The document discusses barbiturate and morphine/opioid poisoning. It provides details on the classification, mechanism of action, signs and symptoms, and management of barbiturate poisoning. It describes how barbiturates bind to GABA receptors and prolong opening of chloride channels, inhibiting the central nervous system. Signs of acute poisoning include depression, amnesia, respiratory issues and death from respiratory arrest. Management involves cardio-respiratory support, preventing drug absorption, and removing barbiturates from the body through charcoal, diuresis or dialysis. For morphine/opioid poisoning, it notes respiratory depression as a major risk and describes treatment with naloxone to reverse effects or intubation to ensure

1. BARBITURATEPOISONING
By
Dr. D. Sandeep
Assistant Professor
CHIPS

2. • Barbiturates are chemical derivatives of barbituric acid.
• Depending on their duration of action, they can be classified as long
acting (>6 hours), intermediate acting (3-6 hours) and short acting (<3
hours).
• They are classified under sedatives and hypnotics category.
• Barbiturates are frequently involved in over dosage, and are generally
taken with suicidal intent.
• The poisoning occurs after the ingestion of total dose of 3g for short
acting drugs and 5g for long acting drugs.
• The poisonous effect of barbiturates is potentiated by alcohol, narcotics,
tranquilisers and antidepressants.

3. MECHANISM OF POISONING
All barbiturates bind to Gamma amino butyric acid (GABA) receptors and prolong the
opening of chloride channels, thus inhibiting excitable cells of the central nervous system.

4. SIGNS AND SYMPTOMS
• It is characterized by progressive CNS depression culminating in paralysis of brainstem and medulla.
• Acute Poisoning - Signs and Symptoms:
• Depression,
• amnesia,
• lowered body temperature,
• depressed circulation (marked fall in blood pressure),
• respiratory embarrassment and cyanosis,
• limbs are flaccid,
• retention of urine is common,
• corneal reflexes may be absent,
• ataxia,
• deep coma,
• possible shock,
• cold extremities,
• death due to respiratory arrest (frequently associated with marked cardio-vascular depression) or pneumonia.

5. • Chronic Poisoning - Signs and Symptoms:
• Skin rash,
• slurred speech,
• cyanosis,
• amnesia,
• anorexia, (reduced appetite)
• emotional instability,
• ataxia and
• constipation.
MANAGEMENT OF BARBITURATE POISONING
1. CARDIO-RESPIRATORY SUPPORT:
• A clear airway is ensured by thorough suctioning and insertion of oral airway.
• The passage of barbiturates across the BBB into CNS may be facilitated during
hypoventilation and respiratory acidosis.
• If the patient is comatose, prompt intubation (without waiting for the partial oxygen to fall
to dangerously low levels) is strongly advocated .
• Dehydration is corrected by guided fluid therapy.
• If hypotension persists, IV infusion of plasma volume expanders and vasopressors are
started.

6. 2. MEASURES TO PREVENT ABSORPTION
• a. Gastric lavage: It is done within 2-4 hours of ingestion.
• b. Activated charcoal:. 1g/Kg is administered through nasogastric tube.
• Cathartic agent like magnesium sulphate can be used along with it for further removal of
barbiturates but hypermagnesemia can occur.
3. MEASURES FOR REMOVAL OF BARBITURATES
• a. Frequent doses of activated charcoal : These adsorb the barbiturates when they
reenter the GIT through enterohepatic circulation. 1g/Kg initial dose is followed by
0.5g/kg every 2-4 hours.
• b. Forced diuresis with alkalinisation of urine:
• This is especially useful in long acting barbiturates which are largely excreted by the
kidney.
• At high rates of urine flow (by the use of diuretics), the renal clearance of barbiturates is
increased.
• Thus, it shortens the duration of coma and decreases plasma concentration of barbiturates.

7. • This should be avoided in older patients as it can cause pulmonary oedema,
hyponatraemia.
• In addition to diuresis, phenobarbitol excretion can be enhanced ten fold by urinary
alkalinization (pH 7.8 -8.0).
• Alkalinising urine causes ionization of phenobarbitone after its filtration into renal tubular
cells and trapping the agent, thereby inhibiting its re-absorption from renal tubules and
increasing its excretion.
• c. Haemodialysis and haemoperfusion: Is now being used extensively.
• Single six hour haemodialysis can remove more amount of barbiturate.
• Removal of short acting barbiturates is more limited because of lower plasma
concentrations and greater binding to plasma proteins.
• Supportive care: The most important aspect of management in these cases is close
observation and quality nursing care.
• Prophylactic antibiotics should be started.
• Good oral hygiene, temperature maintenance, and posture change at regular intervals.

8. MORPHINE/OPIOIDPOISONING
By
Dr. D. Sandeep
Assistant Professor
CHIPS

9. • Morphine is a pain medication belonging to opioid family.
• Naturally extracted from poppy (Papaver somniferum)
• Acts directly on CNS.
• MOST COMMON DRUG OF ABUSE
• Increases feeling of pleasure and warm, relaxation and reduced pain.
• Can be taken through various routes.
• Max effect - within 20min (IV) & 60min (oral)
• Duration of effect - 3 to 7 hours
• General use: Treatment of pain due to myocardial infraction, kidney
stones and during labor.
• Can produce other opioids like hydromorphone, heroin & oxymorphone.

10. Causes:
• Due to excessive consumption of any opioids (may be suicidal/intentional/accidental)
• Majorly due to drug dependence or detoxification.
• Co-ingestion with benzodiazepines or alcohol.
Signs & Symptoms:
• Respiratory depression (major reason for death)
• Hypoxia
• Miosis
• Unconsciousness
• Stupor
• Hepatic injury
• Renal failure
• Hypothermia
• Rhabdomyolysis

11. Mechanism of Poisoning:
• Morphine binds specifically to the neurological opioid receptors called Mu (μ)
receptors.
• Mu (μ) receptors found in cerebral cortex and thalamus.
• It evokes analgesic, sedative and euphoric effects.
• Over activation of Mu (μ) receptors occurs.
• It leads to permanent brain damage
from cerebral hypoxia or neurotoxicity.

12. TREATMENT
• Management of Overdose:
• Patients with Opnea need a pharmacologic or mechanical stimulus in order to breathe. For
patients with stupor, ventilation should be provided.
• Naloxone, the antidote for opioid overdose, is a competitive mu opioid–receptor
antagonist that reverses all signs of opioid intoxication.
• It is active in parenteral, intranasal, or pulmonary route of administration.
• An alternative to administration of naloxone is orotracheal intubation, a procedure that
safely ensures oxygenation and ventilation while providing protection against aspiration.
• Initial dose of naloxone for adults is 0.04 mg;
• If there is no response, the dose should be
increased every 2 minutes according to the
schedule to a maximum of 15 mg.

13. TREATMENT
• Clonidine: Clonidine is generally considered a safe, non-narcotic medication
used to help patients withdraw from opioids.
• It is a centrally acting alpha-2 adrenergic agonist and works to minimize the
noradrenergic hyperactivity seen in opioid withdrawal.
• For opioid withdrawal, clonidine is typically dosed at 0.1 mg to 0.3 mg orally up
to every 6 hours.
• The use of clonidine in opioid withdrawal is limited because of its hypotensive
and sedative adverse effects.
• Naltrexone. Naltrexone is a mu-receptor antagonist.
• It also antagonizes the kappa-receptor, and weakly antagonizes the delta-receptor.
• When used in conjunction with clonidine for opioid withdrawal, naltrexone is
usually dosed between 50 mg and 100 mg daily and can also be dosed 3 times
weekly.