Browse

You are looking at 1 - 2 of 2 items for :

Clear All
Open access

Ilan Rahmani Tzvi-Ran, Judith Olchowski, Merav Fraenkel, Asher Bashiri and Leonid Barski

Summary

A previously healthy 24-year-old female underwent an emergent caesarean section without a major bleeding described. During the first post-operative days (POD) she complained of fatigue, headache and a failure to lactate with no specific and conclusive findings on head CT. On the following days, fever rose with a suspicion of an obstetric surgery-related infection, again with no evidence to support the diagnosis. On POD5 a new-onset hyponatremia was documented. The urine analysis suggested SIADH, and following a treatment failure, further investigation was performed and demonstrated both central hypothyroidism and adrenal insufficiency. The patient was immediately treated with hydrocortisone followed by levothyroxine with a rapid resolution of symptoms and hyponatremia. Further laboratory investigation demonstrated anterior hypopituitarism. The main differential diagnosis was Sheehan’s syndrome vs lymphocytic hypophysitis. Brain MRI was performed as soon as it was available and findings consistent with Sheehan’s syndrome confirmed the diagnosis. Lifelong hormonal replacement therapy was initiated. Further complaints on polyuria and polydipsia have led to a water deprivation testing and the diagnosis of partial central insipidus and appropriate treatment with DDAVP.

Learning points:

  • Sheehan’s syndrome can occur, though rarely, without an obvious major post-partum hemorrhage.

  • The syndrome may resemble lymphocytic hypophysitis clinically and imaging studies may be crucial in order to differentiate both conditions.

  • Hypopituitarism presentation may be variable and depends on the specific hormone deficit.

  • Euvolemic hyponatremia workup must include thyroid function test and 08:00 AM cortisol levels.

Open access

Victoria John, Philip Evans and Atul Kalhan

Summary

A 65-year-old woman was admitted to the emergency unit with a 48 h history of generalised weakness and confusion. On examination, she had mild slurring of speech although there was no other focal neurological deficit. She had profound hyponatraemia (serum sodium level of 100 mmol/L) on admission with the rest of her metabolic parameters being within normal range. Subsequent investigations confirmed the diagnosis of small-cell lung cancer with paraneoplastic syndrome of inappropriate antidiuresis (SIAD). She was monitored closely in high-dependency unit with an attempt to cautiously correct her hyponatraemia to prevent sequelae associated with rapid correction. The patient developed prolonged psychosis (lasting over 2 weeks) and displayed delayed dyskinetic movements, even after a gradual increase in serum sodium levels close to 130 mmol/L. To our knowledge, delayed neurological recovery from profound hyponatraemia (without long-term neurological sequelae) has previously not been reported. This case should alert a clinician regarding the possibility of prolonged although reversible psychosis and dyskinetic movements in a patient presenting with profound symptomatic hyponatraemia.

Learning points:

  • Patients with profound hyponatraemia may develop altered sensorium, dyskinesia and psychotic behaviour.

  • Full recovery from psychotic symptoms and dyskinesia may be delayed despite cautious correction of serum sodium levels.

  • Careful and close monitoring of such patients can help avoid long-term neurological sequelae.