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You are in Home >> Exams >> Mitchell Anaesthetic Notes


Neurology

Created: 1/6/2006
Updated: 8/1/2007
 

Brain death

  • Coma GCS <8, potential for recovery
  • Persistent coma
    • Persistent vegetative state: brainstem function intact
    • Brain death: brainstem function lost (no spontaneous ventilation)
  • Death: “Irreversible cessation of circulatory and respiratory functions or irreversible cessation of all functions of the entire brain, including the brainstem.”

Diagnostic criteria of brain death

  • Deep coma
    • Confirm clearance of depressant drugs
    • Normal body temperature
    • No gross electrolyte or metabolic disturbance
  • Apnoea
    • No relaxants, opioids or other depressants
    • Raised PaCO2, normal PaO2
  • Irreversible structure brain damage

Procedure

  • Pupillary response to light absent
  • Corneal touch reflex absent
  • Vestibulo-ocular reflexes absent
    • 20 ml ice cold water in ear canals, no eye movement
  • Facial motor response to trigeminal distribution pain absent
  • Gag and cough reflexes absent
  • Apnoea in the presence of PaCO2 >60 mmHg, pH < 7.30
  • Two examinations at least 2 h apart by separate qualified doctors
  • Angiography required if no diagnosis or tests incomplete (e.g. eye injury)
  • Modified criteria <1 year of age due to greater recovery potential

Tests

Flicker fusion test

  • Increasing frequency of flashing light
  • Frequency at which light appears steady is recorded
  • Used to assess degree of hypotension producing significant cerebral ischaemia

Neuromuscular disorders and anaesthesia


Literature

  • Little high-quality evidence
  • Many case reports, few series
  • Small numbers for all conditions except myasthenia gravis (thymectomy)

General concerns

  • Preoperative assessment
    • Weakness
      • Respiratory failure
      • Upper airway maintenance
      • Assessment of need for back-up ventilated bed
      • Decreased fitness and exercise tolerance
      • Possible myocardial involvement
      • Documentation of functional state before anaesthesia
    • Deformity
      • Airway assessment
      • Likely ease of intubation
      • Positioning
    • Investigations
      • Respiratory function testing
      • Blood gas analysis
      • ECG, echocardiography if indicated
  • Intraoperative management
    • Risk of aspiration
    • Decision regarding need for muscle relaxants
    • Altered sensitivity to relaxants, need for NMJ monitoring
    • Variable distribution of weakness makes relaxant monitoring unreliable
    • Appropriate management of steroids or other drugs
  • Postoperative management
    • Careful monitoring of recovery to adequate tidal volume
    • Monitoring for respiratory failure post-extubation
    • Possible ICU ventilation

Motor neurone disorders


Multiple sclerosis

  • Aetiology
    • Unknown, environmental and genetic associations
    • Patchy demyelination in the CNS
  • Features
    • Signs
      • Typical onset in females 20-40 years of age
      • Variation in severity over minutes to years
      • Common involvement of optic nerve and oculomotor pathways
      • Exacerbated by:
        • Parturition, elevated temperature, other stresses
      • Progression to motor weakness of limbs
    • Investigations
      • MRI shows “plaques”
      • Abnormal sensory evoked potentials
      • CSF IgG and myelin basic protein elevated
  • Treatment
    • Steroids, ACTH, immunosupressants used with some effect
  • Anaesthetic considerations
    • Hyperthermia may cause exacerbation of weakness
    • Induction agents, volatiles, relaxants (including suxamethonium) all known to be safe
      • Relaxants may exacerbate weakness directly
    • Regional
      • Possible increased permeability of blood-brain barrier
        • Increased risk of CNS toxicity from local anaesthetics
      • Possible increased risk of histotoxicity from spinal local anaesthetic
        • Not supported by clinical data

Guillain-Barré syndrome

  • Aetiology
    • Cell-mediated autoimmune response
    • Causes demyelination of peripheral nerves
    • Commonly post-viral (herpes viruses, influenza, para-’flu, HIV)
    • Possibly post-vaccination (TB, tetanus, typhoid)
  • Features
    • Signs
      • Progressive motor weakness or more than one limb
      • Areflexia or hyporeflexia
      • Symmetrical and progressive
      • Results in flaccid paralysis
      • Mild sensory involvement, mostly vibration and proprioception
      • Cranial nerve involvement in 45%
      • Autonomic dysfunction
        • Circulatory instability: hypo- and hypertension
        • Bradycardia, tachyarrhythmias
        • Ileus, urinary retention
    • Investigations
      • CSF: low WCC, high protein
      • Abnormal nerve conduction studies
    • Time course
      • Recovery 2-4 weeks after onset
  • Treatment
    • Plasma exchange proven effective
    • Immunoglobulin therapy is as effective, but more relapses
    • Steroids commonly used but unproven
    • Supportive management: ventilation etc.
  • Anaesthetic considerations
    • Increased aspiration risk with bulbar palsy
    • Respiratory muscle weakness
    • Circulatory instability on induction
      • Exaggerated response to pressors and vasodilators
    • Suxamethonium contraindicated

Motor neurone disease

  • Aetiology
    • Some inherited, most sporadic (amyotrophic lateral sclerosis)
    • Progressive degeneration of upper and lower motor neurones
  • Features
    • Signs
      • Sensory and autonomic pathways spared
      • Cerebral function largely spared
      • Several patterns of progression
        • Cranial vs somatic
        • Upper vs lower
      • Similar to post-polio syndrome
    • Investigations
      • None specific
      • EMG shows denervation
  • Anaesthetic considerations
    • Upper airway and respiratory muscle weakness
    • Lack of specific treatment raises ethical problems
    • Suxamethonium contraindicated due to potassium release

Neuromuscular junction disorders

Myasthenia gravis

  • Aetiology
    • Autoantibodies (IgG) to α-subunit of ACh receptors on skeletal muscle
    • Thymic abnormalities in 75% of patients
    • Associated with other autoimmune diseases
      • Hypothyroidism, RA, SLE, pernicious anaemia
    • Neonatal variants
      • Children of myasthenic mothers
        • Transient weakness from maternal IgG
      • Hereditary myasthenia
        • No autoantibodies, structurally abnormal receptors
    • Paraneoplastic variant (Eaton-Lambert syndrome)
      • Autoantibodies against voltage-gated Ca2+ channels
      • Decreased ACh release from nerve terminals
      • Association with autonomic dysfunction, reduced gastric motility
      • Predominantly limb involvement
      • Little bulbar involvement
  • Features
    • Signs
      • Ocular involvement first: ptosis and diplopia
      • Commonly bulbar weakness
      • Asymmetrical trunk and limb involvement
    • Investigations
      • Edrophonium (Tensilon™) test
        • 1-6 mg edrophonium, 0.6 mg atropine
      • Autoantibody assay
        • False positives in RA and some family of affected patients
        • False negative immediately after anaesthesia
  • Treatment
    • Anticholinesterase drugs
      • Pyridostigmine 60 mg qid (up to 750 mg/day)
    • Plasma exchange
    • Immunoglobulin (unknown mechanism)
    • High-dose corticosteroids
    • Azathioprine, cyclophosphamide, cyclosporin
    • Thymectomy after medical optimization gives the best results
  • Anaesthetic considerations
    • Decision to continue anticholinesterase drugs depends on severity
    • Anticholinergic agents may be required to cover bowel anastomoses
    • Myasthenic crisis (acute exacerbation)
      • Described worsening with local anaesthetics, muscle relaxants, narcotics, ether, aminoglycosides
    • Weakness can also be due to anticholinesterase overdose
    • Regional anaesthesia is well tolerated
    • General anaesthesia
      • Propofol plus opioid, or
      • Volatile only
        • Produces 50% twitch fade at 1.0 MAC
      • Suxamethonium is safe
        • Possibly decreased sensitivity
        • Decreased metabolism if on high anticholinesterase dose
        • High incidence of phase II block at normal dose
      • Non-depolarizing agents are usually avoided
        • Increased sensitivity, difficulty reversing

Muscle disorders

Myotonia dystrophia

  • Aetiology
    • Disorder of relaxation of skeletal muscle (AD 19q)
      • Slow reuptake of Ca2+ into sarcoplasmic reticulum
      • Multiple tissues affected
    • Myotonia congenita variant present from birth
    • Paramyotonia variant manifest only with cold
  • Features
    • Signs
      • Weakness with myotonia
        • Involving pharyngeal muscles as well as limbs and face
      • Cataracts
      • Frontal balding
      • Variable intellectual disability, somnolence
      • Cardiomyopathy, conduction abnormalities
      • Testicular failure
      • Reduced gastric motility
    • Investigations
      • ECG increased PR interval, atrial flutter, other arrhythmias
      • RFT marked reduction in maximal expiratory pressure, small reduction in VC
    • Treatment
      • Myotonia can be treated with phenytoin, but is not usually a problem
      • Atrophy is not treatable
  • Anaesthetic considerations
    • Prolonged contraction in response to depolarizing relaxants
      • Suxamethonium absolutely contraindicated
      • Also triggered by propranolol, clofibrate, K+
    • Prolonged contraction with shivering
      • Aim to maintain normothermia
      • Relative contraindication to volatiles
    • Myotonia provoked by mechanical stimulus and diathermy
    • Increased risk of apnoea with sedative drugs
    • Myotonia antagonized only by intramuscular local anaesthetic
    • Some relief with quinine, procainamide or phenytoin
    • Non-depolarizing relaxants are effective at normal doses
      • Reversal appears to be safe despite theoretical risk of myotonia
    • Intravenous regional anaesthesia should be effective

Muscular dystrophy

  • Aetiology
    • Familial
      • Duchenne (X-linked), limb girdle (AR), facioscapulohumeral (AD)
    • Atrophy of skeletal muscle with fatty infiltration and fibrosis
  • Features
    • Signs
      • Progressive limb weakness
      • Diaphragm function relatively preserved
      • Late cardiomyopathy, arrhythmias, mitral valve prolapse
      • Kyphoscoliosis with respiratory compromise common
    • Investigations
      • CK typically elevated
      • ECG abnormalities (RSR’ in V1, deep Q in lateral V leads, arrhythmias)
      • RFT VC<30% predicted indicated high risk with GA
  • Anaesthetic considerations
    • Progressive disease so earlier operation is preferable
    • Increased incidence of malignant hyperthermia
    • Suxamethonium contraindicated due to potassium release
    • Decreased margin of safety with non-depolarizing relaxants
    • Gastroparesis reported pre- and postoperatively
    • Increased risk of aspiration with bulbar weakness
    • Avoid tachycardia as increased risk of arrhythmia
    • Rhabdomyolysis and renal failure

Neuroleptic malignant syndrome

Kindly provided by Dr James Mitchell from his pharmacodynamics series


ArticleDate:20060601
SiteSection: Article
 
   
    
                                            
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