All about barbiturate poisoning , causes , clinical symptoms , types of poisoning , barbiturates classification , adverse effects and toxic effects of barbiturate poisoning , Management of barbiturate poisoning , Scandinavian method , support vital function , prevention and further absorption .

1. By:- Shailja Sharma
Assistnt Professor
Pharmacology

2.  Barbiturates are a class of sedative-hypnotic
drugs. They are commonly used as anti epileptics
(phenobarbital) and for the induction of general
anesthesia (thiopental). Some states administer
barbiturates for physician-assisted
suicide/euthanasia and use them for capital
punishment by lethal injection. Their use in
clinical practice has largely been replaced by
benzodiazepines such as alprazolam, diazepam,
and lorazepam due to the lower risk of overdose
and available antidote to reverse toxicity.
Barbiturates are used as a laboratory buffer and
can be found in clinical and research
laboratories.

9. 1. Cardiorespiratory support
2. Measures to prevent absorption
3. Measures for removal of barbiturates
4. Analeptic Drugs
5. Supportive care

10.  A clear airway is ensured by thorough suctioning and
insertion of oral airway. In addition, the passage of
barbiturates across the blood brain barrier into the
central nervous system may be facilitated during
hypoventilation and respiratory acidosis. If the
patient is comatose, prompt intubation (without
waiting for the PaO2 to fall to dangerously low levels)
is strongly advocated because of the fear of
impending, worsening respiratory failure.
 Dehydration is corrected by CVP guided fluid therapy
depending on the serum electrolyte reports. If
hypotension persists, intravenous infusion of plasma
volume expanders and vasopressors is started. In
refractory cases, steroids are given.

11.  a. Gastric lavage : If no more than 2-4 hours
have passed since ingestion of the
barbiturate, gastric lavage is done.
 b. Activated charcoal : Is an inert non toxic
adsorbent which binds high molecular
weight compounds due to intermolecular
attractions. 1gKg-1 is administered through
nasogastric tube.
 Cathartic like magnesium sulphate can be
used along with it for further removal of
barbiturates buthypermagnesemia can occur.

12.  a. Frequent doses of activated charcoal : These adsorb the barbiturates
when they reenter the GIT through enterohepatic circulation. 1gKg-1
initial dose is followed by 0.5gkg-1 every 2-4 hours.
 b. Forced diuresis with alkalinisation of urine: This is especially useful
in long barbiturates which are largely excreted by the kidney. At high
rates of urine flow (by the use of diuretics), the renal clearance of
barbiturates is increased.
 Thus, it shortens the duration of coma and decreases plasma
concentration of barbiturates. This should be avoided in older patients as
it can cause pulmonary oedema, hyponatraemia and increase in ICP.
 In addition to diuresis, phenobarbitol excretion can be enhanced ten fold
by urinary alkalinization (Ph 7.8 -8.0). Alkalinising urine causes ionization
of phenobarbitone after its filtration into renal tubular cells and trapping
the agent, thereby inhibiting its re-absorption from renal tubules and
increasing its excretion.
 c. Haemodialysis and haemoperfusion: Is now being used extensively in
treatment of barbiturate intoxication to increase rate of removal of
barbiturates. Single six hour haemodialysis can remove an amount of
barbiturate which is comparable to that removed during 24 hours of
sustained diuresis or peritoneal dialysis.

13.  These have minimal role now a days because
under their influence, true clinical
assessment of patient becomes impossible.
Also, they are associated with side effects
like convulsions, cardiac arrhythmias,
vomiting, hyperpyrexia.

14.  The most important aspect of management in these
cases is close observation and quality nursing care .
 Prophylactic antibiotics should be started. Good oral
hygiene, temperature maintenance, and posture
change at regular intervals .
 Usually, recovery from barbiturate coma is without
neurologic deficit even after severe poisoning. Our
patient also recovered fully without any deficit.
 The rarity of permanent damage after barbiturate
coma precludes immediate establishment of
adequate pulmonary ventilation as well as control of
shock to be of prime importance .
 We were able to save our patient because of
immediate control of ventilation, temperature
maintenance, early prevention of renal damage and
haemodialysis .

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 MANAGEMENT OF BARBITURATE POISONING– A
CASE REPORT Dr. Shashi Kiran1 Dr. B.
Chhabra2 Dr. Nandini3 ,480 Indian J.
Anaesth. 2002; 46 (6) : 480-482