Barbiturate poisoning

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Barbiturate poisoning
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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

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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

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Properties
Long Long Inter Inter Short Short Ultrashort Ultrashort
Barbital Pheno barbital Amo Buta Pento Seco Thio Metho
Pka 7.74 7.25 7.7 7.74 7.96 7.9 7.6 7.9
Detoxi-fication Renal Renal Renal Renal Hepatic Hepatic Hepatic Hepatic
Duration (hr) gt6 gt6 3-6 3-6 lt3 lt3 0.3 0.3
Half life (hr) X 24-140 8-42 34-42 21-42 20-28 6-46 1-2
Fatal dose (gm) 10 5 X X 30 30 X x
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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.

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• 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

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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

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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

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Clinical features of over dose (contd)

• E. Skin
• Occurs at an early stage
• Bullous
• Not specific
• over pr points dorsum of fingers

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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
• Unconsciousnesslack of bowel sounds? severely
  poisoned

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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

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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)

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• 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

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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

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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 _at_3-4mg/min with IV NaHCO3
  (1.4)
• Urinary pH 7.5-8.5, but plasma pH lt7.5
• Barbiturates are acidic, ionise in alkaline
  urine, not absorbed back and hence excreted

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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

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Thank You
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