1	Toxicological Emergencies & Treatments
2	Objectives After completing this chapter, the student should be able to: Discuss the importance of toxicological emergencies in prehospital care Discuss the role of regional poison centers in the management of the poisoned patient Describe the key historical information required in the management of a toxicological emergency
3	Objectives (cont.) After completing this chapter, the student should be able to: Describe the various routes of exposure to toxic substances Describe the general management of the patient exposed to a toxin, including decontamination and elimination Define the term toxidrome and describe the common toxidromes encountered in prehospital care
4	Objectives (cont.) After completing this chapter, the student should be able to: Describe the signs, symptoms, and management (including antidotes where appropriate) of the following toxic exposures and overdoses: acetaminophen, anticholinergics, neuroleptics, beta-blockers, calcium channel blockers, carbon monoxide, cyanide, cyclic antidepressants, digoxin/digitalis, ethylene glycol, iron, isopropyl alcohol, lithium, methanol, narcotics and narcotic antagonists, organophosphates and carbamates, salicylates, and selective serotonin reuptake inhibitors (SSRIs)
5	Toxicology
6	Toxicology A rapidly evolving science The approach to the poisoned or overdosed patient is like a form of detective work. The clinical clues required to manage these patients are often subtle. Virtually any patient presentation may be directly or indirectly related to a toxicological problem.
7	Specific Toxic Agents Encountered in Prehospital Care and needed treatments
8	Acetaminophen Tylenol ®
9	Route of Exposure Oral
10	Mechanism of Toxicity Metabolism is primarily hepatic 90% is conjugated with glucuronic or sulfuric acid in the liver to form nontoxic compounds that are excreted in the urine 2% is excreted unchanged in the urine When glutathione stores are depleted, as in a massive overdose, hepatotoxicity occurs.
11	Toxic Dose Acute ingestion: Doses > 7.5 g or 140 mg/kg Chronic ingestion: Variable toxicity can occur at low doses In chronic alcoholics who have higher levels of acetaminophen
12	Signs and Symptoms
13	Prehospital Management Supportive care should be provided Airway support as indicated Activated charcoal where permitted by medical direction guidelines
14	In-hospital Management N-acetylcysteine (NAC) either orally or intravenously Lavage if the patient presents within 2 hours of ingestion Liver transplant has been performed as a lifesaving measure in rare cases
15	Anticholinergics ie: antihistamines, atropine, mushrooms, tricyclics
16	Route of Exposure Oral Intravenous (IV) Dermal
17	Mechanism of Toxicity Cholinergic blockade occurs both centrally and peripherally Involves both muscarinic and nicotinic receptors Different agents have different degrees of effect on the two receptor types and, as such, can have slightly different presentations.
18	Toxic Dose Variable
19	Signs and Symptoms Peripheral signs: Dry skin and mucous membranes Thirst Dysphagia Blurred vision Fixed dilated pupils Tachycardia Fine red (scarlatiniform) rash Hyperthermia Abdominal distension with decreased/absent bowel sounds Urinary urgency or retention
20	Signs and Symptoms (cont.) Central signs: Lethargy Confusion Restlessness Delirium Hallucinations Ataxia Seizures In severe cases, cardiopulmonary collapse
21	Prehospital Management Conservative supportive care Monitor airway, breathing, and circulation Establish IV access Cardiac monitoring Activated charcoal may be useful
22	In-hospital Management Supportive care Lavage even late in overdose Seizures and agitation are treated with benzodiazepines. Dysrhythmias can be treated. Class 1a drugs (quinidine, disopyramide, and procainamide) should be avoided.
23	Neuroleptics
24	Route of Exposure Oral Intravenous Intramuscular
25	Mechanism of Toxicity Act by blocking neurotransmission involving dopaminergic, adrenergic, muscarinic, and histaminic receptors Therapeutic and toxicologic effects vary from agent to agent depending on the degree of blockage of each receptor subtype.
26	Toxic Dose Variable
27	Signs and Symptoms Adverse reactions are common and may occur even in the setting of normal therapeutic dosages. Include: Dystonic reaction Akathisia Parkinsonism Tardive dyskinesia
28	Signs and Symptoms (cont.) Neuroleptic malignant syndrome (NMS) Life-threatening condition (10% mortality rate) Hyperthermia Rigidity Altered mental status Autonomic instability Symptoms of acute overdose are highly variable.
29	Prehospital Management ABCs Cardiac monitoring Nalaxone Glucometer reading Treat hypotension with crystalloid and norepinephrine or phenylephrine as needed.
30	Prehospital Management (cont.) Ventricular dysrhythmias – treated with bicarbonate, then lidocaine or phenytoin Torsades de pointes – treated with magnesium, then isoproterenol or overdrive pacing as needed Seizures should be treated using standard methods, including benzodiazepines, phenytoin, or phenobarbital.
31	In-hospital Management Supportive care, including all the prehospital methods Activated charcoal and gastric lavage Class 1A antidysrhythmics should be avoided – may worsen the cardiac toxicity Cooling or warming techniques may be needed
32	Benzodiazepines ie: Valium®, Ambien®, Ativan®
33	Benzodiazepine Overdose Presents with altered mental status and respiratory depression if mixed with other CNS depressants. Care should include airway support and flumazenil
34	Flumazenil Anexate, Romazicon
35	Class Benzodiazepine antagonist
36	Description Used to reverse the sedative effects of benzodiazepines Especially respiratory depression
37	Mechanism of Action Antagonizes the actions of the benzodiazepines in the central nervous system Inhibits their actions on the gamma-aminobutyric acid–benzodiazepine complex Used to reverse the sedative effects of the benzodiazepines
38	Pharmacokinetics Onset 1-5 minutes Peak effects 6-10 minutes Duration 2-4 hours Half-life 54 minutes
39	Indications Complete and partial reversal of CNS and respiratory depression caused by benzodiazepines Should not be used as a diagnostic agent for benzodiazepine overdose
40	Contraindications Known history of hypersensitivity Hypersensitivity to benzodiazepines Patients who have received benzodiazepines to control life-threatening conditions such as status epilepticus Patients with tricyclic antidepressant overdoses
41	Precautions Administer with caution to patients dependent on benzodiazepines. Benzodiazepine withdrawal can be life-threatening. Monitor for signs of resedation.
42	Side Effects Fatigue Headache Agitation Nervousness Dizziness Flushing Confusion Convulsions Dysrhythmias Nausea and vomiting
43	Interactions Few interactions in the emergency setting
44	Dosage 0.2 mg IV administered over 30 seconds Can be repeated as needed Maximum dose of 1.0 mg
45	Beta-Blockers
46	Route of Exposure Generally oral Occasionally ocular
47	Mechanism of Toxicity Cause blockade of both β₁- and β₂- receptors in the adrenergic nervous system Affect several organ systems Cardiovascular (bradycardia, atrioventricular block, or vasodilation) Respiratory (bronchospasm or congestive heart failure)
48	Toxic Dose The toxic dose is highly variable. Toxicity is more likely in the setting of underlying heart disease.
49	Signs and Symptoms Bradycardia AV blockade Hypotension Tachycardia LOC changes Bronchospasm Congestive heart failure Masks S/S of hypoglycemia Impairs recovery from hypoglycemia
50	Prehospital Management Supportive care Activated charcoal may be indicated May respond to atropine or epinephrine Usually require glucagon 3-10 mg IVP Fluid therapy Transcutaneous pacing Treat seizures Treat bronchospasm with a β₂-agonists
51	In-hospital Management Supportive care including all the prehospital methods Intensive care unit support Continuous glucagon infusion With or without pressor therapy (dopamine or epinephrine)
52	Calcium Channel Blockers
53	Route of Exposure Oral Sublingual Intravenous
54	Mechanism of Toxicity Any cell utilizing calcium can be affected: Myocardium Sinoatrial (SA) node AV node AV nodal conduction pathway Metabolism occurs in the liver
55	Toxic Dose Toxic dose is variable Effects are generally more severe in the presence of underlying cardiovascular disease
56	Signs and Symptoms Dependent on the specific agent ingested Hypotension Bradycardia AV conduction blocks Lethargy and slurred speech Nausea and vomiting Coma Respiratory depression
57	Prehospital Management Supportive care as required Activated charcoal may be indicated Calcium therapy, 10 cc of a 10% solution IVP Atropine or isoproteronol Transcutaneous pacing Glucagon IVP has limited success IV fluids Inotropes
58	In-hospital Management Supportive care, including all the prehospital methods Activated charcoal or gastric lavage ICU admission Assisted ventilation Inotropic therapy
59	Carbon Monoxide
60	Route of Exposure Inhalation Caused by blocked ventilation of furnace, chimney, or automobile exhaust systems Common in smoke inhalation Can be seen with ingestion or inhalation of paint thinners, which metabolize into CO
61	Mechanism of Toxicity Binds to hemoglobin Reduces the availability of hemoglobin to carry oxygen Induces hypoxemia Affinity of hemoglobin for CO is 250 times O₂
62	Toxic Dose Variable
63	Signs and Symptoms < 10% – generally asymptomatic 10–20% – headache and dyspnea 20–30% – headache, fatigue, and visual disturbance 40–50% – tachycardia and altered level of consciousness; may precipitate angina > 60% – coma, seizures, cherry-red skin
64	Signs and Symptoms (cont.) Levels can only be measured via blood testing. Levels > 40%, any organ system can be affected Central nervous system Pulmonary system Cardiovascular system
65	Prehospital Management Supportive care as required Airway management Supplemental O₂ via NRB Measuring SpO₂ is unreliable
66	In-hospital Management Supportive care with all prehospital measures Use of hyperbaric oxygen therapy For patients with significant neurological abnormalities Patients with cardiovascular abnormalities Symptomatic pregnant patients
67	Cyanide
68	Route of Exposure Inhalation Ingestion Intravenous Dermal contact
69	Mechanism of Toxicity Cyanide binds a key cellular enzyme, cytochrome oxidase. Causing cellular asphyxia Affecting virtually all organ systems
70	Toxic Dose Highly variable
71	Signs and Symptoms Present very quickly post-exposure Unconscious Noncyanotic Hypotensive Bradycardia Death occurs in seconds to minutes.
72	Signs and Symptoms (cont.) Less severe cases or very early post-exposure: Headache Dyspnea Confusion Seizures with hypotension A bitter almond odor may be detected by care providers.
73	Prehospital Management Recognition of cyanide exposure is the key Initial supportive care, including ABCs A specific antidote, known as the Pasadena Cyanide Antidote Kit, is available. The kit contains three different products: Amyl nitrite pearls for inhalation Sodium nitrite solution for intravenous use Sodium thiosulfate for intravenous use
74	In-hospital Management Supportive care with all prehospital measures Smoke inhalation cases require treatment for cyanide and carbon monoxide toxicity. IV hydroxycobalamin (vitamin B₁₂) can be useful. For oral cyanide ingestion, charcoal may be beneficial.
75	Amyl Nitrite
76	Class Vasodilator/cyanide antidote
77	Description A potent vasodilator An antidote for cyanide poisoning
78	Mechanism of Action Chemically related to nitroglycerin Supplied in a glass inhalant that can be broken and inhaled immediately Causes oxidation of hemoglobin to a compound called methemoglobin Methemoglobin reacts with the toxic cyanide ion to form cyanomethemoglobin, which can be enzymatically degraded and eliminated.
79	Pharmacokinetics Onset 10-30 seconds Peak effects 30 seconds Duration 3-5 minutes Half-life N/A
80	Indications Cyanide poisoning
81	Contraindications None when used in the management of cyanide poisoning
82	Precautions Amyl nitrite is a drug of abuse and should be kept in a secure place with the narcotics. It has an odor resembling dirty sweat socks.
83	Side Effects Severe headache Weakness Dizziness Flushing Cold sweats Tachycardia Syncope Orthostatic hypotension Nausea and vomiting
84	Interactions Hypotensive effects can be potentiated by: Antihypertensive agents β-blockers Certain antiemetics (phenothiazines)
85	Dosage One to two inhalants of amyl nitrite should be crushed and inhaled. Maintained until the patient has reached an emergency department Therapeutic effects diminish after 20 minutes Should be administered by inhalation only
86	Sodium Nitrite
87	Class Nitrate/cyanide antidote
88	Description A nitrate salt Seldom used alone in the treatment of cyanide poisoning Used with sodium thiosulfate and amyl nitrite
89	Mechanism of Action Converts hemoglobin to methemoglobin Methemoglobin can actually draw cyanide from the cells. Must be detoxified by sodium thiosulfate Mechanism of action not fully understood
90	Pharmacokinetics Onset 2-5 minutes Peak effects 30-70 minutes Duration Variable Half-life N/A
91	Indications Cyanide poisoning Part of the Cyanide Antidote Kit
92	Contraindications Should not be administered to asymptomatic patients following exposure to cyanide Should not be administered to smoke inhalation cases until hyperbaric oxygen therapy is available and such therapy has already been initiated
93	Precautions Blood pressure should be monitored carefully. The infusion rate needs to be reduced if hypotension occurs.
94	Side Effects Excessive methemoglobinemia may occur, especially with doses exceeding those recommended. Hypotension may occur with rapid intravenous infusion.
95	Interactions None when used in the setting of cyanide poisoning
96	Dosage Adult dose: After amyl nitrite Administer 300 mg (10 mL of 3% solution) IVP Subsequent doses of 150 mg IVP every 30 minutes as needed Pediatric dose: 10 mg/kg IV 50% of the dose in 30 minutes as needed
97	Sodium Thiosulfate
98	Class Cyanide antidote
99	Description Part of the Cyanide Antidote Kit Seldom used alone in the treatment of cyanide poisoning
100	Mechanism of Action The major route of detoxification of cyanide in the body is conversion to thiocyanate. The thiocyanate is then removed by the kidneys.
101	Pharmacokinetics Onset 2-5 minutes Peak effects Variable Duration Variable Half-life N/A
102	Indications Cyanide poisoning Part of the Cyanide Antidote Kit
103	Contraindications None when used in the treatment of cyanide poisoning
104	Precautions Most effective as a cyanide antidote when used in conjunction with nitrites
105	Side Effects Nausea and vomiting Joint aches Psychosis reported with higher doses Side effects are mild and of minor importance compared to the risks associated with cyanide poisoning.
106	Interactions None when used in the setting of cyanide poisoning
107	Dosage Adult dose: Administer following sodium nitrite and/or amyl nitrite 12.5 g (50 mL of 25% solution) IV over 10 minutes Repeat half original dose if signs recur Pediatric dose: 400 (300 to 500) mg/kg body weight IV over 10 minutes
108	Cyclic Antidepressants Tricyclics
109	Route of Exposure Oral
110	Mechanism of Toxicity Multiple physiological effects lead to clinical toxicity Blocks norepinephrine, dopamine, and serotonin reuptake at the presynaptic receptor, causing norepinephrine depletion Has anticholinergic activity, calcium channel blocking activity, and alpha-blocking activity
111	Mechanism of Toxicity (cont.) Cardiac toxicity results in prolonged QRS complexes and QT interval prolongation Metabolism is almost entirely hepatic, with a half-life of approximately 24 hours at therapeutic doses In the setting of overdose, half-life can be as much as 72 hours
112	Toxic Dose Highly variable
113	Signs and Symptoms Symptoms: Dizziness Confusion Blurred vision Dry mouth Signs classified into three categories: Cardiovascular CNS Anticholinergic
114	Signs and Symptoms (cont.) Cardiovascular signs include: Conduction blocks, hypotension, dysrhythmias, and cardiac arrest CNS signs include: Delirium, agitation, extrapyramidal signs, myoclonus, seizures, and coma Anticholinergic signs include: Tachycardia, mydriasis, decreased bowel sounds, urinary retention, and hyper- or hypothermia
115	Signs and Symptoms (cont.) The earliest and most sensitive sign of cyclic antidepressant overdose is tachycardia. Life-threatening dysrhythmias are generally preceded by prolongation of the QRS complex.
116	Prehospital Management Supportive care, including ABCs Multi-dose activated charcoal IV access and fluid therapy are indicated if hypotensive Sodium bicarbonate remains a mainstay of therapy Hypotension unresponsive to bicarbonate and IV fluid may require inotrope therapy Seizure activity unresponsive to bicarbonate therapy may be treated with benzodiazepines
117	In-hospital Management Supportive care with all prehospital measures Gastric lavage may be indicated if less than 2 hours postingestion Cases of suspected toxicity require an observation period of at least 6 hours.
118	Digoxin and Digitalis
119	Route of Exposure Generally oral Can be related to plant exposure Digitalis is derived from plants. Most notably the purple foxglove plant
120	Mechanism of Toxicity Inhibit the sodium-potassium ATPase Cause potassium efflux and sodium and calcium influx into cells Toxicity is enhanced in hypokalemia, hypomagnesemia, hypercalcemia, and alkalosis.
121	Toxic Dose The toxic dose is highly variable. Patients more prone to toxicity: Underlying heart disease Renal failure Hypothyroidism Hypoxemia Users of nonsteroidal anti-inflammatory drugs
122	Signs and Symptoms Virtually any cardiac dysrhythmia can be seen. Symptoms are nonspecific and include: Fatigue Anorexia Disorientation and confusion Delerium and hallucinations Gastrointestinal upset Visual halos (green or yellow)
123	Prehospital Management Supportive care, including ABCs Fluids and pressor agents for hypotension Multi-dose activated charcoal may be useful. Calcium, which will worsen digoxin toxicity, should not be given.
124	In-hospital Management Supportive care with all prehospital measures Correct electrolyte abnormalities Magnesium may lessen cardiac toxicity. Phenytoin or dilantin may be helpful for ventricular dysrhythmias. Atropine and pacing may be required for symptomatic bradycardias.
125	In-hospital Management (cont.) Procainamide and quinidine may worsen conduction and contractility problems Digibind (digoxin Fab fragments) can be lifesaving in severe overdose Lethal amounts (generally 10 mg in an adult) High serum levels (> 12.8 to 19.2 mmol/L) Marked hyperkalemia Malignant dysrhythmias Resistant bradycardias Hypotension
126	Ethylene Glycol
127	Route of Exposure Generally oral
128	Mechanism of Toxicity Toxic metabolites are formed, causing acidosis and renal damage. Signs and symptoms may not appear until 6 to 12 hours after the ingestion. This delay is even more pronounced if ethanol is also ingested.
129	Toxic Dose The minimal toxic dose is 1 to 2 mL/kg.
130	Signs and Symptoms Phase I: 1 to 12 hours post-ingestion Signs of intoxication without the smell of ethanol CNS symptoms may include ataxia, seizures, and nystagmus. Nausea and vomiting are common.
131	Signs and Symptoms (cont.) Phase II: 12 to 36 hours post-ingestion Cardiopulmonary toxicity Hypertension Tachycardia Tachypnea Pulmonary edema (severe poisoning) Congestive heart failure (severe poisoning) Shock (severe poisoning)
132	Signs and Symptoms (cont.) Phase III: 24 to 72 hours post-ingestion Acute renal toxicity Flank pain Costovertebral angle tenderness Decreased urine output Acute renal failure Not all patients go through these phases Fluorescent additive sometimes seen in urine
133	Prehospital Management Supportive care, including ABCs IV fluids for dehydration and renal perfusion Ethanol therapy is indicated as a means of preventing metabolism to toxic metabolites.
134	In-hospital Management Supportive care with all prehospital measures Metabolism to toxic metabolites is limited by administering ethanol as a competitive inhibitor of alcohol dehydrogenase. Hemodialysis is indicated in cases of renal failure. Bicarbonate is used in cases of profound acidosis.
135	Iron
136	Route of Exposure Oral
137	Mechanism of Toxicity Direct corrosive effect on gastric and intestinal mucosa that can lead to hemorrhage or perforation Fluid loss from the gastrointestinal (GI) tract and vasodilation can cause hypotension An intracellular toxin that causes uncoupling of oxidative phosphorylation, leading to impaired generation of ATP and cellular death
138	Toxic Dose Dependent on the form of iron ingested The elemental amount of iron present that is relevant
139	Signs and Symptoms Stage 1:
140	Signs and Symptoms (cont.) Stage 2: 2 to 12 hours post-ingestion Relatively asymptomatic period
141	Signs and Symptoms (cont.) Stage 3:
142	Signs and Symptoms (cont.) Stage 4: Beyond 48 hours post-ingestion Pyloric (gastric outlet) strictures Either death or recovery occurs
143	Prehospital Management Supportive care including ABCs Fluid resuscitation in cases of volume depletion
144	In-hospital Management Supportive care including prehospital methods Whole-bowel irrigation is the decontamination method of choice. Toxic levels are treated with deferoxamine.
145	Isopropyl Alcohol Rubbing Alcohol
146	Route of Exposure Oral Skin contact Inhalation
147	Mechanism of Toxicity Isopropyl alcohol is a CNS depressant and vasodilator. Metabolized to acetone in the liver
148	Toxic Dose 0.5 to 1 mL/kg of 70% isopropanol
149	Signs and Symptoms Signs of intoxication CNS depression may appear. Twice as potent a CNS depressant as ethanol Hypotension that is unresponsive to fluids Cardiac ischemia or infarction can occur.
150	Prehospital Management Supportive care, including ABCs Assisted ventilation and fluid therapy as needed Gastric lavage and activated charcoal may be indicated for recent ingestions. Ethanol therapy is not indicated.
151	In-hospital Management Supportive care, including prehospital methods Vasopressor therapy, though of limited value, may be tried. Dialysis may be indicated in cases involving severe hypotension.
152	Lithium
153	Route of Exposure Oral
154	Mechanism of Toxicity Replaces sodium Can result in permanent neurological damage Excreted by the kidneys Can enhance its own reabsorption by the kidneys
155	Toxic Dose Highly variable depending on whether it is an acute or chronic ingestion Chronic ingestion is more severe Toxicity is more severe in the setting of poor underlying renal function, diuretic use, and dehydration.
156	Signs and Symptoms Low (serum levels < 1.5 mEq/L) – nausea, vomiting, and diarrhea Moderate (serum levels 1.5 to 3.0 mEq/L) – polyuria followed by urinary and fecal incontinence, muscle weakness, and neurological symptoms Severe (serum levels > 3.0 mEq/L) – seizures, coma, cardiac dysrhythmias, hypotension, and muscle twitching
157	Prehospital Management Supportive care including ABCs Aggressive fluid resuscitation
158	In-hospital Management Supportive care, including prehospital methods Lavage if < 1 hour since ingestion Whole-bowel irrigation Correction of volume depletion is essential Hemodialysis in cases of renal failure, of severe cardiovascular or neurological abnormalities, or with high serum levels
159	Methanol
160	Route of Exposure Generally oral Can be dermal Can be by inhalation
161	Mechanism of Toxicity Toxic metabolites are formed Result in profound acidosis Up to 5% ingested methanol may be excreted unchanged by the kidneys and via respiration.
162	Toxic Dose Death has been reported with as little a dose as 15 to 30 mL (1 to 2 tablespoons).
163	Signs and Symptoms 6-30 hours – signs of intoxication and gastrointestinal irritation Lack of symptoms does not preclude toxicity. Nausea, vomiting, abdominal pain, and CNS symptoms occur. Death is generally related to profound acidosis and severe CNS effects.
164	Prehospital Management Supportive care, including ABCs Oral or IV ethanol therapy has been utilized. Gastric lavage is used in recent ingestions. Charcoal is not helpful.
165	In-hospital Management Supportive care, including prehospital methods IV ethanol therapy Hemodialysis is indicated in the presence of visual symptoms, severe acidosis, high serum levels, or an ingestion of greater than 30 mL. Bicarbonate is reserved for cases of profound acidosis.
166	Narcotics and Opioids
167	Route of Exposure Oral Intravenous Intramuscular Intranasal Dermal
168	Mechanism of Toxicity Narcotics and opioids act directly on opiate receptors within the CNS. Cause CNS depression Some opioids have mixed agonist and antagonist properties.
169	Signs and Symptoms Miosis Respiratory depression Decreased level of consciousness Occasionally seizures, hypotension, and ventricular dysrhythmias can be seen.
170	Prehospital Management Supportive care, including ABCs Naloxone (Narcan) may avert the need for invasive airway control. Ensure patient and care providers safety. Consider prophylactic use of restraints.
171	In-hospital Management Supportive care, including prehospital methods Observe for possible re-sedation Duration of IV naloxone is 20-120 minutes Duration of most opioids is 3-6 hours Continuous naloxone infusion may be indicated.
172	Naloxone Narcan
173	Class Narcotic antagonist
174	Description Proven effective in the reversal of overdoses caused by: Narcotics Synthetic narcotic agents
175	Mechanism of Action Chemically similar to the narcotics Only has antagonistic properties Competes for opiate receptors in the brain Displaces narcotic molecules from opiate receptors Reverses respiratory depression associated with narcotic overdose
176	Pharmacokinetics Onset < 2 minutes (IV), 2-10 minutes (IM, ET) Peak effects < 2 minutes (IV), 2-10 minutes (IM, ET) Duration 20-120 minutes Half-life 60-90 minutes
177	Indications Complete or partial reversal of depression caused by narcotics May be used in the treatment of coma of unknown origin
178	Contraindications Known history of hypersensitivity
179	Precautions Administered cautiously to patients who are known or suspected to be physically dependent on narcotics Abrupt and complete reversal by naloxone can cause withdrawal-type effects Includes newborn infants of mothers with known or suspected narcotic dependence
180	Side Effects Hypotension Hypertension Ventricular dysrhythmias Nausea and vomiting
181	Interactions May cause narcotic withdrawal in the narcotic-dependent patient Only enough of the drug to reverse respiratory depression should be administered
182	Dosage 1 to 2 mg IVP Second dose after 5 minutes 2 mg 500 mL of D₅W Concentration of 4 μg/mL Infuse at 100 mL/hr IM, SC, and ET are acceptable.
183	Nalmefene Revex
184	Class Opioid antagonist
185	Description An opioid antagonist used for the reversal (partial or complete) of opioid effects, including respiratory and CNS depression
186	Mechanism of Action Completely blocks the effects of opioids, including CNS and respiratory depression, without producing any agonist (opioid-like) effects
187	Pharmacokinetics Onset 2-5 minutes (IV), 15 minutes (IM/SC) Peak effects 5 minutes (IV), 2 hours (IM/SC) Duration 4-8 hours Half-life 8.5-10.8 hours
188	Indications Management of known or suspected opioid overdose
189	Contraindications Known history of hypersensitivity
190	Precautions Overdose of long-acting opioids may require repeat dosing Use with caution in: Pregnant patients Opioid dependent patients
191	Side Effects Dysphoria Headache Hypertension and hypotension Tachycardia Vasodilation Abdominal cramps Nausea
192	Interactions None in the emergency setting
193	Dosage 0.5 mg/70 kg IV Incremental doses of 1.0 mg/70 kg Every 2 to 5 minutes Total dose of 1.5 mg/kg
194	Organophosphates and Carbamates
195	Route of Exposure Dermal Oral Ocular Inhalation