scholarly journals A rare cause of postpartum acute hyponatremia

2019 ◽  
Vol 2019 ◽  
Author(s):  
Ilan Rahmani Tzvi-Ran ◽  
Judith Olchowski ◽  
Merav Fraenkel ◽  
Asher Bashiri ◽  
Leonid Barski
Keyword(s):  
Urine Analysis ◽  
Post Partum ◽  
Brain Mri ◽  
Thyroid Function Test ◽  
Lymphocytic Hypophysitis ◽  
List Type ◽  
Sheehan’S Syndrome ◽  
Central Hypothyroidism ◽  
Sheehan's Syndrome ◽  
Acute Hyponatremia

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.

scholarly journals Reversible cardiomyopathy as a rare presentation of sheehan’s syndrome-case report and review of literature

2017 ◽  
Vol 4 (6) ◽  
pp. 1713 ◽  
Author(s):  
Mohmmad Hayat Bhat ◽  
Farhana Bagdadi ◽  
Asma Rafi ◽  
Parvaiz Ahmad Shah
Keyword(s):  
Pituitary Gland ◽  
Post Partum ◽  
Hormone Replacement ◽  
Poor Response ◽  
Sheehan’S Syndrome ◽  
Rare Presentation ◽  
Sheehan's Syndrome ◽  
Post Partum Period ◽  
Pressure Changes ◽  
High Degree

Sheehan’s syndrome is a clinical condition characterised by post-partum panhypopitutarism caused by necrosis of the pituitary gland. The hypervascularity of the pituitary gland during pregnancy makes it vulnerable to arterial pressure changes and prone to haemorrhage in the post-partum period. The cardinal features are lethargy, secondary amenorrhea and lactational failure. The diagnosis in immediate post-partum period is difficult and require a high degree of suspicion. Cardiac involvement in sheehan’s syndrome is known but rare.We hereby present a case of post-partum cardiomyopathy with relatively poor response to anti failure treatment. Patient however responded to hormone replacement including glucocorticoids and levothyroxine, after proper confirmation of the hypopituitary state. Cardiac dysfunction markedly reversed with the institution of replacement therapy.

scholarly journals MON-243 Atypical Presentation of Isolated Adrenocorticotropic Hormone Deficiency and Sheehan’s Syndrome

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Zahira Marie Lugo López ◽  
Nadyeschka Angelique Rivera Santana ◽  
Andrea del Toro Diez ◽  
Michelle Marie Mangual Garcia ◽  
Ernesto Sola Sanchez ◽  
...  
Keyword(s):  
Postpartum Hemorrhage ◽  
Adrenocorticotropic Hormone ◽  
Brain Mri ◽  
Pituitary Hormones ◽  
Hormone Deficiency ◽  
Normal Brain ◽  
Sheehan’S Syndrome ◽  
Isolated Acth Deficiency ◽  
Acth Deficiency ◽  
Sheehan's Syndrome

Abstract Introduction: Isolated adrenocorticotropic hormone (ACTH) deficiency is a rare pituitary hormone deficiency defined by secondary adrenal insufficiency and normal secretion of all other pituitary hormones. Patients present with fatigue, weakness, weight loss, anorexia, nausea, low cortisol levels and low ACTH levels. Isolated ACTH deficiency is more common in males and usually presents in the fifth decade of life. Main mechanisms involved in the pathogenesis are genetics and autoimmune causes, traumatic brain injury and infarction of the pituitary postpartum, known as Sheehan’s syndrome. Sheehan’s syndrome is characterized by postpartum hemorrhage, failure to lactate and menstrual irregularities and it can occur from immediate postpartum period to years after delivery. The most common hormone deficiencies are prolactin and growth hormone. Empty sella is the most common finding on brain MRI. We are reporting a case of a woman in her third decade with isolated ACTH deficiency due to Sheehan’s syndrome two years postpartum, able to lactate, with normal menses and normal brain MRI. Clinical Case: A 33-year-old woman G3P3A0 with hypothyroidism who was referred to Endocrinology clinics due to tiredness, fatigue and weakness. She reported postpartum hemorrhage requiring 4 PRBC transfusions and IV steroids after last pregnancy 5 years ago. Patient was able to lactate after pregnancy and continued in her usual state of health until 3 years ago when she referred loss of consciousness with traumatic head injury due to hypoglycemia. At Endocrinology office physical examination and vital signs were unremarkable, including no blood pressure or heart rate variations with positional changes. Despite hypothyroidism being adequately controlled, she continued with extreme fatigue and weakness affecting her quality of life, for which cortisol and ACTH levels were ordered. Laboratories showed normal electrolytes, negative autoantibodies, cortisol 0.20 μg/dL (5-25 μg/dL) and ACTH 22 pg/mL (10-60 pg/mL) suggesting partial isolated ACTH deficiency. ACTH stimulation test was done and noted with suboptimal response. Evaluation of other anterior pituitary hormones was normal. Brain MRI showed normal pituitary gland. She was started on hydrocortisone in AM and PM and symptoms resolved. Conclusion: Immediate recognition of isolated ACTH deficiency due to Sheehan’s syndrome is necessary due to the availability of effective treatment and morbidity and mortality associated with this serious condition. To our knowledge isolated ACTH deficiency due to Sheehan’s syndrome in which the patient was able to lactate and normal findings on brain MRI has not previously been reported.References: Shivaprasad C. Sheehan’s Syndrome: Newer advances. Indian J Endocrinol Metab. 2011 Sep; 15(3): S203-207. DOI:10.4103/2230-8210.84869.

scholarly journals Colonic pseudo-obstruction in a patient with Sheehan’s syndrome

2019 ◽  
Vol 12 (8) ◽  
pp. e228936
Author(s):  
Navneet Kaur ◽  
Ulrich Schubart ◽  
Adel Mandl
Keyword(s):  
Exploratory Laparotomy ◽  
Sigmoid Resection ◽  
Thyroid Stimulating Hormone ◽  
Primary Hypothyroidism ◽  
Thyroid Function Tests ◽  
Sheehan’S Syndrome ◽  
Central Hypothyroidism ◽  
End Colostomy ◽  
History Of ◽  
Sheehan's Syndrome

A 56-year-old woman with a history of hypothyroidism and chronic constipation presented with an acute abdomen due to colonic pseudo-obstruction. Thyroid function tests were consistent with central hypothyroidism prompting intravenous administration of stress-dose glucocorticoids and levothyroxine. The patient then underwent emergency exploratory laparotomy with sigmoid resection and end-colostomy. The postoperative endocrine evaluation revealed that the patient had panhypopituitarism due to Sheehan’s syndrome (SS). The diagnosis had been missed by physicians who had been treating her for several years for presumed primary hypothyroidism with a low dose of levothyroxine, aimed at normalising a minimally elevated thyroid-stimulating hormone (TSH) level. This is the second reported case of SS presenting with colonic pseudo-obstruction and it illustrates the potential danger of relying on measurement of TSH alone in the evaluation and treatment of thyroid dysfunction.

Acute Hyponatremia in Puerperium: Sheehan's Syndrome

2018 ◽  
Vol 131 (4) ◽  
pp. e147-e148
Author(s):  
Martin Windpessl ◽  
Andreas Karrer ◽  
Christoph Schwarz
Keyword(s):  
Sheehan’S Syndrome ◽  
Sheehan's Syndrome ◽  
Acute Hyponatremia

scholarly journals A Patient with Postpartum Hypopituitarism (Sheehan's Syndrome) Developed Postpartum Autoimmune Thyroiditis (Transient Thyrotoxicosis and Hypothyroidism): A Case Report and Review of the Literature

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Nobuyuki Takasu ◽  
Yoshirou Nakayama
Keyword(s):  
Autoimmune Thyroiditis ◽  
Post Partum ◽  
Empty Sella ◽  
Review Of The Literature ◽  
Sheehan’S Syndrome ◽  
Acth Deficiency ◽  
Regular Menses ◽  
Sheehan's Syndrome ◽  
Secondary Hypoadrenalism ◽  
Immunological Alterations

A 36-year-old woman with postpartum hypopituitarism (Sheehan's syndrome: SS) developed postpartum autoimmune thyroiditis (PPAT). She delivered a baby by Caesarean section (620 mL blood loss). At 1 month post partum, she developed thyrotoxicosis due to painless thyroiditis (autoimmune destructive thyroiditis). She was positive for antithyroid antibodies. Postpartum and hypoadrenalism-induced exacerbation of autoimmune thyroiditis caused the thyrotoxicosis due to autoimmune destructive thyroiditis. ACTH was undetectable. She had ACTH deficiency and secondary hypoadrenalism. Hydrocortisone was started. At 6 months post partum, she was referred to us with hypothyroidism. Thyroxine was administered. She had thyrotoxicosis at 1-2 months post partum and then hypothyroidism. She was diagnosed with PPAT. She had hypopituitarism, ACTH deficiency (secondary hypoadrenalism), low prolactin with agalactia, and low LH with failure to resume regular menses. She had empty sella on MRI. She was diagnosed with SS. Three cases with SS have been reported to develop PPAT. Postpartum immunological rebounds and hypoadrenalism-induced immunological alterations (or a combination of the two) might have been responsible for the PPAT.

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