EPIDEMIOLOGY TCA & MAOI - PowerPoint Presentation

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EPIDEMIOLOGY

TCA & MAOI

first-generation antidepressant.Antidepressants third most common cause of drug-related fatalities .

cyclic antidepressants

the most commonly identified class of antidepressants to cause overdose-related deaths.!

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PHARMACOKINETICS

peak plasma levels :

between 2 and 6 hours Tissue cyclic antidepressant levels :

10 to 100

times greater than plasma levels.

Attempts to remove cyclic antidepressants by hemodialysis,hemoperfusion,

peritoneal dialysis, or forced diuresis generally are

unproductive.

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The average half-life of cyclic antidepressants

24 hours (range, 6 to 36 hours).

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TOXICITY

patients at

higher risk for cyclic antidepressant toxicity include who have medication such as:Cardiotoxic

Sedative-hypnotic

Geriatric

patients, underlying heart or neurologic

disease.

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Desipramine

Most potent sodium channel blocker

Precipitate severe cardiotoxicity (e.g.,

wide QRS

complex,

hypotension) It is associated with a higher fatality rate

than the other cyclic antidepressants

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Amoxapine

and maprotiline

Associated with greater toxicity than other cyclic antidepressants, especially in regard to causing seizures.

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CLINICAL FEATURES

Mild

antimuscarinic symptoms: (dry mouth and

axillae,sinus

tachycardia)

Severe cardiotoxicity secondary to sodium channel blockade.

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Most common symptom

:

Altered mental status.

(GCS of <8 in the ED

is a strong predictor of serious complications such as

seizures and cardiac dysrhythmias

)Most frequent dysrhythmia:

Sinus tachycardia.

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Serious toxicity

within

6 hours of major cyclic antidepressant

ingestion and consists of:

coma

cardiac conduction delays supraventricular

tachycardia hypotension respira

tory depression ventricular tachycardia

seizures

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Secondary complications

Apiration

pneumoniaAnoxic encephalopathyHyperthermia.

Rhabdomyolysis

.

Pulmonary edema

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Seizures

Generalized and of brief duration.

Exception : amoxapine

and

maprotiline

(these agents can cause status epilepticus.)

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DIAGNOSIS

Urine tests

Cannot differentiate between therapeutic and toxic levels. False positive results have been reported for a number of medications such as :

carbamazepine

. cetirizine, cyclobenzaprine

. cyproheptadine. diphenhydramine

, hydroxyzine. quetiapine.

phenothiazines

(e.g.•

thioridazine

).

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ECG abnormalities

The classic ECG with cyclic antidepressant

toxicity:(sinus tachycardia

,

right axis deviation

and prolongation of the PR,QRS. and QT intervals)

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ECG abnormalities

develop within

6 hours of ingestion and typically resolve over 36 to

48

hr.

The identification of either QRS complex widening of >100 ms, right axis deviation of > 120 degrees, or a

Brugada pattern warrants sodium bicarbonat

therapy and admission to a ICU.

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TREATMENT

Evaluation for

: alterations of consciousness.

hemodynamic instability

respiratory impairment.

IV line Continuous cardiac rhythm monitoring

Serial ECGs laboratory studies (electrolyte. creatinine. and glucose level)

Serum acetaminophen level ABG

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Antimuscarinic

symptoms

: urinary catheterization nasogastric

tube

Patients who are initially asymptomatic may deteriorate rapidly and therefore should be

monitored closely for 6 hours.

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GI DECONTAMINATION

ipecac syrup cannot be recommended

charcoal

single 1 gram/kg dose.

gastric lavage

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• SODIUM BICARBONATE THERAPY:

Indications:

- Hypotension refractory to fluid hydration.

-

Cardiac conduction abnormalities

(e.g., prolonged QRS duration or Brugada pattern), -Ventricular

dysrhythmias.

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SODIUM BICARBONATE THERAPY

IV bolus of

1 to 2 mEq/kg.

which can be repeated until patient

improvement

is noted or until blood pH equals 7.50 to 7.55

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ALTERED LEVEL OF CONSCIOUSNESS

Coma

is rapid in onset and serves as a predictive factor for development of cardiotoxicity and/or seizures.Flumazenil

Reassurance. decreased environmental stimulation. and benzodiazepines.

Physostigmine

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SEIZURES

Seizures are

generalized and of brief duration.Focal seizures are atypical and should prompt further neurologic evaluation.

Seizures are common with

maprotiline

& amoxapine ingestions and require aggressive management. Because status epilepticus

is frequently associated with them.

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Benzodiazepines

( diazepam,

lorazepam) are the anticonvulsants of

choice

to stop existing seizure activity

Seizures resistant to benzodiazepine: Barbiturates(e.g .•

phenobarbital)Endotracheal intubation and respiratory support are required when benzodiazepines are combined with barbiturates or

propofol.

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HYPOTENSION

1..Treated with isotonic crystalloid fluids in IV boluses

10 ml/kg.2.. does not improve:

sodium bicarbonate

3.. does not improve:

vasopressor most effective:

norepinephrine (1 microgram/min to 30 micrograms/min.)

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CARDIAC CONDUGION ABNORMALITIES

AND DYSRHYTHMIAS

Asymptomatic patients with

sinus tachycardia

,

isolated PR interval prolongation or first-degree atrioventTicular block do not require specific pharmacologic therapy.

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Asymptomatic or mildly toxic patients with

isolated QRS complex prolongation

(QRS duration is > 100 milliseconds) should be treated with sodium bicarbonate

therapy.

Hyperventilation Hypertonic saline

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Ventricular

dysrhythmias

: sodium bicarbonatesecond agent of choice: Lidocaine

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Contraindicated medications

all class

Ia and Ic antiarrhythmic

agents,

B blockers Calcium channel blockers

all class III antiarrhythmic agents.

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Intravenous lipid emulsion:

20% lipid emulsion 100 mL IV bolus

over 1 minute. followed by 400

mL

IV over 20 minutes in patients with life-thTeatening cyclic antidepressant induced cardiotoxicity that is refractory to other measures

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DISPOSITION AND FOLLOW-UP

Asymptomatic after 6 hours

of observation do not require hospital admission for toxicologic reasons.

All symptomatic patients :

hospital admission

.signs of moderate to severe toxicity: ICU

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