Clinical Overview > Condition/ Syndrome > Traumatic brain injury

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Peter Taylor Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK
Thyroid Research Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff, UK

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Sasan Dehbozorgi Department of Neurosurgery, University Hospital of Wales, Heath Park, Cardiff, UK

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Arshiya Tabasum Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK

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Anna Scholz Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK

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Harsh Bhatt Department of Neurosurgery, University Hospital of Wales, Heath Park, Cardiff, UK

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Philippa Stewart Department of Neurosurgery, University Hospital of Wales, Heath Park, Cardiff, UK

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Pranav Kumar Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK

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Mohd S Draman Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK
Thyroid Research Group, Division of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff, UK

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Alastair Watt Department of Diabetes and Endocrinology, North Devon District Hospital, Barnstaple, UK

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Aled Rees Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK
Institute of Neuroscience and Mental Health Research Institute, School of Medicine, Cardiff University, Cardiff, UK

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Caroline Hayhurst Department of Neurosurgery, University Hospital of Wales, Heath Park, Cardiff, UK

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Stephen Davies Department of Diabetes and Endocrinology, University Hospital of Wales, Heath Park, Cardiff, UK

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Summary

Hyponatraemia is the most commonly encountered electrolyte disturbance in neurological high dependency and intensive care units. Cerebral salt wasting (CSW) is the most elusive and challenging of the causes of hyponatraemia, and it is vital to distinguish it from the more familiar syndrome of inappropriate antidiuretic hormone (SIADH). Managing CSW requires correction of the intravascular volume depletion and hyponatraemia, as well as mitigation of on-going substantial sodium losses. Herein we describe a challenging case of CSW requiring large doses of hypertonic saline and the subsequent substantial benefit with the addition of fludrocortisone.

Learning points:

  • The diagnosis of CSW requires a high index of suspicion. Distinguishing it from SIADH is essential to enable prompt treatment in order to prevent severe hyponatraemia.

  • The hallmarks of substantial CSW are hyponatraemia, reduced volume status and inappropriately high renal sodium loss.

  • Substantial volumes of hypertonic saline may be required for a prolonged period of time to correct volume and sodium deficits.

  • Fludrocortisone has a role in the management of CSW. It likely reduces the doses of hypertonic saline required and can maintain serum sodium levels of hypertonic saline.

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Michael Dick Faculty of Medical and Health Sciences, The University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand

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Sarah R Catford Department of Endocrinology and Diabetes, The Alfred Hospital, Commercial Road, Melbourne, Victoria, 3004, Australia

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Kavita Kumareswaran Department of Endocrinology and Diabetes, The Alfred Hospital, Commercial Road, Melbourne, Victoria, 3004, Australia
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia

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Peter Shane Hamblin Department of Endocrinology and Diabetes, The Alfred Hospital, Commercial Road, Melbourne, Victoria, 3004, Australia
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia

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Duncan J Topliss Department of Endocrinology and Diabetes, The Alfred Hospital, Commercial Road, Melbourne, Victoria, 3004, Australia
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia

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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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