Hyperthyroidism affects 0.8-1.3% of the adult population (1-2). Psychosis is a rare manifestation of hyperthyroidism, estimated to occur in 1% of cases (3).
A 35-year-old female working on a cruise ship presented with a 2-week history of lethargy, emotional lability and feelings of persecution. She had a background of Graves’ disease treated with radioactive iodine ablation 12 months prior and subsequent propylthiouracil 200mg TDS, albeit with medication non-adherence. Examination aboard ship demonstrated tachycardia and investigations showed marked hyperthyroidism with TSH <0.02 mIU/L (0.4-4.8 mIU/L), fT4 49.9 pmol/L (8-16 pmol/L) and fT3 21 pmol/L (4-6 pmol/L). Given concern for thyroid storm, treatment was intensified to propylthiouracil 200mg QID, atenolol 50mg BD and IV hydrocortisone 100mg Q8hr. She was transferred to a shore-based hospital where investigations were consistent with hyperthyroidism secondary to a flare of Graves’ disease (TRAb 19.0 IU/L [(<1.8 IU/L], TSH <0.02 mIU/L, fT4 34.6 pmol/L, fT3 7.1 pmol/L). She was treated with propylthiouracil 150mg TDS and propranolol 20mg BD, with doses titrated as thyrotoxicosis resolved.
Psychiatric review demonstrated incongruent fatuous affect, thought blocking and auditory hallucinations. CT and MRI Brain did not identify a structural cause, and limbic encephalitis panel was negative. Neurological examination was normal. Quetiapine 100mg BD was commenced after hours, but discontinued next working day following Psychiatric Consultant review as it was not expected to assist with hyperthyroidism-induced psychosis . Her mental state progressively improved with normalisation of thyroid function, albeit with a several day lag. By day 10, mental state examination and bedside cognitive testing had normalised. On discharge, her thyroid function was normal (fT4 8.4 pmol/L, fT3 3.4 pmol/L), on propylthiouracil 100mg BD.
This case highlights the diagnostic and management challenge of psychosis in the setting of hyperthyroidism. Resolution of psychosis secondary to hyperthyroidism may lag the biochemical normalisation of thyroid function (4).