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ect in elderly

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

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    1. ECT IN ELDERLY DR:Hisham H.Aly Anaesthetic Dept J.P.H.

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

    3. 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.

    4. 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.

    5. 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.

    6. 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 .

    7. 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.

    8. 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.

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

    10. 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.

    11. Anaesthetic consideration Ageing & coexisting illness. Physiological effects ECT. Drugs interactions.

    12. 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.

    13. 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.

    14. Cerebral effect: Increase cerebral oxygen consumption. Increase cerebral blood flow. Increase intracranial tension.

    15. 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.

    16. 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 > 1.5 mm mol /litre may be fatal toxicity is worse be sod. depletion as may occur with concurrent use of diuretics.

    17. 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.

    18. 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.

    21. MOINITORING SEIZURES ACTIVITY ECT bilateral & unilateral Latent period Tonic phase Clonic phase = 15 sec peripherally and = 25 sec on EEG recording.

    24. 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.

    25. 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

    26. 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 >2min.

    27. 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.

    28. 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

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