Specific poisoning
In therapeutic doses it is known to have very few adverse events.Acetaminophen(paracetamol):
As its most widely used analgic antipyretic so more available for poisoning Normally metabolized by liver; saturation of normal pathways leads to breakdown by p450 to NAPQI (mercapturic acid toxic metabolite) which causes hepatic necrosis.The maximum daily dose of acetaminophen is 4 g in adults and 90 mg/kg in children. A single ingestion of 7.5 g in an adult or more than 150 mg/kg in a child is a potentially toxic dose but smaller doses may also cause liver damage.
Clinical manifestations:
Serum level 4h or more after ingestion can help predict hepatotoxicityStage II: 24-48 hrs after ingestion. Better, less symptoms. Elevated bilirubin, transaminases and PT
Stage III ( 2- 4 days) after ingestion: Hepatic dysfunction (Rarely hepatic failure) Peak elevations in: Bilirubin Transaminases may reach > 1000 IU/L Prolonged PT
Stage IV _ (7-8 days)Depending on the extent of damage: Clinical improvement LFTs returning to normal or….. Death
Probable toxicity should be treated with: N-acetylcysteine oral (effective as many as 24 hours after a toxic ingestion). i.v administration NAC is recommended for selected pt.with potentially toxic plasma levels. Most pediatric patients can be treated with activated charcoal alone. GIT decontmination limited to patients with recent (within 60 min) and potentially life-threatening toxicity.
Iron Poisoning
Five Stages but variable Stage 1: GIT stage: within several hrs of ingestion: V/D, Hematochezia and abdominal pain Severe: fluid loss, bleeding, shock(acidosis, tachycardia +/- hypotension) Fever, Lethargy, ComaStage 2: Quiescent stage: 4-48hrs Clinical improvement Subtle hemodynamic changes: Tachycardia Decreased U.O.P.
Toxic doses occur at absorption of 60mg/Kg of elemental iron.1oTab
Stage 3: Circulatory collapse : 48-96 hrs Metabolic acidosis, hypotension, low Cardiac output i.e. Shock Coagulopathy Multi Organ Failure Syndrome (MOFS)
Stage 4: Hepatic failure: 96 hrs Liver transplant can save lives
Stage 5: Bowel obstruction 2-6 wks Due to scarringManagement: Gastric decontamination: Gastric lavage with 5% NaHCO3 No activated charcoal to be used!!! Secure good IV Get initial then 4hrs levels and TIBC Chelate with Deferoxamine if levels> 300mg/dL
SALICYLATES
Acute toxic dose 150mg/kg; large number of tablets form a concretion in the GI tract resulting in prolonged absorption and toxicity Directly stimulate respiratory centers. Oral ingestion commonest Transdermal lessPhase 1 hyperventilation , leading to respiratory alkalosis and compensatory alkaluria. Both potassium and sodium bicarbonate are excreted in the urine.
Clinical manifestations
phase 2 paradoxic aciduria in the presence of continued respiratory alkalosis occurs when sufficient potassium has been lost from the kidneys.
Phase 3 includes dehydration, hypokalemia, and progressive metabolic acidosis.
CNS changes are an important sign of serious toxicity. Agitation, restlessness, and confusion & even coma may develop secondary to cerebral edema. Pulmonary edema or hemorrhage may develop in more severe cases. Hyperglycemia or hypoglycemia, particularly in infants, has also been observed after dehydration Hepatotoxicity occurs after chronic exposure or very large acute ingestions. Death results from pulmonary edema and respiratory failure, cerebral edema, hemorrhage, severe electrolyte imbalance, or cardiovascular collapse.Lab Studies: Bedside ferric chloride testing Arterial blood gas analysis Salicylate concentration: therapeutic level 15-30 mg/dl (nomogram) Serum electrolytes & glucose (hypoglycemia , hypokalemia) Liver function test Renal function test
Treatment Treat electrolyte imbalance IV hydration Forced alkaline diuresis Hemodialysis Diuretics
Hydrocarbons
Hydrocarbons (HC) are composed of large number of organic compounds made up of carbon and hydrogen atoms that are classified into: High viscosity include substances like vaseline and motor oils. Low viscosity include furniture polish, spirits, kerosene oil and turpentine oil.Low viscosity products are more likely to be ingested and cause more damage to lung and nervous system.
Ingestion is rarely more than 10 ml but as little as 2 ml entering in to the tracheobronchial tree can cause severe chemical pneumonitis.
Pathophysiology:
Hydrocarbon aspiration primarily affects the CNS and respiratory systems. Volatile hydrocarbons are highly lipid soluble. They enter the circulation through the lungs and rapidly diffuse throughout the body and into the CNS .
Kerosene ingestion:Clinical PresentationRespiratory :Choking, gagging, and coughing usually begins immediately or within 2–5 min of the aspiration, and persists. There may be oral pain if an irritating hydrocarbon has been ingested.Vomiting is common, and this may increase the risk of aspiration, but it is not necessary for aspiration.In most children, the initial symptoms resolve without the development of aspiration pneumonitis. Signs of significant exposure are continued cough, tachypnea, increased respiratory effort, rib cage retractions, grunting, wheezes, and rales on chest auscultation.
CVS — Cardiac arrhythmia may occur after inhalation. GIT — local irritation to the pharynx, esophagus, stomach, and small intestine, with edema and mucosal ulceration. Orogastric and intestinal irritation may be associated with nausea and hematemesis .
Hematologic — Leukocytosis (with fever) occurs early in the clinical course . Hemolysis, hemoglobinuria, and consumptive coagulopathy also may occur with significant ingestion . CNS — HC ingestion or inhalation may have direct CNS effects as somnolence, headache, ataxia, dizziness, blurred vision, weakness, stupor, seizures, and coma. In addition, hypoxia caused by HC aspiration may cause 2ry CNS depression, including drowsiness, tremors, or convulsions.
Treatment: Do not induce vomiting !!!!! Do not attempt gastric lavage !!!!!! Bronchospasm should be treated with selective beta 2 agonists. Epinephrine and isoproterenol should be avoided because they can cause fatal ventricular dysrhythmia in the hydrocarbon-sensitized myocardium. If gastric lavage is to be performed, the patient should be intubated with a cuffed ETT to protect the airway from further aspiration. Activated charcoal also is not useful because it does not bind the common hydrocarbons.
Corticosteroid should be avoided.Antibiotcs given if bacterial pneumonia occurs.Treatment is usually supportive, attention to respiratory and CNS symptoms.Observe in ER for 6-8 hrs if no symptoms discharge.
Organophosphorus
InsecticidesInhibition of Cholinesterase enzymes all over.Muscarinic N/V Abdominal pain/ fecal incontinenceCholinergic “SLUDGE” (Salivation, Lacrimation, Urinary incontinence, Diarrhea/Diaphoresis, GI upset/hyperactive bowel, Emesis) cough, resp.secretions , crepitation and even pulmonary edemaCVS : Tachycardia/ bradycardia/ block/ hypotensionNicotinic: restlessness, confusion, coma, meiosis, flaccidity/convulsionWeakness from Pesticides
Diagnosis: blood Cholinesterase levels< 50% indicates poisoning.Atropine as test doseManagement:A….B….C….. StabilizationWash hair and body with soap & waterConsider Gastric lavage if within 1hrAtropine sulphate I.V. till pupils are normal size.Remember…Atropine has no effect on muscle paralysis must support breathingUSECholinestrase reactivator such as Pralidoxime
Tricyclic Antidepressants e.g amitriptyline
Anticholinergic effects cause most of the following presenting symptoms: Dry mouth Flushed skin Blurred vision Urinary retention Constipation Dizziness EmesisPhysical Signs of TCA toxicity include the following: Anticholinergic effects Altered mental status (agitation, confusion, lethargy) Resting sinus tachycardia Dry mucous membranes Mydriasis Fever Cardiac effects Hypertension (early and transient, should not be treated) Tachycardia Orthostasis and hypotension Arrhythmia/ECG changes
CNS effects Coma Seizure Myoclonic twitches/tremor Hyperreflexia Pulmonary effects - Hypoventilation resulting from CNS depression GIT effects - Decreased or absent bowel sounds
Lab Studies: Rapid bedside glucose level determination Serum pH, electrolytes, calcium, Urine toxicology screening
The single most important test to guide therapy and prognosis remains the 12-lead surface ECG. Important ECG changes include the following: Prolongation of the QRS complex Prolongation of the QT interval Tachycardia and arrhythmia
ECG changes in TCA poisoning
Medical Care: Careful attention to ABC, and neurologic parameters are of utmost importance because of the risk of rapid deterioration in patients. Decontamination strategies should be used carefully in selected patients(usually charcoal) Sodium bicarbonate given in doses to achieve PH level 7.45-7.55 to treat and prevent dysrhythmias Lidocain is used to treat dysrhythmias that are unresponsive to serum alkalizationAntidiarrheal agent containing both diphenoxylate and atropine. Both agents are absorbed by the GI tract and absorption may be delayed in overdose due to inhibitory effects on smooth muscle motility. Diphenoxylate is an opoid
Patients manifest signs and symptoms of opiate toxicity(respiratory depression, altered mental status, and miosis). Respond well to naloxone and supportive care. Current recommendations are for a minimum of 24 hour observation.