The document discusses toxicology and poison control. It provides information on common toxic exposures including drugs, chemicals, plants and animals. Poison control centers provide treatment advice and education on poisonings. They are responsible for toxicology consultation, data collection, education and research. Early identification of poisoning is important for successful management. The majority of poisonings occur in the home and involve young children.

1. Toxicology

2.  Overviews of Poisoning Emergencies
 Drug Abuse
 Alcoholism
 Managing Toxic Syndromes

3.  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.

4. • 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

5. • 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.

6.  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

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

8.  Ingestion
 Inhalation
 Injection
 absorption

9.  Accidental poisoning
◦ Dosage errors; Idiosyncratic reactions; Childhood
poisoning; Environmental exposure; occupational
exposure
 Drug/alcohol abuse
 Intentional poisoning/overdose
◦ Chemical warfare; assault/homicide; suicide
attempts

10. • 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

11.  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.

12.  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.

13.  Primary goal is to identify effects on
respiratory, cardiovascular, and CNS.
 Detailed history of event, past significant
medical and/or psychiatric history is
important.

14.  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

15.  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.

16.  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.

17. • 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?

18.  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.

19.  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.

20.  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.

21.  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.

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

23.  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

24.  Altered level of consciousness
 Ingestion of caustic substances
 Loss of gag reflex
 Seizures
 Pregnancy
 Acute myocardial infarction
 Ingestion of: acids, alkalis, ammonia, nontoxic
agents, petroleum distillates, rapidly acting
CNS depressants, rapidly acting CNS irritants,
hydrocarbons.

25.  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.

26.  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)

27.  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.

28.  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.

29.  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)

30.  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

31.  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.

32.  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

33.  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

34.  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.

35.  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

36.  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

37.  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

38.  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.

39.  Primarily supportive
 Airway and ventilatory to ensure adequate
respiratory elimination of acetone
 Gastric lavage
 Fluid resuscitation
 Rapid transport to facility with dialysis
capabilities

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

41.  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.

42.  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.

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

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

45.  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.

46.  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)

47.  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

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

49.  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.

50.  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

51.  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

52.  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

53.  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

54.  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

55.  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

56.  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

57.  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.

58.  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)

59.  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

60.  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

61.  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.

62.  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).

63.  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

64.  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.

65.  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

66.  Burning sensation & swallowing
 N/V, abdominal cramps, weakness,
anesthesia, hallucinations, changes in color
perception, blindness, seizures, coma
 Emergency Care: supportive, rapid transport
for evaluation

67.  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

68.  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.

69.  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

70.  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.

71.  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.

72.  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.

73.  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.

74.  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.

75.  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.

76.  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%.

77.  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.

78.  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).

79.  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.

80.  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,

81.  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.

82.  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.

83.  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.

84.  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

85.  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.

86.  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

87.  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.

88.  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.

89.  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.

90.  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.

91.  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.

92.  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

93.  CNS: anxiety, dizziness, coma, convulsions,
respiratory depression
 Musculoskeletal: fasciculations, flaccid
paralysis
 Skin: diaphoresis
 Other: salivation urination

94.  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.

95.  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

96.  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

97.  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.

98.  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

99.  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,

100.  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

101.  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.

102.  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.

103.  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.

104.  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.

105.  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.

106.  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.

107.  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

108.  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

109.  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

110.  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

111.  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.

112.  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

113.  Suspect intoxication in any patient with a
know psychiatric history who is confused,
ataxic, or tremulous.
 Activated Charcoal does not effectively bind
lithium.

114.  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.

115.  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.

116.  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

117. 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.

118.  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.

119.  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.

120.  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.

121.  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.

122.  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.

123.  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.

124.  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.

125.  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.

126.  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.

127.  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).

128.  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

129.  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

130.  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

131.  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.

132.  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.

133.  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

134.  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.

135.  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.

136.  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.

137.  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.

138.  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.

139.  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.

140.  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.

141.  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.

142.  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.

143.  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.

144.  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.

145.  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.

146.  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.

147.  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.

148.  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

149.  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

150.  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.

151.  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.

152.  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.

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

154.  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

155.  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.

156.  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

157.  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

158.  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

159.  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

160.  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

161.  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

162.  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

163.  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

164.  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

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

166.  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

168.  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,

169.  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.

170.  THIS CHAPTER IS THROUGH!