Excitatory neurotoxicity Sweating, salivation, piloerection

1. EVALUATION OF THE ENVENOMED PATIENTAssessment of type and extent of envenoming Neurotoxic paralysis'Sleepy' or drooping eyelidsDifficulty swallowing, dysarthria and droolingLimb weaknessRespiratory distress

2. Excitatory neurotoxicity • Sweating, salivation, piloerection • Tingling around mouth, tongue or muscle twitching • Dyspnoea (pulmonary oedema)

3. Myolysis • Muscle pain or weakness Coagulopathy • Blood oozing from bite site and/or gums • Bruising • Melaena, haematemesis Local effects • Pain, sweating, blistering, bruising etc.

4. Taking a history in envenoming • When was the patient exposed to a bite/sting? • Was the organism causing it seen and what did it look like (size, colour)? • What were the circumstances (on land, in water etc.)? • Was there more than one bite/sting? • What first aid was used, when and for how long? • What symptoms has the patient had (local and systemic)? • Are there symptoms suggesting systemic envenoming (paralysis, myolysis, coagulopathy etc.)? • Past medical history and medications? • Past exposure to antivenom/venom and allergies

5. Acute poisoning is common, accounting for about 10% of hospital admissions in the UK. In developed countries, the most frequent cause is intentional drug overdose in the context of self-harm and usually involves prescribed or 'over-the-counter' medicines. Accidental poisoning is also common, especially in children and the elderly .Toxicity also may occur as a result of alcohol or recreational substance use, or following occupational or environmental exposure. Poisoning is a major cause of death in young adults, but most deaths occur before patients reach medical attention, and mortality is much lower than 1% in those admitted to hospital.

6. In developing countries, the frequency of self-harm is more difficult to estimate because patients may be reticent in admitting to deliberate poisoning. Household and agricultural products such as pesticides and herbicides are more freely available, are common sources of poisoning and are associated with a much higher case fatality. In China and South-east Asia, pesticides account for about 300 000 suicides each year.

7. Important substances involved in poisoning Analgesics, e.g. paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) • Antidepressants, e.g. tricyclic antidepressants (TCAs), selective serotonin re-uptake inhibitors (SSRIs) and lithium • Cardiovascular agents, e.g. β-blockers, calcium channel blockers and cardiac glycosides • Drugs of misuse, e.g. opiates, benzodiazepines, stimulants (e.g. amphetamines, MDMA, cocaine) • Carbon monoxide* • Alcohol

8. In South and South-east Asia • Organophosphorus* and carbamate insecticides • Aluminium and zinc phosphide • Oleander • Snake venoms • Antimalarial drugs, e.g. chloroquine • Antidiabetic medication

9. Poisoning in old age • Aetiology: commonly results from accidental poisoning (e.g. due to confusion or dementia) or drug toxicity as a consequence of impaired renal or hepatic function or drug interaction. Toxic prescription medicines are more likely to be available. • Psychiatric illness: self-harm is less common than in younger adults but more frequently associated with depression and other psychiatric illness, as well as chronic illness and pain. There is a higher risk of subsequent suicide. • Severity of poisoning: increased morbidity and mortality result from reduced renal and hepatic function, reduced functional reserve, increased sensitivity to sedative agents and frequent comorbidity

10. GENERAL APPROACH TO THE POISONED PATIENT Triage and resuscitation s Patients who are seriously poisoned must be identified early so that appropriate management is not delayed. Triage involves: • immediate measurement of vital signs • identifying the poison(s) involved and obtaining adequate information about them • identifying patients at risk of further attempts at self-harm and removing any remaining hazards from them. Those with possible external contamination with chemical or environmental toxins should undergo appropriate decontamination .Critically ill patients must be resuscitated

11. Substances of very low toxicity • Writing/educational materials • Decorating products • Cleaning/bathroom products (except dishwasher tablets which are corrosive) • Pharmaceuticals: oral contraceptives, most antibiotics (but not tetracyclines and antituberculous drugs), H2-blockers, proton pump inhibitors, emollients and other skin creams, baby lotion • Miscellaneous: plasticine, silica gel, household plants, plant food

12. The Glasgow Coma Scale (GCS) is commonly employed to assess conscious level, although it has not been specifically validated in poisoned patients. The AVPU (alert/verbal/painful/unresponsive) scale is also a rapid and simple method. An electrocardiogram (ECG) should be performed and cardiac monitoring instituted in all patients with cardiovascular features or where exposure to potentially cardiotoxic substances is suspected. Patients who may need antidotes should be weighed when this is feasible, so that appropriate doses can be prescribed. Substances that are unlikely to be toxic in humans should be identified so that inappropriate admission and intervention are avoided

13. Clinical assessment and investigations. Occasionally, patients may be unaware or confused about. what they have taken, or may exaggerate (or less commonly underestimate) the size of the overdose, but rarely mislead medical staff deliberately. In some parts of the world, such as Asia, patients may not readily admit to deliberate self-poisoning.. The patient may have a cluster of clinical features ('toxidrome') suggestive of poisoning with a particular drug Poisoning is a common cause of coma, especially in younger people, but it is important to exclude other potential causes unless the aetiology is certain. Urea, electrolytes and creatinine should be measured in most patients. Arterial blood gases should be checked in those with significant respiratory or circulatory compromise, or when poisoning with substances likely to affect acid-base status is suspected .Calculation of anion and osmolar gaps may help to inform diagnosis and management

14. Causes of acidosis in the poisoned patient • Cause Normal lactate*High lactateToxic Salicylates, Metformin, Methanol, Iron ,Ethylene glycol, Cyanide ,Paraldehyde, Sodium valproate , Carbon monoxide Other ,Renal failure Shock Ketoacidosis , Severe diarrhoea *Unless circulatory shock is present, when it will be high in any case

15. Anion and osmolar gaps in poisoning • Anion gap Osmolar gap Calculation [Na+ + K+] - [Cl- + HCO3-]Osm (measured) - [2Na + K + Urea + Glucose]Normal range12-16 mmol/L< 10 mOsm/kg Common toxic causes of elevation *EthanolEthylene glycolMethanolSalicylatesIronCyanide EthanolEthylene glycolMethanol

16. Psychiatric assessment • All patients presenting with deliberate drug overdose should undergo psychosocial evaluation by a health professional with appropriate training prior to discharge.This should take place once the patient has recovered from any features of poisoning, unless there is an urgent issue such as uncertainty about his or her capacity to decline medical treatment

17. General management • Patients presenting with eye or skin contamination should undergo appropriate local decontamination procedures .Gastrointestinal decontamination .Laboratory analysis in poisoning Acetylcholinesterase • Plasma cholinesterase is reduced more rapidly but is less specific than red cell cholinesterase in organophosphorus poisoning • Antidote use should not be delayed pending results

18. Carboxyhaemoglobin • > 20% indicates significant carbon monoxide exposure Digoxin • Therapeutic range usually 1-2 μg/L • Concentrations > 4 μg/L usually associated with toxicity, especially with chronic poisoning Ethanol • Toxicity at concentrations > 1.8 g/L Iron • Take sample at least 4 hrs after overdose or if there are clinical features of toxicity • Concentrations > 5 mg/L suggest severe toxicity Lithium • Take sample at least 6 hrs after overdose or if there are clinical features of toxicity • Usual therapeutic range 0.4-1.0 mmol/

19. Methaemoglobin • Methaemoglobinaemia associated with toxicity due to nitrites, benzocaine, dapsone, chloroquine, aniline dyes • Concentrations > 20% may require treatment with methylthioninium chloride (methylene blue) Paracetamol • Take sample at least 4 hrs after overdose • Use nomogram to determine need for antidotal treatment Salicylate • Take sample at least 2 hrs (symptomatic patients) or 4 hrs (asymptomatic patients) after overdose • Concentrations > 500 mg/L suggest serious toxicity • Repeat after 2 hrs if severe toxicity is suspected Theophylline • Take sample at least 4 hrs after overdose or if there are clinical features of toxicity • Repeat after 2 hrs if severe toxicity is suspected • Concentrations > 60 mg/L suggest severe toxicity • Patients who have ingested potentially life-threatening quantities of toxins may be considered for gastrointestinal decontamination if poisoning has been recent). Induction of emesis using ipecacuanha is now never recommended

20. Activated charcoal • Use of gastric decontamination methods Single-dose activated charcoal ‘ The administration of activated charcoal may be considered if a patient has ingested a potentially toxic amount of a poison (which is known to be adsorbed to charcoal) up to 1 hr previously. Multiple-dose activated charcoal 1.'Multiple-dose activated charcoal should be considered only if a patient has ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline .'2.Gastric lavage 'Gastric lavage should not be employed routinely, if ever, in the management of poisoned patients. '3.Whole bowel irrigation (WBI)

21. 'WBI should be considered for potentially toxic ingestions of sustained-release or enteric-coated drugs, particularly for those patients presenting more than 2 hrs after drug ingestion. WBI should be considered for patients who have ingested substantial amounts of iron, as the morbidity is high and there is a lack of other options for gastrointestinal decontamination. The use of WBI for the removal of ingested packets of illicit drugs is also a potential indication

22. Given orally as slurry, activated charcoal absorbs toxins in the bowel as a result of its large surface area. If given sufficiently early, it can prevent absorption of an important proportion of the ingested dose of toxin. However, efficacy decreases with time and current guidelines do not advocate use more than 1 hour after overdose in most circumstances However, use. after a longer interval may be reasonable when a delayed-release preparation has been taken or when gastric emptying may be delayed. Some toxins do not bind to activated charcoal .so it will not affect their absorption. In patients with an impaired swallow or a reduced level of consciousness, the use of activated charcoal, even via a nasogastric tube, carries a risk of aspiration pneumonitis. This risk can be reduced but not completely removed by protecting the airway with a cuffed endotracheal tube.