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    Persistent syndrome of inappropriate antidiuretic hormone secretion following traumatic brain injury

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    Author
    Dick, M; Catford, SR; Kumareswaran, K; Hamblin, PS; Topliss, DJ
    Date
    2015-10-01
    Source Title
    Endocrinology, Diabetes and Metabolism Case Reports
    Publisher
    BIOSCIENTIFICA LTD
    University of Melbourne Author/s
    Hamblin, Peter
    Affiliation
    Medicine and Radiology
    Metadata
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    Document Type
    Journal Article
    Citations
    Dick, M., Catford, S. R., Kumareswaran, K., Hamblin, P. S. & Topliss, D. J. (2015). Persistent syndrome of inappropriate antidiuretic hormone secretion following traumatic brain injury. ENDOCRINOLOGY DIABETES AND METABOLISM CASE REPORTS, 2015, https://doi.org/10.1530/EDM-15-0070.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257585
    DOI
    10.1530/EDM-15-0070
    Abstract
    UNLABELLED: The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur following traumatic brain injury (TBI), but is usually transient. There are very few case reports describing chronic SIADH and all resolved within 12 months, except for one case complicated by meningo-encephalitis. Persistent symptomatic hyponatremia due to chronic SIADH was present for 4 years following a TBI in a previously well 32-year-old man. Hyponatremia consistent with SIADH initially occurred in the immediate period following a high-speed motorbike accident in 2010. There were associated complications of post-traumatic amnesia and mild cognitive deficits. Normalization of serum sodium was achieved initially with fluid restriction. However, this was not sustained and he subsequently required a permanent 1.2 l restriction to maintain near normal sodium levels. Multiple episodes of acute symptomatic hyponatremia requiring hospitalization occurred over the following years when he repeatedly stopped the fluid restriction. Given the ongoing nature of his hyponatremia and difficulties complying with strict fluid restriction, demeclocycline was commenced in 2014. Normal sodium levels without fluid restriction have been maintained for 6 months since starting demeclocycline. This case illustrates an important long-term effect of TBI, the challenges of complying with permanent fluid restrictions and the potential role of demeclocycline in patients with chronic hyponatremia due to SIADH. LEARNING POINTS: Hyponatraemia due to SIADH commonly occurs after TBI, but is usually mild and transient.Chronic hyponatraemia due to SIADH following TBI is a rare but important complication.It likely results from damage to the pituitary stalk or posterior pituitary causing inappropriate non-osmotic hypersecretion of ADH.First line management of SIADH is generally fluid restriction, but hypertonic saline may be required in severe cases. Adherence to long-term fluid restriction is challenging. Other options include oral urea, vasopressin receptor antagonists and demeclocycline.While effective, oral urea is poorly tolerated and vasopressin receptor antagonists are currently not licensed for use in Australia or the USA beyond 30 days due to insufficient long-term safety data and specific concerns of hepatotoxicity.Demeclocycline is an effective, well-tolerated and safe option for management of chronic hyponatraemia due to SIADH.

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