Stepped care targeting psychological distress in head and neck cancer and lung cancer patients: a randomized, controlled trial.

BACKGROUND: This study aimed to evaluate the efficacy of stepped care (SC) targeting psychological distress in head and neck cancer (HNC) and lung cancer (LC) patients. PATIENTS AND METHODS: Patients with untreated distress [Hospital Anxiety and Depression Scale (HADS; HADS-D > 7, HADS-A > 7, or HADS-total > 14)] were randomized to SC (n = 75) or care-as-usual (CAU) (n = 81). SC consisted of watchful waiting, guided self-help, problem-solving therapy, and psychotherapy and/or psychotropic medication. The primary outcome measure was the HADS; secondary outcome measures were recovery rate, EORTC QLQ-C30, QLQ-HN35/QLQ-LC13, and IN-PATSAT32. Measures were assessed at baseline, after completion of care, and at 3, 6, 9, and 12 months follow-up. Linear mixed models, t-tests, and effect sizes (ES) were used to assess group differences. RESULTS: Patients with untreated distress were randomized to SC (n = 75) or care-as-usual (CAU) (n = 81). The course of psychological distress was better after SC compared with CAU (HADS-total, P = 0.005; HADS-A, P = 0.046; HADS-D, P = 0.007). The SC group scored better post-treatment (HADS-total, ES = 0.56; HADS-A, ES = 0.38; HADS-D, ES = 0.64) and at 9 months follow-up (HADS-total, ES = 0.42 and HADS-A, ES = 0.40). The recovery rate post-treatment was 55% after SC compared with 29% after CAU (P = 0.002), and 46% and 37% at 12 months follow-up (P = 0.35). Within SC, 28% recovered after watchful waiting, 34% after guided self-help, 9% after problem-solving therapy, and 17% after psychotherapy and/or psychotropic medication. The effect of SC was stronger for patients with a depressive or anxiety disorder compared with patients without such a disorder (HADS-total, P = 0.001; HADS-A, P = 0.003; HADS-D, P = 0.041). CONCLUSIONS: SC is effective and speeds up recovery among HNC and LC patients with untreated psychological distress. TRIAL REGISTRATION: Netherlands Trial Register (NTR1868).

[The syndrome of inappropriate antidiuretic hormone secretion (SIADH) during treatment with the antipsychotic agents haloperidol and quetiapine]. / Het syndroom van inadequate secretie van antidiuretisch hormoon (SIADH) tijdens het gebruik van de antipsychotica haloperidol en quetiapine.

A 45-year-old man with paranoid schizophrenia repeatedly developed hyponatraemia due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH), both after treatment with haloperidol and after taking quetiapine. This side effect did not occur subsequently during clozapine treatment. SIADH has been described in connection with almost all psychotropic drugs. Since the risk of developing SIADH is increased with increasing age, comorbid somatic disorders and polypharmacy, and the mean age of the psychiatric patient will further increase in the years to come, the physician should be alert to the risk factors and the clinical symptoms of disturbances in water balance; moreover, the proper differential diagnostic deliberations should be made. In case of increased risk, it is recommended to monitor the serum sodium during the first 2-4 weeks of pharmacotherapy.

[Sudden death following a single oral administration of haloperidol]. / Plotseling overlijden na eenmalige orale toediening van haloperidol.

A 39-year-old man was admitted with myasthenia, alcoholic hepatitis and electrolyte abnormalities due to an inadequate nutritional state. On admission the ECG showed a prolonged QTc interval (0.46 s). The patient was treated with intravenous fluid and supplementary vitamins and minerals. On the third day of admission the patient developed a delirium, partly due to alcohol withdrawal, and was therefore treated with oxazepam 50 mg 3 times daily and a single dose of haloperidol 5 mg. One hour after ingesting haloperidol, the patient suddenly succumbed and resuscitation was not successful. The autopsy revealed a cardiomyopathy but no explanation for the sudden death. Due to the temporal relationship between the ingestion of haloperidol and this sudden death, we assume that haloperidol induced a fatal arrhythmia in the presence of a preexisting prolonged repolarisation time. To the best of our knowledge, sudden death after a single oral therapeutic dose of haloperidol has not previously been described.