Diagnosis of complications and differential diagnosis
Alcoholism often masks or coexists with other severe pathologies. For example, binge drinking episodes can be equivalent to an epileptic seizure (dipsomania) or occur against the background of depression. In schizophrenia, alcohol consumption may be associated with a loss of volitional control or an attempt to mitigate depersonalization.
The development of alcohol-induced psychoses indicates a severe stage of dependence.
- Alcoholic delirium: a nonspecific exogenous reaction that appears exclusively in patients with a multi-year history of heavy drinking. It is invariably accompanied by somatic manifestations of withdrawal (tachycardia, hyperhidrosis, dyspnea, blood pressure surges).
- Hallucinosis and paranoid psychosis: unlike schizophrenia, they are not accompanied by typical thought disorders, circumstantiality (resonership), or Kandinsky-Clérambault syndrome. Delusions are simple and mundane in character, and the course of the disease most often tends toward symptom regression.
- Encephalopathies: require a thorough exclusion of brain tumors, syphilitic lesions, and trauma. Important "red flags" that rule out a purely alcoholic etiology include nocturnal bursting headaches with vomiting (a sign of intracranial hypertension) and pronounced dysarthria.
Pathogenesis and Risk Factors
The development of pathological craving is driven by a complex interplay of biological, genetic, and social factors. Genetic predisposition is confirmed by high concordance in monozygotic twins.
Biological vulnerability largely depends on the functioning of enzyme systems:
- Aldehyde dehydrogenase: its deficiency leads to the rapid accumulation of toxic acetaldehyde, triggering autonomic storms (flushing, tachycardia) and hindering the development of dependence.
- Alcohol dehydrogenase: a deficiency of this enzyme causes severe forms of intoxication and the rapid development of encephalopathy.
At the neurochemical level, euphoria is mediated through the dopamine reward system. Genetically determined low dopamine activity drives the individual to seek stimulants. Furthermore, serotonin receptor dysfunction in individuals with anxiety and low self-esteem contributes to the chronification of depressive states, which are alleviated by ethanol. Upon abrupt cessation of alcohol, an imbalance occurs: inhibitory systems (GABA) are depleted, while excitatory systems (glutamate) are overly stimulated, leading to psychoses.
Principles of treatment for withdrawal syndrome
Therapy is aimed at safe sobering, relief of withdrawal symptoms, and the prevention of psychoses. All patients must undergo screening for HIV, hepatitis, and syphilis.
The mainstay of pharmacotherapy for withdrawal includes:
- GABAergic agents: tranquilizers (diazepam, phenazepam), barbiturates, carbamazepine. Due to cross-tolerance with ethanol, doses exceeding standard therapeutic levels are required. Intravenous administration is not recommended due to the risk of respiratory arrest.
- Detoxification: forced diuresis, crystalloid infusions (saline, Ringer's solution). Colloids are rarely used. Glucose is contraindicated as it exacerbates vitamin B1 deficiency.
- Nootropics and vitamins: high doses of thiamine (intramuscularly) are mandatory for the prevention of Wernicke-Korsakoff encephalopathy.
- Antipsychotics: used strictly in low doses (haloperidol, thioridazine) for sedation and antiemetic effects. Drugs with pronounced anticholinergic effects and diphenhydramine are excluded due to the risk of provoking delirium.
Briefly: answers to topical questions
What somatovegetative and psychiatric disorders manifest during cannabinoid withdrawal?
Cannabinoid withdrawal syndrome resembles tobacco cessation.
The structure of the syndrome includes:
- Psychiatric disorders — irritability, fatigue, sleep and appetite disturbances.
- Somatovegetative disorders — chills, tremor, pupillary reversal (miosis), and pronounced somatic discomfort.
Somatic discomfort includes chest tightness, air hunger, cardialgia, headache, and throbbing in the temples. The syndrome resolves without treatment within 4–6 days.
What forms of acute intoxication psychoses develop with cannabinoid use?
Cannabinoid use can lead to acute intoxication psychoses that may mimic an acute episode of schizophrenia.
The following variants of psychotic states are distinguished:
- Oneiroid — accompanied by dream-like experiences, delusional ideas, and illusory disorders.
- Paranoid — characterized by anxiety and ideas of persecution.
- Delirious — manifested by hallucinations and disorientation.
- Twilight — proceeds with ambulatory automatisms.
Psychosis can occur both from high doses and as a result of chronic use of small amounts of the drug. The duration of acute psychotic episodes is 3–5 days.
What clinical signs characterize the first stage of cannabinoid addiction?
The initial stage (development of dependence) in cannabinoid addiction is characterized by the emergence of pathological craving and increasing tolerance.
Clinical signs of the onset of the disease include:
- Change in consumption pattern — transition from episodic social use to daily use and smoking alone.
- Domination of need — spending significant time and effort on procuring the drug.
- Increased tolerance — doses significantly exceeding initial ones are required to achieve euphoria, while the body's protective reactions disappear.
Persistent addiction to cannabis preparations typically forms after an average of 3 months of daily use.
Which psychiatric disorders require differential diagnosis with cannabinoid psychosis?
Differential diagnosis of cannabinoid psychosis must be performed with schizophrenia. Acute intoxication with high doses of cannabinoids is accompanied by delusional ideas and illusory disorders, resembles an oneiroid state, and can mimic an acute attack of schizophrenia.
How does tolerance to the drug change upon transition to the second stage of cannabinoid dependence?
The dynamics of tolerance in substance addictions proceeds in two phases, where the second phase (outcome of the disease) is characterized by its decrease.
The change in drug tolerance at this stage is manifested by the following signs:
- Organic basis — the decrease in tolerance occurs against the background of organic damage to the brain and internal organs.
- Loss of resistance — the body loses its ability to withstand intoxication.
- High risk — despite the drop in tolerance, the patient retains the urge to consume large doses of the psychoactive substance, leading to a high risk of fatal poisoning.
To memorize medications for withdrawal, use the "TGD" rule: Thiamine (mandatory!), GABAergic drugs (tranquilizers), Detoxification (crystalloids).
Class and exam questions
Is it permissible to administer glucose for sobering up in severe intoxication?
Administering a 5% glucose solution is permissible only after ruling out hypoglycemia and strictly without adding insulin; however, it is contraindicated during withdrawal syndrome due to the risk of worsening thiamine deficiency.
How does delirium in alcoholic paranoid differ from schizophrenic delirium?
In alcoholism, delusions are mundane and concrete in nature; personality defects, circumstantiality (resonership), and phenomena of psychic automatism (Kandinsky-Clérambault syndrome) are absent.
Why are diphenhydramine or chlorpromazine not used in the treatment of withdrawal syndrome?
Drugs with potent anticholinergic and adrenergic-blocking effects cause severe hemodynamic disturbances and significantly increase the risk of provoking alcoholic delirium.
Is the use of alcohol itself permitted for treating withdrawal syndrome?
Yes, in exceptional cases under the threat of severe delirium and somatic complications, a single dose of up to 50 g of pure alcohol (100–150 ml of vodka) is permitted.
What else to study on this topic
- Acute necrosis of hemorrhoids and giant parotitis as somatic markers
- Specifics of epileptic seizures during alcohol withdrawal
- Pathogenesis of blood-brain barrier damage in alcoholism
- Tactics of non-specific detoxification (unitiol, sodium thiosulfate)
- Symptomatic therapy of cardiovascular disorders during the abstinence period
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Other topics in «Chapter 21. Disorders due to use of alcohol and other psychoactive substances»
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