Neurologic manifestation of hyponatremia
The signs and symptoms associated with hyponatremia are related both to the degree of imbalance as well as the time the imbalance was established. Neurological disorder symptoms can occur as a result of an osmotic gradient between the intra and extra-cellular. This gradient makes the water move into the cells, resulting in tissue edema. This process is clinically more important in the brain because due to the exhaustion of adaptive mechanisms and the confinement of the skull, cell edema here can lead to increased intracranial pressure and damage neurological function/tissues.
This situation occurs more frequently when hyponatremia develops in a short period of time. If severe hyponatremia develops over hours or a few days instead of many days or weeks, the brain’s ability to adapt to osmotic changes and cell edema is exceeded more quickly. This leads to the development of cerebral edema. Patients in whom severe acute hyponatremia has developed in less than 48 hours may present alarming neurological findings, such as coma and seizures.
In addition, they are at risk of death from brain herniation. Severe hyponatremia developed rapidly is a form of disease other than hyponatremia with a slow evolution. The cerebral adaptations present in the evolutionary slow hyponatremia prevent cerebral edema. This occurs through the transport of sodium, chloride, and potassium for ECF. This compensatory mechanism maintains the osmolarity of the FIC equal to the osmolarity of the ECF and thus avoids the large displacement of water into the cells. Over a period of time, organic solutes such as glutamine, glutamate taurine goes to the ECF to maintain osmotic stability. These molecules are known as “organic osmolites”. The clinical result of this compensation is that these patients experience less severe symptoms and generally do not die due to cerebral herniation.
Slowly evolving hyponatremia is often asymptomatic, but there are limits to how low the level can be before it affects physiological processes, regardless of the chronicity of symptoms. Non-specific symptoms usually develop when serum sodium levels fall below 120 mmol / l. These symptoms include fatigue, lethargy, weakness, and confusion. Seizures and coma are uncommon. As well as the range of time, symptoms are also dependent on the patient’s pre-morbid state.
Certain groups, such as children, hypoxic patients, and pre-menopausal women, are at higher risk of cerebral edema