Cerebral Salt-Wasting Syndrome in a Patient With Neuroleptic Malignant Syndrome

Lenhard, Thorsten; Külkens, Sonja; Schwab, Stefan

doi:10.1001/archneur.64.1.122

“…This notion is further supported by the associated elevated CHGA levels. Sympathoadrenal stimulation as a possible cause of salt-wasting is further supported by the finding that BNP-associated hyponatraemia can occur also in neuroleptic malignant syndrome14 that reflects a state of sympathoadrenal dysregulation as well 15…”

Section: Discussionmentioning

confidence: 84%

Renal salt wasting as part of dysautonomia in Guillain-Barre syndrome

Lenhard¹,

Grimm

²

,

Ringleb

³

2010

Journal of Neurology, Neurosurgery & Psychiatry

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Cerebral salt-wasting syndrome and the syndrome of inappropriate antidiuresis (SIAD) are the most important causes of non-iatrogenic hyponatraemia that can significantly complicate various brain diseases. Salt wasting without an underlying CNS disease may have been disregarded so far by clinicians and has been described as renal salt-wasting (RSW) in patients as drug side effect (eg, cisplatin), in older people with various common diseases (eg, hip fracture, pulmonary infections) and other sporadic conditions. In Guillain-Barré Syndrome (GBS), however, hyponatraemia has been described mainly as SIAD. However, symptoms of hyponatraemia rarely develop in GBS. Here, we report on a woman with GBS with dominant symptoms of dysautonomia and moderate severe hyponatraemia. We could identify RSW as part of the autonomic dysfunction that significantly contributed to disease worsening.

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“…The effect of natriuretic peptides is well documented in nephrons, but less clear in the CNS and autonomic nervous system. It has, however, been suggested that dysregulation of the sympathetic response may be responsible for CSW; association of CSW with neuroleptic malignant syndrome suggests the role of the sympathoadrenal system and natriuretic peptides 7 . A direct relationship between ANP and BNP with intracerebral pressure (ICP) has been reported 4 .…”

Section: • Surgerymentioning

confidence: 99%

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

Misra

¹

,

Kalita

²

2021

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Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

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“…The effect of natriuretic peptides is well documented in nephrons, but less clear in the CNS and autonomic nervous system. It has, however, been suggested that dysregulation of the sympathetic response may be responsible for CSW; association of CSW with neuroleptic malignant syndrome suggests the role of the sympathoadrenal system and natriuretic peptides 7 . A direct relationship between ANP and BNP with intracerebral pressure (ICP) has been reported 4 .…”

Section: Pathophysiology Of Hyponatremiamentioning

confidence: 99%

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

Misra

¹

2019

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Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

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Cerebral Salt-Wasting Syndrome in a Patient With Neuroleptic Malignant Syndrome

Cited by 15 publications

References 14 publications

Renal salt wasting as part of dysautonomia in Guillain-Barre syndrome

Renal salt wasting as part of dysautonomia in Guillain-Barre syndrome

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

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