Hyponatremia in the Neurologically Ill Patient: A Review

Lerner, David P.; Shepherd, Starane; Batra, Ayush

doi:10.1177/1941874419895124

Cited by 6 publications

(12 citation statements)

References 74 publications

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“…The entire process can last for up to 48 h, while concurrent downregulation of aquaporin channels may take up to a week or longer before reaching homeostasis. 7 , 17 Considering these pathophysiological changes related to hyponatraemia, the already injured brain cells in a patient with stroke would be more susceptible to further damage.…”

Section: Pathophysiology Of Hyponatraemia and Its Effect On The Brainmentioning

confidence: 99%

“…The most severely affected patients become ‘locked in’, unable to move, speak or swallow due to central pons demyelination. 7 , 17 Therefore, physicians should be alert for such symptoms in order to exclude ODS apart from other stroke-related complications. Although ODS may result in permanent disability or death, many patients, even those who have previously required ventilator support, can fully recover.…”

Section: Clinical Significance Of Hyponatraemia In Patients With Strokementioning

confidence: 99%

“…Although ODS may result in permanent disability or death, many patients, even those who have previously required ventilator support, can fully recover. 7 , 17 Despite these early neurologic symptoms, brain imaging may remain normal for as long as 4 weeks after the onset of ODS. Thus, a normal brain scan does not exclude ODS diagnosis.…”

Section: Clinical Significance Of Hyponatraemia In Patients With Strokementioning

confidence: 99%

“… 1 – 4 Low sodium (Na + ) levels are commonly noticed in neurologic diseases, including stroke, and are present in 38–54% of such patients. 5 – 9 In this setting, hyponatraemia and water balance exhibit detrimental effects on the injured brain and might increase the corresponding mortality by 60%. 6 , 8 , 9 …”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4] Low sodium (Na + ) levels are commonly noticed in neurologic diseases, including stroke, and are present in 38-54% of such patients. [5][6][7][8][9] In this setting, hyponatraemia and water balance exhibit detrimental effects on the injured brain and might increase the corresponding mortality by 60%. 6,8,9 Clinical symptoms owing to hyponatraemia are related with the severity, the onset and rate of change of serum Na + levels.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke

Anastasiou

Liamis

Barkas

2023

Therapeutic Advances in Endocrinology

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Hyponatraemia is common in patients with stroke and associated with adverse outcomes and increased mortality risk. The present review presents the underlying causes and provides a thorough algorithm for the diagnosis and management of hyponatraemia in stroke patients. Concomitant diseases and therapies, such as diabetes, chronic kidney disease and heart failure, along with diuretics, antidepressants and proton pump inhibitors are the most common causes of hyponatraemia in community. In the setting of acute stroke, the emergence of hyponatraemia might be attributed to the administration of hypotonic solutions and drugs (ie. mannitol and antiepileptics), poor solute intake, infections, as well as stroke-related conditions or complications, such as the syndrome of inappropriate secretion of antidiuretic hormone, cerebral salt wasting syndrome and secondary adrenal insufficiency. Diagnostically, the initial step is to differentiate hypotonic from non-hypotonic hyponatraemia, usually caused by hyperglycaemia or recent mannitol administration in patients with stroke. Determining urine osmolality, urine sodium level and volume status are the following steps in the differentiation of hypotonic hyponatraemia. Of note, specific parameters, such as fractional uric acid and urea excretion, along with plasma copeptin concentration, may further improve the diagnostic yield. Therapeutic options are based on the duration and symptoms of hyponatremia. In the case of acute or symptomatic hyponatraemia, hypertonic saline administration is recommended. Hypovolaemic chronic hyponatremia is treated with isotonic solution administration. Although fluid restriction remains the first-line treatment for the rest forms of chronic hyponatraemia, therapies increasing renal free water excretion may be necessary. Loop diuretics and urea serve this purpose in patients with stroke, whereas sodium-glucose transport protein-2 inhibitors appear to be a promising therapy. Nevertheless, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in such patients. Randomized trials designed to compare therapeutic strategies in managing hyponatraemia in patients with stroke are required.

show abstract

Section: Pathophysiology Of Hyponatraemia and Its Effect On The Brainmentioning

confidence: 99%

Section: Clinical Significance Of Hyponatraemia In Patients With Strokementioning

confidence: 99%

Section: Clinical Significance Of Hyponatraemia In Patients With Strokementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke

Anastasiou

Liamis

Barkas

2023

Therapeutic Advances in Endocrinology

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Metabolic values precluding clinical death by neurologic Criteria/Brain death: Survey of neurocritical care society physicians

Lerner

Bassil

Tadevosyan

et al. 2021

Journal of Clinical Neuroscience

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Location‐atypical lesions in non‐ketotic hyperglycemic epilepsy: expanding the clinico‐radiographic phenotype

Amar,

Bhattacharya,

Uzo‐Okereke

et al. 2022

Epileptic Disorders

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Non‐ketotic hyperglycemia (NKH) is associated with a spectrum of symptoms and radiographic findings due to poorly‐controlled diabetes mellitus. These lesions, which predominantly affect the parieto‐occipital cortex, are commonly missed by neurologists and neuroradiologists due to their subtle hypointense appearance on T2‐based imaging. We report four atypical cases of this syndrome to highlight its subtle, protean presentation in order to aid timely diagnosis. Based on our institutional case series, we describe four cases of NKH with atypical presentation and lesion burden affecting the anterior cortex. We review the clinical presentations, laboratory abnormalities, neuroimaging, and corresponding electroencephalography. Four patients with atypical NKH were characterized in our series. Presenting symptoms ranged from rhythmic handtapping to generalized tonic‐clonic status epilepticus. Laboratory values were notable for marked hyperglycemia (range: 447 – 627 mg/dL), mild pseudohyponatremia (range: 127 – 136 mmol/L), and elevated hemoglobin A1C levels (range: 10.9 16.1%). All patients were found to have the classically described pattern of T2‐based hypointensity; three with atypical distributions involving the “anterior” cortex. These lesions corresponded to the electrographic nidus of seizure burden. During follow‐up, both seizures and T2‐based hypointensity resolved within weeks of serum glucose normalization. Our series of four NKH patients with atypical findings of T2‐based signal abnormalities expands the clinico‐radiographic phenotype revealing a more protean distribution than previously described. Knowledge of these atypical imaging features will aid both the neurologist and radiologist in timely diagnosis and care of these patients.

show abstract

Hyponatremia in the Neurologically Ill Patient: A Review

Cited by 6 publications

References 74 publications

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke

A step-by-step guide for the diagnosis and management of hyponatraemia in patients with stroke

Metabolic values precluding clinical death by neurologic Criteria/Brain death: Survey of neurocritical care society physicians

Location‐atypical lesions in non‐ketotic hyperglycemic epilepsy: expanding the clinico‐radiographic phenotype

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