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Barbiturate poisoning

Barbiturate poisoning. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Babiturate poisoning. Substituted derivative of barbituric acid (derived from urea-malonic acid) Classification Long Barbital, Phenobarbital Intermediate Amo barbital, Buta barbital Short Pento barbital

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Barbiturate poisoning

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  1. Barbiturate poisoning www.anaesthesia.co.inanaesthesia.co.in@gmail.com

  2. Babiturate poisoning • Substituted derivative of barbituric acid (derived from urea-malonic acid) • Classification • Long • Barbital, Phenobarbital • Intermediate • Amo barbital, Buta barbital • Short • Pento barbital • Seco barbital • Ultra short • Thio • Methohexital

  3. Mechanism of action • Acts at GABA-BZD receptor-Cl- channel complex • Potentiate GABAnergic inhibition by increasing life time of Cl- channel opening • Increased conc barbiturate   Cl- conductance  depress Na+/K+ channels

  4. Properties

  5. Clinical features of over dose • sign and symptom are variable and depend on stage of intoxication Significant toxicity 4mg/dl(long acting) ,2mg/dl(short) Mild - Resembles Alcohol intoxication Moderate - depression of mental status, response to painful stimuli, deep tendon reflex & slow resp Severe- coma & loss of all reflexes except light reflex. planter extensor, hypothermia & hypotension • Both acute / chronic intoxications are seen but the chronic form occurring at dose higher (ten times) than those required for acute.

  6. A. Central N system • Act as depressant • Primary feature : impaired level of consciousness • Main features include : restlessness, insomnia, delirium, hallucinations, confusion, slurred speech, ataxia, convulsions, coma. • Increased intoxications • Increased depth of coma • Increased loss of neurological function

  7. Clinical features of over dose (contd…) B. Respiratory system • Direct depressant action : on respiratory centre(medulla) • Decreased respiratory rate, hypoventilation • Cyanosis and shallow respiration • Loss of hypoxic drive / influence on sensitization of chemoreceptors • Later part  develop pneumonia, non-cardiogenic pulmonary edema

  8. Clinical features of over dose (contd…) C. Cardiovascular • decreased myocardial contractility • Direct vascular smooth muscle relaxation (vasodilatation) • Excessive capillary exudation  venous pulling  hypovolemia  decrease BP  shock • severe cases : medullary depression of CVS regulation D. Hypothermia • Significant • Due to depression of hypothalamic temp regulation centre vasodilatation effects • During recovery : pyrexia occurs

  9. Clinical features of over dose (contd…) E. Skin • Occurs at an early stage • Bullous • Not specific : over pr points & dorsum of fingers

  10. Clinical features of over dose (contd…) F. Ocular • Nystagmus / dysconjugate eye movements • Miosis  early manifestation • Later hypoxia + paralysis of pupillary sphincter  Mydriasis G. Gastrointestinal system Assess the severity of poisoning Unconsciousness+lack of bowel sounds severely poisoned

  11. Clinical features of over dose (contd…) H. Renal system • Severe hypotension with hypothermia  significant impairment of renal function • ARF shock& hypoxia 16% death • Judicious use of vasopressor drugs like dopamine / dobutamine and timely hypotension correction can prevent rental shut down

  12. Clinical features of over dose (contd…) I. Laboratory evaluation Investigations CBC, serum electrolyte, urea,, creatinine, glucose, ABG analysis, chest x-ray Serum barbiturate level Urine level (common)

  13. If other drugs present :interference in measurement • Depth/duration of coma depend on concentration of barbiturate in brain (not plasma level) • Recently • Gas liquid chromatography  • Based on influence of pH on UV absorption spectrum of drug

  14. Management • No specific antidote • supporting therapy is adequate • Removal of the source gastric lavage Activated charcoal (1gm/kg) Repeat every 2-4 hourly slow continuous administration till patient improves

  15. Management of barbiturate poisoning (contd…) 2. Supportive care • Assessment and stabilisation of the airway oxygenation, mechanical ventilation if required • Maintenance of blood volume / correction of dehydration, fluid infusion and use of vasopressor • Rewarming 3. Forced alkaline diuresis • long acting barbiturate poisoning (phenobarbitone), eliminated primarily by renal excretion • pt adequately hydrated, with stable CVS / renal status • Frusemide 250mg in 25ml @3-4mg/min with IV NaHCO3 (1.4%) • Urinary pH 7.5-8.5, but plasma pH <7.5 • Barbiturates are acidic, ionise in alkaline urine, not absorbed back and hence excreted

  16. Management of barbiturate poisoning (contd…) 4 Hemodialysis and hemoperfusion : (activated charcoal or other adsorbents) - Remove long &short acting barbiturates use of analeptics abandoned Instead of emphasizing the termination of coma, attention directed at • Intensive supportive therapy • Respiratory care / support • Cardiovascular support

  17. Thank You www.anaesthesia.co.inanaesthesia.co.in@gmail.com

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