Beruflich Dokumente
Kultur Dokumente
EMERGENCY
MEDICINE BLOCK
Agustina Cynthia Cesari S
405140066
Group 1
LI 1.
DRUG INTOXICATION
ACETAMINOPHEN
DIGOXIN
WARFARIN
SULFA
OPIOID
PSYCHOTROPIC AGENTS
LI 2.
CHEMICAL AGENTS
INTOXICATION
ORGANOPHOSPHATE
Organophosphates
◦ Commonly used: diazinon, acephate, malathion, parathion, and
chlorpyrifos
◦ Organophosphate and carbamate compounds are the
insecticides most commonly associated with systemic illness
◦ Organophosphate poisoning results primarily from accidental
exposure in the home, recently sprayed or fogged areas using
pesticide applicators, agriculture, industry, and the transport of
these products
◦ Systemic absorption of organophosphates occurs by inhalation
and after mucous membrane, transdermal, transconjunctival,
and GI exposure.
Pathophysiology
◦ Organophosphate and carbamate compounds inhibit the enzyme
cholinesterase acetylcholine accumulation at nerve synapses and
neuromuscular junctions, resulting in overstimulation of acetylcholine
receptors Excess acetylcholine results in a cholinergic crisis that
manifests as a central and peripheral clinical toxidrome
◦ Aging : the permanent, irreversible binding of the organophosphorus
compound to the cholinesterase
◦ The time to aging is highly variable among different agents and can
range from minutes to a day or more
◦ Once aging occurs, the enzymatic activity of cholinesterase is
permanently destroyed, and new enzyme must be resynthesized over
a period of weeks before clinical symptoms resolve and normal
enzymatic function returns Antidotes must be given before aging
occurs to be effective
Signs & symptoms
◦ Four clinical syndromes:
ACUTE POISONING
◦ Most poisoned patients are symptomatic within the first 8 hours
and nearly all within the first 24 hours
◦ Acute organophosphate poisoning results in CNS, muscarinic,
nicotinic, and somatic motor manifestations
INTERMEDIATE SYNDROME
◦ May occur 1-5 days after exposure
◦ Clinical features include paralysis of neck flexor muscles, muscles
innervated by the cranial nerves, proximal limb muscles, and
respiratory muscles respiratory support may be needed
CHRONIC TOXICITY
◦ Is seen primarily in agricultural workers with daily exposure,
manifesting as symmetrical sensorimotor axonopathy begin
with leg cramps and progress to weaknes and paralysis,
mimicking features of the Guillain-Barre syndrome
INORGANIC MERCURY
◦ Mercury salts are caustic, and an acute ingestion produces a
severe hemorrhagic gastroenteritis with abdominal pain often
associated with a characteristic graying of the oral mucosa and
metallic taste
◦ GI symptoms of chronic inorganic mercury toxicity include
metallic taste, burning sensation in the mouth, loose teeth,
mucosal lesions and fissures, excessive salivation, and nausea
ORGANIC MERCURY
◦ After a latent period of weeks to months, orofacial paresthesias
are a common initial symptom, followed by headache, tremor,
and fatigue.
◦ In severe cases, patients may develop ataxia, muscle rigidity and
spasticity, blindness, hearing deficits, and dementia
Diagnosis
◦ History of exposure
◦ 24-hour urine mercury levels: a level >20 micrograms/L (>0.1
micromol/L) may indicate meaningful exposure
◦ Whole blood mercury levels
◦ MRI findings in methyl mercury toxicity from ingestion of
contaminated seafood include marked atrophy of the visual
cortex, cerebellar vermis and hemispheres, and postcentral
cortex
Treatment
◦ Elemental mercury: the severe respiratory failure following
inhalation of volatilized elemental mercury or aspiration of
elemental mercury may require endotracheal intubation and
positive-pressure ventilation
◦ Inorganic mercury salts: treat with aggressive IV hydration and GI
decontamination, including gastric lavage if the patient has not
had significant emesis, and consider activated charcoal
◦ Organic mercury: institute gastric decontamination in the setting
of acute ingestion
◦ Chelation
LI 5.
PSYCHOTIC BREAK