Treatment of Hyponatremia

Sterns, Richard H.; Silver, Solomon; Hix, John K.

doi:10.1007/978-1-4614-6645-1_12

Cited by 31 publications

(45 citation statements)

References 112 publications

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“…The volume expansion activates secondary natriuretic mechanisms (renin-angiotensin-aldosterone or atrial natriuretic peptide), resulting in loss of sodium and water, and in restoration of euvolaemia 10. Patients with SIADH are euvolaemic and urinary sodium excretion is equal to dietary sodium intake 2 10…”

Section: Discussionmentioning

confidence: 99%

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Reset osmostat: a rare cause of hyponatraemia

Vale

Morais²,

Mesquita³

et al. 2015

BMJ Case Reports

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Neonatal hyponatraemia is common, and related to significant morbidity and mortality. We report a case of a preterm newborn (gestational age of 36 weeks) with hyponatraemia, and with a prenatal diagnosis of cleft lip and palate, with a normal fetal karyotype. On the seventh day of life, a biochemical evaluation for jaundice and mild signs of dehydration showed hyponatraemia of 124 mmol/L. Investigation showed normal adrenal and thyroid functions, plasma hyposmolality (258 mOsm/kg); high urinary sodium (73 mmol/L) and high urinary osmolality (165 mOsm/kg). Despite oral sodium supplementation and fludrocortisone treatment, sodium levels remained between 124 and 130 mmol/L. Cranial ultrasound, brain MRI and renal ultrasound were normal. The diagnosis of hyponatraemia was unpredicted and the investigation was suggestive of reset osmostat, a subtype of the syndrome of inappropriate secretion of antidiuretic hormone, characterised by a subnormal threshold for antidiuretic hormone secretion.

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Section: Discussionmentioning

confidence: 99%

“…In patients with SIADH, the corner stone of diagnosis is hyponatraemia in a state of euvolaemia, in which the rate of sodium excretion is determined by sodium intake 2. SIADH is a disorder where the excretion of water is partially limited by an increased secretion of ADH in the absence of an osmotic or hypovolaemic stimulus 1 4 7.…”

Section: Introductionmentioning

confidence: 99%

Reset osmostat: a rare cause of hyponatraemia

Vale

Morais²,

Mesquita³

et al. 2015

BMJ Case Reports

View full text Add to dashboard Cite

show abstract

“…Overly rapid correction of severe, chronic hyponatremia (serum sodium concentration <120 mmol/L and particularly <115 mmol/L) can lead to a severe and sometimes irreversible neurologic disorder, osmotic demyelination syndrome (ODS). 28,29 According to United States and European hyponatremia guidelines, 2 the limit of correction rates in hyponatremia should be around 10 mmol/L per day for both acute and chronic hyponatremia. 2 Of note, the United States guideline recommends a lower limit of 8 mmol/L per day in patients with high risk of ODS (sodium ≤ 105 mmol/L, concurrent hypokalemia, alcoholism, malnutrition, or hepatic disease).…”

Section: Optimal Correction Rates Of Hyponatremiamentioning

confidence: 99%

“…2 Of note, the United States guideline recommends a lower limit of 8 mmol/L per day in patients with high risk of ODS (sodium ≤ 105 mmol/L, concurrent hypokalemia, alcoholism, malnutrition, or hepatic disease). Many physicians advocate a more conservative rate of correction of 6 mmol/L per day, 28,30 although this is likely to be both sufficient and safe, the data to support this are still limited. During treatment, close monitoring of serum sodium is essential and prompt action should be taken to avoid overly rapid correction.…”

Section: Optimal Correction Rates Of Hyponatremiamentioning

confidence: 99%

A case of extreme hyponatremia without neurologic symptoms

Zhou

Chen²

2019

Clinical Case Reports

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“…28 However, some cases have also been reported at a slower correction rate of 9 mmol/L in 24 hours. 29 Therefore, the current recommendation for correction of serum sodium is an increase of no greater than 6-8 mmol/L in 24 hours, because most cases of acute hyponatraemia are suitably corrected within this range without serious complications. [28][29][30] Patients with severe hyponatraemia (≤120 mmol/L) or comorbidities such as alcoholism, liver disease, and malnutrition are at increased risk of developing osmotic demyelination, so a slower rate of correction (4-6 mmol/L in 24 hours) is recommended.…”

Section: Long Answermentioning

confidence: 99%

An unusual case of quadriparesis

Ahmad

Vassallo

Naqvi

et al. 2013

BMJ

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A 48 year old man presented with a four day history of lethargy, dizziness, and an unsteady gait with recurrent falls, on a background of chronic alcohol misuse. The patient was taking desmopressin for nocturnal enuresis and bendroflumethiazide for hypertension, which were both stopped on admission.On physical examination he appeared clinically euvolaemic and he had no focal neurological deficit. Vital signs were within normal limits. Serum biochemistry showed sodium of 110 mmol/L (normal range 137-145; 1 mmol/L=1mEq/L) and potassium of 2.6 mmol/L (normal range 3.5-5.5 mmol/L). A computed tomogram of the brain that was performed to rule out traumatic brain injury was unremarkable.Fluids were subsequently restricted and he was started on parenteral thiamine, oral chlordiazepoxide, and intravenous 0.9% sodium chloride with potassium supplementation. Twenty four hours later, serum sodium was 119 mmol/L and serum potassium was 3.3 mmol/L. Serum sodium eventually reached 130 mmol/L on day 4. Seven days after admission he developed delirium and on examination had bilateral pyramidal weakness, more pronounced on the right. Reflexes were generally brisk, with bilateral extensor plantar responses. He also developed mild dysarthria but there was no dysphagia.

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Treatment of Hyponatremia

Cited by 31 publications

References 112 publications

Reset osmostat: a rare cause of hyponatraemia

Reset osmostat: a rare cause of hyponatraemia

A case of extreme hyponatremia without neurologic symptoms

An unusual case of quadriparesis

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