**13. Digitalis glycosides poisoning**

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].

#### **13.1. Mechanism of action**

**11.3. Treatment**

260 Essentials of Accident and Emergency Medicine

**12.1. Mechanism of action**

prolongation [33, 34].

**12.2. Clinical features**

(cardiovascular, CNS …etc.).

because of rhabdomyolysis [35–37].

**12.3. 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

Cocaine is one of the most potent Sympathomimetic, extracted from the leaves of the coca by indigenous to South America; therapeutically, first time Cocaine was used in 1884 as a local anaesthetic for ophthalmologic procedures. In the United States Cocaine is one of the most

Cocaine stimulates alpha and adrenergic receptors by increasing levels of norepinephrine, causing vasoconstriction in cardiovascular system, also inhibits neuronal serotonin reuptake which lead to euphoria. Cocaine blocks Sodium (Na+) channel causing QRS interval

Cocaine toxicity may cause sympathomimetic and vasoconstrictive effects on variety systems

Cardiovascular: patients with cocaine toxicity present with high blood pressure and dysrhythmias include tachycardia, such as sinus tachycardia, SVT, and AF. ECG changes include rightward shift of the terminal portion of the QRS complex and prolongation the QT interval. Patients may present with acute coronary syndromes (cocaine-associated acute coronary syndrome), aortic and coronary artery dissection, myocarditis and cardiomyopathy. CNS: patients with Cocaine present with a variety CNS clinical features including: agitation, seizures, and coma. Pulmonary: mainly seen in patients who smoke crack cocaine includes pul-

Gastrointestinal: Cocaine may cause intestinal ischemia, bowel necrosis and ischemic colitis, also increase risk for bleeding and ulcer perforation. Renal: acute kidney failure may occur

Securing the airway and adequate breathing are initial steps in treatment. CNS manifestation (agitation, seizure) treated with sedation by Benzodiazepines, patient with Hyperthermia

of drug use history, can be repeated IV every 3 min [30–32].

common causes of acute drug-related emergency department visits.

monary haemorrhage, barotrauma, pneumonitis and asthma.

**12. Sympathomimetic (cocaine) poisoning**

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 repolarization intervals of the atria and ventricles [39].

#### **13.2. Clinical features**

Digoxin toxicity divided to acute and chronic toxicities.

#### **13.3. Acute toxicity**

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 usually marked elevated [40, 41].

#### **13.4. Chronic toxicity**

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].

#### **13.5. Treatment**

General supportive care is an Initial step in treatment of digoxin toxicity; it includes securing airway and adequate ventilation and boluses of fluid IV in case of hypotension. Activated charcoal helps in early acute ingestion [42], Atropine can be given in case of Symptomatic bradycardia). Digoxin-specific antibody fragments (digoxin-Fab) are antidotes for digoxin. The indication to use (digoxin- Fab) includes Life-threatening dysrhythmias unresponsive to standard therapy and hyperkalaemia excess 6 mEq/L. [43] Digoxin-Fab doses are based on the total-body load of digoxin, which can be calculated from either the estimated dose ingested or the serum digoxin level, each vial of Digoxin-Fab reverses approximately 0.5 mg of ingested digoxin. If the amount of ingested digitalis is unknown, digoxin Fab 10 vials for adults empirically can be given. Hyperkalaemia is treated with insulin, dextrose, sodium bicarbonate. The use of calcium salts in digoxin induced hyperkalaemia is controversial because old literature shows increase incidence of ventricular dysrhythmias and increase mortality [44].

decreased automaticity in pacemaker cells, and decreased conduction through the AV node. Non- selective beta blockade results in systemic effects including bronchoconstriction, impaired gluconeogenesis and decreased insulin release. Same Beta blockers (e.g., propranolol) have high lipid solubility leading to rapid cross of the blood brain barrier into the central nervous

Toxicology in Emergency Medicine

263

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

The major system affected by β-blocker toxicity is the cardiovascular system; patients present with bradycardia and hypotensive. The cause of bradycardia is sinus node suppression or conduction abnormalities but ingestion of β-blockers with partial agonist activity may cause hypertension and tachycardia as early presentation. The β-blockers with sodium channel

Β-Blockers also have effect on CNS and pulmonary system. Neurologic features include delirium, coma and seizures with more lipophilic. Β-blockers (propranolol) have more neurological manifestations. Bronchospasm and hypoglycaemia can be in β-blockers toxicity [47, 48].

GI decontamination can be done by giving Activated charcoal within 1 h of ingestion and air way is the main aim treatment in beta-blocker toxicity focusing on restore perfusion to critical organ systems by increasing cardiac output by: fluid resuscitation and glucagon (3–10 mg), vasopressor (e.g., epinephrine) and high dose Insulin- glucose (insulin 1 unit/kg IV bolus). Intravenous lipid emulsion therapy may be used in case of sever toxicity and refractory to treatment. In case of refractory to pharmacologic therapy, haemodialysis, haemoperfusion, cardiac pacing, placement of intra-aortic balloon pumps can be used. Wide QRS-interval dysrhythmias due to sodium channel blockade treated with sodium bicarbonate 2–3 mEq/kg over 1–2 min [49, 50].

Calcium channel blockers (CCBs) are mainly used in the treatment of cardiovascular diseases such as hypertension, coronary artery disseise- CAD and cardiac arrhythmias Calcium channel blockers one most prescribed cardiovascular drugs and can be immediate-release or

The calcium channel blockers (CCBs) can be divided into two major groups based upon their major physiologic effects: the dihydropyridines, group which mainly block the L-type calcium channels in the vasculature and the non-dihydropyridines, which selectively block L-type calcium channels in the myocardium such as verapamil. Dihydropyridine group toxicity causes arterial vasodilation and reflex tachycardia, whereas non-dihydropyridines toxicity

cause peripheral vasodilation decreased cardiac inotropy, and bradycardia [46].

system, causing a neurological manifestation such as seizures and delirium [45, 47].

Sotalol causes potassium channels block leading to prolonging the QT interval.

**14.2. Clinical features**

**14.3. Treatment**

extended-release [17].

**15.1. Mechanism of action**

block affect may cause a wide-complex bradycardia.

**15. Calcium channel blocker poisoning**
