alcoholism Dangerous

Alcohol Withdrawal Syndrome Is Dangerous, Can Lead to Death

Alcohol withdrawal syndrome is an acute condition characterized by a set of self-limiting signs and symptoms of varying severity, secondary to total or partial alcohol withdrawal, and may be associated with numerous clinical problems and / or other psychiatric disorders.

The aim of this article is to review the main psychiatric complications secondary to alcohol withdrawal syndrome with convulsions and delirium tremens, as well as some other psychiatric conditions associated with alcohol dependence such as Wernicke Korsakoff and Marchiava Bignami syndromes.

It is intended to help in the early diagnosis and appropriate treatment, thus minimizing the morbidity and mortality associated with such complications.

Alcohol Withdrawal Syndrome Is Dangerous, Can Kill

It is responsible for a significant increase in morbidity and mortality associated with alcohol consumption and is one of the diagnostic criteria of alcohol dependence syndrome.

It is characterized by signs and symptoms resulting from a total or partial interruption of consumption of alcoholic beverages in dependents that present a significant previous consumption.
Alcohol Withdrawal Syndrome Is Dangerous
These signs and symptoms are not specific only to the alcohol withdrawal syndrome, and may be present in other withdrawal syndromes (eg benzodiazepines).

They are still insidious and unspecific, which makes their recognition and evaluation complex processes; vary in intensity and severity, and may appear, as said, after a partial or total reduction of the dose usually used.

This article aims to describe the main complications secondary to SAA as well as its treatment. Some of them are quite common (seizures and hallucinations); others, more serious and less common (delirium tremens). In addition, it describes and proposes the treatment of other complications associated with alcohol dependence such as Wernicke Korsakoff’s syndrome and Marchiava Bignami’s syndrome).


Convulsive seizures secondary to alcohol abuse / dependence are not uncommon, as well as worsening seizure control in patients with a history of seizures (idiopathic or not) 10. Seizures secondary to alcohol withdrawal are usually of the tonic-clonic type (or “grand mal”), unique, and affect the first 48 hours (with a peak between 13 and 24 hours) after the suspension or reduction of alcohol consumption. alcohol. However, focal symptoms may appear in about 5% of seizures secondary to alcohol withdrawal.
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Almost always, the onset of seizures is associated with more severe alcohol withdrawal, and most patients who are not adequately treated evolve to delirium tremens.

There is an indication for image evaluation of seizure pictures secondary to alcohol withdrawal (eg computed tomography), to detect comorbid diseases (chronic subdural hemorrhage and cranial trauma, for example).

About 4% of the CT scans performed in patients with convulsive conditions secondary to alcohol withdrawal show structural lesions. Computed tomography is also indicated in cases of seizures other than the grand problem type in abstinent patients due to the higher prevalence of co-occurrence of lesions in this group.

The chance of another seizure in 6 months is 41%, and this prevalence increases with time, reaching 55% in three years 11,16. New episodes of seizures could trigger pictures of secondary alterations in the kindling that seem to be summed up, that is, with each new seizure, the picture worsens. Kindling is defined as a phenomenon in which a weak electrical or chemical stimulus, which would normally not cause an important behavioral response, when administered several times, triggers the process. Kindling may result from changes in brain neurotransmitters (GABA and NMDA, mainly) which, consequently, increase cerebral excitability, predisposing to the risk of new seizures, anxious pictures and increased neurotoxicity.
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If structural changes are not identified in patients with seizures secondary to alcohol withdrawal, if they have no previous history of seizures and have not previously used anticonvulsants, anticonvulsants do not appear to be indicated and may in some cases precipitate the occurrence of seizures by abstinence (including anticonvulsants).

The treatment of choice is the control of the convulsive crisis through the infusion of benzodiazepines and specific treatment to control alcohol dependence11. A maximum of 10 mg of diazepam should be administered for 4 minutes without dilution and the intravenous administration of benzodiazepines requires specific and back-up technique for the management of eventual respiratory arrest. 12 Chronic use of anticonvulsants (phenytoin and phenobarbital, among others) a limited action in the prevention of seizures due to alcohol withdrawal, since the central problem of the patient is the use of alcohol and, in the vast majority of cases in which alcohol consumption is maintained (thus, risk of new seizures) , non-adherence to drug treatment is almost a rule, and this action, by itself, precipitate a new seizure crisis. However, in patients with prior anticonvulsants, the medication should be maintained.

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The most effective prevention in this group of patients is undoubtedly the treatment for alcohol withdrawal and the use of long-acting benzodiazepines (diazepam, for example) at a dose of 10 to 20mg or use of lorazepam in an equivalent dose in a hepatopathic or senile patient 1,12. There is no justification for the introduction of anticonvulsants in this population, either for the treatment of seizures or for the prevention of new seizures.

The status epilepticus is a serious condition with a high mortality rate (about 10%) and is not uncommon among patients with alcohol withdrawal syndrome. A 1980 study showed that 21% of the patients in the tonic-clonic type of disease were in abstinence. Treatment of this condition should be instituted as soon as possible in clinical emergency care units.

Delirium Tremens (DT)

Delirium is a common cause of altered behavior in people with some physical illness that has not been properly diagnosed or treated. Several terms over the years have been used to describe this syndrome, including acute confusional states, acute brain syndrome, acute cerebral psychosyndrome, and acute organic reaction.

DT is a specific picture of delirium, related to alcohol withdrawal. Frames of delirium usually exhibit fluctuating symptoms, with significant worsening at night. Cognitive, memory and attention changes and temporomandibular disorientation are common. Decreased attention and disturbances in thinking result in incoherent speech. Relatives and other informants may report a rapid and drastic decline in the pre-morbid functioning of a patient, which differentiates him from those with dementia.

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Sensory-perceptual alterations (hallucinations and illusions) are common, and visual hallucinations are quite common. Delusions are also frequent, usually persecutory and related to temporomandibular disorientation. Mood changes are common and range from intense apathy to intense anxiety; the presence of changes in the sleep-wake cycle is constant. Unfortunately, as said, many cases are not properly detected and therefore are not treated.

Not all abstinence is a DT. In fact, DT is an uncommon condition among alcohol dependents, occurring in less than 5% of the abstinent population. However, it is responsible for the great morbidity and mortality associated with ASD, since DT frames are not, as mentioned, adequately diagnosed. The DT usually begins up to 72 hours (although it can start up to seven days) after abstinence and includes various signs and symptoms, such as mental confusion, hallucinations, tremors, fever (with or without signs of infection) and autonomic hyperresponsiveness, with hypertension, tachycardia and sweating. DT should be suspected in all cases of agitation in a patient with ASA whose blood pressure is above 140 / 90mm Hg, heart rate is greater than 100 bpm, and temperature, higher than 37ºC. Mortality rates are high, ranging from 5% to 15% of patients with this condition.
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Few studies, however, adequately define DT frames taking into account clinical / psychiatric comorbidities, trauma, etc. The most frequent cause of death is cardiorespiratory failure. The pathophysiology of DT frames remains poorly understood. The physiological changes resulting from TD would result from interactions of neuroreceptors (mainly gabaergic and catecholaminergic systems), as well as ionic changes (potassium and magnesium, mainly).

Treatment of this condition is usually done with benzodiazepines, in order to reduce autonomic hyperactivity and the risk of psychomotor agitation. Diazepam is preferred in a higher dose than those usually used (60mg / day) or lorazepam (12mg) if the patient is hepatopathic or senile. Eventually, the association of neuroleptics, at low doses, may be indicated (haloperidol 5mg / day). In the case of neuroleptic-induced dystonia (particularly if given parenterally), it can be controlled with the use of anticholinergics (2mg biperiden).

Wernicke Korsakoff Syndrome (SWK)

SWK is a potentially fatal complication associated with vitamin B1 or thiamine deficiency. It has been described as two distinct entities – Wernicke’s encephalopathy and Korsakoff’s psychosis.

The syndrome is composed of a triad of clinical abnormalities described by Wernicke – ophthalmoplegia, ataxia and mental confusion. These would be the pillars in the diagnosis of the syndrome; However, the presence of all these symptoms is not necessary for the diagnosis of SWK, and isolated signs (of ophthalmoplegia and / or disorientation and / or stupor and / or coma) are more routinely found. Eye movements may consist of horizontal and vertical nystagmus, weakness or paralysis of the lateral rectus muscle and the conjugate gaze. In advanced cases, complete ophthalmoplegia can be found. Mental confusion is characterized by decreased alertness and alertness and sensory-perceptual change and memory. Frames of confabulation are common in this group of patients. Sometimes there is progression to coma.
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Daily thiamine needs are estimated at 1.0 – 1.5 mg / day in normal patients. Thiamine is an important cofactor of the enzyme pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, involved in the metabolism of carbohydrates and transketolase, an important enzyme in the pentoses pathway. Thiamine is naturally present in cereals and many flours. However, the processing of these grains results in the loss of much of that vitamin. Several countries (USA, England, Canada and Denmark) enrich flours with thiamine; with this measure, thiamine deficiency was restricted to some groups of patients. SWK is a syndrome commonly associated with alcohol dependence and, in some cases, some types of cancer, hyperemesis gravidarum, small bowel obstruction, anorexia nervosa and gastroplasty. The chronic consumption of alcohol is related to the low absorption of thiamine by the intestinal cells, as well as the lower phosphorylation of the same, in its active form, and a decrease in the hepatic thiamine stock. These factors, associated with the lower intake of foods containing thiamine, may be one of the causes of the low concentration of thiamine in alcohol dependents.

Several mechanisms have been implicated in the pathogenesis of this syndrome, but are still not fully understood. One of the explanations are neuronal losses, and the mechanisms for this brain death include cerebral energetic deficiency, glutamate-mediated excitoxicity, focal lactic acidosis, and alteration of the blood-brain barrier. Focal lactic acidosis may be one of the mechanisms that lead to a brain thiamine deficiency (reducing the permeability to thiamine in the brain). The most plausible explanation for this phenomenon appears to be a decrease in the pyruvate oxidation resulting from the decreased activity of thiamine-dependent dehydrogenases. With the accumulation of lactate in the neurons, there is a change of pH (acidosis), generating cell death. The intense formation of free radicals is also associated with SWK frames. Chronic alcohol administration in rats, with subsequent SAA, causes an increase in the formation of free radicals in several brain regions, as well as increase of the nitric oxide molecule by the metabolization of ethanol 6.
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In animals in which thiamine deficiency was experimentally induced, microdialysis demonstrated a significant increase in extracellular glutamate, selective for the ventral posterior thalamus. These changes are reversible with administration of thiamine in the cortex and brain bridge, but not in the thalamus. In regions where there is such excess of glutamatergic activity, there may be excitotoxic neurodegeneration. Nevertheless, direct evidence is needed to support a relationship between thiamine deficiency and changes in the NMDA receptor.

Anatomopathological characteristics vary according to the stage and severity of the disease. Patients in the acute phase may have changes in mammillary bodies, hypothalamus, periventricular region of the thalamus (above the aqueduct). The mamillary bodies, especially the medial nuclei, are the structures most frequently affected and are affected in almost all cases. Histopathological exams, in acute cases, demonstrate edema, necrosis, demyelination, discrete neuronal loss, spongy degeneration and enlargement of blood vessels as a result of hyperplasia; when there is petechial hemorrhage, erythrocytes and hemosiderin are present, as well as macrophages. In chronic cases, there is more marked neuronal loss and gliosis 2. The diagnosis is clinical, magnetic resonance imaging being a useful complementary exam in the detection of these brain lesions, whereas brain tomography is in many cases ineffective. SWK is one of the complications of alcohol dependence frequently underdiagnosed

Treatment of this condition is still not adequately established with respect to the route and dose of thiamine necessary for both prevention and treatment, and no well-conducted study is known to the authors of this article; most recommendations for vitamin supplementation are empirical8. The consensus thiamine dose on alcohol withdrawal syndrome was at doses above 300mg of thiamine per day intramuscularly for a period of 7-15 days. Oral use is not indicated for the prevention of Wernicke Korsakoff Syndrome because the absorption of thiamine may be impaired due to alcohol consumption and, therefore, there is a decrease in efficacy in the prevention of Wernicke Korsakoff Syndrome. In England, after the discontinuation of the use of high-potency B vitamins (250mg of thiamine in each ampoule), there was an increase in cases of “alcoholic psychosis” and the authors suggest that the increase in the occurrence of these conditions is secondary to vitamin supplementation in low doses.
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Marchiava Bignami’s Syndrome

Also called “primary degeneration of the corpus callosum”, it is a disease more commonly defined by pathological aspects than by clinicians. The main alteration is found in the medial portion of the corpus callosum where, in the naked eye examination, a decrease in tissue density is observed, with a slight reddish or yellowish depression, depending on the time of the lesion. From the microscopic point of view, areas of demyelination with abundance of macrophages are clearly visible, although there are no inflammatory changes. Less consistent, lesions of a similar nature are found in the central portion of the anterior and posterior commissures and bridge.

It is a rare disease that affects older people and, with few exceptions, all patients affected are alcohol dependent. Some present, in the terminal stage, pictures of stupor and coma, and others, symptoms compatible with chronic intoxication and withdrawal syndrome. In some cases, pictures of progressive dementia have been described, with symptoms such as dysarthria, sluggish and unstable movements, transient sphincter incontinence, hemiparesis, and aphasia. The diagnosis of this pathology is rarely made during life, but, as a rule, at necropsy, by anatomopathological examination. The occurrence of symptoms similar to frontal lobe syndrome, Alzheimer’s disease, or tumor-like symptoms in the frontal region, but spontaneously occurring, suggest a syndrome of Marchiava Bignami, and exams help in the diagnosis. The etiology and pathology of this condition are not well understood until now.


Although serious complications of alcohol dependence have been addressed above, regardless of the level of alcohol consumption, all dependents need and should have access to treatment at any stage of their illness as well as their family members. The article sets out the bases for the recognition of these complications and proposes some interventions for the treatment minimizing morbidity and mortality.
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There are effective interventions and some proposed interventions, such as the use of thiamine in the prevention of Wernicke Korsakoff syndrome, still require further research to establish dosage, route of administration and duration of use.

Others, however, are well established, such as the use of benzodiazepines to prevent the progression of SAA to more severe conditions such as DT. Such use should be instituted as early as possible in a patient with a history of severe SAA in the past in which abstinence is proposed or when the patient has been abstinent for less than three days and presents an important symptomatological picture justifying the use of this medication.

The involvement of the family in the treatment of the patient is fundamental, as it promotes a greater adherence to the treatment as well as a better quality of life for the members of the family nucleus. When outpatient treatment is not possible, or when the condition is severe, hospitalization may be necessary to ensure abstinence. All of these measures can and should be implemented and integrated into public and private health systems and, for this to take place properly, more professionals must be adequately trained to carry them out.

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