Acute intoxication The symptoms of alcohol
intoxication will vary depending on the blood alcohol concentration (BAC),
individual alcohol tolerance, and to some extent the setting in which the
alcohol is taken. In general, as BAC rises from mild intoxication (BAC
<100mg%) to moderate intoxication (BAC 100–200mg%) to severe intoxication
(BAC >200mg%) a characteristic syndrome of acute intoxication is observed.
Initial symptoms are elevated mood, disinhibition, and impaired judgement,
followed by slurred speech, unsteady gait, nystagmus, ataxia, aggressiveness,
lability of mood and impaired concentration, and eventually sopor and coma.
At-risk drinking There are reported benefits to
health (lowered risk of coronary artery disease and strokes) associated with
low levels of alcohol consumption as compared with those who are abstinent (the
‘J-shaped curve’), though this remains a contentious area. Above this low
level, health risks increase with increasing alcohol consumption. It is
therefore arbitrary at which point drinking is considered ‘at risk’. Patient
and situational factors are important (e.g. any alcohol consumption while
driving or in pregnancy carries increased risks; for patients with established
alcohol-related organ damage any consumption is risky).
Harmful drinking (DSM-IV—alcohol abuse) Non-dependent
drinking which continues despite established harm to the patient’s physical or
mental health secondary to the alcohol consumption. ICD-10 diagnosis considers
only physical and mental health harm, not harm related to social sanction.
Alcohol dependence Harmful use of alcohol +
established dependence syndrome (b p. 542). Usually daily, stereotyped
drinking pattern with increased tolerance, withdrawal features on abstinence,
and ‘relief drinking’ (i.e. further drinking to alleviate the effects of
withdrawals).
Pathological intoxication (‘mania à potu’) This
is a medically and legally disputed syndrome which was not included in DSM-IV
due to
lack of empirical evidence. It is described as an
idiosyncratic reaction to a small amount of alcohol characterized by severe
agitation, belligerence, and violent behaviour followed by collapse, profoundly
deep sleep, and amnesia for the events which followed the alcohol consumption.
It is a dubious diagnosis which is mainly sought after by defence lawyers, as
most legal systems do not regard normal self-induced intoxication as a valid
defence. There is of course a strong association between alcohol and violent
crime. Careful re-examination of the history will usually demonstrate that
significant quantities of alcohol have been consumed.
Alcohol-induced amnesia (‘blackouts’ or
‘palimpsest’) This term refers to transient amnesic episodes related
to periods of intoxication. Characteristically the patient will report a ‘gap’
in their memory lasting several hours with global or partial amnesia for their
actions during that time. The patient’s behaviour as reported by witnesses is
usually characteristic of their normal behaviour when intoxicated. This amnesia
seems to be a failure of recall rather than initial registration and represents
a reversible form of brain damage. Its occurrence is not predictive of
longer-term cognitive impairment. It occurs in the later stages of a drinking
career, if at all, and tends to recur once established. Two forms are
described:
- ‘En
bloc’—dense amnesia with well demarcated start and finish points.
- Partial—episodes
with indistinct start and end point with islands of preserved memory and
variable degrees of recall.
There is some degree of state-dependent recall in blackouts
and a return to intoxication may aid recall. Because of the potential confusion
of the term ‘blackout’ with periods of loss of consciousness, the term ‘alcoholic
palimpsest’ is to be preferred.
Alcoholic hallucinosis This is a
substance-induced psychotic illness (defined in ICD-10), which is a rare
complication of prolonged heavy alcohol abuse. The sufferer experiences
hallucinations—usually auditory—in clear consciousness and while sober. The
auditory hallucinations may begin as elemental hallucinations (e.g. bangs or
murmurings) before, with continued alcohol use, being experienced as formed
voices, most usually derogatory in nature. There may be secondary delusional
elaboration. The nature of hallucinations tends to worsen during periods of
alcohol detoxification, and at times, when intoxicated with alcohol.
- Differential
diagnosis Transitory hallucinatory or illusionary experiences
while intoxicated, delirium tremens, psychotic illnesses.
- Course In 795%
of patients there is rapid resolution of these symptoms on ceasing alcohol
consumption but the symptoms rapidly recur on restarting drinking.
In 75% there are prolonged symptoms (<6mths after abstinence) and
an emergence of more typical schizophrenic symptomatology.
- Management Persisting
symptoms may be treated with antipsychotic medication (bearing in mind the
medical comorbidities seen in this population).
Alcohol-induced psychotic disorder with delusions Long
recognized, but only recently included in DSM-IV. Development of persecutory or
grandiose delusions after long history of heavy drinking. No other features of
delirium tremens. Resolves on abstinence.
Alcohol-related cognitive impairment/alcohol-related
brain damage (ARBD)
The classification of alcohol-related cognitive impairment is
unclear, with both ICD-10 and DSM-IV viewing it as a number of discrete
entities, as opposed to a continuum. ICD-10 describes amnesic disorder (F10.6),
dementia (F10.73), and other persisting cognitive disorder (F10.74), DSMIV-TR
using the terms alcohol-induced persisting amnestic disorder and
alcohol-induced persisting dementia. It is worth noting that the DSMIV-TR
categories ignore the possibility of slow recovery over 1–2yrs in this patient
group.
The majority (50–60%) of heavy drinkers display some degree
of cognitive impairment on cognitive testing while sober. There is impairment
in short-term memory, long-term memory recall, new skill acquisition, executive
function, relative preservation of language ability and mildly impaired
visuospatial function. IQ (measured by the WAIS) is generally preserved (in
comparison with pre-morbid IQ, measured using the NART). CT/MRI examination of
the brains of heavy drinkers reveals cortical and subcortical atrophy. White
matter loss is prominent, which correlates with neuropathology findings. Degree
of structural abnormality poorly correlated with degree of functional
impairment. In all patients with alcohol-related brain damage (including those
with ‘alcohol dementia’ and Korsakoff
syndrome), a significant amount of medical comorbidity is
seen, including small vessel disease, repetitive head injuries, and comorbid
alcohol liver disease. The neurotoxic effects of alcohol on the brain are
exacerbated significantly by thiamine deficiency, and there is evidence to
suggest earlier onset in women. Abstinence from alcohol use has been shown to
correlate with functional improvement and MRI improvement at 1yr.
The term alcohol dementia is used at times, describing a
generalized dementia syndrome, in which there is intellectual decline and more
pronounced neuropsychological deficits. The changes correlate with total
lifetime drinking and length of drinking history.
Wernicke–Korsakoff syndrome
This is a monosymptomatic delusional disorder (see b p.
220) seen most commonly secondary to current or previous alcohol abuse. The
form is a primary delusion in which the content is that the patient’s spouse or
partner has been or is being unfaithful. Delusional evidence may be provided to
back up this belief and the patient may go to great lengths to obtain
‘evidence’ (e.g. following her, planting tape recorders, examining discarded
clothing). There is a significant association with violence and even homicide
towards the supposedly unfaithful partner.
Management
- Abstinence
from alcohol with addition of antipsychotic medication.
- It may
be necessary for the couple to separate and advice to this effect may have
to be given to the at-risk partner.
Psychiatric comorbidity
Anxiety and depressive disorders Symptoms such
as generalized anxiety, panic attacks, and low mood are very frequently
reported in alcohol abusers. Many patients with alcohol problems also merit
diagnoses of depressive illness (750%) or anxiety disorder (775%). The
phenomenology of these disorders is similar to that found when the disorders
occur in isolation. The difficulty is deciding the sequence of events, as in
some cases the alcohol problem is secondary to the patient ‘self-medicating’
with alcohol in order to relieve primary anxiety or depressive symptoms.
Nonetheless, chronic alcohol use will act as a direct depressant, its secondary
effects will produce depressogenic life events (e.g. loss of job) and
alcohol-related effects such waking at 04.00hr due to withdrawal, or weight
loss related to nausea may masquerade as, or mask, biological depressive
features.
Patients may emphasize the primacy of the mood or anxiety
features and seek their resolution before tackling the alcohol problem.
Generally a primary mood or anxiety disorder diagnosis should not be made in
the presence of continuing alcohol misuse and psychological or pharmacological
treatment for mood disorder is unlikely to be effective. The correct course is
to initiate detox if indicated and to reassess mood/anxiety symptoms after 4wks
of abstinence, treating residual symptoms at this point. Only a minority will
require formal treatment. An undiagnosed depressive illness preceding the
alcohol problem is more common in women. Alcohol problems can also arise as a
result of self-medication of agoraphobia and social phobia.
Suicide Classically quoted as lifetime risk of
10–15% in dependent drinkers. Now estimated at 74% lifetime risk of
suicide in those with alcohol problems. Psychiatric comorbidity is important,
as is social isolation, physical ill health, and repeated failed attempts at
abstinence.
Schizophrenia High rates of alcohol and
substance use found in schizophrenic patients (750%). Increased risk of
violence, EPSEs, TD, noncompliance, relapses, and rehospitalizations. Alcohol
is an easily available temporary treatment for some of the distressing symptoms
of psychotic illness.
Drug misuse Comorbid alcohol and drug misuse can
be to enhance effects (e.g. euphoriant effect of alcohol and cocaine combined)
or to minimize unpleasant side-effects (e.g. alcohol to relax after taking
stimulants), or as a substitute when the primary drug is unavailable. Comorbid
drug misuse is associated with poorer outcome. Some comorbidity can have an
iatrogenic component where there is mixed abuse or substitution of BDZs for
alcohol. This can result from inappropriate prescribing of anxiolytics,
misdiagnosis of alcohol problems as anxiety disorders, and repeated
unsupervised withdrawals with hoarding of tablets. Aim to limit new
prescriptions, review diagnosis in patients with treatment-resistance anxiety
disorders, and avoid short-acting BDZs (e.g. lorazepam).
Wernicke–Korsakoff syndrome
Wernicke encephalopathy and Korsakoff psychosis represent
the acute and chronic phases of a single disease process—Wernicke–Korsakoff syndrome—which
is caused by neuronal degeneration secondary to thiamine deficiency, most
commonly seen in heavy drinkers.
Neurological Effects
- Wernicke–Korsakoff
syndrome (b p. 572).
- Peripheral
neuropathy.
- Central
pontine myelinolysis (pseudobulbar palsy + quadriplegia).
- Marchiafava–Bignami
disease (corpus callosum degeneration).
- Cerebellar
degeneration.
- Optic
atrophy.
- Alcoholic
myopathy.
- Erectile
problems.
- Hypogonadism
in men.
- Foetal
alcohol syndrome
- Gout.
- Osteoporosis.
- Impaired
absorption and diminished intake of specific vitamins and food overall.
- Contribution
to accidents, particularly RTA.
- Exacerbating
factor in violent crime and assaults.
- Diminished
compliance with treatment for other medical and psychiatric disorders.
Last Updated: 10 Dec 2024