**10. Salicylate (aspirin) poisoning**

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 accidental and intentional toxicity [24].

(WBI) is useful in case of massive ingestions or sustained preparation or enteric-coated. Sever Salicylate toxicity treated with serum Alkalinisation by sodium bicarbonate with a aim of a serum pH of ~7.5.Patients may need haemodialysis and the indications for haemodialysis are clinical deterioration, severe acid-base disturbance, altered mental status, and acute lung

Toxicology in Emergency Medicine

259

http://dx.doi.org/10.5772/intechopen.77011

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

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, respira-

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

Serotonin syndrome (in combination with other agents)

injury, failure of serum and urine alkalinisation and renal failure [26–28].

tory depression, cough suppression, euphoria and decreased GI motility.

**11. Opioids poisoning**

from the poppy plants [29].

**11.1. Mechanism of action**

**11.2. Clinical features**

such as sympathomimetic or anticholinergic.

**Opioids agent Specific clinical feature** Dextromethorphan Serotonin toxicity; at high doses

Meperidine Seizure, normal pupils size

Oxycodone QT interval prolongation

Heroin Acute lung injury

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

Methadone long-acting;

Tramadol Seizure

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

Loperamide QRS and QT prolongation; Wide-complex tachycardia

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.

QT prolongation, Torsade de Pointes

### **10.1. Mechanism of action**

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].

#### **10.2. Clinical features**

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

#### **10.3. Acute toxicity**

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 platelet dysfunction.

#### **10.4. Chronic toxicity**

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.

#### **10.5. Treatment**

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 (WBI) is useful in case of massive ingestions or sustained preparation or enteric-coated. Sever Salicylate toxicity treated with serum Alkalinisation by sodium bicarbonate with a aim of a serum pH of ~7.5.Patients may need haemodialysis and the indications for haemodialysis are clinical deterioration, severe acid-base disturbance, altered mental status, and acute lung injury, failure of serum and urine alkalinisation and renal failure [26–28].
