The Intoxicated Patient 49

They can start as soon as 812 hours after the most recent alco-
hol ingestion. The symptoms are usually relieved by drinking
more alcohol and vary across a wide spectrum from mild nausea
and minor tremulousness through to life-threatening seizures and
delirium tremens (see Table 12.4).
Hallucinations occur in approximately 25% of patients with-
drawing from alcohol. Symptoms consist of predominantly visual
and tactile hallucinations. In the early stage, the patients recognise
hallucinations. However, in the advanced stage, these hallucinations
are perceived as real and may provoke extreme fear and anxiety.
The patient can be seen pulling at imaginary objects, clothing, and
sheets, for example.
Seizures occur in 2333% of patients with signicant alcohol
withdrawal. They are usually brief, generalised, tonic-clonic
without an aura. Most seizures terminate spontaneously or are
easily controlled with a benzodiazepine.
Delirium tremens occurs in 5% of individuals withdrawing from
alcohol within 2472 hours after last ingestion. It is characterised
by altered mental status disorientation, confusion, delusions and
severe agitation. There is associated fever, sweating and tachycardia.
Untreated it has a mortality of 15% from arrhythmias (secondary
to acidosis, electrolyte disturbance) and intercurrent illness.
Head injury causing intracranial pathology
Head injuries are often associated with excessive alcohol.
In fact, alcohol use is thought to be a contributing factor in
50% of all adults with traumatic brain injuries. Excessive
alcohol increases both the likelihood of injury and the seriousness
of injury.
Chronic excessive alcohol use may cause decreased platelets and
impaired clotting factor production by the liver. These patients
are more likely to suffer from an intracranial haematoma from
apparently minimal trauma and must be managed with care.
Symptoms and signs of serious head injury may occur
immediately or may develop over hours after the injury. Some
symptoms of head injury, such as amnesia, decreased conscious
level and vomiting can be mistakenly attributed to alcohol excess
and these patients must be assessed and investigated/observed
as appropriate.
NICE have issued guidance as to which patients with head injury
need urgent CT imaging, i.e. within 1 hour (see Box 12.2).
Table 12.2 Medical problems related to alcohol.
System
Gastrointestinal Liver
Fatty inltration
Alcoholic hepatitis
Cirrhosis
Liver failure
Liver cancer
Upper GI tract
Reux oesophagitis
Mallory Weiss tear
Oesophageal cancer
Gastritis
Peptic ulcers
Other
Malabsorption
Pancreatitis
Malnutrition
Neurological Acute intoxication
Blackouts
Seizures
Persistent damage
Korsakoffs syndrome
Wernickes encephalopathy
Cerebellar degeneration
Dementia
Withdrawal
Tremor
Hallucinations
Seizures
Other
Haemorrhage subarachnoid,
traumatic subdural
Myopathy
Neuropathy
Cardiovascular/ Respiratory Cardiovascular
Atrial brillation
Hypertension
Cardiomyopathy
Respiratory
Aspiration pneumonia
Other Psychiatric
Depression
Anxiety disorders
Schizophrenia
Co-dependence
Marijuana addiction
Cocaine addiction
Smoking
Trauma
Table 12.3 Symptoms of hypoglycaemia.
Sympathetic overactivity Neuroglycopenia
Tachycardia
Palpitations
Sweating
Anxiety
Pallor
Tremor
Confusion
Slurred speech
Focal neurological defects (stroke-like
syndrome)
Seizures
Coma
Table 12.4 Alcohol withdrawal symptoms and signs.
Severity Timing of last alcohol Features
Mild Within 24 hours Tremulousness (shakes)
Insomnia
Anxiety
Nausea
Moderate 2436 hours Sweating
Tachycardia
Irritability
Hallucinations
Seizures
Severe >48 hours Delirium tremens
50 ABC of Emergency Differential Diagnosis
Acute thiamine deciency
Chronic alcohol use, particularly when associated with
malnutrition, can cause vitamin B1 (thiamine) deciency.
Thiamine deciency causes damage to the mamillary bodies,
cranial nerve nuclei, thalamus and cerebellum, termed Wernickes
encephalopathy, a triad of:
Encephalopathy (disorientation, agitation, indifference and 1
inattentiveness, short term memory loss)
Occulomotor disturbance (nystagmus, lateral rectus palsy) 2
Ataxic gait 3
To diagnose Wernickes encephalopathy, however, it is not necessary
to have all three components present.
To protect against Wernickes encephalopathy intravenous
thiamine should be administered to any patient who is confused,
with a history of alcohol abuse. If the blood sugar is also low, it
is important to administer glucose with the thiamine treatment.
If Wernickes encephalopathy is not treated the confusion is liable
to progress to stupor or death.
Korsakoff s psychosis is a late neuropsychiatric manifestation
of Wernickes encephalopathy. It is characterised by confusion,
confabulation and amnesia (anterograde and retrograde). The
memory problems associated with Korsakoff s syndrome are largely
irreversible.
Acute alcohol intoxication
Alcohol affects the brain like an anaesthetic. The effects of alcohol
depend on the amount ingested (see Table 12.5).
Measuring the serum alcohol level has limited use it conrms
approximately how much alcohol has been ingested but does not
exclude other important causes which may co-exist.
This diagnosis is not suggested by the history.
Alcoholic ketosis
This is an acute metabolic acidosis that typically occurs in people
who chronically abuse alcohol and have a recent history of binge
drinking, little or no food intake, and persistent vomiting.
Patients typically present with nausea, vomiting and abdominal
pain. They are usually hypotensive, tachycardic and tachypnoeic
with the fruity odour of ketones present on their breath. They
are usually alert and lucid, but may have mild confusion.
Investigations show a raised anion gap metabolic acidosis, with
normal lactate and raised serum and urine ketone levels.
Systemic infections
People with chronic alcohol dependence are relatively immuno-
compromised, malnourished and more commonly exposed
to infectious agents (e.g. tuberculosis) than others. Infections,
in particular of the nervous system, e.g. meningitis, encephalitis,
can present with non-specic confusion and vomiting.
Case history revisited
Revisiting the case, the diagnosis is not immediately obvious. This
man regularly drinks excessive amounts of alcohol and presents
more than 12 hours after ingesting a large amount of alcohol. This
late presentation would not be typical for a presentation of acute
alcohol intoxication.
On examination, his Glasgow Coma Score (GCS) is 14/15 (E4,
M6, V4) he is confused and disorientated to time and person.
His observations are: blood pressure 160/100 mmHg, pulse
120 beats/minute, respiratory rate 20 breaths/minute and blood
glucose (meter) 4.5 mmol. He appears sweaty and is irritable, but
allows you to perform a limited examination.
Box 12.2 NICE guidelines indications for urgent CT head scan
in head injuries.
GCS <13 on initial assessment in the Emergency Department
GCS <15 when assessed in the Emergency Department 2 hours
post injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture haemotympanum, panda
eyes, cerebrospinal uid leakage from ears or nose, Battles sign
(bruising to the mastoid area)
Post-traumatic seizure
Focal neurological defect
>1 episode of vomiting
Amnesia or loss of consciousness and coagulopathy
Table 12.5 Effects of acute alcohol ingestion.
Stage Effect
Euphoria Overall improvement in mood, becoming more self-condent
and daring. Attention span shortens and judgement becomes
impaired
Lethargy Sleepiness, difculty understanding or remembering things.
Reactions slow and body movements become uncoordinated
Confusion Profound confusion, disorientation, heightened emotional
state aggression, withdrawal or overly affectionate. Nausea
and vomiting
Stupor GCS uctuates between 3 and 13
Coma GCS 3/15, pupil reexes to light diminished, pulse and
respiratory rate lowers
The Intoxicated Patient 51
He has a 4 cm cut to his forehead (partial thickness) with some
surrounding swelling, but no bogginess. He has no post-auric-
ular bruising, haemotympanum, panda eyes or evidence of a
cerebrospinal uid leak.
He has slurred speech and a tremor at rest. Peripheral nervous
system examination reveals normal power, tone, reexes and sensa-
tion but coordination is impaired with dysdiadokinesia. Nystagmus
is noted on eye examination, otherwise cranial nerves are intact.
Whilst you are examining him he appears to be becoming more
agitated. He is pulling at the sheets and grabbing out at the air
periodically and is becoming less cooperative.
Question: Given the history and
examination ndings what is your
principal working diagnosis?
Principal working diagnosis Acute alcohol
withdrawal though one needs to exclude
intracranial pathology and acute thiamine
deciency
The most likely diagnosis for this patient is acute alcohol with-
drawal. He is sweaty and tachycardic, has a tremor and is becoming
increasingly agitated. Pulling at his sheets and grabbing at the air
may be signs of the agitation or of visual hallucinations associated
with the withdrawal.
As previously discussed, it is very important not to miss head
injuries in this group of patients that are notoriously difcult to
assess. If there are signs of a head injury in these patients, brain
imaging should be considered.
This patient also has signs of possible encephalopathy and the eye
signs (nystagmus) could be related to the excess alcohol but could
also be a sign of Wernickes encephalopathy. He should be treated for
possible acute thiamine deciency in addition to the withdrawal, as
this could progress if left untreated, with disastrous results.
Management
This man requires close observation, intravenous thiamine,
treatment for alcohol withdrawal (lorazepam/chlordiazepoxide)
and a CT scan to exclude intracerebral pathology.
Outcome
His CT/head scan was normal and his agitation and confusion
settled with regular thiamine and chlordiazepoxide.
Further reading
Simon C, Everitt H, Kendrick T. Oxford Handbook of General Practice, Second
Edition. Oxford University Press, Oxford, 2002.
Tintinalli J, Kelen G, Stapczynski S, et al. Emergency Medicine: A Comprehensive
Study Guide. Sixth Edition. McGraw-Hill, New York, 2003.
Wyatt JP, Illingworth R, Graham C, et al. Oxford Handbook of Emergency
Medicine, Third Edition. Oxford University Press, Oxford, 2006.
A blood glucose meter.