Poisoning

 
Poisoning refers to the development of dose-related adverse effects following exposure to
chemicals, drugs, or other xenobiotics.
• In excessive amounts, substances that are usually innocuous such as oxygen and water
can cause poisoning.
• Poisoning maybe local (e.g. skin, eyes, or lungs) or systemic depending on the chemical
and physical properties of the xenobiotic, its mechanism of action, and the route of
exposure.
• The severity and reversibility of poisoning also depend on the functional reserve of the
individual or target organ which is influenced by age and preexisting disease.
• All of these factors must be considered when attempting to predict the effects of a
particular exposure.
Clinical Features of Poisoning
• Clinical features should focus initially on
Vital signs
Cardiopulmonary system
Neurologic status
• On the basis of the pulse, blood pressure, respiratory rate, temperature, and mental status,
the physiologic state can be characterized as
Excited
Depressed
Discordant
Normal
• More features are obtained from examination of
Eyes for nystagmus, pupil size, and reactivity
Abdomen for bowel activity and bladder size
Skin for burns, bullae, color, warmth, moisture, pressure sores, and puncture marks
may narrow the diagnosis to a particular disorder.
• Grading the severity of poisoning is useful for assessing the clinical course and response
to treatment.
• the patient should also be examined for evidence of trauma and underlying illnesses.
• Focal findings should prompt evaluation for a structural central nervous system (CNS)
lesion.
• When the history is unclear all orifices should be examined for the presence of chemical
burns and drug packets.
• The odor of breath or vomitus and the color of nails, skin, or urine may provide
diagnostic clues.
Diagnosis of Poisoning
• Although poisoning can mimic other illnesses, the correct diagnosis can usually be
established by
History
Physical examination
Routine and toxicologic laboratory evaluations
• The history should include
Time, the route, and duration of poisoning
Circumstances (location, surrounding events, and intent) of exposure
The name and amount of each drug used
Chemical or ingredient involved
The time of onset, nature, and severity of symptoms
The time and type of first aid measures provided
The medical and psychiatric history
• In In many cases the victim is
Confused
Comatose
Unaware of exposure or unable or unwilling to admit to one
Suspicious circumstances include unexplained illness in a previously healthy person
• Take history of psychiatric problems particularly depression
• Recent changes in health economic status or social relationships
• Onset of illness while working with chemicals or after ingesting food, drink especially
ethanol or medications
• Patients who become ill soon after arriving from a foreign country or being arrested for
criminal activity should be suspected of ‘body packing’ or ‘body stuffing’ (ingesting or
concealing illicit drugs in a body cavity)
• Relevant history may be available from family, friends, paramedics, police, pharmacists,
physicians and employers who should be questioned regarding the patient's habits,
hobbies, behavior changes, available medications, and antecedent events
• A search of clothes, belongings, and place of discovery may reveal a suicide note or a
container of drugs or chemicals
• The imprint code on pills and the label on chemical products may be used to identify the
ingredients and potential toxicity of a suspected poison by consulting a reference text, a
computerized database, the manufacturer, or a regional poison information center
• In the absence of a history of exposure, the clinical course may suggest a diagnosis of
poisoning typically evolves and resolves more rapidly than other disorders
• Signs and symptoms characteristically develop within an hour of acute exposure, peak
within several hours and resolve over hours to days
• The absence of signs and symptoms soon after an overdose does not rule out poisoning
Management Protocols for Poisoning
General Principles
• Monitoring and support of vital signs
• Prevention of further poison absorption
• Enhancement of poison elimination
• Administration of specific antidotes
• Prevention of re-exposure
• Specific treatment depends on the identity of the poison, the route, and the amount of
exposure, the time of presentation relative to the time of exposure, and the severity of
poisoning
• Knowledge of the offending agents' pharmacokinetics and pharmacodynamics is essential
Specific Poisons
Non-steroidal Anti-Inflammatory Drugs
• Inhibit prostaglandin and thromboxane synthesis by blocking cyclo-oxygenase (COX)
isoenzymes
• They are absorbed rapidly and blood concentrations peak 1 to 2 hours after ingestion
• They are highly protein-bound (>90%) and have volumes of distribution of less than 1.0
L/kg body weight
• They are primarily eliminated by hepatic metabolism
• Half-lives range from 1 to 16 h except for phenylbutazone which has a half-life of 2 to 4
days
Clinical Toxicity
• Effects are usually mild and include
Nausea
Vomiting
abdominal pain
Drowsiness
Headache
Glycosuria
Hematuria and proteinuria
Acute renal failure and hepatitis occur rarely but NSAIDS can cause renal failure
even without poisoning.
Diflunisal can cause hyperventilation, tachycardia, and sweating
Coma, respiratory depression, seizures, and cardiovascular collapse may occur with
mefenamic acid and phenylbutazone
Ibuprofen can cause metabolic acidosis, coma, and seizures
Metabolic acidosis is relatively common in phenylbutazone poisoning and occurs
rarely with naproxen
Treatment
Perform Pre-referral Management
• Urgently perform initial resuscitation with priorities to airway, breathing and circulation.
This includes opening an intravenous (I/V) line and initiation of IV fluids
• Maintain a clear airway, extend the neck, support jaw, and suction
• Ensure normal breathing and use mechanical ventilator as indicated
• Stop external bleeding (if any)
• Monitor vital signs
• Immediately refer the patient to a higher center
Further Treatment at Higher Centre
• Activated charcoal is the preferred method of gastrointestinal decontamination
• Repeated doses may enhance the elimination of indomethacin, phenylbutazone and
piroxicam
• Renal excretion is not increased by diuresis and protein binding limits the efficacy of
hemodialysis
• Hemoperfusion might be useful in patients with hepatic or renal failure and severe
clinical toxicity
• Treatment is otherwise supportive
Organophosphate and Carbamate Insecticides
• Organophosphorus compounds such as the insecticides (Chlorpyrifos, Phosphorothioic
acid (Diazinon), Dichlorvos, Fenthion, Malathion, and Parathion), chemical warfare
‘nerve gases’ such as sarin irreversibly inhibit acetylcholinesterase and cause
accumulation of acetylcholine at muscarinic and nicotinic synapses in the CNS.
• Carbamates such as the insecticides (Aldicarb, Propoxur (Baygon), Carbaryl (Sevin),
bendiocarb (Ficam)), therapeutic agents (Ambenonium, Neostigmine, Physostigmine, and
Pyridostigmine) reversibly inhibit this enzyme.
• Agents that directly stimulate cholinergic receptors such as arecholine (from betel nuts),
bethanechol, pilocarpine and urecholine have the same effect.
• Organophosphates are absorbed through the skin, lungs, gastrointestinal tract and are
distributed widely in tissues.
• Also are slowly eliminated by hepatic metabolism
• Oxidative metabolites of parathion and malathion (paraoxon, naloxone) are the active
forms of these agents.
• Carbamates are eliminated rapidly by serum and liver enzymes.
Clinical Toxicity
• The time from exposure to the onset of toxicity varies from minutes to hours but is
usually between 30 minutes and 2 hours.
• Muscarinic effects include
Nausea, vomiting and abdominal cramps
Urinary and fecal incontinence
Increased bronchial secretions
Cough, wheezing and dyspnea
Sweating
Salivation
Miosis, blurred vision, lacrimation, and urinary frequency and incontinence
• In severe poisoning
Bradycardia, conduction block, hypotension, and pulmonary edema may occur.
Nicotinic signs include
Twitching
Fasciculations
Weakness
Hypertension
Tachycardia
Paralysis and respiratory failure
CNS effects include
Anxiety
Restlessness
Tremor
Confusion
Weakness
Seizures
Coma
• Toxicity due to Carbamates is shorter in duration and usually less severe than that due to
organophosphates.
• Most patients recover within 24 to 48 hours but fat-soluble organophosphates may cause
effects for weeks to months.
• Death is most often due to pulmonary toxicity that consequently leading to respiratory
failure.
Treatment
• Perform Pre-referral Management
Urgently perform initial resuscitation with priorities to airway, breathing and
circulation. This includes opening an intravenous (I/V) line and initiation of IV fluids.
Maintain a clear airway, extend the neck, support jaw, and suction.
Ensure normal breathing and use a mechanical ventilator as indicated.
Stop external bleeding (if any).
Monitor vital signs.
Immediately refer the patient to a higher center.
Further Treatment at Higher Centre
• Gastrointestinal decontamination should include the use of activated charcoal
• Supportive measures include
Oxygen administration
Ventilatory assistance
Treatment of Seizures
• Atropine, a muscarinic receptor antagonist should be administered for muscarinic effects
A dose of 0.5 to 2 mg is given intravenously every 5 to 15 minutes until bronchial and
other secretions have dried and the pupils are dilated to the normal levels (watch for signs
of atropine toxicity).
• Do not use morphine or theophylline.
Management of Poisoning
Activated Charcoal
• Have comparable or greater efficacy.
• Fewer contraindications and complications.
• Is less aversive and invasive than ipecac or gastric lavage and is the preferred method of
gastrointestinal decontamination in most situations.
• Activated charcoal is prepared as a suspension in water, either alone or with a cathartic
• It is given orally via a nippled bottle (for infants), or via a cup, straw or small-bore
nasogastric tube.
• Do not give to a comatose patient unless the patient is intubated and you have a
nasogastric tube in place.
• the recommended dose is 1g/kg body weight using 8 ml of diluents per gram of charcoal
if a premixed formulation is not available.
• Charcoal adsorbs ingested poisons within the gut lumen allowing the charcoal-toxin
complex to be evacuated with stool.
• the complex can also be removed from the stomach by induced emesis or lavage.
• In vitro, charcoal adsorbs >90% of most substances when given in an amount equal to 10
times the weight of the substance.
• Compounds that are not well adsorbed by charcoal.
Charged (ionized) chemicals such as:
Mineral acids
Alkalis
Highly dissociated salts of cyanide, fluoride, iron, lithium
Other inorganic compounds
• In animal and human volunteer studies, charcoal decreases the absorption of ingestants by
an average of 73% when given within 5 minutes of ingestant administration, 51% when
given at 30 minutes and 36% at 60 minutes.
Complications
• Mechanical obstruction of the airway
• Aspiration
• Vomiting
• Bowel obstruction and infection caused by inspissated charcoal
• Charcoal is not recommended for patients who have ingested corrosives because it
obscures endoscopy
Gastric Lavage
• Is performed by sequentially administering and aspirating about 5 ml fluid per kilogram
of body weight through a no. 28 French orogastric tube in children and no. 40 French tube
in adults.
• Except for infants tap water is acceptable.
• The patient should be placed in Trendelenburg and left lateral decubitus positions to
prevent aspiration even if an endotracheal tube is in place.
• Lavage decreases ingestant absorption by an average of 52% if performed within 5
minutes of ingestion administration, 26% if performed at 30 minutes, and 16% if
performed at 60 minutes.
• Its efficacy is similar to that of ipecac.
• Significant amounts of the ingested drug are recovered in one-tenth of patients.
• Aspiration is a common complication occurring in up to 10% of patients especially when
lavage is performed improperly.
• Serious complications of tracheal, esophageal, and gastric perforation occur in
approximately 1% of patients.
• For For this reason the physician should personally insert the lavage tube and confirm its
placement and the patient must be cooperative or adequately restrained with
pharmacologic sedation if necessary during the procedure.
• Gastric lavage is contraindicated in corrosive (such as lye) or petroleum distillate
ingestions because of the respective risks of gastroesophageal perforation and aspiration induced
hydrocarbon pneumonitis.
                                                                                                                       
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