ECT therapy and guidelines for trwatmentpptx

Ect therapy

1. Future Design Lorem ipsum dolor sit amet, consectetuer adipiscing elit

2. E l e c t r o c o n v u l s i v e t h e r a p y - a h i s t o r y C on v ul s i on s a n d e l ec t r i c i t y h a v e b een k no w n t o re du ce sy m pto m s i n p e opl e w i t h n e u r ol o g i cal d i s o r d ers f o r m a n y y ear s . H i ppo cra t es s aw th at i n s a n e p a t i e nt s s ho w ed re du ced sy m pto m s a f t er s u ff er i n g f r o m c on v ul si on s b r ou g h t o n b y m a l ar i a There is an account in ad 47, of a physician using an electric eel cure h ea d ac h es o f th e r o m an e m p er o r c l a ud i u s . I n th e 1500 s : a jesuit missionary wrote of ethiopians using electricity to “expel devils.” paracelsus, a swiss physician, used camphor to produce seizures to cure insanity.

3. In the 1700s : Individuals treated with hellebore went into convulsions and coma and were cured of “mania” and “raving madness.” In 1792 John birch used electric shocks to the head to cure patients. In the 1800s there were reports of insanity being cured with electric shock. In 1927 insulin coma therapy was invented by manfred sakel. It involved giving insulin in order to lower levels of glucose, producing coma and convulsions. Mathematician john nash ( a beautiful mind ) was given this treatment in the 1960s. In 1932 Ladislaus von Meduna used camphor to treat schizophrenia. He later used metrazol since it was faster. However research show it would produce immerse terror upon aministration and seizure produce have up to 23-30% of vetebral fracture ( Reads, 2006 ) Myocardial damage and a tendency to hypertension occurred in a relatively small number of patients. E l e c t r o c o n v u l s i v e t h e r a p y - a h i s t o r y

4. In 193 7 two neurologists studying epilepsy, ugo cerletti and lucio bini, decided to use electric shock to induce seizure without the side effects of metrazol. The idea to apply shock therapy to humans came to cerletti when he s a w p ig s b e i n g s h o c k e d i n t o a c o ma b e f o r e b e i n g s l a u g h t e r e d . I n 193 8 t h e f i r st e l ec t r o c onvu l s i v e t h e r a p y treatment was tested on patient with schizophrenia in Rome. He had a full recovery. In 1940 the first electroconvulsive therapy treatment was given in the united states. E l e c t r o c o n v u l s i v e t h e r a p y - a h i s t o r y

5. First Documented ECT trail U nidentified 40- year-old schizophrenic who had been found wandering in Rome and speaking incomprehensible , gibberish , having somehow arrived from Milan by train without a ticket ( Wright, 2011) In between rounds of electric shocks , when his team was figuring out how to titrate dosage and number of rounds to administer the patient began to speak comprehensibly, saying " not again it will kill me ” ! Upon cessation of the last seizure , Cerletti writes that the patient “ sat up of his own accord , looked about him calmly with a vague smile , as though asking what was expected of him. I asked him "what has been happening to you?" He answered, with no more gibberish : " I don't know, perhaps I have been asleep .” Cerletti completed a course of 14 total treatments on the patient who remained completely symptom free for the next two years , after which he was lost to follow up. And so, Cerletti had successfully carried out the first trial of electroconvulsive therapy.

6. What is ECT? ECT is a form of physical therapy It is an artificial induction of grandmal seizure (tonic phase 10-15sec, clonic phase 30-60s) via the delivery of electrical charges to the brain in a controlled manner and of relatively brief duration to treat certain psychiatric illnesses

7. E l e c t r o p h ys i o l o g i c a l P r i n c i p l e s ▶ O h m ’ s L a w : I = E/ R ( I = c u rre nt , E = v olt a g e, a n d R=resistance) ▶ D o s e o f e l ec t r i c i t y i n E C T = 10 - 5 milliCoulombs ▶ Bra i n h as lo w i m p e d a n ce (re s i s t a n ce), sk ul l h as very high impedance . Only 20% of applied charge ac tu a ll y e nt ers th e b ra i n . ▶ Seizure involves propagation of action potentials in a l ar g e p erce nt a g e o f n e u r on s .

8. Mechanism of action ▶ Neurotransmitter levels increase in CSF after seizure. Results in down regulation of Beta Adrenagic receptors ▶ During Seizure - PET studies shows a transient break in continuity of the blood brain barrie r which results in angiogenesis and neurogenesis . Thus increase its permeability , cerebral blood flow and metabolism

9. Mechanism of action cont’ ▶ After the seizure, blood flow and glucose metabolism are decreased, perhaps most markedly in the frontal loves. Some reaseach incades that the degress of decrease in cerebral metabolism is correlated with therapeutic response (Suzuki et al.,2006)

10. The decision to use ECT is based on the risk/benefit analysis for the specific patient Patient’s diagnosis Severity of illness Treatment history Anticipated speed of action and efficacy of ECT Medical risks Anticipated adverse effects The likely speed of action, efficicacy and safety of alternative treatments

11. Indications Selection of patients for Electroconvulsive Therapy (ECT) is of utmost importance to ensure that the treatment is effective , and the risk is kept minimal . Treating practitioners should have a good understanding of the indications for ECT and its potential contraindications before deciding on ECT.

12. Factors to consider when prescribing ECT for the individual patients include: Diagnosis Severity of symptoms Urgency of response needed Potential vulnerability to cognitive and physical adverse effects Previous good response to ECT Co- existing medical conditions Concurrent use of medical and/or psychiatric medications

13. ECT for major psychiatric illnesses: Depressive disorder i.e. major depressive disorder with or without psychotic features with melancholic features with peripartum onset Bipolar disorder , in manic episode major depressive episode mixed episode Psychotic disorders i.e. schizophrenia in acute phase or with treatment- resistant and predominantly disorganized features schizoaffective disorder puerperal psychosis

14. ECT for other conditions: Catatonia A thorough medical and neurological work- up is to be performed prior to initiating ECT to identify any reversible medical conditions. In malignant catatonia , as it is a life- threatening condition, ECT should be administered early. Neuroleptic malignant syndrome (NMS) Antipsychotics should be discontinued and autonomic stability is to be achieved before initiating ECT. Repetitive self- injurious behaviour or challenging behaviour in autism ECT has shown a decrease in self-injury, elimination of catatonic symptoms, acquisition or recovery of functional life skills, and return to baseline functioning. Maintenance ECT is often required to sustain improved clinical status.

15. ECT for other conditions: Challenging behaviour and mood disorder in intellectual disability Evidence mainly derived from case reports and case series involving those with co- morbid unipolar and bipolar depression. Agitation and aggression in patient with dementia ECT has shown to decrease agitation, reduce psychotropic polypharmacy and improve global functioning level. Parkinson’s disease (PD) with motor signs (i.e. tremor, bradykinesia, rigidity) not responding to medications with refractory psychosis, major depression or catatonic stupor May need to consider adjusting dose of antiparkinsonian agent during ECT course, to prevent possibility of treatment- emergent dyskinesia or psychosis

16. ECT as first-line treatment ECT is prescribed as the first- line treatment (primary use) prior to a trial of psychotropic medication in such situations: 1. Rapid and definitive response is required due to severity of the psychiatric or medical illness especially in cases with high suicidal risk or severe psychomotor retardation with associated problems e.g. poor oral intake Risks of other alternative treatments outweigh risks of ECT Previous good response to ECT in particular treatment- resistant depression Patients who prefer ECT as their choice of treatment

17. ECT as second-line treatment ECT is prescribed as a second- line treatment (secondary use) in one of the following: Treatment- resistant cases especially depression Cases with severe adverse effects with or intolerant of medications Deterioration of the psychiatric or medical condition and the need for rapid, definitive response e.g. severe or prolonged mania with persistent or life- threatening symptoms

18. Electrophysiology in ECT Phases of ECT- EEG recording include recruitment , polyspike , polyspike with slow- wave complexes , termination and immediate post- ictal . When seizure is adequately induced, the amplitude, morphology and duration of each of these phases may differ inter- individually as well as intra- individually.

19. Figure 1.2(i): Phases in a sample of ECT- EEG recording

20. Table 1.2(i) : Phases of ECT- EEG recording with corresponding motor and EEG responses ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity 2 Figure 1.2(i): Recruitment phase is observed up to 0.042s Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow- wave complexes Figure 1.2(i): Polyspike with slow- wave complexes from 0.12 to 0.29s Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s Immediate post- ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

21. ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity Figure 1.2(i): Recruitment phase is observed up to 4s

22. Table 1.2(i) : Phases of ECT- EEG recording with corresponding motor and EEG responses ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity 2 Figure 1.2(i): Recruitment phase is observed up to 0.042s Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow- wave complexes Figure 1.2(i): Polyspike with slow- wave complexes from 0.12 to 0.29s Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s Immediate post- ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

23. ECT- EEG recording phases Motor response EEG response Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s

24. Table 1.2(i) : Phases of ECT- EEG recording with corresponding motor and EEG responses ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity 2 Figure 1.2(i): Recruitment phase is observed up to 0.042s Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow-wave complexes Figure 1.2(i): Polyspike with slow-wave complexes from 0.12 to 0.29s Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s Immediate post- ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

25. ECT- EEG recording phases Motor response EEG response Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow- wave complexes Figure 1.2(i): Polyspike with slow- wave complexes from 0.12 to 0.29s

26. Table 1.2(i) : Phases of ECT- EEG recording with corresponding motor and EEG responses ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity 2 Figure 1.2(i): Recruitment phase is observed up to 0.042s Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow- wave complexes Figure 1.2(i): Polyspike with slow- wave complexes from 0.12 to 0.29s Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s Immediate post- ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

27. ECT- EEG recording phases Motor response EEG response Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s

28. Table 1.2(i) : Phases of ECT- EEG recording with corresponding motor and EEG responses ECT- EEG recording phases Motor response EEG response Recruitment - - Initial low amplitude and fast frequency activity 2 Figure 1.2(i): Recruitment phase is observed up to 0.042s Polyspike Tonic muscle contraction High amplitude, fast frequency spike and polyspike (hypersynchronous) activity Figure 1.2(i): Polyspike waveform from 0.042 to 0.12s Polyspike with slow- wave complexes Clonic muscle contraction High amplitude polyspike and slow- wave complexes Figure 1.2(i): Polyspike with slow- wave complexes from 0.12 to 0.29s Termination - - Progressive change in slow- wave amplitude and/or frequency i.e. variable amplitudes become slower and more disorganised Figure 1.2(i): Termination phase from 0.29 to 0.42s Immediate post-ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

29. ECT- EEG recording phases Motor response EEG response Immediate post- ictal - - Bioelectric suppression following seizure termination Figure 1.2(i): Seizure terminates around 0.42s with the start of immediate post- ictal silence

30. Sample 1

31. Sample 2

32. Physiological changes during ECT Cardiovascular response Central Nervous System Other physiologic effect

33. Physiological changes during ECT 1. Cardiovascular response Post- seizure: Gradual return to baseline haemodynamic function. A third phase of parasympathetic discharge may occur following termination of seizure. Parasympathetic vagal outflow Sympathetic surge During ECT stimulation Initial, brief Later, more prominent Haemodynamic changes transient hypotension and bradycardia; rarely, an overly increased vagal stimulation can cause asystole hypertension and tachycardia Corresponds to tonic muscle contraction clonic muscle contraction

34. Physiological changes during ECT Central Nervous System In ECT, it is postulated that post- stimulation causes the brain autoregulatory mechanism to function ineffectively resulting in an increase in cerebral blood flow with higher rate of oxygen consumption. Furthermore, the rapidly increasing systemic blood pressure may have transiently overwhelmed the cerebral autoregulation. Other physiologic effect Transient substantial increase in intraocular pressure post- ECT is well documented in early literatures. However, the magnitude was not of clinical concern to most patients except in those with severe ophthalmic diseases e.g. narrow- angled or closed-angle glaucoma.

35. Adverse Events Injury to mouth Most common, including dental and tongue injury which is c o mm on l y du e t o i n c o rr ec t b i t e b l o c k p l ace m e n t Cognitive adverse events Cognitive adverse events Common cognitive impairments are memory and orientation anterogde memory dysfunction i.e learning new verbal skills, may recover after variable time (from days to month, unlikely long term) retrograde memory dysfunction i.e learnt information prior to ECT (autobiographical and impersonal memory), recoery is slower than anterograde, may have residual (patchy memory) Subjective Memory loss, patient reported despite no evidence in neuropsychological testing

36. Adverse Events Post ECT Delirium Transient – arbitrary to allow not longer than ½ hr Delirium >1/2 hr , must resume EEG monitoring Must rule out prolonged seizure, to abort seizure if it is due to that M u s t b e r e v i e w e d b y p s y c h i a t r i s t i n c h a r g e To prevent further delirium, need to determine correct stimulus dose for next treatment Need to consider the use of unilateral ECT, reduce frequency of treatments, minimize concurrent use of sedative antipsychotics and lithium33 Hypomania or mania ‘switch’ switch from depression ot hypomania or mania may occur case report suggest ECT may be continued as it has mood stabalizing properties

37. Electrodes Placement ▶ 2 methods of electrode placement ▶ i.Bitemporal ▶ Bilaterally one inch above the midpoint of the line connecting external canthus and tragus ▶ ii.Unilateral ▶ 1 inch lateral to the point of intersection of lines connecting 2 auditory tragi and that of the nasion and anion on the non dominant hemisphere for vertex electrode placement and the other at the temporal placement on the non dominant hemisphere ▶ IMPORTANT : in unilateral ECT, cannot use elastic strap and metal plate as in bilateral, must use hand-held electrodes ▶ An additional staff is required to provide counter force so that the patient’s head remains at proper position during ECT

38. Pharmacotherapy in ECT A large proportion of these studies is based only on theoretical considerations and most of the evidences are derived from case reports or case series. Clinicians’ clinical judgement is required and essential in managing ECT cases in particular those with complex pharmacotherapy. Medication should be reviewed before commencing ECT , during the ECT course and post- ECT recovery period . Cautions should be considered on the effects of medications on seizure threshold (ST), seizure duration (SD) and therapeutic effectiveness of ECT, neurophysiological effects of ECT especially cardiovascular risks and post- ECT cognitive sequelae.

39. 1.4.1 Concomitant use of psychotropics: Antidepressants Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Selective serotonin reuptake inhibitor (SSRI) May increase ST theoretically. No or minimal effect on SD. Sertraline may reduce metabolism of propofol. Serotonin syndrome has been reported when SSRI combined with ECT. Generally safe with ECT. Tricyclic antidepressant (TCA) Reduced ST with higher dose of TCA. May increase SD. Amitriptyline can decrease the metabolism of propofol. Propofol may decrease the metabolism of clomipramine. Propofol may increase the CNS depressant effect of imipramine. Exaggerated response to indirect sympathomimetic drugs e.g. ephedrine may cause hypertensive crises. TCAs do not increase risk of prolonged post- ECT confusion despite having high anticholinergic effects. Generally safe with ECT at recommended therapeutic dose with potential better clinical efficacy.

40. Antidepressants Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Venlafaxine No or minimal effect on ST and SD at standard dose. N/A May cause serotonin syndrome and other cardiovascular adverse effects e.g. ventricular tachycardia especially in combination with both lithium and ECT. If indicated, keep dose <300mg/day or possibly <200mg/day to reduce risk of potential cardiovascular adverse effects. Duloxetine N/A Minor risk of orthostatic hypotension and syncope if combined with propofol. Weak association between duloxetine and ventricular tachycardia when combined with lithium during ECT. No recommendation Mirtazapine May minimally increase SD. Propofol may increase mirtazapine’s CNS depressant effect. N/A Use can be continued as it may enhance the therapeutic effect of ECT.

41. Antidepressants Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Agomelatine No study on its effect on ST or SD. May potentiate the CNS depressant effect of inhalational or intravenous anaesthetic drugs (as well as benzodiazepines). Not known to be pro- convulsive in patient with epilepsy. No recommendation Monoamine oxidase inhibitor (MAOI) e.g. Moclobemide No study on its effect on ST or SD. Combined use with propofol and etomidate is safe during ECT. Although Moclobemide, a reversible inhibitor of monoamine oxidase A (RIMA), has lesser interaction with anaesthetic drugs (e.g. ephedrine) to cause hypertensive crisis, its occurrence is still possible. Combined use with pethidine may cause serotonin syndrome. Not known to be pro- convulsive in patients with epilepsy. Recommend to stop MAOI 24 hours before anaesthesia if it is not effective. MAOI may be continued if it is effective. Switching to Moclobemide may be considered if interaction between MAOI and anaesthesia is a concern.

42. Antipsychotic Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Antipsychotic Chlorpromazine and clozapine may increase SD; others, no obvious effect. Combined use of clozapine/olanzapine/ quetiapine and propofol may increase the CNS depressant effect. Minor risk of hypotension with risperidone-propofol combination. No significant increase in QTc when combined with ECT. Clozapine is not associated with post- ECT cognitive impairment e.g. delirium. Continue use with ECT as combination may produce synergistic therapeutic effects.

43. Benzodiazepine Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Benzodiazepine (BDZ) BDZ may theoretically increase ST but the evidence is not robust. Decrease SD. May affect the efficacy of unilateral ECT but not bilateral ECT. Synergistic interaction between midazolam and propofol. May increase cognitive side effects when combined with ECT. BDZ should be avoided or used at reduced doses during ECT. If BDZ use could not be discontinued or unavoidable, may consider: Convert to BDZ with shorter half- life e.g. lorazepam Use higher stimulus dose or bilateral ECT Use flumazenil to temporarily reverse its effect before ECT Use of substitutes e.g. zolpidem

44. Mood Stabiliser Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Lithium No effect on SD. Higher serum lithium level is associated with longer duration of post- ECT recovery due to the synergistic reaction with succinylcholine. Risks of post- ECT confusion, delirium and serotonin syndrome especially in elderly. If no clear indication of lithium use, to discontinue at least 48 hours before ECT; longer washout period is required for high or toxic lithium level. Recommend to maintain lithium level at lower therapeutic end and ensure hydration prior to and during ECT.

45. Mood Stabiliser Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Others May increase ST. Interaction between propofol and valproate may delay recovery. Use of mood stabiliser as an anticonvulsant in epilepsy cases should be continued as risk of unmodified seizures may outweigh risk of higher stimulus doses. As higher stimulus doses may be needed, increased rates of confusion are possible. Consultation with the neurologist or physician is required prior to ECT initiation. No significant adverse effect if ECT combined with lamotrigine, gabapentin or topiramate. Discontinue if possible before the start of an acute ECT course. Alternatively, halve the dose and then withdraw over a 1- week period prior to ECT. Recommence at the end of ECT course.

46. Other Psychotropics Concomitant Psychotropics Effects on ECT Interaction with anaesthetic drugs Additional information Recommendations Acetyl- cholinesterase inhibitor for dementia e.g. donepezil & rivastigmine Theoretically may decrease ST and increase SD due to its cholinomimetic effect but no documented evidence. Theoretical complex interaction with muscle relaxant e.g. succinylcholine may result in prolonged apnoea, muscle paralysis and cardiac arrhythmia. However, no concrete evidence. N/A Safe to continue use in ECT. Psycho- stimulant: Methylphenidate No effect on ECT- induced seizure though theoretically may potentiate seizure activity. N/A N/A No recommendation

47. Generally, non- psychotropics that are necessary to optimise medical conditions should be given before ECT as these medications may have a protective effect to the physiological changes induced by ECT. However, caution should be taken on any potential negative effects. 1.4.2 Concomitant use of non- psychotropics

48. Concomitant non- psychotropics Effects on ECT Effects of ECT on medical conditions Additional information Recommendations Antihypertensive Beta blocker and calcium channel antagonist may increase ST (very weak evidence). Esmolol may reduce SD. ECT may increase risk of hypertension during sympathetic phase if routine dose of anti-hypertensive is not served. Risk of urinary incontinence during ECT and electrolytes imbalance (e.g. Mg 2+ and K + ) especially those on long- term treatment of diuretics. Concurrent use of beta blocker may be associated with post- stimulus asystole (weak evidence). Administer antihypertensive (except diuretic) 2 hours prior to ECT with sips of water. Administer diuretic post- ECT. Theophylline Reduce ST. Increase SD with risk of status epilepticus. Patients with chronic obstructive pulmonary disease (COPD) or asthma are susceptible to hypoxia due to acute exacerbation from bronchial spasm during parasympathetic phase of ECT. Risk of asthmatic exacerbation post- ECT if discontinued. If possible, taper off and substitute with another bronchodilator. Alternatively, administer theophylline at lowest effective dose. Consultation with respiratory physician is required prior to ECT initiation. 1.4.2 Concomitant use of non- psychotropics

49. Concomitant non- psychotropics Effects on ECT Effects of ECT on medical conditions Additional information Recommendations Anti-gastric medication N/A ECT may worsen gastroesophageal reflux disease (GERD) via vagal nerve stimulation and potential aspiration. N/A Antacids or proton pump inhibitor (PPI) can be safely administered pre- ECT. Anti- diabetic agent N/A ECT may cause hyperglycaemia in diabetic patients but insignificant to result in hyperglycaemic crises. Risk of hypoglycaemia as patient fasted from the night before ECT. Perform pre- and post- ECT glucose monitoring. Withhold OHA the morning before ECT as patient fasted from the night before ECT. For insulin dependent diabetic patients, ECT should be done early in the morning; consider to delay the usual morning insulin till after ECT and before breakfast. 1.4.2 Concomitant use of non- psychotropics

50. Concomitant non- psychotropics Effects on ECT Effects of ECT on medical conditions Additional information Recommendations Warfarin N/A ECT does not increase risk of intracranial haemorrhage; safe for patients on long- term warfarin. N/A Continue if no contraindication and maintain INR < 3.5. Decision to withhold on case- by- case basis thus consultation with physician is required prior to ECT initiation. Anti-glaucoma N/A ECT does not worsen glaucoma though theoretically ECT may increase intraocular pressure. Caution is required on the use of long- acting anti- cholinesterase drops e.g. echothiophate due to risk of prolonged succinylcholine-induced apnoea from irreversible cholinesterase inhibition. Although cases reported successful use of ECT, it is recommended to administer anti- glaucoma drops prior to each ECT session. Consultation with ophthalmologist is required prior to ECT initiation. 1.4.2 Concomitant use of non- psychotropics

51. INSTRUMENTS NEEDED FOR ECT ▶ INSTRUMENTS FOR ANESTHESIA ▶ SUCTION APPARATUS ▶ FACE MASK ▶ OXYGEN CYLINDER ▶ TONGUE DEPRESSOR ▶ MOUTH GAG ▶ RESUSCITATION APPARATUS ▶ FULL SET OF EMERGENCY DRUGS, ECT DRUGS ▶ DEFIBRILLATOR

52. N u r s e / M e d i c a l O ff i c e r A ss i s t a n t To finalize the list of patients for ECT a day before ECT session E C T c oo r d i n a t o r / N u r s e i n c h a r g e To send the ECT patients list to the Department of Anaesthesiology before 12 noon the day before ECT session P a t i e n t i s fa s t e d b e f o r e 1 2 m i d n i g h t Personal hygiene is attended N u r s e / M e d i c a l O ff i c e r A ss i s t a n t R e m o v e j e w e ll e r y / d e n t u r e P a t i e n t o f f e r e d u s e o f t o i l e t P r e E CT o b s e r v a t i o n t a k e n a n d d o c u m e n t e d C h e c k p a p e r w o r k : c o n s en t , p r e v i o u s EE G D o c u m e n t s t o a cc o mpa n y p a t i en t M e d i c a t i o n c h a r t N u r s e / E C T C oo r d i n a t o r Medical record I n f o r m e d c o n s en t E CT T r e a t m e n t R e c o r d Pre-ECT Observation Heart Rate, Blood Pressure, SpO2, Temperature checking P s y c h i a t r i s t / M e d i c a l O ff i c e r Right Patient / Electrode Placement / Dentures / Valid Consent / Bite Block Ready Begin treatment with appropriate st imulus dose R e v i e w EE G a n d t o make c l i n i c a l d e c i s i o n o n s u b s e q uen t s t i m u l u s d o s e N u r s e / E C T C oo r d i n a t o r Document the st imulus dose, EEG seizure durat ion, and EEG quality (onset, symmetry, amplitude, durat ion) Post ECT Observation Heart Rate, Blood Pressure, SpO2, Respiration, Temperature St ate of consciousness: Alert, drowsy, or delirium T i me t a k e n t o r e g a i n c o n s c i o u s ne s s Decide transfer out to ward (with anaesthetist permission)

53. ECT AND THE LAW IN MALAYSIA ▶ Based on Mental Health Act 2001 Section 77, ECT is considered as a surgical procedure, therefore consent of ECT is the same consent for surgical procedure in psychiatry. ▶ When a mentally disordered person is required to undergo ECT, consent for any of them may be given : ▶ by patient himself/herself if he/she is capable of giving consent as assessed by a psychiatrist. ▶ by his/her guardian in case of a minor, or a relative in case of an adult, if the p a t i e n t i s i n c a p a b l e o f g i v i n g c o n s e n t . ▶ by 2 psychiatrists, one of whom shall be the attending psychiatrist, if there is no g u a r d i a n o r re l a t i v e a v a i l a b l e o r t r a c e a b l e, a n d t h e p a t i e n t h i m s e l f / h er s e l f i s incapable of giving consent.

54. ECT AND THE LAW IN MALAYSIA ▶ In cases of emergencies, consent for ECT may be given : b y t h e g u a r d i a n / r e l a t i v e O R . by 2 MOs or 2 registered medical practitioners, one of whom shall preferably by a psychiatrist, if there is no guardian/relative immediately available/traceable. ▶ I n D e p a r t m e n t o f P s y c h i a t r y a n d M e n t a l H e a l t h H K L : - consent for ECT only lasts for 14 days - new consent is mandatory if duration of ECT > 14 days. ▶ According to Malaysia Child Act 2001, definition of a child is a person < 18 year-old, therefore consent for ECT must be obtained from the child’s parent / legal guardian.