Virtually all substances found in the home have been ingested either by adults because of poorly labelled bottles or accidentally by children. Occasionally household agents are deliberately taken. Many kitchen products contain bleaches (sodium hypochlorite or hydrogen peroxide), acids or alkalis and the main problem after poisoning with them is their corrosive action on the gut. There is an immediate burning pain in the lips, mouth, throat, retrosternal area and stomach, and ulceration may follow. Vomiting may occur, with blood in severe cases. The major long-term complication is oesophageal stricture. Poisoning with sodium hypochlorite should be treated with sufficient water or milk to dilute it. Gastric lavage is contraindicated unless very substantial quantities have been taken. Alkalis should not be neutralized. Some’ household products contain solvents, e.g. acetone in nail varnish remover or toluene in paints, which may be sniffed accidentally or intentionally.
Over the last few years, accide~tal poisoning with paraquat has become less common in the developed world and deliberate self-poisoning now accounts for most cases. However in some developing countries it is the commonest single cause of poisoning. Paraquat is found in commonly used brands of weedkiller as an aqueous 20% solution (Gramoxone) or 2.5% solution (Weedol). A dose of 1.5 g may be fatal. Clinical features include ulcers in the mouth and oesophagus, diarrhoea and vomiting, epistaxis, pulmonary oedema, and later pulmonary fibrosis, respiratory failure and renal failure. Treatment is with gastric lavage with Fuller’s earth or bentonite and purging with magnesium sulphate. Haemodialysis or haemoperfusion may be useful in removing the paraquat if started early.
The outcome can be predicted by relating the plasma paraquat concentration to the number of hours that have elapsed since ingestion. It is doubtful whether any treatment affects the outcome.
Carbon monoxide poisoning is a worldwide problem. Domestic gas in the UK (except in Northern Ireland) does not contain carbon monoxide, but the combustion of any fuel gas in the absence of adequate oxygen and ventilation may lead to domestic carbon monoxide poisoning. The other common sources of carbon monoxide are the exhaust fumes of petrol engines and from certain gas appliances that use propane and butane gases. Carbon monoxide combines readily with haemoglobin to form carboxyhaemoglobin, thus preventing the formation of oxyhaemoglobin. The clinical features of carbon monoxide poisoning include mental impairment, including coma in severe cases. Headache, nausea and vomiting, and the classic pink colour of the skin due to the carboxyhaemoglobin are seen. More severe toxicity produces widespread effects, including myocardial damage and respiratory distress. Treatment consists of removing the patient from the carbon monoxide source, and giving as high a concentration of oxygen as possible. Hyperbaric oxygen should be considered if the victim is unconscious or has a blood carboxyhaemoglobin level in excess of 10%.
Batteries more than 20 mm in diameter can lodge in the oesophagus and a chest X-ray should always be performed. Batteries should be removed by endoscopy because they may break open liberating mercury and manganese, which have corrosive effects. Most batteries will pass through the gut in 48 hours but, if they do not and are seen on X-ray to be disintegrating, they should be s rgically removed.
Carbamates and organophosphate insecticides are used extensively in the home and agricultural market. They may be ingested accidentally, inhaled, or absorbed through the skin when protective clothing is not worn. These agents are potent inhibitors of cholinesterase and produce an accumulation of acetylcholine. Carbamate poisoning is generally less severe and of shorter duration.The clinical features are due to the muscarinic and nicotinic effects of acetylcholine. They include nausea, vomiting, hypersalivation, muscle weakness, bronchospasm,and respiratory failure; convulsions may also occur. The plasma cholinesterase activity will be low. Treatment involves washing any contaminated skin. Atropine 2 mg i.v. is given repeatedly to obtain full atropinization. Pralidoxime mesylate 1 g i.v., a cholinesterase reactivator, is used in severe cases but its benefit has not been established.
CWorphenoxyphenol poisoning may require treatment with alkaline diuresis.
Cyanide is found in a wide range of industrial compounds, e.g. rodenticide and fertilizers. Hydrogen cyanide is also released from polyurethane foams. Ingestion or inhalation of this agent produces rapid onset of dizziness and headache, followed by acute shortness of breath, shock and eventual coma. Cyanosis is not present and the skin colour is red. There may be an odour of bitter almonds. Cyanide inhibits cytochrome oxidase, preventing cellular respiration, which leads to hypoxia, metabolic acidosis and frequently death. Treatment is urgent; oxygen is given and an intravenous combination of sodium nitrite (300 mg over 3 min) and sodium thiosulphate (12.25 g over 10 min). This is followed by 300 mg of dicobalt edetate intravenously over 1 min and 300 mg given a minute later if no recovery occurs. 50% Dextrose 50 ml i.v. should also be given after the dicobait edetate.
METHANOL, ETHANOL AND ETHYLENE GLYCOL
These agents are all chiefly metabolized by alcohol dehydrogenase in the liver. In poisoning, there is increased lactate formation, which increases the metabolic acidosis found after methanol (due to formate) or ethylene glycol ingestion (due to glycolate). Minor poisoning with methanol causes headache, breathlessness and photophobia. In severe poisoning there is papilloedema and eventually optic atrophy and blindness. Poisoning with methanol is treated with gastric lavage and correction of acidosis with bicarbonate infusion. Ethanol infusion and haemodialysis are used to remove methanol in patients who have taken more than 30 g of methanol and who have a blood level of methanol greater than 500 mg litre”! (15.6 mrnol litre'”). Intravenous folinic acid may prevent ocular toxicity. Ethanol poisoning produces severe depression of consciousness and hypo glycaemia, particularly in children. Treatment usually only consists of gastric lavage with an endotracheal tube in position. The use of fructose is no longer advised and peritoneal dialysis or haemodialysis is only indicated for very severe cases. Chlormethiazole, used for alcohol withdrawal, is dangerous if the patient takes alcohol and should therefore be used as an inpatient therapy only.
Poisoning with ethylene glycol (antifreeze) causes gastrointestinal upset and neurological involvement, including coma, followed by cardiorespiratory collapse and acute renal failure. Treatment is by gastric lavage and correction of the acidosis with intravenous sodium bicarbonate and of the hypocalcaemia with intravenous calcium solutions. Ethanol is given orally or intravenously to maintain an ethanol blood level of 1000 mg Iitre ” in severe cases to inhibit the metabolism of ethylene glycol. Haemodialysis is indicated in patients who have taken more than 50 g of ethylene glycol or who have plasma levels >500 mg litre:” (8.1 mmol litre “).
Chronic mercury poisoning causes tremor (hatters’ shakes), excessive salivation, scanning speech, anxiety and depression. In the hatters’ trade, rabbit fur was stirred in vats of hot mercuric nitrate to make felt, and inhalation of the vapour led to signs of chronic mercury poisoning. Acute mercury poisoning is seen after the ingestion of mercuric salts (e.g. mercuric chloride), inhalation of mercuric vapours or the ingestion of mercuric oxide in ‘button’ batteries. It is treated by induced emesis, lavage and injections of dimercaprol or penicillamine.
Acute lead poisoning is rare. Chronic lead poisoning, however, commonly occurs.
Occupational lead poisoning
This is a notifiable disease in the UK and work with leadis covered by strict regulations. Most lead poisoning occurs in scrap metal or smelting workers. Blood levels in these workers should be lower than 800 fLglitre ” (4 mmol litre “).
Domestic lead poisoning
This usually occurs in children owing to the ingestion of old lead-based paint around the home. Most toys have lead-free paint. Chronic ingestion of water from lead pipes and acute accidental ingestion of fluid from car batteries are other frequent causes of lead poisoning. After absorption, lead interferes with haem and globin synthesis. It also binds to bone, and in patients suffering from chronic exposure small amounts of lead can be found in many tissues.
ANOREXIA, NAUSEA AND VOMITING
A BLUE LINE ON THE GUMS
CONSTIPATION AND SEVERE ABDOMINAL COLIC
DENSE METAPHYSEAL BANDS at the growing end of long bones, particularly the wrist and knee in children (lead lines) ANAEMIA, with erythrocytes showing basophil stippling PERIPHERAL NERVE LESIONS giving wrist drop and foot drop, with muscle involvement
LEAD ENCEPHALOPATHY, wit eventual seizures and impairment of consciousness. The diagnosis is made on the basis of the clinical features. The blood level of lead is very variable; levels above 800 fLglitre ” (4 mmol litre “) are toxic.
It is most important to remove the source of lead intoxication.Sodium calcium edetate (calcium EDT A), D-penicillam ine and dimercaprol have all been used for treatment.
Poisoning with iron tablets is often accidental in children. Symptoms include nausea, vomiting, abdominal pain, diarrhoea and haematemesis due to a direct corrosive effect. In severe cases, hypotension, hepatic damage and coma can occur. Treatment is urgent and a serum iron concentration should be sent off as an emergency. Administer gastric lavage and intragastric desferrioxamine 5-10 g and 2 g i.m. 12-hourly or a slow i.v. infusion of 15 mg kg:” hour:” (maximum 80 mg kg:” in 24 hours). Arsenic Acute poisoning with arsenic causes vomiting. abdominal pain and diarrhoea. It is treated with rehydration and dimercaprol. Chronic poisoning causes excess salivation, weakness, anorexia and polyneuritis. There is a ‘raindrop’
pigmentation of the skin. Arsenic accumulates in the hair and the nails.