Neuro Flashcards
Anaesthetic considerations for patient with SAH requiring aneurysmal coiling?
General considerations:
1. Critically unwell patient undergoing emergency high-risk procedure will require an experienced senior anaesthetist, ODP and emergency help if available
- Time-critical therefore full stomach, aspiration risk
- Remote site anaesthesia - lack of familiar monitoring/equipment, out of hours with less help around, limited access to patient during procedure, lack of appropriate recovery area
Pathology specific considerations:
1. Unsecured aneurysm with potential for bleeding
- Avoidance of extremes of blood pressure and reversal of coagulopathy
- Potential increased ICP
- Maintenance of CPP 60-70mmHg (MAP 80-90)
- PaO2 , PaCO2, normothermia, euglycaemia, venous drainage considerations
- May require EVD before or after if evolving hydrocephalus - Potential medical complications
- Neurogenic pulmonary oedema
- Myocardial dysfunction due to catecholamine surge
- Electrolyte disturbance
Anaesthetic goals for patient with SAH requiring aneurysmal coiling/clipping?
- Haemodynamic control and monitoring
- Minimisation of transmural pressure to avoid rebleeding
- Invasive arterial blood pressure monitoring and CVC for noradrenaline
- Avoidance of acute hypertensive episodes such as pressor response to laryngoscopy
- Keep SBP <160mmHg (AHA guideline 2012)
- Keep MAP>85mmHg to prevent ischaemia - Protection from secondary brain injury
- CPP 60-70, MAP 80-90
- Control ICP (normocapnia, venous drainage)
- Reduce CMRO2 - normothermia, barbiturates
- Euglycaemia (BSL <11mmol/L
- Vasospasm and seizure prophylaxis - Smooth postoperative emergence with good analgesia and prevention of coughing and vomiting (ICP)
Anaesthetic “how to” - myasthenia gravis?
- Pre-operative hx/exam/ix
- Usual anaesthetic history with detailed assessment of respiratory, bulbar and muscle weakness
- Exclusion of other autoimmune conditions e.g. RA
- Hx and optimisation of immunosuppresants and anticholinesterase inhibitors
- Airway assessment - thymoma may rarely cause tracheal obstruction
- Consent to possibility of post-op mechanical ventilation - Peri-operative mx.
- Avoidance of sedative premeds due to resp muscle weakness
- Steroid cover if >5mg prednisilone daily
- Continuation of usual anticholinesterase inibitors
- NM monitoring throughout case
- Deepening of inhalational agents to intubate (avoid NMBDs)
- Much lower dose than normal of NDMDs (10% usual dose)
- Higher dose of Sux (2.6x normal dose)
- Avoidance of using muscle relaxant reversal with neostigmine as may precipitate cholinergic crisis - Post-operative
- Assessment of TOF
- Most patients can be exubated but some may require I+V in ICUs
What are the anaesthetic goals in a patient with Myasthenia Gravis?
- Minimize risk of aspiration (prophylaxis, RSI)
- Minimize risk of perioperative respiratory failure (judicious NMBs & opioids) & anticipate need for post-op ventilation
- Minimize risk of myasthenic or cholinergic crisis
- Optimize neuromuscular function
What 7 nerves are blocked in scalp block?
Supraorbital
Supratrochlear
Zygomaticotemporal
Auricotemporal
Greater auricular nerve
Greater occipital nerve
Lesser occipital nerve
Anaesthetic considerations of Lambert-Eaton syndrome?
- May be first presenting feature of cancer - need to ix
- Autonomic dysfunction
- Inc. pulmonary aspiration risk due to delayed gastric emptying
- Hypotension - Increased sensitivity to depolarising and N-D muscle relaxants
- Titrate against NM monitoring - May need post-op ventilation in ICU
You have a patient with raised ICP. What are the concerns around intubation?
High risk patient group.
1. Will require RSI or modified RSI due to unknown fasting status.
2. Apnoeic period may result in hypoxaemia or hypercapnoea
- Inc. CO2 causing vasodilation and high ICP
- Hypoxaemia causing reduced cerebral o2 delivery and worsening 2ndary brain injury
3. Vasodilatory effect of induction agent risk hypotension below impaired ability of brain to compensate
4. Hypertensive response to laryngoscopy risks hypertension beyond impaired ability to compensate risking further inc. in ICP or worsening bleeding in traumatic H.I
5. Despite low GCS an induction agent is important to reduce cerebral metabolic rate and protect brain from inc. ICP
How might you intubate a patient with raised ICP?
RSI or modified RSI +- MILS (if concern r: H.I)
3-minutes of pre-oxygenation
Rapid acting opioid e.g. alfentanil to obtund sympathetic response to laryngoscopy
Induction with low dose propofol OR thiopentone 4mg/kg OR ketamine 1mg/kg
Suxamethonium achieves intubating conditions in 45s vs 60-90s rocuronium
Consider apnoeic oxygenation with BMV or optiflow
Suggamadex not an option
Tape tube vs. tieing (not obstruct JV drainage)
Principles of managing the ventilated patient with raised ICP
Deep sedation (propofol/opioid)
Frequent NMBD boluses to prevent coughing/straining
Maintain MAP >80 or >90 to maintain CPP >60mmHg
Position pt. head up and remove collar (assuming no C-spine injury)
Aim PaO2 >13kPa
Minimise PEEP
Aim PaCO2 4.5-5.0 or ETCO2 4.0
Consider hyperosmolar therapy if blown pupil, midline shift
- 20% mannitol 0.5g/kg
- 3% hypertonic saline 2mls/kg
Normoglycaemia 4-11mmol/L
What are the indications for intubation and ventilation in GBS patient?
- Bulbar involvement
- Inability to cough, swallow, protect airway - Respiratory muscle fatigue
- Clinical assessment or spirometry (FVC<1L or 10-15ml/kg) - Blood gas analysis showing hypercapnoea
- Autonomic instability
Slow recovery means most patients will require tracheostomy t
What is your anaesthetic approach to a patient with scoliosis?
Pre-op assessment:
Hx, exam, Ix with particular attention to
- Potential co-morbidities such as neuromuscular syndromes duchenne’s M.D (with cardiomyopathy)
- Assessment of restrictive lung deficit - RV function on echo, spirometry, functional capacity
- Pre-op pain, are they a patient with chronic or neuropathic pain pre-op
Intra-operative (PRIMADE TIME) positioning, resus, iv access, monitoring, assistance, drugs, equipment, transpost/transfer, induction, maintanance, emergence
- Prone positioning for long period time
- IV access/monitoring - art line (blood loss potential), wide bore access, consider CVC if co-morbid or surg. factors
- Armoured ETT
- Blood loss factors - TXA, art line, cell salvage, blood products available
- Induction/maintanance ?avoid repeat NMBD, TIVA as >0.5 MAC interferes with spinal monitoring
- Emergence - aim for extubation immediately post op to allow neuro assessment
Post-op (AD) analgesia, disposition
- Multi-modal analgesia with opioid sparing techniques - NSAIDS, ketamine iv, epidural catheter placed surgically
- Allows early mobilisation/physio
- Likely crit care as disposition
Anaesthetic considerations of prone position?
Airway
- Risk of ETT dislodgement on proning/deproning
- Endobronchial intubation
Respiratory
- Abdominal compression can splint diaphragm causing atelectasis, V/Q mismatch
- Allen table allows abdomen to hang freely
Cardiovascular
- Compression of abdomen causes decrease in CO due to IVC compression
- Inc. pressure of epidural/vertebral wall plexuses causes inc. surgical bleeding
Neuro/disability
- Dislodgement or kinking of TIVA lines on proning inc. risk of awareness
Peripheral injuries
- Face (ring not suitable), nose pressure and eye pressure
- Arms - shoulder/elbow angle <90deg, elbows flexed, hands pronated
- Breasts, genitalia
- Knees bent
- Ankles not extended
Complications of prone positioning?
- Brachial plexus injury - in particular ulnar
- Facial damage
- Ophthalmic injury
- External compression, haemorrhage/hypotension, head down all inc. damage
- Perm blindness risk 1:100,000 - Lateral cutaneous nerve of thigh
- Macroglossia - impaired venous drainage via lingual/pharyngeal veins
What are the options for anaesthesia for neuro interventional radiology?
- Conscious sedation
Adv - no time delay (‘time is brain’), clinical neurological monitoring, stable haemodynamics
Disadvan - unprotected airway, patient movement
- General anaesthesia
Adv - airway protection, patient immobility
Disadvan - haemodynamic instability, lack of neuro monitoring, time delay
Problem is that the patients with the biggest compromise and most likely to benefit are more likely to need a GA due to agitation, seizures
What issues are there with neurointerventional environment?
Remote site anaesthethesia. Implications =
Training/familiarity
Equipment, lack of access to airway equipment and drugs
Personnel - may not have anaesthetic assistant
Means of summoning help - further away
Radiation issues
- shielding: lead aprons, thyroid collars, lead screens, eyewear
- Undiagnosed pregnancy risk
What is endovascular coiling?
Feeding microcatheters into cerebral circulation via femoral artery catheter to deploy platinum coils into aneurysm sac until it becomes occluded
Advantages and disadvantages of endovascular coiling?
Advantages:
Less invasive than clipping
Lower cost
Better for posterior circulation aneurysms
ISAT trial 2002 - coiled = 24% death/disability at 1 year vs 31% clipping
Disadvantages:
Cant coil all aneurysms (e.g. wide necked, small aneurysms)
Complications - ischaemia, bleeding, vasospasm
Need neurosurgeon if complication occurs
Higher chance need re-treatment
Anaesthetic “how to” - neuroradiology?
Pre-op assessment:
Usual anaesthetic assessment
Attention to - grading of SAH, ICP monitoring, other co-morbidities
ICP>20mmHg is contraindication
Ix - G+S, coag screen
Be aware of neurosurgery they may have to mx. complications
Location:
Neuroradiology suite. Carries own implications (separate flashcard)
Intra-operative:
Positioning - supine, difficult to access airway/cannulas
Resus drugs - drawn up
IV access+ IABP monitoring, act sampling, maintaining CPP
Monitoring - AAGBI, temp monitoring + warmer, urinary catheter
Assistance - may be difficult, remote
Drugs
Equipment
Transport
Induction - GA vs sedation, smooth, maintain CPP
Maintanence - propofol sedation, dexmed, immobility important
Emergence - smooth emergence
Post-op:
Analgesia/Disposition.
Simple analgesia. NeuroHDU/ICU likely
Dose of hyperosmolar therapy for raised ICP?
20% mannitol 0.5g/kg
3% hypertonic saline 2ml/kg
Patient with spinal cord injury - indications for intubation?
Hypoxaemia despite O2 therapy
Impending airway obstruction for other reasons e.g. laryngeal fracture
Reduced GCS and not maintaining airway
Hypercapnoea/inadequate ventilation e.g. flail
Poor cough
Facilitate imaging
Protect spine in un-coperative patients
Anaesthesia considerations for ACDF surgery?
Haemodynamic instability
- Myelopathy patients may have Aut. involvement causing excessive hypotension risking spinal cord ischaemia
- Therefore art line pre-induction
Laryngoscopy
- Potential for impingement of cord, use VL and bougie
Airway
- Difficult access, reinforced ETT left side of mouth
Positioning
- Supine, head up for venous drainage
Post op considerations
- Haematoma
- Vocal cord palsy
- DIFFICULT re-intubation
What is within the posterior fossa
Most inferior to cranial fossae
Contains cerebellum, brainstem and lower cranial nerves
Comprised of
- Occipital bone postero-inferiorly
- Temporal bone anteriorly and laterally
- Sphenoid bone anteriorly and medially
Roof is tentorium cerebelli
Compact with poor compliance, small tumour = high ICP with risk of brainstem compression
What is within the posterior fossa
Most inferior to cranial fossae
Contains cerebellum, brainstem and lower cranial nerves
Comprised of
- Occipital bone postero-inferiorly
- Temporal bone anteriorly and laterally
- Sphenoid bone anteriorly and medially
Roof is tentorium cerebelli
Compact with poor compliance, small tumour = high ICP with risk of brainstem compression
What is an acoustic neuroma?
AKA vestibular schwannoma
Benign tumour of myelin-forming Schwann cells of vestibular nerve (8th)
Features:
Unilateral hearing loss, tinnitus, imbalance, unsteadiness, vertigo (VIII)
LARGE TUMOURS affect V and VII CN
Proximity to VII necessitates EMG monitoring
Posterior fossa “how to” pre-op
Usual anaesthetic assessment
+
Evaluation of cranial nerve dysfunction
Assessment for presence of raised ICP
Posterior fossa “how to” intra-op
Positioning - supine or park bench
Resus drugs drawn up
IV access secured on uppermost limb
Monitoring including art line awake if high ICP and EMG monitoring + BIS + temp + IDC
Airway = reinforced ETT
Drugs + Ex drawn up
Induction - smooth haemodynamically stable avoid CPP hypoperfusion and hypertension, high dose remi
Single dose muscle relaxant
Maintain with TIVA
Extubation smooth extubation no coughing/straining and ICP spikes
Issues specific to posterior fossa surgery
Intraoperative brainstem handling may cause cardiovascular instability, hypertension and bradycardia
Optimise physiology to maximise CPP
Avoid hypoxia
PaCO2 4.5-5.0
Temp control
Plasma glucose 4-11mmol/L
MAP >80
Obtund sympathetic response
V. emetogenic so antiemetics
What are the classic features of spinal epidural abscess and what other features may be present?
Classic triad
1. Back pain
2. Fever
3. Abnormal neurology
Other features
1. Nerve root pain
2. Motor weakness
3. Sensory deficit
4. Bowel/bladder dysfunction
4 Stages:
1. Back pain affected site
2. Nerve root pain radiating from affected area
3. Motor weakness, sensory deficit, bladder/bowel dysfunction
4. Paralysis
Causes of epidural abscess
90% Staph Aureus
Remainder strep and gram -ve anaerobes
AAGBI BEST EPIDURAL PRACTICE
Monitored by staff aware of significance and action required in response to abnormal values
Monitoring
- HR and BP
- RR
- Sedation score
- Temp
- Pain score
- Degree of motor and sensory block
What is required for venous air embolism to occur
- Source of gas
- Communication between this source and venous system
- Pressure gradient enabling movement of gas
1ml/kg rapidly embolised can be fatal
Signs of venous A.E
Depends on volume of air, rate of entrainment, patient awake/anaesthetised
Rapid entrainment
- Classic cardiovascular embolic phenomenon: tachy, hypotension, hypoxaemia
Neurological - confusion, focal signs, dec. GCS
ECG abnormalities
VAE pathophysiology
AIr lock
- Air in rv occupies it and prevents blood flow into pulmonary circulation
Inflammation in pulmonary arterioles
Small bubbles of air into RV and pulm. circ
Mico emboli in pulmonary arterioles
Paradoxical A.Emboli through patent FO may pass into arterial circ causing coronary or cerebral signs
Prevention of venous A.E
Avoiding sitting position - sitting craniotomy high risk
Raised venous pressure at operative site - iv fluid loading, +ve PEEP
Jugular venous compression has been reported
Minimising time venous circulation open to atmosphere
Minimising bubbles in IV lines
Immediate management of VAE
I would CONFIRM the reading
Send for HElp (may or may not do)
Whilst SCANNING the patient, surgical field, monitors and equipment
Alert SURGEONS and consider stopping surgery
Apply 100% oxygen, hand ventilate patient, CPR and ALS if cardiac arrest, giving vasopressor /fluid if hypotension
Specific measures include
- Surgeon to floor field with sterile saline and compress wound edges
- Raise venous pressure at operative site by increasing venous pressure, lowering below right atrium
-Consider aspirating air from right sided IJV cvc
What procedures are associated with VAE
Craniotomy
Radical neck dissection
Thyroidectomy
THR
C. section
Placenta removal
Anaesthetic
- CVC
- Blood products rapid infuser
What is myotonic dystrophy
A rare multisystem neuromuscular disorder characeterised by skeletal muscle myotonia, cardiac and respiratory sequelae
It poses specific risks to anaesthesia
Clinical features of myotonic dystrophy
Skeletal Muscle
- Myotonia (incomplete relaxation)
- Distal muscle weakness - reduced hand dexterity, foot drop
- Muscle wasting
Cardiac
- Conduction defects
- Cardiomyopathy
Resp
- Restrictive lung defect
- OSA
Neuro
- Intellectual impairment
GI
- Bulbar symptoms
- Aspiration risk
Endrocrine
-Testicular atrophy
- Insulin resistance
Facial features
- Frontal balding
- Wasting of facial muscles
Genetics of myotonic dystrophy
Chromosome 19
Trinucleoside repeat disorder
Autosomal dominant
4/100,000 incidence
Anaesthetic “how to” - myotonic dystrophy
Regional favoured over GA
Pre-op:
- MDT input
- R/v of notes - thorough hx/exam/ix
- Avoidance of premeds
Intra-op
- Monitoring - art line due to risk of conduction abnormality
- Access to external pacing
Induction
- RSI due to risk of aspiration
- Avoid sux –> masseter spasm, laryngospasm, hyperkalaemia
Maintanence
- Volatile or TIVA
Emergence
- Neostigmine may induce myotonia
- NM monitoring may induce myotonia
Post op
- Increased sensitivity to sedatives and analgesics
- HDU/ITU
What is NF1
Neurofibromatosis Type 1,
- Tumours are neurofibromas of peripheral nervous system
What is NF2
Neurofibromatosis Type 2,
- Tumours are neurofibromas of Schwann cells (bilateral vestibular schwannomas)
Complications of posterior fossa surgery
Complications specific to posterior fossa
- Emetogenic +++
- Lower CN palsies including loss of pharyngeal reflexes
- CV instability 2ndary to stimulation of pons/medulla
General complications of neurosurgery
- Hydrocephalus
- CSF leak –> pseudomeningocele
- CNS infection
- Pneumocephalus
Complications specific to positioning
- Sitting position - venous pooling and low CPP
- Venous air embolism
- Macroglossia
- Peripheral nerve injury e.g. brachial plexus, peroneal nerve (lateral / park bench)
Neurofibromatosis and anaesthesia
Airway
- Laryngoscope and intubation difficult by neurofibromas of tongue/pharynx/larynx
Resp
- Mediastinal neurofibromas compress/distort bronchial tree
- Kyphoscoliosis associated with neurofibromas = restrictive defect
CV
- HTN - renal artery stenosis/coarctation/phaechromocytomas
GU
- Difficult catheterisation
CNS
- Vertebral deformities/spinal tumours
- Epilepsy/LD
CNS
Cutaneous features of neurofibromas
Cafe-au-Lait spots
Axillary freckling
Lisch nodules
Doses of agents in status treatment
Pre-hospital
10-20mg diazepam PR
20mg midazolam buccal
IV agents:
Lorazepam
0.1mg/kg
Levitiracetam 60mg/kg over 15mins. Max 4500mg
Phenytoin 15-18mg/kg
Sodium Valproate 40mg/kg. Max 3000mg
Phenobarbital 10-15mg/kg
Definition of status epilepticus
Medical emergency traditionally defined as more than 30 minutes of continuous seizure activity
2015 new definition recognised importance of early treatment which is failure to terminate seizure after 5 minutes
Physiological changes associated with seizure
Compensatory and non-compensatory stage (>30-60mins post activity)
Initial compensatory stage:
- Sig. increase in CMRO2
- Catecholamine release increases CO (tachycardia, hypertension)
- Consequent increase in cerebral blood flow / ICP
- Limb movements generate lactate
Decompensation stage:
- Failure of cerebral autoregulation and failure of increased CO to sustain neuronal activity
- Neuronal ischaemia and death
- Cerebral oedema, raised ICP
Sustained muscle contraction
= Rhabdo, Hyperkalaemia, Acidosis
What anaesthetic drugs caution with in epilepsy
Etomidate use associated with post-op seizures
Alfentanil increases EEG activity
Pethidine risks of seizures
Antiemetics - extrapyramidal side-effects of dopamine antagonists confused with seizure activity (prochlorperazine, metoclopramide, droperidol)