Signs and Symptoms Based on Receptor Stimulation

Organophosphate (OP) poisoning manifests with signs and symptoms categorized by the type of cholinergic receptor stimulated.

Muscarinic Signs and Symptoms

• Characterized by excessive secretions from various bodily locations.

• Mnemonic: “Musc leaks from everywhere” or SLUDGE

  • S – Salivation: Increased production of saliva.

  • L – Lacrimation: Watery eyes, increased tear production.

  • U – Urination: Increased frequency and urgency.

  • D – Defecation: Diarrhea and involuntary bowel movements.

  • G – GI Cramps: Abdominal pain and cramping.

  • E – Emesis: Vomiting.

Nicotinic Signs and Symptoms

• Primarily involve muscle and cardiovascular effects.

• Mnemonic: “Nics give tension, weakness and paralysis” or MT WTF my BP is high, and Paralysis is happening.

  • M – Mydriasis: Pupillary dilation (enlarged pupils).

  • T – Tachycardia: Increased heart rate.

  • W – Muscle Weakness: Generalized muscle weakness.

  • T – Muscle Twitching: Involuntary muscle contractions.

  • F – Muscle Fasciculation: Fine muscle twitching.

  • BP is high – Hypertension: Elevated blood pressure.

  • Paralysis is happening – Muscle Paralysis: Muscle weakness progressing to paralysis.

Complications of Organophosphate Poisoning

Beyond the immediate acute symptoms, organophosphate exposure can lead to several long-term health complications. The severity of these complications is often linked to the extent and duration of the poisoning.

1. Paralysis: Persistent muscle weakness or paralysis, potentially long-lasting.

2. Fertility Issues: Potential adverse effects on reproductive health and fertility.

3. Cancer: Some studies suggest a possible increased risk of certain cancers with OP exposure, although research is ongoing.

4. Metabolic Disorders: Disruption of metabolic processes, including:

   • Hyperglycemia: Elevated blood sugar levels (high blood sugar).

5. Pancreatitis: Inflammation of the pancreas.

6. Acidosis: Metabolic disturbances leading to:

   • Acidemia: Excess acid accumulation in the blood.

7. Neurological Sequelae: Long-term problems affecting the brain and nerves.

Diagnosis of Organophosphate Poisoning

Diagnosis typically involves a combination of clinical assessment and laboratory tests:

1. History: Gathering information about potential exposure circumstances, including:

   • Occupational history (e.g., agricultural work).

   • Recent activities involving potential pesticide contact.

   • Symptoms experienced and their onset.

2. Physical Examination: Assessment of characteristic signs:

   • Pupil size (miosis or mydriasis).

   • Secretions (salivation, lacrimation, etc.).

   • Muscle tone and strength (weakness, fasciculations).

   • Respiratory status (wheezing, dyspnea).

3. Vital Signs: Monitoring for key indicators of poisoning:

   • Depressed Respirations: Slow and shallow breathing.

   • Bradycardia: Slow heart rate.

   • Hypotension: Low blood pressure.

4. Laboratory Investigations: To confirm exposure and assess severity:

   • Plasma Pseudocholinesterase Levels:

     • Normal range: 3000–8000 U/L.

     • Significantly reduced levels (< 1000 U/L) are suggestive of OP poisoning.

   • Red Blood Cell Acetylcholinesterase (RBC AChE) Level: Directly measures AChE activity in red blood cells. Reduced levels indicate OP effect.

   • White Blood Cell Count (WBC):

     • Leukocytosis: Elevated WBC count may be observed, particularly if aspiration pneumonia develops.

   • Arterial Blood Gas (ABG) Analysis:

     • To evaluate acid-base balance and oxygenation.

     • May reveal metabolic and/or respiratory acidosis due to impaired respiration and metabolic effects.

   • Electrolyte Levels:

     • Potassium and Magnesium levels: May be decreased in OP poisoning.

5. Imaging Studies:

   • Chest X-ray: To assess for:

     • Pulmonary edema.

     • Aspiration pneumonia.

   • Electrocardiogram (ECG): To monitor for:

     • Ventricular arrhythmias and other cardiac abnormalities.

Medical Management of Organophosphate Poisoning

Management is a multi-step approach focused on decontamination, supportive care, and specific antidotes:

Step I: Poison Identification

• Determine the type of poisoning agent, if possible. Distinguish between:

  • Organophosphates (OPs).

  • Carbamates.

  • Chlorides.

  • Pyrethroids.

  • This identification guides specific treatment strategies.

Step II: Decontamination

1. Personnel Protection: Prioritize staff safety.

   • Healthcare staff must wear personal protective equipment (PPE) before initiating treatment.

   • PPE includes: masks, gloves, gowns, and eye protection.

   • Staff in contact with patient’s secretions should immediately wash affected areas with soap and water.

2. Gastric Lavage: Consider if ingestion is the route of exposure.

   • Perform gastric lavage only after stabilizing the patient’s airway and breathing.

   • Avoid forced emesis in awake patients due to aspiration risk.

   • Gastric lavage is most effective if performed within 1 hour of OP ingestion.

   • Activated Charcoal:

     • 0.5–1 g/kg dose can be administered orally or via nasogastric tube, ideally within 1 hour of ingestion.

     • However, some studies question the clinical benefit of activated charcoal in OP poisoning.

Step III: Airway, Breathing, and Circulation (ABC) Management

1. Airway Management:

   • Maintain a clear airway to ensure adequate ventilation.

   • Assess gag reflex. If absent, intubate the patient before gastric lavage to prevent aspiration.

2. Breathing Support:

   • Oxygen Administration: Administer supplemental oxygen at 6 L/min via nasal cannula or face mask initially.

   • Intubation and Mechanical Ventilation: Consider endotracheal intubation if:

     • Breathing is inadequate.

     • Pulse oximetry (SpO2) is <90% despite oxygen.

     • Glasgow Coma Scale (GCS) score is <8, indicating reduced consciousness.

   • Atropine Administration: Administer intravenous injection of atropine 0.05 mg/kg (or 2 mg for adults) every 5 minutes.

     • Atropine is a competitive antagonist at muscarinic acetylcholine receptors, counteracting the muscarinic effects of OP poisoning.

     • Continue atropine administration until adequate atropinization is achieved to reduce bronchial and oral secretions.

3. Circulatory Support:

   • Intravenous Fluids: Establish intravenous access using a large-bore cannula.

   • Administer adequate intravenous fluids (e.g., crystalloids like normal saline) to address and replace fluid volume loss due to vomiting, diarrhea, and secretions.

Step IV: Cardiac Monitoring

• Implement continuous cardiac monitoring to detect and manage:

  • Arrhythmias (irregular heartbeats).

Step V: Specific Antidote Therapy

• Atropine:

  • Administer atropine intravenously in intermittent boluses of 2 mg every 5 minutes or via continuous infusion.

  • Goal of Atropinization: Maintain a “dry airway” by reducing excessive secretions.

  • Initiate Atropinization: Begin atropine therapy as soon as OP poisoning is suspected clinically.

  • Clinical Signs of Adequate Atropinization: Monitor for these indicators of effective atropine dosing:

    • Heart rate around 100 beats per minute.

    • Pupils in mid-position (not excessively dilated or constricted).

    • Bowel sounds just audible (indicating reduced GI hyperactivity).

    • Lung sounds clear of excessive secretions (reduced bronchorrhea).

    • Skin dry to the touch (reduced diaphoresis).

  • Atropine Toxicity: Be aware of signs of excessive atropine administration (anticholinergic toxidrome):

    • Dry mucus membranes: “Dry as a bone.”

    • Mental status changes: Agitation, delirium – “Mad as a hatter.”

    • Flushed skin: “Red as a beet.”

    • Mydriasis: Dilated pupils – “Blind as a bat.”

    • Fever: Hyperthermia – “Hot as hell.”

    • Tachycardia: Rapid heart rate.

    • Hypertension: Elevated blood pressure.

    • Decreased bowel sounds/GI motility.

    • Urinary retention.

  • Management of Atropine Toxicity: If atropine toxicity occurs:

    • Administer intramuscular or intravenous injection of haloperidol 5 mg to manage agitation and delirium.

    • Reduce the dose of atropine infusion or bolus frequency.

Step VI: Consideration of Antibiotics

• Routine antibiotics are generally not indicated in uncomplicated OP poisoning.

• Aspiration Pneumonia: Antibiotics may be considered if aspiration pneumonia is suspected. Risk factors for aspiration pneumonia include:

  • Gastric lavage performed without airway protection (unprotected airway).

  • Low Glasgow Coma Scale (GCS) score, indicating impaired consciousness and gag reflex.

  • Clinical signs of aspiration pneumonia: Fever, leukocytosis, new pulmonary infiltrates on chest X-ray, worsening oxygenation.

  • Antibiotic choices, if indicated, may include:

    • Penicillins (e.g., amoxicillin-clavulanate).

    • Cephalosporins (e.g., ceftriaxone).

    • Piperacillin-tazobactam (Piptaz).

Step VII: Sedation Management

• Agitation Management: Agitation in OP poisoning can have multiple causes:

  • Over-atropinization (anticholinergic effects).

  • Hypoxemia (low blood oxygen levels).

  • Pain or discomfort.

  • Address the underlying cause.

• Sedation for Intubated Patients: Intubated and mechanically ventilated patients often require sedation and analgesia.

  • Combination Therapy: Use a combination of:

    • Analgesic: e.g., morphine infusion for pain management.

    • Sedative: e.g., lorazepam infusion for sedation.

  • Haloperidol Caution: Haloperidol is generally not recommended for routine sedation in OP poisoning.

    • It may lower the seizure threshold, potentially increasing seizure risk.

    • Reserve haloperidol for specific situations, such as managing atropine-induced delirium, and only if other sedatives are ineffective.

Step VIII: Management of Persistent Pulmonary Edema

• Pulmonary Edema: If pulmonary edema (fluid in the lungs) persists despite full atropinization and supportive measures, consider:

  • Furosemide (Lasix): Loop diuretic. Lasix is the drug of choice to promote fluid excretion and reduce pulmonary edema in this context.

Nursing Roles During Management of Organophosphate Poisoning

Nurses play a vital role in the comprehensive care of patients with organophosphate poisoning, encompassing respiratory, cardiovascular, and general supportive care.

1. Respiratory Assessment: Continuously monitor and assess:

   • Airway patency: Ensure a clear and open airway.

   • Bilateral Equal Air Entry: Confirm breath sounds are equal and present bilaterally in both lungs.

   • Respiratory Rate and Pattern: Assess the rate, depth, and effort of breathing.

   • Breath Sounds: Auscultate lung sounds for:

     • Wheezing (indicating bronchospasm).

     • Crackles or rhonchi (suggesting secretions or fluid).

2. Cough and Gag Reflex Assessment: Evaluate:

   • Cough reflex: Presence and effectiveness of coughing.

   • Gag reflex: Presence of gag reflex to assess aspiration risk.

   • Monitor for bronchospasm: Observe for signs of airway constriction, such as wheezing and increased respiratory effort.

3. Secretion Mobilization: Implement strategies to clear airway secretions:

   • Position Changes: Turn and reposition the patient every 2 hours to mobilize secretions and prevent atelectasis.

4. Positioning for Lung Expansion: Optimize respiratory mechanics:

   • Semi-Fowler’s Position: Position the patient in semi-Fowler’s position at a 45-degree angle to:

     • Promote lung expansion by allowing for diaphragmatic descent.

     • Reduce the risk of aspiration.

5. Hydration Management: Maintain adequate fluid balance:

   • Intravenous Fluid Administration: Administer prescribed IV fluids to ensure adequate hydration and replace fluid losses.

6. Airway Humidification: Improve secretion clearance:

   • Humidified Oxygen: Provide humidification to airways to help thin and loosen secretions, facilitating expectoration or suctioning.

7. Assessment of Respiratory Muscle Effort: Monitor for signs of respiratory distress:

   • Neck Muscle Weakness: Assess for weakness in neck muscles, which can indicate respiratory muscle fatigue.

   • Accessory Muscle Use: Observe for the use of accessory muscles of respiration (e.g., sternocleidomastoid, intercostal muscles), suggesting increased work of breathing.

8. Single Breath Count: Assess respiratory function quickly:

   • Single Breath Count: Perform a single breath count assessment as an indicator of respiratory capacity and muscle strength.

9. Intubation Assistance: Prepare for and assist with advanced airway management:

   • Intubation Preparation: Prepare equipment and assist the medical team with endotracheal intubation if respiratory failure is imminent or established.

10. Ventilator Management: If mechanical ventilation is required:

    • Ventilator Setting Checks: Regularly check and verify ventilator settings to ensure appropriate ventilatory support.

11. Positioning for Ventilation: Optimize ventilation during mechanical ventilation:

    • Semi-Fowler’s Position: Maintain semi-Fowler’s position even in ventilated patients to:

      • Promote diaphragmatic descent.

      • Maximize lung inflation and gas exchange.

12. Airway Suctioning: Maintain airway clearance:

    • Suctioning: Perform airway suctioning as frequently as needed to remove excessive secretions from the trachea and bronchi.

13. Cardiovascular Assessment: Monitor cardiovascular status closely:

    • Heart Rate and Rhythm: Assess heart rate and rhythm for abnormalities, including arrhythmias.

    • Blood Pressure (BP): Monitor blood pressure for hypotension or hypertension.

    • Capillary Refill Time: Assess capillary refill time as an indicator of peripheral perfusion.

    • Skin Turgor: Evaluate skin turgor to assess hydration status.

    • Vital Signs Frequency: Monitor vital signs frequently, typically every hour, or more often as clinically indicated.

14. Peripheral Perfusion Assessment: Evaluate circulatory adequacy:

    • Peripheral Site Assessment: Regularly assess peripheral sites (e.g., extremities) for signs of adequate perfusion (warmth, color, capillary refill).

15. Urine Output Monitoring: Assess renal perfusion and fluid balance:

    • Hourly Urine Output: Monitor urine output every hour as an indicator of renal function and overall fluid balance.

16. Atropine Infusion Management: Administer and monitor antidote therapy:

    • Atropine Infusion: Administer atropine infusion as prescribed.

    • Heart Rate Target: Adjust atropine infusion rate to maintain the heart rate above 90 beats per minute, or as per physician orders.

17. Vital Sign Monitoring During Atropine Therapy: Closely track response to atropine:

    • Vital Sign Monitoring: Continue frequent monitoring of vital signs during atropine administration to assess therapeutic effect and detect potential atropine toxicity.

18. Infection Prevention: Minimize infection risks:

    • Aseptic Technique: Employ strict aseptic technique when handling invasive lines (IVs, central lines) and during procedures like suctioning to prevent healthcare-associated infections.

19. Oral Hygiene: Maintain oral health, especially in patients with excessive secretions or intubation:

    • Oral Care: Provide regular oral care using an antiseptic solution like chlorhexidine to reduce oral bacterial load and prevent complications like ventilator-associated pneumonia.

20. Secretion Assessment: Characterize airway secretions:

    • Secretion Characteristics: Regularly check and document the color, consistency, and volume of airway secretions to monitor for changes and potential infections.

21. Laboratory and Radiographic Monitoring: Track diagnostic parameters:

    • ABG Value Monitoring: Monitor arterial blood gas (ABG) values to assess respiratory and metabolic status.

    • WBC Count Monitoring: Track white blood cell (WBC) counts to detect infection.

    • Culture and Sensitivity Results: Review culture and sensitivity results if infection is suspected and specimens are obtained.

    • Chest X-ray Monitoring: Monitor chest X-ray findings to assess for pneumonia, pulmonary edema, or other lung pathology.

22. Antibiotic Administration: Administer medications as prescribed:

    • Antibiotic Administration: Administer prescribed intravenous antibiotics, such as piperacillin-tazobactam 4.5 g IV every 8 hours (Piptaz 4.5 g IV q8h), as per physician orders if aspiration pneumonia is diagnosed or suspected.

23. Psychosocial Support: Address patient’s emotional and psychological needs:

    • Emotional Assessment: Evaluate the patient’s feelings and perceptions regarding their condition, including feelings of powerlessness and helplessness.

    • Patient Involvement: Involve the patient in their care to the extent possible to promote a sense of control and autonomy.

    • Belief System Assessment: Identify the patient’s usual beliefs or locus of control (internal vs. external) as this can influence their coping mechanisms and response to illness.

Opium/Opioid Poisoning

Opioid poisoning results from voluntary or accidental overdose of opioid drugs.

Clinical Features

Characteristic signs and symptoms of opioid overdose:

• Respiratory Depression: Slowed or shallow breathing, potentially life-threatening.

• Hypotension: Low blood pressure.

• Hypothermia: Abnormally low body temperature.

• Pinpoint Pupils: Miosis – constricted pupils, often described as “pinpoint.”

• Decreased Mental Status: Reduced level of consciousness, ranging from drowsiness to stupor or:

  • Coma: Unresponsiveness.

Management

The primary aim of management is to restore respiration, not necessarily to fully reverse consciousness initially:

• Antidote Administration: Give naloxone (Narcan), a specific opioid antagonist.

  • Dosage: Initial dose for adults is 0.4-2 mg intravenously (IV) or intramuscularly (IM).

  • Repeat Dosing: If no improvement in respiratory status, repeat the dose every 2-3 minutes, up to a maximum total dose of 10 mg.

  • Pediatric Dosage: For children, the initial dose is 0.1 mg/kg.

Important Note Regarding Naloxone Contraindication

• Naloxone is generally contraindicated for reversing opioid-induced respiratory depression in patients with chronic opioid use for pain management, such as in palliative care for cancer patients.

  • In these chronic pain settings, naloxone can precipitate severe and unmanageable withdrawal symptoms, negating any potential respiratory benefit and causing significant patient distress.

  • Management in chronic opioid users with respiratory depression requires careful titration of opioids and respiratory support, not naloxone reversal.

TOXICOLOGY/POISONING: General Concepts

• Toxicology Definition: Toxicology is the scientific discipline focused on studying the adverse effects of chemicals or poisons on living organisms and systems. It encompasses the mechanisms, detection, and treatment of poisoning.

• Poisoning Definition: Poisoning occurs when a toxic substance enters the body in sufficient quantities to cause dysfunction or damage to bodily systems. Entry routes can include ingestion, inhalation, injection, or absorption.

• Antidote Definition: An antidote is a specific chemical substance designed to counteract or reverse the harmful effects of a particular poison. Antidotes work through various mechanisms, depending on the poison and antidote.

• Causes of Poisoning: Poisoning can arise from diverse sources:

  • Microorganisms: e.g., food poisoning caused by bacterial toxins or pathogens in contaminated food.

  • Inorganic Sources: e.g., heavy metal poisoning from lead, mercury, copper, or other toxic metals.

  • Organic Sources: e.g., exposure to agricultural chemicals (pesticides, herbicides), petroleum products (paraffin, petrol), and other organic toxins.

  • Drug Abuse: e.g., alcohol poisoning or overdose with medications taken in excessive amounts, intentionally or unintentionally.

GENERAL MANAGEMENT OF POISONING: Initial Approach

1. Referral to Admission Area: Initially, direct patients suspected of poisoning to the hospital admission or emergency department for evaluation and stabilization.

2. Hospital Admission: In general hospital practice, admit all patients who present with a history or clinical signs suggestive of poisoning, even if they currently appear well or asymptomatic. Delayed effects are possible with many toxins.

3. Optimal Management Factors: Effective management depends on several key factors:

   • Specific Poison Taken: Identifying the exact substance is crucial to guide treatment strategies and antidote use.

   • Patient’s Presenting Condition: Assess the patient’s clinical status, including vital signs, level of consciousness, and specific symptoms.

   • Suspected Illness Severity: Evaluate the potential severity of the poisoning based on the substance, dose, and patient factors.

   • Time Elapsed Since Exposure: The time interval between exposure and presentation significantly impacts the effectiveness of certain decontamination measures.

General Management Components

Management of poisoning typically involves a combination of these approaches:

1. Supportive Care: Focuses on maintaining vital functions and addressing immediate life threats.

2. Decontamination and Enhanced Elimination Techniques: Aims to remove the poison from the body and prevent further absorption.

3. Antidote Therapy: Administering specific antidotes, if available, to directly counteract the poison’s effects.

Supportive Therapy – Key Elements

1. Airway and Breathing Support:

   • Positioning: Place the patient in a semi-prone (recovery) position to minimize the risk of aspiration of vomitus or secretions.

   • Airway Maintenance: Ensure the airway remains patent (open and clear).

   • Ventilatory Assistance: If necessary, assist with ventilation using bag-valve-mask or mechanical ventilation if respiratory depression is significant.

   • Oxygen Administration: Provide supplemental oxygen to maintain adequate oxygen saturation.

2. Blood Pressure Management:

   • Hypotension: If hypotensive (low blood pressure):

     • Trendelenburg Position: Elevate the foot of the bed to promote venous return to the heart.

     • Intravenous Fluids: Initiate intravenous fluid resuscitation with isotonic crystalloids like normal saline (N/S).

   • Hypertension: If hypertensive (high blood pressure), manage appropriately based on the underlying cause and severity, often with antihypertensive medications.

3. Temperature Regulation:

   • Hypothermia: If hypothermic (low body temperature):

     • Warming Measures: Cover the patient with heavy blankets and use other warming methods to restore normal body temperature.

   • Hyperthermia: If hyperthermic (high body temperature):

     • Cooling Measures: Use tepid sponging (applying lukewarm water to the skin) and administer antipyretic medications (fever reducers) like paracetamol to lower body temperature.

4. Seizure Management:

   • Anticonvulsant Administration: For seizures or convulsions:

     • Diazepam: Administer diazepam 10mg rectally or 5-10mg as a slow intravenous (IV) injection for adults.

       • Maximum Diazepam Dose: Do not exceed a maximum total dose of 30mg diazepam.

     • Pediatric Diazepam Dosage: For children, administer diazepam 0.5mg/kg rectally or 0.2mg/kg as an IV injection.

5. Patient and Family Counseling: Provide emotional support and information:

   • Counseling: Offer counseling and reassurance to the patient and their family members regarding the poisoning incident, treatment plan, and prognosis.

Decontamination Techniques

Decontamination refers to procedures aimed at removing or eliminating the poison from the body and preventing further absorption. It is generally implemented after initial stabilization of vital functions.

Decontamination methods include:

1. Gastric Decontamination (Removal from the Stomach):

   • Avoid Induced Vomiting: Do not routinely induce vomiting as a method of gastric emptying in poisoning management.

   • Balance Risks and Benefits: Carefully weigh the potential dangers of gastric emptying (e.g., aspiration, esophageal injury) against the likely toxicity of the ingested substance and the time elapsed since ingestion.

   • Nasogastric Lavage (Gastric Lavage): Consider nasogastric (NG) tube insertion and gastric lavage.

     • Timeframe of Effectiveness: Gastric lavage is most beneficial if performed within 2 hours of poison ingestion.

     • Contraindications: Gastric lavage is contraindicated in specific situations:

       • Comatose patients without secure airway protection (increased aspiration risk).

       • Ingestion of corrosive substances (risk of further esophageal damage).

       • Ingestion of petroleum products (increased risk of aspiration pneumonitis).

2. Prevention of Absorption and Enhanced Elimination:

   • Activated Charcoal Administration: Administer activated charcoal to bind to the poison in the gastrointestinal tract and reduce its absorption into the bloodstream.

     • Adult Dosage: Give 50g (or 250mg) of activated charcoal orally or via NG tube.

       • Repeated Dosing: Repeat the dose every 4 hours if clinically indicated for certain poisons, according to toxicological guidelines.

       • Preparation: For tablet formulations, grind the tablets into a fine powder and mix with 100mL of water for easier administration.

     • Pediatric Dosage: In children, administer activated charcoal at a dose of 0.5-1g/kg.

     • Timeframe of Effectiveness: Activated charcoal is most effective if administered within 2 hours of poison ingestion.

     • Contraindications: Activated charcoal use is contraindicated in:

       • Intestinal obstruction (charcoal can worsen obstruction).

       • Ingestion of corrosive substances (charcoal may obscure endoscopic view and not be beneficial).

       • Ingestion of petroleum products (no significant binding and aspiration risk).

       • Toxins poorly absorbed by charcoal: e.g., heavy metals, alcohols, iron.

       • Depressed mental status or late presentation when aspiration risk is high and benefit is limited.

Benzodiazepine Toxicity

Benzodiazepines are medications commonly used for anxiety and as sedatives. Overdose, whether intentional or accidental, can occur.

Clinical Presentations

Signs and symptoms of benzodiazepine overdose:

• Central Nervous System Depression:

  • Confusion or Drowsiness: Altered mental status, lethargy.

  • Unresponsiveness or Coma: Severe CNS depression.

• Cardiovascular Effects:

  • Hypotension: Low blood pressure.

• Respiratory Depression: Slowed or shallow breathing.

• Neurological Signs:

  • Nystagmus: Involuntary rapid eye movements.

  • Hallucinations: Sensory disturbances (less common, but possible).

  • Slurred Speech: Dysarthria.

  • Body Weakness/Hypotonia: Muscle weakness and decreased muscle tone.

Management

Management of benzodiazepine toxicity is primarily supportive, with an antidote available:

• Baseline Coagulation Assessment:

  • Prothrombin Time (PT) and International Normalized Ratio (INR): Obtain baseline PT/INR values, especially if co-ingestion of warfarin is suspected or patient has underlying liver disease.

  • Plan for repeat PT/INR measurement in 24-48 hours to monitor for potential coagulopathy.

• Activated Charcoal:

  • Administer activated charcoal orally or via NG tube for recent ingestions (within the last 1-2 hours) to limit drug absorption.

• Gastric Lavage:

  • Gastric lavage is generally unnecessary if rapid administration of activated charcoal is feasible and carried out promptly.

• Flumazenil (Romazicon): A specific benzodiazepine receptor antagonist, is available as an antidote.

  • Use with Caution: Flumazenil should be used selectively and cautiously due to potential risks:

    • Seizure Risk: Can precipitate seizures, especially in patients with benzodiazepine dependence or co-ingestion of pro-convulsant substances.

    • Withdrawal: May induce acute benzodiazepine withdrawal syndrome in dependent individuals.

  • Indications for Flumazenil: Consider flumazenil in cases of:

    • Severe respiratory depression unresponsive to supportive measures.

    • Paradoxical agitation or delirium due to benzodiazepines.

    • To reverse sedation for diagnostic or procedural purposes.

• Supportive Care: Focus on:

  • Respiratory Support: Maintain airway, breathing, and oxygenation.

  • Cardiovascular Support: Manage hypotension with IV fluids and vasopressors if needed.

  • Monitoring: Continuous monitoring of vital signs, respiratory status, and neurological status.

Paracetamol (Acetaminophen) Toxicity

Paracetamol toxicity can result from accidental or intentional overdose.

• Toxic Dose: Ingestion of a dose greater than 150mg/kg or 7.5g in adults is considered potentially toxic.

Clinical Features – Stages of Toxicity

Paracetamol toxicity progresses through distinct clinical stages:

• First 24 Hours (Stage 1):

  • Often asymptomatic or with mild, non-specific symptoms.

  • May present with: nausea, vomiting, malaise (general discomfort), and abdominal pain.

• 24-72 Hours (Stage 2 – Latent Phase):

  • Progressive signs of hepatotoxicity (liver damage) begin to emerge.

  • Symptoms may include: right upper quadrant abdominal pain, enlarged and tender liver (hepatomegaly), and elevated liver function tests (LFTs).

• After 72 Hours (Stage 3 – Hepatic Failure):

  • Followed by either recovery or progression to hepatic failure.

  • Recovery: If liver damage is not severe, recovery may occur over 5-7 days.

  • Hepatic Failure: In severe cases, may progress to fulminant hepatic failure with complications like:

    • Jaundice (yellowing of skin and eyes).

    • Coagulopathy (bleeding disorders).

    • Encephalopathy (brain dysfunction).

    • Renal failure.

Management

Prompt management is crucial to prevent or minimize liver damage:

• Gastric Lavage (if early presentation):

  • If ingestion occurred less than two hours prior to presentation, perform gastric lavage to empty the stomach and remove any unabsorbed paracetamol.

• Activated Charcoal:

  • Administer repeated doses of activated charcoal, such as 25-50g every 4 hours orally or via NG tube, to reduce paracetamol absorption.

• Acetylcysteine (NAC) – Antidote: Administer N-acetylcysteine (NAC) intravenously (IV) as the specific antidote for paracetamol toxicity.

  • Optimal Timing: NAC is most effective when given preferably within 8 hours of paracetamol ingestion, but can still be beneficial if started later.

  • Mechanism of Action: NAC works by:

    • Replenishing glutathione stores in the liver. Glutathione is a critical antioxidant that helps detoxify a toxic metabolite of paracetamol (NAPQI).

    • NAC provides cysteine, a precursor for glutathione synthesis.

    • Glutathione reacts with the toxic metabolite, preventing it from causing liver cell damage and allowing for safe excretion.

  • Intravenous NAC Dosing Regimen: A common IV NAC regimen involves a 21-hour infusion protocol:

    • Loading Dose: 150mg/kg (maximum 15g) in 200mL of D5W (5% dextrose in water) infused over 60 minutes.

    • Second Infusion: 50mg/kg (maximum 5g) in 500mL of D5W infused over 4 hours.

    • Third Infusion: 100mg/kg (maximum 10g) in 1000mL of D5W infused over 16 hours.

    • Note: Dosing and infusion volumes may vary slightly based on institutional protocols and patient weight.

• Monitoring: Closely monitor:

  • Liver function tests (LFTs) at baseline and serially to assess liver damage progression and response to treatment.

  • Renal function.

  • Coagulation parameters.

Aspirin/Acetylsalicylic Acid (ASA) Poisoning

Aspirin overdose occurs with consumption of:

• Greater than 10g in adults.

• Greater than 3g in children.

Clinical Features

Clinical signs and symptoms vary depending on the severity of toxicity:

• Mild to Moderate Toxicity:

  • Hyperventilation: Rapid and deep breathing (respiratory alkalosis initially, potentially mixed acid-base disturbance later).

  • Nausea and Vomiting: Gastrointestinal irritation.

  • Vasodilation: Peripheral vasodilation leading to flushing and sweating.

  • Tinnitus: Ringing in the ears, a classic symptom of salicylate toxicity.

• Severe Toxicity:

  • Hyperpyrexia: High fever, elevated body temperature.

  • Convulsions: Seizures.

  • Altered Mental Status: Confusion, agitation, delirium, coma.

  • Acidosis: Metabolic acidosis, reflecting acid-base imbalance.

Management

Management focuses on reducing absorption, enhancing elimination, and supportive care:

• Activated Charcoal: Administer activated charcoal orally or via NG tube to limit aspirin absorption from the GI tract.

• Alkalinization of Urine: Enhance salicylate elimination by increasing urine pH (making urine more alkaline).

  • Sodium Bicarbonate IV Infusion: Administer intravenous sodium bicarbonate to alkalinize urine. This promotes renal excretion of salicylate.

  • Monitor urine pH to achieve and maintain a target pH of >7.5.

• Fluid and Electrolyte Management: Correct fluid deficits and electrolyte imbalances caused by vomiting, hyperventilation, and altered renal function.

• Supportive Care:

  • Manage hyperthermia with cooling measures.

  • Control seizures with benzodiazepines (e.g., diazepam).

  • Provide respiratory support if needed.

  • Monitor and correct acid-base disturbances.

• Hemodialysis: In severe cases of aspirin poisoning with life-threatening symptoms (e.g., severe acidosis, altered mental status, pulmonary edema), hemodialysis may be necessary to remove salicylate from the blood.

Food Poisoning

Food poisoning is illness caused by consuming contaminated food or water.

• Cause: Typically caused by infections with pathogenic microorganisms, mainly Salmonella typhi, or by toxins released by microorganisms in food.

Clinical Features

Common symptoms of food poisoning:

• Gastrointestinal Distress:

  • Nausea and Vomiting: Often sudden onset.

  • Intermittent Abdominal Pain: Cramping or colicky abdominal pain.

  • Diarrhea: Watery or loose stools, may be bloody in some cases.

• Systemic Symptoms:

  • Fever: Elevated body temperature.

Management

Management is primarily supportive, focusing on rehydration and symptom relief:

1. Rehydration: Address fluid loss due to vomiting and diarrhea:

   • Oral Rehydration Solution (ORS): For mild to moderate dehydration, encourage oral intake of ORS to replace electrolytes and fluids.

   • Intravenous Fluids: For severe dehydration or inability to tolerate oral fluids, administer intravenous fluids such as normal saline (N/S) for rehydration.

2. Pain Relief: Manage abdominal pain:

   • Paracetamol: Administer paracetamol 1g every 6 hours as needed for abdominal pain relief. Avoid NSAIDs initially due to potential GI irritation.

3. Identify and Treat Cause:

   • Establish Cause: Attempt to identify the likely causative agent (bacterial, viral, toxin) based on history and symptoms.

   • Treat Accordingly: Treatment depends on the suspected cause.

4. Antibiotics (Selective Use): Antibiotics are generally not routinely indicated for most cases of food poisoning, as many are viral or toxin-mediated and self-limiting. However, in severe cases or specific bacterial infections:

   • Ciprofloxacin: May consider ciprofloxacin 500mg every 12 hours orally or IV for suspected bacterial causes like Salmonella or Shigella.

   • Metronidazole: Metronidazole 400mg three times daily (tds) may be used if parasitic causes or Clostridium difficile infection is suspected, or for severe bacterial infections.

Prevention of Food Poisoning

Emphasize preventive measures to avoid food poisoning:

• Thorough Cooking: Heat cooked food thoroughly to kill pathogenic microorganisms. Ensure food reaches safe internal temperatures.

• Avoid Leftovers: Avoid eating leftovers if possible, or reheat leftovers thoroughly to a safe temperature before consumption.

• Food and Utensil Hygiene: Practice strict food and utensil hygiene:

  • Wash hands thoroughly before handling food.

  • Clean and sanitize kitchen surfaces and utensils.

  • Prevent cross-contamination between raw and cooked foods.

• Personal Hygiene: Maintain good personal hygiene, including frequent handwashing, especially before eating and after using the restroom.

Carbon Monoxide (CO) Poisoning

Carbon monoxide (CO) is a dangerous colorless, odorless, and non-irritating gas.

• Sources of Exposure: CO poisoning results from inhaling CO, which can originate from:

  • Smoke inhalation during fires.

  • Car exhaust fumes, especially in enclosed spaces.

  • Charcoal stoves or grills used in poorly ventilated rooms or areas.

Clinical Features

Symptoms of carbon monoxide poisoning are often non-specific and can be easily missed:

• Early Symptoms:

  • Headache: Often described as a throbbing headache.

  • Dizziness: Lightheadedness or vertigo.

  • Confusion: Disorientation, impaired thinking.

  • Nausea and Vomiting: Gastrointestinal upset.

• Severe Symptoms: As CO poisoning progresses:

  • Seizures: Convulsions.

  • Collapse: Loss of consciousness.

  • Coma: Unresponsiveness.

Management

Prompt management is critical in carbon monoxide poisoning:

1. Remove from Exposure: Move the person to fresh air immediately. Get them out of the CO-contaminated environment.

2. Airway Management:

   • Clear Airway: Ensure a patent airway and remove any obstructions.

3. High-Flow Oxygen Therapy: Administer 100% oxygen as quickly as possible.

   • Non-Rebreather Mask: Use a non-rebreather mask to deliver the highest possible concentration of oxygen. High-flow oxygen helps to displace CO from hemoglobin and improve oxygen delivery to tissues.

4. Arterial Blood Gas (ABG) Re-assessment:

   • Re-assess ABGs: Repeat arterial blood gas (ABG) analysis to monitor oxygenation, carboxyhemoglobin levels (COHb), and acid-base status.

5. Intravenous Fluids for Hypotension: If hypotensive:

   • IV Fluids: Administer intravenous fluids to manage hypotension and improve circulatory volume.

6. Diazepam for Seizures: If seizures occur:

   • Diazepam: Administer diazepam or other benzodiazepines to control seizures.

7. Hyperbaric Oxygen Therapy (HBO): In severe cases of CO poisoning, especially with neurological symptoms, consider hyperbaric oxygen therapy (HBO) if available. HBO involves breathing 100% oxygen in a pressurized chamber, which further accelerates CO removal from the blood.

Methanol Toxicity

Methanol (methyl alcohol) is a toxic alcohol used as an industrial solvent and a component of methylated spirits.

• Sources of Exposure: Methanol poisoning typically occurs from:

  • Ingestion of methylated spirits (denatured alcohol).

  • Consumption of home-distilled crude alcohol, where methanol may be a byproduct of incomplete alcohol conversion.

• Toxicity Mechanism: Methanol itself is not directly toxic, but it is metabolized in the body into highly toxic products, primarily:

  • Formaldehyde.

  • Formic acid.

  • These toxic metabolites cause severe metabolic acidosis and damage to the optic nerve and retina.

• Lethal Dose: Ingestion of a dose greater than 1g/kg of methanol is considered potentially lethal.

Clinical Features

Methanol poisoning presents with a characteristic progression of symptoms:

• Initial Symptoms: Present early after ingestion:

  • Headache.

  • Dizziness.

  • Nausea and Vomiting.

  • Visual Disturbances: Characteristic visual symptoms are common, including:

    • Blurred vision.

    • “Snow vision” or seeing “snowfall.”

    • Photophobia (sensitivity to light).

• Later Symptoms (Progressive Toxicity): Develop as toxic metabolites accumulate:

  • Central Nervous System Depression: Progressing from lethargy to stupor.

  • Respiratory Failure: Respiratory depression and inadequate breathing.

  • Coma: Unconsciousness.

• Toxic Metabolite Effects:

  • Severe Acidosis: Profound metabolic acidosis due to formic acid accumulation.

  • Retinal and Optic Nerve Damage: Formic acid is particularly toxic to the retina and optic nerve, leading to visual impairment and potential permanent blindness if untreated.

Management

Rapid and aggressive management is essential in methanol poisoning:

1. Gastric Lavage (Early Presentation):

   • If ingestion occurred within 1 hour of arrival, perform gastric lavage to remove unabsorbed methanol from the stomach.

2. Activated Charcoal – Ineffective: Activated charcoal is not effective in significantly binding and removing methanol from the GI tract.

3. Intravenous Fluid Resuscitation:

   • IV Fluids: Administer intravenous fluids (e.g., crystalloids) to manage:

     • Shock: If present due to hypotension.

     • Hypovolemia: To correct dehydration and maintain circulatory volume.

4. Fomepizole (Antizol) – Antidote: Fomepizole is the preferred antidote for methanol poisoning.

   • Mechanism of Action: Fomepizole inhibits alcohol dehydrogenase, the enzyme that metabolizes methanol into its toxic metabolites (formaldehyde and formic acid), thus preventing further metabolite production.

   • Loading Dose: Administer a loading dose of fomepizole intravenously, typically followed by maintenance doses. (Specific dosing protocols should be consulted based on established guidelines).

   • If fomepizole is unavailable, ethanol (ethyl alcohol) can be used as a competitive inhibitor of alcohol dehydrogenase, but it is less convenient to administer and requires careful monitoring to maintain therapeutic blood ethanol levels.

5. Sodium Bicarbonate for Acidosis Correction:

   • Sodium Bicarbonate IV: Administer intravenous sodium bicarbonate to correct the severe metabolic acidosis caused by formic acid.

   • Monitor ABGs and serum bicarbonate levels to guide bicarbonate therapy and achieve adequate acid-base correction.

6. Hemodialysis: Hemodialysis is often necessary in moderate to severe methanol poisoning.

   • Indications for Hemodialysis: Consider hemodialysis for:

     • Severe metabolic acidosis (pH < 7.2).

     • Severe visual disturbances.

     • High methanol blood levels.

     • Renal failure.

     • Failure to respond to supportive care and fomepizole.

   • Hemodialysis effectively removes both methanol and its toxic metabolites (formic acid) from the blood.

7. Folic Acid (Folinic Acid): Administer folic acid or folinic acid (leucovorin).

   • Mechanism: Folic acid may enhance the metabolism of formic acid to less toxic products.

Paraffin and Other Petroleum Products Poisoning

Petroleum products encompass a range of substances including:

• Paraffin (kerosene)

• Petrol (gasoline)

• Paint thinners

• Organic solvents

Clinical Features

Signs and symptoms of petroleum product ingestion or aspiration:

• Odor: Patient’s breath or clothing may have a characteristic paraffin or petroleum odor.

• Local Irritation:

  • Burning Sensation: Burning sensation in the mouth and throat.

• Respiratory Distress:

  • Pale Appearance: Pallor due to hypoxemia.

  • Dyspnea: Shortness of breath, difficulty breathing.

  • Tachypnea: Rapid breathing.

• Gastrointestinal Effects:

  • Vomiting: May be immediate or delayed.

  • Diarrhea: Loose stools.

  • Bloody Stool: Hematochezia, presence of blood in stool (if significant GI irritation).

• Cough: Coughing, often due to aspiration.

• Central Nervous System Effects:

  • Lethargy: Drowsiness, reduced alertness.

Management

Management of petroleum product exposure is primarily supportive, focusing on respiratory and general care:

1. Decontamination – Skin: If skin contamination occurs:

   • Clothing Removal: Remove contaminated clothing immediately.

   • Skin Washing: Wash skin thoroughly with soap and water to remove petroleum product from the skin surface.

2. Gastric Lavage and Enemas – Contraindicated: Avoid gastric lavage (stomach pumping) and the use of enemas. These procedures are generally contraindicated due to the high risk of aspiration and limited benefit.

3. Activated Charcoal – Not Recommended: Do not administer activated charcoal. Charcoal is not effective in binding most petroleum products and may increase aspiration risk.

4. Supportive Care: Treatment is mainly supportive and symptomatic:

   • Respiratory Support:

     • Oxygen Administration: Administer supplemental oxygen if the patient is hypoxic (low blood oxygen saturation).

     • Monitor respiratory status closely and provide ventilatory support if respiratory distress becomes severe.

   • Monitor for Pneumonitis: Observe for signs of chemical pneumonitis (lung inflammation due to aspiration), such as cough, dyspnea, and fever. Chest X-ray may be needed.

   • Manage symptoms as they arise.