Indian J. Anaesth.
2002; 46 (6) : 480-482
480
MANAGEMENT OF BARBITURATE POISONING
– A CASE REPORT
Dr. Shashi Kiran1 Dr. B. Chhabra2 Dr. Nandini3
Introduction
Barbiturates are a leading cause of acute poisoning
because of their ready availability. Most of the cases are
suicidal but some occur through error or ungraded
exploration in children. The poisoning is characterized by
stupor or coma, areflexia and in late cases, severe respiratory
depression and cardiovascular insufficiency. It is a potentially
fatal form of poisoning with overall mortality of about
7%.1The clinical outcome is solely related to the level of
supervision and care provided by attending physician and
nurses. A highly organized intensive care unit can reduce
the mortality rate to less than 2%. We present here case
of a young girl of barbiturate poisoning who was managed
successfully using charcoal adsorption and haemodialysis
with favourable outcome.
Case Report
An 18-year old girl was admitted in the medicine
department in an unconscious state with no response to
deep painful stimuli (Grade III coma). History as elicited
from her attendants was suggestive of oral intake of
phenobarbitone tablets a night before, after which the
patient was not arousable in the morning. There was no
history of convulsions, vomiting, urinary incontinence or
tongue bite. Within few hours of admission, patient became
febrile and tachypnoeic with pulse rate 130 min-1, blood
pressure 120/70 mmHg and arterial oxygen saturation
93%. Pupils were of normal size and reaction. Plantar
and deep tendon reflexes were absent. A diagnosis of
barbiturate poisoning was made and patient was shifted to
ICU. Shortly after admission, she had tonic clonic convulsions
which subsided after few seconds spontaneously. She became
increasingly tachypnoeic and oxygen saturation started falling.
Blood gas analysis done showed hypocarbia with metabolic
acidosis. She was intubated nasally and ventilated by Evita-
1. D.A.,D.N.B.,M.D., Lecturer
2. M.D., Professor and Head
3. M.D., Senior Resident
Department of Anaesthesia and Critical Care,
Post Graduate Institute of Medical Sciences,
Rohtak-124001, Haryana.
Correspond to :
Dr. Nandini
2/9J, Medical Campus, Medical Enclave,
Pt. B. D. Sharma PGIMS, Rohtak-124001, Haryana.
INDIAN JOURNAL OF ANAESTHESIA, DECEMBER 2002
480
2 (Drager) ventilator on intermittent positive pressure
ventilation mode with tidal volume 400 ml, FiO2-80% and
frequency – 14 min-1.
Patient was catheterized. Continuous nasogastric
suction was done. Central venous pressure guided fluid
therapy was started. Continuous temperature monitoring
was done and care was taken to avoid hypothermia.
Antibiotics, phenytoin, rantidine, low dose dopamine and
bronchodilator were started. In addition, ten tablets of
activated charcoal 500mg (5g) with egg albumin were
given four hourly through Ryle’s tube. Forced alkaline
diuresis was started. One litre of lactated Ringer solution
was rushed and injection sodabicarbonate 50cc was given
intravenously six hourly. Aim was to keep urinary pH
between 8-8.5.
Her serum potassium was 2.5.eq lt-1 and SGOT
and SGPT were 118 IU and 99IU respectively. Serum
proteins were 6g%. Urine was positive for ketone bodies
and serum barbiturate assay was positive. As her
consciousness level did not improve, haemodialysis was
planned. Haemodialysis was done using Sresenius
Haemodialyser. Within hours, the patient’s condition
improved and she stared responding to verbal commands.
Her vitals were stable. She was extubated once regular
spontaneous respiration was restored. Oxygen therapy with
ventimask (FiO2 – 60%) was instituted. Gradually, the
patient was weaned to FiO2 of 28%. SGOT and SGPT
were still elevated (222 IU and 240 IU respectively).
Repeat serum assay now revealed no residual barbiturate.
She was discharged home a week later.
Discussion
Barbiturates are chemical derivatives of barbituric
acid and depending on their duration of action, they can
be classified as long acting (>6 hours), intermediate acting
(3-6 hours) and short acting (<3 hours). All barbiturates
bind to Gamma amino butyric acid receptors and prolong
the opening of chloride channels, thus inhibiting excitable
cells of the central nervous system.
Barbiturates are frequently involved in over
dosage, and are generally taken with suicidal intent.
Short acting barbiturates are more dangerous than long
acting. Shock and anoxia appear much more quickly
and coma is more severe with short acting barbiturates
KIRAN, CHHABRA, NANDINI : BARBITURATE POISONING
are 10mg 100ml-1 and 3mg 100ml-1 respectively. These
are achieved after the ingestion of total dose of 3 gm for
short acting drugs and 5 gm for long acting drugs. The
poisonous effect of barbiturates is potentiated by alcohol,
narcotics, tranquilisers and antidepressants. Death occurs
from respiratory failure, severe hypotension, vasomotor
failure, non cardiogenic pulmonary oedema, hypothermia
(which aggravates shock) or oliguria with renal failure.
Acute barbiturate intoxication should be clinically
evaluated to differentiate it from other forms of coma or
central nervous injury. History of possible trauma, previous
psychiatric illnesses, attempts at suicide and drug usage
should be obtained with particular attention directed
towards the type, amount and time of drug ingestion, the
duration of coma and associated ingestion of alcohol.
Evidence of preexisting diseases such as hypertension,
cirrhosis and diabetes mellitus should also be sought. In
our case there was no such history.
Barbiturate poisoning is characterized by progressive
CNS depression culminating in paralysis of brainstem and
medulla. In early stages, patient is confused and lethargic
with poor coordination, ataxia and dysarthria. This
progresses on to deep unremitting coma, total areflexia
and unresponsiveness to other stimuli as in our case.
Corneal reflexes are lost. Conjugate doll’s eye movement
are absent. Pupils are usually constricted but may dilate
in terminal phases. Pupillary response to light is minimal.
In late stages, respiration is feeble, shallow and irregular
and hypotension occurs. Apnea and cardiac arrest may result.
Minimum laboratory evaluation include haematocrit,
urine analysis mainly for ketone bodies, WBC and
differential counts. Plasma concentration of electrolytes,
blood urea, serum creatinine and liver function tests
should be obtained. Chest X-ray and blood gas analysis
are mandatory. A blood sample should be sent for
measurement is of little value except to confirm the
presence of barbiturate in plasma. Serial measurements
provide a valuable guide to the adequacy of therapy.
Management of barbiturate poisoning
1. Cardiorespiratory support
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
481
hypotension persists, intravenous infusion of plasma
volume expanders and vasopressors is started. In refractory
cases, steroids are given.
2. Measures to prevent absorption
a. Gastric lavage : If no more than 2-4 hours have
passed since ingestion of the barbiturate, gastric
lavage is done.2
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 but hypermagnesemia can occur.
3. Measures for removal of barbiturates
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.3
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.
Newer technique of lipid dialysis can extract long
acting drugs such as phenobarbitol in greater quantity.
Removal of short acting barbiturates is more limited
because of lower plasma concentrations and greater binding
to plasma proteins.4 Our patient improved remarkably
well after haemodialysis.
Analeptic Drugs
These have minimal role now a days because under
their influence, true clinical assessment of patient becomes
482
impossible. Also, they are associated with side effects
like convulsions, cardiac arrhythmias, vomiting,
hyperpyrexia.
Supportive care
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.
CORRESPONDENCE
Letters to Editor
To,
The Editor,
Indian Journal of Anaesthesia.
Sir,
Apropos “Undergraduate Anaesthesia Education”,
kudos to MCI for recognizing the importance of ana
esthesiology for undergraduate courses. In a country like
ours, which needs primary care physicians to treat common
diseases and to make arrangements for referrals, knowledge
of basic and advanced life support management,
resuscitation and critical care support; monitoring; trauma,
disaster and airway management and lastly, awareness of
basic pharmacology and pain management is important.
A medical student should be able to demonstrate a
successful basic and advance life support management
before obtaining a medical degree.
Can the anaesthesiologists’ take the entire blame for
not making this discipline more popular amongst
undergraduates? Most of the theatres are managed by residents
and senior residents in anaesthesiology under supervision of
consultants who may be found in coffee room with their
irrelevant discussions or preparing the manuscript of a
research paper. Some junior consultants may take it as a
privilege to enter operation theatre at night during an
emergency case. How may consultants go for pre-operative
check ups and post anaesthesia recovery and pain relief to
the patient? Adding irrelevance to already existing literature,
repeating same old things and providing nothing new and
creating unnecessary doubts will only harm the speciality.
The onus lies on the faculty in the discipline of anaesthesiology
to make the undergraduate students more aware of this
science in whatever time slot allotted.
INDIAN JOURNAL OF ANAESTHESIA, DECEMBER 2002
We were able to save our patient because of immediate
control of ventilation, temperature maintenance, early
prevention of renal damage and haemodialysis.
References
1. Ellenhorn MJ, Barceloux DG. Diagnosis and treatment of
human poisoning. In : Medical toxicology. New York: Elsevier,
1988.
2. Hall AH. Gastrointestinal decontaminations: Shifting through
supportive therapeutic options. Emerg Med Reports 1991;
12: 171-8.
3. Birnbaumer D. Poisonings and ingestions. In : Bongard ES,
Sue Dy, editor. Current Critical Care Diagnosis and Treatment.
London: Appleton and Lange, 1994: 686-715.
4. Henderson LW, Merrill JP. Treatment of barbiturate
intoxication. Ann Intern Med 1966; 64: 876.
So many societies in anaesthesiology, have they
ever proceeded more than holding conferences and issuing
journals (IJA.2002; 46(5): 414). It may be appreciated if
ISA takes responsibility to –
1. Review and form a proper curriculum for
undergraduate and postgraduate students.
2. Define the curriculum of superspecialities – cardiac,
neuro, paediatric, intensive care, pain, obstretrics.
Encouraging more institutions to offer certificate
courses in the same and recognizing these by an
executive body of ISA after thoroughly checking
the credentials.
3. Issuing guidelines for a safe anaesthetic practice in
Indian set up – both at tertiary and primary centers.
4. Encouraging well planned research that will benefit
this science.
5. Reaching out to society. Encouraging anaesthesiologists
to teach basic life support in schools and institutions
and to make people more aware of disaster and
trauma management.
An anaesthesiologist has a distinct identity, as is
every specialist in medical education. Can we manage
Integrated Medical Teaching programmes? A paediatrician
cannot administer anaesthesia and same holds true vice
versa. There are many milestones to be covered in this
glorious field.
Yours truly,
Dr. Abhinav Gupta, M.D., D.N.B.
D.N.B.Fellow in Cardiac Anaesthesiology
New Delhi.