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FRCA CRQs > Neuro > Flashcards

Neuro Flashcards

1
Q

What is the normal range for intracranial pressure in adults and children

A

Adults:
10-15mmHg

  • tissue damage tends to occur >20mmHg
  • start treatment >22mmHg in TBI

Children
5-15mmHg

Infants
3-4mmHg

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2
Q

Describe the normal appearance of the intracranial pressure waveform

A

Triphasic:
P1: percussion wave - represents arterial pulse
P2: tidal wave - represents cerebral compliance
P3: dicrotic wave - represents aortic valve closure

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3
Q

State the equation of cerebral perfusion pressure

A

CPP=MAP-ICP

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4
Q

Symptoms of raised ICP

A
  • Headache worse on bending/coughing/lying flat/straining
  • Vomiting
  • Blurred vision
  • Diplopia
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5
Q

Signs of raised ICP

A
  • Papilloedema
  • Seizures
  • Cushing’s reflex (bradycardia and hypertension)
  • Decreased consciousness level
  • Irregular respiration
  • Fixed dilated pupils
  • Hemiparesis
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6
Q

List invasive monitoring methods of intracranial pressure in a patient with traumatic brain injury

A

Intraventricular catheter (external ventricular drain) - can be used to therapeutically drain
Transducer pressure monitoring in subdural, intraparenchymal, subarachnoid or epidural space - cannot be recalibrated once sited

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7
Q

List management of traumatic brain injury in an ED of a non-neurosurgical centre

A
  • Intubate if GCS≤8, irregular breathing, inadequate gas exchange, loss of laryngeal reflexes, spontaneous hyperventilation
  • Avoid hypoxia, aim pO2 >13kPa
  • Normocarbia, aim pCO2 4.5-5.0 kPa
  • Muscle paralysis if required to aid ventilation
  • Avoid PEEP>12cmH2O
  • Avoid hypotension, aim MAP>80 using non hypotonic fluids, blood or vasopressors if required - aim cerebral perfusion pressure 50-70mmHg
  • Normothermia
  • Avoid hyperglycamia, aim glucose < 10mmol/L
  • Aid cerebral venous drainage with head-up 30-45 degrees, avoid tube ties, head in midline
  • Treat seizures
  • Adequate sedation
  • Discuss with neurosurgical unit to facilitate early transfer
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8
Q

Give temporising measures that can be used to treat acute rises in ICP whilst preparing for definitive neurosurgical intervention

A

Mannitol 0.25-1g/kg
3% Hypertonic saline 2ml/kg
Hyperventilate to PaCO2 4-4.5kPa

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9
Q

Production and flow of CSF

A

Produced by ependymal cells of choroid plexus

Flows from lateral ventricles to:
- Foramina of Munro
- Third ventricle
- Aqueduct of Sylvius
- Fourth ventricle then
- Foramen of Luschka and Magendie
- Subarachnoid space

Absorbed by arachnoid granulations in the superior sagittal sinus.

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10
Q

Roles of CSF

A
  • Buoyancy (reduces effective weight of brain)
  • Shock absorption
  • Acid-base buffer
  • Clears waste
  • Compensates for raised ICP through displacement to spinal canal
  • Provides constant chemical and ionic environment for neurons
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11
Q

How to set up EVD

A
  • Set zero level to external auditory meatus (if supine and head in neutral position)–> same level as foramina of Munro
  • Set the drainage level by moving the drip chamber to align with the given setting e.g. 15cmH2O
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12
Q

Complications of EVDs

A
  • Intracranial haemorrhage
  • Infection
  • Seizure
  • EVD becomes locked/displaced/suboptimal placement
  • Excessive CSF drainage leading to ventricular collapse or subdural haemorrhage
  • Failure of EVD to control hydrocephalus
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13
Q

List the neurological changes that occur immediately after transection of the spinal cord at T4

Sensory,motor, autonomic

A

Sensory: complete loss of sensation below level of nipples. Sensory loss can be from higher dermatomes if secondary injury is present

Motor: flaccid paralysis and arreflexia affecting the lower intercostals, trunk and lower limbs

Autonomic: neurogenic shock due to interrupted sympathetic pathways and unopposed parasympathetic activity, if secondary injury is present affecting T1-T4, bradycardia and reduced myocardial contractility can also occur. Loss of temperature control (anhidrosis, cutaneous dilatation). Loss of bladder and bowel function. Occasionally priapism can occur.

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14
Q

List the neurological changes that occur 3 months after transection of the spinal cord at T4

Sensory, motor, autonomic

A

Sensory: Ongoing sensory loss below lesion (and can extend slightly higher than lesion if secondary injury present). Neuropathic pain below lesion can occur. Nociceptive pain below the lesion can occur due to change in musculoskeletal function e.g. spasms, contractures.

Motor: Spastic paralysis with hyper-reflexia below level of lesion. May have paralysis from higher up if secondary injury.

Autonomic: Autonomic dysreflexia (takes up to a year to develop). Non-noxious stimuli below level of lesion causes disproportionate sympathetic response (vasoconstriction) and can lead to hypertensive crisis. Rising blood pressure stimulates parasympathetic system above the lesion, leading to bradycardia and vasodilation but this is often not sufficient to prevent hypertension. In some cases, bowel, bladder and coital function may return.

Hypertensive crisis: flushing, retinal haemorrhages, headache, nasal congestion, stroke, coma

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15
Q

Where does the sympathetic chain originate?

A

T1-L3

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16
Q

Where do the parasympathetic nerve fibres originate?

A

CN 3, 7, 9, 10
S2-4

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17
Q

List the ventilatory changes associated with transection of the spinal cord at T4

A
  1. Innervation to lower intercostals is lost, impaired expansion of chest wall and reduced vital capacity
  2. Worse ventilation in sitting position - abdominal contents pull diaphragm down increasing residual volume and dead space - causes VQ mismatch and atelectasis
  3. Loss of abdominal muscle contraction - weak forced expiration, impaired cough with retained secretions
  4. Loss of abdominal wall muscle tone results in inefficient ventilation - as the diaphragm contracts, abdominal contents are pushed down and out, chest wall is pulled in
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18
Q

List the gastrointestinal complications of spinal cord injury

A
  1. Reduced GI motility, delayed gastric empyting, paralytic ileus, constipation and pseudoobstruction
  2. Increased risk of gallstones (altered motility of GI structures, also found altered bile lipids)
  3. Prone to stress ulceration (unopposed vagal activity, increased gastric acid production)
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19
Q

Why are patients with recent spinal cord injury at increased risk of VTE?

A
  1. Immobility of lower limbs causing venous stasis
  2. Inability to detect limb changes associated with DVT so late diagnosis
  3. Thrombogenic effects of the stress reponse of trauma
  4. Inflammatory response of trauma
  5. Increased use of central venous lines
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20
Q

Why is poor body temperature regulation associated with spinal cord injury?

A

Vasodilation and anhyidrosis and inability to shiver below level of lesion
Loss of sensation to hot or cold below level of lesion and reduced movement - less able to behaviourally compensate
Decreased muscle bulk and reduced metabolic rate

Sometimes - hyperhydrosis above level of lesion

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21
Q

List four advantages of regional anaesthetic for cystoscopy in a patient with previous spinal cord injury

A
  1. Reduced risk of autonomic dysrefflexia
  2. Avoids need for intubation (patient may have had previous tracheostomy with sequelae e.g. tracheal stenosis)
  3. Avoids deterioration in lung function associated with GA, so reduced risk of post-operative respiratory complications
  4. Avoids systemic opiods associated with respiratory depression in patient with compromised respiratory function
  5. Reduces risk of aspiration associated with delayed gastric emptying
  6. Avoids unopposed parasympathetic response to airway instrumentation - causing bradycardia and cardiac arrest
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22
Q

Why and when is suxamethonium contraindicated in spinal cord injury?

A
  • Upregulation of nicotinic acetylcholine receptors at extrajunctional sites, leads to massive potassium release with use of suxamethonium
  • Seen from 48hrs-6months following injury
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23
Q

What are the causes of acromegaly?

A

Primary: hypersecretion of growth hormone from a pituitary adenoma
Ectopic: lymphoma/pancreatic islet cell tumour secretion of GH
Iatrogenic
Secondary: GHRH excess e.g. from hypothalamic tumours, lung tumours

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24
Q

Where is the pituitary gland located?

A

In the sella turcica, which is part of the sphenoid bone

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25
Q

State the visual impairment characteristically associated with large pituitary tumours

A

Bitemporal hemianopia

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26
Q

Describe the blood supply to the pituitary gland

A

Arterial: supplied by internal carotid artery via the hypophyseal and inferior hypophysial arteries into a plexus. Portal circulation connects dural venous sinuses and hypothalamus.
Venous: drainage into cavernous and petrosal sinuses

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27
Q

List the hormones secreted by the pituitary system and their function

A

Anterior (secretion is stimulated by hormones from the hypothalamus):
* GH - anabolic effect on bone and muscle, impairs sensitivity to insulin
* TSH - stimulates thyroid gland to release thyroxine
* LH/FSH - testes to produce testosterone and sperm, ovaries to produce eggs and oestrogen
* ACTH - stimulates adrenal glands to secrete glucocorticoids and aldosterone
* Prolactin - stimulates mamary glands to produce milk
* Melanocyte secreting hormone (MSH) - skin pigmentation

Posterior (synthesised in hypothalamus, travel to pituitary where secreted):
* Oxytocin - uterine contractions during labour
* ADH/vasopressin - regulates water excreted by the kidneys (increases aquaporins in DCT and CDs to increase water reabsorption)

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28
Q

List the features of acromegaly which are of relevance to anaesthesia

A

Airway: macroglossia, macrognathia, thickening of pharyngeal tissues, laryngeal stenosis
Breathing: OSA with risk of hypoventilation and respiratory failure post-operatively
Circulation: Hypertension, eccentric LVH, cardiomyopathy with diastolic dysfunction, valve regurgitation, heart block
Disability: raised ICP if 3rd ventricle obstructed, spinal cord compression, peripheral neuropathies due to soft tissue/bony overgrowth nerve impingement
Endocrine: diabetes
GI: increased risk of colonic polyps and cancer
Joints: osteoarthritis, bony overgrowth around joints, limited movement (Care with positioning and padding)
Kidneys: renal dysfunction

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29
Q

How do the surgical requirements for a trans-sphenoidal hypophysectomy influence the conduct of anaesthesia?

A
  1. Use of operating microscope: minimise bleeding by avoiding surges in blood pressure and preparation of nasal mucosa e.g. with Moffat’s solution
  2. Periods of intense stimulation and minimal stimulation: invasive arterial monitoring, use of remifentanil for management of intense stimulation
  3. Supine with head-up tilt: potential for venous air embolism, ensure adequate venous filling
  4. Operation on head: reinforced tube, eye protection, tube well secured, nerve stimulator on leg, long circuit and long lines for fluids/TIVA
  5. Risk of bleeding from internal carotid artery or cavernous sinus: group+save, throat pack, cuffed endotracheal tube to protect from soiling
  6. Rapid emergence required to assess neurology as soon as possible: use of reversible or short acting anaesthetic agents
  7. Suprasellar portion of tumour may need pushing into surgical field: lumbar drain with injection of saline
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30
Q

State the complications of trans-sphenoidal hypophysectomy

A
  1. Surgical damage to CN III, IV, V, VI, optic chiasm
  2. Major haemorrhage
  3. Stroke (vasospasm or embolism)
  4. Persistent CSF rhinorrhoea, meningitis
  5. Diabetes insipidus, SIADH, Pan-hypopituitarism - may require steroid replacement with weaning regimen
  6. Pituitary apoplexy
  7. Venous air embolism
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31
Q

List the positions that might be employed for posterior fossa surgery

A
  1. Sitting
  2. Prone (if midline)
  3. Lateral (if lateral)
  4. Park bench
  5. Supine with head turned (if lateral)
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32
Q

List the complications of sitting position

A
  1. Jugular venous obstruction due to flexed neck - airway oedema
  2. Endotracheal tube displacement
  3. Venous air embolism
  4. Hypotension due to reduced venous return/venous pooling in dependent areas
  5. Cord/brainstem ischaemia due to head flexion and hypotension
  6. Sciatic/femoral nerve damage from excessive hip flexion and lower limb oedema
  7. Pneumocephalus
  8. Lumbosacral pressure damage
  9. Compartment syndrome
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33
Q

Give the abnormalities you would see on routine monitoring as a consequence of VAE

A
  1. Drop in SpO2
  2. Decrease in etCO2
  3. ST segment depression on ECG
  4. Tachyarrythmia
  5. Hypotension
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34
Q

Which monitoring techniques can specifically detect VAE

A
  1. Precordial doppler: sound heard if air in cardiac chambers (most sensitive)
  2. Transoesophageal echocardiography: air seen in right sided cardiac chambers (cannot be used in long operations where head is flexed)
  3. Pulmonary artery/right atrial pressure: will rise with sicnificant air embolus and related ventricular outlow tract obstruction
  4. Oesophageal stethoscope: mill wheel murmur
  5. End-tidal nitrogen level: will rise
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35
Q

List the steps in the immediate managment of VAE

A
  1. Call for help
  2. Ask surgeon to flood site with saline and cover with wet packs
  3. Administer fluids
  4. Lower head of patient so that surgical site is below right atrium
  5. Apply sustained positive airway pressure until head is below right atrium
  6. Administer 100% O2, stop nitrous oxide if being used
  7. Aspirate air from right atrium via CVC if present
  8. Left lateral or Trendelenburg may help force bubble above right ventricular outflow
  9. If cardiac arrest, start chest compressions (may assist bubble dispersion)
  10. Inotropes if required
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36
Q

What are the consequences of continuing antiplatelets perioperatively for stereotactic brain biopsy?

A
  1. Significant extracranial bleeding
  2. Intraparenchymal haemorrhage with limited access to control the source
  3. Haematoma development with pressure on brain resulting in raised intracranial pressure or specific neurological deficits
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37
Q

What are the consequences of stopping DAPT for cardiac stent perioperatively for stereotactic brain biopsy

A
  1. Stent thrombosis and subsequent mortality
  2. Myocardial infarction or ischaemia
  3. Rebound increase in tendency to thrombosis
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38
Q

List patient factors which increase the risk of ischaemic event following premature cessation of DAPT for cardiac stent

A
  • Cigarette smoking
  • Diabetes
  • Congestive heart failure or LVEF<30%
  • PCI six months prior to stent insertion
  • Previous MI
  • Stent insertion for acute MI
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39
Q

Give three ways to mitigate risk if decision is made to stop DAPT to facilitate stereotactic brain biopsy

A
  1. Perform brain biopsy in a centre with 24-hour interventional cardiology
  2. Consider bridging with a short acting GP IIb/IIIa inhibitor e.g. tirofiban
  3. Consider bridging with a reversible P2Y12 receptor antagonist cangrelor
  4. Consider continuing aspirin if low risk of bleeding and high risk of stent thrombosis
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40
Q

List contraindications to stereotactic brain biopsy under sedation

A
  1. Patient unable to comply with instructions e.g. learning disability, dementia, poor hearing
  2. Patient refusal
  3. Inability to lie still e.g. cough, movement disorder
  4. Inability to lie flat
  5. Significant sleep apnoea
  6. Difficult airway
  7. Patient anxiety/claustrophobia
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41
Q

Define primary brain injury in TBI and explain the pathology involved

A

Definition: injury that occurs due to the initial insult, severity depends on nature, intensity and duration of impact

Pathology:
* Macroscopically: can involve fracture, contusion, haematoma, cerebral oedema, diffuse brain injury
* Microscopically: cell wall disruption, increased membrane permeability–> disruption of ionic haemostasis

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42
Q

What is secondary brain injury and when does it occur after TBI?

A

Secondary brain injury is further tissue damage after primary injury which occurs in the hours to days following trauma. It can be mediated by oedema, tissue hypoxia, excitotoxicity or metabolic dysfunction. Systemic instability can lead to further damage through cerebral hypoperfusion and hypoxia.

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43
Q

Outline the physiological and cellular changes associated with secondary brain injury

A
  • Secondary brain injury is continuation of damage to the brain resulting from events initiating from primary injury
  • Primary injury leads to widespread depolarisation which:
    * Triggers potassium to leave cells and water and sodium to influx: oedema
    * Aerobic metabolism is overwhelmed and anaerobic metabolism occurs: lactic acidosis and mitochondrial dysfunction, loss of autoregulation, further oedema
    * Large concentrations of neurotransmitters released: glutamate excitotoxicity, oxidative stress, apoptosis
    * Free radicals and nitrous oxide produced: cell damage through oxidative stress
    * Further rise in ICP due to oedema, haemorrhage and seizure leads to reduced CPP and ischaemia
    * Leads to programmed cell death
  • Processes involved in secondary injury= excitotoxicity, oedema, oxidative stress and inflammation, ischaemia and mitochondrial dysfunction, programmed cell death
  • Memory aid: AEIOU
    InflammAtion/oxidative stress
    Excitotoxicity (glutamate -> oxidative stress+ apoptosis)
    Ischaemia
    Oedema
    Unalive

Contributors to secondary brain injury: hypotension, hypoxia, hypercarbia

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44
Q

What is acromegaly?

A

An endocrine condition that results from excessive growth hormone secretion after the growth plates have fused.

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45
Q

How may acromegaly present?

A

Headaches
Bitemporal hemianopia
Cranial nerve palsies
Hydrocephalus (signs and symptoms of raised intracranial pressure) due to third ventricle outflow obstruction
Cushing’s disease (if hypersecretory)
Hyperpituitarism
Hypopituitarism due to apoplexy, internal haemorrhage of the adenoma or inadequate blood supply causing tissue necrosis and swelling

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46
Q

What is Guillain-Barre syndrome?

A

Acute ascending deymelinating poluneuropathy which affects pre-junctional sensory, motor and autonomic nerves. It is immune mediated.

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47
Q

What is the underlying pathology of GBS?

A
  1. Autoantibody damage to the myeline sheath (or less commonly, the axon)
48
Q

List triggers for GBS

A

GI infections e.g. campylobacter
Respiratory infections e.g. influenza, COVID-19, Zika, CMV, EBV, HIV, protozoal
Vaccination

49
Q

List the clinical features of GBS

A
  • Acute onset of symptoms and signs with variable recovery
  • Motor: ascending symmetrical weakness which is flaccid and arreflexic. Can ascend to respiratory muscles (resp failure) and facial nerve (bulbar weakness, opthalmoplegia)
  • Sensory: ascending sensory impairment associated with pain and paraesthesia
  • Autonomic: arrythmias, labile BP, urinary retention, ileus, hyperhydrosis
  • Miller Fisher variant: ataxia, arreflexia, opthalmoplegia +/- respiratory and limb weakness
50
Q

How is GBS diagnosed?

A
  • Antiganlioside antibodies esp if axonal GBS
  • MRI spine: selective anterior spinal root enhancement with gadolinium
  • Lumbar puncture: normal cell count, normal glucose, elevated protein
  • Nerve conduction studies: depends on subtype - majority show demyelinating pattern (reduction in conduction velocity), some show axonal loss (reduction in compound axon potential size)
51
Q

List the anaesthetic considerations for a patient recovering from GBS

A

Airway: may have tracheostomy if requiring ventilatory support or help with secretion clearance. Bulbar weakness, poor cough and risk of aspiration

Breathing: Increased risk of post-operative respiratory adverse events due to poor ventilatory function and risk of aspiration. Reduced ventilatory capacity, may require NIV/IV post-operatively

Circulation: autonomic instability with labile BP, risk of arrhthmia. Would use invasive monitoring including cardiac output monitoring to guide fluid administration. IV access may be tricky as likely prolonged illness with multiple previous lines.

Disability: Commonly suffer from neuropathic pain, may require pain team review

F-Pharmacology: Suxamethonium is contraindicated due to risk of hyper-K from extrajunctional nAChR. Increased sensitivity and prolonged duration of NMB. Increased respiratory depressant effect of opiates.

Haem: risk of DVT due to prolonged immobility

Joints: prolonged illness - may be associated with weight loss, care with positioning and padding

52
Q

What specific treatments are available for GBS

A

IVIG - intravenous immunoglobulin
Plasma exchange

53
Q

Which imaging modality is recommended by NICE to diagnose acute stroke?

A

Non contrast CT head within 24hrs of symptom onset
(ideally within 20 minutes in stroke centre, max 60 minutes)

CT contrast angiography then recommended if thrombectomy might be indicated
CT perfusion imaging or MR equivalent if thrombectomy may be indicated beyond 6 hours of onset

54
Q

List the treatment options for acute thrombotic ischaemic stroke

A
  1. Thrombolysis - alteplase within 4.5hours of stroke onset
  2. Thrombectomy - anterior circulation stroke, thrombectomy within 6 hours of symptoms (or longer if perfusion imaging suggests substantial salvageable brain tissue), thrombolysis not worked or contraindicated, significant disability NIHSS>5, previously independent mRS< 3, proximal vessel occlusion e.g. internal carotid/ M1-2, no new ischaemic changes
  3. Antiplatelets
  4. Anticoagulants - due to cerebral venous thrombosis (heparin +warfarin)
  5. Carotid endarterectomy - stable neurological symptoms from acute non-disabling stroke and 50-99% carotid artery stenosis on doppler
55
Q

What is the potential consequence of severe hypertension in acute ischaemic stroke?

A

Haemorrhagic transformation

56
Q

What blood pressure should you target if thrombolysis is being considered?

A

Systolic< 185mmHg
Diastolic <110mmHg

Thrombectomy: 140-180 systolic

57
Q

A patient has a large hemispheric infarction following stroke. Outline ongoing management following admission to critical care.

A
  1. Intubation if GCS≤8, failure to maintain acceptable oxygenation or bulbar dysfunction
  2. Target pO2>13kPa, target pCO2 4.5-5.0kPa
  3. Invasive blood pressure monitoring, maintaining MAP >85mmHg
  4. Maintain BP <185/110mmHg for first 24 hours if thrombolysis or thrombectomy or <220mmHg systolic in patients who are ineligible for thrombolysis or thrombectomy
  5. Facilitate venous drainage: 30 degree head tilt, avoid tube ties, avoid PEEP >12mmHg or high mean airway pressures, use of NMB agents if coughing
  6. Treat seizures
  7. Maintain BM 4-11mmol/L
  8. Treat pyrexia
  9. Consider ICP monitoring, targeting <20mmHg to help ensure CPP >60mmHg
  10. Sedation to reduce CMRO2
  11. Osmotherapy ( 0.5-2g/kg mannitol, 2ml/kg 3% saline) if cerebral oedema or risk of impending herniation
  12. Consider decompressive hemicraniectomy in patients under 60 years with significant GCS drop, large infarct or evolving cerebral oedema
  13. Serial assessments of neurology via sedation holds, guided by ICP monitoring and clinical condition
  14. Commence aspirin once satisfied haemorrhagic transformation has not occured
  15. General measures PPI, NG feed, VTE prophylaxis with intermittent pneumatic compression devices
58
Q

Presenting features of subarachnoid haemorrhage

A

Thunderclap headache - sudden onset, occipital, severe
Signs of meningism e.g. headache, vomiting, neck stiffness, photophobia
Reducing consciousness
Focal neurology
Seizures
Cardiac arrest
Signs of obstructive hydrocephalus e.g. papilloedema, high pressure headache, vomiting

59
Q

List congenital conditions associated with increased risk of subarachnoid aneurysm development

A

Ehlers-Danlos 4
Marfan’s Syndrome
Pseudoxanthoma Elasticum
Autosomal dominant polycystic kidney disease
Hereditary haemorrhagic Telangectasia
Arterviovenous malformations
Familial intracerebral aneurysm disease

60
Q

List non congenital risk factors for subarachnoid bleeding

A

Poorly controlled hypertension
Cigarette smoking
Cocaine use
Atherosclerosis
Trauma
ETOH excess
Increasing size of existing aneurysm

61
Q

List the imaging modalities used in diagnosis of subarachnoid haemorrhage

A

Non contrast CT brain (if negative, can use LP looking for xanthochromia, RBC and bilirubin)
CT angiogram
Digital subtraction angiography
MRI brain

62
Q

What range of blood pressure should you target in patients presenting with subarachnoid haemorrhage?

A

Systolic 110-160 mmHg, MAP>80mmHg

63
Q

Describe the World Federation of Neurosurgeons Scale

A

Grade 1: GCS 15
Grade 2: GCS 13-14 without motor deficit
Grade 3: GCS 13-14 with motor deficit
Grade 4: GCS 7-12
Grade 5: GCS <7

64
Q

List neurological complications following acute subarachnoid haemorrhage

A
  1. Rebleeding and further brain injury
  2. Hydrocephalus
  3. Seizures
  4. Delayed cerebral ischaemia/vasopasm
  5. Cerebral oedema
  6. Death according to neurological criteria
  7. Cognitive impairment

Non neuro: electrolyte derangement, cardiomyopathy, pulmonary oedema

65
Q

List the specific complications associated with endovascular coiling following subarachnoid haemorrhage

A
  1. Complications at vascular access site: haemorrhage, infection, pseudoaneurysm
  2. Intracranial vessel injury
  3. Aneurysm rupture
  4. Cerebral vascular occlusion due to thrombus, embolus, vasospasm or misplaced catheter/coil
  5. Failure to adequately coil the aneurysm
66
Q

List two indications for ICP monitoring following TBI

A
  1. GCS≤8 and abnormal CT brain
  2. Severe TBI, normal CT brain but two or more from:
    a) Age >40 years
    b) Motor posturing
    c) SBP <90mmHg
67
Q

What is jugular venous oxygen saturation used as a surrogate for?

A

Cerebral oxygenation
Cerebral blood flow

68
Q

Where is a catheter for jugular venous oxygen saturation monitoring placed?

A

Inserted in retrograde fashion into the internal jugular vein, to sit in the jugular bulb on the dominant side
(dominant side is ascertained by compressing the IJV on either side to see which increases ICP to the greater extent)

If malpositioned, extracranial blood will mix in and give error

69
Q

What does high jugular venous oxygen saturation represent?

A
  • Reduced oxygen consumption from coma, hypothermia, cerebral infarction
  • Increased oxygen delivery from hypercapnoea or vasodilation

Normal values are between 55-75%

70
Q

What does low jugular venous saturation represent?

A
  • Increased oxygen consumption due to seizures or pyrexia
  • Reduced oxygen delivery due to raised ICP, cerebral ischaemia, hypoxia

Normal values are between 55-75%

71
Q

Describe the arterial supply to the spinal cord

A
  • Anterior spinal artery formed by union of two vertebral arteries at foramen magnum, supplies 2/3 of cord (spinothalamic and corticospinal tracts)
  • Two posterior spinal arteries formed from vertebral arteries or posterior inferior cerebellar arteries, supply the posterior 1/3 of cord (dorsal columns)
  • Segmental arterial supply with numerous paired branches perfusing the spinal cord along its length from vertebral, deep cervical, intercostal, aortic and pelvic vessels. Artery of Adamkiewicz is the biggest segmental artery and forms major supply to lumbosacral spinal cord arising from T8-L4 (typically T12-L1) and originates from intercostal or lumbar artery.
72
Q

Give the forms of neurophysiological monitoring that may be used during spine surgery

A
  • Somatosensory evoked potential - peripheral sensory nerves are stimulated and electrodes placed on scalp to record cortical response - tests integrity of dorsal column and spinothalamic tracts
  • Motor evoked potential - motor cortex is stimulated and electrodes on peripheral muscles record impulses - mainly tests corticospinal tract. Risks include biting, tongue damage, scalp burns and seizures
  • Electromyography - need electrodes placed into specific muscle groups to detect irritation or damage of a particular nerve - complete transection results in loss of signal
  • EEG - topical scalp electrodes, give information about depth of anaesthesia and cerebral blood flow

Spinal cord ischaemia commonly causes reduced amplitude and increased latency of evoked potentials

73
Q

How might anaesthetic technique need to be altered if neurophysiological monitoring is being used?

A
  • Volatiles reduce amplitude of MEPs, TIVA is normally used
  • NMB results in loss of MEP and EMG signal and should be avoided or reversed
  • Alpha-2 agonists may reduced MEPs
  • Ketamine can increase the amplitude of MEP and SSEP and may be used to enhance low amplitude or poorly defined MEPs
74
Q

Give the physiological approaches to minimise risk of neurolgical injury during cervical spine surgery

A
  • Optimal ventilation to avoid hypoxia and hypercapnoea
  • Maintenance of MAP to ensure spinal cord perfusion pressure
  • Replacement of any significant blood loss
  • Maintainance of normothermia
  • Maintenance of normal acid-base status
75
Q

Give the surgical complications of cervical spine surgery

A
  • Spinal cord or nerve root injury due to direct injury, haematoma or metalwork migration
  • Bleeding or haematoma around airway resulting in post-operative airway compromise
  • Infection leading to discitis, meningitis or cerebral abscess
  • Dural tear or CSF leak
  • Damage to local structures - anterior approach: oesophagus, trachea, vertebral + carotid arteries, recurrent laryngeal + hypoglossal nerves, sympathetic chain. Posterior approach: damage to vertebral arteries
76
Q

State potential complications of general anaesthesia in the prone position

A

Airway: airway oedema, potential for tube dislodgement
Breathing: If large abdomen, compression of this by Montreal mattress can lead to impaired chest expansion and ventilation
Circulation: Compression of abdomen can reduce flow through IVC and so venous return to heart, loss of IABP/PVC access when proning
Disability: abnormal neck flexion/extension impairs cerebral venous drainage, risk of pressure to the eyes resulting in retinal artery occlusion, corneal abrasion and optic ischaemia
Gastrointestinal: increased intra-abdominal pressure can result in gastric acid reflux with oral and eye irritation
Joints: risk of pressure to nerves - neuropraxia, joints - myalgia, skin - pressure sores
Facial swelling, bruising and pressure injuries

77
Q

Give the indications for awake craniotomy

A
  • Tumour excision from eloquent cortex
  • Epilepsy surgery
  • Deep brain stimulation surgery
  • Resection of vascular lesions from vessels supplying functionally important areas of the brain
78
Q

Give the contraindications to awake craniotomy

A
  • Patient refusal
  • Inability for patient to comply e.g. confusion, dementia, learning difficulties, anxiety
  • Inability to lie flat
  • Inability to lie still e.g. movement disorders, cough

Relative
* OSA
* Anticipated difficult airway
* Language barrier
* Epilepsy
* Young age
* Morbid obesity

Surgical:
* Highly vascular lesions
* Significant dural involvement (painful)
* Low occipital lobe lesions (may be unable to tolerate positioning for surgical access)

79
Q

What anaesthetic techniques can be used for awake craniotomy?

A
  • Awake throughout - local anaesthesia with sedation
  • Asleep-awake-awake (+/- sedation)
  • Asleep-awake-asleep
80
Q

Give the advantages and disadvantages of using dexmedetomidine for sedation as part of an awake craniotomy technique

A

Advantages:
* Analgesic properties
* Minimal respiratory depression
* Minimal effects on ICP
* Sedative and axiolytic properties
* Minimal effect on interictal epileptiform activities

Disadvantages:
* Bradycardia and hypotension
* Cost
* User unfamiliarity

81
Q

An intraoperative seizure occurs. What immediate management should take place?

A
  • Surgeons to irrigate the field with ice-cold saline
  • Declare emergency, ask surgeons to stop, call for help
  • A-E assessment and aplication of 100% oxygen
  • Airway management with iGel
  • Antiepileptic drugs:
    Propofol 10-30mg titrated to effect
    Midazolam 0.1mg/kg approximately, 2-5mg titrated to effect
    Thiopentone 25-50mg titrated to effect
82
Q

What are the effects of using drugs to terminate seizures for the ongoing surgery

A
  • Significant sedation may require a secured airway, delaying or compromising the awake phase of surgery and potentially leading to delayed wake-up post-operatively
  • Interference with neurophysiological monitoring
    Thiopentone activates interictal epileptiform activity
    Benzodiazepines suppress interictal epiletiform activity
    Propofol has a variable effect
83
Q

List the intraoperative complications of awake craniotomy

A
  • Airway obstruction or apnoea due to sedation with restricted access to airway
  • Hypoventilation due to sedation causing hypoxia and hypercapnoea (poor surgical conditions due to cerebral oedema)
  • Aspiration
  • Sitting position - hypotension due to venous pooling
  • Patient intolerance of procedure due to pain, catheter irritation
  • Seizures
  • Venous air embolism
84
Q

Which structures are contained within the posterior fossa

A
  • Brainstem
  • Cerebellum
  • Cranial nerves 6/7-12
  • Aqueduct of Slyvius
  • Vertebral arteries
  • Basilar arteries
  • Venous sinuses (sigmoid, transverse and occipital)
85
Q

Which neurological features would you assess prior to posterior fossa surgery in the sitting position?

A
  • Cerebellar function: co-ordination, posture, gait
  • Cranial nerve function: bulbar weakness (can lead to loss of airway protection and need for postoperative intubation)
  • Raised intracranial pressure: reduced consciousness, headache, vomiting
86
Q

What are the contraindications to sitting position for craniotomy?

A

Ventriculo-atrial shunt: shunt blockage could occur in VAE leading to raised ICP
Right-to-left heart shunt: VAE passing to left side could lead to stroke

87
Q

How could you minimise the risk of venous air embolus in the sitting position?

A
  1. Ensure optimal venous filling
  2. Surgeons to minimise open veins
  3. Trendelenburg tilt or leg elevation
88
Q

Give the FVC and maximum expiratory pressure values that would warrant consideration of intubation in a patient with GBS

A

FVC: 20ml/kg
Maximum inspiratory pressure: <30cmH20
Maximum expiratory pressure: <40cmH20

20, 30, 40 rule

89
Q

What is the normal adult volume of CSF?

A

150ml

90
Q

Where is CSF absorbed?

A

Via subarachnoid granulations/arachnoid villi to the cranial venous sinuses

91
Q

What are the causes of hydrocephalus?

A

Congenital:
Communicating: achondroplasia, craniofacial abnormalities associated with syndromes
Non communicating: aqueduct stenosis, chiari malformations, Dandy-Walker malformation

Non-congenital:
Communicating: subarachnoid haemorrhage, choroid plexus papilloma, intracerebral infarction
Non communicating: intracerebral tumour, post-inflammatory adhesions, cerebellar haematoma/infarct

92
Q

Give the clinical features of acute hydrocephalus

A

Headaches
Vomiting
Reduced consciousness level
Seizures
Diplopia, opthalmoplegia
Bulging fontanelle in infants

93
Q

Describe how you would zero an EVD

A
  1. Ensure zero mark is level with external auditory meatus with patient in supine position, head neutral (this is equivalent to the foramen of Monro)
  2. CSF collection chamber is positioned relative to the pressure scale depending on desired ICP
  3. System must be rezeroed if pressure changes
94
Q

List specific anaesthetic considerations for a patient with indwelling ventricular shunt for hydrocephalus presenting for general surgery

A
  • Assess for signs of raised ICP before and after surgery
  • Consider transfer to neruosurgical centre if VP shunt with significant abdominal infection
  • Care with regional anaesthesia for upper limb surgery - shunt may be tunnelled behind posterior border of sternocleidomastoid
  • Care with positioning to prevent external pressure on tunnelled part of shunt
  • Minimisation of duration and pressure of laparoscopic surgery, visualisation by surgeon at the end of procedure that tip of shunt is still draining
  • Avoidance of internal jugular avvess
  • IPPV can cause blockage of ventriculo-pleural shunts (consider this if slow to wake up patient) - also avoid LRTI with postoperative physio and incentive spirometry
95
Q

At what level of spinal cord injury is autonomic dysreflexia more common and why?

A
  • above T6
  • splanchic vasoconstriction at these levels which makes a major contribution to hypertension
96
Q

Cardiovascular effects of autonomic dysreflexia

A

Hypertensive crisis (can lead to myocardial ischaemia, arrhthmia, heart failure, stroke)
Bradycardia

97
Q

List the effects of autonomic dysreflexia

A

Headaches
Cerebral oedema, reduced GCS
Retinal haemorrhage
Cerebral haemorrhage
Seizures
Death
Flushing
Nasal congestion
Sweating
Piloerection
Pallor

98
Q

List common triggers for the development of acute autonomic dysreflexia

A

Urinary retention (blocked urinary catheter)
Constipation

Also:
Pressure ulcers
Uterine contractions
Sexual activity
Acute abdominal pathology
Skeletal fractures

99
Q

List conditions that must be met for surgery to take place without anaesthesia in spinal cord injury

A
  • Consent
  • Anaesthetist on standby
  • Surgical site below level of spinal cord injury
  • Complete spinal cord injury
  • Absence of previous autonomic dysreflexia
  • Absence of muscle spasms or dystonia
100
Q

Acute management of hypertension of autonomic dysreflexia

A

Non pharm:
Remove tight clothing and suport stockings
Sit patient up
Ensure bladder empty (catheterise or flush catheter)
Exclude constipation

Pharmacological:
Sublingual GTN (may need to escalate to IV)
Sublingual nifedipine
IV hydralazine
IV diazoxide
IV magnesium
IV phentolamine

101
Q

Why would a reduced dose of induction agent be required when providing GA for a patient with spinal cord injury?

A
  • Altered pharmacokinetics due to reduced blood volume and muscle mass
  • Possibility of absent sympathetic response to hypotension, resulting in risk of profound hypotension with cerebral and myocardial hypoperfusion if normal doses are used
102
Q

Label the diagram

A
103
Q

What is the definition of delayed neurological deficit

A

Any clinically detectable neurological deterioration after initial stabilization without bleeding

104
Q

Which complications can contribute to delayed neurological deficit

A

Hydrocephalus
Seizures
Vasopasm
Sepsis
Electrolyte abnormality

105
Q

How is vasospasm treated following subarachnoid haemorrhage?

A
  1. Triple H: hypertension, hypervolaemia, haemodilution
  2. Nimodipine for 21 days
  3. Balloon angioplasty/intra-arterial vasodilation e.g. papaverine
106
Q

What is the definition of remote site anaesthesia?

A

Any location in which the anaesthetist is required to provide anaesthesia or sedation away from the main theatre suite and/or anaesthetic department. It cannot be guaranteed that help of another anaesthetist will be immediately available.

107
Q

Describe the goals of anaesthetic technique specific to electric convulsive therapy

A
  1. Rapid onset and offset of consciousness with rapid recovery
  2. Effective attenuation of the haemodynamic response to electrical stimulus
  3. Minimal suppression of seizure activity by anaesthetic technique
108
Q

Describe the cardiovascular response to electric convulsive therapy

A
  1. Generalised activation of autonomic nervous system
  2. Initial parasympathetic discharge lasting 0-15s resulting in bradycardia, hypotension or asystole
  3. A more prominent sympathetic response follows - cardiac arrhythmias may occur, sytolic arterial pressure increases, heart rate increases with peak at 3-5mins. Myocardial oxygen consumption increases which may precipitate ischaemia
  4. Systolic and diastolic function can remain decreased up to 6 hours after ECT due to myocardial stunning
109
Q

How can seizure activity be altered by anaesthetic technique for ECT

A
  1. Intentional hyperventilation to induce hypocapnoea may lower seizure threshold and lengthen seizure duration
  2. Choice of induction agent - some have anticonvulsant properties e.g. propofol
  3. Titration of induction agent dose informed by seizure quality during previous ECT treatments
  4. Premedication is avoided e.g. benzodiazepines
  5. Co-administration of dose sparing IV induction drugs is given e.g. opioids
110
Q

Decribe the role of muscle relaxation during ECT, include an example

A

Suxamethonium 0.5mg/kg is most commonly used
NMB reduces muscular convulsions and decreases the risk of serious injury

111
Q

What class of drug is phenelzine

A

Non-selective, irreversible MAOI

112
Q

What is the clinical significance of phenelzine to anaesthesia

A

Administration of indirectly acting sympathomimetic agents such as ephedrine or metaraminol should be avoided as these may precipitate a severe hypertensive reaction

Phenylephrine would be used as this is direct acting.

113
Q

Reasons to immobilise C-spine in trauma

A
  • Neck pain or focal tenderness
  • GCS < 15 on initial assessment
  • Focal neurological deficit or paraesthesia in extremities
  • Clinical suspicion of c-spine injury
114
Q

Which respiratory muscles are innervated by the following nerve roots:
* above C3
* C5-T8
* T8-L1

A
  • Above C3 - diaphragm
  • C5-T8 - external intercostals
  • T8-L1 - internal intercostals and abdominal muscles
115
Q

What is the defining feature of posterior fossa syndrome and what are the risk factors for its development?

A
  • Loss of speech
  • Midline location or medulloblastoma

FRCA CRQs (9 decks)

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