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toxicology Flashcards

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1
Q

top medication overdoses

A

adults - analgesics, sedatives/hypnotics/anti-psychotics, antidepressants, CV drugs, cleaning substances, alcohol
pediatric - cosmetics, cleaning substances, analgesics, foreign bodies, topicals, vitamins

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2
Q

first things first

A

Stabilization: ABC management***, Vital signs, IV access, Oxygenation
Exposure history: Medications/substances, Dose(s), Time of ingestion, Family/EMS report, Pill count
Assessment: Physical exam, Labs, APAP/ASA concentrations, EtOH/toxic alcohol panel
Decontamination: Activated charcoal, Cathartics, Gastric lavage, Whole bowel irrigation

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3
Q

anticholinergic toxidromes

A 
blind as a bat
hotter than hell
red as a beet
dry as a desert
mad as a hatter
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4
Q

urine drug screens detect…

A

Amphetamines, Barbiturates, Benzodiazepines, Cannabinoids, Cocaine, Opioids, Phencyclidine

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5
Q

anion gap

A

Difference between primary measured cations and primary measured anions
(Na+ + K+) – (Cl- + HCO3-) *
Gap is present if greater than 14
MULEPAK (methanol, uremia, lactic acidosis, ethanol, paraldehyde, aspirin, ketoacidosis)

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6
Q

osmolar gap

A

Presence of additional unmeasured low molecular weight molecules that are osmotically active (reference range: 285-300 mOSm/kg)
Gap = Measured - Calculated
Calculated = (2 x Na+) + (BUN/2.8) + (Glu/18) + (EtOH/4.6) ***
Gap is present if greater than 10

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7
Q

activated charcol

A

44-95% prevention of absorption
Pros: Decreases time related problems, Absorbs most toxins
Cons: Difficult administration, must be given within 4 hours
1-2 gm/kg ABW or 50-100 gm in adults

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8
Q

cathartics

A

Decreases GI transit
-Magnesium citrate 2-4 mL/kg/dose (up to 300 mL)
-Sorbitol 70% solution 1-2 mL/kg (up to 1 gm/kg)
rarely used due to OTC abuse - weight loss

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9
Q

gastric lavage

A

“stomach pump”
Efficacy: 8-59%
Complications: Vomiting, Aspiration, Mechanical injury
Advantages: Difficult to refuse, Comatose patients, Use with other agents
Disadvantages: Proper technique, Delay in implementation, Tablet size

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10
Q

whole bowel irrigation

A

Polyethylene glycol
Sustained-release products, “body packers/stuffers”, iron, lithium
Dosing: 500 mL/hr in children 9 months to 6 years; 1,000 mL/hr in children 6 years to 12 years; 1,000-2,000 mL/hr in adolescents and adults
Patient should remain seated on a bedside toilet
Continue until presence of clear rectal effluent

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11
Q

hemodialysis

A

Effective for the following medications: Alcohols, Lithium, Salicylates, Theophylline
must have low molecular weight and small V(d)

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12
Q

s/sxs of opioid toxicity

A

Nausea/vomiting, Drowsiness, Constipation, Pinpoint pupils, Hypotension, Bradycardia, Respiratory depression, Seizure activity

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13
Q

general management of opioid toxicity

A

ABC management
Monitor vital signs, pulse oximetry, and ECG changes
Monitor signs/symptoms of CNS and respiratory depression
Oxygen supplementation (if needed)
UDS and acetaminophen (APAP)/salicylate concentrations
Administer activated charcoal (if presentation within two hours of ingestion)
Administer naloxone (Narcan®)

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14
Q

opioid antidote

A

naloxone
Mechanism of action - Antagonizes opioid effects by binding to same receptor sites
Dosing - 0.4 to 2 mg IV push, IM, SQ, ET, or intranasally
-Utilize lower doses initially in patients with chronic opioid dependence due to withdrawal symptoms - GI upset, restlessness, piloerection, hypertension, tachycardia
-May consider continuous infusion with longer acting opioids - Prolonged signs/symptoms; RR under 8 breaths/min to prevent intubation

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15
Q

opioid toxicology tidbits

A

Severity dependent on medication, dose, duration of action, and patient
Comprises both prescription and illicit drug use - Methadone, Heroin
Aaron’s Law

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16
Q

risk for APAP OD

A 
Induced p450s (CYP2E1 mainly): Isoniazid, Acetone, Chronic EtOH
Patients with depleted glutathione: Malnourished, Anorexic, Alcoholics
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17
Q

protected for APAP OD

A

Children - Increased sulfation pathway, Large liver-to-body ratio
Acute EtOH
Cimetidine and disulfiram - Inhibit CYP2E1

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18
Q

APAP phases of tocivity

A

1) 0.5 to 24 hours post ingestion - Nausea, vomiting, diaphoresis, malaise, pallor
2) 24-72 hours post ingestion - Hepatic injury (abdominal pain/tenderness, oliguria)
3) 72-96 hours post ingestion - Hepatic failure (jaundice, coagulopathy, encephalopathy, coma)
4) Greater than 96 hours post ingestion - Full recovery or death

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19
Q

APAP tox general management

A

ABC management
Acetaminophen (APAP) concentration at least 4 hours post ingestion
Toxic doses in acute ingestions
-Adults: 150 mg/kg or 7.5-10 gm (OR 4 grams)
-Children: 200 mg/kg
Administer activated charcoal (if presentation within two to four hours of ingestion)
Evaluate for potential N-acetylcysteine (NAC) therapy using Rumack-Matthew nomogram (can only be used after 4+ hours of ingestion - plots time v conc - 2 lines to represent if tox is unlikely or if probable hepatic tox)

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20
Q

APAP antidote

A

N-acetylcysteine (Acetadote®)
Glutathione precursor
Mechanism of action: Increases glutathione stores, Acts as a glutathione substitute, Enhances sulfate conjugation
May also have anti-inflammatory, anti-oxidant, inotropic, and vasodilating effects

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21
Q

acetylcystine dosing

A

IV:
-LD: 150 mg/kg IV over 1 hour
-Second infusion: 50 mg/kg IV over 4 hours
-Third infusion: 100 mg/kg IV over 16 hours
PO:
-LD: 140 mg/kg
-Scheduled regimen: 70 mg/kg PO every 4 hours x 17 doses
capped at 100 kg

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22
Q

salicylate toxicity

A

Mixed acid base disorders: ↑ anion gap - metabolic acidosis; Respiratory alkalosis (early) - hyperventilation
Electrolyte disturbances: Hypokalemia, Hypo/hypernatremia
Salicylate concentrations:
-Analgesic properties: 10-15 mg/dl
-Anti-inflammatory properties: 15-20 mg/dl
-Mild toxicity: > 30 mg/dL (tinnitus, dizziness)
-Severe toxicity: > 80 mg/dL (CNS effects)

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23
Q

salicylate toxicity s/sxs

A

CNS: tinnitus, vertigo, delirium, hallucinations, agitation, hyperactivity, seizures, stupor, lethargy
GI: NV

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24
Q

salicylate toxicity general management

A 
ABC management
Monitor vital signs and pulse oximetry
Salicylate (ASA) concentration
Ventilation, ABG
BMP to measure anion gap
Administer activated charcoal (if presentation within two hours of ingestion)
Fluid/electrolyte management
Hemodialysis
Urine alkalization - Sodium bicarbonate: 1 to 2 mEq/kg (50 to 100 mEq) IV push over 1 to 2 minutes; Continuous infusion may be initiated afterwards and titrated to effect
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25
sedative/hypnotics toxicity s/sxs
``` CNS depression Respiratory depression Hypotension Bradycardia Hypothermia Rhabdomyolysis ```
26
sedative/hypnotics toxicity antidote
Flumazenil (Romazicon®) Mechanism of action - Competes with BZDs at BZD binding site of GABA complex Dosing: 0.2 mg IV push -Use with caution in patients with seizures - Can induce seizure activity**** even in seizure naive patients -Can induce withdrawal symptoms - Nausea/vomiting, agitation
27
TCAs toxicology tidbits
Linked to more drug related deaths than any other prescription medication -Starting to see less in clinical practice due to new antidepressant medications (e.g., SSRIs)
28
TCAs in clinical practice
Indications: depression, neuropathy, insomnia, migraines, bed wetting examples: amitriptyline, doxepin, nortriptyline
29
TCA PKs
Initially, rapidly absorbed from the GI tract - Anticholinergic effects may slow GI motility, Decrease rate of absorption Large Vd (10-50 L/kg) Acidemia increases the percentage of unbound TCA Highly lipophilic t1/2 = 4-93 hours
30
TCA pharmacology
``` Anticholinergic activity Alpha receptor blockade Serotonin, norepinephrine, and dopamine reuptake inhibition Sodium and potassium channel blockade CNS and respiratory depression ```
31
TCA toxicity s/sxs
Altered mental status, Hypotension, Tachycardia, ECG changes (QRS prolongation), Seizure activity, CNS depression, Anticholinergic symptoms, Drowsiness, Respiratory depression, Decreased GI motility, Metabolic acidosis, Rhabdomyolysis
32
TCA toxicity effects of QRS prolongation
QRS interval > 100 msec - Increased risk of seizure activity QRS interval > 150 msec - Increased risk of cardiac arrhythmias May also result in metabolic acidosis - Promotes unbinding of drug from proteins
33
TCAs toxicity general management
ABC management Monitor vital signs and ECG changes UDS, urinalysis, serum electrolytes, and ABG/VBGs Serum TCA concentrations? Fluid hydration +/- vasopressors for hypotension Seizure activity management (if applicable) Consider activated charcoal (if presentation within two hours of ingestion and no signs/symptoms of ileus) Consider sodium bicarbonate based on ECG results (QRS prolongation)
34
TCA tox antidote
Sodium bicarbonate Mechanism of action: Increases sodium gradient of poisoned sodium channels Indications: QRS interval > 100 msec, TCA induced arrhythmias or hypotension, Metabolic acidosis Dosing: 1 to 2 mEq/kg (50 to 100 mEq) IV push over 1 to 2 minutes -Continuous infusion may be initiated afterwards and titrated to effect Monitoring -Serum pH 7.45-7.55 -D/C when: QRS interval under 100 msec, Resolution of ECG abnormalities, Hemodyamically stable
35
Seizure management of TCA toxicity
``` **Benzodiazepines - Lorazepam (Ativan®), diazepam (Valium®), midazolam (Versed®) Phenobarbital (Luminal®) Phenytoin (Dilantin®)? Fosphenytoin (Cerebyx®)? Levetiracetam (Keppra®)? ```
36
antipsychotics: pharmacology
First Generation - D2 antagonism | Second Generation - 5HT2A/D2 antagonism
37
antipsychotic examples
typical: haloperidol, fluphenazine, chlorpromazine, thioridazine, perphanazine, trifluoperazine, pimozide atypical: aripiprazole, clozapine, olanzapine, risperidone, quetiapine, ziprasidone, paliperidone
38
antipsychotic toxicity S/sxs
CV: Hypotension, Tachycardia, QT and QRS prolongation neuro: Extrapyramidal symptoms (EPS), Neuroleptic malignant syndrome (NMS), Sedation, Seizure activity
39
atypical antipsychotics toxicity
``` Toxic doses are not well defined Often co-ingested with other agents Symptoms are typically seen within 1- 2 hours of ingestion Peak symptoms in 4 - 6 hours Duration is roughly 12 - 48 hours ```
40
extrapyramidal sxs
Benztropine 2 mg IM -Onset ~ 15 - 20 minutes -Longer half life Diphenhydramine 1- 2 mg/kg IV/IM (up to 50 mg) over several minutes -Onset ~ 5 minutes -Continue with oral therapy for 3 - 4 days - Diphenhydramine 50 mg PO TID
41
neuroleptic malignant syndrome
Hyperpyrexia up to 42.2C (108F) with altered mental status (delirium or coma) and “lead pipe” muscular rigidity Occurs 3-9 days after initiating therapy or after adding a second agent Often these patients are under 40 years of age and more often males
42
NMS complications
Continues for 5-10 days 84% of cases - Haloperidol, depot fluphenazine, or chlorpromazine use Death is secondary to rhabdomyolysis, renal failure, cardiovascular collapse, respiratory failure, arrhythmias, or thromboembolism
43
NMS treatment
D/C offending agent Rapid external cooling Benzodiazepines Dantrolene - Initial dose of 2.5 mg/kg to a maximum of 10 mg/kg IVP; Maintenance dose is 2.5 mg/kg Q6H until resolved Bromocriptine has also been utilized - 2.5 mg BID initially, increasing to 5 mg TID; Doses as high as 60 mg/day have been used
44
serotonin syndrome
Toxic hyperserotonergic state - Excessive stimulation of the post-synaptic receptors in the CNS Triad of symptoms: Altered mental status, Autonomic instability, Neuromuscular abnormalities Development of serotonin syndrome is rapid - Within six hours of an increase in the precipitating medication
45
serotonin syndrome: pharmacology
Direct agonists: Buspirone, Lithium, Lysergic acid diethylamide (LSD), Sumatriptan Increased release of serotonin: Amphetamines, Cocaine, Mirtazapine, MDMA (“ecstasy”) Inhibitors of serotonin metabolism: Monoamine oxidase inhibitors, Linezolid Reduced uptake of serotonin: -Selective serotonin reuptake inhibitors (SSRIs) - Citalopram, fluoxetine, sertraline, paroxetine -Tricyclic antidepressants (TCAs) - Amitriptyline, imipramine, nortriptyline -Serotonin norepinephrine reuptake inhibitors (SNRIs) - Duloxetine, Venlafaxine -Trazodone -Dextromethorphan
46
treating serotonin syndrome
D/C offending agent Benzodiazepines Aggressive cooling Cyproheptadine (Periactin®) -1st generation histamine receptor blocking agent -Non-specific 5-HT1A and 5-HT2A receptor blocking effects - 4 mg PO Q1H; Maximum dose: 16 mg
47
serotonin syndrome vs NMS
SS: lasts under 24 hours, lower limbs more affected NMS: higher fever, lasts over 24 hours, diffuse lead pipe rigidity
48
digoxin in clinical practice
Indicated for the treatment of atrial fibrillation (AF) and heart failure (HF) Monitored with serum concentrations due to narrow therapeutic index -Goal range usually 0.8 to 2 ng/mL - May be 0.5 to 1 ng/mL in HF -Must be drawn at least 6 hours after previous dose
49
digoxin tox s/sxs
Non Cardiac: Nausea/vomiting, Abdominal pain, Anorexia, Confusion, Vision changes Cardiac: Bradycardia, 2nd or 3rd degree heart block, Arrhythmias, Hyperkalemia( 5 to 6.4 mEq/L ~ 35% mortality, > 6.4 mEq/L ~ 90% mortality)
50
digoxin toxicity general management
Discontinue digoxin ABC management Obtain serum digoxin concentration, BMP Monitor vital signs and ECG changes (arrhythmias, bradycardia) Administer activated charcoal (if presentation within two hours of ingestion) Consider administration of Digibind® Hemodialysis is not* effective
51
digoxin antidote
Mechanism of action: Binds free digoxin and tissue bound digoxin released during equilibrium state Indications: Ventricular arrhythmias, bradycardia/2nd or 3rd degree heart block not responsive to atropine, Hyperkalemia (K > 5.5 mEq/L) with signs/symptoms of toxicity, Serum digoxin concentrations > 10-15 ng/mL drawn at least 6 hours after time of ingestion, Ingestion > 10 mg in adults, > 4 mg in children dosing: Each vial binds approximately 0.5 mg* of digoxin -Based on acute ingestion of known amount - Total body load (TBL) = mg digoxin ingested x 0.8; TBL/0.5 mg = # Digibind ® vials to administer -Based on serum digoxin concentrations in adults --- # Digibind ® vials = digoxin concentration (ng/mL) x patient’s weight (kg) / 100
52
digoxin toxicology tidbits
Toxicity can occur with acute ingestion and chronic therapy Must correlate signs/symptoms with serum concentration - Time of ingestion? Time of concentration? Serum digoxin concentrations are clinically useless after Digibind® administration
53
CCBs and BBs in clinical practice
CCBs: Angina, Hypertension, Arrhythmias (e.g., AF), HF BBs: Angina, Hypertension, Arrhythmias, HF, Myocardial infarction, Migraine headaches, Tremor, Portal hypertension
54
CCB and BB toxicity s/sxs
CCBs: Hyperglycemia, Metabolic acidosis, Pulmonary edema, Ileus (SR) BBs: Hypoglycemia, Bronchospasm both: Hypotension, Bradycardia, Arrhythmias, Cardiogenic shock, CNS depression
55
CCB and BB general management
ABC management Monitor vital signs and ECG changes (arrhythmias, bradycardia) Administer activated charcoal (if presentation within two hours of ingestion) Potential antidotes: Atropine, Calcium, Vasopressor therapy, Glucagon, High dose insulin therapy
56
CCBs and BBs : atropine
Mechanism of action: Blocks parasympathetic activity to increase heart rate Dosing: 0.5 to 1 mg IV push - Maximum dose: 3 mg
57
CCBs and BBs : calcium
Mechanism of action: Enters open voltage sensitive calcium channels to promote calcium release from sarcoplasmic reticulum resulting in myocardial contractility, More effective in CCB overdoses vs BB overdoses Dosing: Calcium chloride: 5 to 10 mL of 10% solution; Calcium gluconate: 10 to 20 mL of 10% solution -Note: Calcium chloride has three times more elemental calcium than calcium gluconate
58
CCBs and BBs : vasopressor therapy
May require higher doses to overcome receptor blockade Medication selection depends on clinical presentation -α stimulates effects on blood pressure -β stimulates effects on heart rate Review patient’s ingestion history and monitor vital signs to select appropriate agent
59
CCBs and BBs : glucagon
Mechanism of action: Bypasses beta receptors and acts directly on Gs to stimulate conversion of ATP to cAMP Dosing: 3 to 10 mg IV bolus (adults); 50 to 150 mcg/kg IV bolus (children) -Initiate infusion at same dose as effective bolus dose (in mg/hr) - Patient responds to 5 mg IV bolus, start infusion at 5 mg/hr
60
CCBs and BBs : high dose insulin therapy
Mechanism of action: Facilitates myocardial utilization of carbohydrates Dosing: Insulin drip at 0.5 to 1 unit/kg/hr IV; Dextrose at 0.5 gm/kg/hr IV -Titrate to systolic blood pressure > 90 to 100 mm Hg or effect every 30 to 60 minutes (improved contractility, decreased symptoms) Monitoring: Improved contractility within 15 to 60 minutes; Goal glucose: 100 to 250 mg/dL; Serum electrolytes every 1 to 2 hours (glucose, potassium)
61
CCBs and BBS: toxicology tidbits
Atropine - Not likely to be effective in either CCB or BB overdoses Calcium - More likely to be effective with CCB overdoses vs BB overdoses; Chloride has three times more elemental calcium vs. gluconate, but extravasation more likely with chloride formulation Vasopressor therapy - Should utilize higher doses to overcome beta receptor blockade Glucagon - May need to pre-medicate with ondansetron (Zofran®) and add PRN regimen due to nausea/vomiting with glucagon High dose insulin therapy - Communicate with health care providers to address patient safety
62
Iron toxicology tidbits
Toxicity can occur at 10 to 60 mg/kg of elemental iron Prenatal vitamins contain approximately 65 mg of elemental iron Children’s vitamins contain approximately 10 to 18 mg of elemental iron Concern is absorption of iron into tissue - Can still experience toxicity with normal serum iron concentrations Human body has no natural mechanism to handle iron overload -Excretion: Male = 1 mg daily; Female = 2 mg daily
63
Iron phases of toxicity
1) 0.5 to 2 hours post ingestion - GI upset, abdominal pain, hematemesis, hematochezia 2) 6 to 24 hours post ingestion - Latent phase resembling recovery; continue to monitor 3) 2 to 24 hours post phase 1 - Shock stage (acidosis, hypotension, hypovolemia, poor cardiac output) 4) 48 to 96 hours post ingestion - Hepatoxicity 5) Days to weeks post ingestion - GI scarring, obstructions, strictures
64
iron tox - general management
``` ABC management Monitor vital signs Fluid hydration Serum iron concentration 4 hours post ingestion Activated charcoal is not effective KUB (kidneys, ureter, and bladder) scan Whole bowel irrigation Consider administration of deferoxamine for chelation ```
65
iron antidote
Deferoxamine (Desferal®) Mechanism of action: Chelates iron and enhances renal elimination Indications: Metabolic acidosis or other signs of shock, Clinical deterioration despite IV fluid administration, Presence of iron tablets on KUB Serum iron concentration > 500 mcg/mL dosing: Start at 15 mg/kg/hour - May increase to 45 mg/kg/hour for patients with severe poisoning; Decrease rate if patient experiences hypotension - Usually continued for 12 to 24 hours; May titrate down based on resolution of symptoms and/or absence of vin rose urine
66
toxic alcohol examples
Ethylene glycol - Antifreeze, brake fluid, and industry solvents Methanol - Windshield washer fluid, paint remover, copier fluid, some antifreeze, and some engine fuels Isopropyl alcohol - Rubbing alcohol, paint remover, cements, cleaners
67
toxic alcohols - clinical presentation
anion gap and osmolar gap (know equations!!!)
68
interpretation of results for alcohol tox
``` Anion gap PLUS osmolar gap -Methanol toxicity -Ethylene glycol toxicity -Alcoholic ketoacidosis Osmolar gap WITHOUT anion gap -Isopropyl alcohol (acetone) toxicity ```
69
ethylene glycol PKs
Rapidly absorbed from the GI tract Rapidly distributed throughout the body t ½ = 2.5-4.5 hrs In the presence of normal renal function; 20% excreted unchanged in the urine Alcohol dehydrogenase in the liver is the first rate-limiting step in the breakdown
70
ethylene glycol phases of toxicity
1) 30 minutes to 12 hours post ingestion - CNS effects, nausea/vomiting, inebriation, lethargy/coma (within 4-8 hours), seizures 2) 12-24 hours post ingestion - Metabolic effects, cardiac compromise, anion gap acidosis*** 3) 2 to 3 days post ingestion - Renal effects (calcium oxalate crystals), ATN within 12-48 hours
71
ethylene glycol toxicology tidbits
Presence of osmolar gap? Ethylene glycol, methanol and ethanol serum concentrations Wood’s lamp evaluation of urine
72
methanol: PKs
t1/2 = 14-30 hrs, peak levels in 20-90 min Oral ingestion, inhalation, or dermal absorption Metabolized by alcohol dehydrogenase to formaldehyde then to formic acid - Reaction is slow, so delay in toxic metabolite formation
73
methanol phases of toxicity
1) Headache, dizziness, ataxia, confusion | 2) During formic acid accumulation, Pronounced visual symptoms, Anion gap
74
ethylene glycol and methanol: general management
Non-Pharmacologic - Gastric lavage and aspiration if presents in less than one hour; Charcoal is NOT effective; Hemodialysis if: EG concentration greater than 100 mg/dL, Methanol concentration greater than 45 mg/dL, Refractory acidosis, Renal Failure, Symptomatic Pharmacologic: -Ethanol and fomepizole - Inhibition of alcohol dehydrogenase limits metabolism of ethylene glycol) -Adjunctive therapy - Shunt metabolism toward nontoxic metabolites (Thiamine (EG), Pyridoxine (EG), Magnesium (EG), Folate (Methanol) ) -sodium bicarb: Large amounts may be necessary to maintain normal pH; Helps in conversion of formic acid to carbon dioxide and water Correct hypocalcemia and hypoglycemia
75
ethanol therapy
Greater affinity for alcohol dehydrogenase 0.6 gm/kg IV bolus then 110 mg/kg/hr - If HD started, increase dose to 250-350 mg/kg/hr Optimal blood ethanol concentration of 100-150 mg/dL Side effects: phlebitis, altered mental status, hypoglycemia
76
fomepizole
to treat ethanol glycol and methanol tox Dose -15 mg/kg IV load followed by 10 mg/kg Q12H x 4 doses -Need to increase to 15 mg/kg IV Q12H if continued -Administer Q4H during hemodialysis Advantages: No CNS depression, ICU stay not required Disadvantage - Cost?
77
isopropyl alcohol PKs
50-80% metabolized by alcohol dehydrogenase to acetone t1/2 of isopropyl = 3 hrs; acetone = 10-20 hrs Acetone eliminated via kidneys and lungs Lethal dose greater than 400 mg/dL Potency is double-strength ethanol Peak levels 30 min after ingestion
78
isopropyl alcohol toxic effects
Prolonged CNS depression Nystagmus or miosis Ketonemia Hemorrhagic gastritis Elevated osmolar gap Increased serum isopropanol concentrations Bradycardia/hypotension at high concentrations
79
isopropyl alcohol treatment
Gastric lavage Hydration Correct electrolyte abnormalities Hemodialysis - Lethal doses, Coma, Refractory shock

ID final (4 decks)

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