**17. Iron toxicity**

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

#### **17.1. Mechanism of action**

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

#### **17.2. Clinical features**

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 5 stages:

**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 apparent recovery).

**Stage 3** (12–48 h after the overdose): Very low blood pressure (shock), fever, bleeding, jaundice, liver failure, metabolic acidosis and seizures can develop.

**Stage 4** (2–5 days after the overdose): The liver fails and people may die from shock, bleeding, and blood-clotting abnormalities. Sugar levels in the blood can decrease. Confusion and sluggishness (lethargy) or coma may develop.

by alcohol dehydrogenase. Glycolaldehyde is then converted to glycolic acid which is then converted to oxalic acid. Oxalic acid combines with serum calcium to form the classic calcium

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Ethylene glycol causes an elevated anion gap metabolic acidosis. The neurologic effects of ethylene glycol are coma, seizures, meningism, muscle spasms, and paralysis of the extraocular muscles. It can also affect the heart and lungs, causing tachycardia, hyperventilation, ARDS, and heart failure. Hypocalcaemia and resulting QT prolongation are due to serum calcium combining with oxalic acid. Lastly, kidney failure is due to these calcium crystals depositing into renal tubules.

Isopropyl alcohol is found in solvents and disinfectants. It is also found in mouthwashes, lotions, as well as rubbing alcohol and hand sanitizers. It is also hepatically metabolized by alcohol dehydrogenase to acetone. Isopropanol produces an increased osmole gap; however, it normally does not produce a metabolic acidosis unless concomitant hypotension causes lactic acidosis. It can cause haemorrhagic gastritis and profound inebriation with cerebellar signs and coma [64–70].

An osmolar gap more than 10 mOsm/kg is suggestive of ethylene glycol, methanol, isopropanol, ethylene oxide, or acetone toxicity. A high anion gap metabolic acidosis may be revealed at later stages of methanol and ethylene glycol poisoning. Hypoglycaemia may be detected with isopropanol, while hyperglycaemia and hypocalcaemia may be detected in methanol and ethylene glycol poisonings, respectively. Hyperkalaemia due to acidosis is observed in methanol and ethylene glycol poisoning, whereas hypokalaemia due to vomiting may occur in ethanol intoxication.

Urine calcium oxalate crystals can be seen in ethylene glycol intoxication. These findings

Any patient with serious poisoning may present in a critical condition. As with all poisoned patients, initial stabilization must be instituted before other possible treatments can be employed Initial evaluation should be focused on the improvement of vital signs: airway,

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap meta-

Fomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the build-up of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid)

Fomepizole is indicated for methanol or ethylene glycol ingestion resulting in a metabolic acidosis with an elevated osmolar gap and a serum Methanol or ethylene glycol level of at

Haemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/ or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end

should be evaluated together with the other manifestations and observations [71, 72].

oxalate crystals found in the urine of patients who have consumed ethylene glycol.

**18.2. Investigations**

**18.3. Treatment**

least 20 mg/dL.

respiration and circulation.

bolic acidosis and elevated osmolar gap.

whose deposition in tissues can cause irreparable damage.

**Stage 5 (**2–5 weeks after the overdose): The stomach or intestines can become blocked by scars [59, 60].

### **17.3. Treatment**

First step stabilize the air way, breathing and circulation. An abdominal x-ray may be helpful to confirm the presence of iron tablets. Consider GI decontamination by whole bowel irrigation if the patient is stable and has no contraindications, especially for large ingestions of modified release products, providing the airway can be protected. Activated charcoal does not bind iron. Asymptomatic patients need observation for 6 h and serum iron levels less than 300–350 mcg/dL may be discharged.

Chelation therapy with deferoxamine is indicated for patients with serum iron levels >350 mcg/dL and have evidence of toxicity, or levels of >500 mcg/dL regardless of signs or symptoms. In patients with significant clinical manifestations of toxicity persistent emesis, metabolic acidosis, chelation therapy should not be delayed while one awaits serum iron levels. Haemodialysis does not remove iron effectively but should be considered on a supportive basis for acute renal failure as this will facilitate removal of the iron-deferoxamine complex [61, 62].
