Poisoning

Refers

to the development of dose

related adverse effects following
exposure to chemicals, or other
xenobiotics

The

severity of reversibility of
poisoning depend on the functional
reserve of the individual or target
organ, which is influenced by age
and pre-existing disease

 The

correct diagnosis can usually be

established by the history, PE and
routine and toxicologic lab
evaluations, and characteristic
clinical course

History should include

1. the time, route, duration and
circumstances of exposure
2. The name and amount of each drug,
chemical or ingredient involved
3. The time of onset, nature and severity
of symptoms
4. The time and type of first aid measures
provided
5. Medical and psychiatric history

Severity of Physiologic Stimulation and

Depression in Poisoning and
Drug

Grade

Grade 1

Grade 2

Physiologic
Stimulation

Physiologic
Depression

Anxious, irritable, tremulous; vital

Awake, lethargic, or sleeping but

signs normal; diaphoresis, flushing

arousable by voice or tactile

or pallor, mydriasis, and

stimulation; able to converse and

hyperreflexia may be present

follow commands; may be confused

Agitated; may have confusion or

Responds to pain but not voice; can

hallucinations but is able to

vocalize but not converse;

converse and follow commands;

spontaneous motor activity present;

vital signs mildly to moderately

brainstem reflexes intact

increased

Grade 3

Grade 4

Delirious; unintelligible speech,

Unresponsive to pain; spontaneous

uncontrollable motor hyperactivity;

motor activity absent; brainstem

moderately to markedly increased

reflexes depressed; motor tone,

vital signs; tachyarrhythmias

respirations, and temperature

possible

decreased
Unresponsive to pain; flaccid

fundamentals of poisoning
management
Supportive

care

Airway protection
Oxygenation/ventilation
Treatment of arrhythmias
Hemodynamic support
Treatment of seizures
Correction of temperature abnormalities
Correction of metabolic derangements
Prevention of secondary complications

 Prevention

of further poison

absorption
Gastrointestinal decontamination
Syrup of ipecac
Gastric lavage
Activated charcoal
Whole-bowel irrigation
Catharsis
Dilution
Endoscopic/surgical removal

 Decontamination of other sites

Eye decontamination
Skin decontamination
Body cavity evacuation

 Enhancement

of poison elimination

Multiple dose activated charcoal

Diuresis
Alteration of urinary pH
Chelation
Extracorporeal removal
Peritoneal dialysis
hemofiltration
Hemodialysis
plasmapheresis
Hemoperfusion
exchange transfusion
Hyperbaric oxygenation

 Administration

of antidotes

Neutralization by anti bodies

Neutralization by chemical binding
Metabolic antagonism
Physiologic antagonism

 Prevention

of re- exposure

Adult education
Child proofing
Notification of regulatory agencies
Psychiatric referral

 Activated

charcoal has comparable

or greater efficacy, fewer
contraindications and complications
Dose 1 g/kg body weight
Charcoal adsorbs ingested poison
within the gut lumen allowing the
charcoal-toxin complex to be
evacuated with stool
Not recommended for pts who have
ingested corrosive

 Activated

charcoal is not effective

for caustics, cyanide, mineral acids,
ferrous sulfate, ingestion and heavy
metals

gastric lavage contraindications

include ingestions of strong acids,
alkalis, petroleum distillates - risks
of gastroesophageal perforation &
aspiration pneumonitis

Isoniazid overdose
NGT,

gastric lavage, activated

charcoal

Antidote

Pyridoxine HCl, given gm

per gm
Diazepam

for active seizure

Organophosphate
poisoning
Decontamination
Activated charcoal, sodium sulfate
Antidote : Atropine Sulfate 0.01 -

05 mg/kg IV q 5 mins
Maintain the ff :
Dry mucosa, HR > 60 bpm, hypoactive

bowel sounds, pupils > 4 mm

Atropine

toxicity temp > 39C,

absence of sweating, psychosis &
restlessness

 Seizure

: diazepam/ phenytoin
Mannitol
Avoid the ff: beta-blockers, lidocaine,
sulfa-containing drugs,
aminoglycosides

Paracetamol overdosage
NGT,

activated charcoal, sodium

sulfate
IV antidote: N-acetylcysteine very
effective in preventing paracetamol
induced hepato-toxicity when
administered during the first 8 hours
after an overdose

Alcoholism and Drug

dependency
Alcohol
at low doses alcohol can have some

beneficial effects such as decreased

rates of MI, stroke, gallstones & possibly
vascular & Alzheimers dementias
the consumption of more than two
standard drinks per day increases the
risk for health problems in many organ
systems

ethanol
a weakly charged molecule that
moves easily through cell
membranes, rapidly equilibrating
between blood and tissues
The level of alcohol in the blood is
expressed as milligrams or grams of
ethanol per deciliter
eg. 100 mg/dl or 0.10 g/dl

 Is

a central nervous system

depressant that decreases neuronal
activity
The rate of alcohol absorption is
increased by
Rapid gastric emptying
Absence of proteins, fats, or CHO
Absence of congeners
By dilution to a modest percentage of

ethanol

Bw 2% and 10% of ethanol is

excreted directly through the lungs,
urine or sweat, but the greater part
is metabolized to acetaldehyde,
primarily in the liver

Effects of blood alcohol in the

absence of tolerance
Blood
0.02

level g/dl usual effect

decreased inhibitions, a slight

feeling of intoxications
0.08
dec. in complex cognitive
functions
& motor performance
0.20
obvious slurred speech, motor
incoordination, irritability & poor
judgment
0.30
light coma & depressed vital
signs
0.40
death

 Tolerance
Is a complex phenomenon involving at

least three types of compensatory

mechanisms
1. metabolic or pharmacokinetic toleranceseen after 1-2 weeks daily drinking with up
to a 30% increase in the rate of hepatic
ethanol metabolism
2.cellular or pharmacodynamic tolerance develops through neurochemical changes
that maintain relatively normal physiologic
functioning despite the presence of alcohol

 3. behavioral tolerance individuals

learn to adopt their behavior so that

they can function better that expected
under influence of the drug
THE EFFECTS OF ETHANOL ON ORGAN

SYSTEMS
Nervous system
1. episode of temporary anterograde amnesia in
which the person forgets all or part of what occurred
during a drinking evening

 2. disturbed sleep alcohol might help a

person to fall asleep, it disrupts sleep

throughout the rest of the night
3. exacerbate sleep apnea
4. impaired judgment & coordination
5. peripheral neuropathy in alcohol
dependent individual
6. cerebellar degeneration or atrophy
7. psychiatric syndromes- temporarily

 A. alcohol- induced mood disorder

B. alcohol-induced anxiety disorder
C. alcohol-induced psychotic disorder,
auditory hallucinations % or paranoid
delusions

Treatment
Keeping pts achieve abstinence
Supportive care talk therapy

 The

Gastrointestinal system

Esophagus and stomach

Result in inflammation of the esophagus and
stomach causing epigastric distress and GI
bleeding
Pancreas and liver
Acute pancreatitis is 3x higher in alcoholics
Alc-induced hepatitis, perivenular sclerosis
and cirrhosis

 Cancer
Womens breast increases 1.4 fold
Oral & esophageal cancer - 3x
Rectal cancer

Hematopoietic

- 1.5 x

system

Hypersegmented neutrophils,

reticulocytopenia
Hyperplastic bone marrow
Mild thrombocytopenia

 Cardiovascular

system

Acutely ethanol decreases myocardial

contractility & causes peripheral

vasodilation, with a resulting mild
decrease in BP & a compensatory
increase in cardiac output
Chronic heavy drinkers have a sixfold
increased risk for coronary artery
disease & cardiomyopathy
Atrial & ventricular arrhythmias

maximum of one to two drinks per

day may decrease the risk for
cardiovascular death, perhaps
through an increase in high-density
lipoprotein (HDL) cholesterol or
changes in clotting mechanisms
GUT system changes, sexual
functioning & fetal development
Modest ethanol doses can increase

sexual drive but also decrease erectile

 High doses of ethanol in women

Amenorrhea
Dec. in ovarian size
Absence of corpora lutea with assoc.
infertility
Inc. risk of spontaneous abortion
Heavy drinking during pregnancy serious
consequences for fetal development

alcoholism

Diagnosis blood test

GGT y-glutamyl transferase (>35 U)
CDT - carbohydrate-deficient transferrin

(>20 U/L)
These serologic markers of heavy drinking
can also be useful in monitoring abstinence,
as they are likely to return toward normal
within several weeks of cessation of drinking

 alcohol

withdrawal syndrome

Once the brain has been repeatedly

exposed to high doses of alcohol, any

sudden decrease in intake can produce
withdrawal symptoms
Features:
Tremors of the hands(shakes or jitters)
Agitations and anxiety
Autonomic nervous system overactivity
including an inc. pulse, RR and Temp
insomnia

 Symptoms generally begin within 5-10 h

of decreasing ethanol intake, peak in

intensity on day 2 0r 3 & improve by day
4 or 5.
Delirium tremens (DTs)
Refers to an uncommon state of intense
acute withdrawal that includes
delirium( mental confusion, agitation ,
&fluctuating levels of consciousness) assoc.
with a tremor & autonomic overactivity

 Treatment
Acute

intoxication

1. assess vital signs and manage respiratory

depression , cardiac arrhythmia or BP

instability if present
2.blood & urine- screen for opioids or other
CNS depressors
3.if with aggressive behavior low doses of a
short-acting benzodiazepines
Lorazepam 1-2 mg po or IV
Haloperidol 0.5 -5 mg

 Withdrawal
1st step thorough PE- search for

evidence of liver failure, GI bleeding,

cardiac arrhythmia, infection & glucose
or electrolyte imbalance
Adequate nutrition ,rest
Multiple vitamins including 50 -100 mg
of thiamine
Decrease agitation- lorazepam,
diazepam

 Rehabilitation
The mainstay of alcoholic rehabilitation

involves counseling, education, &

cognitive approaches, several
medications might be useful
6-12 months recommended tx
Naltrexone 5150 mg/d

Opioid drug abuse &

dependence
All

opioid-drugs are capable of

producing a heroin-like intoxication
as well as tolerance & withdrawal

Pure

synthetic opioids

1. meperidine
2.propoxyphene
3. diphenoxylate
4. methadone

5. fentanyl
6. buprenorphine
7. tramadol
8. pentazocine

 Semi-synthetic

drugs produced from

Morphine
1. hydromorphone
2. diacetylmorphine (heroin)
3. oxycodone

Plasma

half-life

2.5 3 h for morphine

>22 h for methadone

 IV

administration most rapid and

pronounced effect
Liver where metabolism primarily
occur through conjugation with
glucuronic acid

 ACUTE

AND CHRONIC EFFECTS OF

OPIOIDS
1. Effects on Organ systems
CNS effects
Nausea, vomiting, decrease pain perception,
sedation
Acute opioid administration inhibits release of
some hormones from the hypothalamus,
including corticotropin-releasing hormone ,
luteinizing hormone with a subsequent
reduction in some sex hormones contribute
to a decreased sex drive

 Respiratory depression

GI effects
Dec. gut motility, nausea, vomiting, anorexia
and weight loss
Cardiovascular
Orthostatic hypotension can occur prob 2dry
to histamine release & dilation of peripheral
vessels

 Opioid

toxicity & overdosage

Syndrome which occurs immediately

with IV overdose, includes

Shallow and slow respirations

Pupillary miosis
Bradycardia
Hypothermia
Stupor and coma

 Rx

: OPIOID overdose

Support vital signs- intubation if needed

Naloxone - 0.4 2 mg IV or IM
Response should occur in 1-2 min but if needed, the dose
can be repeated every 2-3 min up to 10 mg
Monitor 24 h for heroin overdose

72 h for long-acting drugs- methadone

Activated

charcoal ingestion of large doses of

oral opioid
Gastric lavage to remove any remaining drug

Intubation

aspiration

stuporous/comatose to prevent

 Opioid

abuse & dependence

Genetic factors appear to influence an

individuals specific risk for opioid

dependence as well as a more general
vulnerability toward substance- related
problems
Ie. Variations 2 subunit of the aminobutyric (GABA) A receptor

 Increased

risk for dependence

1. persons with chronic pain syndromes

mis use their prescribed drugs

2. physicians, nurses and pharmacists
3. those who buy illicit drugs to get high
some of these individuals have severeantisocial problems

 Withdrawal
Withdrawal symptoms include nausea,

diarrhea, coughing, lacrimation,

mydriasis, rhinorrhea, profuse sweating,
twitching of muscles, piloerection

Treatment of the withdrawal

syndrome
Physical

examination including neurologic

function
Search for focal and systemic infections
Lab test- including liver function, HIV &
Hep B & C status
10-25 mg Methadone BID to decrease sx
-after several days, the opioid is then decreased by
10-20% of the original drugs dose each day

Clonidine

2 to 4x a day to dec.
sympathetic nervous system overactivity

 REHABILITATION
A long term commitment by the patient

to maintain a lifestyle without illicit

substance as essential for preventing
relapse
Pts are educated about their
responsibility for improving their lives &
motivation for abstinence is increased by
providing information about the medical
& psychological problems that can be
expected if dependence continues

 OPIOID

MAINTENANCE

The goal is to provide a substitute drug

that is legally accessible, safer, can be taken

orally, and has a relatively long half-life so
that it can be taken once a day
A. Methadone
Long acting opioid (80-120 mg/d)
This dose is effective in blocking heroin-induced
euphoria while decreasing craving
6 months to > 1 yr- slowly decrease the dose by
~5% per week

 Buprenorphine- alternative
Advantages
1. low overdose danger
2. Easier detoxification than is seen w/
methadone
3. higher doses do not increase euphoria

OPIOID

ANTAGONISTS

Ie. Naltrexone competes with heroin

and other opioids at receptors, reducing

the effects of the opioid agonists

To avoid precipitating a withdrawal

syndrome, patients must be free of
opioids for a minimum of 5 days before
beginning treatment w/ naltrexone

COCAINE
A

stimulant & local anesthetic with

potent vasoconstrictor properties

Increases

synaptic concentrations of
the monamine neurotransmitters
dopamine, norepinephrine and
serotonin by binding to transporter
proteins in presynaptic neurons &
blocking reuptake

 Produces

a brief, dose- related

stimulation & enhancement of mood
and an increase in cardiac rate &
blood pressure
Neurologic complications
1. gen. seizures
2. headache
3. ischemic or hemorrhagic stroke or

SAH

 Severe

pulmonary disease may

develop in individuals who inhale
crack cocaine
Hepatic necrosis
Chronic cocaine use causes
significant loss of libido & adversely
affects reproductive function
May cause paranoid ideation & visual
& auditory hallucinations

 TREATMENT
Cocaine toxicity produces

hyperadrenergic state characterized by

hypertension, tachycardia, tonic-clonic
seizures, dyspnea & ventricular
arrhythmia
IV Diazepam 0.5 mg/kg to control
seizures
Propranolol IV - 0.5 to 1.0 mg/kg for
ventricular arrhythmia

 Treatment of chronic cocaine abuse

requires the combined efforts of primary

care physicians, psychiatrists, &
psychosocial care providers

Marijuana and cannabis

compounds
Delta-9-tetrahydrocannabinol

psychoactive substance
Hashish

is prepared from
concentrated resin of C. sativa

Smoking

is the most common mode

of marijuana or hashish use

 Specific

cannabinoid receptors (CB1 &

CB2) have been identified in the CNS,
including spinal cord & PNS.

ACUTE

AND CHRONIC INTOXICATION

acute intoxication from marijuana &

cannabis compounds is related to both the

dose of THC & the route of administration
THC is absorbed more rapidly from
marijuana smoking

 Usually consists of subjective perception

of relaxation & mild euphoria,

accompanied by some impairment in
thinking, concentration & perceptual &
psychomotor function
The drug can precipitate severe

emotional disorders in individuals who

have antecedent psychotic or neurotic
problems

 Chronic marijuana use has also been

reported to increase the risk of psychotic

symptoms in individuals
with a past
history of schizophrenia
Physical effects
Conjunctival injection and tachycardia are the
most frequent immediate physical
concomitants of smoking marijuana
Decrements in pulmonary vital capacity

 Tolerance

& Physical dependence

Habitual marijuana users rapidly develop

tolerance to the psychoactive effects of

marijuana and often smoke more
frequently & try to secure more potent
cannabis compound
Tolerance for both behavioral &

physiologic effects of marijuana

decreases rapidly upon cessation of
marijuana use

 Therapeutic

use of marijuana

1. antiemetic effects in chemotherapy

recipients
2. appetite-promoting effects in AIDS pt
3. reduction of intraocular pressure in
glaucoma
4. reduction of spasticity in multiple
sclerosis