COMMON HOUSEHOLD POISONINGS
Dr. M. D. Ravi*
Professor/Paediatrics JSS Medical College, Mysore*
Poisoning represents one of the most common medical emergencies encountered by young children. Poisonings result from the complex interaction of the agent, the child, and the family environment. The peak incidence is at age 2 years. For every fatal accidental poisoning in a child, there are about 100 non-fatal accidental poisonings requiring admission. Most of the poisonings do not require active intervention.

General Approach to the Poisoned Child:
There are six basic modes of exposure to poisoning: ocular exposure, topical exposure, envenomation, inhalation, and transplacental exposure. In essence, poisoning might be viewed as a multiple chemical trauma.

PHARMACOLOGIC PRINCIPLES OF TOXICOLOGY:
Estimates of the LD50 (the amount per kilogram of body weight of a drug required to kill 50% of a group of experimental animals) or MLD (median lethal dose) are of little clinical value in humans. A drug that is water-soluble and has a low volume of distribution may cross the dialysis membrane well and also respond to diuresis. In general, methods of extracorporeal elimination are not effective for toxic agents with a Vd greater than 1 L/kg. The route of excretion or detoxification is important for planning treatment. Care of the poisoned patient should never be guided solely by laboratory measurements. Treatment should be directed first by the clinical signs and symptoms, followed by more specific therapy based on laboratory determinations.

Initial Life Support Phase:
The general approach to recognition and support of vital airway and cardiorespiratory functions (or "ABCDs") is well known.

Evaluation and Detoxification Phase:
A brief and focused historical evaluation should be addressed as soon as the life support phase has been accomplished. The primary goal is to determine the potential severity of the exposure noted. General historical features that suggest the possibility of poisoning include 1) acute onset; 2) age range of 1 to 5 years; 3) history of pica or known, unintentional ingestion; 4) substantial environmental stress, either acute (e.g., arrival of a new baby, serious illness in a parent) or chronic (marital conflict, parental disability); 5) multiple organ system involvement; 6) significant alteration in level of consciousness; and 7) a clinical picture that seems especially puzzling

Physical Examination:
The focused physical examination should begin with a reassessment of vital functions and complete recording of vital signs, including core temperature. With secure airway and cardiorespiratory function confirmed, the examination should then focus on the central and autonomic nervous systems, eye findings, changes in the skin and/or oral and gastrointestinal (GI) mucous membranes, and odors on the breath or clothing of the patient. These features represent those areas most likely affected in toxic syndromes and, when taken together, often form a constellation of signs and symptoms referred to as toxidromes). Such toxidromes may be so characteristic as to provide guidance for early therapeutic trials before precise historical or laboratory confirmation of a specific exposure is available.

The laboratory may be helpful in confirming diagnostic impressions or in demonstrating toxin-induced metabolic aberrations. Differences between calculated and measured serum osmolarity (Calculated = 2 × [Serum Na] + BUN/2.8 + glucose/18 with normal osmolarity = 290 mOsm/kg) may suggest intoxication with ethanol, isopropanol, or more rarely in pediatric patients, methanol or ethylene glycol. An electrocardiogram (ECG) should be performed in all seriously ill patients in whom poisoning is being considered. Detectable conduction delays may precede life-threatening cardiac rhythm disturbances.

Specific Detoxification:
Again, it is important the patient be continually reassessed and managed for impaired vital function. All decisions about further decontamination and/or specific antidotal therapy involve a complex interplay of toxin-related and patient's condition-related factors.

Gastrointestinal Decontamination:
The effort to "get the poison out" has long been a mainstay of the traditional discussion of toxicologic management. Recently, considerable controversy has arisen over the optimal method of gastric emptying and its overall value in the management of poisoned patients. Many authorities now disregard gastric emptying in all but a few select cases, preferring an enlarged role for the early use of activated charcoal. Many studies that support this trend have been published over the past 10 years. It is emphasized here that

Simple Dilution:
Dilution may be indicated only when the toxin produces local irritation or corrosion. Water or milk is an acceptable diluent. For drug ingestion, however, dilution alone should not be used because it may increase absorption by increasing dissolution rates of the tablets or capsules, or it may promote more rapid transit into the lower GI tract.

Gastric Emptying:
The goal of gastric emptying is to rid the stomach of remaining poison to prevent further local effect or systemic absorption. The utility of gastric emptying diminishes with time and is most effective if done within the first hour. In certain circumstances, such as the delayed gastric emptying accompanying intoxication with anticholinergic drugs, benefit may be noted longer after ingestion.

Activated Charcoal:
Activated charcoal minimizes absorption of drugs by adsorbing them onto its surface. Charcoal administration has become the decontamination strategy of choice for most pediatric poisonings and is most effective when used in the first few hours after ingestion. A number of notable compounds, such as iron and lithium, do not adsorb well to activated charcoal. The usual dose of activated charcoal is 1 g/kg; adolescents and adults should receive 50 to 100 g. It should be noted that the once advocated "universal antidote" that consisted of activated charcoal, magnesium oxide, and tannic acid is not recommended. Similarly,burnt toast is not effective.Charcoal might be contraindicated in patients with an unprotected airway or a disrupted GI tract (e.g., after severe caustic ingestion) or in patients in whom charcoal therapy may increase the risk and severity of aspiration (e.g., hydrocarbons).

Catharsis:
Two types of osmotic cathartics have been used to treat poisoned patients: the saccharide cathartics (e.g., sorbitol) and the saline cathartics (e.g., magnesium citrate, magnesium sulfate). Unfortunately, little evidence exists to suggest that standard cathartics accomplish their goal of reducing drug absorption by decreasing GI transit time. Mineral oil or stimulant cathartics such as castor oil are discouraged because they may increase absorption of some poisons or unnecessarily extend the cathartic effect.

Whole Bowel Irrigation:
An additional technique of GI decontamination that has been developed over the past several years is that of intestinal irrigation with large volumes and flow rates of a polyethylene glycol-balanced electrolyte solution. WBI has been found to be particularly useful in pediatric iron overdoses, in which gastric lavage may be limited by tube size and the substance is not bound to charcoal. The technique may be used by mouth in cooperative patients or by NG tube; the usual recommended dosing is 500 mL/hour in toddlers and 2 L/hour in adolescents.

Antidotal Therapy:
The overall number of ingestions for which a specific antidote is necessary or available is small. When a specific antidote can be used, it is vital that it be administered as early as possible and in an appropriately monitored dose. Indiscriminant use of antidotes without other forms of management should be discouraged.

Enhancing Excretion:
The procedures available for enhancing the elimination of an absorbed poison that have the greatest value are multiple-dose activated charcoal, ionized diuresis, dialysis, and hemoperfusion. Because some risk is involved, these measures are indicated only in those cases in which the patient's recovery would be otherwise unlikely or in which a specific significant benefit is expected.

Supportive Care:
The final step in optimizing treatment for the poisoned child is the direction of scrupulous attention to supportive care, including continued close monitoring of ABCDs, fluid and electrolyte status, urine output, and level of consciousness. The value of these efforts usually far outweighs that which may be ascribed to any specific toxicologic interventions in most cases.

NON-TOXIC INGESTION:
Often, the emergency physician will be asked about a childhood ingestion of some common household products, many of which are non-toxic, unless taken in huge amounts. The availability of a list of such non-toxic products often leads to immediate relief of parental anxiety and avoids the institution of unnecessary noxious interventions.

MANAGEMENT OF SPECIFIC COMMON POISONINGS:

Hydrocarbons (Petrol, Kerosene, Petroleum Distillates, Turpentine)
Ingestion of hydrocarbons may cause irritation of mucous membranes, vomiting, blood-tinged diarrhea, respiratory distress, cyanosis, tachycardia, and fever. Although a small amount (10 mL) of certain hydrocarbons is potentially fatal, patients have survived ingestion of several ounces of other petroleum distillates. A history of coughing or choking, as well as vomiting, suggests aspiration with resulting hydrocarbon pneumonia. This is an acute hemorrhagic necrotizing disease that usually develops within 24 hours of the ingestion and resolves without sequelae in 3-5 days. GI irritation that may be associated with nausea and bloody emesis. CNS effects may range from inebriation to coma. Hemolysis with hemoglobinuria has been reported after significant ingestions. Finally, hydrocarbon ingestion may be associated with the development of fever and leukocytosis in up to 15% of patients in the absence of clinically evident pneumonitis. Both emetics and lavage should be avoided when only a small amount has been ingested. Mineral oil should not be given, because it can cause a low-grade lipoid pneumonia. Adrenaline should not be used with halogenated hydrocarbons because it may affect an already sensitized myocardium. Because there is a gradual evolution of abnormal radiographs, an initially negative chest radiograph should be repeated at 4 to 6 hours after ingestion. All patients with abnormal chest radiographs or persistent respiratory symptoms after 4 to 6 hours of immediate care should be admitted for observation. Patients who are asymptomatic after this period of observation may be discharged. Antibiotics should not be used prophylactically but should be reserved for specific infections, should they develop. The use of corticosteroids in the treatment of aspiration from hydrocarbons has been associated with increased morbidity and is not recommended.

Insecticides
The petroleum distillates or other organic solvents used in these products are often as toxic as the insecticide itself. Decontamination may be performed by aspirating the stomach with a nasogastric tube.
  1. Chlorinated Hydrocarbons: Signs of intoxication include salivation, gastrointestinal irritability, abdominal pain, vomiting, diarrhea, CNS depression, and convulsions. Inhalation exposure causes irritation of the eyes, nose, and throat; blurred vision; cough; and pulmonary edema.
    Chlorinated hydrocarbons are absorbed through the skin, respiratory tract, and gastrointestinal tract. Decontamination of skin with soap and evacuation of the stomach contents are critical. All contaminated clothing should be removed. Castor oil, milk, and other substances containing fats or oils should not be left in the stomach because they increase absorption of the chlorinated hydrocarbons. Convulsions should be treated with diazepam, 0.1-0.3 mg/kg intravenously. Adrenaline should not be used because it may cause cardiac arrhythmias.
  2. Organophosphate (Cholinesterase-Inhibiting) Insecticides (e.g., Chlorthion, Diazinon, Malathion, Paraoxon, Parathion, Phosdrin, TEPP, Thio-TEPP)
    Dizziness, headache, blurred vision, miosis, tearing, salivation, nausea, vomiting, diarrhea, hyperglycemia, cyanosis, sense of constriction of the chest, dyspnea, sweating, weakness, muscular twitching, convulsions, loss of reflexes and sphincter control, and coma can occur.

    The clinical findings are the result of cholinesterase inhibition, which causes an accumulation of acetylcholine. The onset of symptoms occurs within 12 hours of the exposure. Red cell cholinesterase levels should be measured as soon as possible. (Some normal individuals have a low serum cholinesterase level.) Normal values vary in different laboratories. In general, a decrease of red cell cholinesterase to below 25% of normal indicates significant e plus a cholinesterase reactivator, pralidoxime, is an antidote for organophosphate insecticide poisoning. After assessment and management of the ABCs, atropine should be given and repeated every few minutes until airway secretions diminish. An appropriate starting dose of atropine is 2-4 mg intravenously in an adult and 0.05 mg/kg in a child. The patient should receive enough atropine to stop secretions (mydriasis in not an appropriate stopping point). Severe poisoning may require gram quantities of atropine administered over 24 hours. Because atropine antagonizes the muscarinic parasympathetic effects of the organophosphates but does not affect the nicotinic receptor, it does not improve muscular weakness. Pralidoxime should also be given immediately in more severe cases and repeated every 6-12 hours as needed (25-50 mg/kg diluted to 5% and infused over 5-30 minutes at a rate of no more than 500 mg/min). Pralidoxime should be used in addition to-not in place of-atropine if red cell cholinesterase is less than 25% of normal. Pralidoxime is most useful within 48 hours after the exposure but has shown some effects 2-6 days later.
  3. Carbamates Carbamate insecticides are reversible inhibitors of cholinesterase. The signs and symptoms of intoxication are similar to those associated with organophosphate poisoning but are generally less severe. Atropine titrated to effect is sufficient treatment. Pralidoxime should not be used with carbaryl poisoning but is of value with other carbamates. In combined exposures to organophosphates, give atropine but reserve pralidoxime for cases in which the red cell cholinesterase is depressed below 25% of normal or marked effects of nicotinic receptor stimulation are present.
  4. Botanical Insecticides: Allergic reactions, asthma-like symptoms, coma, and convulsions have been reported. Pyrethrins, allethrin, and rotenone do not commonly cause signs of toxicity. Antihistamines, short-acting barbiturates, and atropine are helpful as symptomatic treatment.
  5. Aluminium Phosphide: This is a grain preservative which releases phosphene, CO and ammonia gases. Toxic effects are due to enzyme dysfunction. In moderate/severe poisoning, all organ systems are affected - GI such as vomiting, epigastric burning, diarrhea and thirst, CVS - hypotension, arrhythmia, ischemia, myocarditis, pericarditis, ccf, RS - ARDS, GUT - renal failure (Oliguric or nonoliguric), CNS - excitation, convulsions. Treatment is supportive. The role of MgSO4 in children is unclear. The mortality is high.

Caustics
Hydrofluoric acid is a particularly dangerous poison. Dermal exposure creates a penetrating burn that can progress for hours or days. Large dermal exposure or ingestion may produce life-threatening hypocalcaemia abruptly as well as burn reactions.

Emetics and lavage are contraindicated. Water or milk (<15 mL/kg) are used to dilute the acid, because a heat-producing chemical reaction does not occur. Alkalis should not be used. Burned areas of the skin, mucous membranes, or eyes should be washed with copious amounts of warm water. Opioids for pain may be needed. An end tracheal tube may be required to alleviate laryngeal edema. Esophagoscopy should be performed if the patient has significant burns or difficulty in swallowing. Acids are likely to produce gastric burns or esophageal burns. Evidence is not conclusive, but corticosteroids have not proved to be of use.

Severe exposure may require large doses of intravenous calcium. Therapy should be guided by calcium levels, the ECG, and clinical signs.

Bases Alkalies produce more severe injuries than acids. Some substances, such as Drano, are quite toxic, whereas the chlorinated bleaches (3-6% solutions of sodium hypochlorite) are usually not toxic. Chlorinated bleaches, when mixed with a strong acid (toilet bowl cleaners) or ammonia, may produce irritating chlorine or chloramine gas.

Alkalies can burn the skin, mucous membranes, and eyes. Respiratory distress may be due to edema of the epiglottis, pulmonary edema resulting from inhalation of fumes, or pneumonia.

Treatment: The skin and mucous membranes should be cleansed with copious amounts of water. The absence of oral lesions does not rule out the possibility of laryngeal or esophageal burns following granular alkali ingestion. Antibiotics may be needed if mediastinitis is likely, but they should not be used prophylactically.

PEDIATRIC OVERDOSES
Paracetamol:
Accidental ingestion in young children has been associated with little morbidity, although occasional cases of hepatotoxicity occur, particularly in the context of inadvertent repetitive overdosing. Paracetamol is normally metabolized in the liver. Anorexia, malaise, and abdominal pain may progress to signs of liver failure with hepatic coma. Treatment is to supply a surrogate glutathione by giving acetylcysteine. The dose of acetylcysteine is 140 mg/kg orally, diluted to a 5% solution in sweet fruit juice or carbonated soft drink. The primary problems associated with administration are nausea and vomiting. After this loading dose, 70 mg/kg should be administered orally every 4 hours for 72 hours. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), serum bilirubin, and plasma prothrombin time should be followed daily. Significant abnormalities of liver function may not develop until up to 72 hours after ingestion. Repeated miscalculated overdoses given by parents to treat fever are the major source of toxicity in children under age 10 years, and parents are often unaware of the significance of symptoms of toxicity, thus delaying its prompt recognition and therapy.

Iron: Iron poisoning is one of the most common, potentially fatal intoxications in children.

Acidotic or symptomatic patients should be admitted and treated with deferoxamine. Although rarely used today, the deferoxamine challenge test (50 mg/kg IM up to a maximum of 1 g) may be useful when iron levels are unavailable and the patient's screening laboratory studies and clinical status are borderline. The appearance of a pinkish-orange (vin rose) color to the urine indicates the presence of iron-deferoxamine complex and correlates well with a significantly elevated serum iron level. A positive deferoxamine challenge also mandates admission and further treatment. Patients asymptomatic after 6 hours with a negative challenge may be discharged.

Desferioxamine is the treatment of choice. The most efficacious route is a continuous IV infusion, and the maximum recommended dose is 15 mg/kg per hour (maximum daily dose 360 mg/kg, up to 6 g total). A higher infusion rate has been associated with hypotension but may be necessary (in conjunction with blood pressure support) for severe ingestions. Generally, it can be stopped after 12-24 hours if the acidosis has resolved and the patient is improving.

Antihistamines: Antihistamines may depress or stimulate the CNS. A potentially toxic dose is 10-50 mg/kg of the most commonly used antihistamines, but toxic reactions have occurred at much lower doses. Activated charcoal should be used to reduce drug absorption. Diazepam, 0.1-0.2 mg/kg intravenously, can be used to control seizures. Forced diuresis is not helpful.

Scorpion sting: India has 99 species of scorpions but only 2 are poisonous (Mesobuthus tamulus or common red and Palaminus swammerdami). Scorpion venom is a potent stimulus for catecholamine release. It also has neurotoxic toxalbumin, hematotoxic phospholipases, cardiotoxin and a specific inhibitor of high conductance calcium activated potassium channel. Local pain is usually intense. The most prominent early feature is an "autonomic storm" perspiration, salivation, vomiting, lacrimation, mydriasis etc. Enchepalopathy may occur and hyperexcitability is common. Heart failure or shock may occur. ARDS can occur. No first aid measures are of great value. Ligature application may be done immediately. Washing the wound and cooling with ice is helpful. Prazosin, the selective alpha-1 adrenergic blocker is used for control of the autonomic storm. Hypertension can be treated with nifedipine or hydrallazine or sodium nitroprusside infusion. The old "lytic cocktail" is contraindicated because of the increased risk of orthostatic hypotension, respiratory depression and convulsions. Steroids are contraindicated because of their anti-insulin and catabolic effects. Insulin (0.1- 0.2 u/kg/day sc in 3 divided doses) with blood sugar monitoring has been shown to increase myocardial glycogen and antagonize the metabolic effects of excess catechoalmines.
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