ECT IN ELDERLY

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ECT IN ELDERLY

• DRHisham H.Aly
• Anaesthetic Dept J.P.H.

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• The knowledge that malaria induced convulsions
  could be beneficial to the insane was first noted
  by Hippocrates.

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• In 1927, insulin induced coma and convulsions was
  discovered by Manfred J.sekel in Berlin for the
  treatment of schizophrenia.
• In 1934, metrazol induced convulsions was used in
  Budapest by ladislaus for the treatment
  schizophrenia and affective psychosis.

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• cerletti and Bini introduced ECT as an
  effective treatment option for
  psychiatric illness in 1937.
• ECT persisted as mainstay of therapy until 1960s
  when effective antipsychotic,antidepressant and
  antimanic drugs were discovered.

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• Renewed interest in ECT prompted by failure of
  pharmacotherapy in treatment refractory patients
  with several psychiatric illnesses mainly
  depression but also in mania, catatonia and
  schizophrenia.

• The most recent study conducted by national
  institute of mental health indicated that
  patients over 61 years old constilute the largest
  age group who received ECT.

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• Other studies found that elderly patients with
  psychotic depression had significantly lower
  frequency response to pharmacotherapy than ECT.
• ECT is the method of choice for treatment of
  fever depression illness, especially when urgent
  action is indicated like a history of suicidal
  attempt .

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HOW DOES IT WORK?

• It is not clearly known how exactly it works.
• Thought to be like cardiac defibrillation,
  shocking the brain into normal activity.
• ECT activates noradrenergic system, enhances
  dopamine receptor sensitivity and reduces
  serotonin uptake.

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ASSESSMENT OF PATIENTS BEFORE ECT

• Detailed history of coexisting diseases (most of
  the patients are ASA II, III)
• Family history, allergic or adverse effected to
  drugs history e.g. MH.
• Investigations, ECG, FBC, U, Es and serum level
  of drugs with low therapeutic window e.g. lithium
  and digoxin. Other tests can be asked if
  indicated as CXR. Echocardiography P.F.Ts.
  

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CONTRAINDICATIONS

• There are five absolute contraindications
  for ECT.
• Recent intracranial surgery.
• Recent cerebrovascular accident.
• Intracranial mass with raised intracranial
  pressure.
• Recent myocardial infraction.
• Phaeochromocytoma.

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• other conditions are relatively
  contraindication.
• (Risk benefits ratio)
• Glaucoma retinal detachment thrombophelbitis,
  angina, CHF, sever pulmonary diseases. We can use
  ECT in patients with fractures with some
  precautions.
• full relaxation ensured by N.S.
• Precurarization.
• Presence of orthopaedic surgeon.
• Unilateral minimum effective E.C.T.

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Anaesthetic consideration

• Ageing coexisting illness.
• Physiological effects ECT.
• Drugs interactions.

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• Ageing
• C.V.S.
• Increase risk of coexisting C.V.D.
• hypertension, I.H.D., valvular diseases
• Prolonged circulatory time.
• Baroreceptor sensitivity, sympathetic tone and
  the ability to increase heart rate are reduced.
• Respiratory system
• Increase risk of COAD.
• Diminution of protective air way reflexes,
  increases in closing volume and ventilation
  perfusion mismatch which all increases risk of
  hypoxaemia.
• Others reduce cerebral blood flow and GFR so
  increase risk of organ perfusion dysfunctions.

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• Physiological effects of ECT
• Cardiovascular effects
• Immediate parasympathetic stimulation,
  bradycardia, hypotension and possible asystole.
  The risk of asystole can be minimized by the use
  of anticholinergic drugs preoperatively and by
  reducing the dose of suxamethonium.
• Late (after 1 minute) sympathetic stimulation,
  tachycardia, hypertension, arrhythmia and
  increase myocardial oxygen consumption.

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• Cerebral effect
• Increase cerebral oxygen consumption.
• Increase cerebral blood flow.
• Increase intracranial tension.

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• Miscellaneous effects
• Increase intra gastric pressure.
• Increase intra ocular pressure.
• Neuroedocrine effects include increase plasma
  level of ACTH, cortizol, glucagons, catecholamine
  and inhibition of glucose mediated insulin
  secretions.

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• Drugs interactions
• No discontinuation to medication.
• TCA postural hypotension, tachycardia.
• MAOI with pethedine and indirect sympathomimetic
  (ephedrine and tyramine and meterminol)
• Less interaction with moclobemide R.I of MAO
  type A.
• SSRI less sedating and less cardio toxic effect
  and prolonged seizures with ECT.
• Venlafaxine is a serotonin and noradrenalin
  reuptake inhibitor may cause hypertension.
• Lithium serum level gt 1.5 mm mol /litre may be
  fatal toxicity is worse be sod. depletion as may
  occur with concurrent use of diuretics.

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FOR A SAFE ECT

• Senior anaesthetist.
• Well trained ODA and recovery nurse.
• Careful recording of anaesthetic regimens and the
  patients response to each treatment.
• Meticulous checking of the anaesthetic machine,
  monitoring system, drugs and instruments for
  airways management and resuscitation and suction
  machine, and tiltable bed.

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• Anaesthetic technique
• Preoxygenation.
• Sedative premedication is undesirable.
• If ant cholinergic antisialogogue is needed.
  Glycopyrrolate is the drug of choice.
• I.V. induction must be administered slowly
• Methohexiton
• Propofol
• Thiopentone
• Etomidate
• muscle relaxant to prevent forceful and
  potentially damaging convulsion.
• Sux. 0.5mg 1kg
• Denture should be removed and bite block inserted
  once the patient has been anaesthetised and all
  trolleys should be adequately padded.

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MOINITORING SEIZURES ACTIVITY

• ECT bilateral unilateral
• Latent period
• Tonic phase
• Clonic phase 15 sec peripherally and 25 sec
  on EEG recording.

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Methods of monitoring seizures activity

• Timing
• Cuff technique
• EEG monitoring poly spike activity occurs during
  the latent and tonic phases while the three hertz
  spike occurs during the clonic phase.

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Therapeutic Window

• The therapeutic window is the key in ECT
• A dose below seizure threshold will fail to
  induce a generalized seizures and so there is a
  risk of a poor therapeutic response.
• A dose greatly in excess of seizure threshold is
  likely to be associated with more sever cognitive
  side effects without any therapeutic advantage

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ADVERSE EFFECTS OF ECT

• Mortality - 4 100,000 treatment. Similar to
  that of general anaesthesia in minor surgical
  procedure ( lower mortality than the use of
  antidepressant drugs).
• Cardiovascular complications are the main cause
  of mortality.
• Prolonged seizure gt2min.

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• Psychiatric complication-cognitive side effects
  ,memory impairment and confusion. In this case
  the following actions should be taken
• Others Headache, body ache , aspiration
  pneumonitis , rupture bladder.
• Switch from bilateral to unilateral ECT.
• Reducing the number of treatment per week.
• Decrease the dose of the ECT.
• Post Ictial delirium.

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Does ECT cause brain damage?

• No detectable irreversible brain damage appears
  to occur, there remains however the possibility
  of changes in the autobiographic memory function