & ICP increase pre & post-extubation
agents that may be emetogenic risk raising ICP (if cause nausea/vomiting/strain)

Question 175

SS_NS 1.16: Describe the pharmacology and clinical utility of antiepileptic and prophylactic therapy in neurosurgical patients
-What’s the BTF recommendation re: seizure prophylaxis for severe TBI?
-How does phenytoin work?
-administration considerations/complications/adverse effects with phenytoin?
-if a pt with phenytoin toxicity requires intubation, what medication should be avoided?
-What are the doses of phenytoin or levetiracetom? therapeutic serum phenytoin concentration?
-What proportion of pts without a Hx of epilepsy can develop seizure following non traumatic craniotomy?
-Which AED is the most efficacious for craniotomy seizure prophylaxis? benefits of any?
-What’s fosphenytoin? dose?
-How does levetiracetam work?
-administration considerations/complications/adverse effects with levetiracetam?
-How to manage pts taking AEDs preoperatively throughout preoperative period?

Answer 175

-Phenytoin recommended to decrease incidence of early PTS when overall benefit felt to outweigh complications ALTHOUGH early PTS haven’t been associated with worse outcomes

-Phenytoin blocks V-D sodium channels (similar to carbamazepine)

-rapid administration of IV phenytoin —> bradyarrhythmias, hypotension, occasional asystole. Avoid by slow (<50mg/min, <25mg/min in elderly) IV administration.
AVOID EXTRAVASATION as this may cause severe tissue necrosis, inadvertent intra-arterial administration has been ass’d w gangrene.
Dilute w NaCl 0.9% to a concentration of 3-10mg/mL, complete infusion within 2hrs, in-line filter desirable, dedicated IV, flush w NaCl after admin to avoid local venous irritation.
Don’t give w glucose (phenytoin will precipitate).
-w LT use: gingival hypertrophy, rash (incr risk rash w phenytoin if rash or allergy w other anti-epileptics), folic acid depletion, body hair, decrease BMD, hypoCa. neurotoxic: confusion, slurred speech, diplopia, ataxia, neuropathy (LT use)
Has been ass’d w SJS & TEN
phenytoin reduces the effectiveness of hormonal contraception.
pregnancy category D.
risks hyperglycaemia in diabetes.
AVOID IV if sinus bradycardia, sinoatrial or 2nd/3rd deg AV blocks
contraindicated in porphyria
low serum Alb, use of other high PB drugs, renal failure—> decreased PB & increased free [], risk toxicity. Earliest signs generally horizontal nystagmus, unsteady gait, N&V. more severe= slurred speech, lethargy/confusion/coma, occ hyperreflexia, hypothermia.
CYP2C9 polymorphisms affect metabolism, hepatic dysfunction may risk toxicity (reduced metabolic rate)

-avoid lignocaine, also vaughan williams class 1B, shares phenytoin’s dysrhythmic properties

-15mg/kg phenytoin IV for craniotomy seizure prophylaxis. oral is 15mg/kg in 3 divided doses (loading, for obese the upper limit of loading is 1g) then 5/mg/kg daily in 1 or 2 doses, starting 24hrs after the loading dose. 10-20microg/mL.
POBA 70%. 1st-order (fixed percentage eliminated) in therapeutic range, zero-order (fixed amount eliminated) kinetics at higher []. This results in prolonged half life (24-230hrs in OD).
500-1000mg BD for levetiracetam. IV is equivalent to oral, 100% POBA.

15-20%

levetiracetam, phenytoin & fosphenytoin are equally efficacious for seizure prophylaxis; levetiracetam isn’t ass’d w hypoT during admin, has reliable pK & doesn’t require serum monitoring. no concern re: tissue injury w extravasation.

fosphenytoin= water-soluble prodrug of phenytoin, can be IV or IM. 10-20mg/kg phenytoin equivalents, over 30mins (max rate 150mg PE/min).

mechanism unknown, binds to synaptic vesicle protein SV2A, linked to epilepsy. may indirectly modulate GAGA.

Dilute with at least 100mL NaCl 0.9%, infusion over 15mins

Relatively well-tolerated, most adverse effects mild-mod & just during initial titration. Also, levetiracetam has very rapid onset of action- high proportion of pts seizure-free on 1st day of keppra BD cf placebo.
fatigue, somnolence, dizziness, URTI.
Sedation, mood disturbance, psychosis may cause discontinuation.
Has been ass’d w SJS & TEN.
Pregnancy category C.

reduce dose in renal impairment.
plasma [] may decr in pregnancy & incr rapidly postpartum- consider plasma [] monitoring.
While routine monitoring isn’t required, monitoring may be useful during preg, early postnatal, renal insufficiency, concomitant use of enzyme-inducing drugs eg. carbamazepine, to Ax adherence & document level @ which seizure control or adverse effects.
metabolism independent of CYP system so limited Pk interactions with other anti seizure meds, hormonal contraception or immunosuppressants.

Maintain pts on regular AEDs on their regular doses preoperatively to avoid seizures.

Question 176

SS_NS 1.17: Describe the pharmacology and clinical utility of corticosteroids in neurosurgical patients
-What’s dexamethasone?
-What’s hydrocortisone?
-What’s are the the BTF recommendations regarding steroids?
-What’s the role of glucocorticoids in intracranial HTN caused by Tumours or CNS infections?
-What is the role of steroids in patients with ardeno-cortical insufficiency due to pituitary disease?

Answer 176

-Synthetic glucocorticoid, potent anti-inflammatory (no mineralocorticoid), 0.75= pred 5=hydrocort 20. onset of action approx 2 hrs, half life B 36hrs. Duration of action 36-54hrs. also analgesic, anti-emetic (similar efficacy to ondans/droperidol), improves quality of recovery.

-Hydrocortisone= cortisol, a short-acting corticosteroid w minimal Na+-retaining potential. Onset of action IV= 1hr, elimination half-life 2hrs. Duration of action 8-12hrs. 1:1 glucocorticoid:mineralocorticoid potency.

-Level 1 recommendation: use of steroids NOT recommended for improving outcome or reducing ICP for severe TBI, high-dose pred associated with increased mortality
CRASH-1 halted early due to clear difference favouring placebo vs methylpred for mortality @ 2/52, recommended corticosteroids not routinely used to Rx head injury of any severity.

-They do have a role, reducing vasogenic cerebral oedema.
Also has analgesic and anti-emetic properties, useful for attenuating ICP raises with SNS or straining w vomit

-these patients have secondary adrenal insufficiency. they are deficient in cortisol but continue to secrete aldosterone in response to renin. the fluid & electrolyte abnormalities aren’t as severe as primary adrenal insufficiency, however patients still require IV hydrocortisone preoperatively; IV hydrocortisone is required on induction for pituitary surgery in patients with demonstrated adrenal insufficiency, AAGBI recommend 100mg IV on induction & 200mg/24hr infusion while NBM. At our institution typically 50mg as per endocrine consultation & advice, others use dexamethasone 4-8mg.

Question 177

SS_NS 1.18: Discuss the pharmacology and clinical utility of pharmacological agents for prophylaxis and treatment of cerebral vasospasm associated with subarachnoid haemorrhage
-when does vasospasm typically occur after SAH?
-what are risk factors for vasospasm ass’d w SAH?
-why is the distinction between angiographic vasospasm (in 30-70% of angiograms @ D7 after SAH) & clinical or symptomatic vasospasm (in 20-30% of pts) important?
-what’s the role of CT angiography in vasospasm?
-what needs to happen before Rx for vasospasm in aneurysmal SAH?
-What are the strategies for treating vasospasm after any aneurysm ass’d w SAH has been occluded?
-What is NOT useful for treating vasospasm?
-what are anaesthetic goals to limit risk of vasospasm in SAH?
-what’s nimodipine? indication for SAH? when commence? how administer? dose? how long treat? adverse effects?
-what endovascular therapies may be used for symptomatic vasospasm after SAH?
-what are particular communication points vital during endovascular therapy for vasospasm after SAH?

Answer 177

day 3, peaks day 7&8, continues up to 21 days

severity of bleeding & its proximity to the major intra-cerebral BVs
age <50yo
hyperglycaemia
poor clinical grade (eg. GCS <14, H&H grade 4-5)
location & extent of blood on CT scan (Fisher score- grades 3-4 almost always have vasospasm, grades 1-2 almost never).
unclear if the type of aneurysm Rx influences vasospasm risk

symptomatic vasospasm ass’d w clinical decline & poorer prognosis
symptoms include development or worsening of focal neurological deficits, altered level of consciousness, seizure

to identify pts with symptomatic vasospasm who may benefit from Rx; vasospasm is observation of narrowing of intracranial arteries, angiographically or on TC doppler. up to 70% of pts with SAH have vasospasm detected on DSA, 30% have clinical symptoms.

aneurysmal occlusion through surgical clipping or endovascular coiling

1. haemodynamic augmentation to raise MAP hence increase CPP; induced HTN with phenylephrine, NEp or dopamine along w maintenance of euvolaemia (crystalloid OR colloid). Progress the BP augmentation in a stepwise fashion, Ax clinical status @ each MAP. If inadequate response to pressers alone, may need inotropic support (dobutamine or milrinone), monitoring for complications eg. cerebral or pulmonary oedema, volume overload.
2. balloon angioplasty if focal vasospasm of larger cerebral arteries refractory to haemodynamic augmentation- there’s an absence of clinical trial data supporting this but it’s the mainstay at many centres
3. intra-arterial vasodilators: for diffuse vasospasm of smaller arterial branches; verapamil, nimodipine, milrinone, nicardipine, papaverine & intrathecal nitroprusside have all been effective for improving vasospasm in case series.
4. intra-arterial VD & angioplasty may be used in combo.

hypervolaemia- not beneficial & may be harmful. Mg++ & statins have no proven benefits.

euvolaemia, normotension (hypovol/hypoT incr risk cerebral ischaemia in setting of vasospasm)
BGL <10 (but not hypo), since hyperglycaemia may accelerate cerebral vasospasm (pro-inflamm cytokines, incr blood viscosity)

a DHP (acts on BVs > heart) CCB to prevent vasospasm for patients with aneurysmal SAH- while there’s no convincing evidence that it affects incidence of vasospasm, it has been demonstrated to improve outcomes in SAH, NNT to prevent one poor outcome= 13
start within 48hrs of symptom onset or sooner, once the pt stabilised
Give orally or via NGT; inadvertent IV—> serious adverse cardiovascular events incl death (boxed warning)

60mg every 4hrs
half dose in pts w cirrhosis.
continue Rx for 21 days

BP fluctuations & hypotension common so vital to monitor BP to avoid hypoT & defend CPP
bradycardia
headache
nausea

angioplasty, intra-arterial vasodilators

goal BP to be discussed
interventionist to communicate when about to administer intra-arterial vasodilator injection; I anticipate hypotension & Rx immediately

Question 178

SS_NS 1.19: Discuss methods to monitor cerebral blood flow including transcranial Doppler
-How is CPP calculated in clinical practice?
-What are some advanced cerebral monitoring techniques for brain oxygenation & blood flow?
-What’s normal SjvO2?
-What information obtained from jugular venous oxygen saturation & how is it done? limitations & complications?
-What does the BTF recommend re: SjvO2 and brain tissue oxygenation (BtpO2)?
-What is NIRS? What are some uses for it? normal value for rcSO2? limitations of NIRS?
-How may brain tissue oxygenation be measured? what are some limitations? what’s the tissue oxygenation threshold for ischaemia? what trial is underway to Ax utility of PtiO2 combined w ICP measurement for functional outcome after severe TBI?
what’s normal brain tissue oxygenation? CO2? pH?
-How does transcranial doppler work? which artery is most commonly insonated? what’s transcranial colour-coded duplex? What’s transcranial doppler primarily used for? other uses? limitations?
-What imaging methods may be used to monitor CBF?

Answer 178

transducers for MAP & ICP are both zeroed @ the level of foramen of Monro (EAM). CPP=MAP-ICP

arterio-jugular venous O2 (AVDO2 globally measures cerebral O2 extraction- measure at jugular bulb)- this MAY be considered to reduce mortality & improve outcomes @ 3 & 6/12 post-injury
Near-infrared spectroscopy
brain tissue oxygenation
*all oxygenation
transcranial doppler/transcranial colour coded duplex sonography
CT angiography to show narrowing & CT perfusion using iodinated contrast to look at mean transit time to determine blood flow in the region
Xenon-enhanced CT
perfusion-weighted MRI
Nuclear medicine methods

55-75%

global oxygenation & adequacy of CBF; SjvO2 reflects balance between O2 supply (CBF, SpO2) & demand.
normal SjvO2 is 55-75%, values below this suggest hypo perfusion (demand exceeds supply, eg. reduced supply w raised ICP, reduced CBF, hypoxia, profound hypocarbia or incr demand w seizures, pyrexia). high SjvO2 suggests reduced cerebral O2 consumption (coma, hypothermia, cerebral infarction) or incr O2 delivery (hypercapnia, vasodilation).
SjvO2 <55% suggests cerebral ischaemia (eg. may guide interventions eg. hyperventilation) but can’t assume lack of cerebral ischaemia @ higher values.
choose the side of dominance for venous drainage (compress each IJV & determine which is ass’d w greatest ICP change) or worst pathology. Insert a catheter by retrograde cannulation of the IJV, advance to jugular bulb- confirm position w lat XR (catheter tip level w C1/2 disc)
measurements w serial sampling or spectrophotometric catheters for continuous measurement.
limitations: erroneous placement= error due to admixture w extra cranial blood. clot formation on the catheter & poor sampling technique also affect accuracy.
complications= thrombosis, risks w CV cannulation (infection, bleeding, damage to adjacent structures, VAE)

if hyperventilation used, oxygen delivery should be monitored with brain tissue oxygenation or SjvO2

Near-infrared spectroscopy is a non-invasive bedside monitor of regional cerebral oxygenation. Light waves in the near-infrared range (700-1000nm). HBO2 & deoxyHb have different absorption spectra. Light absorption depends on the oxygenation status of the cerebral blood, and detectors sense emergent light. Changes in the [] of the near-infrared light are quantified using reflectance spectroscopy based on modified Beer-Lambert law (beer= absorption of light proportional to [] of solute in solution, lambert abs prop to thickness of absorbing layer).
Used to monitor pts w TBI, intra-op monitor for cardiac surgery & CEA.
Normal cerebral regional O2 saturation (rSO2) is 60-75% but there’s variability ++ btwn NIRS devices.
NIRS reliability reduced by extracratial contamination & interference from ambient light. NIRS is not considered reliable in TBI.

-flexible micro-catheters in the brain parenchyma, measure tissue oxygenation based on Clark electrode (KOH solution & a silver anode & gold cathode). number of oxygen molecules reduced @ the cathode is reflected by a change in voltage—> measure of oxygenation. Tissue oxygenation varies with changes in oxygenation & CBF.
Temperature-dependent process (need to measure temp & correct for variations). Measurement limited to the immediate area. positioning in an area of ischaemia or haematoma may give misleading results.
Devices using luminescence to measure PtiO2 are available, may give consistent & reproducible measurements (higher values, may be due to different probe sizes)
PtiO2 <15-20mmHg is consensus threshold for ischaemia @ which intervention should be considered.
BOOST3 trial (brain oxygen optimisation in severe TBI) aims to compare effectiveness of monitoring with ICP alone or both ICP & brain tissue oxygenation. Goals= keep ICP <22mmHg & PbtO2 >20mmHg. Glasgow outcome scale (functional recovery)

20-35mmHg
PtiCO2 40-70mmHg
pH 7.05-7.25

a non-invasive method for measuring CBF. A 2MHz probe & pulsed-wave doppler is used. Flow velocities of the intracranial arteries are calculated using the doppler effect, where the observed frequency of a signal increases as the source moves towards the observer and the frequency of the sound wave is incorporated into the doppler equation to derive velocity.
Velocity is doppler shift frequency times the speed of the wave, divided by 2x the frequency of the transmitted wave times cos angle of blood flow relative to probe.
The MCA is most commonly insonuated through the trans temporal window, with flow velocity mean range 43-77cm/sec, high values indicate vessel narrowing. ACA & PCA can also be insonated through trans temporal window. The transorbital window allows insonation of ophthalmic artery & carotid circulation. transforaminal window allows insonation of vertebral & basilar arteries. Limitation= 1/5th of pts lack a transcranial window so this technique can’t be used.

transcranial colour-coded duplex combines pulsed-wave doppler with real-time imaging, more accurate measurements.

Transcranial doppler sonography is primarily used for detecting & monitoring vasospasm in SAH. velocity changes detected by TCD typically precede the clinical sequelae of vasospasm so daily recordings offer a window of opportunity to treat pts prior to clinical decline. DSA is generally required to diagnose vasospasm & institute treatment.

also used to detect micro emboli, for intraop monitoring during cardiac or carotid surgery or for estimation of ICP through monitoring changes in pulsatility index (PI= (FVsys-FVdias)/FVmean)

It’s operator-dependent, relatively good but imperfect sensitivity & specificity- S&S increased with use of transcranial colour-coded duplex or by incorporating the Lindegaard index (ratio of mean FV in MCA to mean FV in ICA measured through submandibular window, FV in MCA >120cm/s with Lindegaard index 3-6 highly indicative of vasospasm).

CT angiography may show arterial narrowing & CT perfusion scanning may demonstrate asymmetry in brain perfusion and these may be useful & sensitive methods of predicting delayed cerebral ischaemia.
CT perfusion is widely used in acute stroke & SAH to identify potentially reversible cerebral hypo perfusion (ischaemic penumbra) & differentiate these areas from infarcted areas of brain. Performed rapidly with a spiral CT scanner, images are analysed by commercially available software to produce perfusion maps.
iodinated contrast is injected & calculations are made for mean-transit time (represents the average length of time a certain volume of blood spends in the cerebral art circulation) & cerebral blood volume (ml/100g brain tissue). Ischaemic penumbra= area with increased MTT, reduced or diminished CBF but preserved CBV (due to collateral circulation).
Limitations= risks of recurrent dye loads & radiation exposure.

Xenon-enhanced CT may be used as xenon is inert & highly lipid soluble, readily crosses BBB, is clearly visible on CT. baseline CT. 100% O2 to wash-out nitrogen. inhale Xenon until it equilibrates @ a predetermined %. another CT taken. Xenon washout pattern allows quantification of CBF via modified Kety-Schmidt technique.

Perfusion-weighted MRI techniques either with arterial spin-labelling (non-invasive, no contrast, protons in arterial blood water are magnetically labelled by applying a radio frequency pulse, creating an “endogenous tracer”. cerebral blood flow maps crated by comparing baseline MRI with that when the tracer arrived @ destination of interest. Can use IV gadolinium perform an MRI sequence from which a signal intensity curve produced from which CBF can be calculated. Gadolinium reduces the signal intensity of MRI images.

Can use nuclear medicine methods:
PET using radioactive-labelled water, it distributes into brain tissue proportional to CBF. CBF calculated by analysis of time activity curves generated by the PET scanner.
single PET: radioactive tracers eg. technetium99, lipohilic & readily cross BBB, distribution proportional to CBF, continues to emit gamma radiation for hours.

Question 179

SS_NS 1.20: Describe methods of intracranial pressure monitoring
-What are physiological ICP values up to 1yo and in adults?
-how does the normal ICP trace appear?
-What’s the purpose of ICP monitoring?
-What goal CPP is recommended to improve survival & favourable outcomes in TBI?
-What are some indications for ICP monitoring? and overall benefits
-At what level of ICP does BTF recommend treatment?
-What does the BTF recommend wrt ICP monitoring? and CPP?
-What are the 4 main anatomical sites used in clinical measurement of ICP?
-What’s the gold standard ICP monitoring device?
-What are benefits of intraventricular ICP monitoring? and major disadvantages?
-Advantages & disadvantages of intra-parenchymal ICP monitoring devices?
-Pros & cons of subarachnoid bolts (fluid-coupled systems)?
-For which patient group are epidurally-placed ICP monitors used?
-What are some risks of ICP monitoring?
-What does a positive pressure reactivity index (correlation coefficient between ICP & ABP averaged over a defined time) suggest?

Answer 179

3-4mmHg up to 1yr, 10-15mmHg in adults

pulsatile, reflects cardiac & respiratory cycles
Component related to the cardiac cycle (C waves), 3 peaks: P1 (the percussion wave, correlates w arterial pulsation), P2 (tidal wave, art pulsation & R from intracranial parenchyma), P3 (dicrotic wave, reflects closure of AV). Respiratory component generated by changes in Pit caused by respiration.
Component related to respiration (B waves)
With modern clinical practice with recognition & Rx of raised ICP, plateau waves (A waves with ICP 50-100mmHg) are rarely seen.

Allow maintenance of adequate CPP & oxygenation (CPP = MAP - ICP)

60-70mmHg

suspected @ risk for elevated ICP (up to 1/3 of pts with initially normal CTB can develop raised ICP in the first few days after closed head injury)
GCS <8
diagnosed with a process that merits aggressive medical care (eg. after TBI, SAH, stroke, encephalopathy, hydrocephalus & some neurosurgery)
allow early detection of an expanding lesion & calculation of CPP
may help guide management, optimise cerebral function & prevent secondary brain injury

> 22mmHg, values above that level ass’d w increased mortality

the management of severe TBI patients should be undertaken using information from continuous ICP monitoring (reduces in-hospital & 2/52 post-injury mortality)
using CPP monitoring for these pts decreases 2 wk mortality

intraventricular
intraparenchymal
subarachnoid
epidural

intraventricular catheter

can treat some causes of elevated ICP via CSF drainage
can administer intrathecal drugs
provide a global ICP measurement
infection in up to 20% of pts, 2% risk of haemorrhage during placement (greater risk in coagulopathic pts)
placement may be difficult if small ventricles or cerebral oedema.

ease of placement (these are the most commonly used catheters, micro-transducer or fiberoptic, placed via small burr hole or cranial access device into subdural space), less invasive, low risk of infection & haemorrhage (<1%) cf intraventricular devices, considered accurate
disadvantages= unable to drain CSF for diagnostic or therapeutic purposes, inaccuracy over several days (they show drift, can’t recalibrate, greater risk mechanical failure), measure local pressure

low risk infection or haemorrhage but often clog w debris & are unreliable/less accurate cf ventricular ICP devices

coagulopathic patients with hepatic encephalopathy complicated by cerebral oedema
significantly lower risk intracerebral haemorrhage (4 vs 20-22% for intraparenchymal & intraventricular devices) in this population or fatal haemorrhage (1 vs 5 & 4%)
they are often inaccurate as the dura damps the pressure transmitted to the epidural space.

CNS infection
intracranial haemorrhage

Positive suggests disturbed autoregulation, negative suggests normal auto regulation.

Question 180

SS_NS 1.21: Outline the principles of electrophysiological monitoring (electroencephalogram/sensory and motor evoked potentials) and the implication of neuromuscular blockade

-What is electrophysiologic monitoring, or neuromonitoring, used for?
-What is the EEG? examples of when used? limitations?

-How is EMG used? for what surgeries is cranial nerve EMG monitoring used? which nerves can be monitored with EMG?

-For which surgeries should spinal cord monitoring be considered? What is used?

-What’s evoked potential monitoring?

-Describe how SSEPs are measured? Are they influenced by volatiles? what surgeries may they be used for?

-Describe how MEPs are measured? Are they influenced by NMBDs? how about propofol?

-What’s more effective for detecting motor injury?

-What’s a particular consideration with MEPs?

-what pt factors impact MEP monitoring?

-are SSEPs & MEPs impacted by barbiturates?

-How may ketamine influence neuromonitoring?

-How do BZDs impact neuromonitoring?

-what does etomidate do to neuromonitoring?

-What’s the impact of dexmed on neuromonitoring?

-Opioids influence on neuromonitoring?

-Does lignocaine influence neuromonitoring?

-How do anaesthetic vapours influence MEPs & SSEPs?

-How do volatiles & N2O impact EEG?

-What’s the anaesthetic maintenance of choice when using MEPs? Is there any effect of propofol TIVA on cortically evoked responses?

-Where might continual monitoring of muscles innervated by individual nerve roots be useful?

-How does N2O impact neuromonitoring?

-Do NMBAs impact SSEPs?

-What possible actions may be appropriate when neuromonitoring changes occur?

Answer 180

to assess the functional integrity of the brain, brainstem, spinal cord, peripheral or cranial nerves. The goal is to alert the surgeon & anaesthetist to impending injury to allow modification of management to prevent permanent neurological damage.
In some cases, neuromonitoring may be used to map areas of the nervous system & guide procedural management.
It may include the recording of spontaneous activity (EEG and spont EMG) or evoked responses (SSEPs, MEPs, brainstem AEPs)

Recording of spontaneous electrical potentials (EPSP/IPSP) generated by superficial layer of cortical pyramidal cells. summation of the potential generates a real-time tracing of amplitude vs time from which we can surmise info re: CMRO2 & wakefulness, by analysing freq, amplitude & waveform by pattern recognition. Used to detect ischaemia, reductions in CBF, seizure activity & impact of anaesthetic agents on the brain. Electrodes placed on the scalp in a standardised array.

Use during CEA- to assess cerebral perfusion during XC. EEG slowing or asymmetry suggests ischaemia. intracranial surgery- evaluate cortex for ischaemia. electro-corticography may be used during seizure surgery to identify epileptogenic focus for resection.
All anaesthetics impact the EEG so important for neurophysiologist interpreting the EEG to know drugs & doses administered, however generally the anaes drug isn’t chosen because of effects on EEG unless the procedure requires direct cortical recording (eg. ablation of an epileptic focus).

BIS uses a proprietary algorithm derived from artefact-EEGs of anaesthetised pts not under NMBD. it uses Fourier analysis, converting epochs of raw EEG into component sine waves to create a histogram & uses bispectral analysis to analyse parameters such as spectral edge frequency, biocoherence (synchrony of frequencies), burst suppression to derive a dimensionless value. Displays index, raw EEG, SQI (poor quality if <50), EMG, SR (proportion of isolectric from the epochs of the last 63 secs). 20-30sec lag. limited by contact. interference from diathermy. interpret trend vs single number, unfiltered trace. influenced by N2O, ketamine, decmed, inaccurate in paeds, hypox, hypoth, hypercarbia.

surface electrodes so don’t detect ischaemia in subcortical regions. If pharmacologic methods used for metabolic suppression, EEG can confirm BS but then monitoring for ischaemia is precluded.

to monitor muscle activity of muscles innervated by cranial or spinal nerves that are @ risk during surgery, eg. tumour resection, spine surgery with instrumentation.
with spontaneous EMG, stretch or trauma to nerves generates EMG recordings, while muscle innervated by nonirritated/nonstimulated nerves remain quiet.
For triggered EMG, a stimulator is used & a muscle action potential is recorded. Increase in latency or reduction in muscle AP may indicate nerve injury (similar principle to nerve conduction study)- eg with pedicle screws.
EMG monitoring used for acoustic neuroma, skull base surgery, thyroid or parotid, or radical neck dissection.
only CNs w motor component (III, IV, V, VI, VII, IX, X, XI & XII) can be monitored.

Any procedure where the spinal cord is at risk- eg. deformity correction, spinal cord trauma. SSEPs (where amplitude <50% baseline suggests the SC at risk) & MEPs (described as absent or present) are used.

used to assess the integrity of the tested neural pathway.

Somatosensory applies stimulus to a peripheral site and records response @ central location

motor stimulates the motor cortex & records responses at distal muscles.

changes in evoked responses can be due to surgical (blunt or surgical trauma, mechanical effect eg. retractor, vascular occlusion, local medications, surgical stimulation), pharmacologic (ie. aim to keep level of Anaesthesia constant during critical monitoring periods), physiologic (hypoxia, hypoT, hypothermia, anaemia), technical (lead failure or dislodgement, electrical interference from OT equipment, inaccurate locations of leads) or positioning (extreme head position, peripheral nerve compression, spine F or E) causes.
The amplitude & latency are measured.
loss of, or change in the waveform, indicates need for modification of surgical strategy, pt positioning or pt physiologic management to limit risk neurologic injury.

One of the most commonly used evoked potential monitoring modalities.
Electrical stimuli applied to peripheral nerve- median or ulnar @ wrist for UL & post tibial nerve @ ankle for LL SSEPs. needle or surface electrodes near the nerve.
Both motor & sensory components are stimulated- the motor to show twitch (confirming stimulation & lack of sig NMB), actuation of the sensory component causes low-amplitude potentials to be carried via the dorsal nerve root, posterior columns of the spinal cord, territory supplied by the posterior spinal arteries (which supply the posterior 3rd of the SC), and are measured with a recording montage (active & reference electrode) @ scalp over the sensory cortex. 50% reduction in amplitude or 10% incr in latency considered pathologic.
Since the signal-to-noise ratio of SSEPs is improved by increasing depth of muscle relaxation, SSEPs are not significantly affected by therapeutic concentrations of anaesthetic vapours.
may be used for procedures where the spinal cord @ risk (particularly useful for posterior spine surgery), may be used for ICA or MCA aneurysms or for tumours resections. also used for aortic surgeries.

Short-duration constant current electrical stimuli of 300-700V is applied to the scalp utilising 2 needles- stimulates motor cortex. signal transmission of MEPs relies on integrity of the corticospinal tract, which lies in the territory of the ASA, travels via the anterior horn of the SC, synapses & descends to peripheral nerve to NMJ & produces a response at & measured via needle electrodes in the tib ant, abductor hallucis, lateral gatrocs & vastus medialis or adductor polices brevis. Can also (less commonly) monitor as epidural D waves (epidural electrodes specific for the corticospinal tract but don’t differentiate laterality).
Monitor periodically, incr frequency of monitoring at critical points.
monitor amplitude & latency, for MEPs a decr amplitude is a more common sign of impending neurologic compromise. Since MEPs are large-amplitude & incompatible with profound muscle relaxation, NMBDs interfere.
Very deep propofol [] may impair MEPs but still prop preferred (may use prop/remi to lessen prop requirements)

MEPs vs SEPS (changes in MEPs proceed SSEP changes)

transcranial stimulation activates muscles of mastication so need to place a soft bite block btwn molars after induction to ensure the tongue & cheek are clear of the teeth. check again for position changes & periodically intra-op.

diabetic neuropathy, HTN, age extremes, pre-op motor deficit.

similar to propofol; SSEP & MEP usually recordable @ anaes doses, MEP may be lost @ high doses. SSEPs aren’t affected by barbiturates even @ high doses.

enhances SSEP & MEP amplitude (so a ketamine infusion may be useful during spine surgery when neuromonitoring used). Incr EEG amplitude & freq, can evoke seizures in epilepsy.

don’t impact SSEP & MEP responses at the low doses used for premed & amnesia. They slow EEG amp & freq but no BS or electrical silence (unlike most IV anaes prop, barbiturates etomidate)

incr SSEPs & MEPs @ low doses, depression @ high doses, is ass’d w adrenal suppression & worse outcome in sepsis. also, in low dose it can evoke seizures in epilepsy.

conflicting re: MEPs. impact on SSEPs is minimal. reduces BIS values, it’s EEG mimics sleep.

minimal, dose dependent SSEP & MEP depression but these can still be recorded
they incr amp & decr freq of EEG, no suppression @ high doses.

limited literature but appears to not interfere. anticonvulsant at low doses, proconvulsant at high doses.
if spray cords it may block VC EMG response during ant neck procedures.

Anaesthetic vapours reduce SSEP & MEP amplitude in a dose-dependent manner & anaesthetic vapour concentrations >=0.5MAC & >=1MAC aren’t generally compatible with reliable MEP or SSEP monitoring, respectively, in normal patients. If a pt has any neurological impairment (eg. spinal cord trauma), even low level VA may abolish SSEPs

iso, sevo & des inca freq & amplitude @ low doses, higher doses decr to eventual BS (1.5MAC) & elec silence. sevo may produce seizure activity w high-dose mask induction.
N2O has less amplitude & freq changes @ higher doses than the other volatiles. it is synergistic when administered with a volatile.

propofol TIVA- it does cause a dose-dependent suppression of cortically evoked responses, particularly impacting the spinal cord (glycine receptors), altering MEP waveforms at high [].
A benefit of propofol= ability to quickly titrate level of anaes in response to evoked responses.
Intra-op BIS useful, avoid burst suppression to optimise neuromonitoring conditions.
A good option is propofol (80-150 microg/kg/min) with relatively high dose remi (0.1-0.5microg/kg/min). Useful as movement w motor stimulation reduced.
May be useful to use a NMBD for induction & pin placement than reverse. Use TOFR to ensure adequate reversal (me or the neurophysiologist)- balance against need to prevent pt movement.

For procedures involving vertebral levels below the termination of the spinal cord

Similar impacts on SSEPs & MEPs cf volatile but they increase frequency of EEG (overall no impact on BIS as also reduce low frequency signal)

no

alert room
repeat the signal (if time allows)
surgeon/neuromonitoring tech/anaesthetist work together to determine etiology & correct; eg. localised changes more likely surgical/technical/positional while anaes & physiological impacts on neuromonitoring are more global (but may be worse at side of pre-existing deficit). Temporal relationship with events in OT helps detect cause (eg. cerebral aneurysm clipping, spinal instrumentation, XC of carotid). prompt correction necessary to avoid neurol deficit so go straight to most likely ethology first.
while cause being Ix, limit injury by optimising physiology.

stop surgical stimulation (eg. retractor pressure)
increase MAP to increase tissue perfusion pressure
ensure adequate ventilation (changes in neuromonitoring only occur @ extremes of PaO2 & PaCO2).
ensure normothermia (core temp within 2-2.5 deg of baseline)
ensure adequate haematocrit (very low hct <15% increases latency).
Consider pt position: ideally if neck flexion used during surgery, get baseline MEPs & SSEPs supine then again when prone- if recorded potentials deteriorate, reposition before surgery begins.
ensure electrodes/pt limbs haven’t moved & no pressure on peripheral nerves.

eg. if evoked potentials deteriorate during C spine surgery positioning, reposition & if doesn’t recover, may wake pt for neurol exam.
if EEG or SSEP changes with carotid XC, shunt placement & raise BP asap.
if MEP or SSEP lost after temporary aneurysm clip, release clip if poss & raise BP, finish OT asap.

Question 181

SS_NS 1.24: Describe the typical presentation and natural history of the different types of intracranial haemorrhage
SS_NS 1.25: Discuss the acute resuscitation and management of patients with intracranial/subarachnoid haemorrhage (also refer to the Resuscitation, trauma and crisis management clinical fundamental and the intensive care specialised study unit)

Answer 181

INTRACEREBRAL HAEMORRHAGE= 2nd most common cause of stroke but large cerebrovascular M&M.

CLINICAL FEATURES:
typically hypertensive vasculopathy, amyloid angiopathy (older pts), ruptured vascular malformation (esp AVM), cerebral venous thrombosis, haemorrhagic infarction from large oedematous ischaemic infarcts or if reperfusion therapy, tumour haemorrhage, infection, vasculitis, hyperperfusion after carotid revascularisation, sickle cell, bleeding disorders.

Presentation= sudden onset stroke symptoms (speech/vision/movement/sensation/balance)
ICH vs ischaemic more likely if acute symptoms progressively worsen, severely elevated SBP (>220mmHg- elevated BP common (due to incr ICP & pain from mass effect, may be comorbid)), pt taking anticoagulant
Signs elevated ICP (mass effect)= dilated pupil, progressive drowsiness, cushing triad (brady, resp depression, HTN)

Natural Hx= risk haemorrhagic growth from rebleeding; esp within several hrs of onset, risk elev ICP highest first days after onset, risk early or late seizures.
Risk factors poor porg= higher ICH volume, brainstem/cerebellar vs supratentorilal, intraventricular extension, incr age, initial poor neurologic baseline, prev antithrombotic, elevated admission glucose.

SUBDURAL:
btwn dura & arachnoid, crescent-shaped, usually tearing of bridging vv btwn arachnoid membranes & dura (20-30% arterial).
Trauma= most common etiology, low CSF pressure (intracranial hypoT) spont or iatrogenic. If cerebral atrophy may be trivial trauma.

Higher risk if cerebral atrophy (elderly, chronic ETOH), antithrombotics (esp warfarin) or coagulopathy (eg. thromboytopenia or liver disease)

Clinical manifestations:
wide spectrum depending on if acute (typically more severe or progressive & up to 50% comatose) or chronic (more likely non-focal symptoms) & brain region impacted (eg. frontal speech impairment (dom), exec dysfunction (nondominant), hemiparesis; parietal speech (dominant, sensory (nondom); post fossa h/ache, vomit, unequal pupils, dysphagia, CN palsies, nuchal rigidity, ataxia); interhemispheric: h/ache, falx syndrome (paraparesis sans facial weakness)
-suspect if trauma, progressive neurol symptoms (esp in pts w anticoagulants)
typically new & persistent headache, focal/bilat weakness, confusion, cognitive decline, seizures
Signs of elevated ICP.
Natural Hx= risk progression haematoma (esp older age, HTN, antithrombotics, larger SDH, intraventricular haemorrhage) esp 36hrs after SDH. may get elevated ICP (evacuate if ICP persistently >20mmHg). may develop seizures or ischaemic stroke.

INTRAVENTRICULAR haemorrhage:
may complicate intracerebral or SAH (secondary IVH) or primary (most commonly due to vascular malformation or HTN)
Usually sudden headache, nausea & vomiting, impaired alertness.
immediate non-con CT to exclude SAH & evaluate severity of IVH & potential for obstructive hydrocephalus. If primary, MRI to Ix abnormality eg. vascular malformation.
Monitor since obstructive hydrocephalus often complicates IVH involving 3rd & 4th ventricles, risk haemorrhage extension. optimal BP uncertain; balance btwn avoiding haemorrhage progression & compromising CPP.

EPIDURAL haematoma:
bleeding in potential space btwn dura & skull, usually traumatic.
arterial source most common (15% venous).
variable presentation (altered LOC, h/ache, vomit, drowsy, confused, seizures, hemiparaesis).
head CT: lens-shaped pattern. MRI higher sensitivity.
most have surgery (if >30mL or focal/progressive neurol deficits), reverse anticoagulation if OT (if non-op weight risk:benefit).
Most have good recovery, severe neurol deficits, pupillary abnorm, larger volume & midline shift, coexisting trauma/coag disorders= poorer prognosis.

Acute resus/Mx intracerebral/subarachnoid haemorrhage:

EVALUATION:

ABCD

intubate any pt unable to protect airway, w rapidly deteriorating mental status or GCS<=8

supportive care

GCS, Ax neurologic deficits

Emergency imaging (CT head)
immediate NSx consult if indicates need emergency surgery:
ICH: >=3cm2 or causing brainstem compression, IVH or hemispheric ICH w obstructive hydrocephalus/neurologic deterioration
SAH: signs/imaging (eg. midline shift >5mm, signs brainstem compression or pupillary abnormalities, GCS deterioration)

ECG: cardiac abnormalities common w spont SAH or ICH, esp prol QT & ST-T changes (eg. w catecholamine-induced cardiac injury). characteristic ecg abnormalities with raised ICP= widespread giant TWI, QT prolongation & bradycardia (cushing reflex). may also get ST dep/elevation (may mimic ischaemia or pericarditis), incr U wave amplitude).
other: sinus tachy, arrhythmias.

pulmonary: aspiration, neurogenic pulm oedema (post circulation)
SIRS

Biochem: hyperghycaemia, SIADH (ant circn), DI

Other extracranial manifestations: RWMAs eg. Takusubos (catecholamine surge)
initial labs: CBC, PT, INR, electrolytes, glucose, cardiac-specific troponin, preg test if female childbearing age, hourly monitoring for neurologic deterioration or signs elevated ICP

Goals of initial Rx= prevent haemorrhage expansion, monitor for & manage elevated ICP, manage other neurologic & medical complications, prevent secondary brain injury (rebleed, ischaemia, vasospasm)

prevent haemorrhage expansion

-reverse anticoagulation (warfarin= 4-factor PCC (II, VII, IX, X; 3-factor is II, IX, X- trace 7) with IV vit K 10g, dabigatran= idaricizumab, Xas= 4-factor PCC or andexanet alfa, UFH= protamine, LMWH= andexanet alfa or protamine.only consider plts for selected pts w ICH on antiplatelets undergoing emergency surgery- PATCH trial suggested those having plts w ICH had worse outcomes (death, modified Rankin scale, more serious adverse effects- but groups not balanced @ baseline)- no high quality evidence for or against so individualise. for mod-severe TBI, some centres transfuse aiming plt >75 if thrombocytopenic, utility of plt transfusion in TBI for pts on antiplts is unknown but the risk of neuro worsening in these pts is greater.
intracerebral: rVIIa FAST trial showed Rx didn’t improve death or severe disability @ 90 days, higher rates arterial thromboembolic serious adverse events), rVIIa not used in TBI.

-manage HTN: immediate SBP <220mmHg (labetalol or nicardipine, avoid GTN or SNP (may incr ICP), keep GCS, subsequent SBP 140-160mmHg monitoring neuro status (eg. once contained)

-monitor for (clinical (hourly)/imaging +/- ICP monitor (severe TBI ie. GCS <9, pts w mod tbi but unreliable neuro exam; EVD= most accurate/cost-effective, therapeutic advantage of CSF drainage. intraparenchymal monitors easier to place, lower risk haemorrhage/infection; goal ICP <=22mmHg threshold for survival & favourable outcome.
Standard measures:
HoB 30 deg, neutral neck, avoid tight ties or IJ CVC, sedation+analgesia/anaesthesia w mech vent (reduce CMR w NMB too), normothermia (temp <38deg), Mx seizures (not prophylactic), iso-osmotic fluid & Na+ >=135mEq/L, normo capnia (PaCO2 30-40mmHg)/oxia (PaO2>65-70mmHg)
Tier 1 for elev ICP: further analgesia-based sedation, add prop infusion, EVD (avoid overdrainage), osmotic therapy (goal Na 145-150mEq/L if HTS or mannitol
Tier 2: incr HTS (goal 150-160mEq/L), deeper sedation, incr CPP to >70mmHg (vs 60 for standard) if autoreg preserved, CTB to identify correctable pathology
Tier 3: repeat CTB, decompressive craniectomy or barbiturate coma or therapeutic hypothermia 32-34 degC (BTF don’t recommend PROPHYLACTIC hypothermia since clinical heterogeneity in the good-quality trials so can’t perform meta-analyses, also POLAR trial showed no diff neurol outcome. evidence of therapeutic hypoth for refractory ICP uncertain.

Hypervent as transient salvage therapy (goal paCO2 30-35mmHg (ie. eTCO2 25-30mmHg) ONLY if significant raised ICP risk herniation (otherwise relatively CI in TBI or acute stroke)

manage other neurologic & medical complications
-normoglycaemia (aim <10, avoid hypo)
-Mx fevers
-aspiration risk
-VTE prophylaxis
-pressure injury
-Rx seizures but not prophylaxis
-role of TxA unclear for ICH or SDH; for SHD nonoperative management, suggestion that ass’d w reduced haematoma volume but low-quality evidence.
ICH TxA: TICH-2 no diff function/mort @ 90/7. CRASH-3 was RCT TxA vs placebo, primary outcome in-hospital death within 28 days, admin TxA under 3 hrs from injury for pts w GCS <=12 or intracranial bleed on CT. 12737 pts. Non-sig difference primary outcome (RR 0.94 w CIs crossing 1). became stat sig when excluded pts w unreactive pupils. Death reduced sig in pts w mild-mod TBI but not severe. Time-dependence; Early Rx was more effective than later in mild-mod injury but not severe injury. No difference in disability rating TxA vs placebo. No incr risk vaso-occlusive events or seizures. Very large, good internal validity, but only short-term outcome, overall trend to difference but not significant.
the ULTRA trial looked at 955pts w CT-proven SAH, no diff in mRS @ 6/12 (clinical outcome), or all-cause mort @ 6/12, re-bleed prior to aneurysm Rx, infarction- BUT 53% had TxA discontinued due to aneurysm Rx, TxA Rx was delayed (median time from S&S to Rx 185mins.

For SAH, repeat CTB 6-8hrs & BP control: prevent hypOtension (SBP >100mmHg, isotonic fluids, phenyl if refractory). Mx hypERtension (SBP <220mmHg then <160mmHg while monitoring status)

Question 182

SS_NS 1.22, 1.23: Discuss the implications for anaesthesia of the positions used for neurosurgery, discuss the risks associated with pt positioning for neurosurgical procedures & the methods of risk minimisation

Answer 182

CNS/eyes:
neck flexion risks impaired cerebral blood flow: get baseline MEPs & SSEPs before positioning then again in prone- if recorded potentials deteriorate, reposition before surgery begins.

Prone positioning risk:
-postop visual loss. Strategies haven’t been established but: inform pts re: risk, visual Ax & early ophthalmologist R/V if concerns re: eyes.
-injury after non-ocular surgery in <0.1% of anaesthetics. Independent risk factors= lateral or prone positions, prolonged surgery, surgery to head or neck.
POVL for >30 days is 1:250,000 non-cardiac & 1:1100 cardiac surgery. pts undergoing spinal fusion in prone particularly vulnerable, 1:1800.
-Spinal surgery= highest incidence of POVL after non-ophthalmic surgery, mainly due to ION, less commonly retinal vascular occlusion, very rarely cortical blindness.
-Generally painless loss of vision. ION thought to be due to hypo perfusion of optic nerve but no clear association w intro systemic hypoT or with PVD or DM.
-central retinal artery occlusion= direct pressure on globe causing raised IOP & compromising retinal perfusion. visual loss usually unilat & ass’d w other signs of pressure (ophthalmoplegia, ptosis, altered sensation in supraorbital nerve territory). pale retina & cherry red spot on fundoscopy- urgent ophthalmologist referral. Mx by reducing optic nerve oedema (corticosteroids, osmotic diabetics), normal Hb & MAP. May Mx w vasodilators, thrombolysis, corticosteroids.
If signs of POVL, early ophthalmologist opinion, optimise MAP, O2 & correct anaemia.
-Corneal abrasions: direct trauma, chemical irritation (eg. gastric secretions), exposure keratopathy. Tear production reduced under GA, corneal epithelium dries & is exposed to direct trauma. cornea can be damaged when eyelid reopened. Corneal vulnerability compounded by lagophthalmos w relaxation of orbiculares oculi under GA. Appose & tape eyelids, instil ointment, bio-occlusive dressings. Povidone-iodine 10% solution= only antiseptic skin prep that’s non-toxic to the eye- this should be used when face prepped for surgery. Meticulous eye covering & aspiration prophylaxis prior to steep trendelenburg.
Symptoms of corneal abrasion: pain/sensation of eye grit, tears, redness, photophobia. central abrasions may reduce vision. Dx w fluorescein staining & direct ophthalmoscopy or slit lamp. If exposed to irritant chemicals, irrigate w saline. Urgent ophthalmologist R/V if suspect abrasions & arrange follow-up.

Surgical:
-limit operating time (senior surgeon), consider staging prolonged procedures.

Patient:
-risk factors male, >50yo, anaemia, obesity.
-variations in eye anatomy, atherosclerosis, DM may be risk factors.

Anaesthetic:
-neutral head position @ or above heart
-frequent eye checks (at least 30-minutely, document), avoid pressure on globe (central retinal artery occlusion)
-art line w MAP as close to pre-op baseline as possible to optimise perfusion to optic nerve & spine
-euvolaemia, minimise blood loss (>1L blood loss, anaes duration >6hrs= 96% cases POVL after spinal surgery).
-monitor Hb (correct w blood & colloids along w crystalloids) & keep within pt-specific target (eg. >90 if IHD, no transfusion threshold to prevent POVL), Hct (aim 30%), glucose & oxygen

Drug:

Equipment:
-avoid horseshoe head rest
-ensure eyes & face visible & can access to check regularly
-avoid wilson frame (incr risk ION due to dependent head position)
-evoked potential monitoring; if evoked potentials deteriorate, incr MAP to baseline or slightly above & troubleshoot

Head up position:
care w art line transducer position to ensure targeting MAP to facilitate appropriate CPP; 10cm height of transducer=7.5mmHg pressure

SITTING craniotomy:

BENEFITS:
Gravity; facilitates CSF & venous drainage, lowers ICP, facilitates “bloodless field” so less for need retraction (risks ischaemia)
Helps direct surgical access for post fossa lesions
reduces Pit
reduces Pio
ergonomics

RISKS:
reduced cardiac preload due to venous pooling
risk postop tension pneumocephalus, risks VAE, unfavourale position for CPR, extreme neck F impairs venous/lymph drainage, may kink ETT, risk oropharyngeal/tongue oedema, nerve injury (incl paralysis), risk neuropraxia/pressure sores.

Contraindications to seated craniotomy:
PFO/R)–>L) shunt (large)
Patent ventriculo-atrial shunt
severe aortic stenosis
severe spinal stenosis (risks quadriplegia)
severe CVD

relative:
small PFO
extremes of age
severe HTN
Severe COPD (may not tolerate VAE)

Specific anaes considerations:
reinforced ETT/bite block
IABP transducer @ level of CoW
preload prior to positioning, legs up
likely to place CVC in procedure w high risk VAE; tip 2cm distal to SVC:RA junction
Monitoring; change EtCO2 to sweep speed (only mod sens for detecting VAE; 0.5mL/kg). cf TOE most sensitive (0.02mL/kg) then preordial doppler (0.05mL/kg)
eos steth (1.5mL/kg) & ecg (1.25mL/kg) both have low sensitivity- late signs, as are clinical signs

Incidence of VAE can be as high as 76% for seated crani; determinants are the volume entrained (200-300mL though to cause fatal AE), rate of accumulation.
M&M relates to hypoxia (eventually ARDS-like), pulm HTN & R) heart failure, paradoxical air embolus.
prevent w good surgical technique, vigilance/anticipation (eg. discuss in surgical timeout, have a plan for management), early detection.
communicate
screen machine to pt
prevent further air entrainment: flood field, occlude vessel, posn OT site below heart ?tourniquet neck
reduce volume: 100% O2, aspirate if CVC
overcome mech obstn: position eg. L) lat head down to relieve air lock, PEEP
RESUS +++–> offload RV, inotropes/vasopressors

hyperbaric, ICU

Breathing/airway risks:
Prone:
-ETT dislodgement risk (secure firmly, should have an action plan for intra-op ETT displacement, ensure access to the pilot tube & that it isn’t damaged during positioning.
-Place bite block in before prone & check location
-if tube dislodges: promptly identify & troubleshoot any ventilation system leak. if tube dislodged, alert room & summon help, promptly regain control of airway; oxygenate FiO2 100% w BMV (2-person for occiput counter pressure) or supraglotic device, supine if possible or R) or L) lat decubitus, difficult airway trolley into OT. surgeons close wound asap to allow t/f of pt onto stretcher in supine. If unable to move supine, can use iLMA, flexible bronchoscope w tube railroaded or AEC (position confirmed with FoB or by confirming EtCO2 when ventilating through be exchanger. Could do laryngoscopy w scope in R) hand, feed ETT w L) hand, assistant establish sniffing position & turn pts head to R) & elevating R) shoulder, 99% effective & safe (provided no C-Spine precautions).

-minimise airway oedema (eg. head level, look for signs (facial, orbital, conjunctival oedema, distended neck vv), use of flexible nasopharyngoscope, goal euvolaemia, cuff leak test (deflate cuff, positive leak test is >110mL or >10% of the TV decr in the exhaled volume) suggests +ve leak test & likely tolerate extubation. if fail leak test, keep intubated & Mx head up/steroids/diuretics. If pass cuff leak test but concerns re: oedema, extubatne over AEC & keep it in & secured/labelled & pt ICU.
-otherwise, regional ventilation more uniform in prone vs supine if sport vent, greater in non-dependent (dorsal) areas if IPPV so less heterogeneity than supine, overall V/Q matching less heterogenous prone in either spont vent or IPPV.
-pressure points around eyes a risk- use pillow with no external pressure, keep face/tube visible/accessible

CVS:
-prone thresholds for fluid responsiveness higher so look @ trends
-Ensure bolsters are appropriately positioned; one @ level of chest under axillae & one @ level of ASIS, otherwise risk impairing FRC/ventilation, impair venous return & incr after load. Risk abdominal organ dysfunction: compromised blood flow to liver/pancreas with abdo organ pressure (Ax for metabolic acidosis, incr lactate, decr glucose, liver function (ALT) & haematological parameters (consumptive thrombocytopenia)), risk bleeding as pressure distributed back via valveless epidural veins, also risk LL VTE.
-large-bore IVC x2 accessible & well-secured
-urinary catheter if case >2hrs (enlarging bladder may incr intra-op blood loss, pressure transmitted to valveless epidural veins).
-prone CPR challenge (more strenuous, risk ett dislodgement- only do if can’t immediately/safely turn supine & if have definitive airway. same rate compressions, directly over spine mid scapulae, place defibrillator pads bi-axillary or at L) MAL/R) scapula. observe CO2 trace, art line re; effectiveness.

Musculoskeletal:
-risk neuropraxia/nerve entrapment: arms abducted no >90 degree, slight IR & lying in front of the plane of the body to reduce risk brachial plexus injury. particular attention to pad/protect ulnar nerve.
-if arms by pts side, thumbs down to avoid over-pronation.
Check vulnerable points regularly, move, document in notes.

General injuries during anaesthesia:
Human factors: workload management, decision making, team communication; limit through team training & simulation-used training, promoting vigilance (eg. prompting for pressure area checks)
Equipment failure: check before use, regular checking schedules.
Patient factors: pre-existing poor dentition
Duty to disclose material risks of physical injury as part of consent (test of materiality= whether the patient (or a reasonable person in their position) would attach significance to the risk.
INCLUDE CONSENT & DEBRIEF/OPEN DISCLOSURE/M&M FOLLOW-UP/Q&A PROCESS FOR RISK MITIGATION FOLLOWING ANY ADVERSE EVENT

Airway:
Limit by planned limits to # attempts @ airway instrumentation, correct device size selection, cuff pressure (20-30cmH2O provides adequate seal but reduces risk complications), non-humidified breathing systems, prol surgery, NGT use incr risk sore throat.
50% some soft tissue injury to airways, 40% sore throat from ETT, 20% SGA (usually resolve within 48hrs w simple hydration & analgesia). Symptoms persisting longer: further Ix by anaesthetist, support from ENT.
Major rare (eg tracheal trauma w bougie; indicated by mediastinal & subcut emphysema, cough/pain/fever/dysphagia/dyspnoea- Ix w bronchoscopy & oesophagoscopy).

Dental injury: 1% of GAs. 90% to upper incisors, during intubation or extubation, in pts w pre-existing poor dentition or fragile prostheses, higher risk if difficult intubation. Consider deferral for dental R/V if high risk.
If occurs, remove loose fragment from airway, store the fragment in saline or milk (it may be suitable for bonding after OT. Referral pathway/policy for dental injury, counsel pt post re: need for dental R/V. If tooth avulsed, immediately relocate to socket provided socked healthy & pt not immunocompromised, provide firm pressure for several mins (or store in saline/milk). Care ++ on extubation (further avulsion may occur, w aspiration into trachea or oesophagus). Provide pt explanation & apology, see dentist ASAP for consideration of re-implantation & splinting.

Nerves: mechanical (trauma/lacerations), pressure (stretch, compression), vascular (hypoperfusion/compression—> ischaemia), chemical (neurotoxic material/inflammatory reaction)
Neuropraxia= damage limited to the myelin sheath, eg. w excessive stretch or nerve compression. best prognosis, recovery in weeks to months.
axonotmesis: loss of axonal continuity but endoneurium intact, recovery prolonged & may be incomplete. Neurotmesis: complete nerve transection. requires surgery, gravest prognosis.
When consenting: up to 2% at 3/12, up to 0.8% of patients at 6/12, up to 0.2% of pts at 1 year will have symptoms suggestive of nerve injury after peripheral nerve block. hard to quantify permanent; up to 4:10,000
Higher risk if pre-existing peripheral neuropathy (“double crush theory”). Diabetic neuropathy particular risk (incr risk damage 10x); pre-existing neuropathy isn’t an absolute contraindication to RA but consider w risk:benefit balance, reduce [] & avoid epinephrine, use US of theoretical benefit to maintain distance from nerve. Other risks= smoking, anticoagulants, PVD, HTN, vasculitis.
Limit by (no evidence for use of one technique over the other, multimodal/integrated approach best):
-nerve localisation: do block awake to Ax for elicited paraesthesia, use nerve stimulation (not as accurate as once thought; motor response w current <0.2mA specific for intraneural needle placement but not sensitive. nerve stimulation w current intensity 0.2-0.5mA w PD 0.1ms needle-nerve position sufficient for safe LA. US guidance reduces dose/volume of LA, allow visualisation of injectate spread, decr IV puncture or LAST (but unable to differentiate inter or intrafascicular needle tip), strategies to improve needle tip visualisation (echogenic needle, needle beam angle, needle bevel orientation 0 or 180 deg from beam, larger diameter easy to see but more traumatic, hydrolocation/hydrodissectio,, other US technology (eg. electronic beam steering)). No particular technique found to reduce incidence of LT peripheral nerve injury. Avoid intrafascicular injection (ie. don’t breach the perineurium; extrafascicular injection deep to the paraneural sheath around the sciatic nerve= safe (epineureum not breached)).
-adults should be awake/responsive to monitor for elicited pain/paraesthesia (lack doesn’t exclude needle nerve contact or prevent PNI but paraesthesia does incr likelihood of transient neurologic symptoms after PNB). If paraesthesia, stop advancement, reposition) or early S&S of LAST. Children or adults @ risk of movement during block can be done under anaesthesia.
-smaller gauge & short bevel, non-cutting needles.
-avoid high injection pressure (ass’d w intrafascicular intraneural injection); in-line manometer more accurate than subjective but sensitive w limited specificity, little evidence (<15psi indicates extra-fascicular or extra neural).
-solution used: all LAs potentially neurotoxic in [] & time-dependent manner. Avoid intrafascicular injection, ropivacaine has the lowest neurotoxicity potential. High [] Adr (>5microg/mL, 1:200,000) reduces blood flow in dose-dependent manner; avoid in pts w pre-existing nerve injury or higher than N risk of injury (low [] ie. 2.5microg/mL B-adrenergic predominates & neural blood flow increases. No other adjuvants (opioids, clonidine, dexamethasone, neostigmine, dexmed, ketamine, midaz) are licensed for perineurial injection; dexmed though to be neuroprotective (animals), ketamine & midaz neurotoxic @ hight doses, others not believed to be neurotoxic.

Diagnosis/management:
-early recognition & risk stratification of those needing urgent imaging/neuro/surgical consult affords the best chance of near recovery (eg. reverse intrinsic or extrinsic compression from compartment syndrome, haematoma).
-APS/other follow-up monitoring system (I follow my own blocks) to identify.
-Suspect nerve injury if new onset pain, weakness, numbness, paraesthesia or other abnormal sensation lasting beyond usual duration of specific block (eg. single shot PNB >48hrs)
2 categories:
mild/resolving= pure sensory deficits within territory of peripheral nerve block, often resolve in days to weeks—> reassure pt & arrange f/up within 4 wks to review need for Dx tests
complete or progressive neurological deficits +/- motor deficits= generally more ominous—> there should be early neurol consult & radiology if motor involvement, difficulty localising or reconciling the injury w the expected distribution of the block or surgery, complete absence of nerve function beyond the duration of the PNB, any injury w mod or severe functional limitation, progressive deficit or failure to improve. Consideration of potential surgical causes (eg. haematoma) & possible Rx (eg. decompression). Consider further imaging. Typically electrophysiological studies are delayed 2-3/52 to allow for signs of wallerian degeneration but neurologist may suggest earlier electrophysiological studies (EMG changes in the early period suggest preexisting neurology).
*if suspect space occupying lesion ass’d w CNB, Rx as emergency.
Consider referral to peripheral nerve surgeon if no improvement in 3-5/12.
-Ax for signs of infection esp if catheter.
-Neurophysiological studies= EMG, nerve conduction studies or both. EMG= examine electrical activity generated within a muscle to determine motor units affected by the injury. Nerve conduction studies assess electrical conduction impulses (stimulate a nerve, characteristic waveform of nerve conduction velocity is produced). NCS can localise site of conduction block & confirm or refute a PNI lesion @ site of PNB (may not be possible to distinguish if surgical site/tourniquet in proximity). Electrophys also offers prognostic info re: degree of injury (neuropraxia, axonotmesis, neurotmesis).
No pharmacological therapy impacts neurodegeneration, Rx= physical therapy to maintain muscle mass & prevent flexion contractors, analgesia with neuropathic agents & non-narcotic analgesics

Neuraxial:
permanent harm in 2-4.2 per 100,000 in NAP3, the vast majority were periop (vs labour analgesia).
risk:benefit impacted by coagulopathy, pre-existing spinal disease, suspected or actual infection, immunosuppression, aortic stenosis.
Vertebral canal haematoma: risk incr by coagulopathy, pre-existing spinal canal abnormality, traumatic needle insertion. Signs/symptoms: radicular pain, unexpected weakness, paraesthesia, bl/bowel dysfunction. Prolonged loss of motor power or sensory blockade (esp beyond expected dermatomal distribution or that appears after initial block resolution), should trigger a high index of suspicion. Mx by: stop any LA infusions, senior clinician perform & document full neurological exam every 30mins for up to 4hrs; if Neurol deficit doesn’t resolve in that time, pt should have immediate whole-spine MRI. Emergency decompressive surgery within 6-8hrs from symptom onset may result in recovery of neurol function.

Epidural abscess:
rare. NAP3 reported 20 per 707k neuraxials. inc risk if prolonged catheter, poor aseptic technique, underlying immunocompromise, coagulopathy. Untreated active systemic or local infections= absolute contraindication to neuraxial. S&S= radicular back pain (often localised tenderness) presenting over days to weeks, malaise, fever, sensory deficit, weakness, abnormal bowel or bladder function after neuraxial. Immediate MRI, resus pt, culture site, systemic ABx. Most often MRSA. surgical decompression w prolonged ABx= Mx.

Chemical damage: adhesive arachnoiditis (fibrous collagen band formation, inflammation, hyperaemia of meninges, syringomelia) may occur w chlorhex contamination of epidural or subarachnoid space- poor prognosis, few effective treatments. 0.5% alcoholic chlorhex preferred over 2% as skin asepsis before central neuraxial block. Ensure chlorhex isolated from neuraxial needling equipment. ensure antiseptic dried completely before needling. avoid open systems (eg. gallipots) for injectable solutions for neuraxial

Nerve injury by positioning:
-meticulous communication & planning (eg. team huddle, pre-brief) re: initial positioning & any plans for re-positioning.
-pre-op consent disclose risks of position-related injury, highlighting pts @ risk or if particular material risks. Carefully document any peripheral neuropathy present before operation, carefully document any steps taken to ensure safe positioning in medical record.

Most common= ulnar (1:300)>brachial plexus (1:2000)>CPN (1:4600)

Ulnar nerve (C8-T1): Protect by: reduce pressure on cubital tunnel by avoiding elbow extension w forearm pronation, avoid >90deg elbow flexion & >90deg shoulder abduction. Ensure NIBP cuff doesn’t inflate over cubital tunnel (btwn medial epicondyle humerus & olecranon process of ulna). Provide soft external padding @ cubital tunnel. Forearm position neutral w shoulders abducted.
S&S: Pain/paraesthesia ring & little finger or ulnar side of dorsum of hand or hypothenar eminence, pain @ medial aspect of elbow, weak grip, ulnar claw posture 4th & 5th fingers (atrophied intrinsic muscles) muscle wasting if prolonged nerve injury.

CPN:
classically a risk of lithotomy (CPN compressed against lead of fibula in stirrups), also may be injured in knee arthroplasty.
Limit by: ensure no compression on CPN near fibula in lithotomy. Check that leg supports don’t compress calves. lower legs for minimum 15 mins every 3 hrs.
weak ankle DF, foot eversion, paraestheia or pain over dorsal foot & lateral leg up to knee.

Brachial plexus: inferior trunk @ highest risk if shoulder abducted >90degrees, if below plane of torso in supine, or if head rotated to contralateral side. Superior & middle trunk injury more likely w external compression against shoulder (eg braces in trendelenburg, esp if CL neck flexion).

Peripheral nerve injury is 9x more likely to be due to surgical or pt factors rather than nerve block (eg. HTN, smoking); highest incidence of neurological complications with elbow replacement, TKR, ACL repair.

Muscle/skin injury:
pressure ulcers: reduced perfusion, ischaemia, necrosis. esp risk if elderly, malnourished, immobile, chronic diseases eg DM, obesity. Limit w padding, dissipate pressure over as large an area as possible, vigilance to pressure points (schedule movement/relief/repositioning regularly for prolonged surgery). Non-blanching redness= first sign skin poorly perfused, monitor closely & document f/up postop.

Compartment syndrome 1:50,000. LLs particularly if >4hrs incorrect leg placement in Lloyd Davies (trendelenburg 30 deg, hips flexed 15 deg, LLs abducted to allow perineal access) position or lithotomy.
Dependent UL in lat decubitus. extravasation of fluid from misplaced/displaced IV or IO cannulate, arterial tourniquets, extrinsic compression from instruments or personnel.
cardinal signs= severe pain passive stretch. Urgent ortho R/V, may have decompressive fasciotomy.

Tourniquet injuries: tissue compression or ischaemia. pressure necrosis or friction burns if poorly applied tourniquets move. chemical burns if antiseptics seep beneath tourniquets & held under pressure on skin. Equipment failure or improper use (test/calibrate @ regular intervals). Longer inflation times & higher pressures= risk pressure-related nerve injury.
Radial nerve most frequently impacted in UL, sciatic in LL.
Longer inflation times & higher pressures risk pressure-related nerve injury. Tourniquet cuffs should exceed circumference of the limb by 1/3 & applied @ widest part of limb. Pad skin underneath sans folds. once applied, don’t rotate. seal distal edge to avoid seepage under it. inflate to pressures 40-80mmHg above point where art pulse distal to tourniquet is lost, deflate @ least 10 mins after max 120mins inflation in healthy pts; reduce this time if chronic disease or acute physiological disturbance. sickle cell disease, peripheral neuropathy, limb infection, PVD or prev VTE= relative contraindications to tourniquets.

Burns: warming devices, electrocautery, ETOH-based skin prep or a combo of these factors.
Dispersive pad must be secure in contact w dry, shaved skin away from bony prominences, scar tissue & metal. use of protective quivers, audible signals when electrocautery in use & alarms if malfunctioning of dispersive plate= extra protection. metal contacting tissue (eg. ecg dots) may provide an alternate return pathway if diathermy dispersive plate incorrectly placed.
minimising risk airway burns:
discuss risk in team timeout, close communication re; diathermy/laser use when close to inspired O2.
avoid etoh-based skin prep. use laser-resistant tracheal tubes w saline vs air in cuff, low FiO2 (blender if HFNO) & avoid N2O, minimal exposure of airway to electrosurgery/laser, fire Mx plan/sims, saline

Considerations for PNB on anti coagulated pt: site, compressibility, vascularity, consequences of bleeding if it occurs.

Question 183

SS_NS 1.27: anaes considerations for vestibular schwannoma

Answer 183

Patient: generally young. may have NF2 (multisystem disease strongly ass’d w bilat vestibular schwannomas; also other brain tumours/meningiomas, seizures, spinal tumours, low muscle tone, facial weakness, chronic pain, schwannomas/skin tumours, visual impairment eg. cataracts)

Pathology: generally benign, cerebellopontine angle
May have vestibular or hearing signs/symptoms
larger cerebellopontine angle tumours may affect lower CNs (eg. gag reflex, risk aspiration). If obstruction of 4th ventricle outflow, hydrocephalus & altered LOC.
these pts need swallow Ax, consider NGT.
proximity to brainstem & sinuses; risk haemodynamic instability (eg. bradycardia, hypotension with surgical stimulation around brainstem; esp trigeminal nerve root), bleeding, VAE

Procedure: skull base surgery. PROLONGED (consider positioning/pressure areas, VTE prophyl, normothermia to reduce risk SSI, cardiac events, coagulopathy, fluid input/output monitoring).
Positioning may be park bench (for retrosigmoid which is typically NSx, involves mayfield pins, head flexed, CL rotation & CL 30 deg lat flexion contralaterally) or supine for translabyrinthine (combined w ENT & neurosurgeons).
shared airway.
neuroanaesthesia principles: optimise cerebral perfusion & DO2 while avoiding raised ICP, minimising bleeding (consider permissive hypoT in liaison w surgeons, cognisant of preserving CPP) & being vigilant for VAE.
Need art line, group & hold
may need facial nerve monitoring so non-paralysing anaesthetic
Prolonged surgery but want rapid recovery for neuro Ax; consider prop/remi (for tube tolerance & lack relaxant) or volatile/remi).
smooth cough/strain-less extubation attenuating any HTN.
multimodal anti-emesis
Postop HDU for neuro Ax, haemodynamic Ax/Mx, analgesia (generally orals fine, avoid NSAIDs due to anti-platelet effects, generally avoid LIA due to potential brainstem/CN effects; generally not significant pain unless a fat graft harvested; would drain should be used since pain from pressure w haematoma formation may be an issue)/anti-emesis (vestibular OT emetogenic +++)

Potential complications:
VAE
bleeding
cerebral ischaemia (hypoperfusion, embolism, vasospasm)
haemodynamic instability (eg. brady/hypOtension even asystole w trigeminal cardiac reflex; may require glyco>atropine. surgeons immediately cease stimulation).
facial nerve palsy
aspiration
postoperative neuro dysfunction (consider need for postop vent depending on preop LOC)
VTE; administer prophylaxis (prolonged surgery)

Question 184

antiphospholipid syndrome

Answer 184

venous or art thrombosis or adverse preg outcome w persistent lab evidence of aPL antibodies. either a primary condition or in the setting of disease (eg. SLE)

Question 185

criteria for ECR eligibility
meta-analysis of 4 RCTs for GA vs conscious sedation for endovascular thrombectomy

Answer 185

ischaemic stroke with proven large vessel occlusion on CTA: ICA, MCA, basilar (emetogenic, higher risk vagal symptoms w retracting clot)
independent premorbid function (mRS 0-2)
may be eligible up to 24hrs
IV thrombolysis if eligible

GA vs conscious sedation higher OR successful recanalisation & functional indep (mRS 0-2) @ 3/12

Question 186

why haemodynamic targets so important for ECR?

Answer 186

autoregulation effected; possible loss of compensatory vasodilatory capability distal to occluded vessel, collateral flow can be compromised during hypoT, ischaemic penumbra must be protected before recanalisation. hypoT prior to recanalisation ass’d w larger infarct volumes & worse functional outcomes.

MASTERSTROKE is looking at mRS for lower vs higher target

SNACC: SBP 140-180mmHg with DBP <105mmHg
SpO2 >92%, PaO2 >60mmHg, PaCO2 35-45mmHg
normoglycaemia, propofol may have improved functional indep @ 3/12
currently: 140-180mmHg SBP, DBP <105mm

Question 187

What’s a myelomeningocoele & how repaired?

Answer 187

sac containing meninges & neural elements bulging through a vertebral defect. Closed surgically shortly after birth OR can be done in-utero, underlying spinal cord damage remains however prenatal repair may limit damage since SC damage is progressive during gestation (ie. Prenatal repair may reduce need for shunts for hydrocephalis & may improve chances of independent mobility). Done 23-25wks 6 days. GA, laparotomy, sterile intraop US to map placental & foetal position, open uterus w uterine stapling device (pinches off blood vessels, keeps membranes secured), paediatric neurosurgeon removes MMC sac, returns SC to spinal canal & closes to protect the spinal cord from exposure to amniotic fluid. Foetal cardiologist monitors foetal heart w echo.

Question 188

What’s trigeminal neuralgia & it’s anaesthetic implications

Answer 188

Rare but debilitating facial neuropathic pain condition in trigeminal nerve distribution. Unilateral, superficial, brief, intense, sharp, electric shock-like pains. Abrupt onset & termination.

Cause not apparent; possibly micorvascular compression or processes (eg. MS, tumours, AVMs) abnormalities in afferent neurones of the trigeminal root or ganglion, axonal injury/demyelination hyperexcitability. Central sensitisation likely plays a role.
Thre’s no clinically evident neurological deficit.

DDx= headache disorders (eg. Cluster), dental pain, TMJ disorders, post-herpetic neuralgia, acoustic neuromas.

More common in females (2:1). Risk factors= MS, incr age, stroke, HTN (in women), charcot-marie-tooth disease (hereditary (variable inheritance patterns most often autosomal dominant) motor & sensory polyneuropathy, degenerative, appears adolescence or early adulthood. Muscle weakness, chronic fatigue, muscle atrophy (LLs/Uls), respiratory impairment (restrictive pattern related to chest deformities & muscle weakness, may have central sleep apnoea ass’d w diaphragm dysfunction, may have OSA due to pharyngeal neuropathy, some have VC dysfunction), may be at risk of lung aspiration (VC paraesis), ANS denervation, cardiac manifestations (long QT, cardiomyopathy, AV block) potentially pulm HTN secondary to restrictive long disease, foot drop, restless legs, muscle & nerve pains, cold extremities, may lead to deformities (eg. Scoliosis, claw hand, pes cavus, hammer toes) & functional dependence; avoid sux, NDMR may have prolonged action (monitor where not weak eg. Corrugator supercilli; postop HDU/BiPAP or CPAP may be required depending on severity. More likely malpresentation, bleeding postpartum; higher rates operative delivery & instrumental. Can use epidural or CSE), tumors in trigeminal nerve root

Clinical Dx, MRI useful to exclude secondary causes (MS, tumours), high-res MRI may detect vascular compression

CNV= largest CN, sensory & motor but motor only to V3 (muscles of mastication). PSNS to lacrimal glands (V1,2), nasal (V2), submandibular/sublingual/parotid glands (V3).

Pharmacological therapy 1st line: carbamazepine, NNT 1.8, 200-1200mg. Anticonvulsant, blocks use-dependent Na channels.
Main limitation= side effects of drowsiness, rash, liver damage, hyponatremia, ataxia.
LFTs, blood count, serum electrolytes should be regularly checked.

APMSE: LAs (esp lig) local or systemic, anticonvulsants (phenytoin), sumatriptan, motor cortex stimulation, may reduce pain in acute exac TN. Level IV.
Botox A reduces pain at 4, 12 & 24wks level 1.
APMSE finds topiramate as effective as carbamazepine @ 1/12 after Rx commencement & slightly more effective @ 2/12, studies of poor methadological quality.
Gabapentin, pregabalin & amitryptilline are commonly used in TN due to efficacy for neuropathic pain but evidence in TN not strong. Baclofen may be useful in MS pts suffering TN. Phenytoin w limited benefit in some cases.

Surgical: for pts who don’t benefit from pharmacological therapy or who experience significant side effects.

Peripheral: neurolysis (laser, ETOH, neurectomy) of the branches distal to gasserian ganglion (in middle cranial fossa). Less invasive but pain relief is short-term (6-12 months), risk post-procedure dysaesthesias. Useful in emergency or pts unfit for other procedures.

Ganglion (gasserian aka trigeminal): ablated either radiofrequency (thermal) or chemical (ETOH, glycerol) or mechanical (balloon): usually under LA/sedation (since pts cooperation is necessary), pt supine w neck sl extended, under fluoroscopic guidance, needle passed via foramen ovale. This rhizotomy is effective for 4-5yrs in 50%. Complications: sensory loss & dysaesthesias (4% anaesthesia dolorosa- painful numbness). Balloon compression may  arrhythmias, aseptic meningitis, temporary diplopia.

Microvascular decompression= best outcome for quality & duration of pain relief, HOWEVER less effective for MS-related TN with high relapse rate & more risk sensory dysaesthesia. Pre-op MR tomographic angiography useful for pt selection & outcome prediction for microvascular decompression.

Posterior fossa: suboccipital craniotomy to access trigeminal nerve in posterior fossa. Nerve root is freed from vessels compressing it (most commonly superior cerebellar artery) & Teflon felt placed between. 80-90% success, most sustained pain relief (relapse rate @ end of 10yrs is 30%). MVD is major neurosurgery; 0.5% mort. Other risks aseptic menintigis, hearing loss, sensory loss, CSF leaks, haematomas, infarcts.
Gamma knife stereotactic radiosurgery: delivers focused beam of radiation to trigeminal nerve root in posterior fossa where there’s proven vascular compression. MRI mapping locates exact site of microvascular compression. Complete pain relief in up to 69% of pts @ end of 1 yr but benefits may not be sustained. It can be repeated. May be more useful for MS-related TN. Complications= facial numbness, paraesthesia. Useful if can’t have MVD.

Psychological intervention- limited evidence but multi-D team incl psychologist useful, eg. CBT & ACT.

Question 189

What are some cardiovascular complications of brain injury & their implications?

Answer 189

Common, ass’d w M&M, more likely w more severe neurol insult

High SNS tone persists up to 10 days (may be protective to maintain cerebral perfusion in presence of raised ICP)

Neurogenic cardiac injury is related to brain injury-induced catecholamine release & inflammatory response

Neurogenic stunned myocardium syndrome is dt local release of NE from myocardial SNS terminals

Haemodynamic changes (initially HTN due to catecholamines or hypoT either due to disruption of brainstem haemodynamic control or if develop myocardial ischaemia (demand:supply mismatch) & cardiogenic pulmonary oedema with poor LV output).. typically HTN/tachy followed by hypotension with unopposed VD & ventricular dysfunction, responsive to fluid therapy & NAdr may provide predictable control of arterial pressure & CPP; vasopressin useful for refractory hypoT but is ass’d w cerebral VC & risk brain ischaemia. Dobutamine may assist normalising cardiac index in neurogenic stunned myocardium-related low CO states after SAH.

ECG changes (in 49-100% of cases after SAH, esp ST changes, flat or inverted T waves, prominent U waves, QTc prolongation; Can be difficult to differentiate neurogenic ecg changes (which aren’t related to cardiac hypoperfusion) from acute ischaemic coronary event.
Neurogenic stunned myocardium= a Dx of exclusion, suggested if no Hx cardiac probs, temporal relationship btwn brain injury & CV abnormalities, ECG changes in isolation, modest elev cTnI, new onset LV dysfunction, cardiac WMA’s don’t correspond w coronary vascular territories, inconsistency btwn echo & ecg findings, inconsistency w cTnI & LV EF, spont/early resolution.
Ecg changes may be transient or persistent. Generally asymptomatic but some may be ass’d w delayed ischaemic neurol deficit, poor outcome & death (eg. Persistent prol QTc in SAH ass’d w unfavourable outcome, QTc prolonging drugs should be avoided after brain injury)
Arrhythmias
biomarker changes (elevated cTnI in 20-68% of pts after SAH, generally below the level for Dx MI. Elevated BNP independently ass’d w LV dysfunction, pulm oedema & adverse neurol outcome after SAH (elevated BNP 11x RR of death after SAH)
LV dysfunction usually mild but ass’d w incr mort after SAH; characteristic RWMAs in SAH (basal & middle portions w relative apical sparing). Diastolic dysfunction common, ass’d w pulm oedema. Takotsubo cardiomyopathy is aka L) apical ballooning, is transient, virtually global LV dysfunction. Apical & mid-ventricular akinesia w relative sparing of basal segment. Well-recognised response to sudden physical or emotional stress, generally benign prognosis. Rarely ass’d w SAH but is ass’d w incr mortality in THIS context.

Generally transient cardiac abnormalities, Mx focuses on supportive care (no specific Rx for arrhytmias but standard correction of electrolytes), Rx of injured brain.

Propofol infusion syndrome: metabolic acidosis, CK elevation, rhabdo, widespread ecg changes, may cardiac myocytolysis, rhabdo, acute renal failure. Run propofol infusions no >4mg/kg/hr to avoid. Thought due to impaired utilisation of FAs within mitochondria.

Question 190

Circulatory death

Answer 190

“irreversible cessation of circulation of blood in the body of the person”

Determination of loss of pulsatile arterial blood pressure in context of donation best done by ABSENT PULSE ON ARTERIAL LINE FOR 5 MINUTES. confirm by clinical exam (absent HS or absent central pulse)
If art line not possible/accepted, observe ecg electrical asystole for 5mins (ECG activity may continue for >30mins post cessation of arterial BP)

Question 191

Electrolytes with ectopic acth secretion?

Answer 191

hypokalaemia
metabolic alkalosis
glucose intolerance

Question 192

Electrolytes with ectopic acth secretion?

Answer 192

hypokalaemia
metabolic alkalosis
glucose intolerance

Question 193

What’s SAH, risk factors

Answer 193

extravasation of blood btwn pia & arachnoid maters
rupture due to haemadynamic stress to the thin-walled outpouchings of arterial wall

Generally acquired but can have genetic susceptibility

most common saccular/”Berry”
more common @ arterial bifurcations/areas turbulent flow (a comm/ p comm)

risk factors to aneurysm:
non-modifiable:
female
middle age
connective tissue disorders (EDS, marfan’s, PCKD, NF-1, fibromuscular dysplasia)
modifiable:
smoking, HTN, ETOH excess, cocaine use atherosclerosis

rupture risks:
female, p-comm or large aneurysms
HTN, cocaine, smoking

Question 194

What % BMR is isoelectric EEG?

Answer 194

30-40%

Question 195

If have given mannitol to manage ICP, what’s the end point?

Answer 195

serum osmolality >320mosmol/Kg not effective (may achieve this after 2x 0.5g/kg mannitol)- change to HTS

Question 196

End point for HTS?

Answer 196

give 3mL/kg, Na+ no >155mmol/L

Question 197

Specific MTP considerations for neurotrauma?

Answer 197

lower threshold to give plts (80), avoid albumin, ROTEM-guided

Question 198

DECRA study TBL:

Answer 198

For diffuse TBI, early decompressive craniectomy reduces ICP & ICU LoS but poorer 6/12 functional outcomes.

Question 199

should EVD be open or closed on transport

Answer 199

generally close unless high output