Emergency Drug Guidelines (Fiji) 2008 PDF

 Emergency Drug Guidelines ______________________________________________ Second Edition 2008 Ministry of Health Government of Fiji Islands 2008 "This do...

 Emergency Drug Guidelines ______________________________________________ Second Edition 2008 Ministry of Health Government of Fiji Islands 2008 "This document has been produced with the financial assistance of the European Community and World Health Organization. The views expressed herein are those of the Fiji National Medicine & Therapeutics Committee and can therefore in no way be taken to reflect the official opinion of the European Community and the World Health Organization.”  Disclaimer The authors do not warrant the accuracy of the information contained in nd this 2 Edition of the Emergency Drug Guidelines and do no take responsibility for any death, loss, damage or injury caused by using the information in these guidelines. While every effort has been made to ensure that these guidelines are correct and in accordance with current evidence-based and clinical practices, the dynamic nature of medicine information requires that users exercise in all cases independent professional judgment and understand the individual clinical scenario when referring, prescribing or nd providing information from the Emergency Drug Guidelines, 2 Edition.  Preface The publication of the Second Edition of the Emergency Drug Guidelines represents the culmination of the efforts of the National Drugs and Therapeutics Committee (NDTC) to publish clinical drug guidelines for common diseases seen in Fiji. These guidelines are targeted for health care professionals working at hospitals and at the primary health care settings. It sets the gold standard for the use of drugs in the treatment of emergency medical conditions in Fiji. The guidelines have taken into account the drugs available in the Fiji Essential Medicines Formulary (EMF), 2006 Edition, in recommending treatment approaches. All recommended therapies are either evidence- based or universally accepted standards. It is hoped that these guidelines will be used by all health care workers in their daily care of patients suffering from emergency medical conditions. DR. MARGARET CORNELIUS Chairperson National Drugs and Therapeutics Committee Ministry of Health, Suva, Fiji 2008  Acknowledgements The First Edition of these guidelines was drafted on behalf of the Ministry of Health (MOH) by Nick Adams, MBBS (Melb), FACEM, Principal Medical Officer, Accidents and Emergency Department, Colonial War Memorial Hospital in 1999. The Ministry of Health initially approached Dr Adams to prepare these guidelines as part of an overall effort to develop treatment guidelines in critical areas. Dr Adams prepared these guidelines during his employment as a specialist emergency physician at CWM Hospital. The Ministry of Health gratefully acknowledges the personal enthusiasm and initiative of Dr Adams in producing these guidelines. Dr Adams was assisted by Elizabeth Pemberton, MBBS, FANZCA, Long-Term Advisor in Anaesthesia, Pacific Postgraduate Medical Centre, Fiji School of Medicine, in the preparation of the draft guidelines. The guidelines have been reviewed by a subcommittee of the National Drugs and Therapeutics Committee. Subcommittee on the Preparation of the Second Edition of the Emergency Drug Guidelines Dr Gyaneshwar Rao Consultant Physician, Colonial War Memorial Hospital Prof Robert Moulds Clinical Pharmacologist, Professor of Medicine, Fiji School of Medicine Dr Alan Mamerto Garvez Consultant Physician, Colonial War Memorial Hospital Dr.Adam Jenney Specialist Physician, Colonial War Memorial Hospital Dr Anne Drake Senior Lecturer in Medicine, Fiji School of Medicine Ms Vasiti Nawadra-Taylor Principal Pharmacist, Fiji Pharmaceutical Services  Table of Contents 1 Emergency Drugs 1 1.1 Local anaesthetics 1 1.2 Sedatives and induction agents 1 1.3 Anticholinergics 2 1.4 Opiod analgesics 2 1.5 Antiemetics 3 1.6 Corticosteroids 3 1.7 Antiepileptics 3 1.8 Antiarrhyhtmics 4 1.9 Antihypertensives 5 1.10 Inotropic agents 5 1.11 Diuretics 6 1.12 Muscle relaxants 6 1.13 Neuroleptics 6 1.14 Anti-asthma drugs 7 1.15 Intravenous fluids 7 1.16 Tetanus prophylaxis 8 1.17 Drugs used in cardiac arrest 8 2 Cardiovascular Emergencies 10 2.1 Cardiac arrest 10 2.2 Cardiogenic shock 15 2.3 Unstable angina 16 2.4 Acute myocardial infarction 17 2.5 Cardiac arrhythmias 19 2.6 Acute pulmonary oedema 24 2.7 Hypertensive emergency 26 3 Respiratory Emergencies 27 3.1 Asthma 27 3.2 Exacerbation of chronic obstructive pulmonary disease 29 3.3 Croup 30 3.4 Epiglottitis 31 3.5 Oxygen therapy 32 4 Neurologic Emergencies 34 4.1 Seizures 34 4.2 Migraine 35 4.3 Oculogyric crisis 36 4.4 Tetanus 36 4.5 Acute bacterial meningitis in adults 37 5 Poisoning and Overdoses 38 5.1 General principles 39 5.2 Treatment of specific poisons 40 5.3 Poisons information 47 6 Endocrine Emergencies 48 6.1 Diabetic ketoacidosis 48 6.2 Hyperosmolar, hyperglycaemic state 50 6.3 Adrenal insufficiency 50 6.4 Hypoglycaemia 51 6.5 Thyroid storm 52 6.6 Myxydema coma (hypothyroid crisis) 52  6.7 Phaeochromocytoma 53 7 Fluid and Electrolyte Emergencies 54 7.1 Hyperkalaemia 54 7.2 Hypokalaemia 55 7.3 Hypercalcaemia 55 7.4 Hypocalcaemia 56 7.5 Fluid resuscitation 56 8 Miscellaneous Emergencies 57 8.1 Anaphylaxis 57 8.2 Pre-eclampsia 60 8.3 Septic shock 61 8.4 Acute psychosis 62 Appendix 63 1 Emergency Drugs This section is intended as a brief guide to some of the drugs mentioned in this book. It is by no means exhaustive and does not cover all contraindications or dosage alterations in special situations. Information about these areas should be obtained elsewhere. The dosages below are guides only. Drug therapy should always be adjusted to the individual patient situation. 1.1 Local Anaesthetics Local anaesthetic agents are used to provide anaesthesia through local wound infiltration, nerve blocks or regional techniques. Side effects from systemic absorption include seizures and cardiac arrhythmias. Avoid accidental intravenous administration by aspirating for blood prior to injection. Lignocaine is the agent of choice for local wound infiltration. The 1% solution is suitable for local infiltration of most wounds. A concentration of 2% should be used for digital nerve blocks and any other area where a smaller volume of anaesthetic is desirable. Lignocaine with adrenaline should not be used on the extremities, i.e. nose, fingers, toes, ears or penis. The addition of adrenaline helps control bleeding and also extends the duration of anaesthesia. 1 1.2 Sedatives and Induction Agents These drugs are used to depress the conscious state either for sedation or general anaesthesia. They should be used with great care as unconscious patients are unable to protect their airway and because of the risk of causing hypoventilation and hypotension. Ketamine has anaesthetic and analgesic properties and is less likely to produce hypotension than other sedative agents. It also has a mild bronchodilator action which makes it useful when anaesthetising patients with asthma. Adverse effects include increased salivation, laryngospasm, raised intracranial pressure and unpleasant hallucinations after recovery of consciousness. Ketamine should not be used in patients at risk of raised intracranial pressure (e.g. head injuries, meningitis) or in patients with ischaemic heart disease. It should not be given unless personnel and facilities are available to protect the patient’s airway. Ketamine should be given as an intravenous bolus. The usual dose is 2 mg per kg although some patients may require larger amounts. The onset of action is within 60 seconds and the duration is about 20 minutes. Thiopentone is a barbiturate with a short action because of rapid distribution. Its main adverse effects relate to cardiorespiratory depression. It should be used with great care in patients who are hypotensive and should not be given unless personnel and facilities are available to protect the patient’s 2 airway. It is a potent anticonvulsant and is the drug of choice for anaesthetising patients with status epilepticus. Thiopentone should be given as an intravenous bolus. The usual dose is 3 to 5 mg per kg. The lower dose should be used in the elderly. The onset of action is about 30 seconds and its effects last for 5 to 10 minutes. Midazolam is a short-acting benzodiazepine. It has powerful amnestic properties and produces less cardiorespiratory depression than thiopentone. It is a fairly safe and useful anaesthetic induction agent in the critically ill and is also used to sedate children and agitated patients. Midazolam can be given intramuscularly or as an intravenous bolus. In children, intranasal midazolam is a useful premedication prior to suturing. The onset of action of intravenous midazolam is 1 to 2 minutes and the effects of a single dose last from 60 to 90 minutes. Intranasal midazolam has its maximal effect within 10 minutes and lasts up to 2 hours. In ADULTS: The intravenous dose is 2.5 to 15 mg. The dose should be titrated to its effect. Smaller doses are usually required for the elderly, whereas alcoholics may require higher doses. The intramuscular dose is 5 to 10 mg. In CHILDREN: The intravenous dose is 0.15 to 0.3 mg per kg up to 0.5 mg per kg. The intranasal dose is 0.2 to 0.4 mg per kg (to a maximum of 5 mg), slowly dropped into alternate nostrils 3 over 15 seconds. 1.3 Anticholinergics Anticholinergic drugs block the effects of acetylcholine at muscarinic receptors. The most commonly used anticholinergic agent is atropine. This drug is used for the treatment of bradycardia due to increased vagal tone, to block the cholinergic effects of drugs such as suxamethonium in children, and to reverse some of the adverse effects of anticholinesterase (organophosphate) poisoning. Ipratropium is used in the treatment of asthma and benztropine is used in the treatment of oculogyric crisis. Atropine should be used with care in patients with ischaemic heart disease as it may cause a marked sinus tachycardia. The usual adult dose is 0.6 mg intravenously as a bolus, repeated in 5 minutes if necessary. A dose of 3 mg will produce complete blockade of muscarinic cholinergic receptors in an adult. Much larger doses are used in anticholinesterase poisoning. Atropine may be given via the endotracheal tube in an emergency; use twice the normal intravenous dose and dilute in 10 ml of 0.9% saline. The paediatric dose is 20 micrograms per kg (to a maximum of 0.5 mg). The onset of action is within 5 minutes and the duration of action is 2 to 4 hours. Benztropine is used in the treatment of oculogyric crisis precipitated by prochlorperazine or similar drugs. Overdose of 4 benztropine can cause central anticholinergic syndrome (confusion, hallucinations). The usual dose in adults is 1 to 2 mg orally or intramuscularly. Children should be given 20 micrograms per kg. Its duration of action is shorter than most of the drugs that cause oculogyric crisis so a repeat oral dose should be given 4 hours after the initial dose. 1.4 Opioid Analgesics Opioid agents are mainly used for their analgesic and sedative actions. The main side effects of these drugs are respiratory depression, hypotension, nausea, vomiting, and constipation. NOTE: The use of parenteral opioid drugs is not recommended in patients with chronic or recurrent painful conditions such as migraine or back pain due to the risk of addiction. Morphine is usually used in the treatment of acute myocardial infarction and pulmonary oedema. As an analgesic, it may produce less dysphoria than pethidine. The usual dose in adults is 2.5 mg intravenous bolus repeated every few minutes as required to a maximum of 15 mg. The usual dose in children is 0.05 mg per kg given intravenously every 5 minutes to a maximum of 0.2 mg per kg. The duration of action is about 3 hours. Pethidine is mainly used as an analgesic. This is a highly addictive drug even after a few doses. The best method of administration is a dose of 25 to 50 mg intravenously every 3 to 4 hours. Alternatively, a dose of 25 to 100 mg (maximum 150 5 mg) may be given intramuscularly. The duration of action is 2 to 3 hours with intramuscular dose and shorter with intravenous administration. Fentanyl is a short acting narcotic used to sedate patients prior to painful procedures or intubation (often in combination with midazolam). The usual dose of fentanyl is 1 microgram per kg. The duration of action is 30 to 40 minutes. 1.5 Antiemetics Anti-emetic drugs are used for the temporary relief of nausea and vomiting. Metoclopramide (brand name: Maxolon) should not be given to children less than 16 years of age due to the high incidence of acute dystonic reactions. It should also not be given to patients with bowel obstruction. Metoclopramide is useful in the treatment of migraine and may also help the passage of calculi in renal colic. The usual dose is 10 mg by intravenous bolus or intramuscular injection or orally. Males weighing more than 70 kg may require 15 or 20 mg. Females with low body weight or the elderly should be given 5 mg initially. Prochlorperazine (brand name: Stemetil) is also useful for the treatment of vertigo as well as nausea and vomiting. It should not be given to children less than 16 years of age. The oral dose is 5 to 10 mg 8-hourly. The intramuscular or intravenous dose is 12.5 mg every 8 hours. 6 Promethazine (brand name: Phenergan) is a weaker antiemetic than prochlorperazine and is more sedating. It can be given intravenously, intramuscularly or orally. The usual dose is 0.5 mg per kg. 1.6 Corticosteroids Although very useful in the treatment of asthma, anaphylaxis and many other conditions, the beneficial effects of these drugs are delayed for several hours at least. They should be used with care in patients with diabetes or peptic ulcer disease. All agents have similar anti-inflammatory effects but differ in their mineralocorticoid potency. Their mineralocorticoid (or aldosterone-like) effects may be undesirable and include sodium retention, oedema, and hypokalaemia. Equivalent anti-inflammatory doses are: 100 mg hydrocortisone = 25 mg prednisolone = 4 mg dexamethasone Hydrocortisone has marked mineralocorticoid effects. It should be given intravenously over 5 minutes. The usual dose is 50 to 100 mg intravenously 6-hourly. Dexamethasone has virtually no mineralocorticoid effects. It can be given intramuscularly or intravenously as well as orally. The usual dose is 0.1 mg per kg every 8 hours. Prednisolone has moderate mineralocorticoid effects. It is 7 given orally. The usual dose is 1 mg per kg daily to a maximum of 80 mg. 1.7 Antiepileptics The first line drug in the treatment of epilepsy is diazepam. Phenytoin is useful for the treatment of idiopathic epilepsy but is less effective for seizures due to other causes. Barbiturates such as phenobarbitone are powerful anti-epileptics but also cause cardiorespiratory depression and marked depression of conscious state often necessitating intubation and ventilation. Diazepam is a safe and effective agent for the termination of seizures. It may be given intravenously or rectally. The oral route is too slow in an emergency, whereas the intramuscular route is painful and unpredictable. The onset of action when given intravenously is 1 to 2 minutes, whereas the rectal route may take 5 to 10 minutes to have its full effect. The usual intravenous dose is 0.1 mg per kg repeated every 5 minutes if required. The usual rectal dose is 0.5 mg per kg. Phenytoin must be given by slow intravenous injection. The infusion rate should not exceed 50 mg per minute in adults or 1 mg per kg per minute in children. The drug should be diluted in 0.9% saline only (not 5% dextrose) so that the concentration is no greater than 5 mg per ml. Rapid infusion of concentrated solutions may cause hypotension. The usual loading dose is 15 mg per kg intravenously. 8 1.8 Antiarrhythmics 1.8.1 Lignocaine Lignocaine shortens the action potential duration. It is the drug of first choice in the treatment of ventricular tachycardia although phenytoin is used in the treatment of ventricular tachycardia due to digoxin toxicity. Lignocaine 2% should be given intravenously over one minute in a dose of 1 mg per kg. A further 0.5 mg per kg may be given after 5 minutes if necessary. Lignocaine has a very short half-life so the intravenous bolus should be followed by an infusion at a rate of 40 micrograms per kg per minute. Adverse effects include confusion, coma, seizures and heart block but are not often encountered. Elderly patients may require lower infusion rates. 1.8.2 Propranolol Propranolol is occasionally used to delay conduction through the atrioventricular (AV) node in the treatment of supraventricular tachycardia or atrial fibrillation. It also may be of benefit in the treatment of ventricular tachycardia due to theophylline overdose. Propranolol should not be used in patients with decompensated left ventricular failure, asthma, or bradyarrhythmias. The dose should be titrated according to effect. Give 10 micrograms per kg intravenously every 2 minutes to a maximum of 100 micrograms per kg. 9 1.8.3 Amiodarone Amiodarone prolongs the action potential duration. It is used in the treatment of both ventricular and atrial arrhythmias. At least some of its therapeutic effects are often delayed for up to 24 hours. Amiodarone is not a negative inotrope and is well tolerated by patients with cardiac failure. Intravenous administration is occasionally associated with hypotension due to vasodilation. The usual loading dose of amiodarone is 5 mg per kg given intravenously over 30 minutes. 1.8.4 Verapamil Verapamil is a calcium channel antagonist and depresses sinus node automaticity and AV node conduction. It is therefore used to treat supraventricular tachyarrhythmia. It is a powerful negative inotrope and should be used with great care in patients with impaired left ventricular function. Verapamil should not be given to children less than 2 years of age. It should not be given to patients with left ventricular failure, bradycardia, or hypotension. The effectiveness of vagal manoeuvres is increased following the administration of verapamil. The usual dose in adults is 1 mg intravenous boluses every minute to a maximum of 10 mg. 1.8.5 Digoxin Digoxin is used to control the ventricular rate in atrial fibrillation. It is contraindicated in atrial fibrillation associated 10 with Wolff-Parkinson-White syndrome. The main advantage digoxin has over other drugs available to control conduction through the AV node, is the fact that it is not a negative inotrope. Most patients with atrial fibrillation have significant underlying cardiac disease and often tolerate poorly the myocardial depressant effects of verapamil and propranolol, making digoxin the safest choice. The effects of digoxin are increased in the presence of hypokalaemia, hypothyroidism, hypomagnesaemia, and hypercalcaemia. Digoxin should not be given to patients with bradycardia. The maximum therapeutic effects of digoxin are delayed by 6 to 24 hours after administration. The usual initial dose is 10 micrograms per kg given intravenously over 20 to 30 minutes and the total digitalizing dose should be given within 24 hours. 1.8.6 Adenosine Adenosine is a very short acting agent used in the treatment of supraventricular tachycardia. It is best given in incremental doses according to response (usually 6 mg initially and if no response, give 12 mg and if necessary followed by 18 mg). Adenosine should be given as a rapid intravenous bolus followed by a 20 ml 0.9% saline flush. It should be given with great care to asthmatics as it may occasionally induce severe bronchospasm in these patients. Adenosine is antagonised by theophylline and is unlikely to be effective in patients who are taking this drug. 11 1.9 Antihypertensives Several different drugs are available for the management of hypertensive emergencies. Hydrallazine is a direct acting arteriodilator. It should not be used in patients with ischaemic heart disease who are not being treated with a beta-blocker. Side effects include nausea, tachycardia, and headache. Peak effects are not seen for 10 to 20 minutes after intravenous injection and it has a duration of action of 4 to 8 hours. The usual dose in adults is 10 mg intravenously every 20 minutes to a maximum of 50 mg. Nifedipine is a direct-acting arterial vasodilator. When given by sublingual route, it has unpredictable effects and can precipitate myocardial infarction or stroke by excessive lowering of blood pressure. Hence, it should not given by this route. 1.10 Inotropic Agents Inotropic agents are used in the treatment of cardiogenic and distributive shock. All should be infused via a large vein. Adrenaline is an alpha- and beta-adrenergic agonist. It causes an increase in cardiac output and heart rate plus vasoconstriction. It is given by infusion into a large vein at a rate of 1 to 70 micrograms per minute titrated to effect. 12 Dopamine has similar effects to adrenaline but produces more tachycardia at higher doses. It may preferentially enhance renal blood flow at rates less than 5 micrograms per kg per minute. Dobutamine has positive chronotropic and inotropic effects which are balanced by a mild degree of vasodilation so that myocardial oxygen demand is generally not increased. Dobutamine is generally considered the inotrope of choice in patients with myocardial ischaemia. The usual dose range is 2 to 20 micrograms per kg per minute titrated to effect. 1.11 Diuretics Frusemide is a potent loop diuretic used in the treatment of fluid overload. Its main side effects are hypokalaemia and fluid depletion. Damage to the inner ear may occur with too rapid intravenous injection. Frusemide is ineffective in the acute treatment of hypertension and should not be used except as an adjunct to other more powerful drugs. Intravenous frusemide has an onset of action within 5 minutes, a peak effect at about 30 minutes, and a duration of action of 2 hours. Dosage varies according to renal function; most patients without renal impairment will have a significant diuresis after 40 mg given intravenously. Doses in excess of 250 mg may be required to diurese patients with severe renal failure. Frusemide should not be given intravenously at a rate faster than 40 mg per minute. The absorption of intramuscular frusemide is unpredictable and this route of administration 13 should not be used. 1.12 Muscle Relaxants Suxamethonium is a depolarising muscle relaxant. It is given as an intravenous bolus and has its maximal effect within 60 seconds. The duration of paralysis is usually about 5 minutes. Very rarely, some patients with an atypical plasma cholinesterase enzyme will be paralysed for much longer. The usual dose is 1 to 1.5 mg per kg in adults and 2 mg per kg in children. Suxamethonium is contraindicated in the presence of hyperkalaemia, lower motor neurone diseases, and between 3 days and 2 years after major burns. In the absence of these contraindications, suxamethonium is the drug of first choice for muscle relaxation in rapid sequence intubation. Vecuronium is a non-depolarising muscle relaxant. Given as an intravenous bolus it has its onset in about 3 minutes and lasts 20 to 30 minutes. The usual dose is 0.1 mg per kg. 1.13 Neuroleptics Haloperidol is the safest neuroleptic to use for sedation. It may be given intramuscularly or intravenously. The usual intravenous dose in adults is 2.5 mg repeated every 5 minutes to a maximum of to 10 mg. Chlorpromazine is more likely to cause hypotension than haloperidol. 14 Diazepam can be used as a sedative for short defined periods of treatment to avoid addiction. 1.14 Anti-asthma Drugs Salbutamol is a beta-2 adrenergic agonist. It is best given in the inhaled form (either via an inhaler or a nebulizer). Intravenous salbutamol may occasionally be required for very severe asthma where marked airway obstruction may prevent the inhaled form of the drug from reaching the distal airways. The main side effects of salbutamol are sinus tachycardia, tremor, and anxiety. It can also cause hypokalaemia. Nebulized salbutamol may be given as often as necessary, even continuously. The upper dose limit is defined in each patient by the adverse effects of tachyardia and tremor. The usual dose is 5 mg in adults and older children, and 2.5 mg in children less than 5 years old. The dose should be diluted up to 2 ml using 0.9% saline but may be given without dilution. Intravenous salbutamol is given in a dose of 5 micrograms per kg (up to a maximum of 250 micrograms) over 1 to 2 minutes and repeated once 15 minutes later if necessary. Ipratropium is used in the treatment of asthma and chronic obstructive pulmonary disease (COPD). It has a synergistic effect with salbutamol. Adverse systemic effects are very rare but nebulized ipratropium can inadvertently enters the eye and causes a fixed, dilated pupil. The usual dose in adults is 0.5 mg 15 via a nebulizer every 4 to 6 hours. Children 5 years of age or under should be given 0.25 mg per dose. Corticosteroids are discussed in Section 1.6. Aminophylline is a xanthine derivative that has been used for many years in the treatment of asthma. However, it is a weak bronchodilator and has no additional benefit over optimal doses of salbutamol. It also has a very narrow therapeutic margin and therefore has little place in the management of acute asthma. Adverse effects include ventricular tachycardia, seizures, and hypokalaemia. Its use should be restricted to severe asthma. 1.15 Intravenous Fluids Normal (0.9%) saline contains 154 mmol per liter of sodium chloride. It is essentially isotonic and iso-osmolar, and is distributed to the extracellular fluid space. It is the fluid of first choice in the treatment of hypovolaemia. Normal saline contains too much saline to be used as the sole maintenance fluid, although it may be alternated with 5% dextrose. Dextrose 5% contains 50 g per liter of dextrose. It is distributed to the total body water space and is thus not suitable for emergency rehydration. Although it can be used as the sole maintenance fluid in the short term, prolonged administration of 5% dextrose alone may cause hyponatraemia, especially in children. 16 Dextrose 3% with 0.3 saline contains 51 mmol per liter of sodium chloride and 30 g per liter of dextrose. Its primary use is as a maintenance fluid (with potassium) in children. It may be suitable for rehydration of patients with mild or moderate dehydration. Hartmann’s solution contains a mixture of ions similar to that of the extracellular fluid. It may be substituted for 0.9% saline except in the presence of hyperkalaemia or alkalosis. It contains 140 mmol per liter of sodium, 109 mmol per liter of chloride, 29 mmol per liter of bicarbonate, 5 mmol per liter of potassium, and 2 mmol per liter of calcium. Plasma volume expanding solution (e.g. Haemaccel, Gelofusin): Colloids can be used for patients with hypovolaemic shock in association with crystalloid solutions. 1.16 Tetanus Prophylaxis Regular immunization with tetanus toxoid is the best way to prevent death due to tetanus. Children should receive doses of tetanus toxoid at 6, 10 and 14 weeks of age then booster doses at 6 years. Thereafter, booster doses of tetanus toxoid should be given every 10 years. Patients presenting with a skin wound should be treated as described below. A non-immune patient is one who has never received a full course of tetanus toxoid injections. Tetanus 17 prone wounds include puncture wounds, contaminated or infected wounds and crush wounds. 1.16.1 Non-immune patient with tetanus prone wound ™ Give tetanus toxoid 0.5 ml intramuscularly and complete course (with repeat tetanus toxoid injections at 6 weeks and 6 months), PLUS ™ Give tetanus immune globulin 250 units intramuscularly at a different site than that of the tetanus toxoid injection. 1.16.2 Non-immune patient with clean wound ™ Give tetanus toxoid 0.5 ml intramuscularly and complete course (with repeat tetanus toxoid injections at 6 weeks and 6 months). 1.16.3 Immune patient with tetanus prone wound If more than 5 years since last tetanus toxoid booster THEN ™ Give tetanus toxoid 0.5 ml intramuscularly. 1.16.4 Immune patient with clean wound If more than 10 years since last tetanus toxoid booster THEN 18 ™ Give tetanus toxoid 0.5 ml intramuscularly. 1.17 Drugs Used in Cardiac Arrest Adrenaline is a powerful endogenous catecholamine. The pharmacologic doses used in cardiac arrests far exceed the amounts usually produced by the adrenal glands. Adrenaline has both alpha- and beta-adrenergic agonist effects. It stimulates myocardial contraction, increases the heart rate, and raises the blood pressure. Its most dangerous adverse effect is induction of ventricular arrhythmias, an effect which is far more likely when the myocardium is sensitized to catecholamines. This occurs with myocardial ischaemia (which adrenaline can also induce by increasing myocardial work), and with overdoses of drugs such as amphetamines and cocaine. In the setting of a cardiac arrest, the induction of ventricular arrhythmias is obviously not a problem and a large intravenous bolus doses should be given. However, in situations other than cardiac arrest, such as anaphylaxis or asthma, adrenaline should be used with great care to avoid worsening the patient’s condition. In these circumstances, adrenaline is best given intravenously in small carefully titrated doses. Also see Section 1.10. The absorption of adrenaline given by the subcutaneous or intramuscular routes is unpredictable especially in shock states but administration by these routes can be life-saving in patients in shock states due to anaphylaxis. In ventricular fibrillation or asystole, adrenaline should be given in doses of 1 mg by 19 intravenous bolus. Administration should be by a central line if already present or by a large peripheral vein and followed by a 20 ml 0.9% saline flush to ensure it rapidly reaches the central circulation. If there is no intravenous access then adrenaline can be given via the endotracheal tube. When given by this route it should be diluted in 10 ml of 0.9% saline and the dose should be 5 times the intravenous dose. There is no role for intracardiac injection of adrenaline (or any other drug). Lignocaine is recommended for the treatment of ventricular fibrillation and ventricular tachycardia. Its effectiveness has not been proven but it is unlikely to be harmful. The usual dose is 1 mg per kg intravenously given over 1 minute. Lignocaine has a short therapeutic half-life so a successful bolus dose should be followed by a lignocaine infusion. Lignocaine may be given via the endotracheal tube if intravenous access is unavailable. Twice the intravenous dose is used and it should be diluted in 10 ml of 0.9% saline. Also see Section 1.8.1. Atropine is used in the treatment of asystole and severe bradycardia. It acts to block the effects of the vagus nerve on the heart. A dose of 3 mg in an adult produces complete atropinization, blocking all the cholinergic receptors. The main adverse effect of atropine is to produce a sinus tachycardia which may be harmful in the presence of ischaemic heart disease. The usual total dose of atropine used in cardiac arrest is 40 micrograms per kg which may be given as a single bolus or in several divided doses a few minutes apart. Also see Section 1.3. 20 Sodium bicarbonate is used to treat the metabolic acidosis associated with cardiac arrest. Its effectiveness has not been proven and it has many potential adverse effects. Most authorities recommend that it be given in prolonged cardiac arrests (i.e. those greater than 10 minutes in duration). It should be given earlier in the presence of acute renal failure, hyperkalaemia, or tricyclic antidepressant overdose. The usual dose is 1 mmol per kg intravenously over 1 to 2 minutes. 21 2 Cardiovascular Emergencies 2.1 Cardiac Arrest 2.1.1 Basic cardiac life support (BCLS) Prompt and effective cardiopulmonary resuscitation (CPR) has been shown to increase survival after cardiac arrest. It should begin as early as possible after the onset of cardiac arrest and continued with as little interruption as possible until the patient either recovers spontaneous circulation or a decision is made to cease the resuscitation efforts. a. Call for help Proper CPR requires at least two people. At least one other person is required to obtain the drugs and equipment needed for advanced cardiac life support. b. Check for response Assess the patient’s conscious state quickly by shaking the patient and yelling his or her name. Loss of consciousness always accompanies cardiac arrest. Unconscious patients are unable to protect their own airway. 22 c. Airway Look in the mouth for a foreign body or vomitus. Listen for breath sounds. Noisy breath sounds are a sign of a partly obstructed airway. The absence of breath sounds may indicate complete airway obstruction. Act to protect and maintain the airway. Perform appropriate procedures including suctioning, head tilt, chin lift, jaw thrust, and insertion of an oral airway. The correct size oral airway can be estimated by holding it against the side of the patient’s face – it should reach from the corner of the mouth to the ear lobe. d. Breathing Look for movement of the chest wall and listen to the lungs for breath sounds on both sides of the chest. Asymmetry of breath sounds may be a sign of a pneumothorax. Act by ventilating the patient with a bag and mask. Be sure to use an appropriate size face mask that fits the patient’s face. Mouth to mouth ventilation should be performed if a bag and mask are unavailable. e. Circulation Feel for the carotid or femoral pulse and listen for heart sounds. (The brachial pulse is often the easier to feel in neonates, rather than the carotid or femoral). If there is no palpable pulse, act 23 by starting external cardiac massage. Cardiac massage should be performed on the lower 1/2 of the sternum, depressing it about 5 cm in adults and older children. In young children and babies, it should be depressed about 1/4 of the distance between the front and the back of the chest. The rate should be 80 per minute in adults and 100 per minute in children and babies. The ratio of ventilations to compressions depends on the number of persons doing CPR and is as follows: If one person, 2:30 in children and ??? in adults If two persons, 2:15 in children and ??? in adults Start advanced cardiac life support as soon as possible. 2.1.2 Advanced cardiac life support (ACLS) Cardiac arrest most commonly occurs due to life-threatening arrhythmias. The first step in ACLS is to determine what the cardiac rhythm is by attaching a cardiac monitor. Cardiac arrest rhythms can be divided into three basic types: “Shockable” rhythm ƒ Pulseless ventricular tachycardia (VT) ƒ Ventricular fibrillation (VF) “Non-shockable” rhythm ƒ Asystole or severe bradycardia ƒ Pulseless ventricular activity. 24 a. Pulseless ventricular tachycardia or ventricular fibrillation (VF) Ventricular tachycardia without an adequate cardiac output should be treated as for ventricular fibrillation. The most important feature of the treatment of these arrhythmias is prompt defibrillation. Defibrillation is the only treatment that has been definitely shown to increase survival after cardiac arrest – it should be performed as early as possible. The primary drug in the treatment of VF is adrenaline – all other drugs are of secondary importance. Provide basic cardiac life support as described above. Defibrillate with 360 joules (first shock) once only. Immediately continue CPR for 2 minutes continuously. During CPR, establish intravenous access (if not yet available) and secure airway and ventilate with 100% oxygen. Check heart rhythm after 2 minutes of CPR. If no response: Defibrillate again (second shock) with 360 joules and resume CPR immediately and continue for 2 minutes. Check heart rhythm. If still no response: 25  Give adrenaline 1 mg bolus intravenously (1 ml of 1:1,000 or 10 ml of 1:10,000) and defibrillate (third shock) with 360 joules, followed by CPR for 2 minutes. Check heart rhythm. NOTE: Adrenaline dose should be followed by a 20 ml normal saline flush. Adrenaline may also be given down the endotracheal tube – the dose is 5 times the intravenous dose and it should be diluted in 10 ml of normal saline. If still no response: Give amiodarone 300 mg slow bolus intravenously (if available), OR Lignocaine 2%, 100 mg bolus intravenously, and defibrillate (fourth shock) with 360 joules, followed by CPR for 2 minutes. Check heart rhythm. If still no response: Give adrenaline 1 mg bolus intravenously (1 ml of 1:1,000 or 10 ml of 1:10,000) and defibrillate (fifth shock) with 360 joules, followed by CPR for 2 minutes. 26  Continue defibrillation and CPR for 2 minutes, giving adrenaline every alternate cycle. Sodium bicarbonate is generally not indicated unless cause of arrest is secondary to hyperkalaemia or tricyclic overdose. NOTES: If there is no spontaneous circulation 20 minutes after cardiac arrest then the chance of recovery is essentially zero and resuscitation should usually be ceased. If sinus rhythm is restored, check for pulse and blood pressure. The patient may require an adrenaline infusion to maintain blood pressure. Lignocaine or amiodarone infusion should be continued (refer to Annex). In children: ™ Defibrillate at 2 joules per kg then 4 joules per kg. ™ Give adrenaline 10 micrograms per kg (0.1 ml per kg of 1: 10, 000 up to 1 ml). Ventricular tachyarrhythmias in special circumstances Other drugs may be indicated in some special circumstances: Digoxin Toxicity (see Section 5.2.14) – Ventricular 27  tachycardia in the presence of digoxin toxicity may respond to phenytoin and magnesium sulphate. If defibrillation is necessary then 25 joules may be all that is required. Higher defibrillation energies may induce ventricular fibrillation. Theophylline Toxicity (see Section 5.2.16) – Administration of intravenous propranolol may be helpful for ventricular tachyarrhythmias. b. Asystole or severe bradycardia Asystole has a very poor survival rate compared to VF. It is wise to make sure that the rhythm is indeed asystole by inspecting more than one lead on the ECG monitor. Very occasionally, VF may look like asystole in one of the ECG leads. Provide basic cardiac life support as described above. Obtain intravenous access. Secure airway and continue to ventilate with maximum oxygen available. Give adrenaline 1 mg intravenous bolus (1ml of 1:1, 000 or 10 ml of 1:10 ,000 ). Continue external cardiac massage. If no response: Give atropine 3 mg intravenous bolus. Continue external cardiac massage. If no response: 28  Give adrenaline 5 mg intravenous bolus. Continue external cardiac massage. Further doses of adrenaline 1 mg intravenously may be given at 3- to 5-minute intervals until return of spontaneous circulation or cessation of resuscitation efforts. NOTES: In children ™ Give adrenaline 10 micrograms per kg ( 0.1 ml per kg of 1: 10,000 up to 1 ml) and repeat as necessary every 5 minutes. ™ Give atropine 50 micrograms per kg. If there is no spontaneous circulation 20 minutes after cardiac arrest then the chance of recovery is essentially zero and resuscitation should usually be ceased. c. Pulseless ventricular activity (formerly called electromechanical dissociation (EMD) This term refers to patients who have a cardiac rhythm other than VF, VT, or asystole but without a detectable cardiac output. Most cases are due to severe and irreversible cardiac muscle dysfunction but occasionally pulseless ventricular activity may be due to a treatable cause. 29 Treatment is as for ventricular asystole with the addition of the need to exclude potentially reversible causes (“4Hs and 4Ts”) such as: hypoxia hypovolemia, severe hypothermia or hyperthermia hypokalemia or hyperkalemia and metabolic acidosis cardiac tamponade tension pneumothorax toxins, poisons, drugs thrombosis – pulmonary or coronary. Tension pneumothorax Insert a wide-bore intravenous cannula in the second intercostal space in the midclavicular line on the side of the pneumothorax. Hypovolaemia ™ Administer Haemaccel 10 m per kg intravenous bolus stat. Severe hyperkalaemia or acidosis ™ Give 0.1 ml per kg of 10% calcium chloride (to a maximum dose of 10 ml) intravenous bolus and repeat in 5 minute, if necessary, 30  PLUS ™ Give 8.4% sodium bicarbonate 1 mmol per kg intravenous bolus. Calcium channel blocker overdose or hypocalcaemia ™ Give 0.1 ml per kg of 10% calcium chloride (to a maximum of 10 ml) intravenous bolus and repeat in 5 minutes, if necessary. Beta-adrenergic antagonist overdose (see Section 5.2.7) ™ Give glucagon 5 mg intravenous bolus. NOTE: This is not available in the EDL (Essential Drug List). Obtain intravenous access. Secure airway and continue to ventilate with maximum oxygen available. Give adrenaline 1 mg intravenous bolus. Continue external cardiac massage. Give adrenaline 5 mg intravenous bolus. Continue external cardiac massage. 31 2.1.3 Intubation Endotracheal intubation should be attempted as soon as possible during cardiopulmonary resuscitation to ensure adequate ventilation. 2.2 Cardiogenic Shock Cardiogenic shock is defined as a state where the cardiac output is inadequate to maintain tissue perfusion. It is usually characterised by hypotension, compensatory peripheral vasoconstriction, and signs of congestive cardiac failure. It is very important to distinguish cardiogenic shock from hypovolaemic shock and distributive shock (due to anaphylaxis or sepsis). Cardiogenic shock has many different causes, the usual being acute myocardial infarction. Treatment of the underlying cause, whenever possible, is essential. Administration of inotropic agents should be viewed only as a temporary measure while the underlying cause is reversed. Close monitoring in an intensive care unit is highly desirable. The prognosis of cardiogenic shock is dismal and most patients will not recover despite the following therapy. 2.2.1 Maintain airway and breathing The usual maneuvers to maintain an adequate airway and adequate ventilation, up to and including endotracheal 32 intubation should be used. All patients should at least receive high flow oxygen via face mask. ™ Give oxygen to maintain arterial oxygen saturation greater than 95%. 2.2.2 Optimise intravascular volume Insertion of a central venous line allows accurate measurement of central venous pressures (CVP) and also makes administration of inotropic agents safer. If CVP line is not available, examination of neck veins must be used. Correct anaemia with administration of blood or otherwise use boluses of normal saline to achieve an optimal CVP (5 to 10 cm water). Note that patients with right ventricular infarction usually require a much higher central venous filling pressure (e.g. 20 cm water) than other patients. ™ Give 0.9% saline boluses of 100 ml intravenously to obtain an optimal central venous filling pressure. 2.2.3 Inotropic agents The initial agent of choice in cardiogenic shock is dobutamine, if available. Dopamine is a suitable alternative. In ADULTS: ™ Give dobutamine 2 micrograms per kg per minute by intravenous infusion and increase rate by 1 to 2 33  micrograms per kg per minute every 5 minutes to a maximum of 20 micrograms per kg per minute; OR ™ Give dopamine 2 micrograms per kg per minute by intravenous infusion and increase to 20 micrograms per kg per minute, if necessary. In CHILDREN: ™ Give dobutamine 2 micrograms per kg per minute by intravenous infusion and increase rate by 1 to 2 micrograms per kg per minute every 5 minutes according to response to a maximum of 20 micrograms per kg per minute; OR ™ Give dopamine 2 micrograms per kg per minute by intravenous infusion and increase rate by 1 microgram per kg per minute every 5 minutes according to response to a maximum of 20 micrograms per kg per minute. NOTE: Ideally, inotropic agents should be infused via a central venous line. Otherwise, a large peripheral vein (such as the femoral vein or the cubital veins) should be used. In some situations, a combination of dopamine and dobutamine can be more effective than either agent alone. 34 2.3 Unstable Angina This coronary syndrome is characterized by anginal pain which is severe, of recent onset, or which has recently become abruptly worse. Angina occurring at rest or following recent myocardial infarction is also classified as unstable angina. There is evidence that the reason for unstable angina is a sudden change in a previously stable plaque within an atheromatous coronary artery. Rupture of the endothelium over and around the plaque leads to vasoconstriction, platelet adhesion, and an inflammatory response. If the vessel becomes completely occluded, a myocardial infarct will result. However, commonly, occlusion is not complete and the area around the plaque settles down over a period of a few weeks. All patients diagnosed to be suffering from unstable angina should be referred for admission preferably to the Coronary Care Unit (CCU). The most important distinction to make is between unstable angina and an acute myocardial infarction. The factors favouring an acute myocardial infarction include pain of more than 15 to 20 minutes duration; pain not responsive to nitrates or requiring narcotics; and systemic features such as pallor, sweating, vomiting, and hypotension. If any or all of these are present, refer immediately to hospital. An electrocardiogram (ECG) is critically important in making the diagnosis. The aim of treatment in unstable angina is to relieve the pain and to modify the environment around the “active” plaque to 35 reduce the likelihood of coronary artery occlusion and subsequent myocardial infarction. However, it should be borne in mind that chest pain might be secondary to other serious conditions like acute myocardial infarction, pericarditis, aortic dissection, and pulmonary embolism. For initial treatment: ™ Oxygen therapy. ™ Aspirin 150 to 300 mg orally stat, AND ™ Morphine 2.5 to 5 mg intravenously as needed, AND ™ Atenolol 50 to 100 mg orally daily, OR ™ Propranolol 40 to 80 mg orally two to three times daily. If pain still persists, in addition, heparin should be given as follows: ™ Heparin 5,000 units intravenous bolus dose followed by 1,000 units per hour by intravenous infusion. The infusion rate should be adjusted to keep the PTTK (partial thromboplastin time with kaolin) between 60 and 85 seconds. 36 The PTTK should be measured 6-hourly until stable, then daily thereafter. Heparin will normally be required for at least 3 days and possibly longer depending on clinical response. If pain persists and if the patient’s hemodynamic status allows, ADD: ™ Nifedipine SR 20 to 40 mg orally twice daily, AND, if required, ADD ™ Isosorbide dinitrate 10 to 40 mg orally three times daily. If symptoms persist despite all of the above treatment, cardiological intervention, if available, is required with a view to further investigation and revascularization. 2.4 Acute Myocardial Infarction Complete occlusion of a coronary artery leads to the death of the cardiac muscle it supplies. Occlusion of a large, proximal vessel may cause myocardial ischaemia of such an extent that the patient dies rapidly of pump failure. Alternatively, a ventricular arrhythmia (tachycardia, fibrillation) may reduce cardiac output to such a drastic extent that, if the abnormal rhythm cannot be reversed, death is most likely. 37 Severity of pain by itself is a poor indicator of the extent of myocardial damage especially in a diabetic patient. Poor cerebral function, peripheral circulatory signs such as pallor, sweating, and hypotension combined with extensive ECG changes with or without arrhythmias point to a large infarct. The aims of immediate management are to: relieve pain achieve coronary reperfusion and minimize infarct size prevent and treat heart failure and shock allay the patient’s anxiety All patients with suspected myocardial infarction should be admitted to hospital and preferably to a unit where cardiac monitoring can be performed. 2.4.1 Immediate management ™ Aspirin 300 mg chewed or dissolved before swallowing. ™ Oxygen 4 to 6 liters per minute by mask. ™ Morphine 2.5 to 5 mg intravenously with repeat doses as necessary for pain relief, AND ™ Glyceryl trinitrate 600 micrograms sublingually with a repeat dose in 5 minutes if no response. It should not be given in hypotension and if right ventricular infarction is suspected. 38 Unless the patient is very anxious, routine use of a sedative drug (e.g. diazepam) is not recommended. 2.4.2 Thrombolytic therapy The indications for thrombolytic therapy includes chest pain that has developed within the previous 12 hours with either ST segment elevation myocardial infarction (STEMI) or development of new left bundle branch block (LBBB). Streptokinase Administer streptokinase (STK) 1.5 million international units (IU) by intravenous infusion over 30 to 60 minutes. If blood pressure falls as a result of the infusion, reduce the rate or stop briefly and restart at half the previous rate. Streptokinase induces antibody formation that makes it unsuitable for use in subsequent episodes of coronary occlusion. It may also produce allergic symptoms (i.e. bronchospasm, angio-oedema, urticaria, flushing, and musculoskeletal pain). The contraindications to thrombolytic therapy are shown in Table 1. Patients most likely to benefit from thrombolytic treatment are those presenting early with large anterior infarcts especially if complicated by heart failure. 39 Those presenting after 24 hours have less chance of benefit and increased risk of cardiac rupture. For mild or moderate allergic reactions to streptokinase: ™ Promethazine 25 mg intravenously, AND / OR ™ Hydrocortisone 100 mg intravenously. Severe allergic reactions should be treated as for anaphylaxis. Give ™ Adrenaline 1 in 1,000 solution, 0.5 to 1 ml ( 0.5 to 1 mg) intravenously over 5 minutes. If response is poor, increase dose to: ™ Adrenaline 1 in 1,000 solution 2 to 5 ml (2 to 5 mg) intravenously over 5 minute, AND ADD ™ Promethazine 25 mg intravenously, OR ™ Hydrocortisone 100 mg intravenously. 40 NOTE: Refer to Cardiovascular Guidelines for details on the subsequent management of unstable angina and acute myocardial infarction. 2.5 Cardiac Arrhythmias Cardiac arrhythmias range from trivial ectopic beats to the life- threatening ventricular fibrillation. Whether or not an arrhythmia requires intervention depends largely on its capacity to make a significant impact on cardiac output. In a patient whose myocardial function is already impaired (e.g. by a large infarct) a change from normal sinus rhythm to atrial fibrillation with an increased ventricular rate of 140 beats per minute may be sufficient to cause heart failure. By contrast, a young person with a normal myocardium may sustain a supraventricular tachycardia at the same rate for days without any evidence of cardiac decompensation. The urgency for intervention and the nature of that intervention are dictated equally by the situation in which the arrhythmia occurs and by the nature of the arrhythmia itself. Most arrhythmias are benign and injudicious use of antiarrhythmic drugs can be harmful as many of them are proarrhythmic in their own right. 41 Table 1. Contraindications to thrombolytic therapy Absolute contraindications Relative contraindications Active internal bleeding Previous peptic ulcer disease Recent surgery, biopsy or Warfarin therapy trauma Liver disease Prior cardiopulmonary Previous streptokinase resuscitation therapy within the last Known bleeding disease four years (haemophilia, platelet Previous hypersensitivity to disorders) streptokinase Ischemic stroke within 6 Heavy perivaginal bleeding months Diabetic proliferative Neurosurgery within 6 months retinopathy A previous intracranial bleed Pregnancy Severe uncontrolled hypertension (a blood pressure greater than 180/110 mm Hg during presentation) Aortic dissection Coma Oesophageal varices 42 2.5.1 Tachyarrhythmias a. Atrial tachyarrhythmias i. Sinus tachycardia This implies a persistent heart rate over 100 per minute in a resting patient. It usually has an underlying cause such as anxiety, thyroid overactivity, or systemic illness. The first approach should be to identify and treat the underlying cause. If no obvious underlying cause is apparent, treatment is generally not needed. ii. Atrial premature complexes Treatment is seldom required. If patient is symptomatic, ™ Atenolol 25 to 100 mg orally daily, OR ™ Propranolol 40 to 80 mg orally two to three times daily. 43 iii. Paroxysmal supraventricular tachycardia (PSVT) This occurs intermittently and sometimes can be converted to sinus rhythm by carotid sinus massage, by the Valsalva manoeuvre, or by holding ice cold water in the mouth. If these are ineffective, ™ Verapamil 5 mg intravenously slowly, repeat if needed up to 15 mg; OR ™ Adenosine 6 mg bolus intravenously over 5 to 10 seconds, if unsuccessful, followed by 12 mg intravenously 2 minutes later, and if needed, 18 mg intravenously thereafter. Adenosine can produce chest pain and large falls in blood pressure. However, the half-life of the drug is short and recovery will occur within one minute normally without intervention. If the symptoms persist, aminophylline intravenously can be used. If above drugs are not available, ™ Digoxin 0.25 to 0.50 mg orally stat, repeat same dose orally 6 hours later, followed by 0.25 mg orally 6 hours after the second dose, 44  followed by 0.25 mg orally 6 hours after the third dose, and continue at 0.25 orally mg daily. If rapid control is needed, digoxin may be given intravenously (see below under section on atrial fibrillation). The maintenance digoxin dose should be adjusted depending on the patient’s renal function and serum potassium level. Verapamil must never be given to a patient with a wide-complex undiagnosed tachycardia – QRS > 0.12 seconds. If there is any possibility that the rhythm is a ventricular tachycardia, either use adenosine or treat as for ventricular tachycardia. Once arrhythmia has been stabilized, prophylaxis against further attacks of PSVT, if frequent, must be initiated. Drugs that can be used for prophylaxis include digoxin, beta-blockers, calcium channel blockers, and amiodarone (in difficult cases). iv. Atrial flutter and fibrillation Atrial flutter usually presents with a 2:1 atrioventricular block and a regular rate of around 150 beats per minute. Atrial fibrillation presents with a similar rate which is however quite irregular. The aims of treatment are discussed below. 45 ƒ Control ventricular rate This is only required if the ventricular rate is >100 per minute. The urgency to control the rate depends on the pre-existing ventricular rate. ™ Digitalization: Digoxin 0.25 to 0.50 mg orally stat, repeat same dose orally 6 hours later, followed by 0.25 mg orally 6 hours after the second dose, followed by 0.25 mg orally 6 hours after the third dose, and continue at 0.25 orally mg daily. The intravenous route is rarely necessary because oral digititalization is just as effective. However, if rapid digitalization is needed, digoxin may be given intravenously. The total loading dosage is 0.5 to 1.5 mg. A loading dose of 0.5 mg in 20 ml of normal saline is given as an intravenous infusion for 20 minutes. The remaining dose is also given intravenously over 20 minutes at intervals of 4 to 6 hours depending on the response over a period of 24 hours. The total digitalizing dose will need to be reduced if the patient has had digoxin in the preceding 2 weeks. 46  OR ™ Verapamil 5 mg intravenously up to 15 mg with careful monitoring of pulse and blood pressure. For long-term control, the drugs that can be used are similar to that mentioned under the section on PSVT. ƒ Treatment of underlying cause Whenever possible, the underlying cause should be identified and treated (e.g. hypokalaemia, thyrotoxicosis). ƒ Reversal to sinus rhythm For atrial fibrillation of recent onset, consideration should be given to convert it to sinus rhythm by electrocardioversion. Medical therapy with amiodarone or sotalol might be effective. In chronic AF, recent evidence suggests that rate control is just as effective as rhythm control. ƒ Anticoagulant therapy Unless contraindicated and impractical (i.e. poor patient compliance, difficulty in monitoring), anticoagulant therapy should be considered in every patient with chronic AF to prevent thromboembolic event. If warfarin cannot be used for one reason or another, aspirin can be used as alternative but is not as 47  effective as warfarin. The risk of thromboembolism increases in patients with previous thromboembolism, mitral valve disease, heart failure, hypertension, and in older patients – especially women over the age of 75 years. b. Ventricular arrhythmias i. Premature ventricular ectopics including bigeminy These are benign unless patients have underlying heart disease. If no obvious cause is found, the following measures are advisable: reduction of coffee and tea intake cessation of smoking reduction alcohol intake. Drug treatment is not normally required but in symptomatic cases beta-blockade may be of value. ™ Atenolol 25 to 100 mg orally daily, OR ™ Propranolol 40 to 80 mg orally two to three times daily. 48 ii. Ventricular tachycardia (VT) ƒ Non-sustained ventricular tachycardia In hospitals where ECG monitoring is possible, treat only prolonged episodes that cause cardiovascular haemodynamic instability. ™ Lignocaine 2%, 50 to 100 mg intravenously over 1 to 2 minute, followed by 4 mg per minute intravenous infusion for a maximum of one hour, then 1 to 2 mg per minute by intravenous infusion for 24 hours (see Appendix). If patient is unresponsive or if lignocaine is contraindicated use: ™ Amiodarone 5 mg per kg intravenously (preferably through a central venous line) over 1 to 2 hours, followed by 10 to 15 mg per kg infused over a 24- hour period (see Appendix). ƒ Sustained ventricular tachycardia - With haemodynamic stability Treatment is the same as for non-sustained ventricular tachycardia. - With haemodynamic instability (“pulseless VT”) – Refer to Section 2.1. 49 iii. Ventricular fibrillation – Refer to Section 2.1. iv. Ventricular asystole – Refer to Section 2.1. v. Torsades de pointes This is a rare, polymorphic ventricular tachycardia in which the QRS axis is constantly shifting (turning, “torsade”). Patients usually have a prolonged QTc (greater than 0.45 seconds) on the ECG. The rhythm is particularly prone to occur as a result of drug therapy including treatment with tricyclic antidepressants, phenothiazines, erythromycin, and ketoconazole. Any drug suspected of causing the arrhythmia should be stopped immediately. Patients should be managed in hospital with ECG monitoring. No consensus exists about the most effective treatment. Lignocaine can be effective. ™ Lignocaine 2%, 75 to 100 mg intravenously over 1-2 minutes, followed by 4 mg per minute for a maximum of one hour. Maintenance infusion thereafter of 1 to 2 mg per minute by intravenous infusion (see Appendix). Alternatively, 50  ™ Magnesium sulphate 50%, 2 grams intravenously over 10 to 15 minutes, followed, if necessary, by 0.5 to 0.75 gram per hour by intravenous infusion for 12 to 24 hours. DO NOT use amiodarone to treat this arrhythmia as it may provoke it. 2.5.2 Bradyarrhythmias a. Sinus bradycardia Treat only if symptomatic. Exclude hypothyroidism, pituitary failure, and drugs (e.g. beta-blockers, digoxin, and verapamil). If intervention is required: ™ Atropine 0.6 to 1.8 mg intravenously and repeat as needed. b. Atrioventricular block Drugs (digoxin, beta-blockers, or verapamil) may be the cause and should be withheld if this appears to be the case. i. First degree AV block There is prolonged PR interval on ECG. This requires no treatment. 51 ii. Second degree AV block There are two types. ƒ Wenckebach phenomenon (Mobitz type I) In this type of AV block, there is successive prolongation of the PR interval followed by a dropped beat and the whole cycle repeats. ƒ Mobitz type II There is a fixed ratio between the atrial and ventricular contractions in this type of arrhythmia, e.g. 2:1 or 3:1. Generally, both types of AV block do not require treatment. Rarely, pacing may be required in Mobitz type II AV block. iii. Third degree heart block This may be an acute and potentially spontaneously reversible complication of, for example, an acute anterior or inferior myocardial infarction. In centers where cardiac pacing is possible, this is the treatment of choice. If pacing is not available give ™ Isoprenaline 20 micrograms intravenously, 52  repeat according to clinical response, and follow with an infusion of 1 to 4 micrograms per minute, or occasionally higher in patients who have been on beta-blockers (see Appendix). There is anecdotal evidence for the efficacy of ephedrine, salbutamol, and theophylline in maintaining response if the block has responded to isoprenaline. The treatment of choice for chronic heart block is permanent cardiac pacing. iv. Sinoatrial block and sick sinus syndrome These conditions require pacemaker therapy if persistent. However, this therapeutic option is currently not available in Fiji. 2.6 Acute Pulmonary Oedema Acute pulmonary oedema is a medical emergency that requires prompt treatment. Oxygen, morphine, vasodilators, and diuretics should be used. If the patient becomes hypotensive (systolic blood pressure 4 years). NOTE: Patients who fail to respond to nebulized adrenaline may require endotracheal intubation. Nebulized adrenaline provides only temporary relief of airway obstruction lasting 1 to 2 hours. Patients should be closely observed after this period for recurrence of obstruction. 67 3.4 Epiglottitis Epiglottitis is a medical emergency and failure to provide prompt treatment may be fatal. It is due to infection of the epiglottis with Haemophilus influenzae bacteria. Epiglottitis mainly affects children between the ages of 3 and 8 years but is occasionally seen in adults as well. It is characterized by fever, inspiratory and expiratory upper airway noises, a severe sore throat, dysphagia, and drooling. The patient usually looks very unwell. There is a very high risk of acute airway obstruction. All patients should be referred immediately to an anaesthetist and admitted to an intensive care unit. Attempting to view the throat or otherwise upsetting the child may cause airway obstruction and should be avoided. Keep the patient sitting up. ™ Give ceftriaxone 100 mg per kg stat then 50 mg per kg intravenously daily, OR ™ Give chloramphenicol 40 mg per kg stat then 25 mg per kg intravenously daily. 3.5 Oxygen Therapy Oxygen is essential for human metabolism and lack of oxygen is generally fatal within 5 to 6 minutes. Oxygen has almost no 68 adverse effects in the acute situation and should not be withheld if there is any suggestion of it being needed. Indications for oxygen therapy include: cardiac or respiratory arrest hypoxia of any cause cardiac failure myocardial infarction shock of any cause carbon monoxide poisoning. Oxygen therapy should be monitored with pulse oximetry and ABGs estimation, if available. In general, aim to achieve an oxygen saturation of at least 92% (except in patients who are carbon dioxide retainers). Humidification of oxygen is not necessary. 3.5.1 Methods of oxygen delivery a. Intranasal catheters These provide a low concentration of oxygen of between 25% and 40%. They should be used with an oxygen flow rate of between 1 and 4 liters per minute (1 to 2 liters per minute in children). Higher flow rates cause drying of the nasal mucosa and are uncomfortable. They should only be used in patients with mild hypoxia or cardiac failure or myocardial ischaemia. They do not provide a high enough oxygen concentration for patients with significant hypoxia, carbon monoxide poisoning, shock, or cardiac arrest. 69 b. Plastic face masks These provide oxygen concentrations of between 35% and 70%. The oxygen flow rate should be set between 4 and 15 liters per minute. Do not use face masks with an oxygen flow rate less than 4 liters per minute. This method of oxygen delivery is suitable for patients with moderate hypoxia or shock. c. Tight fitting face masks (e.g. Laerdal, CPAP masks) These devices can provide oxygen concentrations close to 100%, if available. They should be used in patients with severe hypoxia or with cardiac arrest. 3.5.2 Adverse effects of oxygen Patients with COPD and elevated carbon dioxide levels may occasionally have a hypoxia-dependent respiratory drive. In these patients, the administration of oxygen causes hypoventilation and an increase in the carbon dioxide level. Although this may cause problems it is usually far less dangerous than hypoxia itself. In the emergency situation, it is important that hypoxia is corrected – problems with carbon dioxide retention can be handled later. Do not hesitate to give oxygen to hypoxic patients with COPD, but they should be observed for possible deterioration caused by worsening hypercapnea. 70 Administration of 100% oxygen sometimes causes pulmonary toxicity but this only occurs after 24 hours and therefore is not a problem in the emergency situation. NOTE: If arterial blood gases or pulse oximetry measurement is available, then they should be undertaken before the commencement of oxygen to establish the baseline in significantly hypoxic patients or those at risk of carbon dioxide retention. 71 4 Neurologic Emergencies 4.1 Seizures There are numerous causes of epileptic seizures. In adults, the majority occur in known epileptics with idiopathic epilepsy while in children febrile convulsions are a common cause. However, it is important to exclude less common, reversible, and serious causes of seizures such as hypoglycaemia, hyponatraemia, hypocalcaemia, eclampsia, drug overdose, meningitis, or intracranial lesions. Most seizures are self-limiting and brief. Emergency drug treatment is only necessary if the seizures are prolonged (>5 minutes) or recurrent. Initial treatment is gentle restraint of the patient in the left lateral position and administration of high flow oxygen via face mask. 4.1.1 Treatment in adults ™ Give diazepam 5 mg intravenous bolus and repeat every 2 minutes as required to a maximum dose of 20 mg. This dose may be repeated 30 minutes later if necessary, OR, if there is no intravenous access, 72 ™ Give diazepam 0.5 mg per kg per rectum (use intravenous solution); PLUS, if seizures persist or are recurrent, ™ Give phenytoin 15 mg per kg via intravenous infusion over 20 minutes. NOTE: If seizures persist despite diazepam and phenytoin, THEN diazepam or thiopentone infusions should be considered. a. Diazepam infusion ™ Diazepam 100 mg in normal saline to make a total of 100 ml solution (strength: 1 mg per ml) and infuse at a rate of 2 mg per hour. Patient must be carefully monitored for respiratory depression. b. Thiopentone infusion The patient should be intubated before the thiopentone infusion is begun. ™ For induction, give thiopentone 5 mg per kg intravenous bolus, THEN 73 ™ Commence thiopentone infusion at a rate of 50 mg per hour. 4.1.2 Treatment in children ™ Give diazepam 0.2 mg per kg intravenous bolus and repeat after 5 minutes to a maximum dose of 6 to 12 mg, OR, if there is no intravenous access, ™ Give diazepam 0.5 mg per kg per rectum; PLUS, if seizures persist, ™ Give phenytoin 15 to 20 mg per kg via intravenous infusion over 20 minutes, OR ™ Give phenobarbitone 20 mg per kg intravenously or intramuscularly stat which may be repeated 10 mg per kg as required to a maximum dose of 40 mg per kg. If seizures persist and last for more than 60 minutes, give ™ Midazolam infusion 1 to 4 micrograms per kg per minute (3 mg per kg in 50 ml of dextrose saline or normal saline to run at 1 to 4 ml per hour). If seizures persist, consider thiopentone infusion: 74 ™ For induction, give thiopentone 5 mg per kg intravenous bolus, THEN ™ Commence thiopentone infusion at a rate of 1 mg per kg per hour. 4.2 Migraine Migraines are recurrent, often unilateral, throbbing headaches associated with nausea, photophobia, and sometimes visual disturbance. The diagnosis is usually fairly obvious but it is important to consider other causes of headache (e.g. meningitis, subarachnoid haemorrhage) if there are atypical features. 4.2.1 Treatment in adults Patients should rest in a quiet dark room after treatment. ™ Give metoclopramide 10 mg orally or intramuscularly, OR ™ Give prochlorperazine 5 mg orally or 12.5 mg intramuscularly; THEN 15 minutes later, 75 ™ Give aspirin 900 mg orally, repeat in 4 hours, if required; PLUS ™ Give paracetamol 1.5 gram orally, repeat in 4 hours, if required. NOTE: Other drugs that can be used in the treatment of acute migraine include ergotamine preparations and sumatriptan but they are not available in the Fiji EDL. 4.2.2 Treatment in children Paracetamol alone is usually sufficient along with rest in a quiet dark room. ™ Give paracetamol 20 mg per kg orally or rectally. 4.3 Oculogyric Crisis Oculogyric crisis is an acute focal dystonic reaction to neuroleptic agents and anti-emetic drugs such as metoclopramide. It most commonly affects young women. It is characterised by involuntary deviation of the eyes upward often with torticollis (spasm of the neck muscles). ™ Give benztropine 2 mg orally or intramuscularly. NOTE: A further dose of benztropine should be given 4 hours 76 later to prevent recurrence. 4.4 Tetanus Tetanus is a severe life-threatening disease caused by the toxin producing bacterium Clostridium tetani. It usually follows local wound contamination in an improperly immunized individual. Clinical features include muscle rigidity (esp. trismus), painful muscle spasms, fever, labile hypertension, and abnormalities of cardiac rhythm. Patients should be managed in an intensive care unit if possible. 4.4.1 Airway and breathing Give high flow oxygen via face mask. Cardiorespiratory status should be closely monitored. Patients with respiratory muscle involvement will need early intubation, muscle paralysis and ventilation. 4.4.2 Tetanus immune globulin and immunization Tetanus immunoglobulin neutralizes circulating toxin. Large doses are required. ™ Give tetanus immune globulin 4,000 units intravenously over 30 minutes. Commence active immunization with tetanus toxoid. ™ Give tetanus toxoid 0.5 ml intramuscularly. 77 4.4.3 Wound debridement Aggressive wound debridement is essential. 4.4.4 Antibiotics Penicillin or metronidazole is effective against C. tetani: ™ Give benzylpenicillin 100,000 units per kg (maximum dose of 4 megaunits) intravenously 4-hourly, OR, if penicillin sensitive, ™ Give metronidazole 7.5 mg per kg (maximum dose 500 mg) intravenously 8-hourly. 4.4.5 Muscle spasms Morphine and diazepam are used to control muscle spasms. Very large doses may be required. A quiet environment should be maintained. 4.5 Acute Bacterial Meningitis in Adults In adults, Streptococcus pneumoniae is the most likely organism. Haemophilus influenzae and Neisseria meningitidis are less common. Cerebrospinal fluid (CSF) microscopy and culture are vital in directing antibiotic therapy. Therefore, a lumbar puncture and blood culture should be performed as 78 soon as possible. Caution is required with lumbar puncture if the patient is in coma, has signs of increased intracranial pressure, or has focal neurological signs. A computed tomography (CT) scan of the head is preferred before lumbar puncture if available. Bacterial meningitis is a medical emergency and antibiotic therapy should not be delayed if there is difficulty in obtaining a CSF sample. In such cases, empirical therapy should be started immediately. In rural areas or where there is a delay in transferring patient to a major hospital, if meningitis is suspected, antibiotics should be started immediately, either with: ™ Penicillin G 4 megaunits intravenously or intramuscularly 6-hourly, OR ™ Ceftriaxone 2 grams intravenously as a single dose (if available). Penicillin, chloramphenicol, and ceftriaxone have proven to be effective in the treatment of meningitis. Chloramphenicol in oral doses achieves good CSF penetration. Dexamethasone has been found to be useful in children. Recent literature suggests that it has a role in the management of bacterial meningitis in adults and is to be given just before 79 the first antibiotic dose. ™ Dexamethasone 10 mg intravenously just before the first dose of antibiotic followed by 10 mg intravenously 6- hourly for 4 days. 4.5.1 Empirical therapy ™ Penicillin G 1.8 gram (3 megaunits) intravenously 4- hourly for 10 days, PLUS ™ Chloramphenicol 750 mg to 1 gram intravenously 6-hourly for 10 days. In patients hypersensitive to penicillin: ™ Chloramphenicol alone, OR ™ Ceftriaxone 4 grams intravenously daily in one or two divided doses. Change to appropriate regimen once the organism and susceptibility result are available. If no organism is identified, continue empirical therapy for a total of 10 days. 80 4.5.2 Specific therapy a. Streptococcus pneumoniae and Neisseria meningitidis meningitis ™ Penicillin G 1.8 gram (3 megaunits) intravenously 4- hourly. In penicillin hypersensitive patients: ™ Ceftriaxone 4 grams intravenously daily in two divided doses. Pneumococcal meningitis is to be treated for 10 to 14 days. Some very ill patients may require treatment for 21 days. Meningitis due to Neisseria meningitidis usually requires treatment for 7 days only. NOTE: At the end of penicillin therapy, rifampicin 10 mg per kg per dose (up to 600 mg) orally 12-hourly for 4 doses should be given to eradicate nasopharyngeal carriage in cases of meningococcal meningitis. This treatment should also be given to all close contacts. b. Gram negative bacterial meningitis Consultation is advisable. Generally, for gram-negative meningitis not due to H. influenzae, a combination of ceftriaxone and gentamicin is useful and the treatment is for 21 days. 81 5 Poisoning and Overdoses Poisoning may occur with both chemicals (e.g. insecticides) or with therapeutic drugs, many of which can be toxic in overdose. Poisoning and overdose may or may not be life- threatening, depending on the type and amount of substance ingested. Treatment is most often supportive only and care should be taken that any intervention does not worsen the situation. Below are the steps to be taken in most cases of poisoning. 5.1 General Principles 5.1.1 Resuscitation (see Section 2.1) Rapidly assess the airway, breathing, and circulation. Maintain the airway, if necessary. Administer oxygen. Obtain intravenous access. Give intravenous fluids if the patient is hypotensive. NOTE: Oxygen should be avoided unless absolutely necessary in patients with paraquat poisoning as it may increase toxicity. 82 5.1.2 Gastric decontamination The best method of preventing absorption of ingested poisons is with the use of activated charcoal. ™ Give activated charcoal 1 gram per kg (to a maximum of 50 grams) orally or via nasogastric tube. Patients who are unable to protect their airway (i.e. excessive drowsiness) should be intubated BEFORE insertion of a nasogastric tube and administration of activated charcoal. In CHILDREN: ™ Give activated charcoal 15 to 30 grams if under 12 years old and 50 to 60 grams if over 12 years of age. NOTE: Ipecac syrup has no role in the treatment of poisoning. Gastric lavage should be performed only in exceptional circumstances such as recent ingestion of large doses of paracetamol. Gastric lavage is contraindicated in ingestion of hydrocarbons, caustics, and corrosives. Administration of activated charcoal is the easiest, safest, and most effective method of decontamination of the gut in almost all situations. In paraquat poisoning, Fuller’s earth (if available) should be substituted for activated charcoal. Activated charcoal does not effectively absorb hydrocarbons, anticholinesterase insecticides, heavy metals, or acids and alkalis, but it is unlikely to cause harm in these situations and 83 may still be given, especially if there is doubt about exactly what the patient has ingested. 5.1.3 Supportive care Continued observation and the provision of oxygen, intravenous fluids and airway support as required. Knowledge of the pharmacologic effects of the substance ingested allows anticipation of possible problems. 5.1.4 Specific antidotes Antidotes to a number of drugs exist and their use is described in the sections below. 5.1.5 Psychiatric evaluation Self-administered overdoses are more often expressions of distress due to emotional crises than true suicide attempts. All patients should be assessed for suicidal intent and treated appropriately. Appropriate counseling should be given prior to discharge. 5.2 Treatment of Specific Poisons 5.2.1 Opiates (e.g. codeine, heroin, pethidine, morphine, methadone) These drugs cause depression of conscious state and 84 hypoventilation. Particular attention should be paid to the maintenance of the airway and adequate ventilation. The specific antidote naloxone is highly effective. ™ Give naloxone 0.4 mg intravenously or intramuscularly and repeat in 5 minutes if necessary to a maximum of 2 mg. NOTE: Failure to respond to a dose of 2 mg of naloxone is an indication that the depression of conscious state is not due to opiate ingestion alone – other possible causes should be considered. Naloxone has a short half-life and further intramuscular doses may be required after 1 to 2 hours. Naloxone may induce pulmonary oedema. 5.2.2 Paracetamol Overdose of this drug is common and can be fatal. Initial symptoms are mild with nausea, vomiting, and sometimes abdominal pain. Hepatic failure and death may follow in days to weeks. The minimum toxic dose is 150 mg per kg and almost all patients who ingest more than 350 mg per kg will develop hepatic failure. Acetylcysteine is the specific antidote and if given within 8 hours may largely prevent hepatic damage. It may still be useful when given from 8 to 24 hours after the ingestion. 85 If urgent serum paracetamol levels are available, then an assessment of the risk of hepatic damage is done using the Rumack-Matthew nomogram which relates serum paracetamol levels to time since ingestion. If a paracetamol level is available within 8 hours of ingestion then withhold acetylcysteine until a toxic level is confirmed. If a paracetamol level will not be available within 8 hours of ingestion, then acetylcysteine should be commenced immediately. If there is any doubt about the time of ingestion or if paracetamol levels are not available, then acetylcysteine should be given to all patients in whom it is reasonably certain that they have ingested an overdose of paracetamol. ™ Give acetylcysteine 150 mg per kg intravenously over 15 minutes, THEN ™ Give acetylcysteine 50 mg per kg intravenously over 4 hours. THEN ™ Give acetylcysteine 100 mg per intravenously over 16 hours. NOTE: Acetylcysteine may cause severe bronchospasm in some individuals. If this occurs the infusion should be ceased and salbutamol administered. Hydroxycobalmin has been used as an alternative antidote. 86 5.2.3 Anticholinesterases (e.g. insecticides) These substances cause severe cholinergic effects including vomiting, diarrhoea, bradycardia, hypotension, hypersalivation, bronchospasm, urinary incontinence, muscle weakness, constricted pupils, and pulmonary oedema. Poisoning may occur with skin exposure or inhalation, as well as with oral ingestion. The specific antidote is atropine and very large doses may be required. Atropine will not reverse muscle weakness so intubation and mechanical support of ventilation may be required. Pralidoxime, which is an acetylcholinesterase reactivator, may also be useful, particularly if administered in conjunction with atropine. a. Treatment in adults ™ Give atropine 3 mg intravenously every 5 to 15 minutes until atropinization is achieved (dry mouth, tachycardia, pupillary dilatation). There is no maximum dose; however, 20 or 30 mg may be required; PLUS ™ Pralidoxime 1gram intravenously over 30 minutes and repeat every 12 hours if symptoms persist. b. Treatment in children ™ Give atropine 1.2 mg intravenously every 5 minutes until the patient develops sinus tachycardia (heart rate of up to 87  120 beats per minute). There is no maximum dose. PLUS ™ Pralidoxime 20 mg per kg intravenously over 30 minutes and repeat every 12 hours if symptoms persist. NOTE: Further doses of atropine may be needed for 24 to 48 hours after exposure. 5.2.4 Aliphatic hydrocarbons (e.g. kerosene, petroleum) Hydrocarbons cause irritation of the gastrointestinal tract, with common symptoms being abdominal pain, vomiting, and diarrhoea. Their most dangerous toxic effects occur when they are aspirated into the lungs causing a chemical pneumonitis. This may occur either during the primary ingestion or when the patient subsequently vomits. Hydrocarbons are not absorbed by activated charcoal so this should not be given. Patients who have any signs or symptoms of aspiration pneumonitis (e.g. fever, cough, dyspnea, wheeze) should be given oxygen, admitted for observation, and administration of intravenous antibiotics should be considered. Patients with severe vomiting and diarrhoea may need intravenous hydration. There is no specific antidote for these chemicals. 5.2.5 Alkali ingestion (e.g. bleach, drain cleaner) Gastric decontamination is not indicated in alkali ingestion and 88 vomiting should be avoided. There is no specific antidote; the treatment is supportive only. Ingestion of an alkaline substance causes damage to the oropharynx and oesophagus. Household bleach (5% sodium hypochlorite) is not a very strongly alkaline substance and is unlikely to cause serious injury. These patients need only symptomatic treatment with intravenous fluids and admission for observation. Stronger alkalis such as drain cleaner may cause severe chemical burns the complications of which include airway obstruction and oesophageal or gastric perforation. These patients should be admitted for rehydration and consideration of upper gastrointestinal endoscopy to determine the extent of the damage. 5.2.6 Oral anticoagulants (e.g. warfarin, rat poison) Overdose of these substances causes prolongation of the prothrombin time and increased risk of bleeding. Patients who have active bleeding or who are at high risk of developing bleeding (e.g. post-operative) should be actively treated. Vitamin K reverses the effect of oral anticoagulants over 12 to 24 hours whereas fresh frozen plasma provides immediate replacement of coagulation factors. In patients not at immediate risk, ceasing warfarin temporarily until the prothrombin time is in the therapeutic range is all that is required. The potency of rat poisons vary – some may require large doses of vitamin K over several weeks. 89 a. Treatment in adults ™ Give vitamin K 5 to10 mg intravenously slowly stat; PLUS, if necessary, ™ Give fresh frozen plasma 2 units intravenously and repeat as necessary to a maximum of 8 units using repeated measurements of the prothrombin time as a guide to therapy. Refer to consultant physician for subsequent management. b. Treatment in children ™ Give vitamin K, 0.3 mg per kg (maximum 10 mg) intramuscularly daily; PLUS, if necessary, ™ Give fresh frozen plasma 20 ml per kg (maximum 2 units) intravenously and repeat as necessary using repeated measurements of the prothrombin time as a guide to therapy 5.2.7 Beta-adrenergic antagonists (e.g. propranolol, atenolol) Beta-blocker overdose causes bradycardia, AV node block and hypotension, sometimes complicated by bronchospasm, 90 congestive cardiac failure, and confusion. Hypoglycaemia may also occur in children. These overdoses may be fatal and patients with significant toxic effects may need a central venous line, ECG monitoring, and monitoring in an intensive care unit (if available). a. Treatment in adults ™ Give adrenaline infusion 10 micrograms per minute and increase by 5 micrograms per minute every 2 minutes until the systolic blood pressure is >90 mmHg, to a maximum of 100 micrograms per minute. b. Treatment in children ™ Give adrenaline infusion 0.5 micrograms per kg per minute and increase by 5 micrograms per minute every 2 minutes until the systolic blood pressure is >90 mmHg, to a maximum of 100 micrograms per minute; OR ™ Give isoprenaline infusion 0.5 to 10 micrograms per kg per minute. 5.2.8 Iron Overdose of iron initially causes vomiting, diarrhoea, abdominal pain, and sometimes haematemesis. After a variable 91 quiescent period during which these gastrointestinal symptoms resolve, the patient may develop shock and hypoglycaemia plus cardiac, hepatic, and renal failure. The specific antidote is desferrioxamine but supportive care including intravenous fluid and glucose (if necessary) is important as well. Iron is not well absorbed by activated charcoal. The following patients should receive desferrioxamine: all symptomatic patients all patients who have iron tablets visible on a plain abdominal X-ray all patients in whom the serum iron level (if available) is greater than 350 micrograms per dl (90 micromoles per liter). ™ Give desferrioxamine 15 mg per kg per hour by intravenous infusion continued until the patient is asymptomatic (usually 12 to 24 hours). 5.2.9 Benzodiazepines (e.g. diazepam) These substances are very safe in overdose generally causing only drowsiness. Supportive care and observation is usually all that is necessary. 5.2.10 Nonsteroidal anti-inflammatory dugs (e.g. indomethacin, ibuprofen, aspirin) Overdose of these drugs causes nausea, vomiting, abdominal 92 pain, and drowsiness. Treatment is supportive only. 5.2.11 Phenytoin In overdose, phenytoin causes cerebellar dysfunction (nystagmus, ataxia, dysarthria, nausea, and vomiting) plus confusion, coma and paradoxically, seizures. Treatment is essentially supportive. Diazepam should be used to control seizures. 5.2.12 Aspirin This commonly used drug can be highly toxic in overdose. The clinical features include gastrointestinal (nausea, vomiting, haematemesis), neurologic (confusion, coma, seizures), and metabolic (fever, tachypnea, and hypokalaemia) manifestations. Metabolic acidosis and hypoglycaemia may occur in children. Cardiac failure and acute respiratory distress syndrome are uncommon complications. The potentially toxic dose is greater than 150 mg per kg. Patients with manifestations of aspirin overdose should be admitted and treated as follows: ™ Give 0.9% saline (or 0.3% saline with 3% dextrose in children) intravenously at a rate necessary to maintain a urine output greater than 2 ml per kg per hour; PLUS ™ Give sodium bicarbonate 1 mmol per kg intravenously 93  every 4 hours to maintain a urine pH greater than 7.5 if facilities are available; PLUS ™ Give potassium chloride 0.25 mmol per kg intravenously over at least one hour, every 4 hours to maintain serum potassium levels > 4 mmol per liter. NOTE: Frequent measurement of urine output, urine pH, and serum potassium should be performed (e.g. every 2 to 4 hours). Larger or smaller doses of sodium bicarbonate and potassium chloride than those listed above may be required. 5.2.13 Carbon monoxide (e.g. car exhaust) This odourless and colourless gas competes with oxygen for the binding sites on the haemoglobin molecule. Toxic effects include headache, nausea, confusion, coma, seizures, and cardiac arrhythmias. Treatment for symptomatic patients is with 100% oxygen for at least 12 hours. 5.2.14 Digoxin Poisoning with this drug may be acute (usually intentional self- poisoning) or chronic (gradual accumulation in a patient taking digoxin for therapeutic reasons). Patients with significant toxicity always complain of nausea and vomiting. Other clinical features include headache, diarrhoea, visual disorders, confusion, and coma. Acute poisoning causes marked 94 hyperkalaemia whereas chronic toxicity cases are often hypokalaemic. Digoxin toxicity has been known to cause just about every type of cardiac arrhythmia from complete heart block to ventricular tachycardia. In addition to the usual supportive care, complications should be treated as follows: a. Ventricular tachycardia ™ Give phenytoin 15 mg per kg intravenously, infused no faster than 50 mg per minute; PLUS ™ Give magnesium sulphate 50 mg per kg intravenously (maximum dose 5 grams) over 5 minutes. THEN, if arrhythmia persists, ™ Give lignocaine 1 mg per kg intravenous bolus. NOTE: Use cardioversion only as a last resort as it may induce intractable ventricular fibrillation. If it is absolutely necessary then use low energies (e.g. 25 joules in an adult). b. Bradyarrhythmias ™ Give atropine 10 micrograms per kg intravenous bolus and repeat in 5 minutes, if necessary. 95 c. Hyperkalaemia (serum potassium >6 mmol per liter) i. Treatment in adults ™ Give short-acting insulin 10 units intravenous bolus, PLUS, at the same time, ™ Give 50 ml of 50% glucose intravenously over 5 minutes. ii. Treatment in children ™ Give short-acting insulin 0.1 unit per kg intravenous bolus, PLUS, at the same time, ™ Give 50% glucose 2 ml per kg intravenously over 5 minutes. NOTE: Serum glucose should be monitored hourly over the next 4 hours. Calcium should not be given to patients with digoxin toxicity. The above treatment for hyperkalaemia may be repeated in 2 hours if necessary. Refer to Section 7.1 for subsequent management. 96 5.2.15 Barbiturates (e.g. phenobarbitone) In overdose, barbiturates can cause severe central nervous system depression with coma, hypoventilation, and hypotension. Patients with significant ingestions will need intensive supportive care. There is no specific antidote. 5.2.16 Theophylline Theophylline poisoning may occur because of deliberate ingestion of an overdose or due to gradual accumulation of the drug in those taking it for therapeutic reasons. Toxicity affects several organ systems: cardiovascular – supraventricular and ventricular tachycardia, atrial fibrillation gastrointestinal – nausea, vomiting, and diarrhoea neurologic – agitation, confusion, seizures metabolic – hypokalaemia, hyperglycaemia. Seizures may be resistant to treatment with benzodiazepines; intubation and sedation with barbiturates may be required. Hypokalaemia should be treated with intravenous potassium replacement (see Section 7.2), while tachyarrhythmias may respond to beta-adrenergic antagonists. For supraventricular or ventricular tachycardia: ™ Give propranolol 0.5 mg intravenous bolus and repeat every 2 minutes up to a maximum of 10 mg. 97  Note: Propranolol is contraindicated in patients with asthma. 5.2.17 Chloroquine This drug is highly toxic in overdose causing hypotension and cardiac arrhythmias. Treatment involves adrenaline and very large doses of diazepam. Most patients will require intubation and management in an intensive care unit (if available). ™ Give adrenaline 0.25 microgram per kg per minute via intravenous infusion and increase rate by 5 mic