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Neuro & Spine

Sheet 04Anaesthesia

Neuro & Spine

Perfusion and intracranial pressure, the craniotomy and its positions, neuromuscular disease, neuromonitoring and brain death, and spinal cord injury.

Cards
24
Minutes
about18
Scenarios
23

Start at card 1Review the rules

Core rulesRead these first3 cards · about 2 min

  1. 01Perfusion pressure: the number everything turns on
  2. 02Lowering intracranial pressure
  3. 03Protect the injured brain

Perfusion pressure: the number everything turns on

01 / 24

Cerebral perfusion pressure (CPP) is mean arterial pressure (MAP) minus the higher of intracranial pressure (ICP) or central venous pressure (CVP): hold 60-70, treat ICP over 20-22.

Perfusion pressure target

MeasureValue
CVP higher than ICP, open its explanationCPP = MAP minus CVP, the higher pressure
Parameter to target in brain injury, open its explanationCPP
CPP goal, severe head injury, open its explanation60–70 mmHg (Brain Trauma Foundation)
CPP floor and ceiling, open its explanationNever below 50; don't push above 70

Intracranial pressure thresholds

MeasureValue
ICP treatment threshold, open its explanationTreat sustained ICP above 20‑22 mmHg
ICP band linked to poor outcome, open its explanationAbove 20–25 mmHg; normal 7–15

When to monitor intracranial pressure (Brain Trauma Foundation)

CT in severe head injuryICP monitoring
Abnormal CT, open its explanationMonitor ICP
Normal CT, open its explanationMonitor if two or more: over 40, posturing, systolic below 90

Report a problem with card 1: Perfusion pressure: the number everything turns on

Lowering intracranial pressure

02 / 24

Raised ICP: head up, sedate, osmotherapy; brief hyperventilation only if refractory; steroids only for tumour oedema.

Tight brain at craniotomy

FindingAction
High PaCO2, open its explanationHyperventilate
Further measures, open its explanationOsmotic diuretic, with or without furosemide; raise head
Phenytoin, open its explanationNot a brain relaxant
Coughing or bucking on the tube, open its explanationGreatest ICP rise: keep deep and paralysed

Raised ICP after head injury: first line, then rescue

OrderMeasure
Position, open its explanationHead up 30–45 degrees, neck neutral; never head‑down
First line, open its explanationSedation, analgesia and bolus osmotherapy
Refractory to sedation and osmotherapy, open its explanationBrief hyperventilation only; never prophylactic

Hyperventilation limits

SituationRule
Surgeon wants deeper hyperventilation, PaCO2 already low, open its explanationNo further; add mannitol; hold PaCO2 30–35
Abrupt PaCO2 fall after sustained hypercapnia, open its explanationCerebral ischaemia; change PaCO2 gradually
Cerebrospinal fluid (CSF) pH renormalises, open its explanationAbout 6 hours (Barash, Stoelting); Miller 8–12

Osmotherapy and steroids

AgentEffect
Mannitol, open its explanationNeeds an intact blood–brain barrier
Hypertonic saline, open its explanationAlso barrier‑dependent (Miller)
Steroids, open its explanationShrink vasogenic oedema of brain tumour
Dexamethasone in cytotoxic, interstitial or osmotic oedema, open its explanationNo effect

Report a problem with card 2: Lowering intracranial pressure

Protect the injured brain

03 / 24

After brain injury prevent the second hit: hypoxia, hypotension, hypercarbia, fever, hyperglycaemia, hypotonic fluid, steroids.

Threat after brain injuryWhat to do
Targets after severe head injury, open its explanationPaO2 >60, PaCO2 35–40, MAP >80, temperature ≤37
Glucose after head injury, open its explanationKeep below 180; no tight control
Glasgow Coma Scale (GCS) 8 or less, or rising PaCO2, open its explanationIntubate and ventilate; then normocapnia
Resuscitation fluid, open its explanationNormal saline; no hypotonic fluid, no albumin
Corticosteroids (methylprednisolone), open its explanationRaise mortality about 20% in a large trial; contraindicated

Report a problem with card 3: Protect the injured brain

Part 1 · DecisionsWhat to do7 cards · about 5 min

  1. 04Chronic disease before surgery
  2. 05Which test
  3. 06Relaxants in neuromuscular disease
  4. 07Technique in neuromuscular disease
  5. 08Position and reference points
  6. 09The craniotomy, and procedures with their own rule
  7. 10Vascular lesions: pressure by phase

Chronic disease before surgery

04 / 24

Continue the patient's drugs, switch off their devices, screen and protect what the disease threatens.

Which test

05 / 24

Image the part the signs point to, at once when a new deficit follows surgery.

Signs pointing to the test

PresentationTest
Neck pain, weakness in both arms, open its explanationImage the cervical spine (CT or MRI), not carotids
Transient hemispheric weakness plus transient monocular blindness, open its explanationCarotid duplex ultrasound first, to grade stenosis

Postoperative deficit

Postoperative deficitTest
Four‑limb weakness, cervical sensory level, spondylosis, open its explanationCervical cord injury: cervical spine MRI
New deficit on waking after spine surgery, open its explanationEpidural haematoma until disproved: urgent MRI, then decompression

Report a problem with card 5: Which test

Relaxants in neuromuscular disease

06 / 24

Denervation, myotonia and bulbar disease bar succinylcholine; myasthenia is sensitive, anticonvulsant users resistant, to non-depolarisers.

DiseaseRelaxant decision
Myasthenia gravis: depolariser, open its explanationResistant: needs a higher succinylcholine dose
Myasthenia gravis: relaxation without blockers, open its explanationVolatile agent for intubation and maintenance
Myasthenia gravis: intubation, open its explanationOften possible without any neuromuscular blocker
Myasthenia gravis: blockade needed, open its explanationHalf to two‑thirds dose steroidal blocker; sugammadex reversal
Guillain–Barré syndrome (denervation), open its explanationAcetylcholine receptors up‑regulated, not down‑regulated; avoid succinylcholine
Myotonic dystrophy, open its explanationAvoid succinylcholine (contracture); short‑acting non‑depolariser if needed
Cerebral palsy on long‑term anticonvulsants, open its explanationResistant to non‑depolarising blockers

Report a problem with card 6: Relaxants in neuromuscular disease

Technique in neuromuscular disease

07 / 24

In neuromuscular disease favour neuraxial amide local anaesthetic; if general, intubate.

Disease and operationTechnique
Prior Guillain–Barré, limb surgery, open its explanationNeuraxial acceptable after documenting deficits; never succinylcholine
Myotonic dystrophy, lower‑limb surgery, open its explanationSpinal or lumbar epidural; peripheral block ultrasound‑guided only
Myotonic dystrophy, if general anaesthesia, open its explanationRapid sequence intubation with tracheal tube; no laryngeal mask
Bulbar amyotrophic lateral sclerosis (ALS), lower‑body surgery, open its explanationSpinal with plain bupivacaine; no intrathecal opioid, no succinylcholine
Myasthenia gravis, labour epidural, open its explanationAmide local anaesthetic; avoid esters

Report a problem with card 7: Technique in neuromuscular disease

Position and reference points

08 / 24

Zero pressures at the brain, keep the head above the heart, never force the neck.

The craniotomy, and procedures with their own rule

09 / 24

Craniotomy: test the function at risk, wake smoothly, treat pain; carotid clamping: keep pressure up.

Craniotomy, by phase

PhaseRule
Awake resection near Wernicke's area, open its explanationTest receptive speech, not speech output or limb movement
Awake phase: commonest complication, open its explanationNausea and vomiting; other cohorts rank hypertension or seizures
Emergence and extubation, open its explanationStop volatile; low‑dose propofol bridge; keep opioid cover
Emergence coughing or hypertension, open its explanationAdd lidocaine or antihypertensives as needed
Recovery, pain after extubation, open its explanationTitrated short‑acting opioid, not sedating doses

Shunt and pituitary surgery

ProcedureRule
Shunt revision, raised ICP, full stomach, open its explanationRapid sequence, rocuronium 1.2 mg/kg; avoid succinylcholine (raises ICP)
Transsphenoidal pituitary resection, heavy blood loss, open its explanationHead‑up, group and screen, only mild hypotension

Carotid endarterectomy

MomentRule
Handling the bifurcation, open its explanationReflex haemodynamic swings; infiltrate local anaesthetic there
Low pressure before clamping, open its explanationLighten anaesthesia or phenylephrine; never deepen or vasodilate
Brain monitoring under general anaesthesia, open its explanationTranscranial Doppler of the middle cerebral artery

Electroconvulsive therapy (ECT)

PointRule
Absolute contraindications, open its explanationIntracranial mass, head injury, aneurysm; recent myocardial infarction (MI) or stroke
Glaucoma, retinal detachment, severe osteoporosis, open its explanationRelative, not absolute, contraindications
Hypnotic dose, open its explanationSmall, brief, just unaware; not deep or prolonged

Report a problem with card 9: The craniotomy, and procedures with their own rule

Vascular lesions: pressure by phase

10 / 24

Secure the aneurysm early, nimodipine for all; pressure up for clipping and vasospasm, never surging.

Securing the lesion

Lesion and phaseDecision
Aneurysmal subarachnoid haemorrhage: leading cause of death, open its explanationRebleeding; secure by coiling or clipping within 24 hours
Unsecured arteriovenous malformation: airway, open its explanationSupraglottic airway when aspiration risk allows; avoid laryngoscopy
Coiling after subarachnoid haemorrhage, open its explanationGeneral anaesthesia, muscle relaxation, invasive arterial line
Temporary clip on cerebral aneurysm, open its explanationRaise BP to high‑normal before and during clamp

After the bleed: nimodipine and vasospasm

SituationDecision
Every aneurysmal subarachnoid haemorrhage, open its explanationEnteral nimodipine 60 mg every 4 hours, 21 days
Other calcium‑channel blockers, open its explanationNo outcome benefit; nimodipine only
Symptomatic vasospasm, open its explanationKeep pressure up, euvolaemic; no hypervolaemia or haemodilution

Report a problem with card 10: Vascular lesions: pressure by phase

Part 2 · RecognitionWhat it is6 cards · about 6 min

  1. 11Neuromonitoring: evoked potentials, jugular bulb, EEG
  2. 12Scores and grades
  3. 13Consciousness and brain death
  4. 14Localise the lesion
  5. 15Name the neuromuscular disease
  6. 16The body after a brain insult

Neuromonitoring: evoked potentials, jugular bulb, EEG

11 / 24

Each monitor warns at a threshold: amplitude down 50%, latency up 10%, jugular saturation under 50%.

Warning thresholds

MonitorThreshold
Somatosensory evoked potential (SSEP), open its explanationAlert at 50% amplitude fall or 10% latency rise
Jugular bulb venous saturation, open its explanationBelow 50% is ischaemic desaturation; normal 55–75%
Jugular bulb saturation, Barash early warning, open its explanationStay above 55%
EEG during cooling, open its explanationFlat at about 18–20 °C; some need 15–18

SSEP change in spine surgery

ChangeMeaning
SSEP amplitude down, latency up, open its explanationSpinal cord ischaemia
Sudden SSEP loss, stable anaesthesia and physiology, open its explanationSurgical cord compression or distraction: surgeon relieves immediately

Other influences on SSEPs

FactorEffect
Volatile agents, sevoflurane included, open its explanationDepress cortical SSEPs: favour intravenous agents
Mild hypothermia, open its explanationProlongs SSEP latency, even small falls
Mild acidaemia, moderate neck flexion, open its explanationLittle effect; one source: pH below 7.2 matters

Choosing the monitor

SettingMonitor
Open thoracoabdominal aneurysm repair, open its explanationAdd sensory and motor evoked potentials
Cranial nerve VIII in brainstem surgery, open its explanationBrainstem auditory evoked potential (BAEP); facial nerve uses electromyography (EMG)

Report a problem with card 11: Neuromonitoring: evoked potentials, jugular bulb, EEG

Scores and grades

12 / 24

GCS sums eyes, verbal, motor; American Spinal Injury Association (ASIA) turns on S4–5 sparing; Leventhal 10 points predicts ventilation.

Glasgow Coma Scale (Stoelting): add the best response in each, 3–15

ComponentScores
Eye opening (1–4), open its explanation4 spontaneous · 3 to voice · 2 to pain · 1 none
Verbal response (1–5), open its explanation5 oriented · 4 confused · 3 inappropriate words · 2 incomprehensible sounds · 1 none
Motor response (1–6), open its explanation6 obeys · 5 localises · 4 withdraws · 3 abnormal flexion · 2 extension · 1 none
Total 8 or less, open its explanationIntubate and ventilate (Miller)

GCS worked examples (eyes + verbal + motor)

PatientTotal
Eyes to command, incomprehensible sounds, localises pain, open its explanation3 + 2 + 5 = GCS 10
No eye opening, moans, abnormal flexion to pain, open its explanation1 + 2 + 3 = GCS 6
No eye opening, incomprehensible sounds, withdraws from pain, open its explanation1 + 2 + 4 = GCS 7: withdrawal, not abnormal flexion

ASIA impairment scale (Barash, Miller): decided by S4–5 sparing

GradeCriteria
ASIA A, open its explanationComplete: no motor or sensation, including S4–5
ASIA B, open its explanationSensory incomplete: sensation but no motor below the level, including S4–5
ASIA C, open its explanationMotor incomplete: more than half of key muscles below the level grade under 3
ASIA D, open its explanationMotor incomplete: at least half of key muscles grade 3 or more
ASIA E, open its explanationNormal motor power and sensation

Hunt and Hess grades (Stoelting): subarachnoid haemorrhage

GradeClinical state; mortality
Grade 0, open its explanationUnruptured aneurysm; mortality 0–2%
Grade 1, open its explanationMinimal headache, no deficit; mortality 2–5%
Grade 2, open its explanationModerate to severe headache, cranial nerve palsy only; mortality 5–10%
Grade 3, open its explanationDrowsy, confused or mild focal motor deficit; mortality 5–10%
Grade 4, open its explanationStupor, marked hemiparesis or early decerebration; mortality 25–30%
Grade 5, open its explanationDeep coma, decerebrate rigidity; mortality 40–50%
Miller's version, open its explanationLists survival, not mortality: grade 4 survival 20%

Leventhal score: ventilation after thymectomy in myasthenia

PredictorPoints
Myasthenia symptoms over 6 years, open its explanation12
Chronic lung disease not caused by myasthenia, open its explanation10
Pyridostigmine above 750 mg/day, open its explanation8
Forced vital capacity below 2.9 L, open its explanation4
Total of 10 points or more, open its explanationPostoperative ventilation predicted (Leventhal 1980)

Report a problem with card 12: Scores and grades

Consciousness and brain death

13 / 24

Name the state from eye opening and awareness; brain death needs brainstem silence under set conditions.

Coma, vegetative state and locked-in syndrome

FindingState
Eyes closed, unrousable, no awareness, open its explanationComa
Eyes open, unresponsive, no awareness, open its explanationVegetative state
Aware but paralysed, blinks or vertical gaze only, open its explanationLocked‑in syndrome
Breathing pattern, open its explanationSeparates none of them; eyes and awareness decide

The EEG in coma

StateEEG
Deep coma, open its explanationDelta waves, 0.5 to 4 Hz; not theta or alpha

Brain-death tests

FindingIn brain death
Brainstem reflexes, open its explanationAll absent: pupillary, corneal, oculovestibular (cold caloric), gag, cough
Limb movements or spinal reflexes, open its explanationMay persist; they do not exclude brain death

Before brain-death testing (American Academy of Neurology)

PrerequisiteRequired value
Core temperature and systolic pressure, open its explanation≥36 °C and ≥100 mmHg
PaCO2 before the apnoea test, open its explanation40 ± 5 mmHg, with adequate oxygenation

Report a problem with card 13: Consciousness and brain death

Localise the lesion

14 / 24

Root, nerve, cord and brainstem each have a signature: reflex, muscle, sensory pattern, breathing, crossed signs.

Name the neuromuscular disease

15 / 24

Ascending after infection is Guillain–Barré; fatigable is myasthenia; better with use is Lambert–Eaton.

The body after a brain insult

16 / 24

Read sodium with volume and urine; the heart and glucose change from the catecholamine surge.

Part 3 · SituationsWhat now5 cards · about 3 min

  1. 17Hypertension or hypotension with bradycardia
  2. 18Air embolism
  3. 19Spinal cord injury
  4. 20Acute weakness
  5. 21Complications after neurosurgery

Hypertension or hypotension with bradycardia

17 / 24

Hypertension with bradycardia is pins, rising ICP or rupture; hypotension with bradycardia is a reflex.

Hypertension with bradycardia: the cause

EventCause
Sudden hypertension then bradycardia during coiling, open its explanationAneurysm rupture until proven otherwise
Hypertension with bradycardia, rising intracranial pressure, open its explanationCushing reflex; impending herniation

Rupture during coiling: what to do

FindingAction
Rupture during coiling, open its explanationReverse heparin with protamine
Cushing signs during coiling, open its explanationHyperventilate briefly on 100% oxygen
Blood pressure after rupture, open its explanationLower pressure without cerebral vasodilators

Trigeminocardiac reflex and skull pins

FindingAction
Bradycardia in trigeminal or posterior fossa surgery, open its explanationStop surgical manipulation first
Severe or recurrent bradycardia after stopping, open its explanationAtropine
Surge at pinning or adrenaline scalp infiltration, open its explanationDeepen anaesthesia; slow rate is baroreflex; no IV adrenaline

Report a problem with card 17: Hypertension or hypotension with bradycardia

Air embolism

18 / 24

Falling end-tidal CO2 head-up is air: flood the field, then support; precordial Doppler detects it non-invasively.

Venous air embolism: management

FindingAction
Falling end‑tidal CO2 with hypotension, posterior fossa, open its explanationSurgeon floods the field with saline first
Venous air embolism once field flooded, open its explanationOxygen, aspirate air, support circulation

Detecting venous air embolism

MonitorSensitivity
Precordial (transthoracic) Doppler, open its explanationMost sensitive non‑invasive monitor for venous air embolism
Transoesophageal echo, open its explanationMore sensitive overall, but invasive; not the non‑invasive choice

Report a problem with card 18: Air embolism

Spinal cord injury

19 / 24

Cord injury: decompress within 24 hours; neurogenic shock early, autonomic dysreflexia later, remove its trigger first.

Acute weakness

20 / 24

Failing ventilation comes first; edrophonium separates myasthenic from cholinergic crisis; Guillain–Barré gets intravenous immunoglobulin (IVIG), never steroids.

FindingAction
Hypercapnia and tiring in myasthenia, open its explanationIntubate and ventilate; atropine treats only muscarinic signs
Myasthenia weaker after edrophonium test, open its explanationDiagnose cholinergic crisis, not myasthenic crisis
Weak on anticholinesterase, before edrophonium, open its explanationEither crisis: signs and edrophonium response decide; airway first
Weakness on anticholinesterase, edrophonium worsens, open its explanationCholinergic crisis: stop the drug, atropine, support ventilation
Weakness on anticholinesterase, edrophonium improves, open its explanationMyasthenic crisis: give more anticholinesterase
Guillain–Barré syndrome leg weakness after vaccination, open its explanationIVIG or plasma exchange within two weeks; never steroids

Report a problem with card 20: Acute weakness

Complications after neurosurgery

21 / 24

A new deficit after surgery is ischaemia or compression until imaging says otherwise.

Part 4 · Conditions and mechanismsWhy it is true2 cards · about 1 min

  1. 22What sets cerebral blood flow
  2. 23Anatomy and physiology worth holding

What sets cerebral blood flow

22 / 24

Carbon dioxide and metabolism set flow, autoregulation holds it; anaesthetics lower both, volatiles uncouple, ketamine raises.

Physiology

FactorEffect on flow and metabolism
Arterial carbon dioxide, open its explanationDominant regulator of cerebral blood flow
Hypercapnia versus hypocapnia, open its explanationRaises flow versus lowers flow, roughly linearly
Rise in regional metabolic rate, open its explanationFlow–metabolism coupling, not pressure–flow coupling
Chronic hypertension, open its explanationShifts autoregulation curve rightward
Raised ICP (infant hydrocephalus), open its explanationReduces cerebral blood flow
Therapeutic hypothermia, open its explanationLowers basal metabolism and neuronal function; flow falls

Anaesthetic drugs

DrugEffect on flow and metabolism
Volatile agent, open its explanationLowers metabolic rate; flow rises above 1 minimum alveolar concentration (MAC)
Thiopental or propofol, open its explanationLower cerebral blood flow most, equally
Midazolam, open its explanationLittle change at sedative doses; falls at anaesthetic doses
Fentanyl (opioids), open its explanationLeast effect among IV agents, ventilation controlled
Ketamine, open its explanationRaises both flow and metabolic rate

Report a problem with card 22: What sets cerebral blood flow

Anatomy and physiology worth holding

23 / 24

Plain facts: outflow levels, carbon dioxide raises eye pressure, stroke risk and its salvageable penumbra.

Outflow

OutflowCord segments
Sympathetic preganglionic cell bodies, open its explanationLateral (intermediolateral) grey horn, T1 to L2
Parasympathetic preganglionic outflow, open its explanationCraniosacral: cranial nerves and sacral cord, not thoracolumbar

Eye pressure and stroke

StateFact
Raised PaCO2, open its explanationRaises intraocular pressure; keep PaCO2 normal
Underperfused penumbra around infarct core, open its explanationSalvageable; infarcts over time unless reperfused
Family history of stroke, open its explanationFixed stroke risk factor, like age and male sex

Report a problem with card 23: Anatomy and physiology worth holding

TrapsCheck these before you finish1 card · about 1 min

  1. 24Traps

Traps

24 / 24

The tempting choice is the familiar one; the books often name another.

Clinical situationWhat the books say, not the familiar choice
Drug raising mortality after head injury, open its explanationCorticosteroids (methylprednisolone), not propofol
IV agent lowering cerebral blood flow most, open its explanationThiopental or propofol equally; not midazolam
Phenytoin for a bulging brain, open its explanationDoes not relax the brain; furosemide helps mannitol
Leading cause of death after SAH admission, open its explanationRebleeding, not vasospasm; secure aneurysm within 24 hours
Surgery months after Guillain–Barré, open its explanationNeuraxial acceptable after documenting deficits; never succinylcholine
Cerebral palsy on anticonvulsants: relaxant response, open its explanationResistance to non‑depolarising blockers
Long QT after SAH with low calcium, open its explanationNeurogenic catecholamine surge; not the hypocalcaemia
CPP when CVP exceeds ICP, open its explanationMAP minus CVP, the larger; not MAP minus ICP
Surgeon asks for deeper hyperventilation, brain injury, open its explanationOsmotherapy first; brief hyperventilation only for refractory ICP
Single agent needing an intact blood–brain barrier, open its explanationMannitol (classic); Miller: hypertonic saline also barrier‑dependent
Painless one‑eye visual loss after prone spine surgery, open its explanationPosterior ischaemic optic neuropathy, not retinal artery occlusion
Hypertension and bradycardia right after coil deployment, open its explanationHyperventilate on 100% oxygen (fastest); protamine; mannitol slower
Duration of hyperventilation's effect on ICP, open its explanationAbout 6 h (Barash, Stoelting); 8–12 h (Miller); not minutes

Report a problem with card 24: Traps

QuizCheck yourself23 practice scenarios · one to a screen

QuizCheck yourself23 practice scenariosAnswers checked against the books and guidelines.

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