Treatment Administration of oxygen when available is the most important ?rst-aid management. Rescuers should be trained, must not put themselves at risk, and should use protective clothing and breathing apparatus. In unconscious victims, establish a clear airway and give 100 per cent oxygen. If breathing stops and oxygen is unavailable, initiate expired-air resuscitation. If cyanide salts were ingested, mouth-to-mouth contact must be avoided and a mask with a one-way valve employed instead. Some commercially available ?rst-aid kits contain AMYL NITRATE as an antidote which may be employed if oxygen is unavailable.
Once in hospital, or if a trained physician is on the scene, then antidotes may be administered. There are several di?erent intravenous antidotes that may be used either alone or in combination. In mild to moderate cases, sodium thiosulphate is usually given. In more severe cases either dicobalt edetate or sodium nitrite may be used, followed by sodium thio-sulphate. Some of these (e.g. dicobalt edetate) should be given only where diagnosis is certain, otherwise serious adverse reations or toxicity due to the antidotes may occur.... cyanide poisoning
– although lead-containing paints are no longer used for items that children may be in contact with.
Acute poisonings are rare. Clinical features include metallic taste, abdominal pain, vomiting, diarrhoea, ANOREXIA, fatigue, muscle weakness and SHOCK. Neurological effects may include headache, drowsiness, CONVULSIONS and COMA. Inhalation results in severe respiratory-tract irritation and systemic symptoms as above.
Chronic poisonings cause gastrointestinal disturbances and constipation. Other effects are ANAEMIA, weakness, pallor, anorexia, insomnia, renal HYPERTENSION and mental fatigue. There may be a bluish ‘lead line’ on the gums, although this is rarely seen. Neuromuscular dysfunction may result in motor weakness and paralysis of the extensor muscles of the wrist and ankles. ENCEPHALOPATHY and nephropathy are severe effects. Chronic low-level exposures in children are linked with reduced intelligence and behavioural and learning disorders.
Treatment Management of patients who have been poisoned is supportive, with removal from source, gastric decontamination if required, and X-RAYS to monitor the passage of metallic lead through the gut if ingested. It is essential to ensure adequate hydration and renal function. Concentrations of lead in the blood should be monitored; where these are found to be toxic, chelation therapy should be started. Several CHELATING AGENTS are now available, such as DMSA (Meso-2,3dimercaptosuccinic acid), sodium calcium edetate (see EDTA) and PENICILLAMINE. (See also POISONS.)... lead poisoning
EDTA (ethylenediaminetetraacetic acid) see edetate.... edrophonium
lead1 n. a soft bluish-grey metallic element that forms several poisonous compounds. Acute lead poisoning, which may follow inhalation of lead fumes or dust, causes abdominal pains, vomiting, and diarrhoea, with paralysis and convulsions and sometimes *encephalitis. In chronic poisoning a characteristic bluish marking of the gums (‘lead line’) is seen and the peripheral nerves are affected; there is also anaemia. Treatment is with *edetate. The use of lead in paints is now strictly controlled. Symbol: Pb.
lead2 n. 1. a portion of an electrocardiographic record that is obtained from a single electrode or a combination of electrodes placed on a particular part of the body (see electrocardiogram; electrocardiography). In the conventional ECG, 12 leads are recorded. Each lead represents the electrical activity of the heart as ‘viewed’ from a different position on the body surface and may help to localize myocardial damage. 2. a flexible steerable insulated wire introduced into the heart under X-ray control to allow electrical stimulation of the heart for the purpose of pacing (see pacemaker).... l-dopa
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