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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
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
Properties
Long Inter Short 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 Hepatic Hepatic
Duration (hr)
>6 >6 3-6 <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
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.
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
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
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
Clinical features of over dose (contd…)
E. Skin– Occurs at an early stage – Bullous– Not specific: over pr points & dorsum of fingers
Clinical features of over dose (contd…)
F. Ocular– Nystagmus / dysconjugate eye movements– Miosis early manifestation– Later hypoxia + paralysis of pupillary sphincter
Mydriasis
G. Gastrointestinal systemAssess the severity of poisoning Unconsciousness+lack of bowel sounds severely
poisoned
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
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)
• 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
Management• No specific antidote
• supporting therapy is adequate
1. Removal of the source
gastric lavage
Activated charcoal (1gm/kg)
Repeat every 2-4 hourly
slow continuous administration till patient improves
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
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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