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LBMON140 Central Diabetes Insipidus Manifesting After Vasopressin Withdrawal In A Critically Ill Patient
INTRODUCTION: Central diabetes insipidus is a rare clinical entity characterized by a lack of vasopressin secretion from the posterior pituitary. We present a case of central diabetes insipidus manifesting after the withdrawal of vasopressin in a critically ill patient. CASE PRESENTATION: A 19 year...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9707045/ http://dx.doi.org/10.1210/jendso/bvac150.976 |
Sumario: | INTRODUCTION: Central diabetes insipidus is a rare clinical entity characterized by a lack of vasopressin secretion from the posterior pituitary. We present a case of central diabetes insipidus manifesting after the withdrawal of vasopressin in a critically ill patient. CASE PRESENTATION: A 19 year old female with a history of Hodgkin's Lymphoma treated with chemotherapy was transferred from another medical facility while intubated and sedated for management of severe ARDS. She had undergone extensive infectious workup and the etiology was attributed to COVID-19 pneumonia and or bleomycin toxicity. She was started on Methylprednisolone for management of bleomycin toxicity and suspected organizing pneumonia. During her hospitalization, she developed septic shock for which she received broad spectrum antibiotics and pressor support. On day 12 of her hospitalization, vasopressin was discontinued and within 12 hours, there was a rise in serum sodium from 134 to 146 along with polyuria with dilute urine (daily urine output of ∼6-7 liters, urine osmolality decreased from 771 to 279 and urine specific gravity decreased from 1. 037 to 1. 026). No diuretics were administered and serum glucose was without excursions. With administration of 2 mcg DDAVP, urine osmolality increased by more than 50% from 279 to 497, serum sodium decreased from 146 to 141 and urine specific gravity increased from 1. 004 to 1. 026 confirming the diagnosis of central DI. CT head was negative. MRI brain could not be done due to hemodynamic instability. Endocrinology was consulted and concomitant adrenal insufficiency testing was not sought due to chronic steroid therapy. The dose of DDAVP was titrated to ∼1-2 mcg per day based on serum sodium levels and daily urine output. Approximately 10 days later, Vasopressin was restarted due to hemodynamic instability and with ongoing DDAVP therapy, hyponatremia was noted. Thus, DDAVP was discontinued while on vasopressin. She was continued on vasopressin for the remainder of her hospitalization ∼ 11 more days until she unfortunately passed away. DISCUSSION: Our patient developed central diabetes insipidus after withdrawal of vasopressin. She continued to require DDAVP for ∼10 days before Vasopressin had to be restarted due to hemodynamic instability, after which DDAVP had to be discontinued due to concern of SIADH. Central diabetes has been linked to critical illness in a transient state driven by depletion of endogenous stores, negative feedback repression and posterior pituitary hypoperfusion. However, our patient continued to require exogenous supplementation. More research is needed in this regard to elucidate the differing etiologies and characteristics of transient versus permanent DI. Critical illness is a rare but extremely important cause of central DI and can quickly prove to be life threatening without timely diagnosis and treatment. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m. |
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