**11. Opioids poisoning**

**10. Salicylate (aspirin) poisoning**

Salicylate toxicity divided to **acute** and **chronic** toxicities.

tal and intentional toxicity [24].

258 Essentials of Accident and Emergency Medicine

**10.1. Mechanism of action**

**10.2. Clinical features**

**10.3. Acute toxicity**

platelet dysfunction.

**10.4. Chronic toxicity**

**10.5. Treatment**

Aspirin is the most common analgesic antiplatelet therapy used in cardiovascular and cerebrovascular disease. Aspirin is over-the-counter drugs and widespread used lead to acciden-

Salicylate Inhibit cyclooxygenase leads to decreased synthesis of prostaglandins; prostacyclin and thromboxane. It also leads to platelet dysfunction and gastric mucosal injury. Salicylate Stimulate the chemoreceptor trigger zone in the medulla which causes nausea and vomiting. Also activate respiratory centre of the medulla leading to hyperventilation and respiratory alkalosis. Uncoupling of oxidative and Inhibit the Krebs which lead to metabolic acidosis [25].

Acute salicylate toxicity manifests initially through GI, CNS effects and metabolic effects. Gastric irritation, vomiting and nausea may predominate early in the course and are more predominant in the acute poisoning. Rising CNS salicylate concentrations produce tinnitus, diminished auditory acuity, vertigo and hyperventilation. As the poisoning continues, the CNS effects may progress to agitation, hallucinations, delirium, seizure and lethargy. The metabolic effects of salicylate toxicity cause uncoupling of oxidative phosphorylation leading to temperature elevation (an indicator of severe toxicity) and a large anion gap metabolic acidosis. Subsequent squeal of salicylate toxicity include renal failure, acute lung injury and

In contrast, chronic poisoning occurs over a longer period of time, when patients ingest more drug than they can eliminate over a prolonged period. These patients tend to be older and the overdose is unintentional. The initial presenting signs and symptoms include those of acute toxicity although with slower onset and lesser severity. Chronic toxicity may easily be confused in the elderly for sepsis, ketoacidosis, delirium, dementia, CHF or respiratory failure. Diagnostic delay in the chronically poisoned patient has been shown to cause increased morbidity and mortality.

Stabilization of the airway, breathing and circulation are the first steps in management. Intubation may increases the severity of the aspirin toxicity, so it is better to be avoided, but if intubation is necessary patients need appropriately high minute ventilation sitting. In case of volume depleted and acidosis, start treatment with I. V fluid. Gastrointestinal decontamination with Activated charcoal may help in early ingestion. Whole bowel irrigation Opioid abuse is a significant medical and social problem in the world. In the past 10 years, the number of abuses and deaths from opioid overdoses had been increased. Opioids are all substances related to opium. They have analgesic and sedative effects. Opiate is extracted from the poppy plants [29].

#### **11.1. Mechanism of action**

There are three main opioid receptors: μ (mu), κ (kappa), and δ (delta), and Opioids have agonists effect on this receptors. Stimulation of opioids receptors will cause miosis, respiratory depression, cough suppression, euphoria and decreased GI motility.

#### **11.2. Clinical features**

Classic signs of opioid intoxication toxidrome, depressed mental status, decreased respiratory rate miosis, (constricted) pupils. Other finding includes: decreased bowel sounds orthostatic hypotension, urinary retention and localized urticaria. Normal pupil examination can be seen, meperidine diphenoxylate, propoxyphene toxicity and co-ingestion of other toxin such as sympathomimetic or anticholinergic.


Same opioids have specific clinical feature (**Table 2**) [30, 32]:

Body packing: swallowing packets or containers of drug for the purposes of smuggling. Body stuffing: swallowing of a smaller quantity of drug because of fear of arrest.

**Table 2.** Opioids with specific clinical feature.

#### **11.3. Treatment**

Secure Airway and maintain adequate oxygenation and ventilation by using bag-valve mask are the first important steps in treatment; serum glucose should be checked. After that administer naloxone 0.4 mg IV, in non-opioid-dependent with minimal respiratory depression abut if patient is opioid-dependent present with minimal respiratory depression, administer small dose of naloxone, 0.1 mg IV, because larger doses can induce opioid withdrawal symptoms. Patients presenting with apnea or near-apnea and cyanosis, start naloxone, 2 mg IV regardless of drug use history, can be repeated IV every 3 min [30–32].

should be cooled rapidly, severe hypertension not responding to sedation can be treated with a sodium nitroprusside infusion or phentolamine; (avoid Β-ac blockers). Cocaine toxicity with acute coronary syndrome are treated with aspirin and nitroglycerin also may add calcium channel blockers, wide-complex tachycardia with cocaine toxicity treated with serum alkalinisation by sodium bicarbonate, make sure serum Ph do not exceed 7.55. Intravenous lipid emulsion can be used in severe cocaine toxicity, with refractory cardiovascular instability or

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Cardiac glycosides were used in treatment of heart failure since long time. Since 1785 glycosides found in plants like lily of the valley foxglove and oleander. Digoxin is most common digitalis drug used today for treatment of atrial fibrillation and congestive heart failure [38].

Digoxin inhibits Na + -K + -ATPase during repolarization which leading to increase in intracellular sodium and a decrease in intracellular potassium leading to increase in the intracellular concentration of calcium causing Positive inotropic, also increase automaticity and shorten

The cause of acute toxicity is usually intentional or accidental ingestion, symptoms usually abrupt in onset, patients present with nausea, vomiting, non-specific abdominal pain, headache and dizziness. Sever toxicity may cause confusion and coma, Bradydysrhythmia and atrioventricular block or supraventricular tachydysrhythmia and hyperkalaemia. Xanthopsia is a classic eye future in digoxin toxicity (viewing yellow-green halos around objects), but the most common finding is nonspecific changes in their colour vision. Serum digoxin level

Chronic toxicity is commonly and mainly seen in elderly patients and common causes are interaction with other medications (calcium channel antagonists, amiodarone, β-receptor antagonists, and diuretics) or renal insufficiency which causes decree the clearance of digoxin. In contract of acute toxicity, where Gastrointestinal symptoms are prominent in chronic toxicity CNS symptoms (weakness, fatigue, confusion, or delirium) are more prominent. Ventricular dysrhythmias are commonly seen in chronic toxicity. Serum potassium level can

be normal or decreased, also serum digoxin level usually minimally elevated [40, 41].

refractory wide-complex tachycardia [37].

**13. Digitalis glycosides poisoning**

the repolarization intervals of the atria and ventricles [39].

Digoxin toxicity divided to acute and chronic toxicities.

**13.1. Mechanism of action**

**13.2. Clinical features**

**13.3. Acute toxicity**

usually marked elevated [40, 41].

**13.4. Chronic toxicity**
