199 ACE INHIBITOR POISONING 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 w ith plants containing cardiac glycosides (foxglove, oleander and yew). Clinical features Nausea, vomiting, malaise, delirium, xanthopsia (yellow \202 ashes or d iscolouration of vision). Acute poisoning usually causes bradycardia with PR and QRS prolon gation. There may be AV block, AV disso- ciation and escape rhythms, sometimes with ventric ular ectopics or VT. Hyperkalaemia occurs, and in severe cases metabolic acidosis due to hy potension and d tissue perfusion. Management Provide supportive treatment. Monitor ECG and BP. Obtain venous access. Give act ivated charcoal to d absorption and prevent entero-hepatic recycling of digoxin ( b p.185). Measure U&E, plasma digoxin, and ABG in severe poisoning. Get expert help for patients who are severely poisoned. Correct severe metabolic acidosis with sodium bicarbonate. Treat hy per- kalaemia > 6mmol/L ( b p.162). Bradycardia and AV block often respond to atropine IV t otal 1 \200\2232mg (child 0.02mg/kg). Cardiac pacing is not always effective and a high vol tage is often needed for capture. VT may respond to lidocaine or a B -blocker. Treat severe poisoning with digoxin anti- bodies (Digibind ), which rapidly correct arrhythmias and hyperkalaemia. Digibind is expensive and rarely needed, so is not stocked in many hospi- tals: Poisons Information Services (b p.181) can advise about emergency supplies and the d ose required for the patient \200\231s body weight and plasma digoxin concentration or the quantity taken. ACE inhibitor poisoning Overdosage with angiotensin converting enzyme (ACE) inhibitors (eg captopril, enalapril, lisinopril) may cause drowsiness, hypotension, hyperkalaemia and rare ly, renal failure. Monitor BP and ECG. Give IV 0.9 % saline if BP is low. Check U&E. Consid er activated charcoal ( b p.185). 200 CHAPTER 4 Toxicology Theophylline poisoning Theophylline and aminophylline can cause fatal poisoning. Many prepa rations are slow-release and may not produce serious toxicity until 12 \200\22324 hours aft er ingestion, so careful observation is essential. Features Nausea, vomiting (often severe and not helped by anti-emetics), abdominal pain, haematemesis, restlessness, i muscle tone, i re \202 exes, headache, convulsions. Coma, hyperventilation, hyperpyrexia and rhabdomyo lysis may occur. Sinus tachycardia may be followed by supraventricular and ventricular arrh ythmias and VF. BP may initially i , but later d in severe poisoning. Complex metabolic dis turbances include a respiratory alkalosis followed by metabolic acidosis, hyperglycaemia, a nd severe hypokalaemia. Management \200 Treat supportively. \200 Monitor ECG, heart rat e and BP. \200 Obtain venous access and measure U&E, glucose, ABG, plasma theo- phylline (repeated after a few hours). Repeat K + hourly if patient is symptomatic, since early corr ection of hypokalaemia may prevent dan- gerous arrhythmias. Correct hypokalaemia with K + ( large amounts may be needed, but no faster than 20mmol/hr). Perform gastric lavage if <1hr since ingestion. Give repeated activated charcoal ( b p.185), by NG tube if necessary. Intractable vomiting may respond to ondansetron (8mg slowly IV in adult). \200 GI bleedin g 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-select ive B -blockers (eg propranolol) may help severe tachyarrhythmias and hypokalaemia, but cau se bronchospasm in asth- matics. Lidocaine and mexiletine may precipitate \201 ts, so dis opyramide is preferable for ventricular arrhythmias. Control convulsions with diazepam or lorazepam. Paralyze, intubate, and provide IPPV if the airway is at risk from coma, \201 ts and vomiting. \200 Charcoal haemoperfusion may be needed in severe poisoning, especially if oral or NG activated charcoal is impracticable b ecause of vomiting. Serious hyperkalaemia may occur during recovery from theophylline poiso ning if large amounts of K + were given earlier. Salbutamol poisoning B 2 -agonists (eg salbutamol, terbutaline) may cause Poisoning with vo miting, agitation, tremor, tachycardia, palpitations, hypokalaemia and hypertension. Rarely , there may be hallucinations, hyperglycaemia, ventricular tachyarrhythmias, myocardial isc haemia, and convulsions. Treat supportively: \200 Correct hypokalaemia by infusion of K + (max 20 mmol/hour). \200 Monitor ECG and BP. \200 Activated charcoal may d drug absorp tion. \200 Do not treat tachycardia if there is an adequate cardiac output. Propranolol m ay help severe tachyarrhythmias and hypokalaemia, but can precipitate bronchospasm in asthm atics. 201 IRON POISONING Iron poisoning Small children often eat iron tablets, many of which resemble sweets. Seriou s poisoning is uncommon, but fatalities can occur. Note that iron is present in some weed/s eed preparations. Different preparations contain the equivalent of 35 \200\223110mg of elemental iron per tab let, sometimes in slow-release form. Serious toxicity is unlikely unless > 60mg elemental iron/kg body weight has been taken. Th e estimated lethal dose is about 150 \200\223300mg/kg. Features In the \201 rst few hours after ingestion nausea, vomiting, diarrhea and abdomin al pain are common. Vomit and stools are often gray or black and may contain blood. Hypergl ycaemia and i WCC may occur. Most patients do not develop further features. In severe poisoning, early effects include haematemesis, drowsiness, convulsions, coma, met abolic acidosis and shock. Early symptoms settle after 6 \200\22312hr, but a few patients then deteriorate 24 \200\223 48hr after ingestion, with shock, hypoglycaemia, jaundice, metabolic acidosis, hepatic ence phalopathy, renal failure, and occasionally bowel infarction. Survivors may develop gastric strictures or pyloric obstruction 2 \200\2235 weeks after the overdose. Management \200 Check serum iron, FBC, glucose, and also ABG in severe poisoning. \200 Perform gastric lavage if > 20mg elemental iron/kg body weight has been taken in the previo us 1hr. Do not give charcoal, which does not absorb iron. Iron tablets are radio-opaque and can be counted on a plain abdominal X-ray \201 lm. Whole-bowel irrigation ( b p.185) may be useful if many tablets remain in the gut, especially with slow-release formulations. Use supportive measures if required. \200 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 24hr). Desferrioxamine should also be given if the se rum iron exceeds the expected total iron binding capacity (about 54 \200\22375mmol/L): meas urement of total iron binding capacity may give misleading results after iron poisoning. De sferrioxamine causes hypotension if infused too rapidly and can produce rashes and rarely, anaphylaxis, pulmonary oedema or ARDS. The iron-desferrioxamine complex makes the urine ora nge or red, which con \201 rms that free iron has been bound and that desferrioxamine was required. Reduce desferrioxamine dosage when there is clinical improvement and serum iron i s less than the expected total iron binding capacity. Patients who still have no symptoms 6 hours after an iron overdose have probably not ingest ed toxic amounts and may be discharged, with advice to return if symptoms develop. Pregnancy does not alter the treatment needed for iron poisoning; use desferrioxamine if indicated. 202 CHAPTER 4 Toxicology Ethanol poisoning Features Overdosage of ethanol (ethyl alcohol or \200\230alcohol \200 \231) is very common. Alcohol potentiates the CNS depressant effects of many drugs. It init ially causes disinhibition and later ataxia, dizziness, dysarthria and drowsiness. In sever e poisoning there may be coma with respiratory depression, hypotension, hypothermia and a m etabolic acidosis. Hypoglycaemia is a particular problem in children and may occur after so me hours. Death may result from respiratory failure or aspiration of vomit. For an adult, t he fatal dose of ethanol alone is 8300 \200\223500mL of absolute alcohol: whisky and gin us ually contain 40 \200\22350 % ethanol. Do not assume that d GCS is due to alcohol until oth er causes have been excluded. Rarely, alcohol causes lactic acidosis (especially in patient s with liver disease or taking biguanide hypoglycaemic drugs) or ketoacidosis (due to dehyd ration and hypoglycaemia in alcoholics) \200\224 see b p.622. Treatment \200 Maintain a clear airway and adequate ventilation. \200 Check blood glucose every 1 \200\2232 hours i n severe poisoning. \200 Correct hypoglycaemia with glucose, not with glucagon. \200 Lo ok for signs of injury, especially head injury. \200 Emergency measurement of blood ethan ol rarely alters management. \200 Gastric lavage and activated charcoal are ineffective i n ethanol intoxication. Methanol poisoning Methanol is used as a solvent and in antifreeze. Ingestion of 10mL of pu re methanol may cause blindness and 30mL can be fatal, the toxic effects being due to the m etabolites formaldehyde and formic acid. Methylated spirits is a mixture of ethanol and wat er with about 5 % methanol: toxicity is almost entirely due to ethanol. Clinical features Methanol initially causes only mild transient drowsiness. Serious toxicit y develops after a latent period of 12 \200\22324 hours with vomiting, abdominal pain, head ache, dizziness, blurring of vision, and drowsiness leading to coma. There is a severe meta bolic acidosis, hyperglycaemia and i serum amylase. Survivors may be blind from optic nerve damage and develop Parkinsonian problems. Management \200 Consider gastric lavage if <1h r since ingestion. Do not give charcoal. \200 Measure ABG, U&E, Cl \200\223 , HCO 3 \200\223 , glucose, FBC, LFTs and osmolality, and plasma methanol if possible. Calculate os molal gap and anion gap. Read Toxbase advice ( b p.181). Discuss with Poisons Information Service. \200 Observe fo r at least 6hr after ingestion, even if asymptomatic. \200 Early use of fomepizole or eth anol (as for ethylene glycol, b p.203) minimizes methanol toxicity and should be started if poisoning is likely, especially if there is a high anion gap metabolic acidosis. Use sodium bicarbonate to correct metabolic acidosis (aim for pH 7.5). Large amounts may be needed and hypernatraemia may occur. Give folinic acid (1mg/kg, max 50mg, IV every 6hr for 48hr). \200 In severe poisoning, re fer to ICU for haemodialysis and possibly IPPV. 203 ETHYLENE GLYCOL POISONING Ethylene glycol poisoning Ethylene glycol is used mainly as antifreeze. Fatal dose for an a dult is about 100g (90mL of pure ethylene glycol). Toxic effects are due to metabolites gly colaldehyde, glycolic acid and oxalic acid. Fomepizole or ethanol block ethylene glycol met abolism, preventing toxicity. Clinical features In the \201 rst 12hr after ingestion the patient looks drunk, but does not smell of alcohol. Ataxia, dysarthria, nausea, vomiting, and sometimes haematem- esis oc cur, followed by convulsions, coma and severe metabolic acidosis. From 12 \200\22324hr after ingestion hyperventilation, pulmonary oedema, tachycardia, cardi ac arrhythmias and cardiac failure may develop. Hypocalcaemia may be severe. Acute tubular necrosis and renal failure occur at 24 \200\22372hr. Cranial nerve palsies may develop. Urine microscopy shows calcium oxalate monohydrate crystals which are diagnostic of ethylen e glycol poisoning. Some makes of antifreeze contain \202 uorescein, which makes urine \202 uoresce in ultraviolet light (eg a Wood \200\231s lamp from a dermatology department). This helps to con \201 rm ethylene glycol poisoning, but the absence of \202 uorescence does not exclude poisoning. Management \200 Consider gastric lavage if <1hr since ingestion. Do not give charcoal. \200 Measure ABG, U&E, Cl \200\223 , HCO 3 \200\223 , glucose, FBC, LFTs, osmolality, an d plasma ethylene glycol if possible. Calculate osmolal gap and anion gap. \200 Read Toxb ase advice (b p.181). Discuss with Poisons Information Service. Observe for at least 6hr after ingestion, even if asymptomatic. \200 Monitor ECG, pulse, blood pressure, respiratory rate, and urine output. \200 Early use of fomepizole or ethan ol minimizes toxicity and should be started if poisoning is likely. High anion gap metabolic acidosis ( b p.99) occurs in ethylene glycol poisoning (and also m ethanol poisoning, diabetic ketoacidosis, alcoholic ketoacidosis, and renal failure), but a cidosis only develops after some ethylene glycol has been metabolized. Consider fomepizole: discuss with Poisons (b p.181) about indications, dosage, and where to obtain i t. Information Service If fomepizole is not available give ethanol orally as whisky, gin or vodka (adult 125 \200 \223150mL, child 2mL/kg) followed by IVI of ethanol, preferably as 5 % solution in glucose. Initial IV adult dose is 12g ethanol/hr, i for alcoholics and during haemodialysis and adj usted to maintain blood ethanol at 81g/L (discuss dose with Poisons Information Service). Use sodium bicarbonate to correct metabolic acidosis (aim for pH 7.5). Large amounts may be needed and hypernatraemia may occur. Correct severe hypocalcaemia with calcium gluconate (10mL of 10 % slowly IV). Haemodialysis may be required in severe poisoning, with frequent measurements of blood ethy lene glycol concentrations (and ethanol if this is used). Intensive care and ventilation ma y be needed. 204 CHAPTER 4 Toxicology Paraquat poisoning Paraquat is an effective weedkiller which is very toxic if ingested: dea th is likely after 10mL of liquid paraquat (100 or 200g/L). Paraquat poisoning is now rare in the UK, where paraquat is no longer approved for sale or use, but accidental or delibera te poisoning still occurs in many developing countries. Inhalation of dilute paraquat spray may cause sore throat and epistaxis, but not systemic p oisoning. No speci \201 c treatment is needed and symptoms resolve in a few days. Prolonge d contact of paraquat with the skin causes erythema and sometimes ulceration, but absorptio n is rarely suf \201 cient to cause systemic toxicity. Remove soiled clothing and wash the skin thoroughly with water. Splashes in the eyes cause pain and corneal ulceration. Immediately irrigate with water and refer 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 diarrhea. Large amounts ( > 6g) of paraquat result in rapid deterioration with shock, pulmonary oedem a, metabolic acidosis, coma, convulsions, and death within 24hr. Smaller quantities (3 \200\2236g) do not produce shock. After 24hr, chemical burns of the m outh and throat cause pain and dif \201 culty in swallowing and speaking. The burns look w hite until the surface sloughs after about 3 days, leaving painful raw areas. Renal failure occurs at 1 \200\2232 days and there is mild jaundice. Paraquat lung usually develops by 5 \200\2237 days, with pulmonary oedema and \201 brosis causing breathlessness and cyanosis. Lung shadowing is seen on CXR. Death from hypoxia occ urs 7 \200\22314 days after poisoning. 1.5 \200\2232g of paraquat may produce slower respir atory failure, with gradual deteriora- tion until death up to 6 weeks after ingestion. Surv ival with lung damage is uncommon. Management \200 Do not give O 2 , which increases pulmonary toxicity of paraquat. \200 Consider gastric lavage if <1hr since ingestion. \200 Give oral activated charcoal immedi ately, with IV analgesia and anti-emetics. \200 Send urine (and gastric \202 uid if ava ilable) for the laboratory to test for paraquat, which can be done very quickly using sodiu m dithionite. A negative test within 4 hours of suspected ingestion excludes signi \201 - cant poisoning. If paraquat is present, measure the plasma concentra- tion if possible, sin ce it helps assessment of the prognosis: the Poisons Information Services ( b p.181) can ad vise about paraquat measurement and the interpretation of results. Unfortunately, no treatment improves the outcome of paraquat poisoning. Keep patients who are likely to die as comfortable as possible. 205 gasoline AND PARAFFIN POISONING Gasoline and paraf \201 n poisoning Gasoline, paraf \201 n (kerosene), and other petroleu m distillates are used as fuels and solvents. They contain mixtures of hydrocarbons, often with small quantities of other chemicals. Unintentional poisoning occurs after liquids have been stored in inappropriate and unlabelled containers. The major problem is pneumonitis c aused by aspiration of hydrocarbons into the lungs. Clinical features In many cases no symptoms occur. There may be nausea, vomiting, and occas ionally diarrhea. Aspiration into the lungs causes choking, coughing, wheeze, breathlessnes s, cyanosis and fever. X-ray changes of pneumonitis (shadowing in the mid or lower zones) m ay occur without respiratory symptoms or signs. Occasionally, pleural effusions or pneumato celes develop. In severe cases, there may be pulmonary oedema, drowsiness, convulsions or c oma. 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 conce rn about another poison: in these rare cases lavage may be done on specialist advice if the patient has a good cough re \202 ex or the airway is protected by a cuffed ET tube. Obtai n a CXR and observe for respiratory problems. Patients with a normal initial CXR who have n o symptoms or signs 6 hours after ingestion may be discharged with advice to return if symp toms develop. If symptoms occur, treat supportively with O 2 and bronchodilators as necessary. Steroids a nd prophylactic antibiotics are unhelpful. IPPV is occasionally needed because of severe pu lmonary oedema. 206 CHAPTER 4 Toxicology Organophosphate poisoning Organophosphates are widely used as insecticides. Poisoning with these chemicals is rare in the UK, but common in many developing countries. Organophosphate s are absorbed through the skin, bronchial mucosa and gut, and inhibit cholinesterases, cau sing 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 ( \200\230ageing \200\231) develops after some minutes or hours. Pralidoxime reactivates cholinesterase if given promptly, before ageing occurs. Organophosphate nerve gas agents such as sarin may be released deliberately by terrorists. Information is available from Toxbase ( b p.181). Carbamate insecticides act similarly to o rganophosphates, but poisoning with carbamates is generally less severe and pralidoxime is not needed. Clinical features Minor exposure to organophosphates may cause subclinical poisoning with d cholinesterase levels, but no symptoms or signs. Symptoms may be delayed by 12 \200\22324h r after skin exposure. Early features of toxicity include anxiety, restlessness, insomnia, tiredness, headache, na usea, vomiting, abdominal colic, diarrhea, sweating, hyper- salivation, and miosis. Muscle weakness and fasciculation may develop. In severe poisoning there is widespread paralysis with respiratory failure, pulmonary oedem a, profuse bronchial secretions, bronchospasm, convulsions and coma. Hyperglycaemia and car diac arrhythmias may occur. Occasionally, delayed effects of poisoning develop 1 \200\2234 days after acute poisoning, with cranial nerve palsies, muscle weakness and respiratory fai lure which resolve after 2 \200\2233 weeks. A peripheral neuropathy may develop after 2 wee ks, usually involving the legs. Management 1 \200 Wear protective clothing and avoid getting contaminated yourself. \200 Give supportive treatment as needed. \200 Clear the airway and remove secretions. Give O 2 and IPPV if needed. \200 Insert two IV cannulae. Take blood for cholinesterase. \200 If there are profuse bronchial secretions or bronchospasm, give atro- pine IV (adult 2mg, child 0.02mg/kg), repeated every 5min with the dose doubled each time until the chest soun ds clear, systolic BP > 80mmHg and pulse > 80. Some patients need > 100mg of atropine. \200 Give diazepam to treat agitation and control convulsions. \200 In moderate or sever e poisoning give pralidoxime mesylate (also called P2S). The dose of pralidoxime is 30mg/kg IV over 5 \200\22310min, repeated if necessary every 4hr. Improvement is usually apparent within 30min. \200 Poisons Information Services can advise on pralidoxime supply and use: in the UK the Blood Transfusion Service will supply pralidoxime if there are multiple casu alties with organophosphate poisoning. 1 Eddleston M et al . ( 2008 ) Management of acute organophosphorus pesticide poisoning . L ancet . 371 : 597 \200\223 607 . 207 CYANIDE POISONING Cyanide poisoning Cyanide compounds are widely used in industry and may be ingested or inha led inadvertently or deliberately. Cyanides produced by burning polyurethane foam i mortali ty from smoke inhalation: if there is severe acidosis consider cyanide toxicity. Cyanide po isoning may be caused by the drug sodium nitroprusside or ingestion of amygdalin (laetrile) from the kernels of apricots, cherries and other fruits. Solutions for removing arti \201 cial \201 ngernails may contain acetonitrile (methyl cyanide). Cyanides inhibit cytochrome oxidase, blocking the tricarboxylic acid cycle and stopping cel lular respiration. This process is reversible. Inhalation of hydrogen cyanide often causes death within minutes. Ingestion of cyanides can produce rapid poisoning, but food in the st omach may delay absorption and the onset of symptoms. Delayed poisoning may follow absorpti on of cyanides through the skin. Ingested cyanide compounds react with gastric acid to form hydrogen cyanide, which could poison \201 rst-aiders giving mouth to mouth resuscitation . Clinical features Acute poisoning causes dizziness, anxiety, headache, palpitations, breath - lessness, and drowsiness. In severe cases, there may be coma, convulsions, paralysis, pul monary oedema, cardiac arrhythmias and cardiorespiratory failure, with metabolic acidosis. Most of the clinical features result from severe hypoxia, but cyanosis is uncommon. Classic ally, there is a smell of bitter almonds on the breath, but many people cannot detect this. Management \200 Avoid getting contaminated yourself. \200 Provide supportive measures: give 100 % O 2 and monitor ECG. \200 Remove contaminated clothing and wash exposed skin. \200 Consider activated charcoal or gastric lavage within 1hr of ingestion. \200 In mil d poisoning, reassurance, O 2 and observation may be all that is required. Exposure to cyan ide causes great anxiety and it may be dif- \201 cult to distinguish between fear of pois oning and early symptoms of toxicity. Speci \201 c antidotes should be available, but are not always needed. Some speci \201 c antidotes to cyanide are dangerous in the absence of cyanide \200\224 only give if poisoni ng is moderate or severe (eg coma). In severe cyanide poisoning, give dicobalt edetate (Kel ocyanor ) 300mg IV over 1min, repeated if there is no improvement after 1min. In the abs ence of cyanide, dicobalt edetate may cause cobalt poisoning with facial, laryngeal and pul monary oedema, vomiting, tachycardia and hypotension. Alternative treatment is sodium thios ulphate (adult dose 25mL of 50 % solution IV over 10min; child 400mg/kg) with sodium nitrit e (adult dose 10mL of 3 % solution IV over 5 \200\22320min; child dose 0.13 \200\2230.33mL of 3 % solution/kg, ie 4 \200\22310mg/kg). Sodium thiosulphate often causes vomiting. Sodiu m nitrite may cause hypotension. High doses of hydroxocobalamin (5 \200\22310g, Cyanokit ) are useful and relatively safe in cyanide poisoning, especially in victims of smoke inha lation. 208 CHAPTER 4 Toxicology Carbon monoxide poisoning Carbon monoxide (CO) is a tasteless and odorless gas produced by incomplete combustion. Poisoning may occur from car exhausts, \201 res and faulty gas hea ters. CO is also produced by metabolism of methylene chloride (used in paint strippers and as an industrial solvent). CO d the O 2 -carrying capacity of the blood by binding hemoglob in (Hb) to form carboxyhaemoglobin (COHb). This impairs O 2 delivery from blood to the tiss ues and also inhibits cytochrome oxidase, blocking O 2 utilization. These effects combine t o cause severe tissue hypoxia. The elimination half-life of CO is about 4hr on breathing ai r, 1hr on 100 % O 2 , and 23min on O 2 at 3 atmospheres pressure. Clinical features Early features are headache, malaise, nausea and vomiting (sometimes misd iagnosed as a viral illness or gastroenteritis, especially if several members of a family a re affected). In severe poisoning , there is coma with hyperventilation, hypotension, i mus cle tone, i re \202 exes, extensor plantars and convulsions. Cherry-red coloring of the sk in may be seen in fatal CO poisoning, but is rare in live patients. Skin blisters and rhabd omyolysis may occur after prolonged immobility. Pulmonary oedema, MI and cerebral oedema ca n occur. Neurological and psychiatric problems sometimes develop some weeks after CO poison ing, but usually improve over the following year. Management \200 Remove from exposure. \200 Clear the airway and maintain ventilation wi th as high a concentration of O 2 as possible. For a conscious patient use a tight- \201 t ting mask with an O 2 reservoir, but if unconscious intubate and provide IPPV on 100 % O 2 . \200 Record ECG and monitor heart rhythm: look for arrhythmias and signs of acute MI. Check ABG \200\224 SpO 2 measurements are misleading in CO poisoning, as are p a O 2 values, but acidosis indicates tissue hypoxia. Check COHb levels (in blood or with a special pulse oximeter): although these correlate poo rly with clinical features, COHb > 15 % after arrival at hospital suggests serious poisonin g. COHb may be up to 8 % in smokers without CO poisoning. A nomogram ( b p.395) can help to estimate COHb at the time of exposure. Correct metabolic acidosis by ventilation and O 2 : try to avoid bicarbo- nate, which may worsen tissue hypoxia. Consider mannitol if cerebral oedema is suspected. \200 Hyperbaric O 2 therapy is logical , but of no proven bene \201 t for CO poisoning. Transfer to a hyperbaric chamber and pres surization may take hours and so hyperbaric treatment may be no more effective than ventila tion on 100 % normobaric O 2 . Caring for a critically ill patient in a small pressure cham ber may be impracticable. Discuss with a Poisons Information Service ( b p.181) and conside r 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. The Poisons Information Service can advise on the location and telephone numbers of hyperbaric chamber s. Some details are in Table 6.1, b p.261. 209 CS GAS (TEAR GAS) Chlorine poisoning Chlorine gas causes lacrimation, conjunctivitis, coughing, wheezing, bre athlessness, and chest pain. Laryngeal and pulmonary oedema may develop within a few hours. \200 Remove from exposure and give O 2 , with bronchodilators if necessary. If there is laryngeal or pulmonary oedema, consult an expert and give prednisolone in high dosage (adul t 60 \200\22380mg/day initially). In severe cases, IPPV in ICU may be needed. If the eyes are painful, irrigate with water or saline, and examine with \202 uorescein 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. \200 Patients with symptoms when seen in hospital usually need admission for at least 12 hours for observation. Record serial peak expirator y \202 ow rates, which may warn of deterioration. CS gas (tear gas) CS (orthochlorobenzylidene malononitrile) is used for riot control, polic e 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 che st. Vomiting may occur. These symptoms usually disappear within 10min in fresh air, but con junctivitis may persist for 30min. Exposure in a con \201 ned space may cause symptoms for some hours 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 a nd close- \201 tting goggles. Remove contaminated clothes and wash affected skin thoroughl y. Give O 2 and bronchodilators if necessary. Reassure the patient that the symptoms will r esolve. 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 minutes. Alternatively, irrigate the eyes with sal ine (although this may cause a transient worsening of symptoms). When symptoms have settled , record visual acuity and examine the corneas using \202 uorescein. Refer to an ophthalm ologist if symptoms persist. CN gas (chloroacetophenone) is used in some countries for riot control and in personal defe nse devices. CN has similar effects to CS, but is more toxic. 210 CHAPTER 4 Toxicology Chemical incidents Chemical incidents involving single or multiple casualties may result fr om accidents (eg release of chlorine gas) or deliberate release of chemicals (by terrorists or others). CBRN (Chemical, Biological, Radiological and Nuclear) incidents have many feat ures in common. If you know or suspect that a patient has been involved in a chemical incident: \200 Info rm senior ED staff. \200 Avoid contaminating other staff or patients. \200 Ensure that you are wearing suitable personal protective equipment (PPE), unless the patient has already been decontaminated. Decontaminate the patient according to departmental guidelines if this has not been done already (see b p.211). Resuscitate as necessary: airway, breathing, and circulation. \200 Assess the clinical fe atures and toxic agent. \200 Give antidotes if appropriate, and reassess the patient. \200 Enquire whether other patients are expected. \200 Inform the local Health Protectio n Team. \200 Get expert advice from Toxbase, Poisons Information Service ( b p.181) or HP A Chemical Hazards and Poisons Division (ChaPD tel. 0870 606 4444). If deliberate release is suspected inform the Police and involve other agencies and the press of \201 cer. Chemical agents which might cause a chemical incident include: \200 Chlorine \200\224 se e b p.209. \200 CS gas (tear gas) \200\224 see b CS gas (tear gas), p.209. \200 Cyanid e \200\224 see b p.207. \200 Organophosphates \200\224 see b p.206. Information about chemical incidents \200 Health Protection Agency advice on CBRN and che mical incidents: www.hpa.org.uk/emergency/CBRN.htm TOXBASE (see b p.181) section on Deliberate Release gives details of toxicity and antidotes , with medical, public health and public brie \201 ng documents about 60 chemicals that mi ght be deliberately released. \200 Home Of \201 ce guidance on decontamination after CBR N incidents: http://www.cabinetof \201 ce.gov.uk/ukresilience/emergencies/cbrn.aspx Infection control and prevention: see b p.32. Major incidents: see b p.38. Radiation incide nts: see b p.268. 211 DECONTAMINATION OF PATIENTS Decontamination of patients Decontamination after exposure to a chemical, biological, or ra diation hazard is intended to reduce the risks to the patient and to other people. Casualties should be decontaminated at the scene after a CBRN inci- dent, but some contamin ated patients are likely to arrive at EDs without warning. Many people will be worried abou t contamination, but not actually at risk. Patients injured by industrial incidents, road t raf \201 c collisions, bombs, or other incidents may also be contaminated. Even with advance planning it will be challenging to organize the ED, keep \200\230clean \200\231 areas clean, maintain order, and communicate between the \200\230decon \200\231 t eam (in PPE) and other ED staff. Equipment for decontamination \200 Scissors. Buckets. Sponges, soft brushes, wash cloths. Liquid soap. \200 Disposable towels. Disposable gowns and slippers. Blankets. \200 Pla stic bags (large for clothing, small for valuables). \200 ID labels and waterproof markin g pens (for patients and property bags). \200 Plastic bins with polythene liners (for use d decontamination equipment). \200 Warm or tepid water (hot water might increase chemical absorption). \200 0.9 % saline and drip sets for eye and wound irrigation. LA eye drops. Decontaminating non-ambulant patients \200 Keep contaminated patients outside the ED. \200 Clear, prepare, and secure the decontamination area. \200 Protect yourself with app ropriate PPE and use it properly. \200 Work in teams of 2 \200\2234 people. Look after ea ch other. \200 Tell the team what to look for and what to do. \200 In severe poisoning resuscitation, antidote administration, and decon- tamination may have to be done simultaneously. Tell casualties what you are doing. \200 Record patient \200\231s name and number on wris t band and property bags. \200 Remove or cut off clothing (which removes 80 \200\22390 % of contamination). Do not pull clothing off over the head. Fold clothing outside-in and put it in property bags. \200 Put valuables in a separate ba g. Wash glasses and keep with patient. \200 Clean face (protecting airway), open wounds, and sites for IV access, then from head to toes, front and back (log roll) including skin c reases. Rinse affected areas with soapy water (saline for wounds and eyes). \200 Wipe affected ar eas gently with a sponge to remove chemicals. \200 Rinse with clean water. \200 Dry pat ient. Cover in gown and blanket. Transfer to \200\230clean \200\231 trolley. \200 Move p atient to \200\230clean \200\231 area for further assessment and treatment. \200 Put con taminated equipment in appropriate containers. \200 Contain waste water if possible; if n ot, inform water/sewage agency. \200 Rest and rotate staff as needed. \200 Ensure staff are decontaminated before leaving the \200\230dirty \200\231 area. \200 Record names of staff involved in decontamination. \200 Warn staff of possible symptoms and check for si gns of poisoning. \200 Debrief staff and record events. 212 CHAPTER 4 Toxicology Plants, berries and mushrooms Plants and berries Many children eat plant leaves or brightly -colored berries, but serious poisoning from plants is very rare. Identify the plant if pos sible, using reference books 1 , 2 , 3 or the CD-ROM computer software Poisonous plants and fungi in Britain and Ireland ( b p.180). Advice on toxicity and any nec- essary 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 one death recorded in the UK in 50 years. No treatment needs to be provided for children who eat laburnum seeds, except for th e very few with symptoms (nausea, salivation, vomiting, headache, rarely convulsions). Mushroom poisoning Serious poisoning from mushrooms or fungi is rare. Most deaths are due t o Amanita phalloides (death cap mushroom). Reference books 1 , 4 are useful, but identi \201 cation of mushrooms from the description or fragments available is often uncertain. Ad vice on toxicity and treatment is available from Poisons Information Services ( b p.181). M ushrooms found in gardens are unlikely to produce severe poisoning, but may cause vomiting and occasionally hallucinations, usually within 2hr of ingestion. Mushrooms which cause sym ptoms within 6hr are unlikely to be seriously toxic. Delayed toxicity occurs with Amanita p halloides and some other species, which grow throughout the UK. Amanita phalloides poisoning causes vomiting and profuse watery diarrhea after a latent per iod of 6 \200\22312hr, followed by hepatic and renal failure. The interval between ingestio n and the onset of symptoms is crucial in distin- guishing between non-serious and potentia lly fatal poisoning. Try to ascertain if: \200 More than one variety of mushroom was eaten (since poisonous an d edible mushrooms often grow together). Whether the mushrooms were cooked (since some toxins are inacti- vated by heat). Whether alcohol was taken (since disul \201 ram-like effects may occur with Coprinus species, ink cap mushrooms). For most toxic mushrooms only symptomatic treatment is required. Activated charcoal may d a bsorption if given within 1hr. Get expert advice immediately if Amanita poisoning is suspec ted ( b p.181). 1 Cooper MR , Johnson AW , Dauncey EA ( 2003 ) Poisonous Plants and Fungi, An Illustrated G uide , 2 nd edn. TSO , London . 2 Dauncey EA ( 2010 ) Poisonous Plants: A Guide for Childcare Providers . Royal Botanic Gar dens , Kew . 3 Frohne D , Pf nder HJ ( 2004 ) Poisonous Plants , 2 nd edn. Manson Publishing Ltd , Lond on . 4 Bresinsky A , Besl H ( 1990 ). A Color Atlas of Poisonous Fungi . CRC Press , London . 213 BUTTON BATTERIES Button batteries Small children often swallow button or disc batteries intended for toys, w atches, hearing aids, and other electrical equipment. The larger batteries may become stuck in the esophagus, causing perforation or later stenosis. Most batteries that reach the sto mach pass through the gut without any problem. Corrosive damage could occur from electrical discharge, but toxicity from battery contents is rare. Mercury poisoning is very unlikely since mercuric oxide batteries are no longer sold. The Poisons Information Service may iden tify the type of battery involved from the reference number, if this is available on the pa cket or on a similar battery to that ingested. Management X-ray the chest and abdomen or use a metal detector to \201 nd the battery. A battery stuck in the esophagus should be removed immediately by endoscopy (which allows ins pection for oesophageal damage and so is preferable to a magnet or Foley catheter). An asymptomatic child with a battery in the stomach or bowel can be sent home with advice t o return if any symptoms develop. If the battery has not been passed after 2 or 3 days, and is causing concern use a metal detector or repeat X-ray to look for the battery. If it is still in the stomach (which is rare) consider removal by endoscopy to avoid any risk of per foration or absorption of battery contents. Batteries in the small or large bowel almost always pass spontaneously and should be left t o do so, unless they cause symptoms. If abdominal pain, vomiting, diarrhea or rectal bleedi ng occur an abdominal X-ray is needed to localize the battery, which may require removal by endoscopy or surgery.