Causes and initial manifestations
The pathology develops against the background of severe somatic diseases, acute cerebrovascular accidents (stroke), febrile infections, acute poisoning (e.g., with anticholinergics), and as part of withdrawal syndrome in alcoholism or substance abuse.
The development of psychosis proceeds sequentially. In the prodromal period, there is increasing anxiety towards evening or night, persistent insomnia, and nightmares upon falling asleep.
In the fully developed stage, abundant scene-like true hallucinations (predominantly visual) come to the fore. The patient is completely disoriented in time and place, confused, and exhibits pronounced psychomotor agitation.
Severe forms of delirium
There are several variants of an extremely severe course of psychosis that require transferring the patient to the intensive care unit:
- Mussitant (muttering): productive contact is impossible. The patient is severely exhausted, blood pressure is lowered. Characterized by meaningless muttering and small, chaotic movements that do not extend beyond the bed (picking/fumbling).
- Hyperkinetic: extreme, chaotic motor agitation. Contact is completely lost. The condition is accompanied by arterial hypertension, pronounced hyperthermia, and impaired coordination of movements.
- Professional: deep clouding of consciousness in which the patient automatically performs actions habitual to their profession (mimicking work with tools, giving orders to imaginary "subordinates").
Principles of treatment and nursing care
Etiopathogenetic therapy is of decisive importance: elimination of intoxication, combating infection, normalization of blood circulation and acid-base balance, oxygen inhalation. Antioxidants, antibiotics, nootropics, specific antidotes, and extracorporeal methods (plasmapheresis) are used. For fluid retention against the background of massive infusions, furosemide is administered intravenously as a bolus.
Agitation that is dangerous to others and to the patient is managed with medications: diazepam, haloperidol, droperidol, or sodium oxybutyrate. Caution: sedatives can sharply lower blood pressure and depress respiration.
Features of sedation and care: One should not strive to completely suppress productive symptoms in the first days—excessive sedation will put the patient into drug-induced sleep, which will prolong the course of psychosis. Maximum doses of drugs are given in the evening, taking into account the nocturnal escalation of symptoms. During the day, care is critically important for the prevention of pressure sores and hypostatic pneumonia: the patient needs to be turned, propped up, given drinks, and, whenever possible, helped to stand.
Complications in alcoholism: Wernicke's encephalopathy
Severe alcohol delirium can mark the onset of Wernicke's encephalopathy. Precursors include symptoms of general exhaustion and severe polyneuropathy occurring even before the development of psychosis. With a critical deterioration, typical delirious agitation is replaced by passivity and stereotyped movements in bed, and consciousness rapidly declines to amence or coma.
Gross disorders join:
- Neurological: oculomotor disorders (nystagmus, ptosis, diplopia, inability to converge), pathological pupillary reactions (miosis, anisocoria), cerebellar ataxia, hyperkinesias (choreiform, athetoid), nuchal rigidity, seizures, and paraparesis.
- Somatic: drug-resistant hyperthermia, tachycardia, drop in blood pressure. The skin acquires an earthy hue with petechiae, and pressure sores form rapidly. The tongue becomes dry with a dark coating, and breathing becomes rapid.
Mortality from this complication is extremely high (40-50%). The majority of survivors retain severe organic consequences: Korsakoff's syndrome, pronounced dementia, or gross personality changes.
Forms of severe delirium can be remembered by the acronym MGP: Mussitant (muttering quietly in bed), Hyperkinetic (tossing about chaotically with blood pressure changes), Professional (imitating working movements).
Class and exam questions
Is it necessary to completely suppress hallucinations and delusions in the first days of psychosis?
No, they should not. Excessive doses of sedatives cause drug-induced sleep, which prolongs psychosis and hinders normal recovery of brain function.
What is the main danger of using psychopharmacotherapy in delirium?
Sedatives used to relieve agitation can depress the respiratory center and cause a sharp, life-threatening drop in blood pressure.
What clinical signs indicate the transition of delirium into Wernicke's encephalopathy?
The replacement of motor agitation with passivity, depression of consciousness to coma, the appearance of oculomotor disorders (ptosis, nystagmus), pupil pathologies, hyperthermia, and hemodynamic instability.
What else to study on this topic
- Mechanisms of hyperthermia development in severe forms of exogenous psychoses
- Features of the differential diagnosis of delirium and twilight clouding of consciousness
- Specific antidotes in anticholinergic delirium
- Tactics of infusion therapy management and diuresis control in elderly patients
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Other topics in "Chapter 19. Organic, Exogenous, and Somatogenic Mental Disorders"
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