Toxicology

Overviews of Poisoning Emergencies Drug Abuse Alcoholism Managing Toxic Syndromes

Our environment contains many harmful substances including animal and plant toxins, industrial and household chemicals, therapeutic pharmaceuticals, and drugs of abuse.

Early identification is crucial to successful management of patients.

• Responsible for 10% of all ED visits, 9% of all ambulance transports, 5-10% of medical admissions to hospitals.

• Poison control centers exist in the United States to help manage poisoning emergencies.

• Carolinas Poison Control Center can be contacted at 800-222-1222.

• CHEMTREC 1-800-262-8200• Available 24 hours a day

• Each year, more than 4.7 million poisonings are reported to centers.

• 90% of these happen in the home• 51% of poisoning victims are children

younger than 6 years of age.• Information and treatment advice are

provided on toxic substances including drugs, chemicals, plants, animals, insects, fish, snakes, cosmetics, and hazardous materials.

Responsible for the following 6 elements:◦ Treatment info and toxicological consultation with

health care providers and the public◦ Professional education ◦ Data collection on all poisoning for evaluation◦ Public education and prevention◦ Research◦ Regional EMS poison system development

Specific agent or agents Amount ingested Time of exposure Weight and medical condition of the patient Treatment rendered before EMS arrival

Ingestion Inhalation Injection absorption

Accidental poisoning◦ Dosage errors; Idiosyncratic reactions; Childhood

poisoning; Environmental exposure; occupational exposure

Drug/alcohol abuse Intentional poisoning/overdose

◦ Chemical warfare; assault/homicide; suicide attempts

• Most require only supportive therapy• Ensure adequate airway, ventilation, and

circulation• Obtain thorough history & focused exam• Consider hypoglycemia in pt with ALOC• Administer narcan to pt with respiratory

depression• Obtain OD history from pt, family, friends• Consult with medical direction or poison control

center for specific treatment.• Reassess frequently, obtain substance or

containers, transport for evaluation.• SCENE SAFETY

80% of unintentional ingestions occur in children 1-3 years of age

Most result from household products (petroleum based agents, cleaning agents, cosmetics, medications, toxic plants, contaminated foods)

In adults poisoning is usually intentional, often suicide attempt or recreational drug abuse.

Corrosive substances may produce immediate tissue damage.

Medications and toxic plants require absorption and distribution through bloodstream to produce toxic effects

Early management focuses on: removing toxin from stomach; binding it to prevent absorption before poison enters intestines.

Primary goal is to identify effects on respiratory, cardiovascular, and CNS.

Detailed history of event, past significant medical and/or psychiatric history is important.

Scene safety, secure airway, provide adequate ventilatory support with high concentration oxygen and aggressive airway management.

Early development of noncardiogenic pulmonary edema

Later development of ARDS & Bronchospasm

Most common complication is cardiac rhythm disturbances

Tachy or brady dysrhythmias may indicate hypoxia, acidosis

Other complications include hypotension & hypertension (rarely), which may lead to cerebral vascular hemorrhage.

Perform and document baseline neuro exam

Deviations from normal can range from mild drowsiness and agitation to hallucinations, seizures, cardiopulmonary depression, death.

Complications can result from the toxin itself, or secondary to underlying metabolic or perfusion problem.

• Information obtained may not be reliable• Ascertain: what was ingested, when

ingested, how much, was vomiting attempted, antidote administered?

• If intentional, look for multiple drugs.• If one child has ingested something, likely

siblings or playmates have also ingested.• Does patient have psychiatric history

pertinent to suicide attempts or recent episodes of depressions?

Goal of treating serious poisoning by ingestion is to prevent toxic substance from reaching small intestine.

May be accomplished through use of activated charcoal, gastric lavage, or syrup of ipecac.

Using activated charcoal alone is considered equivalent or superior to other methods and has fewer complications.

Product of wood material that has been heated to extremely, high temps

Able to absorbs molecules of chemical toxins while in intestinal tract. (as much as 50%)

Administered unless strong acids, alkali or ethanol is the toxicant.

Not well absorbed by cyanide, ferrous sulfate, and methanol.

May be withheld when specific oral antidotes are available, or ingestion occurred 1 or more hours before presentation.

Comes mixed in aqueous solution with or without a cathartic.

Advantage is recovery of some gastric contents if performed within 1 hour after ingestion.

Provides method for administration of activated charcoal.

Performed using large bore OG tube (36-40Fr in adults, 24-28 in children).

After tube insertion, aspirate gastric contents to confirm placement.

Infuse tap water or NS until return fluid appears clear.

Unprotected airway Altered level of consciousness Those who have ingested low viscosity

hydrocarbons or caustic agents. Can be performed in patients with

depressed consciousness, but airway should be protected with ETI before the procedure.

Agitation of the patient Inadvertent tracheal intubation Esophageal perforation Aspiration pneumonitis Fluid and electrolyte imbalances in pediatric

patients.

Reduces absorption by 30% May interfere with efficacy of activated

charcoal Potential complications:

◦ Mallory-Weiss tear of esophagus◦ Pneumomediastinum◦ Fatal diaphragmatic or gastric rupture◦ Aspiration pneumonitis

Altered level of consciousness Ingestion of caustic substancesLoss of gag reflexSeizuresPregnancyAcute myocardial infarction Ingestion of: acids, alkalis, ammonia,

nontoxic agents, petroleum distillates, rapidly acting CNS depressants, rapidly acting CNS irritants, hydrocarbons.

May cause burns to mouth, pharynx, esophagus, upper respiratory and GI tracts.

Ingestion of substances generally produce immediate damage to mucous membrane & GI tract.

Acids generally complete damage within 1-2 minutes after exposure

Alkalis, may continue to cause liquefaction of tissue and damage for minutes to hours.

Prehospital care is usually limited to airway & ventilatory support, IV fluid replacement, and rapid transport

May receive orders to dilute with oral administration of milk or water (200-300mL in adult, 15 mL/Kg in child)

Saturated and unsaturated compounds derived from crude oil, coal, or plant substances.

Mixtures vary in viscosity, surface tension, and volatility, which, with other factors determine toxic effects of these agents.

Found in household products (spot removers, paints, pesticides) and petroleum distillates (turpentine, kerosene, gasoline, lighter fluids).

Also are halogenated hydrocarbons (carbon tetrachloride) and aromatic hydrocarbons (toluene, benzene).

Account for 7% of all ingestions in children < 5 yo.

Most important physical characteristic in potential toxicity◦Lower viscosity, higher risk of aspiration and

associated complications◦EX: agent like gasoline rapidly disperses over

pharyngeal and glottic surfaces, more volatile components becoming gas on contact with warm, mucous membranes

◦Exposure causes irritation, coughing, and possible aspiration, which may allow a toxic amount of hydrocarbon to enter tracheobronchial tree.

GI: Immediate (up to 6 hours: mucous membrane hyperemia, irritation, abdominal pain, N/V, belching) Delayed(diarrhea, hepatic toxicity)

Respiratory: Immediate(cough, choking, inspiratory stridor, tachypnea, cyanosis, dyspnea) Delayed(bacterial pneumonia, dyspnea, sputum production, atelectasis, pulmonary edema)

Neurological: lethargy, coma, seizures Systemic: Immediate(fever, malaise) Delayed

(spontaneous hemorrhage, hemolytic & aplastic anemias)

Ensure patent airway, provide support Identify substance & contact medical direction

or poison control. Gastric decontamination generally avoided,

medical direction may recommend gastric emptying of petroleum product containing significant amounts of camphor, benzene and its derivatives, organophosphates, halogenated hydrocarbons, heavy metals such as arsenicals, lead, and mercury.

Initiate IV fluids Monitor cardiac rhythm transport

Common solvent obtained from distillation of wood Found in gas line antifreeze, windshield washer

fluid, paints, paint removers, varnished, canned fuels such as sterno.

Poisoning can result from intentional or accidental ingestions, absorption through skin, or inhalation

Deliberate use of agent by chronic alcoholics to maintain inebriated state

Accidental ingestion resulting from misuse or distribution of methanol for ethanol

Accidental ingestions in children As absorbed, rapidly converted in liver to

formaldehyde and in minutes to formic acid.

Accumulation of formic acid causes: CNS depression, GI pain, N/V, blindness with as little as 4 mL, development of metabolic acidosis.

Onset of symptoms range from 40 minutes to 72 hours.

Symptoms of methanol poisoning may include: ◦ CNS depression: lethargy, confusion, coma, seizures◦ GI: N/V, abdominal pain◦ Visual: blurred or indistinct vision, pupils dilated and

sluggish to react to light, “spots before eyes”, “snow-filled vision”, blindness

◦ Metabolic Acidosis: shortness of breath, tachypnea, shock, multisystem failure, death

Supportive Secure airway & provide adequate ventilatory &

circulatory support IV Cardiac Monitor If pt seen within 1 hour after ingestion, gastric

lavage indicated Attempts to correct acidosis with Sodium

Bicarbonate may be recommended, hemodialysis will probably be necessary

Prevention of conversion of methanol to formic acid may be prevented by administration of ethanol. (30-60mL of 80 proof ethanol by mouth or gastric lavage).

Rapidly transport

Colorless, odorless, water-soluble liquid commonly used in windshield de-icers, detergents, paints, radiator antifreeze, and coolants.

Commonly ingested by children due to color & warm, sweet taste; by alcoholics as a substitute for ethanol.

Toxicity caused by accumulation of intermediary metabolites in primarily liver and kidneys. They may affect CNS and Cardiopulmonary and renal and result in hypocalcemia.

Stage1: CNS effects occur 1-12 hours after ingestion: slurred speech, ataxia, somnolence, N/V, focal or generalized convulsions, hallucinations, stupor, coma

Stage 2: cardiopulmonary system effects occurring 12-36 hours after ingestion: rapidly progressive tachypnea, cyanosis, pulmonary edema, cardiac failure.

Stage 3: renal system effects occurring 24-72 hours after ingestion: flank pain, oliguria, crystalluria, proteinuria, anuria, hematuria, uremia

ABC’s Gastric lavage in pt. presents within 1 hour after

ingestion; administer activated charcoal IV therapy to maintain adequate urine output Sodium bicarbonate to correct acidosis 80 proof ethanol to block conversion into toxic

metabolites Rapid transport for definitive treatment, which

may include hemodialysis and continued ethanol administration.

Poison Control Center may also recommend: Thiamine, Calcium Gluconate or Chloride, Diazepam

Rubbing alcohol most common source Used in disinfectants, degreasers,

cosmetics, industrial solvents, cleaning agents

Routes of Exposure: Ingestion, inhalation Potentially Lethal Dose: 150-240mL After ingestion, 80% metabolized to

acetone; rest excreted unchanged by kidneys.

Affects CNS, GI, and Renal Systems

Occur within 30 minutes after ingestion CNS and Respiratory Depression Abdominal pain Gastritis Hematemesis Hypovolemia Causes acetonemia & ketonuria, but usually

no metabolic acidosis, unless see hypotension.

Primarily supportive Airway and ventilatory to ensure adequate

respiratory elimination of acetone Gastric lavage Fluid resuscitation Rapid transport to facility with dialysis

capabilities

Infants and children are high risk groups for unintentional iron, lead, and mercury poisoning

When ingested iron exceeds body’s ability to store it, free iron circulates and is deposited into other tissues.

Most poisoning result from ingestion of multivitamins of children < 6 years old.

Is corrosive to GI tract, may produce bloody vomitus, painless bloody diarrhea, dark stools.

In severe cases (ingestion >20 mg/kg) iron toxicity can produce cardiovascular collapse and death 12-48 hours after ingestion.

Prehospital care: supportive measures and GI decontamination, charcoal gen. not recommended.

Can be found in: homes, esp. painted before 1978

Soil around a home Painted toys and furniture Food and liquid stored in lead crystal or lead

glazed pottery or porcelain Lead smelters or other industries Hobbies that use lead Folk Remedies (“greta” or “azarcon” Children most common victims, usually

result from ingestion of lead based paint.

Damage to brain and nervous system Behavioral and learning problems Hyperactivity Slowed growth Hearing problems headaches

Difficulties during pregnancy Reproductive problems Hypertension GI disorders Nerve disorders Memory and concentration problems Muscle and joint pain

Slow in onset, eventually results in toxicity Metal is excreted by body slowly and

accumulates primarily in the bone tissue Nonspecific symptoms such as: malaise,

mental disturbances, incoordination, abdominal pain, diarrhea, vomiting.

Acute Intoxication: anemia, weakness or paralysis, seizures and death.

Pt’s who survive will likely have brain damage

Prehospital: focus on recognizing potential and transport for evaluation.

Liquid at room temperature Used in thermometers, sphygmomanometers,

dental fillings, paints, pesticides, cosmetics, drugs, industrial processes

All forms except for dental is poisonous. Highly volatile, and vapor is readily absorbed

into body via lungs. Inhalation (shortness of breath, lung

damage); absorption (severe inflammation); intestines (N/V/D, abdominal pain)

After enters body, passes into bloodstream, principally accumulates in brain and kidneys.

Symptoms include: Malaise Incoordination Excitability Tremors Numbness in limbs Vision impairment Nausea and emesis (sy of renal failure) Mental status changes Care: supportive, possible hemodialysis, GI evacuation,

chelation therapy

Any illness of sudden onset associated with stomach pain, vomiting, diarrhea suspected of being caused by food eaten within previous 48 hours.

Salmonella: Staph: causes formation of toxins Causes Diarrhea: E.coli, campylobacter, shigella Botulism: found in soil and untreated water,

spore forming properties resist boiling, salting, smoking, pickling; more common in US; can be used as biological weapon. Associated with severe CNS symptoms in head to toe progression: HA, blurred or double vision, dysphagia, respiratory paralysis, quadriplegia.

Clostridum difficile can produce life threatening diarrhea associated with long term antibiotic administration.

Most Common: Norwalk, is a contaminant of shellfish, and rotavirus

May be responsible for illness when raw or partly cooked foodstuffs have been in contact with water contaminated by human excrement

Can result from consuming mushrooms, toadstools, eating fresh foods and vegetables contaminated with insecticides.

Chemical food poisoning can result from food stored in contaminated containers, improperly preparing and cooking various exotic foods

Symptoms usually develop within:◦ 30 minutes for chemical poisoning◦ 1-12 hours for bacterial toxins◦ 12-48 hours for viral and bacterial toxins

Use precautions to avoid contamination Ensure adequate ABC’s Complete history IV with crystalloid Transport

Frequently reported category 2nd to ingestion of cleaning substances.

Toxic manifestations are predictable and categorized by chemical and physical properties of plant.

Anticholinergic crisis may result form ingestion of alklaoid components (jimsonweed, lantana), with tachycardia, dilated pupils, hot dry skin, decreased bowel sounds, altered vision, abnormal mental status

Cholinergic – usually from ingestion of some mushrooms, manifested by: bradycardia, miosis, salivation, hyperactive bowel sounds, diarrhea

Nicotinic Alkaloids: (poison hemlock & delphinium) initially act as stimulants followed by depression and weakness

Customize to the patient’s symptoms rather than particular type of ingestion

Bring sample of plant to ED if possible. Ensure adequate ABC’s IV with fluids VS and monitor Most are hospitalized for observation and

treatment

Physical Properties –type and location of injury caused by toxic inhalation depend on the specific actions and behaviors of the chemical involved.

Large concentrations or prolonged exposure are more likely to cause contact with lungs and damage to lung tissue.

Solubility influences injury◦ Soluble chemicals (chlorine) can be converted to HCL

when they contact moisture in respiratory tract mucus producing injury I nasopharynx and conducting airway.

◦ Insoluble chemicals (phosgene) can produce severe damage to alveoli & bronchioles

Chemicals can be inhaled as gases and vapors, mists, fumes, or particles◦ Gases and vapors mix with air and distribute

freely throughout lung and its airways◦ Mists are droplets and toxic effect depends on

droplet size◦ Fumes contain fine particles of dust dispersed in

air. Large particles likely to be trapped in nasopharynx and conducting airways, small particles penetrate lower airways.

As a rule more reactive a chemical more severe and rapid the injury than a less reactive chemical.

Reactivity determined by: pH (<2 & > 11.5), direct-acting potential (produce injury w/o being transformed or changed, ex: HFL Acid); indirect-acting potential (must be transformed before can produce injury, ex:Phosgene); allergic potential (stimulate allergic reactions, EX: formaldehyde)

3 categories:◦ Simple asphyxiants (methane, propane, & inert

gases) displace or lower ambient O2 concentration

◦ Chemical asphyxiants (CO, Cyanide) possess intrinsic systemic toxicity manifested after absorption into circulation

◦ Irritants/Corrosives (chlorine, ammonia) cause cellular destruction and inflammation as they come into contact with moisture

Scene safety PPE Rapid removal Surface decontamination ABC’s Assessment Irrigation of eyes if needed IV VS and ECG monitoring Rapid transport to appropriate facility

Used in electroplating, ore extraction, fumigation, fertilizer, gas chambers

Poisoning can result from: inhalation of gas, ingestion of cyanide salts, nitriles, or cyanogenic glycosides, absorption,

Combines and reacts with ferric ions of respiratory enzyme cytochrome oxidase to inhibit cellular oxygenation. Produces rapid progression of symptoms from dyspnea to paralysis, unconsciousness & death, large doses usually fatal within minutes.

May produce characteristic odor of bitter almonds on pt’s breath or body.

Ensure personal safety Aggressive airway management Convert ferrous ions in HgB to ferric ions,

methemoglobin. Cyanide has a greater affinity for ferric ions,

is released from cytochrome oxidase and combines with methemoglobin, allowing cytochrome oxidase to resume normal function. (antidote kits induce methemoglobin).

3 steps:◦ Amyl nitrite by inhalation (converts 5% of HgB to

methemoglobin◦ Sodium nitrite 300 mg IV (yields methemoglobinemia

of 25-30%)◦ Sodium thiosulfate 12.5 mg IV (enhances conversion of

cyanide to thiocyanate for renal excretion. Consult with medical direction or poison control

if using Anticipate hypotension as a consequence of

antidote. IV fluids, and possible vasopressors Rapid transport for evaluation

Causes local pulmonary complications after inhalation

Results in inflammation, irritation, erosion of mucosal tissue of all respiratory structures as combines with water, producing caustic alkaline compound.

Pt develops coughing, choking, congestion, burning and tightness in chest, and feeling of suffocation, burning and lacrimation of eyes.

In severe cases may develop bronchospasm and pulmonary edema.

Along with general guidelines patient may require positive pressure ventilation and administration of diuretics and bronchodilators.

Most risky are those that have low viscosity, high volatility, high surface tension or adhesion of molecules along a surface

Cause aspiration pneumonia, CNS depression, live, kidney, or bone marrow toxicity.

Result from recreational use of carbon tetrachloride & methylene chloride, aromatic hydrocarbons like benzene & toluene.

Produce state of inebriation or euphoria through sniffing or huffing; Onset is rapid, followed by CNS depression, respiratory failure, cardiac dysrhythmias

Burning sensation & swallowing N/V, abdominal cramps, weakness,

anesthesia, hallucinations, changes in color perception, blindness, seizures, coma

Emergency Care: supportive, rapid transport for evaluation

Arthropod bites and stings – hymenoptera (bees, wasps, ants) and Arachnida (including spiders, scorpions, ticks)

Reactions to venoms are classified as local, toxic, systemic & delayed

Hymenoptera – usually causes instant pain followed by wheal and flare reaction

Large local reactions spread more than 15cm beyond the sting site & persist for more than 24 hours

Ant species of greatest concern is fire ant, venom results in necrotic activity, may produce systemic reactions, and are managed like other hymenoptera stings. Secondary infections can occur requiring antibiotic therapy, and extensive scarring can require skin grafts.

If stinger is present it should be scraped or brushed off , do not squeeze.

2 major types of reactions are neurotoxic reactions, from black widow; and necrotic from most other spiders.

Black Widow-shiny black, with red hourglass marking on surface of abdomen, usually found in undisturbed areas. Bites usually occur in rural and suburban areas of southern & western states between April & October.

Bite usually described as pinprick, can find 2 small fang marks about 1 mm apart surrounded by small papule. Within 1 hour of envenomation have characteristic muscle spasms and cramps, which can lead to abdominal rigidity (w/o tenderness), intense pain

Associated sy: paresthesia (burning sensation in soles of feet or body); pain in muscles of shoulders, back, and chest, HA, Dizziness, N/V, Edema of eyelids, increased perspiration and salivation.

Severe envenomation can cause HTN & ECG abnormalities

Care: ABC’s; clean area with saline, cover with sterile dressing, and intermittently apply ice

For moderate to severe sy: can be managed with valium and morphine

Transport for evaluation; antivenom should be administered in hospital setting.

Prefers hot, dry, abandoned environments, frequently found in closets

Fawn to dark brown in color, 1-2 cm long; have 6 white eyes in semicircle on head, dark violin shaped marking on top of cephalothorax; most active from April to October.

Initially bite causes little pain and is often overlooked, 1-2 hours later localized pain & erythema develop, 1-2 days blister or vesicle. Lesion surrounded by ischemic ring that further outlined by erythematous halo, giving “bulls-eye” appearance.

Next 24-72 hours area becomes larger, necrosis may occur with center yielding purple or black eschar, which sloughs in 2-5 weeks, leaving ulcer.

Systemic involvement may occur with S+S that include fever, chills, malaise, N/V, rash, hemolytic anemia, hemoglobinuria, & hypotension.

Death occasionally occurs from disturbance of coagulation system or hepatic injury

Care is supportive: cold compresses, sterile dressings, transport.

Sculptured or bark scorpion found in SW US dangerous to humans. Is nocturnal, favors wooded areas, clings upside down in it hideouts, under bark of eucalyptus and cottonwood tress esp. Occasionally invades homes, is small and yellow to brown some have tail stripe.

Most active April-August, hibernates in winter. Venom is mix of proteins with effect on sodium

channels. Acts at presynaptic terminals, releasing acetylcholine, stimulates sympathetic nerves is neurotoxic & can cause hyperactivity & convulsions.

Hyperesthesia at site of sting Pain, tingling, and burning sensation along

nerves at location of bite SLUDGE Bradycardia followed by tachycardia,

dysrhythmias Muscle twitching, convulsions, roving eye

movements, temporary blindness Majority produce minimal pain Mild analgesics, cool compresses,

observation are usually all required.

Can cause disease by transmitting microorganisms, or secreting toxins or venoms.

Reactions may vary from small pruritic nodule to extensive ulcerations. Can be accompanied by fever, chills, and malaise unrelated to infection.

Diseases that ticks are vectors for include: Rocky Mountain spotted fever, Lyme disease, tick paralysis.

Transmitted by bites of wood and dog tick More common on Atlantic Seaboard Accounts for more than 40 deaths/yr in US S+S usually develop within 5-7 days of bite,

includes HA, High Fever, loss of appetite. Within 2-3 days of onset of symptoms small

pink spots appear on wrists & ankles, which eventually spreads over body, spots darken, enlarge, and become petechial.

Mild cases recovery is within 20 days. If untreated, mortality rate is 8-25%.

Most cases of occurrence: NE coast from Maryland to Massachusetts, Wisconsin, and NW coast of California & Oregon.

Most commonly reported tick-born disease in US.

Caused by spirochete Course of disease of has several stages:

◦ Red dot appears at site of bite, expands in reddened annular rash with central clearing

◦ 2nd stage can follow in 4-6 weeks with cardiac abnormalities (AV blocks), neurological deficits (CN palsies)

◦ 3rd stage with arthritis as primary symptom◦ Unless treated sy may continue for several years,

gradually declining in severity.

From prolonged bite by female wood tick Caused by neurotoxin secreted from tick’s

salivary glands during blood meal Develops within 6 days after tick attaches to

host Initially pt presents with restlessness, c/o

paresthesia in hands & feet Over 24-48 hours an ascending, symmetrical,

flaccid paralysis may develop with loss of DTR’s (death can result from respiratory paralysis)

Removal of tick usually results in rapid improvement with complete resolution in several days. (Resembles Guillain-Barre syndrome).

Proper removal of tick Grasp as close to skin as possible with

forceps, tweezers, protected fingers, and pull out with steady pressure.◦ Do not crush or squeeze body of tick, other

methods of removal (fingernail polish, isopropanol, hot match) may induce tick to salivate or regurgitate into wind.

After removal, bite should be disinfected with soap, water, cover with sterile dressing.

2 main: pit vipers, coral snakes Pits: rattlesnakes, cottonmouth, copperhead,

pigmy rattlesnake, massauga Majority of bites caused by rattlesnake family Identifying characteristics: depression or pit

in maxillary bone, vertical elliptical pupils, triangular head distinct from rest of body.

Venom composed of variety of proteins designed to immobilize, kill, digest prey

S+S of mild envenomation: fang marks, local swelling & pain, lack of systemic sy,

Moderate: fang marks, pain & edema beyond site, systemic S+S (weakness, diaphoresis, N/V, paresthesias)

Severe: fang marks, massive edema, subcutaneous ecchymosis, severe systemic sy, shock

Mojave rattlesnake: s+s of envenomation may be delayed, onset of muscle weakness, ptosis, respiratory arrest may occur several hours after envenomation.

Description: round pupils, small, fixed fangs near anterior end of maxilla, 3 color pattern with red, black, yellow, white bands with black snout.

“Red on yellow, kill a fellow; red on black, venom lack.”

Small mouth makes it difficult to bite anything larger than finger, toe, or fold of skin, tends to hang and chew.

Venom neurotoxic, blocks acetylcholine receptor sites, early S+S are slurred speech, dilated pupils, dysphagia. Within 8-24 hours flaccid paralysis, death.

Tissue damage increases as venom spreads into lymph and blood

Care directed at retarding systemic spread of venom

If snake has been destroyed transport in closed container, do not try to destroy.

ABC’s; IV in unaffected extremity with fluids. Immobilize extremity in dependent position; if

coral snake wrap bandage snugly around extremity, keep pt. at rest.

Prepare for transport to appropriate facility, use of tourniquets, restricting bands controversial.

Most likely involved: coelenterates, echinoderms, stingrays

Coelenterates: those that carry venomous stinging cells (nematocysts) known as Cnidaria

Severity related to toxicity of venom, number of nematocysts discharged, physical condition of victim

Jellyfish, which Portuguese-man-of-war is largest and most dangerous, occur through Atlantic & Pacific. Tentacles can be up to 100 feet long. Contact can produce systemic S+S.

Sea Anemones – possess slender projections to sting & paralyze passing fish, can produce mild-moderate pain in humans.

Fire Corals – often mistaken for seaweed, may grow 2 m in height & have razor sharp exoskeleton with thousands of nematocyst bearing tentacles.

Envenomation ranges from irritant dermatitis to excruciating pain, respiratory depression, anaphylaxis, cardiovascular collapse.

Most often mild with stinging, paresthesias, pruritis, reddish-brown linear wheals of tentacle prints.

Systemic: N/V, abdominal pain, HA, bronchospasm, pulmonary edema, respiratory arrest

Care: stabilization & counteract effects of venom

Stabilize: ABC’s as needed, be prepared to provide aggressive airway mgmnt for systemic reactions.

Counteract: rinse with seawater, apply copious amounts of vinegar, isopropanol, baking soda slurry, household ammonia to inactivate venom. Paste of unseasoned meat tenderizer, no more than 5-10 minutes. Remove visible tentacles with forceps. Lather with shaving cream and shave area. Rinse again until pain alleviated.

Sea Urchins: globular dome shaped body, found on rocky bottoms or burrowed in sand or crevices. Have tiny spines thought to be poisonous.

Starfish: covered with thorny spines of calcium carbonate that secrete toxins. As spine enters skin, carries venom into wound with immediate pain, copious bleeding, mild edema. Can have systemic reactions.

Sea Cucumbers: sausage shaped animals, produce toxin that is secreted into surrounding ocean producing minor dermatitis or conjunctivitis in swimmers and divers.

Usually caring for puncture wounds and inactivating venom.

Remove spines with forceps, larger may require surgical removal.

Delayed toxic effects may include respiratory distress, paresthesia of lips and face, respiratory paralysis, atonia.

If patient is stable immerse affected area n extremely warm water before and during transport.

Venom organ consists of 2-4 sting on dorsum of whip like tail. Usually by person stepping on ray.

Venom has local and systemic complications: immediate intense pain, edema, variable bleeding, necrosis. Systemic: weakness, N/V/D, vertigo, seizures, cardiac conduction abnormalities, paralysis, hypotension, death.

TX: ABC’s, copiously irrigate with NS or fresh water. Immerse affected part in warm water. Possible orders for constricting bands, analgesics. Transport.

Many result from exposure to organophosphates, carbamates available for use as flea collars, home and commercial insecticides.

Compounds inhibit effects of acetylcholinesterase (degrades acetylcholine), which leads to accumulation of acetylcholine and a cholinergic “overdrive” occurs with resulting signs and symptoms characteristic of organophosphate and carbamate poisoning.

Early: nonspecific, include HA, dizziness, weakness, nausea

As overstimulation and distribution occurs see: SLUDGE, rapidly changing pupils with miosis common with vapor exposure or organophosphates, muscle fasciculation rapidly follow.

Cardiovascular: bradycardia, variable BP (hypo ten. Us.)

Respiratory: rhinorrhea, bronchoconstriction, wheezing, dyspnea

GI: cramps, emesis, defecation, increased bowel sounds

Vision: miosis, rapidly changing pupil size, lacrimation, blurred version

CNS: anxiety, dizziness, coma, convulsions, respiratory depression

Musculoskeletal: fasciculations, flaccid paralysis

Skin: diaphoresis Other: salivation urination

Scene safety by qualified personnel Respiratory support – paralysis may occur

suddenly. Aggressive mngmnt, suctioning, PPV, PEEP due to bronchoconstriction.

Drug administration – inhibit release of acetylcholine, separate cholinesterase and suppress seizures. Only after pt. exhibits 2 or more S+S of poisoning and consulting with medical control or poison control.

ECG monitoring – may see idioventricular, PVCs, VT, Torsades, Complete Heart Block, Asystole.

Atropine – reverses muscarinic effects (bradycardia, bronchoconstriction, respiratory secretions, miosis). Antagonizes actions of acetylcholine. Initial dose: 2 mg IVP q 5-15 (Ped: 0.05mg/kg q 15 min.) min. to dry secretions and decrease pulmonary resistance to ventilation.

Medical control may recommend IM admin during decon. DOC for carbamate poisons.

Cholinergic poisoning cause pt. to be wet, anticholinergic dry. “wet” pt requires atropine, “dry” patient pralidoxime.

Pralidoxime DOC for organophosphate poisoning

3 desirable effects: frees and reactivates acetylcholinesterase, detoxifies organophosphorous molecules, anticholinergic “atropine-like” effect.

Initial adult dose: 600 mg IM or 1-2 g IV over 15-30 min.

Ped: 20-50 mg/kg IV over 15-30 minutes May repeat in 1-2 hours. Diazepam: if needed before decon give in

2mg increments IM

Dysrhythmias usually occur in 2 phases: transient episodes of sympathetic tone that results in Sinus Tachycardia. Followed by extreme parasympathetic tone that results in Sinus Bradycardia, AV blocks, ST-segment & T-wave abnormalities.

Significant ventricular bradydysrhythmias may need overdrive pacing.

Common Drugs: Narcotics, Sedative-Hypnotics, Stimulants, PCP, Hallucinogens, TCAs, Lithium, Cardiac Meds, MAOIs, Nonprescription pain medications, salicylates, acetaminophen, for sexual purposes or gratification, metals

Emergencies that result include: adverse effects caused by drug, impurities, or contaminants. Infection from IV, intradermal injections; accidents during intoxication; drug dependence or withdrawal syndrome

General Management: scene safety; ABC’s; history of event, past medical, psychiatric.

Contact medical control or poison control about substance.

GI decon for oral substance. Look for track marks, evidence of body

packing,

Heroin accounts for 90%, also morphine, methadone, meperidine, oxycodone.

CNS depressants, hypotension, profound shock, pulmonary edema.

S+S: euphoria, arousable somnolence “nodding”, nausea, PINPOINT PUPIL (except with Meperidine), coma, seizures.

Antidote: naloxone, reverses opiate triad (respiratory depression, coma, miosis). If pt does not respond consider intubation

Desired end points of reversal: adequate airway reflexes and ventilation.

S+S of WD: gooseflesh, tachycardia, diaphoresis, irritability, insomnia, abdominal cramps, tremors, N/V/D, pulmonary edema, severe agitation, Vent. Dysrhythmias., anorexia, cold sweats or chills, fever, malaise

Includes: benzo’s and barb’s; usually taken PO can be diluted and injected IV, use with ETOH greatly increases effects, known as downers.

Benzo’s: depress brain function, abused for sedative effects, class of “ams”

Barb’s: inhibit impulse conduction in ascending reticular activating system, once used to anxiety and insomnia. Ex: phenobarbital, secobarbital.

Related to CNS and cardiovascular system: drowsiness, staggering gait, paradoxical excitability, comatose, respiratory depression, hypotension, shock.

Pupils may be constricted, often become fixed and dilated.

Airway and ventilatory management are essential points in treatmetn

Flumazenil for benzo’s, CI in pt prone to seizures, TCA OD. Not routinely recommended.

Amphetamines: produce mood elevation, improve task performance, suppress appetite, prevent sleepiness.

Similar to endogenous catecholamine, more pronounced effects on CNS.

Adverse effects: tachycardia, increased BP, tachypnea, agitation, dilated pupils, tremors, disorganized behavior, psychosis, paranoia, hallucinations.

Sudden withdrawal may result in “crash” stage with depression, suicidal, incoherent, or near coma.

Know as speed or uppers. Methamphetamine: meth, speed, crank, crystal, water, ice.

Cocaine: vary in purity fro 25-90%. Taken by snorting, IV, SC, IM, speed-ball is cocaine & heroin combo. Crack more potent formula prepared by mixing powdered street with alkaline soln, than adding solvent such as ether. Free base combined with marijuana or tobacco and smoked in pipe or cigarette.

Major CNS stimulant that causes profound sympathetic discharge: euphoria, talkativeness, agitation.

Drug can precipitate significant cardio and neuro complications.

Adult fatal dose thought to be about 1200 mg, but fatalities have been reported with 25-30mg.

Treatmetn: ABC’s, benzo’s, rapid transport.

Dissociative analgesic with sympathomimetic and CNS stimulant and depressant properties.

Psychoactive drug sold in table or powder, taken PO, intranasally, or smoked with other drugs (Sherman).

Most tablets contain 5 mg, in powder relatively pure.

Chronic use results in permanent memory impairment and loss of higher brain functions.

Produces unpredictable state that can resemble drunkenness, may see euphoria, confusion, disorientation, agitation, sudden rage. Intoxicated pt often has blank stare, stumbling gait, dissociative state.

Pupils reactive, flushing, diaphoresis, facial grimacing, hypersalivation, vomiting, nystagmus with burst like quality.

Death usually r/t behavioral disturbances from spatial disorientation, drug induced immobility, insensitivity to pain

TX by keeping sensory stimulation to minimum, monitor VS, LOC, safeguard for violence, increasing motor activity and muscle strength often precedes seizures.

More than 10 mg. Pt may be in coma, respiratory depression,

hypertension, tachycardia, HTN crisis with cardiac failure in severe

cases, HTN encephalopathy, seizures, intracerebral hemorrhage.

Manage life threatening comps, rapid transport

True psychiatric emergency that may mimic schizophrenia

Usually acute onset, may last from days to weeks

Syndromes range from catatonic, unresponsive, to bizarre & violent behavior.

See agitation, suspicious pt, with auditory hallucinations, paranoia

TX: hospitalization, antipsychotics, personal safety of paramount importance

Cause perceptual distortions Most common: PCP, LSD. Other: mescaline,

psilocybin mushrooms, marijuana, morning glory, nutmeg, mace, MDMA, MDEA

Effects range from minor visual illusions, classic anticholinergic syndromes resembling TCA toxicity, to permanent psychosis, flashbacks, respiratory & CNS depression (esp with LSD).

TX: usually supportive, calming measures, transport, pharmacological agents to counteract anticholinergic effects

Prescribed in treatment of depression Work by blocking uptake of norepinephrine,

serotonin into presynaptic neurons and alter the sensitivity of brain tissue to the actions of these chemicals.

Toxicity thought to result form central & peripheral atropine-like anticholinergic effects and direct depressant effects on myocardial function

EX: amitriptyline, desipramine, nortriptyline Examples of SSRIs: Prozac, Zoloft, Paxil

Early Sy: dry mouth, blurred vision, confusion, inability to concentrate, visual hallucinations.

Severe Sy: delirium, depressed resps, HTN, Hypotension, hyperthermia, hypothermia, seizures, coma

Cardiac Effects: tachy to brady, dysrhythmias 2ndary to AV block, prolonged QRS, GCS < 8, or both are finding that should alert to major toxicity. Sudden death from arrest may occur several days later.

TX: Sodium Bicarbonate 1-2 mEq/kg to reverse cardiac toxicity, ABCs, ECG monitoring. Transport.

Used to treat bipolar disorders, OD is common, pt frequently have levels checked.

Helps to prevent mood swings by interfering with hormonal responses to cAMP & augmenting reuptake of norepinephrine.

Effects include: muscle tremor, thirst, nausea, increased urination, abdominal cramping, diarrhea.

With toxic ingestion (20 mg/kg or more) S+S: muscle weakness, slurred speech, severe trembling, blurred vision, confusion, seizure, apnea, coma

TX: ABC’s, control of seizure activity

Suspect intoxication in any patient with a know psychiatric history who is confused, ataxic, or tremulous.

Activated Charcoal does not effectively bind lithium.

Common cause of poisioning fatalities in children and adults.

Major drugs responsible: digoxin, propanolol, beta blockers, calcium channel blockers.

All pt’s require high concentration oxygen administration, IV access, monitoring of VS and ECG.

Exerts direct and indirect effects on SA and AV fibers. At toxic levels can halt impulses in SA node, depress

conduction through AV node, increase sensitivity of SA & AV node to catecholamines.

Can increase rate of PVC’s, and produce almost any dysrhythmia or conduction block

Common S+S: nause, anorexia, fatigue, visual disturbances, disorders of GI, opthamological and neurological systems.

Oral OD managed with Activated Charcoal, Gastric Lavage, drugs to treat life-threatening dysrhythmias.

Severe OD’s treated with Digibind.

Rapidly absorbed after ingestion Toxicity impairs SA & AV node function, leading

to bradycardias & AV blocks. Ventricular conduction makes pt’s susceptible to wide QRS complexes, ventricular dysrhythmias (rarely VT or VF).

S+S: CNS, respiratory depression, hypotension, seizures

Care: activated charcoal, drugs to manage hypotension, dysrhythmias.

In-hospital: infusion of glucagon, various catecholamines, possible hemodialysis

Toxic Ingestion: myocardial depression, peripheral vasodilation with negative inotropic, chronotropic, dromotropic, and vasotropic effects.

Hypotension and bradycardia early manifestations.OD may result in dysrhythmias including AV Block

of all degrees, sinus arrest, AV dissociation, junctional rhythm, asystole. Ventricular dysrhythmias uncommon.

Other S+S: N/V, hypotension, CNS & Respiratory Depression

Care may include use of antidysrhythmics, vasopressors, activated charcoal, gastric lavage.

Block or diminish activitiy of monoamines (norepi, dopamine, serotonin).

Prescribed as antidepressants, antineoplastics, antibiotics, antihypertensives.

Some (phenelzine & tranylcypromine) have significant amount of amphetamine & methamphetamine & sometimes abused for their effects.

Signs of toxicity are usually delayed (6-24 hours after ingestion) and may last for several days.

Neuromuscular: agitation, rigidity, hyperreflexia, nystagmus, hallucinations, seizure.

Cardiovascular: sinus tachycardia, hypotension with vascular collapse, HTN, bradyasystolic rhythms

Severe: severe HTN, intracranial hemorrhage, delirium, hyperthermia, CV collapse, multisystem failure.

Care: supportive, ABC’s, activated charcoal for all, gastric lavage with recent ingestion.

Have analgesic & antipyretic action, reduces inflammation of joints, soft tissues such as muscle & ligaments.

Block production of prostaglandins (trigger transmission of pain signals to brain)

Used to relieve symptoms caused by types of arthritis, back pain, menstrual pain, HA, minor postoperative pain, soft tissue injuries.

Common: difunisal, fenoprofen, ibuprofen, naproxen.

Most commonly ingested NSAID in overdose. Effects usually reversible, seldom life-

threatening (can result in coma, seizure, hypotension, ARF).

Common SY: (more than 300mg/kg), include mild GI and CNS disturbances that usually resolve within 24 hours after ingestion.

Less common: mild metabolic acidosis, muscle fasciculations, chills, hyperventilation, hypotension, asymptomatic bradycardia

Care: gastric decontamination with activated charcoal, monitoring for hypotension, dysrhythmias.

Available as ASA, cold preparations, oil of wintergreen (methyl salicylate), and in combination with propoxyphene, oxycodone.

Due to association with Reye’s syndrome, not recommended for children > 16 yo who have viral symptoms.

Mechanism of toxicity includes direct CNS stimulation, interference with cellular glucose uptake, inhibition of Krebs cycle.

Complications from chronic or acute ingesiton include CNS stimulation, GI irritation, glucose metabolism, fluid and electrolyte imbalance, neurological symptoms, coagulation effects.

Initially direct stimulation of respiratory center causing increased rate and depth of respiration.

Respiratory alkalosis follwed by compensatory elimination of bicarbonate ions by kidneys and subsequent compensatory metabolic acidosis.

Next, accumulation of intermediate acides involved in energy metabolism, leading to profound metabolic acidosis.

Confusion, lethargy, convulsions, respiratory arrest, coma, brain death can occur in severe poisoning.

GI Irritation: N/V, hematemesis. Glucose metabolism: accumulation of serum

glucose. Eventually cellular glucose is depleted, pt. can demonstate tissue effects of hypoglycemia. Pt’s who die frequently demonstrate primary CNS tissue toxicity & severe cerebral edema.

Fluid and Electrolyte Imbalance: total body fluids adversely affected by hypermetabolism. Losses occur via GI fluids, emesis, renal clearance. Acid base disturbances may result in hypokalemia, hyperchloremia. Cardiac dysrhythmias: PVCs, VT, VF.

Neurological Sy: Mild (tinnitus, lethargy); Severe(hallucination, seizure, coma).

Coagulation: alter normal platelet funciotn, increased risk for significant bleeding.

Prehospital Care: activated charcoal, IV glucose to manage hypoglycemia, possible administration of sodium bicarbonate to produce alkaline urine.

Definitive Care: in-hospital intensive care observation, continued support of vital functions, hemodialysis.

One of tem nost commonly used drugs for intention self-poisoning & is associated with significant morbidity & mortality.

Can cause life threatening hepatic toxicity if not mangaed within 16-24 hours of ingestion. 30 (325mg) tablets can be toxic in the average adult.

Toxic effects (doses of 140mg/kg or >) can be classified in 4 stages.

Begin with mild sy that may be overlooked or masked by more dramatic effects of other agents, followed by transient clinical improvement, and finally peak liver abnormalities. If treated withing 16-24 hrs, complete recovery should occur.

Respiratory, cardiac, hemodynamic support in critically ill patients.

If inestion is recent (<1 hour) and pt. is alert, may recommend gastric decontamination & administration of activated charcoal.

Definitive care: administration of antidote, N-acetlycysteine (Mucomyst).

Commonly classified as “uppers”(CNS stimulants), “downers”(CNS depressants) or “all arounders” (anesthetics & mood altering agents that are taken alone or in combination to produce:◦ Euphorical sense◦ Excitation (“rush”)◦ Relaxation (“blissed out”)◦ Loss of inhibition

Uppers: Ecstasy, Speed/Meth/Crystal, Coke/Crack, Anabolic Steroids

Downers: Alcohol, Heroin, Benzodiazepines, Gamma hydroxybutyrate (GHB)

All-arounders: Ketamine, Cannabis/skunk, Poppers (alkyl nitrates), LSD

S+S of abuse: mild N/V to life threatenin respiratory depression, coma, death

Care: Personal safety, supportive, ABC’s, rapid transport

Key factor in:◦ 40% of vehicle fatalities◦ 68% of manslaughters◦ 62% of assaults◦ 54% of murder attempts◦ 48% of robberies◦ Economic Cost: 61.8 billion annually

Disorder characterized by chronic, excessive consumption of alcohol that results in injury to health or in inadequate social function and the development of withdrawal symptoms when patient stops drinking suddenly.

Should be considered chronic, progressive, potentially fatal disease characterized by remissions, relapses, & cures.

3 causative factors: personality, environment, addictive nature of drug. Generally thought that any person, regardless of these factors can become dependent on drug when consumed for long periods.

1: tolerance develops in social drinker, allowing individual to consume larger quantities of ETOH before experiencing ill effects.

2: drinker experiences memory lapses r/t events during drinking episodes.

3: characterized by lack of control over alcohol; drinker can no longer be certain of discontinuing alcohol consumption at will.

4: prolonged binges of intoxication with associated mental & physical complications.

Active ingredient; all alcoholic drinks rated based on ethanol percentage. Distilled liquors are proofed.

Metabolism: total of 80-90% ingested alcohol absorbed within 30 minutes. Then rapidly distributed through vascular space and reaches organ systems. 3-5% excreted unchanged via lungs & kidney. Rest metabolized in lever to CO2 & H2O. Generally metabolized atrate of 20 mg/dL/hr

Measured in mg or alcohol / given volume of blood (deciliter)

Widely used to evaluated CNS status of intoxicated person, there is marked individual variation in BAC and degree of intoxication. In NC can assist in conducting blood test to detect alcohol or drug intoxication.

Neurological Disorders: Potent CNS depressan, in moderate amount reduces anxiety, tension, provides most drinkers with feeling of relaxation and confidence. Initial feeling give way to impaired judgmetn, discrimination, prolonged reflexes, incoordination, drowsiness, and may progress to stupor and coma.

Long term neuro effects: short-term memory deficit, problems with coordination, difficulty with concentration & abstraction.

Potential for decreased dietary intake, malabsorption, leading to multipl vitamin & mineral deficiencies.

Clinical manifestations: altered immunity, anorexia, cardiac dysrhythmias, coma, irritability & disorientation, muscle cramps, paresthesias, poor wound healing, seizure, tremor & ataxia.

Wernicke-Korsakoff Syndrome: from chronic thiamine deficiency combined with inability to use thiamine from a heritable disorder or reduction in intestinal absorption and metabolism of thiamine by alcohol.

Affects brain & nervous system by disrupting central & peripheral nerve function.

2 stages: Wenicke’s encephalopathy, Korsakoff’s psychosis, or combo of 2

Wernicke’s encephalopathy develops suddenly with clinical manifestations of ataxia, ocular changes (nystagmus), disturbances of speech & gait, signs of neuropathy (paresthesias, impaired reflexes), stupor, or coma (rare). May be precipitated by IV administration of glucose. Is cause of coma in 1% of all alcoholics. IV admin. Of thiamine before glucose.

After receiving thiamine, patients usually become more alert, attentive, but gait and mental difficulties often persis for days or months; fewer than half of patient’s recover completely.

Mental disorder often found with Wernicke’s encephalopathy.

Signs include apathy, poor retentive memory, retrograde amnesia, confabulation, dementia.

Usually considered irreversible, leaves patient permanently handicapped by memory loss and in need of continual supervision.

Fluid & Electrolyte Imbalances: Urinary Output increases after ETOH consumption. Diuresis results from inhibition of ADH, which can lead to dehydration as well as electrolyte imbalances.

GI Hemorrhage: 4 primary causes are gastritis, ulcer formation, esophageal tear (Mallory-Weiss syndrome), variceal hemorrhage.

Gastritis: from toxic effects of ethanol on gastric mucosa, lead to areas of erosion. In chronic form blood can contiunaly ooze from mucosal lining & ulcers may develop.

Esophageal Tear: usually follow severe or protracted vomiting or retching. Results when gastric contents are forced against unrelaxed gastroesophageal junction, which produces sudden increase in pressure & mucosal tear with subsequent bleeding. Bleeding can be exacerbated by clotting abnormalities.

Varices: result of portal HTN caused by cirrhosis. Any veins subject to ruputre, most common site is esophagus. One of most difficult conditions to treat. Severe hematemesis requires aggressive supportive care through large bore IV’s and fluid resuscitation.

Cirrhosis: caused by chronic damage to lever cells that result in inflammation & necrosis. Bands of fibrosis develop & break up normal structure of liver, leads to portal HTN, with complicaitons of ascites, splenomegaly, bleeding esophageal and gastric varices.

Can also lead to hepatic encephalopathy by accumulation of toxic metabolic waste products, which would normally by detoxified by a healthy liver and has an adverse effect on the brain.

ETOH is most common cause of acute & chronic pancreatitis, exact mechanism is not clear.

May be caused by activation of pancreatic proenzymes, obstruction of pancreatic ducts, stimulation of enzymatic secretion. Also may be direct toxic effect.

Chronic: usually severe pain that can last from several hours to several days. Other effects include malabsorption, electrolyte imbalances (hypocalcemia, DM)

Complications of pancreatitis, hemorrhagic pancreatitis, sepsis, pancreatic abscess are associated with high mortality.

Thought to result from direct toxic effect of ETOH or its metabolites.

Pathological changes include intracellular edema, formation of lipid droplets, excessive cellular glycogen, deranged sarcoplasmin reticula and mitochondria.

In heart muscle, have decreased force of contraction (neg. inotrope), dysrhythmias, tendency to develop CHF.

In skeletal muscle, symptons are weakness and muscle wasting

Clinical prevalence estimated between 50-60% of all chronic alcoholics.

Suppresses bone marrow production of WBC’s, RBC’s, and platelet production also decreased.

Has specific effects on lung tissue which impairs macrophage mobilization and mucociliary function. Therefore, ability to fight pulmonary function altered, making person more susceptible to viral & bacterial pneumonia, which may occur 2ndary to aspiration during alcoholic stupor or for other reasons.

Increased incidence of cancer in alcoholic patients.

Suppresses 11 of 12 blood clotting factors produced in liver. Makes one more susceptible to bruising & internal hemorrhage and adds to frequency of subdural bleeding.

Causes increased myocardial irritability & decrease in tidal & minute volume, which may alter trauma pt’s ability to compensate for metabolic acidosis seen in shock.

Acute Alcohol Intoxication: at toxic levels, hypoventilation, hypotension, and hypothermia may develop.

Pt with S+S look out for: occult trauma, hypoglycemia, cardiac myopathy & dysrhythmias, GI bleeding, polydrug abuse, ethylene glycol or methanol ingesiton, never assume one is just inebriated.

Mildly toxicated: transport, monitor VS & LOC, thorough physical to R/O illness or injury, protect from further harm & maintain vital functions.

After scene safety: ABC’s, with spinal precautions, Initiate IV, per protocol thiamine, 50% dextrose (if hypoglycemia likely or confirmed), and naloxone is opiate OD suspected; ECG and monitor for dysrhythmias, transport.

Severity of syndrom depens on: magnitude of BAL, length of time level was obtained, abruptness of cessation, tissue tolerance to alcohol, general condition of patient.

Pathophysiological mechanism thought to result from CNS hyper-excitability, biochemical changes such as respiratory alkalosis & hypomagnesemia.

Can be divided into 4 categories: minor reactions, hallucinations, alcohol withdrawal seizures, DT’s

Begin 6-8 hours after cessation or reduction of intake

Symptoms peak within 24-36 hours and may persist for 10-14 days

Prognosis for recovery excellent with management

Reactions include: sudden and unexpected startle, flushed face & diaphoresis, anorexia, N/V, Insomnia, general muscle weakness, slight disorientation, generalized tremor, mild tachycardia, HTN, hyperreflexia

Occur 24-36 hours after cessation Disorders of perception are common and

vary from auditory & visual illusions to frank hallucinations, which can produce agitation, fear, & panic

Pt. may show signs of suicidal & homicidal tendencies, & minor reactions may be more pronounced

Prognosis good with appropriate management.

7-48 hours after ethanol cessation, with peak between 13 & 24 hours.

Seizure can occur singly or in groups of 2-6 Most often grand mal and of short duration,

associated with varying degrees of tremor, anorexia, hallucinations, autonomic hyperactivity.

May be self-limiting or progress to DT’s, with or without lucid interval

Seizure activity may require IV administration of large doses of diazepam, 5 mg every 5 minutes up to 30 mg.

Most dramatic and serious form of withdrawal Occurs 72-96 after cessation of alcohol but may be

delayed up to 14 days. Characterized by psychomotor, speech, autonomic

hyperactivity; profound confusion; disorientation; delusion; vivid hallucinations; tremor; agitation; & insomnia

Single episode may last 1-3 days, and with multiple recurrences last up to 1 month.

Autonomic hyperactivity is most distinguishing feature of DTs: tachycardia, fever, HTN, dilated pupils, profuse diaphoresis, cardiovascular collapse may be present.

True medical emergency, with mortality rate as high as 15%. Associated illnesses frequent contributing cause of death.

Prehospital primarily supportive: scene safety, ABC’s, IV with Saline for rehydration, pharmacological therapy as needed, calm, frequent reorientation, transport.

Antabuse prescribe to help abstain from ETOH, inhibits ethanol metabolism & allows accumulation of metabolite acetaldehyde.

Acetaldehyde produces ill effects on GI, CV, autonomic nervous system, and thought to be responsible for hangover.

When mixed with ethanol pt can experience unpleasant & potentially lifethreatening physiological response. (Can also occur in pt’s taking Flagyl for trichomonas & other types of infections).

Reaction begins 15-30 minutes after ingestion of 2-5 alcoholic drinks and continues for 1-2 hours

Pt experiences vertigo, HA, vomiting, flushing, dyspnea, diaphoresis, abdominal pain, CP

Also hypotension, shock, dysrhythmias Sudden death, myocardial & cerebral

infarction and hemorrhage have been reported after as little as one drink

TX: ABC’s, IV fluids to treat hypotension, meds to treat dysrhythmias, transport.

Most pt’s require supportive therapy Ensure scene safety, provide ABC’s Thorough history, focused physical exam Consider hypoglycema, narcan or

nalmefene for respiratory depression. If OD suspected, obtain history, consult with

poison control or medical direction. Frequently monitor VS & ECG, transport

container or substance if possible, transport

Common signs: confusion, CNS depression, weakness, SLUDGE, bradycardia, wheezing, bronchoconstriction, myosis, coma, convulsion, diaphoresis, seizures

Causative agents: organophosphate and carbamate insecticides, nerve agents, some mushrooms

TX: atropine, pralidoxime, diazepam, activated charcoal

Common signs: delirium, tachycardia, dry, flushed skin, dilated pupils, seizures, dysrhythmias

Causative Agents: antihistamines, antiparkinson meds, atropine, antipsychotics, antidepressants, skeletal muscle relaxants, many plants (jimson weed)

TX: diazepam, activated charcoal, physostigmine

Common signs: visual illusion, delusions, bizzare behavior, flashbacks, respiratory & CNS depression

Causative agents: LSD, PCP, mescaline, some mushroom, marijuana, jimsom weed, nutmeg, mace, some amphetamines

TX: mimimal sensory stimulation and calming measures

Common signs: euphoria, hypotension, respiratory depression/arrest, nausea, pinpoint pupils, seizures, coma

Causative agents: heroin, morphine, codeine, meperidine, propozyphene, oxycodone, hydrocodone, fentanyl

TX: naloxone, nalmefene

Common signs: delusions, paranoia, tachycardia or bradycardia, HTN, diaphoresis, seizures, hypotension and dysrhythmias in severe cases

Causative agents: cocaine, amphetamine, methamphetamine, OTC decongestants

TX: minimal sensory, calming measures

Atropine seldom helpful, not harmful Lifesaving in organophosphate or carbamate

with starting dose of 2-4 mg for adults Isupre may induce or aggravate hypotension

and ventricular dysrhythmias, do not give unless massive beta-blocker poisoning, then in high doses may be effective.

Cardiac Pacing often effective, if still resistant manage with vasopressors with greater beta agonist activity

May induce myocardial ischemia, MI, dysrhythmias, high output heart failure, shock

Avoid adenosine, cardioversion, Cardizem & Verapamil relatively CI.

Drug therapy preferred when rate control necessary, benzo in doses that do not produce a decreased LOC or respiratory depression is safe & effective

When due to sympathomimetic poisoning cautious use of nonselective beta blocker

Usually do not require aggressive therapies Benzo’s first line therapy Short acting (nitroprusside) 2nd line agents. Carefully titrated doses of labetalol 3rd line

therapy

Tx similar to HTN emergencies Benzo’s and NTG 1st line agents Phetolamine 2nd line Propranolol CI Fibrinolytics CI

Should be cardioverted Antidysrhythmics indicated Procainamide CI in TCA OD’s Lidocaine safe in cocaine poisoning Consider correctable factors in Torsades Rhythm may respond to electrical &

pharmacological therapy:◦ Magnesium◦ Lidocaine◦ Electrical or pharmacological OD pacing◦ Potassium

Usually results when drug induces: decerases in intravascular volume, falls in SVR, diminished myocardial contractility, combination of factors

Give fluid challenge, dopamine, for hypovolemic

For distributive: potent vasoconstrictors (levophed)

For cardiogenic: inotropics, glucagons, isuprel, dobutamine,

Cardioversion or defibrillation appropriate Resuscitation usually terminated after 20-

30 minutes Prolonged resuscitation may be warranted

in some patients Organ donation can be an option.

THIS CHAPTER IS THROUGH!