PE14.1-3 | Childhood Poisoning — Glossary

The enzyme responsible for hydrolysing acetylcholine at synaptic clefts, thereby terminating cholinergic transmission; irreversibly inhibited by organophosphorus compounds.

An adsorbent used in some poisonings to bind toxins in the GI tract and prevent systemic absorption; NOT effective for hydrocarbons (poor adsorption) and poses aspiration risk.

The irreversible structural change in the organophosphate-AChE bond that occurs within 24–48 hours of exposure, after which oximes (pralidoxime) cannot reactivate the enzyme.

A non-IgE-mediated hypersensitivity reaction to IV N-acetylcysteine, presenting with urticaria, bronchospasm, or angioedema during the loading infusion; treated with antihistamine and slowing the infusion rate.

Proactive counselling provided to parents about potential safety hazards (such as household chemical storage) before an adverse event occurs; a key preventive paediatric practice.

The entry of foreign material (liquid, food, or vomitus) into the larynx and lower respiratory tract, bypassing normal protective reflexes; the primary mechanism of injury in kerosene ingestion.

Chemical inflammation of the lungs caused by inhalation of irritant material (such as hydrocarbons or gastric contents) into the airways, leading to surfactant disruption, alveolar injury, and V/Q mismatch.

A competitive muscarinic antagonist used as the primary antidote in organophosphorus poisoning; titrated to drying of secretions with no fixed maximum dose; does not treat nicotinic or CNS effects.

The clinical state achieved by adequate atropine dosing in OP poisoning: secretions dried, bronchospasm cleared, heart rate >80/min, pupils dilated — the therapeutic endpoint, not a fixed dose.

Constriction of the bronchial smooth muscle causing airway narrowing and wheeze; may occur in kerosene ingestion due to mucosal irritation and is treated with bronchodilators.

Hepatocellular death in zone 3 (perivenular) of the hepatic acinus, the characteristic pattern of paracetamol-induced hepatotoxicity; this zone has the highest CYP2E1 activity and lowest oxygen tension.

Non-infectious pulmonary inflammation caused by direct chemical irritation of the airways and alveoli, distinguished from bacterial pneumonia by its early onset, chemical aetiology, and lack of response to antibiotics.

The clinical syndrome of acetylcholine excess caused by cholinesterase inhibition, comprising muscarinic features (SLUDGE/DUMBELS), nicotinic features (fasciculations, paralysis), and CNS features (seizures, coma).

A cytochrome P450 isoenzyme responsible for the minor CYP-mediated oxidation of paracetamol to NAPQI; induced by alcohol and fasting, contributing to increased susceptibility to toxicity.

The process of removing an absorbed or absorbed toxin from a patient; in OP poisoning, involves removing contaminated clothing and washing skin to stop ongoing dermal absorption, and gastric lavage for recent ingestion in an alert, airway-protected child.

Visible, spontaneous contractions of muscle fibres or motor units caused by repetitive ACh stimulation at the neuromuscular junction; a hallmark nicotinic feature of OP poisoning.

The procedure of introducing fluid via a nasogastric tube and draining it out to wash the stomach contents; contraindicated in hydrocarbon ingestion because it increases the risk of aspiration.

A tripeptide antioxidant (glutamate-cysteine-glycine) in hepatocytes that detoxifies NAPQI by conjugation; stores become depleted in paracetamol overdose, allowing toxic metabolite accumulation.

A neuropsychiatric syndrome complicating severe liver failure, ranging from mild confusion to deep coma; in paracetamol poisoning, it appears in Phase III and indicates fulminant hepatic failure.

Functional renal failure complicating severe hepatic injury, caused by systemic vasodilatation and renal vasoconstriction; occurs in Phase III paracetamol hepatic failure and is a marker of poor prognosis.

A formula for calculating daily maintenance fluid requirements in children: 100 mL/kg/day for the first 10 kg of body weight, plus 50 mL/kg/day for the next 10 kg, plus 20 mL/kg/day for each kilogram above 20 kg.

A neuromuscular complication of OP poisoning occurring 24–96 hours after the acute cholinergic crisis, characterised by proximal muscle weakness and cranial nerve palsies, potentially requiring prolonged ventilatory support.

An aliphatic petroleum distillate hydrocarbon used as a domestic cooking and lighting fuel in India, characterised by low viscosity and low surface tension that make aspiration into the airways particularly dangerous.

Clinical and biochemical criteria used to identify paracetamol-induced acute liver failure patients who require urgent liver transplantation: arterial pH <7.3, or INR >6.5 + creatinine >300 µmol/L + Grade III/IV encephalopathy.

Bilateral constriction of the pupils to pinpoint size; a highly characteristic finding in organophosphorus poisoning due to muscarinic stimulation of the circular pupillary constrictor muscle.

G-protein coupled acetylcholine receptors located on cardiac muscle, smooth muscle, and glands; targeted by atropine (antagonist) and responsible for the SLUDGE features of OP poisoning.

The antidote for paracetamol poisoning; a cysteine prodrug that replenishes hepatic glutathione stores and directly scavenges NAPQI; most effective within 8–10 hours of ingestion; given IV (150/50/100 mg/kg over 21 hours) or orally.

The toxic metabolite of paracetamol produced by CYP2E1 oxidation; normally detoxified by glutathione, but accumulates when glutathione is depleted in overdose, causing covalent hepatocyte injury.

Ligand-gated ion channel acetylcholine receptors at the neuromuscular junction and autonomic ganglia; responsible for muscle fasciculations, weakness, and paralysis in OP poisoning — not blocked by atropine.

A class of cholinesterase-inhibiting chemicals used as agricultural pesticides and chemical warfare agents that covalently bind to and inhibit acetylcholinesterase, causing accumulation of acetylcholine at cholinergic synapses.

An analgesic and antipyretic metabolised primarily by hepatic glucuronidation and sulfation; in overdose, excess CYP2E1-mediated conversion to the toxic metabolite NAPQI causes centrilobular hepatic necrosis.

The second clinical phase of paracetamol poisoning (24–72 hours), characterised by resolution of initial nausea/vomiting and apparent clinical well-being despite ongoing hepatocellular necrosis and rising transaminases.

A 24-hour national telephone resource (India: 1800-116-117) providing expert advice on poisoning management; families should be advised to call immediately on suspicion of any toxic ingestion.

An oxime compound that reactivates acetylcholinesterase by displacing the organophosphate from the enzyme active site; effective only within 24–48 hours of exposure before irreversible ageing of the OP-AChE bond.

Non-invasive measurement of haemoglobin oxygen saturation (SpO2) using a photoelectric probe; the most useful bedside monitoring tool in kerosene ingestion.

A validated clinical tool that plots plasma paracetamol concentration (y-axis) against time since ingestion (x-axis); a level above the treatment line at ≥4 hours post-ingestion indicates need for NAC therapy.

A short-acting beta-2 agonist bronchodilator given by nebulisation or MDI to relieve bronchospasm in kerosene-induced airway irritation; dose 2.5 mg nebulised in children.

A plasma enzyme whose activity is reduced in OP poisoning; activity <50% of normal indicates significant poisoning; used to confirm diagnosis and monitor recovery, but does not guide acute management decisions.

Mnemonic for muscarinic features of cholinergic toxidrome: Salivation, Lacrimation, Urination, Defaecation, GI cramps, Emesis.

A lipoprotein complex secreted by type II pneumocytes that reduces alveolar surface tension, preventing collapse during expiration; disruption by hydrocarbons leads to alveolar instability and atelectasis.

An abnormally elevated respiratory rate — in children aged 1–5 years, defined as >40 breaths/minute; an early and sensitive indicator of respiratory distress.

Unintentional paracetamol toxicity from repeated supratherapeutic doses given over days, commonly occurring in febrile, fasting, or malnourished children where glutathione stores are reduced.

The threshold above which significant hepatotoxicity may occur; in children, generally accepted as >150 mg/kg of body weight; state the dose in mg/kg for all paediatric calculations.

A condition in which lung segments are perfused by blood but not ventilated with air (or vice versa), resulting in impaired gas exchange and hypoxaemia — the primary mechanism of respiratory failure in aspiration pneumonitis.