scholarly journals Challenges of Managing and Diagnosing Reset Osmostat vs SIADH in a Patient With Personal and Family History of Chronic Hyponatremia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A576-A577
Author(s):  
Hasan Syed ◽  
Praveen Attele ◽  
Joseph Theressa Nehu Parimi ◽  
Sowjanya Naha ◽  
Timur Gusov ◽  
...  

Abstract Background: Distinguishing between a reset osmostat and SIADH in a hyponatremic patient can prove to be challenging in certain circumstances. Reset osmostat is an uncommon and under recognized cause of hyponatremia. Thus, it is important to recognize it as it does not require any treatment. Clinical Case: A 48 year old male with history of chronic hyponatremia of unknown cause, fatty liver, hypertension, was in the hospital post operatively after resection of a meningioma along dura. Endocrine was consulted for management of his chronic hyponatremia. Had chronic hyponatremia for over 20 years and was always asymptomatic. Normally drank 6-7 L of water at home, mostly at night. Also found to have a spinal compression fracture of unknown cause. Both his father and brother had chronic hyponatremia of unknown cause as well, suggesting possible familial component. His baseline sodium levels were 129-133 mmol/L. In the hospital, serum sodium levels decreased to the 120s. TSH was 0.307mcunit/mL (0.27-4.2). Was also placed on 1.5 L fluid restriction. Urine osmolality was 900 mOsm/kg (500-800) with sodium of 123 mmol/L (136-145), consistent with SIADH. A rare inherited disorder, nephrogenic SIADH (NSIADH), was considered. However, it has an X-linked inheritance pattern. Fluid restriction was removed, then did fluid load with 2L of water and obtained urine sodium, serum sodium, urine osmolality, serum osmolality, Copeptin (pro-AVP) before fluid load and 1 hour after fluid load. Serum sodium level went from 127mmol/L before to 125 mmol/L after. Urine osmolality improved from 984 mOsm/kg prior to 575 mOsm/kg after. Urine sodium went from 183 mmol/L prior to 91 mmol/L after. Serum osmolality went from 278 mOsm/kg (270-310) to 268 mOsm/kg after. His co-peptin pro-AVP levels were 16.4 pmol/L (ref. <13.1). They are found to be low in NSIADH. It was decided that his chronic hyponatremia was likely due to reset osmostat. After discharge and follow up, his serum sodium was rechecked and was 128 mmol/L. It would have been challenging, but useful, to try a vaptan for diagnostic purposes and possibly to increase serum sodium. However, there are complications from overcorrection. Since patient had long standing asymptomatic chronic hyponatremia with family history, it was decided not to pursue aggressive measures just to “normalize” serum sodium. Otherwise, it would have been an example of treating the numbers and not the patient. Conclusions: Case demonstrates the importance of keeping the patient, their symptoms, and clinical picture in mind, and to not just follow numbers, as difficult as it may be, especially when managing conditions in which diagnosis may be uncertain or unclear. Sometimes no intervention is needed at all, however tempting it may be to do one, it is important to keep the former option in mind. An asymptomatic patient with longstanding chronic hyponatremia due to reset osmostat is an example of that.

2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Hafiz Muhammad Sharjeel Arshad ◽  
Aleida Rodriguez ◽  
Faten Suhail

Background. The Syndrome of Inappropriate Antidiuretic Hormone (SIADH) is considered to be the most common cause of euvolemic hyponatremia. The most common malignancy associated with SIADH is small cell lung cancer. We present a rare case of a patient with SIADH secondary to well differentiated squamous cell carcinoma of the naso-oropharynx.Case. A 46-year-old Caucasian woman presented to emergency department with four-week history of progressive dysphagia. On examination, she was found to have a pharyngeal mass. CT scan and MRI of neck confirmed a mass highly suspicious of carcinoma. Patient’s serum sodium level decreased to 118 mEq/L and other labs including serum and urine osmolality confirmed SIADH. She was started on fluid restriction and oral sodium tablets which gradually improved her serum sodium levels. Biopsy confirmed diagnosis of squamous cell carcinoma of pharynx.Conclusion. SIADH can be caused by squamous cell carcinoma. Appropriate management includes fluid restriction.


2017 ◽  
Vol 12 (2) ◽  
Author(s):  
Kirstie Lithgow ◽  
Bernard Corenblum

A 22-year-old man presented with a 3-week history of increased thirst, polydipsia, and polyuria. He described consuming large volumes of water and waking up multiple times throughout the night to drink and urinate. He also endorsed symptoms of fatigue and frequent headaches. Prior to this, he had been well. There was no history of diuretic use, lithium use, or renal disease. There was no prior head trauma, cranial irradiation, or intracranial pathology. He denied consumption of nutritional or protein supplements. Clinical exam revealed a well appearing young man with normal heart rate and blood pressure. Visual fields and general neurologic exam were grossly normal.Baselines investigations revealed serum sodium ranging from 141–142 mmol/L (reference range 133–145 mmol/L), creatinine 92 umol/L (50–120 umol/L), random glucose 5.4  mmol/L (3.3–11.0 mmol/L), potassium 4.0 (3.3–5.1 mmol/L) and ionized calcium 1.25 mmol/L (1.15–1.35 mmol/L).A 24-hour urine collection was arranged, and returned a urine volume of 5.6L (normal less than 3 litres/24  hours). Further investigations revealed a serum sodium of 142 mmol/L, serum osmolality 306 mmol/kg (280–300 mmol/kg), and urine osmolality of 102 mmol/kg (50–1200 mmol/kg). AM cortisol was 372 nmol/L (200–690 nmol/L). These results demonstrated inability to concentrate the urine, despite the physiologic stimulus of hyperosmolarity. Based on this, a presumptive diagnosis of diabetes insipidus was made. The patient was instructed to drink as much as he needed to satiate his thirst, and to avoid fluid restriction. The patient was started on DDAVP intranasal spray, which provided immediate relief from his symptoms. Magnetic resonance imaging of the brain revealed an unremarkable pituitary gland with abnormal thickening of the pituitary stalk and loss of the posterior pituitary bright spot. This confirmed the diagnosis of central diabetes insipidus, presumed secondary to infiltrative disease affecting the pituitary stalk.


2021 ◽  
Vol 14 (8) ◽  
pp. e241407
Author(s):  
Isabel Saunders ◽  
David M Williams ◽  
Aliya Mohd Ruslan ◽  
Thinzar Min

Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.


2016 ◽  
Vol 33 (S1) ◽  
pp. S469-S469 ◽  
Author(s):  
E. García Fernández ◽  
D.M.I. Ramos García

IntroductionDesvenlafaxine is a prescription medication approved for the treatment of major depressive disorder in adults. Hyponatremia secondary to inappropriate secretion of antidiuretic hormone (SIADH) is a possible side effect in patients receiving serotonin-norepinephrine reuptake inhibitors (SNRIS)MethodTo report a case of SIADH associated with desvenlafaxine.ResultsWe present a 80-year-old female patient who required hospitalization due to an episode of psychotic depression. During the hospitalization, the patient developed hyponatremia after commencing treatment with desvenlafaxine. The serum sodium at this time was 117 mmol/L, serum osmolality was 249 mosmol/kg, urine osmolality 395 mosmol/kg and urine sodium 160 mmol/L, consistent with a diagnosis of SIADH. Desvenlafaxine was ceased and fluid restriction implemented. The mental status improved, and electrolyte studies 6 days later revealed serum sodium and osmolality values of 135 mEq/L during treatment with duoxetine.ConclusionsSIADH has been reported with a range of antidepressants in elderly patients. This case report suggests that desvenlafaxine might cause clinically significant hyponatremia. Close monitoring is recommended in patients starting therapy with antidepressant treatment to study and prevent possible adverse effects.Disclosure of interestThe authors have not supplied their declaration of competing interest.


Author(s):  
Jatuporn Duangpetsang

Objective: Febrile seizure is a common disorder in children that occurs in 2.5% of children 6-60 months of age. The study was conducted to ascertain the role of serum sodium as a predictor of seizure recurrence within the same febrile illness.Material and Methods: A retrospective study was conducted in children with febrile seizures who were admitted to Kaengkhro Hospital between 1 January 2014 and 31 December 2017. The data collected from medical records included age, gender, serum sodium level, body temperature, duration of fever, and family history of febrile seizures.Results: Two hundred ten children were diagnosed with febrile seizures; 190 had a single febrile seizure and 20 had recurrent febrile seizures. Mean±standard deviation ages of children with a single febrile seizure and recurrent febrile seizures were 22.95 ± 0.95 and 22.34 ± 0.89 months, respectively. Serum sodium levels in children with recurrent seizures within 24 hours (130.80 mmol/L) were significantly lower than in children with a single febrile seizure (132.37 mmol/L, p-value=0.02). A family history of febrile seizures was significant for predicting recurrent seizures within 24 hours (p−value= 0.006).Conclusion: Serum sodium levels predict the recurrence of febrile seizure within 24 hours.


Author(s):  
Swapna Talluri ◽  
Raghu Charumathi ◽  
Muhammad Khan ◽  
Kerri Kissell

Summary Central pontine myelinolysis (CPM) usually occurs with rapid correction of severe chronic hyponatremia. Despite the pronounced fluctuations in serum osmolality, CPM is rarely seen in diabetics. This is a case report of CPM associated with hyperglycemia. A 45-year-old non-smoking and non-alcoholic African American male with past medical history of type 2 diabetes, hypertension, stage V chronic kidney disease and hypothyroidism presented with a two-week history of intermittent episodes of gait imbalance, slurred speech and inappropriate laughter. Physical examination including complete neurological assessment and fundoscopic examination were unremarkable. Laboratory evaluation was significant for serum sodium: 140 mmol/L, potassium: 3.9 mmol/L, serum glucose: 178 mg/dL and serum osmolality: 317 mosmol/kg. His ambulatory blood sugars fluctuated between 100 and 600 mg/dL in the six weeks prior to presentation, without any significant or rapid changes in his corrected serum sodium or other electrolyte levels. MRI brain demonstrated a symmetric lesion in the central pons with increased signal intensity on T2- and diffusion-weighted images. After neurological consultation and MRI confirmation, the patient was diagnosed with CPM secondary to hyperosmolar hyperglycemia. Eight-week follow-up with neurology was notable for near-complete resolution of symptoms. This case report highlights the importance of adequate blood glucose control in diabetics. Physicians should be aware of complications like CPM, which can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion. Learning points: Despite the pronounced fluctuations in serum osmolality, central pontine myelinolysis (CPM) is rarely seen in diabetics. This case report of CPM associated with hyperglycemia highlights the importance of adequate blood glucose control in diabetics. Physicians should be aware of complications like CPM in diabetics. CPM can present atypically in diabetics and is only diagnosed in the presence of a high index of clinical suspicion.


2020 ◽  
Vol 7 (7) ◽  
pp. 1606
Author(s):  
Sara Benny

Background: Simple febrile seizures are the common childhood seizures, usually affecting 1 in 20 children between the age group of 6 months to 60 months. Earlier studies have shown an association between low serum sodium as a cause for febrile seizures and its recurrences. The present study was to determine the role of serum sodium in predicting febrile seizure recurrence within 24 hrs and recurrent episodes.Methods: Children aged between 6 months to 60 months with first episode of febrile seizures, admitted to the Paediatric ward of MOSC medical college Kolenchery, were recruited in the study. Inclusion criteria were demographic data, family history, clinical examinations, and laboratory investigations (serum sodium and hemoglobin).Results: Of the total study population of 100 children 33 had recurrences in 24 hours and 16 had recurrent episodes. About 57 children had a family history of febrile seizures, out which 28 children had recurrence of febrile seizure within 24 hours. 26 children had family history of epilepsy, of which only 8 had recurrences in 24 hours and 5 had recurrent episodes. Serum sodium levels of 69 children was above 130 mmol/l and 31 children had sodium level below 130mmol/l. Of 31 children, with low serum sodium levels (<130mmol/l), 29 had recurrence within 24 hours, which was not statistically significant. The sodium levels of 16 children who had recurrent episodes of seizure, was also between 130.1-135mmol/. No significant differences were seen between the serum sodium levels in simple febrile seizures and recurrent episodes.Conclusions: Study showed low serum sodium is not statistically significant to predict a recurrence within 24 hours, but a relative hyponatremia can predispose, a febrile child to occurrence of simple febrile seizure.


PEDIATRICS ◽  
1989 ◽  
Vol 83 (5) ◽  
pp. 700-705
Author(s):  
Guadalupe Padilla ◽  
John A. Leake ◽  
Robert Castro ◽  
M. Gore Ervin ◽  
Michael G. Ross ◽  
...  

The syndrome of inappropriate secretion of antidiuretic hormone is associated with head trauma; however, there are no reports concerning vasopressin levels in pediatric patients with head trauma. Urine vasopressin in eight children (mean ± SEM, age 7.5 ± 1.6 years, range 1 to 15 years) was measured by radio-immunoassay during their hospitalization for head trauma. Urine vasopressin values for ten healthy children (mean age 5.4 ± 1.3 years) and for eight children hospitalized for systemic antibiotic treatment of infections (age 5.9 ± 1.8 years) also were obtained. Urine vasopressin, urine and serum sodium concentration and osmolality, urea nitrogen, creatinine, and fluid intake were measured within 24 hours of admission and daily for the following two days. For the first three days following head trauma, mean urine vasopressin levels in pediatric patients with head trauma were increased (P &lt; .05) compared with those of healthy children. Despite fluid restriction to 85% of maintenance level, 25% of patients with head trauma exhibited the clinical syndrome of inappropriate secretion of antidiuretic hormone (hyponatremia, increased urinary sodium, diminished serum osmolality, and urine osmolality greater than serum osmolality). Urine osmolality greater than 800 mosm/kg was associated with markedly increased urine vasopressin levels (200 to 1,650 pg/mL); children with this finding may be at particular risk for the syndrome of inappropriate secretion of antidiuretic hormone without restrictive water intake.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Roberto Kenji Mitsui Akagi ◽  
Omolola Bolaji Olajide

Abstract Background: Diabetes insipidus (DI) is characterized by hypotonic polyuria and polydipsia. Nephrogenic DI is the result of an inadequate response of the kidneys to arginine vasopressin (AVP), either due to hereditary causes or acquired from various drugs, most commonly lithium. Clinical case: A 30 year old male with past medical history of Hashimoto’s thyroiditis, severe mental impairment was admitted to the hospital for abdominal pain. Medical history was difficult to obtain since the patient was nonverbal. His thyroid function tests, electrolytes including sodium, potassium were all normal on admission. During the hospital course, he was made NPO for both an upper and lower GI endoscopy. He notably had a mild increase in sodium level with subsequent improvement after restitution of diet. Two days after the procedure, he was found to be drinking out of the toilet and also attempting to drink from the urine jug. Due to this odd behavior, he had to be put on physical restraints. The day after, he was found to have a serum sodium of 158 mEq/L. Hypotonic saline was started and urine output was notably ranging from 6-10 L/day with a negative balance. Desmopressin (DDAVP) test was done with a resultant urine osmolality of 170, 237, 257 and 264 mOsm/kg after 30, 60, 90 and 180 mins. Subcutaneous DDAVP was started with some improvement of serum sodium and decrease in urine output. Endocrinology service was consulted for the evaluation of hypernatremia and polyuria. Initial review of his medications did not show any potential cause of DI. Further inquiry of his prior medication history revealed that he had taken Lithium for over 10 years and stopped 4 months prior to the admission due to polyuria. After excluding other causes of polyuria, with partial improvement of urine osmolality to a level &lt;300 mOsm/kg and a clinical history of prior Lithium therapy, a diagnosis of partial nephrogenic DI was made. Patient was started on HCTZ and given adequate water intake with subsequent improvement of his serum sodium back to normal. Conclusion: Nephrogenic DI due to Lithium use usually recovers after treatment is stopped but could be persistent for several years after. In our case, the patient compensated for his polyuria with increased water intake. When his water intake was restricted due to physical restraints, polyuria and subsequently hypernatremia became evident. A thorough medication history including past drug use is essential as it can help unravel the offending agent which was Lithium in our case. There needs to be an increased awareness that the effect of Lithium in the kidneys could be persistent even after stopping the drug for up to many years. References: Thompson CJ. Persistent nephrogenic diabetes insipidus following lithium therapy. Scott Med J 1997; 42:16-17.


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