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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 4 – Poisoning Chapter 4 Poisoning P.174
Poisons: general principles Emergency treatment Clear and maintain the airway (p316). If breathing appears inadequate ventilate with O2 using bag and mask or ET tube (not mouth-to-mouth in poisoned patients). Give naloxone for respiratory depression due to opioids (p182). Circulation Check pulse: if unconscious and pulseless start CPR. Types of poisoning Unintentional or ‘accidental’ poisoning is most common in inquisitive small children (age 1-4yrs) who eat tablets, household chemicals and plants. Older children and adults may be poisoned by chemicals at school or work, or by drinking toxic fluids decanted into drinks bottles. Poisoning by drugs may result from miscalculation or confusion of doses or by taking the same drug under different names. Drug smugglers who swallow drugs wrapped in condoms or polythene, or stuff them in the rectum or vagina, may suffer poisoning if the packages leak (p207). Deliberate self-poisoning is the commonest form of poisoning in adults and may occur in children as young as 6yrs (usually with a family history of self-poisoning). Drugs or poisons are often taken impulsively, sometimes to manipulate relatives or friends. Suicidal intent is relatively uncommon, but all patients must be assessed for this (p587). A few patients leave suicide notes and conceal the drugs or poison to evade detection. Non-accidental poisoning of children is a form of fabricated or induced illness (previously known as Munchausen’s syndrome by proxy—p693), in which a parent deliberately poisons a child. Homicidal poisoning is rare and may involve acute or chronic poisoning with chemicals such as arsenic or thallium. Terrorism poses potential threats to large populations. Information about poisons Tablets may be identified from MIMS Colour Index and descriptions in the BNF and Data Sheet Compendium. Drug Information and Poisons Information Centres (see below) have access to TICTAC, a computer-aided tablet and capsule identification system. Martindale1 gives information on many drugs and poisons and detailed constituents of non-prescription drugs. Identification of plants and fungi from reference books may be difficult, especially if only vague descriptions or chewed fragments are available. The CD-ROM computer software Poisonous Plants and Fungi in Britain and Ireland2 helps with identification and details of toxicity. Local botanic gardens may provide additional help. TOXBASE is the UK National Poisons Information Service’s database on clinical toxicology. It includes information about poisoning with drugs, household products, plants and fungi as well as industrial and agricultural chemicals. TOXBASE is available on the internet (http://www.spib.axl.co.uk). Access is restricted to hospitals and general practitioners in the UK and some hospitals in Ireland. Toxbase or reference books provide sufficient information for most routine cases of poisoning. More detailed information and advice on severely poisoned patients is available at all times from Poisons Information Centres (see below). Footnote 1 Sweetman S (ed). Martindale: The Complete Drug Reference. Pharmaceutical Press, London 2002. 2 Dauncey EA (ed). Poisonous Plants and Fungi in Britain and Ireland. (interactive identification system on CD-ROM) Royal Botanic Gardens, Kew, 2000. P.175
Poisons Information Centres in the UK Use TOXBASE (http://www.spib.axl.co.uk) if possible for poisons enquiries, as this will provide sufficient information in most cases. Telephone advice is available at all times and is especially useful for complex cases or severe poisoning. The single telephone number 0870 600 6266 for the UK National Poisons Information Service directs the call automatically to the relevant local centre. Individual centres can still be contacted directly on the following numbers:

Belfast 028 9024 0503
Birmingham 0121 507 5588 or 0121 507 5589
Cardiff 029 2070 9901
Edinburgh 0131 536 2300
London 020 7635 9191
Newcastle 0191 282 0300

Ireland National Poisons Information Centre, Dublin 018092566 Enquiries to Poisons Information Centres are usually answered initially by an information officer using TOXBASE and other reference sources. Medical staff with specialist toxicology experience are available for advice about seriously poisoned patients. The Poisons Information Centres can also advise about sources of supply of antidotes which are needed only occasionally and also about laboratory analytical services which may be helpful in the management of some patients. Deliberate release of chemicals Information and advice about chemicals which might be deliberately released by terrorists are also available on TOXBASE (http://www.spib.axl.co.uk). P.176
Diagnosis of poisoning The patient or relatives/friends may state what drugs or poison have been taken, but this information is not always accurate. Self-poisoning is often an impulsive act whilst under the influence of alcohol: the patient may not know which tablets he/she took. The amount involved is often unclear. Check any bottles or packets for the names and quantities of drugs or poisons that were available. If a patient is unconscious or severely poisoned, look in hospital notes for details of previous overdoses and find out from the GP what drugs had been prescribed. Record the time of ingestion of the drug or poison. Examine the patient all over for signs of poisoning, injection marks or self-injury. Exclude other diverse processes mimicking poisoning (eg head injury, meningitis). Symptoms and signs which may suggest a particular poison Coma with dilated pupils, divergent squint, tachycardia, ↑muscle tone, ↑reflexes and extensor plantars suggests tricyclic antidepressant or orphenadrine poisoning (p188). Coma with hypotension, respiratory depression and ↓muscle tone suggests barbiturates, clomethiazole, benzodiazepines with alcohol, or severe tricyclic antidepressant poisoning (p188). Coma with pinpoint pupils and slow respiration is typical of opioid poisoning (give naloxone, p182). Tinnitus, deafness, hyperventilation, sweating, nausea and tachycardia are typical of salicylate poisoning (p183). Agitation, tremor, dilated pupils, tachycardia, suggest amphetamines, ecstasy, cocaine, sympathomimetics (p206), tricyclic antidepressants (p188) or selective serotonin re-uptake inhibitors. Assessment and monitoring

  • Assess and record conscious level (GCS, p349)
  • Observe frequently. If unconscious, check BMG and blood glucose.
  • Monitor breathing: record respiratory rate
  • Observe pulse oximeter (NB oximetry SaO2 is low in methaemoglobinaemia, misleadingly high in CO poisoning—see p202)
  • Check ABG if patient is deeply unconscious or breathing abnormally
  • Record and monitor ECG if patient is unconscious, has tachy- or bradycardia or has taken drugs/poisons with risk of arrhythmias
  • Record BP and T°

Investigations in poisoned patients The most useful investigations are paracetamol and salicylate levels, BMG, blood glucose, ABG and U&E. Measure paracetamol levels if there is any possibility of paracetamol poisoning (this includes all unconscious patients). Record the time of the sample on the bottle and in the notes. Many labs can measure salicylate, iron and lithium and also check for paraquat if necessary. Comprehensive drug screening is rarely needed and is only available in a few specialist centres (ask Poisons Information Service). P.177
Poisons: supportive care Protect the airway In an unconscious patient use a cuffed ET tube if there is no gag reflex. If an oral or nasal airway are used, nurse in the recovery position to minimize risk of aspiration should vomiting or regurgitation occur. Monitor breathing and ventilate if necessary Hypoxia and CO2 retention are common in deep coma. Hypotension This may result from relative hypovolaemia, arrhythmias and cardiodepressive effects of drugs. Treat according to the cause. Elevate the foot of the trolley. If BP <90mmHg consider a plasma expander, such as gelatin 500mL (with CVP monitoring if patient is elderly or has cardiac disease). Occasionally, inotropes such as dopamine (2-5micrograms/kg/min) or dobutamine (2.5-10micrograms/kg/min) are also needed, under expert guidance. Cardiac arrhythmias Generally rare in poisoned patients. The most likely drugs responsible are tricyclic antidepressants, ß-blockers, chloral hydrate, digoxin, potassium, bronchodilators, verapamil and amphetamines. Look for and correct hypoxia, respiratory depression, metabolic acidosis and electrolyte abnormalities. Anti-arrhythmic drugs are rarely needed: consult a poisons expert first. Convulsions Dangerous because they cause hypoxia and acidosis and may precipitate cardiac arrest. Drugs responsible include tricyclic antidepressants, mefenamic acid and theophylline. Check for and correct hypoxia and hypoglycaemia. Single brief fits do not require anticonvulsant treatment, but if fits are repeated or prolonged give IV lorazepam 4mg (or PR diazepam if venous access is difficult). Hypothermia May occur with any drug causing coma, especially barbiturates, clomethiazole and phenothiazines. Check rectal T° with a low-reading ther- mometer. Insulation and passive rewarming are usually adequate. Hyperthermia (p260) May occur with amphetamines, cocaine, ecstasy, MAOIs, sympathomimetics and theophylline. Convulsions and rhabdomyolysis are common. Active cooling, chlorpromazine and possibly dantrolene are needed. Get expert help. Blisters Prolonged immobility (eg due to tricyclics and barbiturates) risks pressure areas. Treat blisters like minor burns. Immobility may cause rhabdomyolysis (leading to renal failure), nerve palsies and compartment syndrome: if suspected obtain urgent orthopaedic advice about measuring compartment pressures. Urinary retention Common in coma, especially after tricyclic poisoning. Suprapubic pressure often stimulates reflex bladder emptying. Catheterization is sometimes needed to empty the bladder or to measure urine output. P.178
Reducing absorption of poison Background information If a poison has been swallowed it is logical to try to remove it and prevent absorption from the gut. Possible measures include gastric lavage, induced emesis (eg with ipecacuanha), oral adsorbents (especially activated charcoal) and whole-bowel irrigation. However, none of these can be recommended routinely. They may cause significant morbidity and there is very little evidence that they improve the outcome of poisoning. Gastric lavage This does not empty the stomach of solids and may force gastric contents through the pylorus into the small bowel. It may cause hypoxia, aspiration pneumonia and occasionally oesophageal perforation. Gastric lavage >1h after overdose is ineffective in ↓absorption of poisons. However, it may possibly be helpful for longer in patients in deep coma, especially with tricyclic antidepressants or opioid drugs, which delay gastric emptying. No study has shown that gastric lavage ↓mortality from poisoning. It does not deter patients from further episodes of self-poisoning. Practical advice on use of gastric lavage Only consider this if the patient has taken a life-threatening amount of poison within the previous 1h or is deeply unconscious because of poisoning. It must only be performed if there is a strong cough reflex or the airway is protected by a cuffed tracheal tube. Do not use lavage for poisoning with corrosives (risk of perforation) or petrol/paraffin compounds (risk of pneumonitis), except rarely in severe poisoning on specialist advice.

  • Before starting gastric lavage, check that powerful suction is immediately available.
  • Elevate the foot of the trolley and place the patient in the left lateral position.
  • Give O2 via nasal cannulae. Monitor ECG
  • Lubricate large disposable stomach tube (36 or 40FG) and pass it through the mouth into the stomach: confirm position by aspirating gastric contents or blowing air down the tube while listening over the stomach.
  • Aspirate gastric contents and keep labelled sample for later analysis if necessary.
  • Perform lavage by pouring 300mL aliquots of tepid tap water down the tube and siphoning it back, while massaging over stomach to help dislodge tablet debris.
  • Continue until the effluent is clear.
  • Consider leaving activated charcoal (50g) in the stomach.
  • While withdrawing the tube, occlude it between the fingers to prevent aspiration of fluid from the tube.

Salt and ipecacuanha-induced emesis Never use either of these: Ipecacuanha has been widely used, but several studies have shown that it does not ↓drug absorption. It occasionally causes prolonged vomiting, drowsiness and aspiration pneumonia. There is now no indication for using ipecac. Salt solutions may cause fatal hypernatraemia and must never be used as an emetic. P.179
Activated charcoal Given within 1h, this ↓absorption of therapeutic doses of many drugs, but there is little evidence of clinical benefit after overdosage. Charcoal ↓half-life of some drugs (eg digoxin) which undergo entero-hepatic recycling. However, charcoal is messy, unpleasant to take and often causes vomiting. Aspiration into the lungs can result in fatal pneumonitis, but this is rare. Various formulations of activated charcoal are available. Actidose Aqua Advance® is a new product which is easier to use and less unpalatable than some of the other formulations. Carbomix® may cause severe constipation, especially if given in repeated doses. Do not give activated charcoal for substances which do not bind to it. These include: iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, organophosphates, petroleum distillates and strong acids and alkalis. Charcoal is most likely to be useful for poisons which are toxic in small quantities (eg tricyclic antidepressants and theophylline derivatives). If a dangerous overdose has been taken in the previous 1h, give charcoal (PO or via an orogastric tube: adults 50g; children 25g). Charcoal may be effective for >1h for sustained release formulations or drugs which delay gastric emptying (eg tricyclic antidepressants and opioids). Obtain expert advice before giving charcoal in repeated doses, which are only helpful in life-threatening poisoning with a few drugs (eg carbemazepine, dapsone, digoxin, phenobarbitone, quinine, theophylline and possibly salicylate, and a few other drugs rarely taken in overdose). Whole-bowel irrigation The aim of this is to empty the bowel rapidly of solid contents by giving fluid down an NG tube until the rectal effluent becomes clear. The value of whole-bowel irrigation in poisoning is uncertain, but it may be useful for sustained-release drug formulations or for poisons such as iron or lithium which are not absorbed by activated charcoal. It has also been used to remove packets of cocaine from bodypackers and button batteries from children. Whole-bowel irrigation should be achieved with bowel cleansing solutions of polyethylene glycol and electrolytes (eg KleanPrep®), rather than with normal saline, which may cause fluid overload and hypokalaemia. Nausea, vomiting, abdominal pain and electrolyte disturbances may occur. Whole-bowel irrigation is rarely needed—only use it on expert advice. Use bowel cleansing solution (eg Klean-Prep®) at 2L/h in adults (500mL/h in small children) for 2h, or occasionally for longer. Activated charcoal may be given by NG tube, if appropriate, before whole-bowel irrigation is started. Continue this irrigation until the rectal effluent is clear. Monitor U&E and renal function. P.180
Antidotes for poisons The provision of supportive care is essential in all patients. Antidotes are available for only a few drugs and poisons and are not always necessary. More information is available from reference books, TOXBASE and Poisons Information Centres (p175).

Poison Antidote Notes
ß-blockers Glucagon, atropine p192
Carbon monoxide O2 p202
Cyanide Sodium nitrite, sodium thiosulphate, dicobalt edetate p201
Digoxin Digibind† p193
Ethylene glycol Ethanol, fomepizole† p197
Iron salts Desferrioxamine p195
Methanol Ethanol, fomepizole† p196
Opioids Naloxone p182
Organophosphates Atropine, pralidoxime† p200
Paracetamol N-acetylcysteine, methionine p184
Sulphonylureas Glucose, octreotide p191
Warfarin Vitamin K, clotting factors, FFP
Adder bites Zagreb antivenom p402
Foreign snakes Antivenoms† Specialist advice

Antidotes are also available for arsenic, lead, mercury, thallium and other metals: specialist advice is essential. Some antidotes (marked†) are very rarely needed: get expert advice about when and how to use these antidotes and where to obtain them. Note that although frequently referred to as an ‘antidote’, flumazenil is not licensed for benzodiazepine poisoning. Flumazenil is useful in reversing the sedative effects of benzodiazepines in anaesthetic and diagnostic procedures. Considerable problems may result when it is used following suspected benzodiazepine overdose (see p190). Increasing elimination of poisons The vast majority of poisoned patients recover with supportive care, plus appropriate antidotes if necessary. Active removal of absorbed poison is only needed in special circumstances. Alkalinization of the urine is useful in salicylate poisoning (p183), but forced alkaline diuresis is no longer recommended. Haemodialysis is occasionally helpful for severe poisoning with salicylates, ethylene glycol, methanol, lithium, phenobarbitone and chlorates. Haemoperfusion is rarely needed, but might be helpful in severe poisoning with barbiturates, chloral hydrate or theophylline: specialist advice is essential. P.181
Admission and psychiatric assessment after poisoning Adults Patients who are seriously poisoned need admission to a medical ward, or if appropriate, to ITU. However, most patients who take overdoses suffer no serious ill effects and may be treated satisfactorily on an A&E observation ward or may be admitted to a medical ward, depending on local policies. Even if there is no risk of toxicity, admission overnight is often helpful since it provides a ‘cooling off’ period for the patient to get away from the situation that precipitated the overdose. This should allow a more rational appraisal of the problems and may ↓risk of further self-poisoning. The causes of every episode of self-poisoning and self-injury must be considered. A patient who seems suicidal must be observed carefully in A&E and on the ward, because of the risk of further self-harm. Children with poisoning Serious poisoning is uncommon in children. Often a child appears well, but has possibly taken a toxic compound, although the quantity is usually unknown. Admit such children to a paediatric ward for observation: they can often be discharged after a few hours if no toxic effects occur. A child may be discharged home directly from A&E if the substance taken is known to be non-toxic. The health visitor may usefully visit the home to advise about poisoning prevention. In children >6yrs consider the possibility of deliberate self-poisoning and the need for assessment by a child psychiatrist. P.182
Opioid poisoning The opioids include morphine, diamorphine (heroin), pethidine, codeine, dihydrocodeine, dextropropoxyphene, buprenorphine, nalbuphine, methadone, diphenoxylate, loperamide and related drugs. These are used as analgesics (sometimes in combination with paracetamol, as in co-dydramol and co-proxamol), and also as cough suppressants and anti-diarrhoeal agents. Acute opioid poisoning often occurs in addicts, who may have venepuncture marks and thrombosed veins (and a high risk of HIV and hepatitis infection). Clinical features Opioid poisoning causes coma, pinpoint pupils, ↓respiratory rate and sometimes cyanosis, apnoea, convulsions and hypotension. Hypertension may occur in pentazocine poisoning. Non-cardiogenic pulmonary oedema may result from ‘main-lining’ heroin or other opioids. Respiratory depression may cause death within 1hr of an opioid overdosage. However, delayed respiratory depression can occur in poisoning with co-phenotrope (diphenoxylate and atropine), in which the opioid effects usually predominate over atropine toxicity. Delayed toxicity may occur with slow-release formulations of drugs and also with methadone which has a very long duration of action. Treatment Clear and maintain the airway. If breathing appears inadequate ventilate with a bag and mask or tracheal tube. Naloxone is the specific antagonist for opioids and reverses coma and respiratory depression if given in sufficient dosage. It is only partially effective against buprenorphine. Naloxone may be used as a therapeutic trial in suspected opioid poisoning: record the coma level, pupil size and respiratory rate and check for any response. The initial dose of naloxone for adults is 0.8-2mg IV, with repeated doses of 0.8-2mg IV at 2-3min intervals if necessary. For children, give 10micrograms/kg initially, repeated as necessary. If venous access is not available give naloxone IM. Naloxone has a short duration of action: coma and respiratory depression often recur. Careful observation is essential. Further naloxone is usually needed and may be given IM or by IV infusion, the dose adjusted depending on the response (occasionally as much as 75mg in 24h). Observation is needed for at least 6hrs after the last dose of naloxone. Dissuade or prevent patients at risk of respiratory depression from leaving hospital: rather than reversing an opioid fully it may be preferable to keep a patient sedated but safe by constant observation and titration of naloxone dosage. A patient who insists on leaving earlier could be given a dose of naloxone IM, but may still be at risk of developing fatal respiratory depression. In opioid addicts naloxone may precipitate a withdrawal syndrome with abdominal cramps, nausea and diarrhoea, but these usually settle within 2hrs. Ventricular tachyarrhythmias occur occasionally. Consider activated charcoal (p179) if a sustained release opioid formulation has been taken. P.183
Salicylate poisoning Standard aspirin tablets contain 300mg acetylsalicylic acid. Ingestion of 150mg/kg body weight usually produces mild toxicity; 500mg/kg will cause severe and possibly fatal poisoning. Poisoning can result from absorption of salicylate ointment through the skin. Clinical features Commonly vomiting, tinnitus, deafness, sweating, vasodilatation, hyper-ventilation and dehydration. Hypokalaemia may occur. Severe poisoning may produce confusion, coma and convulsions. Children are particularly prone to develop hyperpyrexia and hypoglycaemia. Rare features include non-cardiogenic pulmonary oedema, cerebral oedema and renal failure. Metabolic and acid-base disturbances These may be complex: adults usually have a mixed metabolic acidosis and respiratory alkalosis, but the respiratory effects predominate. In small children and a few adults, acidosis predominates and is often associated with confusion or coma. Management Gastric lavage if an adult has ingested >4.5 g (15 standard tablets) in the previous 1hr. After ingestion of >4.5 g (or 2g in a child) give 50g activated charcoal (25g in a child) to ↓absorption and ↑elimination of salicylate. Measure plasma salicylate concentration (and repeat after a few hrs if further symptoms occur, since salicylate level may ↑ due to continuing absorption). Check U&E, glucose and ABG if there are CNS features or signs of severe poisoning. A second dose of activated charcoal may be useful if the plasma salicylate increases, suggesting delayed gastic emptying, or if enteric coated tablets have been taken. Mild poisoning Children with plasma salicylate <350mg/litre (2.5mmol/L) and adults with <450mg/L (3.3mmol/litre) usually need only ↑oral fluids. Moderate poisoning Children with salicylate >350mg/L and adults with >450mg/L need IV fluids to correct dehydration and ↑elimination of salicylate: sodium bicarbonate 1.26% (adults 500mL hrly for 3h) corrects any metabolic acidosis and alkalinises the urine (which is much more effective than a massive diuresis in ↑salicylate excretion). Urine pH should be >7.5, ideally 8.0-8.5. Repeat salicylate level, check U&E and add K+ as necessary. Severe poisoning CNS features, acidosis or salicylate >700mg/L (5.1mmol/L) are associated with significant mortality. Get expert advice (p175) and consider urgent referral for haemodialysis. Correct acidosis and give repeated activated charcoal via NG tube. In life-threatening poisoning with coma and extreme hyperventilation: paralysis and IPPV may help while haemodialysis removes salicylate and corrects the electrolyte disturbances. Give additional glucose IV, since brain glucose levels may be low despite normal blood glucose concentrations. Do not use forced diuresis: not only is it ineffective, but it may cause pulmonary oedema. P.184
Paracetamol poisoning 1 Paracetamol (‘acetaminophen’ in USA) may cause severe liver damage if 12g (24 tablets) or >150mg paracetamol/kg body weight are taken. A metabolite of paracetamol binds glutathione in the liver and causes hepatic necrosis when stores of glutathione are exhausted. Renal tubular necrosis may also occur, usually in association with liver damage. Alcoholics and patients on drugs which induce hepatic enzymes are at greater risk of toxicity, because of ↑production of the toxic metabolite of paracetamol. Patients with malnutrition may have ↓glutathione stores and be more susceptible to paracetamol toxicity. Clinical features Nausea, vomiting and abdominal discomfort are common within a few hrs. In untreated patients developing liver damage, vomiting continues beyond 12h and there is pain and tenderness over the liver (from 24h), jaundice (at 2-4days) and sometimes coma from hypoglycaemia (at 1-3days) and hepatic encephalopathy (from 3-5days). Loin pain, haematuria and proteinuria suggest incipient renal failure. Hepatic failure causes hyperventilation from metabolic acidosis and bleeding from coagulation abnormalities. In fatal cases there is often cerebral oedema, septicaemia and DIC. However, many patients survive severe liver damage and recover completely. LFTs are normal until at least 18h after the overdose. The most sensitive lab evidence of liver damage is often a prolonged INR (from 24h after overdose). Liver enzymes (ALT and AST) may reach >10,000 units/L at 3-4days. Bilirubin rises more slowly (max at ≈5 days). Paracetamol antidotes N-acetylcysteine (NAC, ‘Parvolex’®) is given by IV infusion in 5% dextrose. Initial dose is 150mg NAC/kg body weight in 200mL dextrose over 15mins, then 50mg/kg in 500mL over 4h, then 100mg/kg in 1000mL over 16h. NAC occasionally causes side effects: erythema and urticaria localised to the area of the infusion site or more generalized rashes, itching, nausea, angioedema, bronchospasm and rarely hypotension or hypertension. Side effects usually occur in the first hour of treatment and appear to be dose related. If they occur, stop the infusion and give an antihistamine (eg chlorphenamine 10mg IV over 1min). When the symptoms have settled, NAC can usually be resumed at the lowest infusion rate (100mg/kg body weight over 16h). Methionine is given orally as capsules or tablets, 2.5g every 4h to a total of 10g. Methionine has no significant adverse effects. It is less effective than NAC in patients who are vomiting or who present >8h after ingestion. Methionine may be ineffective in patients treated with activated charcoal. Interference with blood glucose analysis High concentrations of paracetamol can affect some lab methods for measuring glucose and cause apparent hyperglycaemia when the blood glucose is normal. Management of paracetamol poisoning The time interval since ingestion is crucial in interpreting paracetamol concentrations and assessing the need for specific treatment. Record the time of ingestion as accurately as possible. When taking blood for paracetamol levels record the precise time in the notes and on the blood bottles and forms. Start treatment if there is doubt about the time of ingestion or if tablets have been taken at different times. If in doubt treat immediately. Treatment with N-acetylcysteine (NAC) or methionine within 8h of an overdose is very effective in preventing liver and renal damage. Later treatment is less effective, but still worthwhile. P.185
P.186
Paracetamol poisoning 2 Patients who present late are more likely to be severely poisoned than those who present soon after ingestion. The treatment graph below may be unreliable at >15h, because of insufficient data on untreated patients. Management within 4h of ingestion In an adult, consider activated charcoal (50g) if >12g paracetamol has been taken in the previous 1hr. Take blood at 4h from ingestion and use graph (below) to assess risk of liver damage: for most patients use line A; for high risk patients (alcoholics, those on anticonvulsants, rifampicin) use line B. If the result is above the relevant line, give IV N-acetylcysteine (NAC) or oral methionine (for doses see p184). Management at 4-8h from ingestion Measure paracetamol and use the graph to assess risk of liver damage: for most patients use line A, for high risk patients use line B. If above relevant line or only just below it, give IV NAC or oral methionine (for doses see p184). Treatment is most effective if started before 8h: start it at once if paracetamol level is not available by this time and >150mg/kg has been taken. Patients treated with NAC or methionine within 8h of an overdose should be medically fit for discharge at the end of the treatment course. Management at 8-15h from ingestion Urgent action is needed: start treatment with IV NAC immediately if >150mg/kg or 12g paracetamol have been taken. Measure plasma paracetamol and use the graph to assess the risk of liver damage: for most patients use line A; for high risk patients (alcoholics, anticonvulsants, rifampicin) use line B. If the paracetamol level is below the appropriate line and patient is asymptomatic stop NAC treatment. Continue NAC if level is above the relevant line, if there is doubt about the time of ingestion or if the patient has nausea or vomiting. At the end of NAC treatment check INR and plasma creatinine: if these are normal and the patient asymptomatic he/she is medically fit for discharge. Management at 15-24h from ingestion Urgent action is needed: give IV NAC immediately if >150 mg/kg or >12g paracetamol have been taken. Measure plasma paracetamol, creatinine and INR. If at 24h after ingestion a patient is asymptomatic, with normal INR, normal creatinine and plasma paracetamol <10mg/L he/she may be discharged. Other patients need continuing monitoring and possibly further treatment with NAC. Management at >24h from ingestion Measure paracetamol, LFTs, U&E, creatinine, INR and ABG. Start treatment with IV NAC if >150mg/kg or 12g paracetamol have been taken, investigations are abnormal or patient is symptomatic. Seek expert advice. Children Serious paracetamol poisoning is uncommon in children. Young children metabolize paracetamol differently from adults and have a ↓risk of hepatotoxicity. However, use the same treatment guidelines as for adults, but with smaller volumes of fluid for IV infusion of NAC. Paracetamol poisoning in pregnancy Follow the same treatment as for non-pregnant patients. NAC and methionine do not seem to carry any risk to the foetus and may protect the foetal liver from damage. Paracetamol overdosage does not appear to cause teratogenic effects. P.187

Figure. Paracetamol treatment graph

Normal treatment line A. High risk treatment line B (for alcoholics, malnourished patients, patients with HIV and patients on anticonvulsants, St John’s wort or rifampicin). Note If in doubt about the time of the overdose, or if the plasma paracetamol is only just below the relevant treatment line, it is best to start treatment as soon as possible. NB Before using the paracetamol treatment graph check whether the lab reports paracetamol levels in mg/L or mmol/L. P.188
Tricyclic antidepressant poisoning Anticholinergic poisoning is most often caused by overdosage of tricyclic antidepressants such as amitriptyline, imipramine or dothiepin, but may result from other drugs (eg procyclidine and atropine—the latter is also present in Atropa belladonna, ‘deadly nightshade’). Clinical features Common features are tachycardia, dry skin, dry mouth, dilated pupils, urinary retention, ataxia, jerky limb movements and drowsiness leading to coma. Unconscious patients often have a divergent squint, ↑muscle tone and reflexes, myoclonus and extensor plantar responses. The pupils may be dilated and unreactive. In deep coma there may be muscle flaccidity with no detectable reflexes and respiratory depression requiring IPPV. Convulsions occur in ≈10% of unconscious patients and may precipitate cardiac arrest. Patients recovering from coma often suffer delirium and hallucinations and have jerky limb movements and severe dysarthria. ECG changes Sinus tachycardia is usual, but as the severity of poisoning↑ the PR interval and QRS duration ↑. These changes may help confirm the clinical diagnosis of tricyclic poisoning in an unconscious patient. The P wave may be superimposed on the preceding T wave, giving the appearance of VT when the rhythm is actually sinus tachycardia with prolonged conduction. In very severe poisoning, ventricular arrhythmias and bradycardia may occur, especially in patients who are hypoxic. Death may result from cardio-respiratory depression and acidosis. Management

  • Clear airway, intubate if necessary, maintain ventilation and give supportive treatment/nursing care.
  • Observe continuously, in view of the potential for rapid deterioration.
  • Monitor ECG and check ABG in unconscious or post-ictal patients.
  • Give activated charcoal by mouth or gastric tube if more than 4mg/kg has been taken within 1hr and the airway is safe or can be protected. Consider further doses of charcoal if a sustained release drug has been taken. Single brief fits do not need anticonvulsant treatment, but give lorazepam or diazepam IV if fits are frequent or prolonged.
  • Most cardiac arrhythmias occur in unconscious patients within a few hrs of overdose. Arrhythmias are best treated by correction of hypoxia and acidosis. 8.4% sodium bicarbonate (adult: 50-100mL; child: 1mL/kg) may produce a dramatic improvement in cardiac rhythm and output (apparently by altering protein binding and ↓ active free tricyclic drug). Further doses of bicarbonate may be needed, depending upon the clinical response and the ECG.
  • Avoid antiarrhythmic drugs. If arrhythmias are unresponsive to bicarbonate, discuss with a poisons specialist (p175).
  • Correct hypotension by elevating the foot of the trolley and giving IV fluids. Glucagon 1mg IV (repeated if necessary) may help in severe hypotension. Dopamine (2-10micrograms/kg) is occasionally indicated for unresponsive hypotension on specialist advice.
  • Do not use physostigmine or flumazenil (p190), which may precipitate fits.
  • Unconscious patients usually improve over 12h and regain consciousness within 36h. Delirium and hallucinations may persist for 2-3days and require sedation with diazepam in large doses (often 20-30mg PO every 2h initially).

P.189

Figure. ECG changes in tricyclic antidepressant poisoning

P.190
Benzodiazepine poisoning Benzodiazepine drugs (eg diazepam, nitrazepam and temazepam), rarely cause serious poisoning when taken alone in overdosage. However, they potentiate the effects of other CNS depressants such as alcohol, tricyclic antidepressants and barbiturates. Clinical features Drowsiness, dizziness, ataxia, dysarthria. Rarely, coma, respiratory depression, mild hypotension. Fatal poisoning is unusual, but may occur from respiratory depression in elderly patients and those with COPD. Management Clear the airway and maintain ventilation if necessary. Provide supportive care. Gastric lavage and activated charcoal are not indicated if only a benzodiazepine has been taken. Many benzodiazepines have long-acting metabolites which may affect driving and other motor skills for several days or even wks after an overdose: give appropriate warnings about this. Flumazenil is a specific benzodiazepine antagonist, but is not officially approved in the UK for treating overdosage. It reverses the effects of benzodiazepines within 1 min, but has a short duration of action (<1h)—as a result, toxic effects often recur. Flumazenil can cause convulsions and cardiac arrhythmias and may precipitate a withdrawal syndrome in patients dependent on benzodiazepines. It is particularly dangerous in patients with combined benzodiazepine and tricyclic antidepressant poisoning, in whom it may cause convulsions and cardiac arrest. Flumazenil may occasionally be used by experts managing very severe benzodiazepine poisoning, but there is no place for its use by the non-specialist. Clomethiazole poisoning Clomethiazole (Heminevrin®) overdosage may cause coma, respiratory depression, ↓muscle tone, hypotension and hypothermia. Excessive salivation and a characteristic smell of clomethiazole on the breath are often noticeable. Treat supportively. IPPV may be necessary. Phenothiazine poisoning The phenothiazines (eg chlorpromazine), butyrophenones (eg haloperidol) and related drugs are used as antipsychotic drugs and antiemetics. In overdosage they may cause drowsiness, coma, hypotension and hypothermia. Deep coma and respiratory depression are uncommon. Some conscious patients suffer dystonic reactions with oculogyric crises and muscle spasms causing torticollis or opisthotonus. Convulsions may occur. ECG changes of prolonged PR, QRS and ST intervals and arrhythmias are seen particularly with thioridazine poisoning. Treat supportively. Activated charcoal may be helpful. If cardiac arrhythmias occur, correct hypoxia, acidosis and electrolyte abnormalities before giving any antiarrhythmic drug. Treat dystonic reactions with procyclidine (5mg IV or 5-10mg IM) or benztropine mesylate (1-2mg IV or IM), repeated if symptoms recur. P.191
Barbiturate poisoning Now uncommon, except in drug addicts. Overdosage with phenobarbitone is seen occasionally. Barbiturate poisoning may cause coma, respiratory depression, hypotension and hypothermia. There are no specific neurological signs. Skin blisters and rhabdomyolysis may result from prolonged immobility. Treat supportively, with IPPV if necessary. Repeated doses of activated charcoal may help to remove barbiturates. Very rarely, charcoal haemoperfusion is indicated in some patients with deep and prolonged coma and respiratory complications. Lithium poisoning Clinical features Often due to therapeutic overdosage or drug interactions (eg with diuretics or NSAIDs) rather than deliberate self-harm. Symptoms may start up to 24hrs after an overdose, especially with slow-release tablets. Nausea, vomiting and diarrhoea are followed by tremor, ataxia, confusion, ↑muscle tone and clonus. In severe cases there may be convulsions, coma and renal failure. Lithium-induced nephrogenic diabetes insipidus may complicate treatment. Investigations Measure U&E and lithium (plain tube, not lithium heparin!). Therapeutic lithium levels are <1.2 mmol/L. Toxic effects are often seen at >1.5mmol/L. Soon after a large overdose, higher levels may occur with little clinical effects, before lithium is distributed to tissues. Management Activated charcoal does not absorb lithium. Gastric lavage is indicated within 1hr of a single large overdose, except for slow-release tablets, which are too large to pass up a gastric tube. Whole-bowel irrigation (p179) may be considered for slow-release tablets: discuss this with a poisons specialist (p175). Observe all patients for at least 24hrs. Encourage oral fluids in conscious patients. Use standard supportive measures and control convulsions with diazepam. Forced diuresis is contraindicated. Haemodialysis is the best treatment in severe poisoning, but often has to be repeated because of rebound of lithium from tissue stores. Sulphonylurea poisoning Sulphonylurea drugs are used to treat non-insulin-dependent diabetes. Accidental or deliberate overdosage causes hypoglycaemia, which may recur over several days after long-acting drugs such as chlorpropamide or glibenclamide. Check blood glucose and U&E. Correct hypoglycaemia with oral or IV glucose (p147). Observe for at least 24h (72h for long-acting drugs) and check BMG hourly. To prevent recurrent hypoglycaemia give 10% dextrose IV infusion; in severe cases 20% dextrose may be needed, via central line because of venous irritation. Hypokalaemia may occur. Check U&E and add potassium as needed. In severe poisoning get expert advice (p175) and consider octreotide which blocks pancreatic insulin release (unlicensed indication): initial dose for adults 50 micrograms SC or IV. P.192
Beta-blocker poisoning Clinical features Overdosage with ß-adrenoceptor blocking drugs (propranolol, oxprenolol, atenolol, labetolol, sotalol) may cause rapid and severe toxicity with hypotension and cardiogenic shock. There is usually a sinus bradycardia, but sometimes the heart rate remains normal. Coma, convulsions and cardiac arrest may occur. ECG changes include marked QRS prolongation and ST and T wave abnormalities. Sotalol can cause a prolonged QTc and VT, sometimes with torsades de pointes. Propranolol may cause bronchospasm in asthmatics and hypoglycaemia in children. Management Monitor ECG, heart rate and BP. Obtain reliable venous access. Check U&E and blood glucose. Consider activated charcoal (p179). Bradycardia and hypotension may respond to atropine (1-2mg for adult; 0.02mg/kg for child), but this is often ineffective. Glucagon is the best treatment for severe cardiotoxicity and seems to work by activating myocardial adenylcyclase in a way not blocked by ß-blockade. Glucagon 5-10mg IV (50-150micrograms/kg for child) usually produces a dramatic improvement in pulse and BP, with return of cardiac output and consciousness. Glucagon may cause sudden vomiting, which must be expected and the patient positioned appropriately. In severe poisoning, the benefits of glucagon may be transient and further doses or an infusion are needed (4mg/h, reducing gradually). Some patients need a total of 50mg of glucagon. If glucagon is not available or is ineffective, use isoprenaline (5-10micrograms/min) or dobutamine (2.5-10micrograms/kg/min), increasing the dose as necessary, depending upon the response. Discuss with Poisons Information Service (p175) in severe poisoning. Cardiac pacing may be needed for bradycardia but is not always effective. Occasionally, circulatory support has to be provided by prolonged cardiac massage, an intra-aortic balloon pump or extracorporeal cardiac bypass while supplies of glucagon are obtained or the ß-blocker is metabolized. Calcium antagonist poisoning Clinical features Poisoning with verapamil, nifedipine, diltiazem or other calcium-channel blockers is rare, but may be fatal. Nausea, vomiting, dizziness and confusion may occur. Bradycardia and AV block may lead to AV dissociation, with hypotension and cardiac arrest (especially in patients taking ß-adrenergic blockers). Metabolic acidosis, hyperkalaemia and hyperglycaemia may occur. Management Provide supportive treatment. Monitor ECG and BP. Obtain venous access. Give activated charcoal. Check U&E, glucose, calcium. Give atropine (1-2mg, child 0.02mg/kg) for symptomatic bradycardia. Get expert help. Pacing may be needed. Calcium gluconate (10-20mL of 10% slowly IV, observing ECG) may reverse prolonged intra-cardiac conduction. Glucagon may help, as in ß-blocker poisoning (see above). Inotropic support with dobutamine or epinephrine (adrenaline) may be needed to maintain cardiac output. P.193
ACE inhibitor poisoning Overdosage with angiotensin converting enzyme (ACE) inhibitors (eg captopril, enalapril, lisinopril) may cause drowsiness, hypotension, hyperkalaemia and rarely, renal failure. Monitor BP and ECG. Give IV saline if BP low. Check U&E. Consider activated charcoal (p179). Digoxin poisoning Toxicity from the therapeutic use of digoxin is relatively common. Acute poisoning is rare, but may be fatal. Similar effects occur with digitoxin and very rarely with plants containing cardiac glycosides (foxglove, oleander and yew). Clinical features Nausea, vomiting, malaise, delirium, xanthopsia (yellow flashes or discolouration of vision). Acute poisoning usually causes bradycardia with PR and QRS prolongation. There may be AV block, AV dissociation and escape rhythms, sometimes with ventricular ectopics or VT. Hyperkalaemia occurs and in severe cases metabolic acidosis due to hypotension and ↓tissue perfusion. Management Provide supportive treatment. Monitor ECG and BP. Obtain venous access. Consider repeated activated charcoal to ↓absorption and prevent entero-hepatic recycling of digoxin (p179). Measure U&E, plasma digoxin and ABG in severe poisoning. Patients who are severely poisoned require expert attention. Correct metabolic acidosis with sodium bicarbonate. Treat hyperkalaemia >6mmol/L (p158). Bradycardia and AV block often respond to atropine IV total 1-2mg (child 0.02mg/kg). Cardiac pacing is not always effective and a high voltage is often needed for capture. VT may respond to lidocaine or a ß-blocker. Severe poisoning is best treated with digoxin antibodies (Digibind®), which rapidly correct arrhythmias and hyperkalaemia. Digibind is expensive and rarely needed, so is not stocked in many hospitals: Poisons Information Services (p175) can advise about emergency supplies and the dose required for the patient’s body weight and plasma digoxin concentration or the quantity taken. P.194
Theophylline poisoning Theophylline and aminophylline can cause fatal poisoning. Many preparations are slow-release and may not produce serious toxicity until 12-24h after ingestion. Careful observation is essential. Features Nausea, vomiting (often severe and not helped by anti-emetics), abdominal pain, haematemesis, restlessness, ↑muscle tone, ↑reflexes, headache, convulsions. Coma, hyperventilation, hyperpyrexia and rhabdomyolysis may occur. Sinus tachycardia may be followed by supraventricular and ventricular arrhythmias and VF. BP may initially↑, but later ↓ in severe poisoning. Complex metabolic disturbances include a respiratory alkalosis followed by metabolic acidosis, hyperglycaemia and severe hypokalaemia. Management

  • Treat supportively.
  • Monitor ECG, heart rate and BP.
  • Obtain venous access and measure U&E, glucose, ABG, plasma theophylline (repeated after a few hrs). Repeat K+ hrly if patient is symptomatic, since early correction of hypokalaemia may prevent dangerous arrhythmias. Correct hypokalaemia with K+ (large amounts may be needed).
  • Perform gastric lavage if <1h since ingestion. Give repeated activated charcoal (p179), by NG tube if necessary.
  • Intractable vomiting may respond to ondansetron (8mg slowly IV in adult).
  • GI bleeding may require transfusion and ranitidine (but not cimetidine, which slows metabolism of theophylline).
  • Tachycardia with an adequate cardiac output should be observed, but not treated. Non-selective ß-blockers (eg propranolol) may help severe tachyarrhythmias and hypokalaemia, but cause bronchospasm in asthmatics. Lidocaine and mexiletine may precipitate fits, so disopyramide is preferable for ventricular arrhythmias.
  • Control convulsions with diazepam. Paralyse, intubate and provide IPPV if the airway is at risk from coma, fits and vomiting.
  • Charcoal haemoperfusion may be needed in severe poisoning, especially if oral or NG activated charcoal is impracticable because of vomiting. Serious hyperkalaemia may occur during recovery from theophylline poisoning if large amounts of potassium were given earlier.

Salbutamol poisoning Poisoning with ß2-agonists (eg salbutamol, terbutaline) may cause vomiting, agitation, tremor, tachycardia, palpitations, hypokalaemia and hypertension. Rarely, there may be hallucinations, hyperglycaemia, ventricular tachyarrhythmias, myocardial ischaemia and convulsions. Treat supportively:

  • correct hypokalaemia by infusion of K+
  • monitor ECG and BP
  • activated charcoal may ↓drug absorption
  • do not treat tachycardia if there is an adequate cardiac output. Propranolol may help severe tachyarrhythmias and hypokalaemia, but can precipitate bronchospasm in asthmatics.

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Iron poisoning Small children often eat iron tablets, many of which resemble sweets. Serious poisoning is uncommon, but fatalities occur. Note that iron is present in some weed/seed preparations. Different preparations contain the equivalent of 35-110mg of elemental iron per tablet, sometimes in slow-release form. Serious toxicity is unlikely unless >60mg elemental iron/kg body weight has been taken. The estimated lethal dose is ap;150-300mg/kg. Features In the first few hours after ingestion nausea, vomiting, diarrhoea and abdominal pain are common. Vomit and stools are often grey or black and may contain blood. ↑blood sugar and ↑WCC occur. Most patients do not develop further features. In severe poisoning, early effects include haematemesis, drowsiness, convulsions, coma, metabolic acidosis and shock. Early symptoms settle after 6-12h, but a few patients then deteriorate 24-48h after ingestion, with shock, hypoglycaemia, jaundice, metabolic acidosis, hepatic encephalopathy, renal failure and occasionally bowel infarction. Survivors may develop gastric strictures or pyloric obstruction 2-5wks after the overdose. Management

  • check serum iron, FBC, glucose, and also ABG in severe poisoning.
  • perform gastric lavage if >20mg elemental iron/kg body weight has been taken in the previous 1h. Do not give charcoal, which does not absorb iron. Iron tablets are radio-opaque and can be counted on a plain abdominal X-ray film. Whole-bowel irrigation (p179) may be useful if many tablets remain in the gut, especially with slow-release formulations.
  • use supportive measures if required.
  • obtain expert advice in serious poisoning. Coma and shock indicate severe poisoning needing immediate treatment with desferrioxamine by IV infusion (15mg/kg/hr, max 80mg/kg in 24h). Desferrioxamine should also be given if the serum iron exceeds the expected total iron binding capacity (about 54-75micromol/L): measurement of total iron binding capacity may give misleading results after iron poisoning. Desferrioxamine causes hypotension if infused too rapidly and can produce rashes and, rarely, anaphylaxis, pulmonary oedema or ARDS. The iron-desferrioxamine complex makes the urine orange or red, which confirms that free iron has been bound and that desferrioxamine was required. ↓desferrioxamine dosage when there is clinical improvement and serum iron is less than the expected total iron binding capacity.
  • patients who have developed no symptoms by 6h after a suspected iron overdose have probably not ingested toxic amounts and may be discharged.
  • pregnancy does not alter the treatment needed for iron poisoning: use desferrioxamine if indicated.

P.196
Ethanol poisoning Features Overdosage of ethanol (ethyl alcohol or ‘alcohol’) is very common. Alcohol potentiates the CNS depressant effects of many drugs. It initially causes disinhibition and later ataxia, dizziness, dysarthria and drowsiness. In severe poisoning, there may be coma with respiratory depression, hypotension, hypothermia and a metabolic acidosis. Hypoglycaemia is a particular problem in children and may occur after some hrs. Death may result from respiratory failure or aspiration of vomit. For an adult, the fatal dose of ethanol alone is ≈300-500mL absolute alcohol: whisky and gin usually contain 40-50% ethanol. Do not assume that ↓GCS is solely due to alcohol until other causes have been excluded. Rarely, alcohol intoxication causes lactic acidosis (especially in patients with liver disease or taking biguanide hypoglycaemic drugs) or ketoacidosis (due to dehydration and hypoglycaemia in alcoholics)—see p595. Treatment

  • maintain a clear airway and adequate ventilation.
  • check blood glucose every 1-2h in severe poisoning.
  • emergency measurement of blood ethanol is rarely helpful.
  • correct hypoglycaemia with glucose, not with glucagon.
  • look for signs of injury, especially head injury.
  • gastric lavage and activated charcoal are ineffective in ethanol intoxication.
  • do not give fructose.

Methanol poisoning Methanol is used as a solvent and in antifreeze. Ingestion of >60mL of methanol (in adults) may cause fatal poisoning, the toxic effects being due to the metabolites formaldehyde and formic acid. Methylated spirits is a mixture of ethanol and water with only ≈5% methanol: toxicity is almost entirely due to ethanol. Clinical features Methanol initially causes only mild transient drowsiness. Serious toxicity develops after a latent period of 8-36h with vomiting, abdominal pain, headache, dizziness, blurring of vision and drowsiness leading to coma. There is a severe metabolic acidosis, hyperglycaemia and ↑serum amylase. Survivors may be blind due to optic nerve damage and develop Parkinsonian problems. Management

  • provide gastric lavage if <1h since ingestion. Do not give charcoal.
  • measure ABG, U&E, blood glucose and plasma methanol.
  • correct metabolic acidosis to keep arterial pH>7.2—large amounts of bicarbonate may be needed and hypernatraemia may occur.
  • give ethanol orally as whisky, gin or vodka (adult 125-150mL; child 2mL/kg) and then IVI (dose as for ethylene glycol).
  • consider fomepizole (as used in ethylene glycol poisoning): discuss with Poisons Information Centre (p175).
  • give folinic acid (30mg IV, every 6h).
  • in severe poisoning: refer to ITU for haemodialysis and possibly IPPV.

P.197
Ethylene glycol poisoning Ethylene glycol is used mainly as antifreeze. The minimum fatal dose for an adult is ≈100mL. Toxic effects are due to metabolites, including glycolaldehyde and oxalic acid. Ethanol and fomepizole block metabolism of ethylene glycol, preventing toxicity. Clinical features In the first 12h after ingestion the patient looks drunk, but does not smell of alcohol. Ataxia, dysarthria, nausea, vomiting and sometimes haematemesis occur, followed by convulsions, coma and severe metabolic acidosis. From ≈12-24h post-ingestion there is hyperventilation, tachycardia, pulmonary oedema, cardiac arrhythmias and cardiac failure. Hypocalcaemia may be severe. Acute tubular necrosis and renal failure occur at 24-72h. Cranial nerve palsies may develop. Some makes of antifreeze contain sodium fluorescein, which causes urine to fluoresce in ultraviolet light (eg using a Wood’s lamp, typically available from dermatology units). This could be helpful to confirm ethylene glycol poisoning, but the absence of fluorescence does not exclude poisoning. Management

  • perform gastric lavage
  • measure ABG, U&E, calcium and plasma ethylene glycol.
  • monitor ECG.
  • correct metabolic acidosis to keep arterial pH > 7.2—large amounts of bicarbonate may be needed and hypernatraemia may occur.
  • give ethanol orally as whisky, gin or vodka (adult 125-150mL, child 2mL/kg) followed by IVI of ethanol, preferably as 5% solution in dextrose. Initial IV adult dose is 12g ethanol/hr, ↑ for alcoholics and during haemodialysis and adjusted to maintain blood ethanol at ≈1g/litre (discuss dose with Poisons Information Service, p175).
  • consider fomepizole: discuss with Poisons Information Service about indications, dosage and where to obtain it.
  • correct severe hypocalcaemia with calcium gluconate (10mL of 10% slowly IV).
  • in severe poisoning, haemodialysis may be required, with frequent measurements of blood ethylene glycol and ethanol concentrations. Ventilation may be needed if pulmonary oedema develops.

P.198
Paraquat poisoning Paraquat is an effective weedkiller which is very toxic if ingested. It is available in several formulations, often in combination with other chemicals. ‘Weedol’ and ‘Pathclear’ are granules containing paraquat 25g/kg, one 60g sachet of which may cause fatal poisoning. Fatalities may result from 10-20mL of the liquid formulations containing paraquat 100 or 200g/litre, but these are not on public sale. Inhalation of dilute paraquat spray may cause sore throat and epistaxis, but not systemic poisoning. No specific treatment is needed and symptoms resolve in a few days. Prolonged contact of paraquat with the skin causes erythema and sometimes ulceration, but absorption is rarely sufficient to cause systemic toxicity. Remove soiled clothing and wash the skin thoroughly with water. Splashes in the eyes cause pain and corneal ulceration and need immediate irrigation with water and referral for ophthalmological review. Clinical features of paraquat ingestion Paraquat is corrosive and causes immediate burning pain in the mouth and throat, nausea and vomiting, followed by abdominal pain and diarrhoea. Large amounts (>6g) of paraquat result in rapid deterioration with shock, pulmonary oedema, metabolic acidosis, coma, convulsions and death within ≈24h. Smaller quantities (3-6g) do not produce shock. After 24h, painful burns of the mouth and throat cause difficulty in swallowing and speaking. The burns look white until the surface sloughs after ≈3 days, leaving painful raw areas. Renal failure occurs at 1-2days and there is mild jaundice. Paraquat lung usually develops by 5-7days, with pulmonary oedema and fibrosis causing ↑breathlessness and cyanosis. Lung shadowing is seen on CXR. Death from hypoxia occurs ≈7-14days after poisoning. 1.5-2g of paraquat may produce slower respiratory failure, with gradual deterioration until death up to 6wks after ingestion. Survival with lung damage is uncommon. Management

  • do not give O2, which ↑toxicity of paraquat.
  • consider gastric lavage if <1h since ingestion.
  • give oral activated charcoal immediately, with IV analgesia and antiemetics.
  • send urine (and gastric fluid if available) for the lab to test for paraquat, which can be done very quickly using sodium dithionite. A -ve test within 4h of suspected ingestion excludes significant poisoning. If paraquat is present measure the plasma concentration if possible, since it helps assessment of the prognosis: the Poisons Information Services (p175) can advise about the interpretation of results.
  • unfortunately, no treatment improves the outcome of paraquat poisoning.
  • keep patients who are likely to die as comfortable as possible.

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Petrol and paraffin poisoning Petrol, paraffin (kerosene) and other petroleum distillates are used as fuels and solvents. They contain mixtures of hydrocarbons, often with small quantities of other chemicals. Accidental poisoning occurs after liquids have been stored in inappropriate and unlabelled containers. The major problem is pneumonitis caused by aspiration of hydrocarbons into the lungs. Clinical features In many cases no symptoms occur. There may be nausea, vomiting and occasionally diarrhoea. Aspiration into the lungs causes choking, coughing, wheeze, breathlessness, cyanosis and fever. X-ray changes of pneumonitis (shadowing in the mid or lower zones) may occur without respiratory symptoms or signs. Occasionally, pleural effusions or pneumatoceles develop. In severe cases, there may be pulmonary oedema, drowsiness, convulsions or coma. Rare problems include renal failure and intravascular haemolysis. Management Many patients remain well and need no treatment. Avoid gastric lavage, unless very large quantities have been taken or there is serious concern about another poison: in these rare cases lavage may be done on specialist advice if the patient has a good cough reflex or the airway is protected by a cuffed ET tube. Obtain a CXR and observe for respiratory problems. Patients with a normal initial CXR who have no symptoms or signs 6hrs after ingestion may be discharged with advice to return if symptoms develop. If symptoms occur, treat supportively with O2 and bronchodilators as necessary. Steroids and prophylactic antibiotics are unhelpful. IPPV is occasionally needed because of severe pulmonary oedema. P.200
Organophosphate poisoning Organophosphates are widely used as insecticides. Poisoning with these chemicals is rare in the UK, but common in many developing countries. Organophosphates are absorbed through the skin, bronchial mucosa and gut and inhibit cholinesterases, causing accumulation of acetylcholine at nerve endings and neuromuscular junctions. The speed of onset, severity and duration of toxicity vary between different compounds. Irreversible binding of cholinesterase (‘ageing’) develops after some mins or hrs. Pralidoxime reactivates cholinesterase if given promptly, before ageing occurs. Organophosphate nerve gas agents such as sarin may be released deliberately by terrorists. Information and advice are available from TOXBASE (p175). Carbamate insecticides act similarly to organophosphates, but poisoning with carbamates is generally less severe and pralidoxime is not needed. Clinical features Minor exposure to organophosphates may cause subclinical poisoning with ↓cholinesterase levels, but no symptoms or signs. Symptoms may be delayed by 12-24h after skin exposure. Early features of toxicity include anxiety, restlessness, insomnia, tiredness, headache, nausea, vomiting, abdominal colic, diarrhoea, sweating, hyper-salivation and miosis. Muscle weakness and fasciculation may develop. In severe poisoning there is widespread paralysis with respiratory failure, pulmonary oedema, profuse bronchial secretions, bronchospasm, convulsions and coma. Hyperglycaemia and cardiac arrhythmias may occur. Occasionally, delayed effects of poisoning develop 1-4days after acute poisoning, with cranial nerve palsies, muscle weakness and respiratory failure which resolve after 2-3wks. A peripheral neuropathy sometimes occurs after ≈2wks, usually involving the legs. Management

  • Wear protective clothing and avoid getting contaminated yourself.
  • Give supportive treatment as needed.
  • Clear the airway and remove bronchial secretions.
  • Give O2 and IPPV if necessary.
  • Prevent further absorption by removing soiled clothing and washing the skin, or by gastric lavage after ingestion in the previous 1h.
  • Take blood for cholinesterase.
  • If there are profuse bronchial secretions and/or bronchospasm, give atropine IV (adult 2mg, child 0.02mg/kg), repeated every 10-30mins until there is improvement or obvious signs of atropinization (dry mouth, tachycardia, dilated pupils): very large quantities may be needed.
  • In moderate or severe poisoning give pralidoxime mesylate (also called P2S). The dose of pralidoxime is 30mg/kg IV over 5-10mins, repeated if necessary every 4hrs. Improvement is usually apparent within 30mins. The Poisons Information Services can advise on the supply and use of pralidoxime. In the UK, large quantities of pralidoxime are available via the Blood Transfusion Service if there are multiple casualties with organophosphate poisoning.
  • Give diazepam to ↓agitation and control convulsions.

P.201
Cyanide poisoning Cyanide compounds are widely used in industry and may be ingested or inhaled inadvertently or deliberately. Cyanides produced by burning polyurethane foam ↑ the mortality from smoke inhalation. Cyanide poisoning may follow excessive use of the drug sodium nitroprusside or ingestion of amygdalin (laetrile) from the kernels of apricots, cherries and other fruits. Solutions for removing artificial fingernails may contain acetonitrile (methyl cyanide). Cyanides inhibit cytochrome oxidase, blocking the tricarboxylic acid cycle and stopping cellular respiration. This process is reversible. Inhalation of hydrogen cyanide often causes death within minutes. Ingestion of cyanides may produce rapid poisoning, but food in the stomach sometimes delays absorption and the onset of symptoms. Delayed poisoning may also follow absorption of cyanides through the skin. Ingested cyanide compounds react with gastric acid to form hydrogen cyanide gas which has the potential to poison other people (eg first aiders providing mouth to mouth resuscitation). Clinical features Acute poisoning causes dizziness, anxiety, headache, palpitations, breathlessness and drowsiness. In severe cases, there may be coma, convulsions, paralysis, pulmonary oedema, cardiac arrhythmias and cardiorespiratory failure, with metabolic acidosis. Most of the clinical features result from severe hypoxia, but cyanosis is uncommon. Classically, there is a smell of bitter almonds on the breath, but many people cannot detect this. Management

  • Avoid getting contaminated yourself.
  • Provide supportive measures.
  • Remove contaminated clothing and wash exposed skin.
  • Give 100% O2 and monitor ECG.
  • Consider activated charcoal or gastric lavage within 1hr of ingestion.
  • In mild poisoning, reassurance, O2 and observation may be all that is required. Exposure to cyanide causes great anxiety and it may be difficult to distinguish between fear of poisoning and early symptoms of toxicity.
  • Specific antidotes should be available but are not always needed.

Some specific antidotes to cyanide are potentially dangerous in the absence of cyanide and should only be given if poisoning is moderate or severe (eg coma). In severe cyanide poisoning, give dicobalt edetate (Kelocyanor®) 300mg IV over 1min, repeated if there is no improvement after 1min. In the absence of cyanide, dicobalt edetate may cause cobalt poisoning with facial, laryngeal and pulmonary oedema, vomiting, tachycardia and hypotension. The alternative treatment is sodium thiosulphate (adult dose 25mL of 50% solution IV over 10mins; child 400mg/kg) with sodium nitrite (adult dose 10mL of 3% solution IV over 5-20mins; child 0.13-0.33mL of 3% solution/kg, ie 4-10mg/kg). Sodium thiosulphate often causes vomiting. Sodium nitrite may cause hypotension. High doses of hydroxocobalamin (5-10g) are useful and relatively safe in cyanide poisoning, but no suitable formulation is currently available in the UK. P.202
Carbon monoxide poisoning Carbon monoxide (CO) is a tasteless and odourless gas produced by incomplete combustion. Poisoning may occur from car exhausts, fires and faulty gas heaters. CO is also produced by metabolism of methylene chloride (used in paint strippers and as an industrial solvent). CO ↓ the O2-carrying capacity of the blood by binding Hb to form carboxyhaemoglobin (COHb). This impairs O2 delivery from blood to the tissues and also inhibits cytochrome oxidase, blocking O2 utilization. These effects combine to cause severe tissue hypoxia. The elimination half-life of CO is ≈4hrs on breathing air, ≈1hr on 100% O2 and ≈23mins on O2 at 3 atmospheres pressure. Clinical features Early features are headache, malaise, nausea and vomiting (sometimes misdiagnosed as a viral illness or gastroenteritis, especially if several members of a family are affected). In severe poisoning, there is coma with hyperventilation, hypotension, ↑muscle tone, ↑reflexes, extensor plantars and convulsions. Cherry-red colouring of the skin is sometimes seen in fatal CO poisoning but is rare in live patients. Skin blisters and rhabdomyolysis may occur after prolonged immobility. Pulmonary oedema, MI and cerebral oedema can occur. Neurological and psychiatric problems sometimes develop some wks after CO poisoning, but usually improve over the following yr. Management

  • Remove from exposure.
  • Clear the airway and maintain ventilation with as high a concentration of O2 as possible: for a conscious patient use a tight-fitting mask with an O2 reservoir, but if unconscious intubate and provide IPPV on 100% O2.
  • Record ECG and monitor heart rhythm: look for arrhythmias and signs of acute MI.
  • Check ABG—pulse oximetry SaO2 measurements are incorrect in CO poisoning, as are pO2 values, but acidosis indicates tissue hypoxia.
  • Check COHb levels: although these correlate poorly with clinical features, COHb >15% after arrival at hospital suggests serious poisoning. COHb may be up to 8% in smokers without CO poisoning. A nomogram (p381) can be used to help to estimate COHb at the time of exposure.
  • Correct metabolic acidosis by ventilation and O2: try to avoid bicarbonate, which may worsen tissue hypoxia.
  • Consider mannitol if cerebral oedema is suspected.
  • Hyperbaric O2 therapy is logical and theoretically useful, but of no proven benefit after CO poisoning. Transfer to a hyperbaric chamber and pressurization may take some hrs and so hyperbaric treatment is not necessarily more effective than ventilation on 100% normobaric O2. Also, caring for a critically ill patient in a small pressure chamber may be impracticable. Discuss with a Poisons Information Service (p175) and consider hyperbaric treatment if a patient has been unconscious at any time, has COHb >20%, is pregnant or has cardiac complications or neurological or psychiatric features after CO poisoning. The Poisons Information Service can advise on the location and telephone numbers of hyperbaric chambers.

P.203
Chlorine poisoning Chlorine gas causes lacrimation, conjunctivitis, coughing, wheezing, breathlessness and chest pain. Laryngeal and pulmonary oedema may develop within a few hrs. Remove from exposure and give O2, with bronchodilators if necessary. If there is laryngeal or pulmonary oedema, consult an expert and give prednisolone in high dosage (adult 60-80mg/day initially). In severe cases, IPPV in ITU may be needed. If the eyes are painful, irrigate with water or saline and examine with fluorescein for corneal damage. Casualties with minor exposure to chlorine but no symptoms may be allowed home with advice to rest and return if symptoms develop. Patients with symptoms when seen in hospital usually need admission for 12h for observation. Record serial peak expiratory flow rates, which may warn of deterioration. CS gas (tear gas) poisoning CS (orthochlorobenzylidene malononitrile) is used for riot control, police self-protection and sometimes as a weapon in assaults. It is an aerosol or smoke rather than a gas. Exposure to CS causes immediate blepharospasm and lacrimation, uncontrollable sneezing and coughing, a burning sensation in the skin and throat and tightness of the chest. Vomiting may occur. These symptoms usually disappear within 10mins in fresh air, but conjunctivitis may persist for 30mins. Exposure in a confined space may cause symptoms for some hrs and is particularly dangerous in people with pre-existing lung disease. Redness or blistering of the skin may develop, due to the solvent in the spray. Treat patients exposed to CS gas in a well ventilated area. Ensure that staff wear gloves and close-fitting goggles. Remove contaminated clothes and wash affected skin thoroughly. Give O2 and bronchodilators if necessary. Reassure the patient that the symptoms will resolve. If the eyes are painful, blow dry air on them with a fan to vaporize any remaining CS gas. The irritation should disappear in a few mins. Alternatively, irrigate the eyes with saline (this may cause a transient worsening of symptoms). When symptoms have settled, record VA and examine the corneas using fluorescein. Refer to an ophthalmologist if symptoms persist. CN (chloroacetophenone) gas is used in some countries for riot control and in personal defence devices. CN has similar effects to CS but is more toxic. P.204
Ingestion of plants, berries and mushrooms Plants and berries Many children eat plant leaves or brightly-coloured berries, but serious poisoning from plants is very rare. Identify the plant if possible, using reference books1,2 or the CD-ROM computer software ‘Poisonous plants and fungi in Britain and Ireland’ (p174). Advice on toxicity and any necessary treatment is available from Poisons Information Services. Many garden and house plants are non-toxic and no treatment is needed after ingestion. Serious poisoning from laburnum is very rare, with only 1 death recorded in the UK in 50yrs. No treatment needs to be provided for children who eat laburnum seeds, except for the very few with symptoms (nausea, salivation, vomiting, headache, rarely convulsions). Mushroom poisoning Serious poisoning from mushrooms or fungi is rare. Most deaths are due to Amanita phalloides (death cap mushroom). Reference books3 are useful, but identification of mushrooms from the description or fragments available is often uncertain. Advice on toxicity and treatment is available from Poisons Information Services (p175). Mushrooms found in gardens are very unlikely to produce severe poisoning, but may cause vomiting and occasionally hallucinations, usually within 2hrs of ingestion. Mushrooms which cause symptoms within 6hrs are unlikely to be seriously toxic. Delayed toxicity occurs with Amanita phalloides and some other species which occur throughout the UK. Amanita phalloides poisoning causes vomiting and profuse watery diarrhoea after a latent period of 6-12hrs, followed by hepatic and renal failure. The interval between ingestion and the onset of symptoms is crucial in distinguishing between non-serious and potentially fatal poisoning. It is important to try to ascertain if:

  • >1 variety of mushroom was eaten (since poisonous and edible mushrooms often grow together)
  • whether the mushrooms were cooked (since some toxins are inactivated by heat)
  • whether alcohol was taken (since disulfiram-like effects may occur with Coprinus species, ink cap mushrooms).

For most toxic mushrooms only symptomatic treatment is required. Activated charcoal may ↓absorption if given within 1hr. Obtain expert advice immediately if Amanita poisoning is suspected. Footnote 1 Cooper MR, Johnson AW. Poisonous Plants in Britain: Animal and Human Poisoning. The Stationery Office, London, 1998. 2 Frohne D, Pfander HJ. A Colour Atlas of Poisonous Plants. Manson Publishing Ltd, London 2004, second edition. 3 Bresinsky A, Besl H. A Colour Atlas of Poisonous Fungi. Manson Publishing Ltd, London, 1989. P.205
Ingestion of button batteries Small children often swallow button or disc batteries intended for toys, watches, hearing aids and other electrical equipment. The larger batteries may become stuck in the oesophagus, causing perforation or later stenosis. Corrosive damage may occur from battery contents and electrical discharge. Mercury may be absorbed from leaking batteries, but significant poisoning is rare. Problems are less likely from old spent batteries than from new batteries. The Poisons Information Service should be able to identify the type of battery involved from the reference number, if this is available from the packet or on a similar battery to that ingested. Management X-ray the chest and abdomen to determine the position of the battery. Batteries stuck in the oesophagus must be removed immediately using endoscopy, a Foley catheter or a magnet. Batteries in the stomach should be removed if they are leaking, are causing symptoms or have been present for several days. It is not essential to remove intact batteries which are causing no symptoms, since many batteries pass uneventfully through the gut, but batteries can usually be retrieved from the stomach without anaesthesia using an orogastric magnet and fluoroscopy. Emetics are ineffective and should not be used. If a battery is not removed repeat the abdominal X-ray at 3-4 days to check the position of the battery and see if it is disintegrating. Batteries in the small or large bowel usually pass spontaneously and should be left to do so, unless they open or cause symptoms (pain, diarrhoea, bleeding). If removal is needed, consider whole-bowel irrigation (p179) before surgery. If a mercury battery disintegrates, measure serum mercury levels. Obtain expert advice before giving chelating agents, which are potentially toxic and rarely needed. Batteries in the nose Button batteries lodged in the nose may cause corrosive burns and bleeding, sometimes with septal perforation after a few weeks. Liaise with an ENT specialist to remove batteries from the nose as soon as possible. P.206
‘Ecstasy’, other illicit drugs and ‘body packers’ Ecstasy and amphetamines ‘Ecstasy’ (3,4-methylenedioxymetamphetamine, MDMA) is an amphetamine derivative which is used as an illegal stimulant drug. It is taken orally as tablets or capsules, or occasionally in powder form. ‘Eve’ (3,4-methylenedioxyethamphetamine, MDEA) and other amphetamines have similar effects. These drugs are often diluted and contaminated with other toxic compounds. Clinical features Agitation, headache, muscle pains, ↑muscle tone, sweating, dilated pupils, tachycardia, hypertension followed by hypotension, pyrexia. In severe cases, there may be heat stroke with hyperthermia, muscle rigidity, convulsions, coma, rhabdomyolysis, cardiac arrhythmias, jaundice, renal failure, DIC and cerebral haemorrhage. Metabolic acidosis and hyperkalaemia are common and hyponatraemia and hypoglycaemia may occur. Treatment Give oral activated charcoal (p179) if less than 1hr since ingestion. Observe aymptomatic patients for at least 4hrs. Monitor ECG, BP and T°. Record ECG. measure U&E, creatinine, glucose, LFTs and CK. In severe cases, check ABG and coagulation. Provide intensive supportive treatment, with maintenance of airway, breathing and circulation. Trismus and fits may prevent airway control and necessitate specialist anaesthetic involvement before intubation. Control fits with clomethiazole (which also helps to ↓hyperthermia) or diazepam. Immediate ↓ in T° is essential, as for heat stroke (p260). If rectal T°> 40°C, give dantrolene 1mg/kg IV, repeated if necessary up to 10mg/kg in 24h. Correct metabolic acidosis with sodium bicarbonate. If hyperkalaemia occurs, give glucose and insulin (p158). Severe tachycardia may require ß- blockade (eg metoprolol 5mg IV). For severe hypertension, consider nifedipine (5-10mg PO) or phentolamine 2-5mg IV). Monitor renal and liver function. Cocaine Cocaine and its derivative ‘crack’ are usually sniffed or smoked, but severe poisoning may occur in ‘body packers’. Euphoria, agitation, dilated pupils, tachycardia, nausea, vomiting, headache and hallucinations may occur. Complications of cocaine overdosage These include hyperpyrexia, convulsions, hypertension and tachyarrhythmias. Severe hypertension can cause cerebral haemorrhage or aortic dissection. Coronary vasoconstriction may produce myocardial ischaemia or infarction. Rhabdomyolysis and renal failure may occur. Treat supportively Maintain a clear airway and adequate ventilation. Give activated charcoal (p179) if cocaine has been ingested within 1hr. Use diazepam to control convulsions and agitation: large amounts of diazepam may be needed. If hypertension is severe, give IV GTN and consider a calcium antagonist. Avoid ß-blockers. Treat chest pain with GTN, aspirin and diazepam, and obtain expert advice if the ECG suggests acute MI. Hyperpyrexia requires cooling and sedation with diazepam, and dantrolene (see above) if core temperature exceeds 40°C. Smoking cocaine may result in phayngeal burns, due to hot gases and the anaesthetic action of cocaine. Intubation may be needed to protect the airway. LSD (lysergic acid diethylamide) LSD causes visual hallucinations, agitation, excitement, tachycardia and dilated pupils. Hypertension and pyrexia may occur. Some patients develop paranoid delusions and require sedation. Massive overdose of LSD is rare, but may cause coma, respiratory arrest and coagulation disturbances. Treat supportively. P.207
Phencyclidine (PCP) Phencyclidine is used illegally as a hallucinogenic drug. It is often smoked mixed with tobacco or cannabis, but may be injected or taken orally. It initially causes euphoria, dissociation and hallucinations, but ‘bad trips’ are common. Features of intoxication These include agitation, sweating, salivation, hypertension, muscle spasms and behavioural disturbances. Hypoglycaemia, convulsions, coma, respiratory failure, and rhabdomyolysis may occur. Treat supportively Check for and correct hypoglycaemia. Observe agitated patients carefully, but disturb them as little as possible to ↓risk of violence. Sedate with diazepam if necessary. Adrenergic blocking agents (eg phentolamine) may be needed for severe hypertension. Gammahydroxybutyric acid (GHB, GBH) GHB is used illegally as a body-building agent and psychedelic drug. It is ingested or injected. Intoxication may cause vomiting, diarrhoea, drowsiness, confusion, ataxia and agitation. Severe poisoning results in coma, respiratory depression, fits, bradycardia and hypotension. Treatment Consider activated charcoal (p179) if <1hr since ingestion. Observe for at least 4hrs and monitor pulse rate, BP and breathing. Provide supportive treatment as needed. Control agitation and convulsions with diazepam. Naloxone may reverse some of the effects of GHB. Body packers Body packers try to smuggle drugs such as cocaine or heroin by ingesting multiple packages of drugs wrapped in condoms or latex. Packages may also be hidden in the rectum or vagina. Fatal poisoning may occur if any packages leak and the drugs are absorbed. Suspected body packers need careful assessment and observation. Check for rectal and vaginal packages. Try to determine the drug involved and the number of packages and type of packaging used. Observe for signs of toxicity and monitor heart rate, BP, ECG, and SaO2. Give activated charcoal (p179). Consider a naloxone infusion (p182) for heroin body packers. Abdominal X-rays may show packets of drugs. Whole bowel irrigation (p179) is usually the best method of removing swallowed packages. Surgery is occasionally needed for bowel obstruction. Endoscopic removal of packets is liable to result in damage to packaging and leakage of the drug. Advice is available from Poisons Information Centres (p175).

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