Download 20. poisoning - UMF IASI 2015

POISONING
Epidemiology
• 99% of ingestions by children under 6 are
unintentional.
• Approximately 40% of ingestions reported to
the poison center by adolescents are
intentional.
• Approximately 56% of adolescent ingestions
are by females.
Physiologic Differences
• Blood brain barrier still more permeable to toxicologic
substances until around 4 months.
– toxicity noted with smaller doses than expected.
• Higher metabolic demands.
• Decreased ability to glucuronidate in the infant period.
Second trimester pregnancies that were terminated
showed only 10% activity of the cytocrome P-450 system.
– between ages 2-4 years that glucuronidation is
equivalent to adults.
• Decreased glycogen stores.
Physiologic Differences
• Increased body surface area can lead to
thermoregulatory issues.
• Children reside lower to the ground. This puts them
at higher risk for ingesting compounds heavier than
air. Often adults will NOT have the same exposure.
• Inability to avoid hazards – they do not read warning
labels or “Do Not Enter” signs.
ANTIDOTES
• A common antidote is N-acetylcysteine
(Mucomyst), which is used to neutralize
acetaminophen, paracetamol.Acetaminophen,
in normal doses, is one of the safest
medications known, but after a massive
overdose, the liver is damaged, and hepatitis
and liver failure develop
• Calcium Disodium EDTA treats lead poisoning
Vitamin K
Anticoagulants
Methylene Blue
Agents that produce
Methemoglobinemia
Methyl Alcohol
Ethanol
D Penicillamine
Copper, Gold, Mercury,
Lead, Arsenic
Deferoxamine Mesylate Iron
Naloxone
Narcotics
Pesticides
• Specifically
organophosphates and
carbamates.
• They work by inhibiting
acetylcholinesterase.
• Present with cholinergic
symptoms
• The mechanism of toxicity is the inhibition of
acetylcholinesterase, resulting in an
accumulation of the neurotransmitter
acetylcholine and the continued stimulation
of acetylcholine receptors. The standard
treatment consists of reactivation of the
inhibited acetylcholinesterase with an oxime
antidote and reversal of the biochemical
effects of acetylcholine with atropine
Cholinergic Symptoms
Nicotinic Symptoms
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•
•
•
•
•
•
Remember the days of the week !
Mydriasis
Tachypnea
Weakness
Tachycardia
Fasiculations
Pediatric patients tend to present with a
predominance of nicotinic symptoms!!!
First Aid Treatment of Pesticide
Poisoning: General Principles
• TERMINATE EXPOSURE by removing the person
from the scene of contamination. Avoid further
skin contact and/or inhalation of fumes or dust.
• REMOVE CONTAMINATED CLOTHING quickly and
completely, including footwear
• REMOVE PESTICIDES FROM SKIN, HAIR AND EYES
by using large quantities of water. Pay particular
attention to the washing of the eyes, hold eyelids
apart and rinse thoroughly for at least 10 minutes
• Swallowed Pesticide
• Induce vomiting when the chemical
swallowed is highly toxic and would likely
prove fatal and if medical assistance is not
readily available.
• If the person is unconscious, the doctor will
put a flexible, soft, plastic tube into the
windpipe to protect the person from
suffocating in his or her own vomit and to
provide artificial breathing (intubation).
• Activated charcoal acts as a "super" absorber
of many poisons, the poison cannot get
absorbed into the bloodstream.
3
3
Treatment
• Atropine 0.02 mg / Kg IV. Repeat as needed and
titrate to respiratory secretions. It will likely take
massive doses!!
• Pralidoxime (2-Pam) 20-40 mg / Kg bolus
followed by 10-20 mg / Kg /hour infusion.
• Remember to send RBC and Plasma
Cholinesterase levels upon arrival and daily.
Mushroom Poisoning Classification
according to the toxic effects of mycotoxins →
there are a few syndromes caused by certain
mushrooms
 hepatotoxic syndromes
death cap (Amanita phalloides)
destroying angel (Amanita virosa)
spring amanita (Amanita verna)
luggies (e. g., Gyromitra esculenta)
little poison parasol mushrooms (Lepiota spec.)
Galerina spec.
 nefrotoxic syndrome
Cortinarius spec.; e. g., web-cap (Cortinarius bulbosus)
 neurotoxic syndromes
cholinomimetic (muscarinic)
some forms of fly agaric intoxication (Amanita muscaria) and panther cap intoxication
(Amanita pantherina)
Inocybe spec.; e. g., fibrecap (Inocybe erubescens)
Clitocybe spec.; e. g., tawny funnel cap (Clitocybe flaccida)
cholinolytic (mycoatropine)
some forms of fly agaric intoxication (Amanita muscaria) and panther fungus
intoxication (Amanita pantherina)
mixed syndromes
– gastrointestinal dyspetic syndromes
• gastric dyspepsia syndromes – satan´s boletus (Boletus
satanas)
• gastric-bowel dyspepsia syndromes
– Scleroderma spec.; e. g., earthball (Scleroderma citricum)
– Russula spec.; e. g., the sickener (russulas) (Russula emetica)
– Lactarius spec.; hazel milkcap (Lactarius pyrogalus)
• bowel dyspepsia syndromes – Ramaria spec.; e. g., beech
ramaria (Ramaria botrytis)
– vasotoxic syndrome
• Coprinus spec.; e. g., common ink-cap (Coprinus
atramentarius)
– hallucinogenic syndrome
• magic mushrooms (Psilocybe)
• fly agaric (Amanita muscaria)
Amanita phalloides
• symptoms
– 6 – 24 hours (approx. 10 – 12 hours)
• between the consummation and occuring symptoms
• cruel abdominal pain, malaise, vomiting, profound diarrhoea
(blood can be present)
• fever, tachycardia, hyperglycemia, dehydration, electrolyte
imbalance
– latency phase (24 hours)
• symptoms remit during water and electrolytic balance improving
• subclinic elevation of serum transaminases
– hepatorenal icteric phase (in 3 – 4 days)
• fuzziness, delirium, hypoglycemia, coma, exitus in 1 week
• complications
– coagulopathy, metabolic acidosis, hemorrhage, sepsis, renal
failure
Treatment
 gastric lavage
 up to 36 hours after consummation
 repeated big doses of activated carbon
 1 gramm/1 kilogramm every 2 – 4 hours
 block amatoxins and their enterohepatic cycle
 water and electrolyte imbalance correction
 save for glomerular filtration
 danger of the brain edema!
 antidote: silibinin (Legalon SIL)
 start the admistration as soon as possible (for 3 – 5 days, till transaminase achieve
the normal serum level, the administration can be terminated even after 1 day use
when misdiagnosed)
 decreases the hepatic content of amatoxins
 blocks the trasport system for amatoxins (into the hepatic cells) → prevention and
diminishing of necrosis
 stimulates hepatic cell RNA-polymerase and hepatic metabolism
 stabilizes extra- and endoplasmatic membranes
 regeneration of hepatocytes
antidote of the second choice: acetylcysteine (ACC INJEKT)
 if silibinin is not available
 for 3 days
benzylpenicilline
 its administration is not recommended more (for unclear benefit)
complex and intensive supporting care!
 central venous pressure monitoring
 fluid resuscitation
 intensive supporting care in hepatorenal failure and
ecephalopathy (glucose, K1 vitamine, fresh frozen plasma in
coagulopathy, lactulose)
liver transplantation, indications
 severe prognosis
 prothrombine time less than 20% of the normal value without any
improvement after the third day
 increasing creatinine level with no reactions after rehydration (in
4 days) accompanied by bilirubin level elevation
Muscarinic Syndromes Due To
Mushroom Poisoning:
Inocybe spec., Clinocybe spec.
symptoms
 latency phase (very short, sometimes the symptoms
occur during the meal)
 muscarinic symptoms and others
sweating, salivation, lachrymation, miosis, colics,
diarrhoea, hypotension, bronchoconstriction
treatment
 gastric lavage
 activated carbon
 atropine
 symptomatic treatment (and supporting care)
Gastrointestinal Dyspeptic Syndromes: Clitocybe
Spec., yellow coral fungus (Ramaria), satan´s boletus
(Boletus satanas), Scleroderma Spec.
• after consuming also of unsufficiently cooked
or bad stored mushrooms
• symptoms
– vomiting, diarrhoea
• treatment
– activated carbon
– symptomatic treatment, supporting care
Hallucinogenic Syndromes: Magic
mushrooms (Psilocybe)
symptoms
 mydriasis, elevated heart rate and blood pressure, sweating, tremor
 hallucinations
acoustic, visual
changed perception of the reality, emotions, mood, desorientation, fuzziness
danger of suicide!!!
treatment
 activated carbon
 sedatives (remember the risk of suicide!)
in long-term abuse averse effects on the personality and psyche!
hallucinogenic syndromes can also be caused by fly agaric
(Amanita muscaria) intoxication
ALCOHOL POISONING The Stages of
Intoxication
• 50 mg/dL: Loss of emotional
restraint, vivaciousness, feeling
of warmth, flushing of skin, mild
impairment of judgment
• 100 mg/dL: Slight slurring of
speech, loss of control of fine
motor movements (such as
writing), confusion when faced
with tasks requiring thinking,
emotionally unstable,
inappropriate laughter
• 200 mg/dL: Very slurred
speech, staggering gait, double
vision, lethargic but able to be
aroused by voice, difficulty
sitting upright in a chair,
memory loss, vomiting
• 300 mg/dL: Stuporous, able to
be aroused only briefly by
strong physical stimulus (such
as a face slap or deep pinch),
deep snoring
• 400 mg/dL: Comatose, not able
to be aroused, incontinent
(wets self), low blood pressure,
irregular breathing
• 500 mg/dL: Death possible,
either from cessation of
breathing, excessively low blood
pressure, or vomit entering the
lungs without the presence of
the protective reflex to cough it
out
• Intoxicated people often
receive IV fluids and B
complex vitamins for
dehydration (alcohol is a
diuretic and increases urine
output) and as a precaution
or treatment for vitamin
deficiency.
• In severe cases - those of
severe stupor and coma - the
person should be intubated
(a breathing tube placed in
the patient's airway) to
support respirations (which
may stop spontaneously) and
to protect the lungs from
filling with vomit/secretions.
– Intubation involves placing a
short, flexible plastic tube
into the windpipe (trachea)
below the vocal cords and
connecting the tube to a
respirator machine. The tip of
the tube has a small donutshaped balloon around it,
which is inflated to seal the
end of the tube to the inside
of the windpipe. This
accomplishes two things:
• It prevents the air from the
respirator from leaking out into
the mouth instead of going into
the lungs.
• It provides a protective seal so
that a large amount of vomit in
the mouth is prevented from
entering the lungs where it
could cause damage and
possible suffocation.
• Hemodialysis is frequently required in patients
with significant methanol ingestions.[13, 17]
Indications for hemodialysis include (1)
arterial pH < 7.10, (2) a decline of >0.05 in the
arterial pH despite bicarbonate infusion, (3)
pH < 7.3 despite bicarbonate therapy, (4) rise
in serum creatinine level by 90 mmol/L
Signs and symptoms
• The peripheral autonomic nervous system, central nervous
system and the heart are the main systems that are
affected following overdose. Initial or mild symptoms
typically develop within 2 hours and include tachycardia,
drowsiness, a dry mouth, nausea and vomiting, urinary
retention, confusion, agitation, and headache.
• More severe complications include hypotension, cardiac
rhythm disturbances, hallucinations, and seizures.
Electrocardiogram (ECG) abnormalities are frequent and a
wide variety of cardiac dysrhythmias can occur, the most
common being sinus tachycardia and intraventricular
conduction delay resulting in prolongation of the QRS
complex and the PR/QT intervals. Seizures, cardiac
dysrhythmias, and apnea
Triciclic antidepressants
• ingestions of 10 to 20 mg per kilogram of body weight
are a risk for moderate to severe poisoning
• Most of the toxic effects of TCAs are caused by four
major pharmacological effects. TCAs have
anticholinergic effects, cause excessive blockade of
norepinephrine reuptake at the preganglionic synapse,
direct alpha adrenergic blockade, and importantly they
block sodium membrane channels with slowing of
membrane depolarization, thus having quinidine like
effects on the myocardium
Treatment
• gastric decontamination of the patient. This is achieved by
administering activated charcoal lavage
• stomach pumps, ipecac induced emesis, or whole bowel
irrigation are not recommended in TCA poisoning.
• maintenance of the airways, along with monitoring of
blood pressure, arterial pH, and continuous ECG
monitoring.
• intravenous sodium bicarbonate as an antidote, which has
been shown to be an effective treatment for resolving the
metabolic acidosis and cardiovascular complications of TCA
poisoning
• Seizures often resolve without treatment but
administration of a benzodiazepine or other anticonvulsive
• Benzodiazepine overdose
• Following an acute overdose of a benzodiazepine the
onset of symptoms is typically rapid with most
developing symptoms within 4 hours.
• Patients initially present with mild to moderate
impairment of central nervous system function. Initial
signs and symptoms include intoxication, somnolence,
diplopia, impaired balance, impaired motor function,
anterograde amnesia, ataxia, and slurred speech.
• The symptoms of an overdose such as sleepiness,
agitation and ataxia occur much more frequently and
severely in children. Hypotonia may also occur in
severe cases
• The diagnosis of benzodiazepine overdose may be
difficult, but is usually made based on the clinical
presentation of the patient along with a history of
overdose.
• Obtaining a laboratory test for benzodiazepine
blood concentrations can be useful in patients
presenting with CNS depression or coma of
unknown origin. Techniques available to measure
blood concentrations include thin layer
chromatography, gas liquid chromatography with or
without a mass spectrometer, and
radioimmunoassay
Treatment
• Gastric decontamination with activated charcoal is not
beneficial in pure benzodiazepine overdose as the risk
of adverse effects would outweigh any potential
benefit from the procedure. It is recommended only if
benzodiazepines have been taken in combination with
other drugs that may benefit from decontamination.
Gastric lavage (stomach pumping) or whole bowel
irrigation are also not recommended Enhancing
elimination of the drug with hemodialysis,
hemoperfusion, or forced diuresis is unlikely to be
beneficial as these procedures have little effect on the
clearance of benzodiazepines due to their large
volume of distribution and lipid solubility.[42]
Glasgow Coma Scale
Eye opening
Motor Response
Verbal Response
Spontaneously
Obeys Commands
=4 Points
=6 Points
Oriented when speaking to
person, place and time)
=5 Points
To speech and
commands
Unconscious but can localize
pain
Confused Disoriented to
person, place and time)
=3 Points
=5 Points
=4 Points
To pain
Withdrawal Response to pain
(but can’t localize pain)
Words only unconscious but
responds to painful stimuli by
words)
=2 Points
= 4 Points
=3 Points
No Response
= 1 Point
Decortication(spastic flexion
of the upper limbs and
extension of the lower
limbs)+Rigidiy
Sounds Only
=2 Points
= 3 Points
Decerebration(extension and
outwards turning of the arms
and legs)+ Rigidity
= 2 Points
No Response
=1 Point
No Response
=1 Point
Glasgow Coma Scale
•
1.
2.
3.
•
•
Generally, comas are classified as:
Severe, with GCS ≤ 8
Moderate, GCS 9 - 12
Minor, GCS ≥ 13.
Highest score is 15/15.the person in this case is
alert and oriented to person, place and time
Lowest score is 3/15 there’s no 0.The patient is in
deep coma and is considered brain dead if he can’t
breath without a ventilator
• Hypotension is corrected with fluid replacement, although
catecholamines such as norepinephrine or dopamine may
be require
• Flumazenil (Anexate) is a competitive benzodiazepine
receptor antagonist that can be used as an antidote for
benzodiazepine overdose. Its use, however, is controversial
as it has numerous contraindications.
• It is contraindicated in who have tachycardia, widened QRS
complex on ECG, anticholinergic signs, or a history of
seizures.
• Due to these contraindications and the possibility of it
causing severe adverse effects including seizures, adverse
cardiac effects, and death due to increase blood pressure
Barbiturates
• Symptoms of an overdose typically include
sluggishness, incoordination, difficulty in
thinking, slowness of speech, faulty judgment,
drowsiness, shallow breathing, and staggering.
In severe cases, coma and death can result
• The treatment of barbiturate abuse or
overdose is generally supportive
• Supportive treatment often includes the following:
• Activated charcoal may be given via nasogastric tube.
• Intravenous administration of saline, naloxone,
thiamine, and/or glucose.
• NaHCO3 to alkalize the urine to increase rate of
excretion
• Observation in the Emergency Department for a
number of hours or admission to the hospital for
several days of observation if symptoms are severe.
• Advise the patient about drug misuse or refer for
psychiatric consult
Carbon Monoxide Poisoning
CO is found in combustion fumes, such as those
produced by cars and trucks, small gasoline engines,
stoves, lanterns, burning charcoal and wood, and gas
ranges and heating systems. CO from these sources can
build up in enclosed or semi-enclosed spaces.
People and animals in these spaces can be poisoned by
breathing it.
Carbon Monoxide Poisoning
• CO prevents oxygen from attaching to the
hemoglobin molecule in your blood
• Oxygen cannot be delivered to the brain and
other tissues
• SYMPTOMS
• Confusion, hallucinations, headache, nausea,
fatigue, dizziness, palpitations, seizures
• COMA and DEATH
• Severe: Hospitalization and adminstration of 100%
oxygen
35 ppm (0.0035%)
Headache and dizziness within six to eight
hours of constant exposure
100 ppm (0.01%)
Slight headache in two to three hours
200 ppm (0.02%)
Slight headache within two to three hours;
loss of judgment
400 ppm (0.04%)
Frontal headache within one to two hours
800 ppm (0.08%)
Dizziness, nausea, and convulsions within
45 min; insensible within 2 hours
1,600 ppm (0.16%)
Headache, tachycardia, dizziness, and
nausea within 20 min; death in less than 2
hours
3,200 ppm (0.32%)
Headache, dizziness and nausea in five to
ten minutes. Death within 30 minutes.
6,400 ppm (0.64%)
Headache and dizziness in one to two
minutes. Convulsions, respiratory arrest,
and death in less than 20 minutes.
12,800 ppm (1.28%)
Unconsciousness after 2–3 breaths. Death
in less than three minutes.
• Administering oxygen via non-rebreather
mask shortens the half life of carbon monoxide
to 80 minutes from 320 minutes on normal air
• Hyperbaric oxygen is also used in the treatment
of carbon monoxide poisoning, as it may hasten
dissociation of CO from
carboxyhemoglobin[6]and cytochrome oxidase
• treatment for other complications such
as seizure, hypotension, cardiac
abnormalities, pulmonary edema, and acidosis