Barbiturate poisoning. Clinical Manifestation and Management

SonomaMaria 48 views 10 slides Sep 09, 2025
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About This Presentation

Barbiturate poisoning is a serious medical condition that arises from the excessive intake of barbiturates, a class of drugs that act as central nervous system depressants. Below is an outline for a PowerPoint presentation on barbiturate poisoning, including key points to cover in each slide:

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Barbiturate poisoning Dr. Sonoma Maria K.B Assistant Professor Department of Pharmacy Practice Bapuji Pharmacy College

Introduction The barbiturates are derivatives of barbituric acid (2,4,6-triox ohexahydropyrimidine ) and were extensively used as sedative hypnotics till the 1960s when the benzodiazepines arrived and quickly displaced them. Category Duration of Action Examples 1. Long acting 6–12 hours Mephobarbitone, Phenobarbitone 2. Intermediate acting 3–6 hours Amobarbitone , Aprobarbitone , Butobarbitone 3. Short acting < 3 hours Hexobarbitone , Pentobarbitone, Secobarbitone 4. Ultra-short acting < 15–20 minutes Thiopentone, Methohexitone

Uses 1. Sedative-hypnotic. 2. Pre-operative sedation. 3. Treatment of seizure disorders. Usual Fatal Dose Phenobarbitone: 6 to 10 grams. Amobarbitone , pentobarbitone, secobarbitone : 2 to 3 grams. Lethal blood level for short- and intermediate-acting barbiturates varies from 3 to 4 mg/100 ml, while for phenobarbitone it ranges from 8 to 15 mg/100 ml.

Toxicokinetics Most barbiturates which are used as sedative-hypnotics are administered orally. Intravenous route is usually reserved for management of status epilepticus or induction/maintenance of general anaesthesia . Following absorption, barbiturates are distributed widely. The long acting barbiturates have a plasma half-life of about 80 hours. Metabolism of most of these drugs occurs by oxidation in the liver resulting in the formation of alcohols, ketones, phenols, or carboxylic acids which are excreted in the urine as such or in the form of glucuronic acid conjugates. Metabolism of barbiturates is more rapid in children and is slower in the elderly

Clinical /Toxic Features 1 Slurred speech, ataxia, lethargy, confusion, headache, nystagmus 2 CNS depression, coma, shock 3 Pupils initially constricted, later dilated due to hypoxia 4 Hypothermia 5 Cutaneous bullae ("barb burns", barbiturate blisters): Clear, erythematous or hemorrhagic blisters, commonly over pressure points like hands, buttocks, ankles, knees; also found on fingers, toes, and conjunctiva 6 Death causes: Respiratory arrest or cardiovascular collapse. Delayed death: Acute renal failure, pneumonia, pulmonary edema, cerebral edema 7 Chronic barbiturate use: Leads to tolerance (therapeutic effect only at 5–6× normal dose). Withdrawal symptoms: Anorexia, tremor, insomnia, cramps, seizures, delirium, orthostatic hypotension

Diagnosis Serial plasma levels may be useful in the management of phenobarbitone overdose. Plasma levels exceeding 8 mg/ dL (80 mcg/mL) (344 mcmol /L) are generally associated with some degree of coma. In the absence of tolerance, plasma levels exceeding 2 to 3 mg/dL may be associated with CNS depression. 2. EEG: alpha coma* indicates poor prognosis

Treatment Parameter Details Tests to Monitor CBC, Serum electrolytes, Glucose, BUN, Creatinine, Urine Myoglobin in patients with significant intoxication. Onset of Toxicity Within 2 hours Peak Toxicity May not occur for18 hours or more Phenobarbitone Monitoring Repeat serum phenobarbitone level at approximately 6 hours after the initial level If Repeat Level is within Therapeutic range Patient is decontaminated, Asymptomatic and Not at risk of toxicity If Repeat Level is Higher than Initial Indicates ongoing absorption, Additional serum levels required to monitor overdose progression

Intervention Details Gastric Lavage Use a large-bore, double-lumen tube; effective up to 12–24 hours post ingestion. Activated Charcoal Usual dose; multiple doses increase phenobarbitone elimination significantly (shown effective in animals, volunteers, and overdose patients). Forced Alkaline Diuresis Particularly useful in phenobarbitone poisoning (not effective in short-acting barbiturates). Haemodialysis / Haemoperfusion Enhances barbiturate elimination, but rarely needed . Reserved for patients with refractory haemodynamic compromise . - Haemoperfusion clears barbiturates 2–4× faster than dialysis, but does not correct electrolytes. - Associated risks: hypothermia, hypotension, ↓calcium

Exchange Transfusion May be beneficial in severe cases . Management of Hypotension First: Administer 10–20 mL/kg isotonic IV fluids + Trendelenburg position. Repeat fluids if needed- Use dopamine or noradrenaline if no response Supportive Measures Supplemental oxygen, intubation, assisted ventilation, IV fluids Withdrawal Management Reintroduce phenobarbitone, followed by gradual taper (10% reduction every 3 days over 3 weeks).

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