1 / 17

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

errin
Download Presentation

Barbiturate poisoning

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  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

More Related