Category Archives: Adverse drug reactions and poisoning

Poison Information Services

Information on poisoning can be obtained from the poisons information services at the following numbers:

Poisons Information Service

Laboratory analysis may help in the diagnosis and management of some cases. Information on the available services can be obtained from the Poisons Information Service in London or the local services in each country.

Drug abuse


Solvent abuse has become a common problem, particularly in teenagers who inhale volatile organic solvents such as toluene in glues (‘glue sniffing’). Many other solvents, such as aerosols (hair lacquer), antifreeze and petrol, can also be misused. Solvents are applied to a piece of cloth or put into a plastic bag and inhaled, often until consciousness is lost. The patient presents either in the acute intoxicated state or as a chronic abuser with excoriation and rashes over the face and a peripheral neuropathy. Sudden death can occur and is probably due to cardiac arrhythmias. Stigmata of solvent abuse include sores or a rash around the nose and mouth and glue on the clothing.

Other drugs

Drug addicts frequently overdose themselves and are commonly admitted to hospital with the signs of opiate injection. Tell-tale injection sites and pin-point pupils are important clues. Naloxone is given in the same dosage as for co-proxamol overdose.


Cannabis is usually smoked and often taken casually. Initially there is euphoria, followed by drowsiness and sleep. Redness of the conjunctivae and pupil dilatation are seen. No specific treatment is required.


Amphetamines are taken for their stimulatory effect. In overdose there is confusion, delirium, hallucinations and violent behaviour. Cardiac arrhythmias can be a major problem. Treatment is with sedatives, such as diazepam. Forced acid diuresis may be used but is rarely required.


Cocaine can be taken by injection, inhalation or ingestion. It produces excitement, over-alertness, euphoria and restlessness. This is followed by delirium, tremor, convulsions, pyrexia and cardiac arrhythmias, which may cause cardiac failure. Respiratory failure may also occur. Treatment is symptomatic and supportive. There is no specific antidote. 13-Blockers should not be used to treat hypertension or tachycardia.


This drug is also known as MDMA (3,4- methylenedioxymethamphetamine) and is a semisynthetic hallucinogenic drug whose initial effects are sympathomimetic and may cause tachyarrhythmias, hyperpyrexia, clonic movements and convulsions, coagulopathy, rhabdomyolysis and renal failure. Treatment consists of gastric lavage, chlorpromazine, a- and J3-adrenergic blockade, intravenous fluids and passive cooling.


There are many poisonous mushrooms that can be confused with edible fungi and be eaten by mistake. Nevertheless, apart from transient nausea, vomiting and diarrhoea, which can occur with many species, very severe reactions are rare.
Fatal mushroom poisoning is almost invariably due to Amanita phalloides (the death-cap mushroom). This fungus contains phallotoxins and amatoxins, both of which interfere with cell metabolism. Toxicity is increased if the mushrooms are eaten raw, as some toxins are inactivated by heat. In general, the sooner the symptoms occur, the less serious the poisoning, depending on the type of mushroom ingested. Within 2 hours, nausea, vomiting, diarrhoea and sweating occur. After about 6 hours, patients complain of headache and dizziness, and severe vomiting occurs at about 12 hours. After 72 hours, the more serious complications of hepatocellular and renal failure may occur, which have a high mortality. The diagnosis is made by obtaining a careful history, with identification of the mushroom if possible. Amatoxins can be measured in the blood by radioimmunoassay. Treatment should include gastric aspiration and lavage and general support. There is some evidence that haemodialysis may be of some value.
Other mushrooms that are poisonous include:
FLY AGARIC (Amanita muscaria), which contains a little muscarine and other hallucinogenic substances
INK CAP (Coprinus atramentarius), which contains a dehydrogenase inhibitor with a disulfiram-like effect, producing flushing, swelling, a rash on the face and hands, and cardiovascular effects, particularly after alcohol
FALSE BLUSHER (Amanita pantherinai, which produces similar features to deadly nightshade because of its atropine-like effects.


Many plants are known to be poisonous, but in practice it is unusual for severe poisoning to occur. Children are the usual victims. Only two people are known to have died from plant poisoning in the UK since the early 1970s. The commonest effects of nettles and poison ivy are dermatitis followed by vomiting. Poisonous plants commonly ingested include hemlock, laburnum, deadly nightshade and green potatoes. Deadly nightshade (Atropa belladonna) contains hyoscyamine and hyoscine. When ingested these cause the anticholinergic effects of a dry mouth, nausea and vomiting, eventually leading to blurring of the vision, hallucinations, confusion and hyperpyrexia.

Venomous animals


The adder (Vipera berus) is the only poisonous snake native to the UK. However, a number of dangerous snakes are kept as pets, and worldwide venomous snakes still cause significant mortality. There are three types of venomous snake:

1 Viperidae have long erectile fangs. They are subdivided into two types:
(a) Viperinae (true vipers, e.g. Russell’s viper [dabora], European adder), which are found in all parts of the world except America and the Asian Pacific.
(b) Crotalinae (pit-vipers, e.g. rattlesnakes, Malayan pit-viper), which are found in Asia and America. They have small heat-sensitive pits between the eyes and the nostrils. The venom of both of these classes of snake is vasculotoxic.
2 Elapidae (cobras, mambas, kraits, coral-snakes) are found in all parts of the world except Europe. They have short, unmoving fangs and the venom produces neurotoxic features. Venom from the Asian cobra and the African spitting cobra also produces local tissue necrosis.
3 Hydrophiidae (sea-snakes) are found in Asian Pacific coastal waters. They have short fangs and flattened tails. The venom is myotoxic.



Russell’s viper is the most important cause of snake-bite mortality in India, Pakistan and Burma. There is local swelling at the site of the bite, which may become massive. Local tissue necrosis may occur, particularly with cobra bites. Evidence of systemic involvement occurs within 30 min, including vomiting, evidence of shock and hypotension; haemorrhage due to incoaguable blood can be fatal.


There is not usually any swelling at the site of the bite, except with Asian cobras and the African spitting cobrahere the bite is painful and is followed by local tissue necrosis. Vomiting occurs first followed by shock and then neurological symptoms and muscle weakness, with paralysis of the respiratory muscles in severe cases. Cardiac muscle can also be involved.


Systemic features are muscle involvement, myalgia and myoglobinuria, which can lead to acute renal failure. Cardiac and respiratory paralysis may occur.


A firm pressure bandage should be placed over the bite and the limb immobilized. This greatly delays the spread of the venom. Arterial tourniquets should not be used and incision or excision of the bite area should not be performed. The type of snake should be identified if possible. In about 50% of cases no venom has been injected by the snake bite and antivenoms are not generally indicated (unless systemic effects are present) as they can cause severe allergic reactions. Nevertheless, careful observation for 12-24 hours is necessary and antivenom must always be given when indicated, as the mortality of snake bite is 10-15% with certain snakes. General supportive measures should be given as necessary, as for all poisoning. These include diazepam for anxiety and intravenous fluids with volume expanders for hypotension. Treatment of acute respiratory, cardiac and renal failure is instituted as necessary. Specific measures, i.e. antivenoms, can rapidly neutralize venom, but only if an amount in excess of the amount of venom is given. Antivenoms cannot reverse the effects of the venom so they must be given early. They do minimize some of the local effects and may prevent necrosis at the site of the bite. Antivenoms should be administered intravenously by slow infusion, the same dose being given to children and adults. Allergic reactions are frequent, and adrenaline (1 in 1000 solution) should be available. Antivenoms are usually rapidly effective. In severe cases the antivenom infusion should be continued even with allergic reactions, with subcutaneous injections of adrenaline being given as necessary. Large quantities of anti venom may be required. Some forms of neurotoxicity, such as those induced by the death adder, respond to anticholinesterase therapy with neostigmine and atropine. Local wounds often require little treatment. If necrosis is present, antibiotics should be given together with initially minimal surgical treatment. Skin grafting may be required later. Antitetanus prophylaxis must be given. Antivenoms must be kept readily available in all snakeinfested areas.


Scorpion stings are a serious problem in the tropics and cause 1000 deaths per year in Mexico. The poison glands are situated in the end of the tail. Severe pain occurs immediately at the site of puncture, followed by swelling. This should be treated by a firm pressure bandage to avoid the spread of the neurotoxic venom. Signs of systemic involvement include vomiting, respiratory depression and haemorrhage. Treatment is supportive. Antivenom is available in certain countries.


The black widow spider (Latrodectus mactans) is found in North America and the tropics and occasionally in Mediterranean countries. The bite quickly becomes painful and generalized muscle pain, sweating, headache and shock occur due to absorption of rapidly acting neurotoxins. No systemic treatment is required except in cases of severe systemic toxicity, when specific antivenom should be given where this is available. Intravenous calcium gluconate may help the muscle spasms.
Loxosceles causes many bites in Central and South America. L. reclusa, the brown recluse spider, is also found in the southern USA. Spiders are often found in bedrooms, so that patients are often bitten at night. There is a burning pain at the site of the bite, followed by a necrotic ulcer in some cases. Systemic effects, which include fever, vomiting and haemolysis, are rare. No treatment is indicated except in severe cases, when an anti venom should be given if available. Phoneutria nigriventer, the banana spider, and Atrax robustus, the Sydney funnel-web spider, can both give nasty bites, which are occasionally fatal.


Insect stings, e.g. from wasps and bees, and bites, e.g. from ants, produce pain and swelling at the puncture site. Death occurs (12 per year in the UK) and is usually due to anaphylaxis, which requires urgent treatment. Patients who have severe local reactions to stings or a mild anaphylactic reaction should carry a Medi-jet syringe for self-administration of adrenaline should a further sting occur. Desensitization can be carried out, but the course is prolonged and often needs to be repeated.
Marine animals There are many poisonous fish that can be dangerous. They are usually found in tropical waters but cases have
been described worldwide. Stringrays and scorpion fish are two examples that sting by injecting venom through barbed spines. There is immediate severe local pain and swelling, which may be followed by tissue necrosis. Systemic effects include diarrhoea, vomiting, hypotension, cardiac arrhythmias and convulsions. Treatment is supportive. Care should always be taken in waters where these fish are known to be present. Venomous Coelenterata include jellyfish, sea anemones and the Portuguese man-of-war. The tentacles contain toxin that, following a sting, produces painful wheals at the site of contact. These wheals may become necrotic. Rarely there are systemic side-effects, including abdominal pain, diarrhoea and vomiting, hypotension and convulsions. Treatment consists of removing the tentacles, having first applied acetic acid (vinegar) to them. Alcohol compounds should not be used.


Only the octopus and cone-shells are venomous to humans. The blue-ringed octopus, which is found in Australia, has saliva which contains the neurotoxin tetrodotoxin. This flows into the wounds from the beak of the octopus and can cause serious systemic effects. In cone-shells the venom is found in association with their radular teeth. A bite initially produces local numbness, which can then spread over the body and may even tually lead to paralysis.

Seafood poisoning

This can occur with fish and shellfish. In some cases it is attributable to toxins, but most poisonings occur as a result of pathogens such as Salmonella or hepatitis A virus. Ichthyosarcotoxic fish contain toxins in their blood, skin and muscle and are the commonest cause of poisoning.
CIGUATERA. Poisoning occurs chiefly with the reefdwelling fish from around the Pacific and Caribbean. The fish contain ciguatoxins from the plankton Gambier discus. Most cases of poisoning are due to the red snapper, grouper, barracuda and amberjack fish but many other species may be responsible. The poisonous fish cannot be distinguished from identical fish that do not contain the poison. The toxin is unaffected by cooking. Symptoms occur from a few minutes to 30 hours after ingestion of the fish. They include numbness and paraesthesia of the lips, abdominal pain, nausea, vomiting and diarrhoea. Visual blurring, photophobia, metallic taste in the mouth, myositis and eventual hypotension and shock can also occur. Treatment is symptomatic, but symptoms can last for up to 2 weeks.
SCROMBOID FISH. Fish such as tuna, mackerel and skipjack contain a high degree of histidine. This is decarboxylated by bacteria to histamine and, particularly if the fish are allowed to spoil, large amounts can accumulate in the fish, producing flushing, burning, pruritus, headache, urticaria, nausea, vomiting and bronchospasm 2-3 hours after ingestion. Treatment is symptomatic; care should be taken only to eat fresh fish.
Tetrodotoxin-containing puffer-fish are found in both sea and freshwater areas of Asia, India and the Caribbean. Symptoms that follow ingestion are circumoral paraesthesia, malaise and hypotension, with more severe cases producing ataxia and neuromuscular paralysis. The mortality is 50-60%.
SHELLFISH. Bivalve molluscs, e.g. mussels, oysters, scallops and clams, can acquire the neurotoxin saxitoxin from the dinoflagellate Gonyaulax. These protozoa colour the sea red and molluscs should never be taken from such areas. Symptoms are similar to those caused by tetrodotoxin, but are usually less severe. Treatment is symptomatic.

Household and industrial poisons

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.


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.





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.



Benzodiazepines are commonly taken in cases of selfpoisoning, accounting for 40% of all drug overdosages in the UK. On their own they are remarkably safe but they potentiate the CNS-depressant effects of other drugs taken with them, such as barbiturates or ethanol. Benzodiazepines produce drowsiness, ataxia, dysarthria, nystagmus and sometimes coma. Mild hypotension and respiratory depression may occur. Most patients recover within 24 hours. Deaths from benzodiazepines alone are rare. Flumazenil, a benzodiazepine antagonist, is only useful for severe respiratory depression but the patient should be carefully monitored.


Monoamine oxidase inhibitors

Self-poisoning with MAOIs is uncommon and has a lower toxicity than with tricyclic antidepressants. Symptoms do not usually develop for at least 12 hours after the overdose, when catecholamine levels in the tissues have risen. The clinical features include CNS overactivity, with agitation, hallucinations and muscle rigidity. Facial grimacing and writhing movements of the limbs and trunk may occur. There is usually dilatation of the pupils, tachycardia, a rising blood pressure and profuse sweating, although hypotension may occur. Muscle tone may be exaggerated and convulsions are common.

Hyperpyrexia also occurs

Gastric lavage is performed

Tricyclic antidepressants

Most of the features of self-poisoning with these agents are due to the anticholinergic effects of the drugs. Clinical features include a decrease in the level of consciousness, but deep coma does not usually occur. Convulsions, increased muscle tone, hyperreflexia and extensor plantar responses sometimes occur. The pupils are usually fixed and dilated and there may be ophthalmoplegia and gaze paralysis. Urinary retention may be present. Cardiovascular effects include hypotension and sinus tachycardia. More serious tachyarrhythmias and conduction defects are uncommon and are thought to be due to the quinidine- like action of these drugs. Ventricular arrhythmias are a cause of death in the first few hours following overdose.
If more than 15 tablets have been taken within 4 hours of admission or if the patient is unconscious, gastric lavage should be performed, followed by instillation of a single large dose of activated charcoal. Cardiac arrhythmias may need treatment but often this is not necessary. Anti-arrhythmic therapy is often not effective; correction of any accompanying acidosis and hypoxia is more important.
Most patients recover consciousness within 24 hours, while most cardiac abnormalities settle within 12 hours. Antidepressants such as mianserin produce only mild clinical effects, with drowsiness, hypotension and sinus tachycardia, which are less severe than with the tricyclic antidepressants.



Self-poisoning with this agent usually occurs in patients on long-term maintenance therapy. It is sometimes accidental owing to:
IMPAIRMENT OF LITHIUM ELIMINATION BY THE KIDNEY, owing to the administration of a diuretic
OTHER FACTORS AFFECTING WATER AND ELECTROLYTE BALANCE, such as nausea, vomiting, diarrhoea or exposure to high temperatures In acute overdoses there is a delayed onset of symptoms of more than 12 hours due to the slow entry of lithium into the tissues.
Clinical features include nausea, vomiting, diarrhoea, coarse tremor, apathy and decreased consciousness. There may be restlessness and ataxia with increased muscle tone and rigidity. Electrolyte disturbances, such as hypokalaemia, occur with ECG changes. Acute renal failure is a rare complication. Coma is associated with a bad prognosis. Serum lithium concentrations correlate poorly with the severity of acute lithium poisoning but, nevertheless, levels in excess of 2 mmol litre'” can be fatal. Intravenous fluids are necessary to maintain a good urinary output. Forced diuresis should not be used but peritoneal or haemodialysis may be helpful in severe cases (when levels >5 mmol litre ” are detected).


Clinical features include hypotension, hypothermia, CNS and respiratory depression, arrhythmias and dyskinesia. The latter can be treated with benztropine 2 mg i.v.


These may be taken deliberately or sometimes accidentallyby the elderly, often when one tablet is mistaken  for another.

I3-Adrenoceptor blocking drugs

A small overdose of these drugs produces a bradycardia, but a large overdose can produce convulsions, hallucinations, coma, severe bradycardia, hypoglycaemia and hypotension. Atropine 0.6-1.2 mg i.v. is given. Glucagon in a bolus dose of 10 mg i.v. followed by an infusion of 3 mg hour-1 should be used for severe hypotension. This agent activates adenyl cyclase, promoting formation of cAMP, which is a direct ,a-stimulant of the heart. If this isunavailable, isoprenaline 2 mg diluted in 500 ml normal saline or 5% dextrose at a rate of 20-40 drops per minute should be given.


Self-poisoning with this agent is uncommon but chronic poisoning in patients on digoxin is frequent. Clinical features include nausea, vomiting and cardiac arrhythmias, such as heart block and various tachyarrhythmias, including ventricular tachycardia.
Treatment is supportive. Cardiac abnormalities are treated, and hypokalaemia should be corrected. Digoxin-specific antibody is available for life-threatening overdosage and can be used for severe digitoxin as well as digoxin poisoning.


Overdosage causes vormtmg, restlessness, agitation, tachycardia and dilated pupils. Convulsions, arrhythmias, gastric haemorrhage and hypokalaemia are seen in severecases. Gastric lavage is performed and activated charcoal given with intravenous diazepam to control convulsions.


Self-poisoning by cardiorespiratory drugs is becoming more frequent. Overdosage results in an exaggerated pharmacological effect and treatment should be aimed at counteracting this, e.g. an overdose of salbutamol is treated with a ,a-blocker.

Specific Drug Problems

In this section only specific treatment regimens will be discussed. The general principles of management of selfpoisoning will always be required.


Analgesic poisoning is common in some areas, accounting for one-third of all cases of self-poisoning admitted to hospital. Salicylate poisoning has decreased over the past decade, while paracetamol poisoning has increased. Combinations of aspirin or paracetamol and narcotic analgesics such as codeine or dextropropoxyphene are frequently taken. Co-proxamol, a combination of paracetamol and dextropropoxyphene can cause severe respiratory depression and is a major cause of death. Accidental poisoning with analgesics has decreased since the introduction of child-resistant bottles.


Salicylates are well absorbed from the stomach and small intestine. They are metabolized to form salicyluric acid and salicyl phenolic glucuronides, a process that is saturated at therapeutic dosage. At high doses, renal excretion becomes important. Overdosage stimulates the respiratory centre, directly increasing the depth and rate of respiration and thereby producing a respiratory alkalosis. Compensatory mechanisms include renal excretion of bicarbonate and potassium, which results in a metabolic acidosis. Salicylates also interfere with carbohydrate, fat and protein metabolism, as well as with oxidative phosphorylation. This gives rise to increased lactate, pyruvate and ketone bodies, all of which contribute to the acidosis. Symptoms and signs of salicylate poisoning include tinnitus, nausea and vomiting, overbreathing, hyperpyrexia and sweating with a tachycardia. Alternatively, the patient may appear completely well, even with high blood levels of salicylate. The ingestion of 10-20 g of aspirin by an adult (or one-tenth of this amount for a child) is likely to cause moderate or severe toxicity.With severe intoxication (salicylate levels 800- 1000 mg litre:”: 5.6-7.2 mmol litre “), confusion delirium, convulsions and coma result. Coma is common in children. It should be remembered that consciousness is not impaired unless the blood salicylate level is very high or, more commonly, another drug has been taken. Cerebral and pulmonary oedema are serious complications, and may be exacerbated by forced diuresis.


Aspirin delays gastric emptying and gastric lavage should be performed up to 12 hours after the ingestion in all but the mildest cases and in severe cases up to 24 hours. Activated charcoal in repeated doses should be given. Intravenous fluids may be necessary to correct dehy dration and hypokalaemia. Occasionally intramuscular vitamin K is required to correct hypoprothrombinaemia. Making the urine alkaline is also effective in increasing urine salicylate excretion.
Forced alkaline diuresis is used if the blood level exceeds 500 mg litre-1 (3.6 mmol Iitre”) in adults, 300 mg litre”! (2.2 mmol litre “) in children. Increasing the pH of the urine from 7 to 8 increases the renal excretion of salicylic acid by about a factor of 10. In the first hour, 1500 ml of fluid should be given as 500 rnl 5% dextrose, 500 ml 1.4% sodium bicarbonate and then 500 ml 5% dextrose again. Sufficient potassium should be mixed with each 500 mI bag to keep the serum potassium level above 3.5 mmol litre “. If less than 200 rnl of urine is produced in the first hour, diuresis should be discontinued. The urine pH should be measured regularly  every 15 or 30 min) and kept at between 7.5 and 8.5. The plasma pH and arterial blood gases should be monitored at least 2-hourly to ensure that pH does not rise above 7.6; the plasma electrolytes should also be measured. If facilities are not available for constant observation by medical and nursing staff, alkaline diuresis may be more dangerous than the salicylate poisoning itself and should not be used.


Self-poisoning with paracetamol is common and the outcome can often be fatal. Paracetamol is converted to a toxic metabolite, N-acetyl-p-benzoquinonimine, which is normally inactivated by conjugation with reduced glutathione. After a large overdose, glutathione is depleted and the toxic metabolite binds covalently with sulphydryl groups on liver cell membranes causing necrosis. Marked liver necrosis can occur with as little as 10 g (20 tablets), and death with 15 g. The prothrombin time (the The International Normalized Ratio, INR) is the best guide to the severity of the damage.
The clinical features in the first 24 hours include nausea and vomiting, but the patient is fully conscious. Most patients recover within 48 hours, but some develop liver failure, which usually becomes apparent in 72-96 hours. Acute renal failure can occur, sometimes in the absence of severe liver damage.


Treatment depends on the interval between overdose and presentation and on the plasma concentration of paracetamol. Blood for paracetamol level should be taken immediately.
Within 4 hours of ingestion, gastric lavage should be considered in adults who have taken a single dose of 7.5 g or more, and in children after a single dose of 150 mg kg-lor more. The antidote of choice is acetylcysteine given intravenously; it provides sulphydryl groups that increase the availability of hepatic glutathione. The decision to give treatment is based on the plasma paracetamol concentration, measured 4 hours after the overdose, or later by referring to a graph of log concentration against time, with a line joining 200 mg litre”! (1.32 mmol litre “) at 4 hours and 50 mg Iitre ” (0.33 rnmol litre “) at 12 hours (Fig. 14.5). If the concentration is above, on, or even slightly below, the line, treatment should be given. Care must be taken concerning the units in which the results of estimations are reported.
Some patients, including chronic alcoholics and those taking enzyme-inducing drugs such as phenytoin and carbamazepine, are at greater risk of liver damage and should be treated at concentrations of paracetamol half as great as those indicated by the standard treatment graph. For maximum protective action, treatment should be started within 8 hours. If a potentially toxic dose of paracetamol has been taken, treatment must be given at once. Therapy with acetylcysteine can be stopped if the concentration of paracetamol is subsequently found to be below the treatment line.
Acetylcysteine is given as an intravenous infusion diluted with 5% glucose solution with an initial dose of 150 mg kg’ in 200 rnl over 15 min followed by 50 mg kg:’ in 500 ml in 4 hours, and then 100 mg kg-l  in 1 litre in the following 16 hours. Occasionally, patients develop a pseudoallergic reaction with wheezing, flushing and hypotension, and if this occurs the infusion should be suspended. Intravenous hydrocortisone and chlorpheniramine should be injected and the infusion restarted at a lower rate when the reaction has subsided.

Nomogram for paracetamol.

Nomogram for paracetamol.

Oral methionine is an alternative and is significantly cheaper than acetylcysteine but absorption and efficacy is unreliable if the patient is vomiting. The benefit of methionine in patients presenting late has not been determined. The dose is 2.5 g by mouth every 4 hours for a total of four doses.
Pregnant women should be treated in the same way as other patients and there is no evidence that either acetylcysteine or methionine are teratogenic or fetotoxic. Concentrations of paracetamol are not a reliable guide to the value of treatment in patients who present more than 16 hours after ingestion of the drug. The benefit of treatment with acetylcysteine after 24 hours has been established only in patients who have evidence of encephalopathy but it is worth treating all patients who have taken a potentially dangerous overdose (more than 150 mg kg:’) and who present 16-24 hours later. Treatment can be stopped 24 hours after ingestion if the patient is asymptomatic, if the plasma paracetamol level is below 10 mg litre’? and if the INR is normal. The risk of severe liver damage is assessed from measurement of the INR, serum creatinine concentration and blood pH. A poor prognosis is indicated by an INR above 3, raised serum creatinine concentration or a blood pH below 7.3 recorded more than 24 hours after overdose. If any of these abnormalities are present, advice should be sought from a specialist liver or poisons treatment unit.

Further treatment

In patients who present within 8 hours of the overdose, the INR and serum creatinine should be measured about 24 hours after the overdose or when treatment with the antidote is complete. Patients with normal values can be discharged. For patients presenting after 8 hours, the INR and serum creatinine should be measured after completion of treatment and at 48 hours after overdose. Patients should remain in hospital until it is clear that the tests are not dangerously abnormal and the values are returning towards normal.
If a combination of paracetamol and dextropropoxyphene has been ingested, naloxone should be given intravenously in an initial dose of 0.8-2 mg and repeated at 2-3 min intervals up to a total of 10 mg if necessary. If this combination is taken with alcohol, then death from respiratory depression may occur rapidly.
In patients who present after 16 hours it is important to monitor and maintain fluid and electrolyte balance and glucose levels and to monitor for signals of encephalopathy. Haemorrhage should be treated with fresh frozen plasma. Patients with incipient or established hepatic failure may be candidates for haemoperfusion or liver transplantation. Those who develop severe hepatic damage and then recover do not develop long-term sequelae and can be treated with normal therapeutic doses of paracetamol. Non-steroidal anti-inflammatory

drugs (NSAIDS)

Self-poisoning with NSAIDs has increased, particularly as ibuprofen is available without prescription. Overdoses will produce a variety of effects including nausea, vomiting, headache, tinnitus and gastrointestinal bleeding. Severe poisoning causes widespread metabolic abnormalities, hepatic and renal damage, and convulsions occur with mefenamic acid. Treatment is with gastric lavage leaving 50 g activated charcoal in the stomach, oral activated charcoal 50 g every 4 hours, intravenous cimetidine 200- 600 mg 6-hourly and diazepam for convulsions.


Opiates produce respiratory depression leading  to coma. Pin-point pupils are seen. Naloxone 0.8-2 mg i.v. is a competitive antagonist but, as it is short -acting, repeated injections may be required.


Many techniques have been developed to decrease drug absorption and increase drug elimination, but most of these manoeuvres are only helpful with a few drugs. These, as well as antidotes to specific drugs, are described below.

Decreasing drug absorption

Vigorous attempts to empty the gastrointestinal tract are indicated when drugs that cause potentially fatal complications other than coma or respiratory depression have been ingested. Examples of such drugs are aspirin, paracetamol, colchicine, organophosphates, iron salts and tricyclic antidepressants. It is important to remember that the risk of aspiration into the lungs associated with the use of gastric lavage may well cause more problems than the effects of the drugs themselves. Gastric lavage does not remove stomach contents completely.

Induced emesis

Induced emesis may be useful in small children as they are more difficult to lavage. It is rarely used in adults, as only small amounts of drug are recovered. Paediatric ipecacuanha emetic mixture (not the undiluted fluid extract) is the emetic of choice. The dose is 10 ml for a child and is given to children over 6 months old. Other emetics such as apomorphine, saline, copper sulphate and mustard are dangerous and should not be used.


Basicdrugs such as quinidine or tricyclic antidepressants,where gastric emptying is delayed Paracetamol

Gastric lavage

This procedure is of use only when a large quantity of drug has been taken. The earlier gastric lavage is performed, the greater the amount of drug that is retrieved. It is of little value after 4 hours except for the drugs. Lavage is contraindicated for some poisons, e.g. corrosives, petrol or paraffin.


If administered promptly (within 4 hours) and in sufficient quantity, activated charcoal significantly reduces the gastrointestinal absorption of many drugs. The ratio of charcoal to the amount of poison to be absorbed is about 10: 1 and hence is most useful when relatively small doses of drugs are toxic, as with tricyclic antidepressants, and when emesis, gastric lavage and aspiration are contraindicated. It can be administered by mouth or down a nasogastric tube.

Skin decontamination

Absorption should be minimized for those poisons which are absorbed through the skin by removal of contaminated clothing and careful washing of the skin with soapy water.

Should be performed by an experienced nurse and doctor
The main danger is from pulmonary aspiration, and it is vital that the tracheobronchial tree is protected either by an intact cough reflex or by a cuffed endotracheal tube
The patient should be positioned lying on the left side, with the head over the end or side of the bed so that the mouth and throat are at a lower level than the larynx and trachea
A wide-bore tube (Jacques’gauge 30) is lubricated with glycerine or Vaseline and passedinto the stomach. Aspiration is performed first, and then followed by lavage using 300 ml of water at body temperature for the first washing
This processshould be repeated at least three or four times, using up to 500ml of water on each occasion An aliquot of the washing should be saved in caseit is needed for drug analysis

Increasing drug elimination

Forced alkaline diuresis

This potentially lethal technique is rarely necessary, as few drugs are excreted in their unchanged form. Its benefits have been shown to be outweighed by its serious complications unless monitoring of fluid balance and urine pH is scrupulous. It is mainly used in salicylate poisoning, which is discussed below.

Peritoneal dialysis

The use of this technique is limited by its low efficacy but it may be indicated for patients severely poisoned by ethylene glycol.


This technique may be useful for patients with severe poisoning by lithium salts or methyl or ethyl alcohols. Rarely, patients with severe salicylate poisoning (blood salicylate level >900 mg litre-lor 6.5 mmol litre “) refractory to forced alkaline diuresis may be helped by haemodialysis.


This involves the passage of heparinized blood through devices containing absorbent particles, such as activated charcoal or resins, to which drugs are adsorbed. Its use should be considered in patients severely poisoned with certain drugs (e.g. theophylline, short- and mediumacting barbiturates and glutethimide) who fail to improve despite the use of adequate supportive measures. Antagonizing the effects of poisons These techniques will be considered under the individual drugs. Specific antidotes are available for a small number of drugs. Antidotes act in a number of ways:
ACCELERATION OR DETOXIFICATION OF A POISON, e.g. methionine, N-acetylcysteine in paracetamol poisoning
PREVENTION OF THE FORMATION OF A MORE TOXIC COMPOUND, e.g. ethanol used as a competitive substrate for the metabolizing enzyme to prevent formation of toxic metabolites in methanol poisoning
BLOCKADE OF RECEPTORS THROUGH WHICH THE TOXIC EFFECTS ARE MEDIATED, e.g. atropine used to block cholinergic receptors in organophosphate poisoning

Principles of management

Most patients with self-poisoning require only general care and support of the vital systems. However, for a few drugs additional therapy is required. Blood and urine samples should always be taken on admission for the determination of drug levels, as these are invaluable for the management of certain poisons and are helpful in legal problems. Drug screens of blood and urine are occasionally indicated in the seriously ill, unconscious patient in whom the cause of coma is unknown.
Routine haematological and biochemical investigations are of value, particularly in the differential diagnosis of coma.

Care of the unconscious patient

In all cases the patient should be nursed in the lateral position with the lower leg straight and the upper leg flexed; in this position the risk of aspiration is reduced. A clear passage for air should be ensured by the removal of any obstructing object, vomit or dentures, and by backward elevation of the mandible. Nursing care of the mouth and pressure areas should be instituted. Catheterization of the bladder is usually unnecessary as bladders can be emptied by gentle suprapubic pressure. Insertion of venous cannulae and intravenous fluids are usually unnecessary unless the patient has been unconscious for more than 24 hours .

Physical signs in poisoning.

Physical signs in poisoning.

Respiratory support

If respiratory depression is minimal, oxygen (approximately 60%) should be administered via a mask. A nasopharyngeal or oropharyngeal airway should be inserted and constant monitoring with a Wright spirometer is mandatory to detect any further depression of ventilation.
Loss of the cough or gag reflex is the prime indication for intubation. The gag reflex is assessed by positioning the patients on their side and making them gag using a sucker. In most patients the reflexes are depressed sufficiently to allow intubation without the use of sedatives or relaxants. The complications of endotracheal tubes are discussed on p. 730.
If ventilation remains inadequate, intermittent positive- pressure ventilation (IPPV) should be instituted. Blood gas analysis is useful to confirm the need for IPPV. Hypoxaemia is common in the unconscious patient, particularly after the ingestion of opiates and barbiturates, and can easily go undetected without blood gas analysis.

Cardiovascular support

Hypotension (blood pressure below 80 mmHg) is a common feature of drug overdose and is caused by the physiological effects listed. The classic features of shock-tachycardia and pale cold skin-may be present, but vasodilatation may also be seen, e.g. with barbiturate overdose.
In the majority of cases, hypotension is mild and elevation of the feet is the only treatment required. In patients with more severe hypotension, volume expanders such as dextran should be used. In severely hypotensive patients, the measurement of central venous pressure (CVP) is helpful. Urine output (aiming for 0.5 ml kg:” hour-I) is also an important longer-term guide to the adequacy of the circulation, as many vasodilated overdose patients are adequately perfused with a systolic blood pressure of as low as 90-100 mmHg. Some hypotensive patients may need to be catheterized in order to monitor urine output. If a patient fails to respond to the above measures, intensive therapy is required.
Arrhythmias are commonly seen with tricyclic antidepressants. All shocked patients should have ECG monitoring. Known arrhythmogenic factors such as hypoxia, acidosis and hypokalaemia should be corrected.

Special problems


Defined as a rectal temperature of below 35°C, this is a common problem, especially in older patients or those poisoned with chlorpromazine or a similar neuroleptic. Hypothyroidism should always be excluded. Hypothermia is compounded by drug-induced vasodilatation and environmental exposure. The patient should be covered with a ‘space blanket’ and given intravenous and intragastric fluids at normal body temperature. Inspired gases should also be warmed to 37°C.

An expanded venous bed due to venous vasodilatation Hypovolaemia due to inadequate fluid intake in prolonged coma Institution of IPPV in an already hypovolaemic patient Myocardial depression due to the direct effect of the drug, exaggerated by hypoxia, acidosis and hypothermia.

IPPV, intermittent positive-pressure ventilation.


Rhabdomyolysis can occur from pressure necrosis in drug-induced coma or it may complicate heroin abuse without coma. The risk of renal failure from myoglobinaemia is potentiated by dehydration and acidosis.


These may occur in serious tricyclic antidepressant poisoning, and in antihistamine, anticonvulsant or phenothiazine poisoning. Diazepam 10 mg i.v. is the standard treatment for fits of any cause. The patient should also receive a loading dose of phenytoin (1 g administered intravenously over 4 hours via a central vein) and a maintenance dose of 100 mg 8-hourly if the fits are not immediately controlled. Persistent fits must be controlled rapidly, as they may otherwise result in severe hypoxia, brain damage and laryngeal trauma.

Stress bleeding

Measures to prevent stress ulceration of the stomach should be started on admission in all patients who are unconscious and require intensive care. Administration of antacid by intragastric tube is usually adequate although H2 antagonists are often used.