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      Persistent syndrome of inappropriate antidiuretic hormone secretion following traumatic brain injury

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          Summary

          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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          Most cited references6

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          Hyponatremia and brain injury: historical and contemporary perspectives.

          Hyponatremia is common in neurocritical care patients and is associated with significant morbidity and mortality. Despite decades of research into the syndrome of inappropriate antidiuretic hormone (SIADH) and cerebral salt wasting (CSW), their underlying pathophysiological mechanisms are still not fully understood. This paper reviews the history behind our understanding of hyponatremia in patients with neurologic injury, including the first reports of CSW and SIADH, and current and future challenges to diagnosis and management in this setting. Such challenges include distinguishing CSW, SIADH, and hypovolemic hyponatremia due to a normal pressure natriuresis from the administration of large volumes of fluids, and hyponatremia due to certain medications used in the neurocritical care population. Potential treatments for hyponatremia include mineralocorticoids and vasopressin 2 receptor antagonists, but further work is required to validate their usage. Ultimately, a greater understanding of the pathophysiological mechanisms underlining hyponatremia in neurocritical care patients remains our biggest obstacle to optimizing patient outcomes in this challenging population.
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            Recurrent hyponatremia after traumatic brain injury.

            Dysregulation of the neuroendocrine system is a frequent complication after traumatic brain injury (TBI). Symptoms of these hormonal abnormalities might be subtle and thus easily ignored. Hyponatremia usually indicates underlying disorders that disrupt fluid homeostasis. In most patients with TBI, hyponatremia is a feature of the syndrome of inappropriate antidiuretic hormone (SIADH) secretion due to pituitary dysfunction after head injury. Usually TBI-associated hyponatremia is transient and reversible. We report the case of a 48-year-old man with TBI-associated hyponatremia with delayed recovery and recurrent hyponatremia precipitated by subsequent surgery. In this report, we emphasize the importance of identifying patients with slow recovery of the injured brain, which could complicate with SIADH and acute hyponatremia. Differentiating TBI-associated SIADH from other important causes of hyponatremia such as cerebral salt wasting, and hypocortisonism are also reviewed. Prevention of its recurrence by avoiding further risk is mandatory in managing patients with TBI.
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              Syndrome of inappropriate secretion of antidiuretic hormone after severe head injury.

              This study is based on 109 patients with severe head injury who had a Glasgow coma score equal to or less than 7 and a Liège coma score equal to or less than 12 in the first 24 hours. The syndrome of inappropriate secretion of antidiuretic hormone seems to us to be a frequent complication of severe craniocerebral trauma. It has been discovered in 33% of our patients. On the other hand, diabetes insipidus was rarely diagnosed (2.8%). We propose, in cranial trauma, to subdivide the syndrome of inappropriate secretion of antidiuretic hormone into two clinical forms: an early syndrome (5%) that becomes apparent towards the second day and is significantly associated with lesions at the base of the skull; and a delayed syndrome that occurs at the end of the first week and is related to different factors inherent in intensive care procedures. Surgical intervention, in the case of acute craniocerebral trauma, does not result in a higher frequency of inappropriate secretion of antidiuretic hormone.

                Author and article information

                Journal
                Endocrinol Diabetes Metab Case Rep
                Endocrinol Diabetes Metab Case Rep
                edm
                EDM Case Reports
                Endocrinology, Diabetes & Metabolism Case Reports
                Bioscientifica Ltd (Bristol )
                2052-0573
                27 August 2015
                2015
                : 2015
                : 150070
                Affiliations
                [1 ]Faculty of Medical and Health Sciences, The University of Auckland , 85 Park Road, Grafton, Auckland, New Zealand
                [2 ]Department of Endocrinology and Diabetes, The Alfred Hospital , Commercial Road, Melbourne, Victoria, 3004, Australia
                [3 ]Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University , Clayton, Victoria, 3168, Australia
                Author notes
                Correspondence should be addressed to S R Catford Email: Sarah.Catford@ 123456monashhealth.org
                Article
                EDM150070
                10.1530/EDM-15-0070
                4626642
                26527077
                70048bd4-824b-4858-9fcb-24a1b4efbe15
                © 2015 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                : 25 August 2015
                : 27 August 2015
                Categories
                Novel Treatment

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