Organophosphates poisoning

Table of Contents

Organophosphates Poisoning is when a person develops an illness as a result of organophosphate exposure.

Organophosphates are chemicals in insecticide used extensively in agriculture. When people, such as agricultural workers, are exposed to large quantities of organophosphates, these chemicals can be harmful.

Organophosphates include: parathion, fenthion, malathion, diazinon, dursban, quinalphos and prothoate.

Fast facts on organophosphate poisoning

Nearly 25 million cases of unintentional pesticide poisoning occur in the agricultural industry across the world each year.
Globally, it is reported that 3 million or more people are exposed to OPs every year, accounting for 300,000 mortalities.
In the United States, there are around 8000 exposures per year, with fewer deaths. Poisoning leads to significant morbidity and mortality each year in India. According to the National Crime Records Bureau of India, there were 27,657 deaths and suicides by poisoning in 2015.
Cases are most common in regions where workers do not use or do not have access to protective gear, such as suits or masks.
Symptoms and complications vary but can include death.

Definitions

Poison: A foreign chemical that is capable of producing a harmful effect on a biologic system (xenobiotic)
Poisoning: The development of harmful effects on normal body functions following exposure to chemicals after it is swallowed, inhaled, injected or absorbed.

Pathophysiology of Organophosphates Poisoning.

Organophosphates exert their acute effects by causing overstimulation at cholinergic nerve terminals. Acetylcholine (Ach) is found in the central and peripheral nervous systems, neuromuscular junctions and red blood cells (RBCs). Normally, acetylcholinesterase (AChE) catalyzes the degradation of the neurotransmitter Ach into choline and acetic acid in the synapse. OP pesticides act by binding irreversibly to the AChE, thereby reducing the ability of the enzyme to break down the neurotransmitter. This produces an accumulation of Ach in the central and peripheral nervous systems, resulting in an acute cholinergic syndrome via continuous neurotransmission. The clinical onset of cholinergic overstimulation can vary from almost instantaneous to several hours after exposure. Although most patients rapidly become symptomatic, the onset and severity of symptoms depend on the specific compound, amount, route of exposure and rate of metabolic degradation.

Routes of absorption during organophosphate poisoning

Ingestion – Gastrointestinal (GI) tract (accidental, deliberate)
Cutaneous – Skin
Inhalation – Lungs.

Signs and symptoms of organophosphates poisoning

Organophosphate poisoning symptoms can range from mild to severe. In more severe cases, a person may die from the toxicity.

The length and strength of the exposure will determine the nature of someone’s symptoms. Symptoms may start in as little as a few minutes or after several hours.

Symptoms of mild exposure to organophosphates include:

Blurry or impaired vision
Watery eyes
Narrowed pupils
Stinging eyes
Nausea
Runny nose
Muscle twitching
Glassy eyes
Extra saliva
Headache
Muscle fatigue or weakness
Agitation

Symptoms of moderate exposure to organophosphate include:

Dizziness
Very narrow pupils
Fatigue
Muscle tremors
Muscle twitching
Drooling
Disorientation
Wheezing or coughing
Severe diarrhea
Difficulty breathing
Sneezing
Uncontrolled urination or bowel movements
Excessive phlegm
Muscle weakness
Severe vomiting

Symptoms of emergency-level exposure to organophosphate include:

Confusion
Narrow pupils
Convulsions
Coma
Agitation
Excessive secretions, such as saliva, sweat, tears, and mucus
Irregular or slow heartbeat
Collapsing
Breathing that is ineffective stops

Signs and Symptoms according to stimulation

Muscarinic signs and symptoms

“Musc leaks from everywhere”

Remember this mnemonic SLUDGE, there is excessive secretions from everywhere in muscarinic overstimulation.

S – salivation
L- lacrimation
U- urination
D- defecation
G- GI cramps
E- emesis

Nicotinic signs and symptoms

“Nics give tension (hypertension), weakness and paralysis”

Remember this mnemonic MT WTF my BP is high, and Paralysis is happening.

M-Mydriasis
T-Tachycardia
W-muscle weakness
T-muscle twitching
F-muscle fasciculation
BP is high- hypertension
Paralysis is happening – muscle paralysis

Complications

In addition to immediate signs and symptoms, organophosphate exposure can cause a number of long- term complications. Again, the severity of the complications depends on the extent and length of exposure.

Paralysis
Fertility issues
Cancer
Metabolic disorders, such as high blood sugar levels
Inflammation of the pancreas
Excess acid in the blood
Brain and nerve problems

Diagnosis of Organophosphate Poisoning

1. History

2. Physical examination

3. Vital signs

Depressed respirations, bradycardia and hypotension are possible findings.

4. Laboratory investigations:

Plasma pseudocholinesterase levels: Normal 3000–8000 U/L. Serum levels may be < 1000 U/L
RBC AChE level:
White blood cells (WBC) – Leucocytosis is seen
ABG values to rule out acidosis – Metabolic and/or respiratory acidosis
Potassium and magnesium levels are decreased.

5. Imaging studies

Chest X-ray for
Electrocardiogram for ventricular

Medical management

Step 1: Identify the nature of poison i.e. OP, carbamate, chloride, pyrethroid.

Step II: Decontamination

Staff must have on protective equipment before commencing treatment including mask, gloves, gowns and eye protection. Staff involved in direct contact with patient’s bodily secretions should immediately and thoroughly wash the affected area with soap and water.
Gastric lavage should be done only after stabilizing the forced emesis if patient is awake. Gastric lavage is given within 1 hour of ingestion of Organophosphates. Activated charcoal 0.5–1 g/kg can be given within 1 hour of ingestion, but studies have shown no benefit.

Step III: Maintaining airway, breathing and circulation

Airway: Maintain clear airway and ensure adequate oxygenation. Check gag reflex. If absent, intubate before stomach wash.
Breathing: Administer oxygen 6 L/min by Intubation if breathing is inadequate, oximetry is <90%, or Glasgow coma scale (GCS) <8. Administer injection atropine 0.05 mg/kg (2 mg in adults) every 5 min to reduce bronchial and oral secretions until adequately atropinised.
Circulation: Administer adequate intravenous (IV) fluids through a wide bore cannula to replace volume loss.

Step IV: Cardiac monitoring

Monitor for arrythmias.

Step V: Specific therapy Antidotes

Atropine is given in intermittent boluses 2 mg every 5 min or as an infusion. The aim is to keep patient airway dry.
Atropinisation is to be initiated as soon as diagnosis is suspected.
Signs of atropinisation: Heart rate about 100/min, pupils mid position, bowel sounds just heard, clear lung sounds, dry skin
Protocol for atropinisation: Injection atropine 2 mg IV bolus is administered, and then the dose is doubled every 5 min till atropinisation is achieved.
Signs of atropine toxicity (anticholinergic toxidrome): Dry mucus membranes (dry as a bone), mental status changes (mad as a hatter), flushed skin (red as a beet), mydriasis (blind as a bat), fever (hot as hell), tachycardia, hypertension, decreased bowel sounds/GI motility and urinary retention.
Atropine toxicity is treated with injection haloperidol 5 mg intramuscular or IV and by reducing the dose of atropine.

Antibiotics

Antibiotics are not usually indicated for OP.
Gastric lavage with an unprotected airway and/or a low GCS in the setting of poisoning are the risk factors for aspiration.
If aspiration pneumonia is suspected (fever, leucocytosis, pulmonary infiltrates with worsening oxygenation), antibiotics such as penicillin (ceftriaxone, amoxycillin or clauvulenic acid, piperacillin tazobacterium [Piptaz]) may be considered.

Sedation

Agitation in the setting of OP poisoning may indicate over atropinisation, hypoxaemia, or distress due to pain/discomfort. Intubated patients need a combination of an analgesic and a sedative such as morphine + lorazepam as an infusion. Haloperidol may increase seizure threshold and is not recommended unless patients are unresponsive to other drugs.
Lasix is the drug of choice if pulmonary oedema persists even after full atropinisation

Nurses roles during management of organophosphate poisoning

Assessing the airway for bilateral equal air entry, respiratory rate and breath sounds
Assessing for cough and gag reflex and for bronchospasms.
Changed position every 2 hourly to mobilize secretions.
Positioning him in semi-fowlers at 45° to promote lung expansion and to prevent aspiration.
Maintaining adequate hydration by administering IV fluids.
Providing humidification to airways to thin secretions.
Checking for neck muscle weakness, use of accessory muscles for breathing.
Assessing single breath count.
Assisting for intubation.
Checking the ventilator settings of the patient.
Positioning patient in semi-fowler’s position to promote diaphragmatic descent and maximal inhalation.
Performing suctioning whenever necessary.
Assessing heart rate, rhythm for arrhythmias, BP, capillary refill time, skin turgor, vital signs every hour.
Assessing peripheral sites for perfusion.
Monitoring urine output every hour.
Administered atropine infusion to maintain the heart rate above 90/min.
Monitoring vital signs.
Following strict aseptic technique while handling invasive lines and while performing suctioning.
Providing oral care with chlorhexidine solution.
Checking for the colour, consistency and volume of secretions.
Monitored ABG values, WBC counts, culture and sensitivity results, chest X-ray.
Administering injection Piptaz 4.5 g IV q 8 hourly as per the order.
Evaluating his feelings and perception of the reasons for lack of power and sense of helplessness.
Involving him in care.
Identifying his usual belief/locus of control that influences his life.

Opium/Opioid poisoning

Voluntary or accidental overdose of opioid drugs

Clinical features

Respiratory depression
Hypotension
Hypothermia
Pinpoint pupils
Decreased mental status or coma

Management

Aim at restoring respiration not consciousness
Give antidote; naloxone 4-2mg IV or IM repeat dose every 2-3minutes if not improving up to max of 10mg
For children give 0.1mg/kg

Naloxone is contraindicated opioid-induced respiratory depression in chronic opioid use like in palliative care of cancer patients

TOXICOLOGY/POISONING:

Toxicology is a scientific study of adverse effects of chemicals/poisons and their effect on living system

Poisoning refers to bodily entry of toxic substance in amounts that cause dysfunction of body system

Antidote is a chemical substance that stops or counteracts effects of a poison

It is caused by;

Micro organism e.g. in food poisoning
Inorganic sources e.g. lead, mercury, copper metal poisoning
Organic sources e.g. agriculture chemical, paraffin, petrol
Drug abuse e.g. alcohol or medicines in excess amounts

GENERAL MANAGEMENT OF POISONING

Refer patients to the admission
In hospital, admit all patients with history or signs of poisoning even if they are well.
Optimal management depends on the specific poison taken, presenting and suspected illness and time has elapsed between exposure and presentation.

Management includes;

Supportive care
Decontamination and enhanced elimination techniques
Antidote therapy

Supportive therapy

Airway and breathing support
Position in semi prone to minimize risk of aspiration of vomitus
Maintain airway patent and if necessary assist in ventilation
Administer oxygen
Blood pressure

If hypotensive, raise foot of bed and start IV N/S
If hypertensive manage appropriately

6. Temperature

If hypothermic, cover with heavy blanket
If hyperthermic, tepid sponging and give antipyretics

7 .Convulsion

Give diazepam 10mg rectally of 5-10mg as slow IV in adults. Max dose is 30mg
In children 0.5mg/kg rectally or 0.2mg/kg as IV

8. Counsel patient and families on poisoning

Decontamination

It refers to removal and elimination of poison.

It has to be implemented after stabilization of vitals.

It involves;

Removal of the stomach, Do not induce vomiting
Balance dangers of gastric emptying against the likely toxicity of swallowed medicine
Insert NG tube perform gastric lavage. It is useful if done within 2 hours of ingestion of poison and is contraindicated in comatose patients, and in corrosive or petroleum products
Prevention of absorption and enhance active elimination
Administer activated charcoal to bind the poison in the stomach and reduce absorption. Give 50g (250mg) repeated every 4 hours if necessary. Grind the tablet into fine powered then mix with 100mls of water. In children give 0.5-1g/kg.

This is effective within 2 hours of ingestion of poison and is contraindicated in intestinal obstruction, corrosive or petroleum products, toxins that are poorly absorbed by charcoal, depressed mental status in late presentation

Benzodiazepine toxicity

Benzodiazepines are used in anxiety and as a sedative drug its overdose can be international or accidental

Clinical presentations

Confusion or drowsiness
Hypotension
Unresponsiveness or coma
Respiratory depression
Nystagmus
Hallucinations
Slurred speech
Body weakness/ hypotonia

Management

Obtain a baseline prothrombin time and international normalized ratio (PT/INR) and make arrangements for a repeat measurement in 24-48 hours
Administer activated charcoal for recent (within the last 1-2 hours)
Gastric lavage is unnecessary if rapid administration of activated charcoal is feasible/ carried out
If the patient is elevated, the effects of wafarin can be reversed with vitamin K₁ is appropriate; 10mg orally or by slow IV infusion or flesh frozen plasma (FFP)
For urgent reversal of the effects, prothrombin complex concentrate (PCC) also known as factor IX complex, has been approved in urgent reversal of acquired coagulation factor deficiency induced by wafarin

Paracetamol toxicity

Accidental or international consumption of paracetamol
Toxic dose>150mg/kg or 7.5g

Clinical features

First 24 hours, the individual may be asymptomatic or may present with nausea, vomiting, malaise and abdominal pain
In 24-72 hours, progressive signs of hepatoxicity appear such as right upper quadrant pain, enlarged tender liver and raised LFT
After 72 hours, its followed by either recovery after 5-7 days or progression to hepatic failure

Management

If ingestion occurred less than two hours, perform gastric lavage to empty the stomach and remove any remaining medicine
Give repeated doses of activated charcoal like 25-50g every 4 hours
Give acetylcysteine IV preferably within 8 hours from ingestion. It work to reduce paracetamol toxicity by providing cysteine for glutat5haione synthesis which is an antioxidant. Glutathione reacts with the toxic metabolite so that it does not damage cells and can be safely excreted.

It can be given as follows;

150mg/kg (max 15g) in 200mls D5 in 60 minutes followed by
50mg/kg (max5g) in 500ml D5 in 4 hours followed by
100mg/kg (max 10g) in 100ml D5 in 16 hours

Aspirin/acetylsalicylic poisoning

Overdose of ASA occurs when there is consumption of > 10g in adults and 3g in children

Clinical features

Mild to moderate toxicity; hyperventilation, nausea, vomiting, vasodilation and tinnitus
Severe toxicity; hyperpyrexia, convulsions, altered mental status,
Acidosis

Food poisoning

This is illness caused by consumption of food or water caused by pathogenic micro-organism.

It caused by infections with mainly salmonella typhi or toxins released by micro-organisms

Clinical features

Nausea and vomiting
Intermittent abdominal pain
Diarrhoea
Fever

Management

Give ORS or IV fluids normal saline to rehydrate the patient
Give paracetamol 1g 6 hourly incase of abdominal pain
Establish the cause and treat accordingly
In severe cases, give antibiotics like ciprofloxacin 500mg 12 hourly or metronidazole 400mg tds

Prevention

Heat cooked food thoroughly before eating and avoid leftovers
Ensure food and utensil hygiene
Ensure personal hygiene

Carbon monoxide poisoning

Carbon monoxide is a colourless, odourless and non-irritating gas. The poisoning can result from inhalation of smoke, car exhaust or fumes or use charcoal stoves in unventilated rooms

Clinical features

Headache, dizziness and confusion
Nausea and vomiting
Seizures, collapse and coma

Management

Move person to fresh air
Clear airway
Give 100% oxygen via non-rebreather mask
Re-assess the ABGS
IV fluids incase of hypotension
Diazepam for seizures

Methanol toxicity

Methanol is used as an industrial solvent and is an ingredient of methylated spirits

Methanol is a product of incomplete conversion of alcohol to ethanol especially in home- distilled crude alcohol. When taken, it’s transformed into toxic products in the body that cause acidosis

Ingestion of a dose >1g/kg is lethal

Clinical features

Initially presents with; headache, dizziness, nausea, vomiting and visual disturbances
Later CNS depression, respiratory failure and coma
Toxic metabolites may cause severe acidosis and retinal optical nerve damage

Management

Gastric lavage if ingestion occurred within 1 hour to arrival
Charcoal is not effective
Give IV fluids to manage shock and hypovolemia
Administer deferoxamine as an antidote for iron toxicity. Give a continuous infusion of 5mg/kg/hr in N/S or D5. Continue until metabolic acidosis clears or symptoms improve. Do not use for more than 2 hours
Avoid the drug in cases of renal failure

Paraffin and other petroleum products

Petroleum products include; paraffin, petrol, paint thinners and organic solvents

Clinical features

Patient may smell paraffin or other petroleum products
Burning sensation in the mouth and throat
Patient looks pale, dyspnea and tachypnea
Vomiting, diarrhoea and bloody stool
Cough
Lethargy

Management

Remove clothes and wash skin with soap and water if contaminated
Avoid gastric lavage or use of enemas.
Do not give charcoal
Treatment is supportive or symptomatic
Administer oxygen if hypoxic

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