**18. Toxic alcohol poisoning**

The term toxic alcohol has generally referred to isopropanol, methanol, and ethylene glycol (EG). Poisoning involving toxic alcohols are relatively uncommon, but remain important causes of suicide or epidemic poisonings; Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly [63, 64].

#### **18.1. .Mechanism of action and clinical features**

Methanol also called methyl alcohol is found in paint removers or photocopying fluid, deicing products and windshield wiper fluid. Methanol metabolism in the liver by alcohol dehydrogenase to formaldehyde. Aldehyde dehydrogenase then rapidly converts formaldehyde to formic acid with no appreciable accumulation of formaldehyde in the blood.

The formic acid inhibits cytochrome c in the mitochondria, shifting the cell to anaerobic glycolysis, leading to lactic acid accumulation. The clinical features of methanol poisoning are the triad of severe anion gap metabolic acidosis, visual changes, and mental status depression. Other methanol intoxication symptoms include headache, light-headedness, nausea, vomiting, abdominal pain and dyspnoea. Methanol may produce pancreatitis by direct toxic effect on the pancreas.

Ethylene glycol is found in radiator antifreeze, metal cleaners, and degreasing agents. It has no smell or colour and tastes sweet. Ethylene glycol is metabolized in the liver to glycolaldehyde 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 oxalate crystals found in the urine of patients who have consumed ethylene glycol.

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].

#### **18.2. Investigations**

**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 slug-

**Stage 5 (**2–5 weeks after the overdose): The stomach or intestines can become blocked by scars

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

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

The term toxic alcohol has generally referred to isopropanol, methanol, and ethylene glycol (EG). Poisoning involving toxic alcohols are relatively uncommon, but remain important causes of suicide or epidemic poisonings; Mortality and morbidity of toxic alcohols are high

Methanol also called methyl alcohol is found in paint removers or photocopying fluid, deicing products and windshield wiper fluid. Methanol metabolism in the liver by alcohol dehydrogenase to formaldehyde. Aldehyde dehydrogenase then rapidly converts formaldehyde

The formic acid inhibits cytochrome c in the mitochondria, shifting the cell to anaerobic glycolysis, leading to lactic acid accumulation. The clinical features of methanol poisoning are the triad of severe anion gap metabolic acidosis, visual changes, and mental status depression. Other methanol intoxication symptoms include headache, light-headedness, nausea, vomiting, abdominal pain and dyspnoea. Methanol may produce pancreatitis by direct toxic

Ethylene glycol is found in radiator antifreeze, metal cleaners, and degreasing agents. It has no smell or colour and tastes sweet. Ethylene glycol is metabolized in the liver to glycolaldehyde

to formic acid with no appreciable accumulation of formaldehyde in the blood.

failure as this will facilitate removal of the iron-deferoxamine complex [61, 62].

if prompt diagnosis and treatment are not initiated rapidly [63, 64].

**18.1. .Mechanism of action and clinical features**

gishness (lethargy) or coma may develop.

266 Essentials of Accident and Emergency Medicine

300–350 mcg/dL may be discharged.

**18. Toxic alcohol poisoning**

effect on the pancreas.

[59, 60].

**17.3. Treatment**

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

#### **18.3. Treatment**

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, respiration and circulation.

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap.

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) whose deposition in tissues can cause irreparable damage.

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 least 20 mg/dL.

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 organ damage (i.e. acute renal failure. Vitamin Supplementation: Give folic or folinic acid to patients with methanol toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites [73–76].

cholinesterase enzyme for a prolonged time, causing clinical effects to persist for a prolonged time. On average, some aging for commercial organophosphorus agents will occur by 48 h but may take longer. The intermediate syndrome is distinct from OP in the following ways: start within 24–96 h after recovery from acute cholinergic crisis, cranial nerves INNERVATED muscle and proximal muscles weakness, and rapid clinical recovery over 4–18 days. Any patient with a clinically apparent cholinergic syndrome should be treated empirically without

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

Medical management of OP pesticide poisoning demands close observation, timely institution of antidote in adequate doses and duration and good supportive. The Treating staff should wear protective clothing. The patient's clothes should be removed and destroyed and

Treatment includes: resuscitation of patients giving oxygen, a muscarinic antagonist (usually atropine), fluids and an acetylcholinesterase reactivator (an oxime that reactivates acetylcho-

Respiratory support is given as necessary. Patients must be carefully observed after stabilization for changes in atropine needs, worsening respiratory function because of intermediate

Poisoned patient in emergency department have unique Approach because of difficulties in obtain history, poisoned patients need careful physical examination looking for toxidromes or sign of illegal drugs abuse. Intoxicated patient's management started with resuscitation and stabilization of air way, breathing and circulation. Consider decontamination in early time post ingestion. Most of the patient need laboratory test includes full cell count and electrolytes and kidney functions, specific drug level. Paracetamol level must be send for every present with history intestinal over dose. Symptomatic treatment is cornerstone treatment for post intoxicated patient also antidotes need for specific substances in specific conditions. Finally physicians in emergency department need to call the local poisoning centre to help

syndrome, and recurrent cholinergic features occurring with fat-soluble OP [79].

waiting for laboratory confirmation of decreased cholinesterase activity [78].

the patient should be showered in a designated decontamination area.

linesterase by removal of the phosphate group).

Ehab Said Aki\*, Waleed Awad Salem and Jalal Alessai

Hamad Medical Corporation, Doha, Qatar

\*Address all correspondence to: akiehab2004@gmail.com

**19.3. Treatment**

**20. Conclusion**

them in management.

**Author details**
