**19. Organophosphates poisoning**

Organophosphates (OP) are used in insecticides for domestic and agricultural use. They are also the main toxins in nerve gases like Sarin. OP pesticide self-poisoning is a major clinical and public-health problem across much of rural Asia [77].

#### **19.1. Mechanism of action**

The most serious poisoning of OP occurs by ingestion; cutaneous absorption and inhalation of sprays rarely cause serious toxicity. OP is extremely toxic pesticides, which produce acetylcholine excess with muscarinic, nicotinic and CNS effects.

#### **19.2. Clinical features**

Patients present with degrees of cholinergic crisis, usually within 4 h of ingestion or exposure. Specific manifestations include: Muscarinic manifestations like bronchospasm, vomiting, pinpoint pupils, bradycardia and hypotension, excessive sweating, lacrimation, salivation, profuse diarrhoea and urination (**Table 4**).

Over-stimulation of nicotinic receptors causes tachycardia, hypertension and sweating. Accumulation of acetylcholine at the neuromuscular junction causes initial stimulation followed by depolarization and paralysis. This appears first as fasciculations, cramps and muscle weakness. Central nervous system (CNS) effects include delirium, coma and seizures. Most deaths are due to respiratory failure. Toxicity from gradual, cumulative exposure may be much more subtle. These patients commonly exhibit vague confusion or other central nervous system complaints; mild visual disturbances; or chronic abdominal cramping, nausea, and diarrhoea. A unique effect of organophosphorus insecticides results from "aging," the irreversible conformational change that occurs when the organophosphorus agent is bound to the


**Table 4.** DUMBELS mnemonic for signs of cholinergic excess.

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

#### **19.3. Treatment**

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

Organophosphates (OP) are used in insecticides for domestic and agricultural use. They are also the main toxins in nerve gases like Sarin. OP pesticide self-poisoning is a major clinical

The most serious poisoning of OP occurs by ingestion; cutaneous absorption and inhalation of sprays rarely cause serious toxicity. OP is extremely toxic pesticides, which produce acetyl-

Patients present with degrees of cholinergic crisis, usually within 4 h of ingestion or exposure. Specific manifestations include: Muscarinic manifestations like bronchospasm, vomiting, pinpoint pupils, bradycardia and hypotension, excessive sweating, lacrimation, salivation,

Over-stimulation of nicotinic receptors causes tachycardia, hypertension and sweating. Accumulation of acetylcholine at the neuromuscular junction causes initial stimulation followed by depolarization and paralysis. This appears first as fasciculations, cramps and muscle weakness. Central nervous system (CNS) effects include delirium, coma and seizures. Most deaths are due to respiratory failure. Toxicity from gradual, cumulative exposure may be much more subtle. These patients commonly exhibit vague confusion or other central nervous system complaints; mild visual disturbances; or chronic abdominal cramping, nausea, and diarrhoea. A unique effect of organophosphorus insecticides results from "aging," the irreversible conformational change that occurs when the organophosphorus agent is bound to the

metabolism to nontoxic metabolites [73–76].

268 Essentials of Accident and Emergency Medicine

**19. Organophosphates poisoning**

profuse diarrhoea and urination (**Table 4**).

**Table 4.** DUMBELS mnemonic for signs of cholinergic excess.

**19.1. Mechanism of action**

**19.2. Clinical features**

Diarrhoea Urination Miosis

Bronchospasm Emesis Lacrimation Salivation

and public-health problem across much of rural Asia [77].

choline excess with muscarinic, nicotinic and CNS effects.

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 the patient should be showered in a designated decontamination area.

Treatment includes: resuscitation of patients giving oxygen, a muscarinic antagonist (usually atropine), fluids and an acetylcholinesterase reactivator (an oxime that reactivates acetylcholinesterase by removal of the phosphate group).

Respiratory support is given as necessary. Patients must be carefully observed after stabilization for changes in atropine needs, worsening respiratory function because of intermediate syndrome, and recurrent cholinergic features occurring with fat-soluble OP [79].
