When there is a condition affecting the CNS, CSW (cerebral salt wasting) may be a contributing factor to hyponatremia. The symptoms of CSW include hyponatremia, hypovolemia, and increased urinary sodium levels. Professionals disagree on whether CSW is a unique illness or a variant of the SIADH (syndrome of inadequate antidiuretic hormone secretion in the present research).
Because SIADH and CSW are treated differently, it’s critical to make the distinction between the two. Liquids and sodium replenishment are given to the patient in order to treat CSW. The patient has a fluid restriction due to SIADH. While CSW might persist, it usually resolves within a few weeks to several months of its commencement.
The release of BNP (brain natriuretic peptide) or injury to the hypothalamus with a consequent malfunction of the sympathetic system is two leading hypotheses for the pathogenesis of CSW.
Epidemiology
The precise frequency and incidence of CSW, a disorder that is still up for debate, may be difficult to determine. The most frequent cause of CSW is aneurysmal subarachnoid bleeding. However, it can also occur from various injuries to the CNS.
There have been reports of CSW in the following conditions: following surgery for a calvarial remodeling procedure, an auditory neuroma, a pituitary lesion, glioma, viral and tuberculous meningitis, cerebral trauma, and metastatic cancer. According to some estimates, CSW causes up to 25% of the serious hyponatremia that occurs following aneurysmal subarachnoid bleeding.
Most instances of cerebral salt wasting, along with other CNS injuries, are case reports. Outside of patients with CNS injury, the prevalence and incidence of CSW are not consistently recorded.
Anatomy
Pathophysiology
The actual cause of CSW is still under investigation. As said, some contend that cerebral salt wasting is a form of SIADH and does not actually occur. There are now two hypotheses for the cause of CSW: the impact of a circulating component or a problem with the nervous system’s sympathetic nerves.
According to certain studies, after an injury, the brain releases (BNP) brain natriuretic peptide, which then crosses the BBB (blood-brain barrier) and circulates throughout the body. The BNP suppresses sodium reabsorption and lessens renin release by acting on the collecting ducts of the kidney tubules.
According to the second hypothesis, damage to the hypothalamus prevents the sympathetic system from stimulating renin secretion and promoting salt absorption. There is disagreement on the precise mechanism behind CSW.
Etiology
The cause of CSW is still not fully known. The most frequently occurring following a CNS injury is CSW. Aneurysmal subarachnoid bleeding is the initiating insult that is most frequently mentioned.
It is unclear why aneurysmal subarachnoid bleeding causes CSW more commonly than trauma subarachnoid bleeding or any CNS injury. It is also unclear why CSW is infrequent following other illnesses or traumas.
Genetics
Prognostic Factors
Clinical History
Physical Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
Medication
Future Trends
Media Gallary
References
https://www.ncbi.nlm.nih.gov/books/NBK534855/
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When there is a condition affecting the CNS, CSW (cerebral salt wasting) may be a contributing factor to hyponatremia. The symptoms of CSW include hyponatremia, hypovolemia, and increased urinary sodium levels. Professionals disagree on whether CSW is a unique illness or a variant of the SIADH (syndrome of inadequate antidiuretic hormone secretion in the present research).
Because SIADH and CSW are treated differently, it’s critical to make the distinction between the two. Liquids and sodium replenishment are given to the patient in order to treat CSW. The patient has a fluid restriction due to SIADH. While CSW might persist, it usually resolves within a few weeks to several months of its commencement.
The release of BNP (brain natriuretic peptide) or injury to the hypothalamus with a consequent malfunction of the sympathetic system is two leading hypotheses for the pathogenesis of CSW.
The precise frequency and incidence of CSW, a disorder that is still up for debate, may be difficult to determine. The most frequent cause of CSW is aneurysmal subarachnoid bleeding. However, it can also occur from various injuries to the CNS.
There have been reports of CSW in the following conditions: following surgery for a calvarial remodeling procedure, an auditory neuroma, a pituitary lesion, glioma, viral and tuberculous meningitis, cerebral trauma, and metastatic cancer. According to some estimates, CSW causes up to 25% of the serious hyponatremia that occurs following aneurysmal subarachnoid bleeding.
Most instances of cerebral salt wasting, along with other CNS injuries, are case reports. Outside of patients with CNS injury, the prevalence and incidence of CSW are not consistently recorded.
The actual cause of CSW is still under investigation. As said, some contend that cerebral salt wasting is a form of SIADH and does not actually occur. There are now two hypotheses for the cause of CSW: the impact of a circulating component or a problem with the nervous system’s sympathetic nerves.
According to certain studies, after an injury, the brain releases (BNP) brain natriuretic peptide, which then crosses the BBB (blood-brain barrier) and circulates throughout the body. The BNP suppresses sodium reabsorption and lessens renin release by acting on the collecting ducts of the kidney tubules.
According to the second hypothesis, damage to the hypothalamus prevents the sympathetic system from stimulating renin secretion and promoting salt absorption. There is disagreement on the precise mechanism behind CSW.
The cause of CSW is still not fully known. The most frequently occurring following a CNS injury is CSW. Aneurysmal subarachnoid bleeding is the initiating insult that is most frequently mentioned.
It is unclear why aneurysmal subarachnoid bleeding causes CSW more commonly than trauma subarachnoid bleeding or any CNS injury. It is also unclear why CSW is infrequent following other illnesses or traumas.
https://www.ncbi.nlm.nih.gov/books/NBK534855/
medtigo
Cerebral Salt-Wasting Syndrome
Updated :
September 28, 2022
When there is a condition affecting the CNS, CSW (cerebral salt wasting) may be a contributing factor to hyponatremia. The symptoms of CSW include hyponatremia, hypovolemia, and increased urinary sodium levels. Professionals disagree on whether CSW is a unique illness or a variant of the SIADH (syndrome of inadequate antidiuretic hormone secretion in the present research).
Because SIADH and CSW are treated differently, it’s critical to make the distinction between the two. Liquids and sodium replenishment are given to the patient in order to treat CSW. The patient has a fluid restriction due to SIADH. While CSW might persist, it usually resolves within a few weeks to several months of its commencement.
The release of BNP (brain natriuretic peptide) or injury to the hypothalamus with a consequent malfunction of the sympathetic system is two leading hypotheses for the pathogenesis of CSW.
The precise frequency and incidence of CSW, a disorder that is still up for debate, may be difficult to determine. The most frequent cause of CSW is aneurysmal subarachnoid bleeding. However, it can also occur from various injuries to the CNS.
There have been reports of CSW in the following conditions: following surgery for a calvarial remodeling procedure, an auditory neuroma, a pituitary lesion, glioma, viral and tuberculous meningitis, cerebral trauma, and metastatic cancer. According to some estimates, CSW causes up to 25% of the serious hyponatremia that occurs following aneurysmal subarachnoid bleeding.
Most instances of cerebral salt wasting, along with other CNS injuries, are case reports. Outside of patients with CNS injury, the prevalence and incidence of CSW are not consistently recorded.
The actual cause of CSW is still under investigation. As said, some contend that cerebral salt wasting is a form of SIADH and does not actually occur. There are now two hypotheses for the cause of CSW: the impact of a circulating component or a problem with the nervous system’s sympathetic nerves.
According to certain studies, after an injury, the brain releases (BNP) brain natriuretic peptide, which then crosses the BBB (blood-brain barrier) and circulates throughout the body. The BNP suppresses sodium reabsorption and lessens renin release by acting on the collecting ducts of the kidney tubules.
According to the second hypothesis, damage to the hypothalamus prevents the sympathetic system from stimulating renin secretion and promoting salt absorption. There is disagreement on the precise mechanism behind CSW.
The cause of CSW is still not fully known. The most frequently occurring following a CNS injury is CSW. Aneurysmal subarachnoid bleeding is the initiating insult that is most frequently mentioned.
It is unclear why aneurysmal subarachnoid bleeding causes CSW more commonly than trauma subarachnoid bleeding or any CNS injury. It is also unclear why CSW is infrequent following other illnesses or traumas.
https://www.ncbi.nlm.nih.gov/books/NBK534855/
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