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Open access

Ramesh Srinivasan, Stephen Ball, Martin Ward-Platt, David Bourn, Ciaron McAnulty, and Tim Cheetham

Background Familial cranial diabetes insipidus (FCDI) is a rare inherited disorder that may have an autosomal dominant inheritance pattern. Polyuria and polydipsia typically develop in childhood due to a progressive decline in AVP secretion

Open access

Pedro Marques, Kavinga Gunawardana, and Ashley Grossman

balance is controlled by thirst and the secretion of arginine vasopressin (AVP), which in turn is primarily regulated by serum osmolality (6) . In pregnancy, water metabolism is remarkably changed, with increased total body water, an expanded plasma

Open access

Jennifer Hague, Ruth Casey, Jonathan Bruty, Tom Legerton, Stephen Abbs, Susan Oddy, Andrew S Powlson, Mohamed Majeed, Mark Gurnell, Soo-Mi Park, and Helen Simpson

AVPR2 . Furthermore, we demonstrate that measurement of co-peptin levels can be used as an alternative to direct AVP measurement during the water load test. Case presentation Our patient was an only child and was born to non-consanguineous white

Open access

Ruben H Willemsen, Violeta Delgado-Carballar, Daniela Elleri, Ajay Thankamony, G A Amos Burke, James C Nicholson, and David B Dunger

become available – the vaptans ( 2 ). Vaptans are vasopressin receptor antagonists. There are three types of vasopressin receptors: V1a, V1b and V2. Binding of AVP to the V2 receptor in the renal collecting duct leads to insertion of aquaporin 2 water

Open access

Matthieu St-Jean, Jessica MacKenzie-Feder, Isabelle Bourdeau, and André Lacroix

hCG, AVP DC, PCR, IHC for LHCGR and Mc2R Trinh 2016 ( 10 ) Adenoma 5–8 pmol/L Elevated ND Abnormal Adrenalectomy during pregnancy ND IHC for LHCGR Xu 2013 ( 15 ) BMAH <1.1 nmol/L 7 ND Abnormal Remission

Open access

Navira Samad and Ian Fraser


Colonoscopy is a useful tool in modern medicine and is increasingly employed for both diagnostic and treatment reasons. However, its effectiveness is highly reliant on the quality of bowel cleansing. Among different bowel-cleansing agents available, PEG (polyethylene glycol) is considered to be the safest cleansing agent, especially in relation to fluid and electrolyte problems. We present here a case of severe symptomatic hyponatremia that developed after the use of PEG for an elective colonoscopy. This case highlights that despite the use of PEG-based preparations, life-threatening fluid and electrolyte disturbances can still occur in patients with risk factors, such as old age, use of thiazide diuretics and SSRIs, chronic kidney disease, heart failure and a history of electrolyte problems. These patients should be closely monitored when undertaking bowel cleansing and should receive prompt care in the event of complications, to avoid permanent neurological sequelae and death. Rapid correction of sodium levels in patients requiring treatment of hyponatremia should be avoided to prevent complications such as osmotic demyelination syndrome.

Learning points:

  • PEG is considered to be the safest bowel-cleansing agents among different options available, but it can still cause significant side effects in susceptible individuals.

  • Those at risk of developing adverse events include elderly individuals, patients with chronic kidney disease, heart failure or previous history of electrolyte problems and those taking thiazide diuretics and SSRIs.

  • All such patients should be closely monitored i.e. have their metabolic profile checked prior to the commencement of bowel cleansing and a low threshold should be kept for the initiation of investigations and treatment in case of development of symptoms.

  • Medications with a potential of causing fluid and electrolytes such as thiazide diuretics and SSRIs should be withheld while patient is undertaking bowel preparation.

  • Hyponatremia in a hospitalized patient can be multifactorial, and the treatment principles are based on duration of onset, presence of symptoms and patients volume status.

  • Overzealous correction of sodium levels during treatment of hyponatremia can result in serious complications such as osmotic demyelination syndrome.

Open access

Victoria John, Philip Evans, and Atul Kalhan


A 65-year-old woman was admitted to the emergency unit with a 48 h history of generalised weakness and confusion. On examination, she had mild slurring of speech although there was no other focal neurological deficit. She had profound hyponatraemia (serum sodium level of 100 mmol/L) on admission with the rest of her metabolic parameters being within normal range. Subsequent investigations confirmed the diagnosis of small-cell lung cancer with paraneoplastic syndrome of inappropriate antidiuresis (SIAD). She was monitored closely in high-dependency unit with an attempt to cautiously correct her hyponatraemia to prevent sequelae associated with rapid correction. The patient developed prolonged psychosis (lasting over 2 weeks) and displayed delayed dyskinetic movements, even after a gradual increase in serum sodium levels close to 130 mmol/L. To our knowledge, delayed neurological recovery from profound hyponatraemia (without long-term neurological sequelae) has previously not been reported. This case should alert a clinician regarding the possibility of prolonged although reversible psychosis and dyskinetic movements in a patient presenting with profound symptomatic hyponatraemia.

Learning points:

  • Patients with profound hyponatraemia may develop altered sensorium, dyskinesia and psychotic behaviour.

  • Full recovery from psychotic symptoms and dyskinesia may be delayed despite cautious correction of serum sodium levels.

  • Careful and close monitoring of such patients can help avoid long-term neurological sequelae.

Open access

Michael Dick, Sarah R Catford, Kavita Kumareswaran, Peter Shane Hamblin, and Duncan J Topliss


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.

Open access

Janani Devaraja, Sarah Sloan, Vicki Lee, and Paul Dimitri

Background Central diabetes insipidus (CDI) is a disease caused by arginine-vasopressin (AVP) deficiency leading to polyuria and polydipsia ( 1 ). The destruction of neurons in the paraventricular and supraoptic nuclei of the posterior

Open access

Raku Son, Masahiko Nagahama, Fumiaki Tanemoto, Yugo Ito, Fumika Taki, Ryosuke Tsugitomi, and Masaaki Nakayama


The etiology of hyponatremia is assessed based on urine osmolality and sodium. We herein describe a 35-year-old Asian man with pulmonary tuberculosis and perforated duodenal ulcer who presented with hyponatremia with hourly fluctuating urine osmolality ranging from 100 to 600 mosmol/kg, which resembled urine osmolality observed in typical polydipsia and SIADH simultaneously. Further review revealed correlation of body temperature and urine osmolality. Since fever is a known non-osmotic stimulus of ADH secretion, we theorized that hyponatremia in this patient was due to transient ADH secretion due to fever. In our case, empiric exogenous glucocorticoid suppressed transient non-osmotic ADH secretion and urine osmolality showed highly variable concentrations. Transient ADH secretion-related hyponatremia may be underrecognized due to occasional empiric glucocorticoid administration in patients with critical illnesses. Repeatedly monitoring of urine chemistries and interpretation of urine chemistries with careful review of non-osmotic stimuli of ADH including fever is crucial in recognition of this etiology.

Learning points:

  • Hourly fluctuations in urine osmolality can be observed in patients with fever, which is a non-osmotic stimulant of ADH secretion.

  • Repeated monitoring of urine chemistries aids in the diagnosis of the etiology underlying hyponatremia, including fever, in patients with transient ADH secretion.

  • Glucocorticoid administration suppresses ADH secretion and improves hyponatremia even in the absence of adrenal insufficiency; the etiology of hyponatremia should be determined carefully in these patients.