HOW TO TREAT ACUTE AND TRANSIENT PSYCHOTIC DISORDER 2025

HOW TO TREAT ACUTE AND TRANSIENT PSYCHOTIC DISORDER 2025

GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF COMMON MENTAL DISORDERS

(Enacted under Decision No. 2058/QĐ-BYT dated May 14, 2020, by the Minister of Health)

Article 16

ACUTE AND TRANSIENT PSYCHOTIC DISORDER

CHIEF EDITOR

Associate Professor, PhD Nguyễn Trường Sơn

CO-EDITOR

Associate Professor, PhD Lương Ngọc Khuê

PhD Nguyễn Doãn Phương

CONTRIBUTING AUTHORS

PhD Trần Thị Hà An

MSc Trịnh Thị Vân Anh

PhD Vũ Thy Cầm

MSc Trần Mạnh Cường

PhD Nguyễn Văn Dũng

PhD Vương Ánh Dương

PhD Lê Thị Thu Hà

MSc Trần Thị Thu Hà

MSc Phạm Công Huân

MSc Đoàn Thị Huệ

Specialist Doctor II Nguyễn Thị Minh Hương

MSc Vũ Thị Lan

1. Nguyễn Phương Linh

Specialist Doctor II Nguyễn Thị Phương Loan

MSc Bùi Văn Lợi

MSc Nguyễn Thị Phương Mai

PhD Trần Nguyễn Ngọc

MSc Bùi Nguyễn Hồng Bảo Ngọc

MSc Trương Lê Vân Ngọc

MSc Bùi Văn San

PhD Dương Minh Tâm

MSc Phạm Xuân Thắng

MSc Lê Thị Phương Thảo

MSc Lê Công Thiện

MSc Vương Đình Thủy

Associate Professor, PhD Nguyễn Văn Tuấn

Specialist Doctor II Ngô Văn Tuất

MSc Đặng Thanh Tùng

MSc Vũ Sơn Tùng

MSc Cao Thị Ánh Tuyết

MSc Nguyễn Thị Ái Vân

Specialist Doctor II Hồ Thu Yến

MSc Nguyễn Hoàng Yến

CONTRIBUTORS TO EVALUATION AND FEEDBACK

Associate Professor, PhD Nguyễn Thanh Bình

PhD Vũ Thy Cầm

PhD Nguyễn Hữu Chiến

Specialist Doctor II Võ Thành Đông

PhD Lê Thị Thu Hà

Specialist Doctor II Đỗ Huy Hùng

PhD Nguyễn Mạnh Hùng

MSc Nguyễn Trọng Khoa

Specialist Doctor II Ngô Hùng Lâm

Associate Professor, PhD Phạm Văn Mạnh

Specialist Doctor II Trần Ngọc Nhân

PhD Dương Minh Tâm

MSc Đặng Duy Thanh

PhD Vương Văn Tịnh

Specialist Doctor II Lâm Tứ Trung

PhD Lại Đức Trường

PhD Cao Văn Tuân

Associate Professor, PhD Nguyễn Văn Tuấn

SECRETARIAT TEAM

MSc Đặng Thanh Tùng

MSc Trương Lê Vân Ngọc

BA Đỗ Thị Thư

Article 16

ACUTE AND TRANSIENT PSYCHOTIC DISORDER

I. DEFINITION  

Acute and transient psychotic disorder involves a rapid shift from a non-psychotic state to a clearly psychotic state within two weeks or less, with or without associated stress. Recovery is typically complete within 2-3 months, often within weeks or days, with only a small proportion of cases persisting or resulting in lasting impairment.

II. ETIOLOGY  

1. Family Factors: Studies indicate 20-33% of patients have a family history of psychiatric disorders, such as schizophrenia, mood disorders (depression, bipolar disorder), or acute psychotic disorders.  
2. Psychological Trauma (Stress):Approximately 20-30% of cases are linked to stressors like bereavement, financial loss, marital breakdown, or romantic rejection.  
3. Personality Traits: Pre-existing abnormal personality traits may contribute, including sensitivity, vulnerability, or schizoid features (introversion, aloofness, limited relationships).

III. DIAGNOSIS  

1. Diagnostic Criteria (ICD-10)  

– Acute onset of psychosis within 2 weeks, lasting up to 1 month.  

– Clinical features include psychotic symptoms (delusions, hallucinations), emotional and behavioral disturbances, and impaired social/occupational functioning.  

– If mood disturbances occur during the psychotic phase, they do not meet criteria for mania or depression.  

– No evidence of organic disease, alcohol, or drug use causally linked to the condition in the patient’s history.

2. Clinical Subtypes (ICD-10)  

– Acute Polymorphic Psychotic Disorder Without Schizophrenic Symptoms (F23.0):  

  – Acute onset within 2 weeks or less.  

  – Rapidly changing delusions and hallucinations, varying in content and intensity, sometimes within a day. Mood swings align with psychotic symptoms.  

  – Does not meet criteria for schizophrenia or mood disorders.  

– Acute Polymorphic Psychotic Disorder With Schizophrenic Symptoms (F23.1):  

  – Acute onset within 2 weeks or less.  

  – Delusions and hallucinations fluctuate daily in content and intensity, with mood changes tied to psychosis.  

  – Meets symptomatic criteria for schizophrenia.  

– Acute Schizophrenia-Like Psychotic Disorder (F23.2):  

  – Acute onset within 2 weeks or less.  

  – Relatively stable psychotic symptoms (delusions, hallucinations) meeting schizophrenia criteria.  

  – Does not fit polymorphic psychotic disorder criteria.  

– Other Acute Predominantly Delusional Psychotic Disorder (F23.3):  

  – Acute onset within 2 weeks or less.  

  – Relatively persistent delusions.  

  – Does not meet criteria for schizophrenia or polymorphic psychotic disorders.  

– Other Acute and Transient Psychotic Disorders (F23.8): For cases not fitting above subtypes.  

– Unspecified Acute and Transient Psychotic Disorder (F23.9): Includes unspecified brief reactive psychosis.

3. Differential Diagnosis  

– Organic Psychosis: Caused by brain-related or systemic conditions affecting brain function. Symptoms resemble schizophrenia but lack full criteria. Neurological and lab findings indicate organic pathology.  

– Substance-Induced Psychosis (Alcohol, Cocaine, Amphetamines): Psychosis (hallucinations, delusions) during or post-substance use, or withdrawal. History and exams link symptoms to substance use; lab tests confirm intoxication or drug presence.  

– Schizophrenia: Gradual onset over months, with persistent delusions (e.g., control, intrusion, bizarre content), minimal content change, and possible negative symptoms or Schneiderian first-rank symptoms lasting over a month.  

– Persistent Delusional Disorder: Systematized delusions lasting at least 3 months.  

– Mood Disorders: Distinct from psychotic features unless mood symptoms predominate.

4. Ancillary Testing  

4.1. Basic Labs  

– Blood: Hematology, biochemistry, microbiology (HIV, HBV, HCV).  

– Urine: General analysis, drug screening, syphilis serology.  

4.2. Imaging/Functional Tests  

– Chest X-ray, abdominal ultrasound.  

– EEG, ECG, cerebral blood flow, transcranial Doppler.  

– CT/MRI brain (select cases).  

4.3. Psychological Assessments  

– PANSS (Positive and Negative Symptom Scale).  

– Personality: EPI, MMPI.  

– Others: BDI, Zung, HDRS, HARS, HAD, MMSE.

IV. TREATMENT  

1. Treatment Principles  

– Multiple etiologies, emphasizing biological and psychosocial factors. Treatment focuses on pharmacotherapy and psychotherapy.  

– Pharmacotherapy is critical for positive symptoms; combine with psychotherapy, occupational therapy, and social reintegration, especially for negative symptoms.  

– Start with monotherapy; if response is poor, combine two antipsychotics, avoiding three or more to limit side effects.  

– Monitor drug use closely to detect and manage antipsychotic side effects promptly.  

– Educate families/communities to reduce stigma and foster collaboration with healthcare providers.  

– Identify and address relapse triggers; maintain treatment post-first episode with community monitoring.

2. Treatment Framework  

– Pharmacotherapy alongside psychotherapy and community rehabilitation.

3. Specific Treatments  

3.1. Pharmacotherapy  

– Antipsychotics: 1-3 agents (prefer monotherapy; switch or combine up to 3 if ineffective):  

  – Typical:  

    – Chlorpromazine (25 mg tabs/vials; 50-250 mg/24h).  

    – Levomepromazine (25 mg tabs; 25-250 mg/24h).  

    – Haloperidol (1.5-5 mg tabs, 5 mg vials; 5-30 mg/24h).  

    – Thioridazine (50 mg tabs; 100-300 mg/day).  

  – Atypical:  

    – Amisulpride (50-400 mg tabs; 200-800 mg/24h).  

    – Clozapine (25-100 mg tabs; 50-800 mg/24h).  

    – Risperidone (1-2 mg tabs; 1-12 mg/24h).  

    – Olanzapine (5-10 mg tabs; 5-60 mg/24h).  

    – Quetiapine (50-300 mg tabs; 600-800 mg/day).  

    – Aripiprazole (5-30 mg tabs; 10-30 mg/day).  

  – Doses may increase based on condition and response.  

– Long-Acting Injectables (LAIs): For non-compliant patients; test short-acting equivalents first:  

  – Haldol Decanoate (50 mg/ml IM; 25-50 mg every 4 weeks).  

  – Flupentixol Decanoate (20 mg/ml IM; 20-40 mg every 2-4 weeks).  

  – Fluphenazine Decanoate (25 mg/ml IM; 12.5-50 mg, max 100 mg/day, every 3-4 weeks).  

  – Aripiprazole (300-400 mg IM every 4 weeks).  

– Adjunctive Treatments:  

  – Anxiolytics: Benzodiazepines (diazepam, lorazepam, bromazepam, alprazolam), non-benzodiazepines (etifoxine, zopiclone).  

  – Beta-Blockers: Propranolol.  

  – Antidepressants: SSRIs, TCAs, SNRIs, NaSSAs.  

  – Mood Stabilizers: Valproate, divalproex, carbamazepine, oxcarbazepine.  

  – Neuroprotection: Piracetam, ginkgo biloba, vinpocetine, choline alfoscerate, nicergoline.  

  – Nutrition: Vitamins (B-group), minerals, IV feeding if needed.  

  – Hepatic support, cognitive enhancers.  

– Monitoring:  

  – Side Effects:  

    – Extrapyramidal symptoms: Cholinesterase inhibitors (trihexyphenidyl, benztropine), beta-blockers, sedatives.  

    – Neuroleptic malignant syndrome: Early detection, ICU management.  

    – Metabolic disorders: Monitor BMI, blood tests every 3-6 months.  

    – Clozapine: White blood cell count every 3 months.  

    – Tardive dyskinesia: Muscle relaxants, sedatives, vitamin E, anticholinergics.

3.2. Electroconvulsive Therapy (ECT) and Transcranial Magnetic Stimulation (TMS)  

– ECT: Effective for catatonia, suicidal behavior driven by delusions/hallucinations, or agitation unresponsive to drugs.  

– TMS: Useful for persistent auditory hallucinations.

3.3. Psychotherapy  

– Individual, family, or group therapy to build a supportive clinician-patient-family relationship, aiding psychological recovery. Individual therapy enhances illness insight; family therapy stabilizes family dynamics.

3.4. Occupational and Rehabilitation Therapy  

– Start activities at the patient’s capability level to rebuild confidence, gradually increasing intensity without causing stress.  

– Tailor vocational rehabilitation to socio-economic-cultural context.

3.5. Physical Therapy and Community Management  

– Ongoing monitoring and treatment in the community.

V. PROGNOSIS AND COMPLICATIONS  

– Favorable Prognosis:  

  – Adaptive premorbid personality.  

  – External triggers present.  

  – Minimal genetic loading.  

– Less Favorable Prognosis:  

  – Onset in youth.  

  – Pre-illness introversion/isolation.  

  – No external triggers.  

  – Strong genetic loading.  

– Most recover fully without personality changes, but a minority may progress to schizophrenia, persistent delusional disorder, or mood disorders.

VI. PREVENTION  

– Exact cause unknown, so prevention focuses on:  

  – Fostering independence and adaptability to life’s challenges.  

  – Reducing stress through sharing and coping strategies.  

  – Monitoring individuals with a family history of schizophrenia or related disorders for early detection and treatment.  

  – Post-discharge follow-up, sustained specialist treatment, avoiding overexertion/stress, and proactive management of physical illnesses to prevent relapse.

REFERENCES

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