Section 6: Drugs Flashcards
6.1 Given an exposure, identify a drug that when ingested in small amounts is potentially life
threatening.
6.1 Given an exposure, identify a drug that when ingested in small amounts is potentially life
threatening.
- Cyclic antidepressants (amitriptyline; imipramine; desipramine; nortriptyline; doxepin)
a. Of note, imipramine is used for childhood enuresis. Comes in 150mg tabs. One tab for a 10kg toddler can be fatal.
b. amoxapine has less cardiotoicity but sz and coma are frequent presenting signs
- Phenothiazines (chlorpromazine; thioridazine; thorazine)
a. anticholinergic, CNS effects, quinidine like cardiotoxicity, rigidity
- Beta blockers (metoprolol; propranolol)
a. bradycardia/hypotension generally well tolerated in peds
b. *hypoglycemic coma and sz in peds
c. Propranolol - may cause sz and altered cardiac conductivity
d. Sotalol - may cause QT prolongation/torsades
- Calcium channel blockers (amlodipine; diltiazem; nicardipine; nifedipine, verapamil)
a. bradycardia and hypotension
b. cardiovascular collapse and sz (verapamil)
- Quinidine (antimalarial medication)
a. type 1a antiarrhythmic
b. cardiac rhythm disturbances
- Clonidine
a. coma, miosis, bradycardia, hypotension in children
b. patches have caused critical cardiovascular depression.
- Imidazoline eye drops
a. Similar to clonidine. SA node arrest
- Lomotil (combination formula - diphenoxylate and atropine)
a. Diphenoxylate is an opiod. 2 tabs have been fatal. Can have confusing constellation with anticholinergic component, but coma and respiratory depression are most common
- Methadone
a. CNS and respiratory depression
* QTc prolongation*
- Topicals
a. Benzocaine
i. Methemoglobinemia (cyanosis)
ii. Sz (common with local anesthetics but uncommon with benzocaine)
b. Camphor
i. CNS, resp depression, sz (usually within an hour)
c. Lindane
i. Organochlorine (chlorinated hydrocarbon)
- topical scabicide
- Sz and CNS depression when ingested
(permethrin - less toxic alternative)
d. Methyl salicylate
i. ASA toxicity
- Chloroquine
a. Cardiac dysfunction
1 tab/300g - fatal to a 1 y/o
- Phenylpropanolamine (amphetamine)
a. Common ingredient in OTC decongestants. Narrow therapeutic-toxic margin
b. B-agonist action
c. HTN with compensatory bradycardia
d. Cerebral infarction noted in adults
e. SVT in infant
- Quinine
a. Used to treat malaria and nocturnal muscle cramps
b. Similar to quinidine but less cardiotoxic
c. Causes direct retinal toxicity
d. Hypersensitivity reactions:
i. Blackwater fever (hemolysis, hemoglobinemia, renal failure)
- Sulfonylureas
a. Ex glyburide; glipizide; chlorpropamide
b. Hypoglycemia: can be delayed and persistent
- Theophylline
a. Used to treat asthma, COPD, apnea of prematurity
b. Sz, cardiac arrhythmias
c. Action:
i. Beta 1 and 2 stimulation
ii. Increase heart rate/contractility; bronchodilation; skeletal muscle vasodilation; uterine relaxation
iii. Inhibition of phosphodiesterase and adenosine receptors
iv. Refractory sz with decreased cerebral blood flow in OD
d. Narrow therapeutic window; Toxicity at 80-100mg/kg blood level
e. Chronic toxicity more dangerous than acute
f. Usually sustained release
g. Should draw levels Q2-4 hrs as levels can peak 12-16 hrs post ingestion
h. Caffeine OD has similar s/s and can create false positive on old blood tests
i. S/S of Theophylline
i. Mild
1. GI: n/v
2. CNS: anxiety; tremor
3. Labs: Metabolic acidosis; electrolyte abnormalities
ii. Severe
1. GI: vomiting
2. Cardiac: hypotension, dysrhythmias
3. CNS: seizures (often refractory)
4. Labs: metabolic acidosis
iii. Chronic
1. Vomiting occasionally
2. Tachycardia common
3. Hypotension rare
j. Metabolic effects (hypokalemia and hyperglycemia) do occur
k. Seizures with low blood levels
l. Labs (Theophylline):
i. LOW: potassium, phosphorus; magnesium
ii. HIGH: calcium, glucose
m. Treatment (Theophylline)
i. Supportive
ii. Consider nonselective beta blockers for tachycardia and hypotension (propranolol or esmolol)
iii. Caution for hx of asthma/wheezing
iv. Consider multi-dose activated charcoal (enteroenteric recirculation)
v. Dialysis for severe toxicity (status or level > 200mg/L)
- Also consider iron, antidepressants, other cardiovascular drugs, salicylates, anticonvulsants.
6.2 Identify the toxicity and symptoms of exposure to analgesics including over-the-counter or
prescription.
Analgesics, Antipyretics, and Anti-inflammatory agents:
- Acetaminophen
a. Normal max dose
i. 75mg/kg/day or 4g/day for a normal adult
b. Single acute ingestion toxic dose
i. Adult local referral 140 mg/kg local - national is >200mg/kg or 10g, whichever is less.
ii. Child 200mg/kg
c. High risk pts
i. Chronic alcoholics (will have more P450 thus create more NAPQI)
ii. Malnutrition (have less substrate to bind NAPQI thus creates more liver damage)
iii. Pregnant patients (fetal death)
iv. Pts taking CYP2E1/cytochrome P-450 inducers (isoniazid)
[1. This is principal enzyme responsible for breaking acetaminophen into toxic metabolites (thus inducers worsen hepatic injury)]
v. Kids < 5 y/o use sulfation pathway more; so they have less NAPQI production
d. S/S of OD (Acetaminophen)
Stage 1; (0-24hrs)
1. Anorexia, n/v
Stage 2; (24-72hrs)
1. Elevated AST/ALT (AST greater); bilirubin and PT; n/v resolve
Stage 3; (72-96hrs)
1. Hepatic necrosis with increasing AST/ALT; coagulopathy; jaundice; hepatic and renal failure; encephalopathy; death or stage 4
Stage 4; (>96hrs)
1. Healing of liver damage with resolution of enzymatic and metabolic abnormalities
e. Labs (Acetaminophen)
i. APAP 4 hrs post ingestion (for extended release check 4+6 hour levels)
ii. BUN/Cr
iii. AST/ALT
iv. PT/INR
v. Glucose
f. Four hr treatment level on Rumack/Matthew Nomogram
i. Treatment level is 150 mcg/ml
ii. Excludes chronic ingestion
iii. Excludes extended release, diphenhydramine containing, or anticholinergic products
iv. In these cases with elevated LFTs (AST usually > than ALT) start NAC with any positive APAP level
g. Treatment (Acetaminophen)
i. Activated Charcoal (<1-2 hrs)
ii. NAC (best started w/i 8 hrs)
iii. Anti-emetics (Zofran preferred)
NOTE: large OD can act as a metabolic poison and cause anion gap metabolic acidosis.
i. Dialysis is effective, but rarely used. May be consideration in later term pregnancy or with significant acidosis in massive ingestion.
Kings College Criteria
Ph < 7.3 or
INR >6.5, Cr > 3.4, and grade 3-4 encephalopathy
- Aspirin
a. Analgesia, anti-inflammatory, antipyretic
iii. Common forms ASA: Oil of Wintergreen (ACF - 1.39/Sp.G - 1.18), Bismuth salicylate (ACF - 0.49)
b. Delayed absorption in OD (bezoar formation)
c. Is an UNcoupler
d. S/S (Aspirin)
i. Respiratory alkalosis (protective as alkalotic environment prevents crossing into CNS)
ii. Possible metabolic alkalosis from emesis
iii. Final Metabolic acidosis from mitochondrial uncoupling
iv. GI upset, tinnitus/auditory changes, tachypnea followed by
v. Coma, seizures, hyperthermia, muscle rigidity
vi. Chronic OD more toxic
e. Treatment (Aspirin)
i. Bicarb for acidosis (Goal pH 7.5) and/or ASA > 40mg/dL (national ASA > 30 and rising)
ii. Dialysis for severe OD (level >100 mg/dL, coma, seizures).
1. dialysis for inability to tolerate fluids/bicarb treatment (renal failure or pulmonary edema)
iii. Monitor ASA; BMP level Q2H
iv. May need glucose with ASA associated AMS
1. Decreased BS in brain even when BS is normal in blood
v. Standard hydration changing to LR
1. NS could create some anion gap acidosis and increase distribution across blood/brain barrier
- Colchicine
a. General cellular poison, inhibits dividing cells, rapidly absorbed, extensively distributed to body tissues
b. Multiorgan effects can occur from days to weeks
i. s/s delayed 2-12 hrs in acute OD
ii. severe gastritis: abd pain, n/v/bloody diarrhea
iii. shock, sz, coma, lactic acidosis
iv. rhabdo, kidney failure, DIC
v. Late: bone marrow suppression, alopecia, myopathy, neuropathy
c. Renal insufficiency, erythromycin, cimetidine and cyclosporine inhibit colchicine clearance
d. Treatment: supportive care, AC, dialysis not effective
- Nonsteroidal anti-inflammatory drugs
a. Act by prostaglandin inhibition (COX inhibitors); inflammatory mediators
b. Five kinds of NSAIDS
i. Propionic acids (ibuprofen)
ii. Acetic acids (toradol)
iii. Fenamic acid (can cause seizures; requires aggressive management)
[1. Ex mefenamic acid/Ponstel]
iv. Oxicams (piroxicam)
v. Pyrazolines (require aggressive management)
c. S/S (Nonsteroidal anti-inflammatory drugs)
i. GI c/o
ii. Mild CNS disturbances (drowsiness, h/a)
iii. Massive OD
1. Sz, hypotension, metabolic acidosis, renal and hepatic dysfunction
iv. S/S may occur in children after OD >100mg/kg
d. Treatment (Nonsteroidal anti-inflammatory drugs)
i. Symptomatic
ii. Charcoal
iii. Dialysis not useful
- Opioids
a. Slang terms: China white, brown, superbuick, black tar, hot shot, bird’s eye, homicide
b. Use: snorted, smoked, injected, oral
c. Three receptors: Delta, Kappa, Mu
d. S/S
i. CNS and respiratory depression
ii. Miosis
iii. Noncardiogenic pulmonary edema (complication)
e. Atypical Opioids
i. Have serotonergic properties:
1. Meperidine
ii. Do not cause miosis/may cause seizures:
1. Meperidine/Demerol (sz from metabolite which accumulates with renal
insufficiency as well as from serotonergic effect)
2. Propoxyphene/Darvon (sz)
3. Tramadol (sz)
f. Treatment (opioids)
i. Supportive
ii. Narcan
1. Monitor 4-6 hrs s/p last dose of narcan. Increase time with renal insufficiency as narcan is renally eliminated.
g. Withdrawal (opioids)
i. CNS excitation (restless)
ii. GI (n/v/d/abd pain)
iii. Piloerection, lacrimation, rhinorrhea, diaphoresis
iv. ***FEVER and AMS are not associated with opioid withdrawal
h. Meds for opioid withdrawal (Methadone, Clonidine, Buprenorphine)
i. Methadone (causes QT prolongation)
ii. Clonidine (causes sleepiness/HTN followed by apnea, coma, bradycardia, hypotension)
iii. Buprenorphine (Suboxone). Has opioid antagonist and agonist in the same medication. Can trigger a mild withdrawal in an opioid using patient.
- Serotonin receptor agonists (i.e. sumatriptan)
a. In therapeutic use cause cerebral vasoconstriction, theoretically antagonizing cerebral vasodilation that causes migraines.
b. In overdose lose cerebral selectivity and cause excessive vasoconstriction. This causes HTN and end organ ischemia. Can cause serotonin syndrome.
c. Treatment: supportive care. Treat HTN with nitroprusside or nitroglycerin. Labetalol and dihydropyridine calcium channel blockers may be effective.
d. AC okay. Hemodialysis not effective
- Tramadol
a. Opioid analgesic, also inhibits norepi and serotonin reuptake
S/S:
Euphoria, CNS depression, n/v, serotonergic, sz, no miosis
Treatment:
i. Narcan, charcoal with caution d/t CNS depression, hemodialysis not effective
6.3 Identify the toxicity and symptoms of exposure to anticonvulsants.
6.3 Identify the toxicity and symptoms of exposure to anticonvulsants.
- General s/s of anticonvulsant OD
a. AMS (anxiety, confusion, irritability, lethargy, somnolence)
b. Ataxia
c. N/V
d. Coma, resp depression, hypotension (LARGE OD)
Anticonvulsant Hypersensitivity Syndrome
i. Seen with drugs with an aromatic amine or sulfonamides (Phenobarbital, Primidone)
ii. S/S:
- Skin eruption (SJS); eosinophilia, hepatitis, interstitial nephritis, hypothyroid
Carbamazepine/Oxcarbazepine (Tegratol/Trileptal)
a. Nystagmus, ataxia, hyperreflexia, CNS depression, dystonia, mild anticholinergic s/s
b. Can progress to coma, seizures, rhabdo, renal failure, cardiac interval changes
i. Sz potential close to therapeutic dose
ii. hyponatremia (trileptal)
c. AHS (anticonvulsant hypersensitivity syndrome)
Lamotrigine (Lamictal)
a. Sz, Rash (SJS), AHS (anticonvulsant hypersensitivity syndrome)
b. CNS depression, dizziness, ataxia, nystagmus, hypertonia, QRS prolongation, n/v, hypokalemia, fever, hepatitis, renal failure
Levetiracetam (Keppra)
a. drowsiness
Gabapentin
a. Somnolence, ataxia, dizziness, mild tremor, slurred speech, diplopia
Phenytoin (Dilantin)
a. Rash (DRESS), IV formulation causes cardiotoxicity, AHS (anticonvulsant hypersensitivity syndrome)
b. IV use: bradycardia, hypotension, dysrhythmias. Cardiotoxicity believed from diluent propylene glycol/Na channel blockade
c. Oral: n/v, *NYSTAGMUS, ataxia, CNS depression
d. Chronic use risk of DRESS (resembles viral infection with multiorgan/system involvement)
Pregabalin (Lyrica)
a. Limited data. Large ingestions minimal symptoms. CNS depression to coma.
Tiagabine
a. Somnolence, confusion, agitation, dizziness, ataxia, tremor, clonus, sz
Topiramate (Topamax)
a. Sz, non AG acidosis, hyperkalemia
b. Sedation, confusion, slurred speech, ataxia, tremor, anxiety, sz
Valproic Acid (Depakote)
a. Hyperammonemia, cerebral edema
b. CNS depression, emesis, tachycardia, QTc prolongation, resp depression, sz, cerebral edema, hyperammonemia, high sodium, low calcium
Zonisamide
a. Na channel blockade. Somnolence, ataxia, agitation, bradycardia, hypotension, resp depression, sz
6.4 Identify the toxicity and symptoms of exposure to non-cyclic antidepressants.
- General s/s expected to cause ataxia, sedation, coma. Noncyclic or tetracyclic antidepressants less toxic than tricyclic or MAOIs.
- Bupropion (Wellbutrin)
a. Stimulant that can cause sz. Acts more like amphetamine than serotonergic
b. Tachycardia and mild HTN, agitation/lethargy, hallucinations, sz, tremors, clonus, hyperreflexia
c. In larger ingestions may see status, hyperthermia, hypotension, coma, cardiac interval prolongation.
d. *increased sz risk for 24 hrs with >600mg of ER product
- UDS false + for amphetamines
- sometimes prescribed for smoking cessation
- Desvenlafaxine/Venlafaxine (SNRI)
a. Serotonergic effects in mild toxicity
b. Serotonin syndrome, QRS and QT prolongation. Rhabdo. Sz.
c. Somnolence in mild toxicity progressing to delirium in more severe toxicity
d. Exacerbation of CHF
- Duloxetine (Cymbalta) - (SNRI)
a. OD rare.
b. Mild to moderate: sleepy, GI upset, tachy, diaphoresis, agitation, confusion, HTN
c. Severe toxicity: serotonin syndrome, sz, hypotension, coma
- Escitalopram (Lexapro) - (SSRI)
a. Serotonergic s/s mild to severe. Citalopram causes delayed QT prolongation. Sz
- Lithium
Acute or Chronic (chronic worse)
S/S OD ACUTE
i. n/v ii. delayed neuro effects
S/S OD CHRONIC
i. Tremor, confusion, ataxia, slurred speech, myoclonus, hyperreflexia ii. **severe** agitated delirium, coma, hyperthermia, convulsions, cerebellar effects, Parkinson like, Diabetes Insipidus
ECG changes
i. T wave flattening ii. Prolonged QT
Labs
i. Obtain serial blood levels Q2H 1. Lithium and BMP ii. Goal Na+ 145-150 for max renal lithium excretion
f. Treatment (Lithium)
i. NO ACTIVATED CHARCOAL
ii. IVF (watch for hypernatremia)
iii. Dialysis for severe cases (Sz or AMS)
Interactions
i. Lithium with SSRIs can precipitate serotonin syndrome
- Monoamine Oxidase Inhibitors
a. Mechanism of action
i. Makes dopamine, norepi and serotonin more available
b. Food interactions
i. Tyramine containing products (beer, fava beans, aged cheese, aged meats, pickled foods, red wine, yeast extract and pepperoni)
ii. MAO-A found in the liver and intestinal wall; metabolizes tyramine (tyramine releases catecholamines from neurons)
MAOI Types
c. 1 st generation Ex: Marplan, Nardil, Parnate are nonselective for MAO-A/MAO-B
d. Newer MAOI have selectivity for MAO-B)
i. Ex selegiline will not interact with foods
ii. Note: selectivity is lost in overdose
iii. Metabolized to amphetamines: causes + amphetamine on UDS
e. Other products with MAO effect: linezolid (abx for MRSA), PMA (mistaken for MDMA), St John’s Wort
f. Associated syndromes (MAOI)
i. Sympathomimetic syndrome
1. When MAOIs used with amphetamines, cocaine, phentermine, PCP
ii. Serotonin syndrome
1. Can result from MAOI use with other serotonergic meds [SSRIs, LSD, dextromethorphan, meperidine, and tramadol]
iii. Use with foods high in tyramine can cause hyperthermic/hypertensive crisis
g. S/S of OD (MAOI):
i. Tachycardia, HTN, flushing, headache in mild toxicity
ii. Hyperadrenergic, hypertensive crisis in severe toxicity (hypertension, hyperthermia, delirium, seizures, cardiovascular collapse, multi-organ failure)
h. Treatment (MAOI)
i. Supportive care
ii. Short acting anti-hypertensives (NO BETA BLOCKERS)
iii. Benzos for seizures
iv. Cyproheptadine for oral serotonergic antidote
- Selective Serotonin Reuptake Inhibitors (antidepressants)
a. Ex fluoxetine (Prozac), citalopram (Celexa), sertraline (Zoloft), paroxetine (Paxil), fluvoxamine, venlafaxine (Effexor), trazodone (Desyrel)
b. May interact with one another or MAOIs to produce serotonin syndrome (The classic clinical triad is altered mental status, neuromuscular abnormalities (tremors, clonus, hyperreflexia, rigidity), and autonomic instability (eg, hypertension, tachycardia, hyperthermia). Mydriasis
- Trazodone (Desyrel)
a. Peripheral alpha-adrenergic blockade causing hypotension (and orthostatic hypotension) w/ reflex tachycardia. May see bradycardia
b. Serotonin syndrome, CNS depression, sz, QT prolongation, priapism, tremors, clonus, hyperreflexia
6.5 Identify the toxicity and symptoms of exposure to tricyclic antidepressants.
6.5 Identify the toxicity and symptoms of exposure to tricyclic antidepressants. Amitriptyline. Amoxapine. Desipramine (Norpramin) Doxepin. Imipramine (Tofranil) Nortriptyline
- Signs and symptoms of tricyclic antidepressants.
a. s/s generally appear within 1 hr but may be delayed if mixed ingestion or delayed gastric emptying
b. initial s/s are often anticholinergic (dry mouth, blurred vision, urinary retention, dizziness, n/v)
c. Cardiac (tricyclic antidepressants)
i. Tachycardia
1. Biogenic amine reuptake inhibitor (serotonin and norepi) causes initial hypertension/tachycardia
ii. Initial hypertension then hypotension
iii. QRS prolongation (Na channel blockade)
1. Treat with Bicarb
2. 50 mEq IVP. If QRS narrows, assume drug related and start drip
3. Drip = 3 amps bicarb in 1L D5W w/ 40meq KCl
4. Rate = 2cc/kg/hr or 2x maintenance
iv. QTc prolongation (K channel blockade)
1. Treat with 2g Mag Q6H
*Note: do not use procainamide or other type 1a or 1c antiarrhythmic agents for vtach as may aggravate cardiotoxicity
d. Neuro (tricyclic antidepressants)
i. Seizures
1. From GABA inhibition or antihistamine effect
2. Treat with Benzos
ii. CNS depression & coma
1. resembles brain death. May last 3-4 d
2. Do not withdraw care
e. Hypotension (tricyclic antidepressants)
i. Alpha blockade causes vasodilation
Treat with
1. IVF
2. norepi (alpha 1&2 agonist)
3. phenylephrine (alpha 1 agonist)
**no dopamine (beta agonist) as it relies on body’s release of catecholamines which may be depleted
6.6 Identify the toxicity and symptoms of exposure to antimicrobials and antimalarials.
6.6 Identify the toxicity and symptoms of exposure to antimicrobials and antimalarials.
- Severe toxicity in acute ingestion of antibiotics is rare.
a. Some IV preparations may contain preservatives such as benzyl alcohol or large amounts of potassium or sodium.
b. Quinolones (ciprofloxacin/Cipro;
levofloxacin/Levaquin) and macrolides (azithromycin and erythromycin) cause prolonged QT/torsades.
c. Sulfonamides can cause sulfhemoglobenemia.
d. Linazolid (Zyvox) is MAOI and serotonergic.
Aminoglycosides (gentamicin, tobramycin, amikacin, plazomicin, streptomycin, neomycin)
a. Toxicity more closely associated with trough levels of drug.
b. Renal damage (acute tubular necrosis), ototoxicity (irreversible), and vestibular toxicity (irreversible).
i. Renal injury may go unnoticed until significant.
c. Crosses placenta and some may cause fetal ototoxicity.
Examples:
gentamicin, amikacin, tobramycin, neomycin, and streptomycin
Cephalosporins
a. Expect GI upset in oral ingestion
b. Sz have occurred after parenternal OD
c. Ceftriaxone has caused pseudoithiasis (gall bladder sludge) when administered rapidly
d. Some have caused coagulopathy
Examples:
Ancef and Kefazol (cefazolin)
Ceclor and Cefaclor (cefaclor)
Cefdinir.
Ceftin and Zinacef (cefuroxime)
Duricef (cefadroxil)
Keflex and Keftabs (cephalexin)
Maxipime (cefepime)
Rocephin (ceftriaxone)
Chloroquine and related drugs
Treatment of malaria, parasitic diseases, lupus, and rheumatoid arthritis
Examples:
Chloroquine (more potent), hydroxychloroquine/ Plaquenil, Primaquine
ii. Mild to moderate ingestion may see GI upset, dizziness, headache, visual disturbances (can cause blindness), and auditory disturbances (can cause deafness) . iii. Severe ingestion may see coma, sz, shock, cardiac interval changes, respiratory and cardiac arrest.
- Extremely long half life
1. Primaquine causes GI upset and may cause methemoblobinemia & hemolysis.
- Findings of gastritis, visual disturbances and neuromuscular excitability especially if accompanied by hypotension, QRS /QT prolongation, or ventricular
arrhythmias, should suggest chloroquine.
Fluoroquinolones
a. Cipro associated with crysatalluria. Inhibits cytochrome P450 1A2, GI upset
* Severe SE: tendon ruptures, extreme fatigue, joint and muscle pains, nerve pains, nervous system disturbances
Examples:
ciprofloxacin (Cipro), gemifloxacin (Factive), levofloxacin (Levaquin), moxifloxacin (Avelox), norfloxacin (Noroxin), and ofloxacin (Floxin)
Isoniazid (treatment for TB)
Seizures, metabolic acidosis
Oxazolidinones
MAOI, serotonergic, thrombocytopenia, anemia, peripheral neuropathy.
*Give pyridoxine for seizures
Examples:
linezolid (Zyvox), tedizolid (Sivextro)
Penicillins
a. Seizures in pts with renal dysfunction, kidney problems, leukopenia, neutropenia, bleeding disorder, hypokalemia. Risk of toxicity higher in pts with renal insufficiency
Metronidazole (Flagyl) and Septra
Can cause Antabuse (disulfiram) type reactions
*When ingested with alcohol. The disulfiram reaction is a very uncomfortable reaction characterized by severe flushing, and may be accompanied by tachycardia and hypotension.
6.7 Identify the toxicity and symptoms of exposure to antipsychotic agents (neuroleptics).
6.7 Identify the toxicity and symptoms of exposure to antipsychotic agents (neuroleptics).
aripiprazole (Abilify) asenapine (Saphris) cariprazine (Vraylar) clozapine (Clozaril) lurasidone (Latuda) olanzapine (Zyprexa) quetiapine (Seroquel) risperidone (Risperdal)
- S/S of antipsychotic agents (neuroleptics)
a. Anticholinergic
i. tachycardia, dry mouth, dry skin, urinary retention
b. CNS depression/sedation
c. Alpha-adrenergic blockers
i. hypotension and miosis
d. QT prolongation (occasional QRS prolongation)
e. Extrapyramidal symptoms
i. torticollis, jaw muscle spasm, oculogyric crisis, rigidity, bradykinesia, pill rolling tremor
ii. Often caused by dopamine receptor blockade.
f. Disturbed temperature regulation
i. hypo or hyperthermia
g. Neuroleptic malignant syndrome
i. Rigidity, hyperthermia, sweating, lactic acidosis, rhabdomyolysis
- Dystonias in children should always suggest the possibility of antipsychotic exposure
Labs and Treatment (antipsychotic agents (neuroleptics)
Labs:
a. Electrolytes, Glucose, BUN, Cr, CK, ABG
Treatment:
a. Benadryl for dystonic reactions (consider Haldol)
b. Bicarb for QRS prolongation
c. IVF and norepi or phenyl for hypotension
* Drugs with beta 2 activity may worsen hypotension (vasodilation)
d. Mag or pacing for QT prolongation
e. Charcoal for decontamination
f. Dialysis NOT recommended
