We describe a young patient diagnosed with postpartum psychosis, and managed with antipsychotics. She presented with hyponatremia after an episode of gastroenteritis. Further probing revealed a history of amenorrhea after the delivery. Workup showed panhypopituitarism. This treatable cause can mimic postpartum psychosis.
Keywords: Panhypopituitarism, postpartum psychosis, Sheehan's syndrome
| Introduction|| |
Postpartum psychosis can be seen in 1 in 500 postpartum women. Rarely, an organic cause like hypopituitatism can mimic this presentation and needs to be diagnosed early for successful management.
| Case Report|| |
A 31-year-old woman Mrs. X presented to the emergency medicine department, with a 3-day history of severe acute gastroenteritis and 1 day of altered sensorium. On admission, she was hypotensive and hypoglycemic, and laboratories revealed hyponatremia with a serum sodium of 119 meq/l (normal 136–145 meq/L). She was stabilized with intravenous (IV) fluids and inotropic supports and shifted to the medical intensive therapy unit.
One year ago, Mrs. X had a full-term pregnancy that resulted in a stillbirth after which she had developed behavioral changes in the form of anger outbursts, decreased social interaction, and occasional hallucinations. Two months after the onset of these symptoms, she consulted a psychiatrist. Investigations done at the time were a completed blood count, renal function tests, liver function tests, thyroid-stimulating hormone (TSH), and an ultrasound abdomen. All the reports were normal except for serum sodium being 130 meq/L. She was diagnosed to have postpartum psychosis and depression due to loss of her baby. She received varying doses of amitriptyline, olanzapine, alprazolam, and aripiprazole over 1 year. She had been hospitalized elsewhere with a diagnosis of neuroleptic malignant syndrome 2 months before the current admission after which all her psychiatric medications were discontinued.
During her stay in our hospital, Mrs. X's gastroenteritis resolved and her BP normalized. Her sensorium improved, but she remained agitated and fearful. She kept repeating the phrase “I have made mistakes” and refused to interact with her attenders. A psychiatry consult was sought in view of her past medical history, and risperidone was started. As the hyponatremia persisted (serum sodium – 129 meq/l) despite resolution of the gastrointestinal loss, an alternate diagnosis was looked for. A detailed history revealed secondary amenorrhea after the stillbirth, and a provisional diagnosis of secondary adrenal insufficiency was made. Random cortisol sent at admission was 6.38 mcg/dL, which was low in the context of her hypotension and stress. As the patient had received steroids in the emergency department, a repeat morning cortisol was not sent. Her hormonal profile showed a normal TSH of 2.72 mIU/l (normal 0.35–4.94 mIU/l) and low Free T4 of 0.28 ng/dl (normal 0.7–1.48 ng/dl) suggestive of central hypothyroidism. The estradiol level was <5 pg/ml and luteinizing hormone and FSH were 8.36 IU/l and 13.06 IU/I, respectively. A magnetic resonance imaging brain showed a partial empty sella [Figure 1].
|Figure 1: Magnetic resonance imaging brain sagittal section showing empty sella|
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A diagnosis of panhypopituitarism was made, and the patient was started on IV hydrocortisone which was later changed to an oral replacement dose of 20 mg per day. Risperidone was discontinued, and she was discharged as her symptoms resolved and sodium levels were maintained in the normal range. Mrs. X has been on follow-up for the last 1 year and is doing well. Her family reports that she is cheerful and has no further hallucinations or abnormal behavior.
| Discussion|| |
Secondary empty sella is known to occur after inflammatory, ischemic, hemorrhagic, granulomatous, or autoimmune processes. This comprises <10% of the causes of hypopituitarism. The enlargement of the pituitary gland during pregnancy makes it vulnerable to a spectrum of disorders, which can lead to hypopituitarism. This includes Sheehan's syndrome, lymphocytic hypophysitis, and rarely, apoplexy of pituitary adenomas. The most common of these, Sheehan's syndrome is due to the hemorrhagic infarction of the enlarged pituitary gland due to blood loss at the time of delivery. Low prolactin with failure to lactate is a common feature of this condition. Other clinical manifestations may be due to thyroid, adrenal, gonadal, or growth hormone deficiencies. The differential diagnosis of lymphocytic hypophysitis may be associated with pituitary enlargement in the immediate postpartum period, but the natural history may be similar to Sheehan's syndrome presenting with empty sella and hypopituitarism. Other clues to the diagnosis of lymphocytic hypophysitis include hyperprolactinemia in 40% of the cases and the presence of other autoimmune diseases as opposed to low baseline prolactin and a history of postpartum hemorrhage in Sheehan's syndrome. Our patient did not have a definite history of postpartum hemorrhage, and unfortunately, a serum prolactin was not measured, so the exact cause for her panhypopituitarism could not be ascertained. Our patient was diagnosed with postpartum psychosis and treated with antipsychotic medication. There are few reports of psychoses as a presenting feature of panhypopituitarism.,,, The pathophysiological basis of psychosis in hypopituitarism is not well understood. There have been postulations of the interaction between pituitary hormones and neurotransmitters.
It is important for psychiatrists and internists to be aware of this uncommon presentation, especially in women. A careful history and appropriate investigations can reveal this imminently treatable cause of mental health disorders.
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Conflicts of interest
There are no conflicts of interest.
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Department of Medicine, St. John's Medical College and Hospital, Bengaluru - 560 034, Karnataka
Source of Support: None, Conflict of Interest: None