**15. Calcium channel blocker poisoning**

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 extended-release [17].

#### **15.1. Mechanism of action**

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].

#### **15.2. Clinical features**

Cardiovascular system is the most affected system in CCBs toxicity. Patient present with hypotension and bradycardia or reflex tachycardia. Verapamil or diltiazem toxicity usually patients present with sinus bradycardia, on the hand dihydropyridine overdoses cause peripheral vasodilatation causing reflex tachycardia [55]. CCBs have not primary effect on pulmonary and CNS System; CNS symptoms (seizures, delirium, and coma) occur secondary to decrease organ perfusion. Cardiogenic pulmonary oedema and acute lung injury (noncardiogenic pulmonary oedema) have also been reported in severe toxicity [48].

severe cases characterized with different symptoms including cognitive deficiency, movement disorders and focal neurologic deficit. The standard pulse oximetry cannot differentiate carboxyhaemoglobin from oxyhaemoglobin, so it is unreliable in the diagnosis or screen carbon monoxide poisoning, so measuring carboxyhaemoglobin level in an arterial blood gas

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After securing the airway, the most important step in treatment is oxygen 100% via nonrebreathing mask or intubation and mechanically ventilation with 100% oxygen if the patient is comatose and cannot secure his air way, half-life of carboxyhaemoglobin in room air 250–320 min while via non-rebreathing with 100% oxygen decreased to 90 min. Hyperbaric oxygen therapy could be considered in certain cases, the indication for Hyperbaric oxygen includes Pregnancy with carboxyhaemoglobin level > 15%, Carboxyhaemoglobin >25%, evi-

Iron tablets are usually available in homes with small children and young women especially pregnant women. Because of its colour, sugar taste and appearance like a candy make iron

Iron exerts a direct corrosive effect on the gastrointestinal tract at high plasma concentrations; it also possesses cytotoxic actions, particularly on the liver, leading to hepatocellular necrosis. Additionally, iron has a direct cardio- toxic effect acting as a negative inotrope and inhibits thrombin leading to a coagulopathy independent of hepatotoxicity. The direct corrosive

Serious iron poisoning usually causes symptoms within 6 h of the overdose and if the ingested elemental iron more than 20 mg/kg body, the symptoms of iron poisoning typically occur in

**Stage 1** (within 6 h after the overdose): Symptoms include vomiting, vomiting blood, diarrhoea, abdominal pain, irritability and drowsiness. If poisoning is very serious, rapid breathing, a rapid heart rate, coma, unconsciousness, seizures, and low blood pressure may develop. **Stage 2** (6–48 h after the overdose): condition can appear to improve (there is often a latent phase with minimal symptoms which may last up to 24 h and may be misinterpreted as an

**Stage 3** (12–48 h after the overdose): Very low blood pressure (shock), fever, bleeding, jaun-

dence of acute myocardial ischemia, and severe metabolic acidosis [56].

tablet more attractive for accidental ingestion for children [57].

effects and cellular toxicity contribute to metabolic acidosis [58].

dice, liver failure, metabolic acidosis and seizures can develop.

helps in diagnosis [52–55].

**16.3. Treatment**

**17. Iron toxicity**

**17.1. Mechanism of action**

**17.2. Clinical features**

apparent recovery).

5 stages:

#### **15.3. Treatment**

First step in management is secure airway, stabilize ventilation and circulation.

Decontamination can be done by oral activated charcoal if patient present within 1 h of ingestion also the whole-bowel irrigation is useful in case of extended-release CCBs. Hypotension treated with IV fluid, Calcium chloride or calcium gluconate, glucagon (3–10 mg), if not responding start Vasopressors (e.g., norepinephrine). If symptoms refractory to vasopressor therapy start, high dose Insulin -glucose. If patient still not responding, lipid emulsion can be started. Finally, circulatory support measures, such as the placement of intra-aortic balloon pumps may be used in case of sever toxicity not responding to standard therapy [49–51].
