Delirium tremens

Most serious alcohol withdrawal phenomena

Mortality of up to 5%
 Defi nition
• The fully developed syndrome consists of
• vivid hallucinations,
• delusions,
• profound confusion,
• tremor, agitation,
• sleeplessness and autonomic overactivity
• Delirium tremens is relatively uncommon in
defined way
• only 5% of a consecutive series of 266patients
admitted to Boston City Hospital (Victor &
Adams 1953).
In contrast,in the same series
• Acute tremulousness occurredin 34%,
transient hallucinosis with tremor in 11%,
• Auditoryhallucinosis in 2%, fits in 12% and
Wernicke–Korsakoffsyndrome in 3%.
 Diagnosing delirium tremens
McNichol (1970)
Presence of hallucinations along with at least
two of the following
• confusion and disorientation
• Tremulousness,increased psychomotor activity,
• fearfulness andsigns of autonomic disturbance.
• He recognised three grades first,
mentalsluggishness with tremor and evidence of
residual intoxication
• Later, emotional lability, agitation, fearfulness,
increasedpsychomotor activity, autonomic
disturbance, nightmaresand disorientation

• finally the onset of definitive delirium tremens

with the appearance of hallucinations.

• Thepresence of autonomic hyperactivity

(tachycardia, sweating,fever)
 Clinical features.
• Frequently presents in a dramatic manner and
appears to have had an explosive onset
• However, when opportunities arise for observation
during the evolution of the llness, a prodromal phase
is commonly seen
• The onset is usually at night, with restlessness,
insomnia and fear.
• The patient startles at the least sound, has vivid
nightmares and wakes repeatedly in panic.
• Transient illusions and hallucinations may occur even
at this stage, and typically arouse intense anxiety
even though insight may still be largely retained
• As the illness becomes more fully declared
• Face anxious or terror stricken. The patient is
tremulous, and if out of bed is usually seen to be
ataxic.
• There is evidence of dehydration, with dry lips, a
coated tongue and scanty urine.
• Restlessness is extreme, with agitated activity by day
and night, preventing sleep and leading ultimately to
dangerous physical exhaustion.
• Autonomic disturbance -perspiration,flushing or pallor,
dilated pupils, a weak rapidpulse and mild pyrexia.
Epileptic seizures occur in up to one-third of cases,
 Illusions and hallucinations
occur in great profusion
• visual hallucinations- fleeting, recurrent and
changeable images
• Rats, snakes and other small animals are said to be
typical, and can appear in colorful and vivid forms.
• They are frequently lilliputianin size, and invested with
rapid ceaseless activity
• Other hallucinations may be normal in size, such as
threatening faces or fantasticscenes depicting
terrifying situations
 Illusions and hallucinations

• The patient’s occupation and experience may

colour the perceptual disorders, the station
master seeing trains rapidly approaching him
• the factory worker seeing his bench before him
Auditory hallucinations
• Commonly threatening or persecutory nature
• Vestibular disturbances are frequent
• Felt by the patient as rotation of the room or
movement ofthe floor. Insects may be felt to be
crawling over the skin
 Speech
• Usually slurred and with par aphasic errors.
• In severe examples it may be incoherent and
fragmented.
• Delusions are secondarily elaborated on the faulty
perceptual experiences, but are usually fragmented,
transitory and as changeable as the hallucinations
EEG
• Typically shows fast activity in delirium tremens.
• In this it is in marked contrast to the picture seen in
most other forms of delirium, where slowing of the
dominant rhythmsis the characteristic pattern
 Outcome
• The disorder is usually short-lived,
• Lessthan 3 days in the majority of cases. Very rarely
recurrent phases may be seen over a longer period of time.
• Typically it terminates in a prolonged sleep after which the
patient feels fully recovered apart from residual weakness
• Death when it occurs is usually due to cardiovascular
collapse, infection, hyperthermia, or self-injury during the
phase of intense restlessness.
• Any infective process, particularly pneumonia, markedly
increases the mortality.
 Pathophysiology
• The precise patho physiology is unknown.
• Cerebral oedema was formerly thought to be
responsible but has not been adequately confirmed.
• A primary disorder of the reticular formation is
strongly suggested by the clinical components of
profound inattention coupled with Alertness, over
activity and insomnia.
• The remarkable association with disturbance of
REM sleep has already been described
• Cerebral blood flow studies- indicated a state of
increased CNS excitability during the course of
delirium, in keeping with the characteristic fast
frequencies seen on EEG
• Hemmingsen et al. (1988) performed xenon-labelled
single photon emission computed tomography (SPECT)
in patients with actual or impending delirium tremens,
with repeat examination on recovery. Increased
hemispheric blood flow correlated
significantly with the presence of visual hallucinations
and psychomotor agitation
• Trauma or infection are present from the outset in up
to half of cases, many others having liver failure,
gastrointestinal bleeding or hypoglycemia
• Lundquist (1961) found biochemical evidence
of acute liver damage in up to 90% of patients
with delirium tremens.

• A multifactorial aetiology will probably prove

to be the complete explanation, involving
complex metabolic and neuro physiological
pathways
 Treatment

• Minor withdrawal symptoms-outpatient basis with

the help of sedation from Chlordiazepoxide
• patients with a history of withdrawal seizures, and
those with any indication of impending delirium
tremensshould be admitted to hospitalimmediately
• Management –close nursing observation at regular
intervals, so that the dosage of sedative drugs can
be titrated against the symptoms displayed.
• Edwards (1982) recommends chlordiazepoxide upto 40 mg three or four
times daily, starting if necessary withan intramuscular dose of 50–100 mg.
• Alternative treatment clomethiazole(chlormethiazole)
• Fluid replacement and adequate sedation are the first essentials, with
careful examination to detect complicating pathologies which aggravate
the delirium and greatly worsen prognosis.
• Head injury and infection must always be borne in mind.
• Skull and chest radiography will be required. Coincident
intoxication with sedative drugs may lead to particularly
severe withdrawal manifestations.
Hypoglycaemia, hepatic failure, uraemia and electrolyte imbalance will
need to be excluded
• Wernicke’s encephalopathy must be detected early and treated vigorously.
• Cardiac failure, gastroduodenal bleeding or bleeding from esophageal
varices may be present. A close watch must be kept at all stages for
seizures or circulatory collapse.