Where can I invite a psychiatrist to examine a patient in a state of psychosis at home?
There are three types of institutions from which you can call a psychiatrist.
- Psychoneurological dispensary (PND). This is a government institution, like a clinic, where psychiatrists work. In cities, each psychiatrist is even assigned his own precinct, that is, each city resident has his own local psychiatrist! The responsibilities of such a psychiatrist include home visits to examine seriously ill patients (and psychosis is a serious condition). You, as a relative or loved one, can contact a psychiatrist (in person, through the registry, or by telephone) with a request for an examination at home. An experienced doctor, during a conversation with you (relatives or friends), will draw a conclusion about the patient’s condition and give advice on what to do while you wait for the doctor to arrive.
Ambulance. If the patient is agitated, aggressive, poses a danger to himself or others, there is no way to leave him alone and there is no time, then call an ambulance for psychiatric help. For more details on how to do this, see here- Private psychiatric clinics. In recent years, their number has been increasing. You can invite a psychiatrist from a private psychiatric clinic to examine the patient. Or call a special team of specialists to provide emergency psychiatric care or hospitalization. The ROSA Clinic is one of the leading private psychiatric clinics in Russia, which operates around the clock and has its own comfortable inpatient department for the treatment of psychosis, and also has a staff of psychiatrists who provide consultations at home.
Diagnosis
The diagnosis is made on the basis of anamnesis data indicating the effect of a certain poison (or poisons) on the body, laboratory tests that reveal the presence of toxic substances (mercury, phenamine, antipsychotics, etc.) or their metabolites in biol, liquids, parallelism (often incomplete) between continuation and cessation of the action of the toxic factor and the dynamics of mental disorders. If a group of toxic substances causes characteristic (preferred) syndromes, then their characteristics can help the diagnosis. Preferred syndromes include: delirium - under the influence of anticholinergic drugs, hallucinatory-paranoid syndromes - under the action of c. stimulants. n. pp., depression - when taking antipsychotics, mania - when using antidepressants and quinacrine, amnestic syndrome - when poisoning with carbon monoxide, etc. The nature of somatic disorders can provide significant help - various changes in the skin and mucous membranes (skin rashes with bromism, brown pigmentation due to fluoride poisoning), internal organs (during alcohol intoxication), changes in. n. With. (in case of poisoning with various drugs) and c. n. With. (damage to the basal ganglia due to manganese and carbon monoxide poisoning).
Differential diagnosis
Distinguishing I. p. from other symptomatic psychoses (for example, drug psychosis from somatogenic or infectious) can be difficult due to the similarity of symptoms and course. The main criterion in this case is to establish a relationship between the influence of a toxic factor and the occurrence or reduction of psychosis, and sometimes the presence of characteristic somatic symptoms. I.'s delimitation from endogenous psychoses and organic lesions of c. n. With. is based on anamnesis data, the connection between the dynamics of mental disorders and the onset, continuation or cessation of the action of a toxic substance.
Treatment of psychosis in a hospital
The duration of treatment for psychosis in a hospital takes, on average, from 10 to 30 days. The necessary research (tests, pathopsychological diagnostics, electroencephalography, etc.) and observations are carried out in the hospital, and the patient is examined by specialists. The causes and mechanisms of development of psychosis are clarified. Antipsychotic treatment is carried out under the supervision of staff: antipsychotics, mood stabilizers, neurometabolic therapy and other methods for which indications will be found. In psychiatric hospitals, a special supervision system is observed to ensure safety for patients: a patient in a state of psychosis is under constant supervision, and there is a medical worker’s post next to his bed. Such observation is reminiscent of looking after a baby who cannot be left alone. As the patient’s condition improves, the patient is transferred from a special “supervision ward” to a regular ward, where there is no longer strict supervision. In the first days of treatment, drug therapies play a large role; closer to discharge, they are joined by psychotherapeutic sessions in the form of conversations, sessions with a psychologist, and group trainings.
Clinical picture
The variety of toxic substances and mechanisms of their action determines the diversity of the wedge. pictures of I. p.—practically all psychopathols, symptoms and syndromes occur with them. The emergence of new, previously unknown poisons (organophosphorus compounds, new drugs, psychotomimetics) has not led to the emergence of new symptoms and syndromes. Thus, the concept of E. Kraepelin (1912), according to which each poison causes mental disorders specific to it, did not come true. It has been established that the same poison can cause various mental disorders. Thus, poisoning with tricyclic antidepressants can cause coma, epileptiform seizures, manic states, delirium, twilight states; Teturam poisoning - asthenia, delirious, delirious-oneiric, twilight states, depressive, manic, catatonic, paranoid and hallucinatory-paranoid, pseudoparalytic syndromes, convulsive seizures. Poisoning with completely different substances can lead to similar mental disorders; Thus, delirious states have been described after poisoning with carbon monoxide, lead, ether, barbiturates, anticholinergic drugs, etc. Attempts to identify shades specific to the action of a particular substance in the structure of similar syndromes have not received universal recognition. However, it is also unjustified to assert that there is nothing characteristic in the wedge, the picture of I. p. and that any substance can lead to the development of any syndrome with equal probability. Schematically, three main forms of I. p. can be distinguished.
Acute forms
- “quantitative” disturbances of consciousness (coma, stupor, stupor) - more often occur with short-term exposure to massive doses or a sharp increase in doses of a long-acting substance, less often with chronic intoxication with the same dose. Against the background of impaired consciousness, chaotic, undirected motor excitation and fragmentary hallucinations can usually be observed.
Forms with a predominantly long course
- mental disorders characteristic of the action of a specific substance or group of substances. Their occurrence is often associated with exposure (short-term or long-term) to moderate doses of poison. It is in this group of Intoxication psychoses that a variety of psychopathols are observed. syndromes: syndromes of clouded consciousness, most often delirium-type (with intoxication with atropine, bromine, digitalis preparations), less often oneiric, twilight, amentive states, convulsive seizures (with intoxication with lead, penicillin), manic (with intoxication with tricyclic antidepressants, quinine), depressive syndromes (with intoxication with reserpine, phenothiazide derivatives, dopegit, l-dopa), verbal hallucinosis syndromes (with bromine intoxication), paranoid and hallucinatory-paranoid (with cocaine, phenamine, teturam intoxication), catatonic, Hebephrenic syndromes (with bulbocapnine intoxication, carbon monoxide, acetylsalicylic acid). Picture I.p. may have significant similarities with endogenous psychoses - manic-depressive psychosis (with intoxication with quinine), schizophrenia (with intoxication with phenamine, hashish, mercury). The similarity with schizophrenia is not limited to the presence of verbal hallucinations and delusions of attitude, persecution, physical influence against the background of clear consciousness; Peculiar disturbances in thinking, emotional and volitional spheres, which are considered characteristic of schizophrenia, can also be observed (with intoxication with hashish, ephedrine, phenamine). Sometimes there is a rapid change of syndromes, polymorphism of psychopathological symptoms that do not fit into the framework of a specific syndrome (with intoxication with corticosteroids and ACTH). With IP, syndromes of organic brain damage also develop - pseudoparalytic (with intoxication with barbiturates), Korsakovsky (with intoxication with alcohol, carbon monoxide), parkinsonian (with intoxication with manganese, neuroleptics), etc.
These syndromes can be transient, for example, Korsakoff's syndrome caused by carbon monoxide poisoning, neuroleptic parkinsonism, pseudoparalytic syndrome caused by barbiturate poisoning disappear. But the opposite dynamics are also possible: some motor impairments caused by neuroleptics are initially similar to psychogenic ones, i.e. they arise or disappear under the influence of excitement, suggestion, etc., but as the medication continues to be taken, they lose connection with psychogenicity and become permanent and subsequently irreversible in some patients. Thus, the development of syndromes of organic brain damage in itself does not allow us to draw a conclusion about the organic nature of the damage to c. n. With. The personality characteristics of the patient in this group of disorders play a secondary role, reflected in Ch. arr. on the specific content of painful (hallucinatory and delusional) experiences, but with little effect on the structure of the syndrome.
Relatively easy-flowing forms
- borderline mental disorders. They usually develop during exposure, often long-term, to small doses of a toxic substance, but they can also appear after the disappearance of more severe mental disorders caused by the action of large doses of a toxic substance. The concept of “small doses” is relative, since we are talking about doses that cause a toxic effect, and therefore excessive. The constant in these cases is asthenic syndrome, against the background of which various neurosis- and psychopathic changes and the personality’s reaction to the disease can develop. The personality characteristics of the patient in this group of disorders play a more significant role; the characteristics of the toxic factor influence the wedge, the picture, only in some cases (for example, uncontrolled laughter and crying, impulsive affective reactions in case of manganese poisoning).
A. V. Snezhnevsky (1940) noted that the specificity of symptomatic psychoses, including intoxication psychoses, is determined not by the characteristics of this or that psychopathol syndrome, but by the patterns of change in these syndromes. This position was further developed in the doctrine of transitional Vic syndromes (see Symptomatic psychoses). These syndromes may be the result of partial restoration of the functions of c. n. pp., with which mental disorders are revealed, previously masked by its more severe disorders. Thus, after the patient’s symptoms of a coma have disappeared, disturbances in memory functions that have not yet been restored may be detected, for example, in the form of Korsakov’s syndrome. Smoothing out memory impairments can lead to the identification of asthenic syndrome, which the patient had before, but was covered by severe mnestic disorders. Such dynamics were described by Wieck (HH Wieck, 1956), for example, in barbiturate poisoning. The search for specific patterns of changes in syndromes is promising, but for many I. p. such a pattern has not been established.
The course of I. p. is different. Mental disorders can develop both directly after a single action of the poison, and during chronic exposure to it - months and years from the onset of intoxication. Acute poisoning usually leads to psychosis, mainly in the form of various syndromes of clouded consciousness and convulsive seizures, which, if death does not occur, completely disappear or are smoothed out within a short time. With the gradual disappearance of mental disorders, transitional syndromes are observed, when more severe and profound disorders are replaced by lighter ones (from coma to borderline mental disorders). Long-term action of poisons can lead to prolonged and chronic. I. p., in which a change of syndromes can also be observed, but in the reverse order - from mild mental disorders to more complex psychopathol. syndromes, and then to stupefaction up to coma. Cessation of the action of toxic substances in this case usually leads to a complete or partial reduction of symptoms, the edges can be both rapid (most phenamine psychoses) and extended over long periods (mercury, lead poisoning). Reduction of symptoms in both chronic and acute I. p. is manifested by a mitigation of the severity of disorders within one syndrome and a change in the syndromes themselves - from deeper to milder disorders. The occurrence of I. p. in response to the cessation of the action of the poison (withdrawal delirium or convulsive seizures) is possible with substance abuse (see Drug addiction).
If the effect of the poison stops in the first hours or days after the onset of I. p., the psychosis stops quickly. If, despite the appearance of symptoms of I. i., the action of the toxic factor continues, I. p. even after the cessation of this action persists the longer, the longer the period of combination of the action of the poison with I. p. The progressive course is associated with the ongoing effect. poison, but in rare cases (poisoning with manganese, carbon monoxide) it is observed even after the rapid cessation of the action of the poison. Chronic psychoses (with intoxication with phenamine, alcohol) are also rare. The connection between such psychoses and the effects of poison is not always clear. Relapses of I. p., as a rule, occur only in connection with repeated exposure to a toxic factor. In a number of patients, after the end of psychosis, increased sensitivity to the substance that caused it remains for some time. In these cases, relapse may occur with repeated exposure to a small dose of this substance (for example, after the end of atropine delirium, the administration of a therapeutic dose of atropine can cause recurrent delirium). I.P. usually end with complete recovery, but partial improvement is also possible with the formation of residual disorders (dementia, parkinsonism, personality psychopathization, etc.).
Drugs to treat psychosis
Medications for the treatment of psychosis are selected individually. There is no one-size-fits-all cure for psychosis. Drugs can act on the cause of psychosis, for example carbamazepine for epileptic psychosis. Or on the mechanism of development of psychosis, this is how neuroleptics, mood stabilizers, and tranquilizers work. The most effective group of drugs are antipsychotics (more about them HERE).
In addition to antipsychotics, other groups of drugs are also used: tranquilizers, mood stabilizers and lithium preparations, antidepressants (for depressive psychosis), neurometabolic and restorative therapy. To quickly achieve an effect, the drugs are administered intravenously at the beginning of treatment. Conventional sedatives are not effective in treating psychosis.
Etiology and pathogenesis
The etiology of IP can be considered known, since a connection between mental disorders and the effect of a toxic substance has been established. Difference chem. structure and mechanisms of action of substances capable of causing I. p., the multicomponent action of a number of such substances determines the complexity and heterogeneity of the pathogenesis of I. p. This, however, does not exclude the presence of some common links in pathogenesis, for example, Selye’s general adaptation syndrome (see Adaptation syndrome ), which is a reaction to any harmful effect on the body. Another common mechanism is the mechanism of protiregulation - an increase in the potential activity of systems whose activity is suppressed by a toxic agent. This mechanism underlies withdrawal psychoses and, possibly, some I. p. that occur against the background of long-term use of standard dosages of the drug. K. Bongeffer (1910) put forward the concept of a common “intermediate link” that determines the wedge, the similarity of IP caused by different substances, but it is more accurate to talk about the general final effect of various toxic substances. Thus, brain hypoxia, which apparently plays an important role in the genesis of IP, may be a consequence of insufficient blood flow to the brain, insufficient oxygen saturation, and impaired oxygen utilization by nerve cells; Moreover, each of the disorders can be caused by different mechanisms. Although the end effect of these diverse disorders may be similar (eg, hypoxia), the means of eliminating it must be different.
Intoxication psychoses are the result of the interaction of an exogenous factor with the body. An important role is played by the dose of a toxic substance, the duration and rate of its intake, and the characteristics of its metabolism. Massive doses, especially at a rapid rate of action, are toxic for almost any healthy person (with the exception of addiction to narcotic and toxic substances) and lead to general disorganization of the activity of the c. n. pp., expressed in nonspecific reactions (coma, stunning). When exposed to smaller, but toxic doses, the selectivity of the action of various substances on certain systems is manifested and the role of the characteristics of the organism increases. These characteristics (age, gender, nutrition, the presence of somatic diseases, constitutional features) change the reaction to the action of the poison. Part of intoxication psychoses is a manifestation of allergies (see).
Prevention
Prevention varies depending on which group the toxic substance that caused psychosis belongs to (industrial poisons, drugs, etc.).
Bibliography:
Avrutsky G. Ya., Gurovich I. Ya. and Gromova V. V. Pharmacotherapy of mental illnesses, M., 1974; Goldenberg M. A. Mental disorders in acute infections and intoxications, Kharkov, 1941; Experience of Soviet medicine in the Great Patriotic War of 1941-1945, vol. 26, p. 237, M., 1949; Ravkin I. G. Mental disorders in tetraethyl lead poisoning (TEP), in the book: Neuropsychic disorders in tetraethyl lead poisoning (TEP), ed. F. X. Chekhlaty and S. M. Genkin, p. 5, M., 1948; Stolyarov G.V. Drug psychoses and psychotomimetic drugs, M., 1964; Emotions, ed. by L. Levi, p. 677, NY 1975; Granville-Grossman K. Recent advances in clinical psychiatry, L., 1971; Psychiatric complications of medical drugs, ed. by R.I. Shder, NY, 1972.
G. V. Stolyarov.
