ABSTRACT
Sodium is the main extracellular cation, with its distribution in extracellular compartments, such as plasma and cerebrospinal fluid being tightly regulated and affecting cell function, especially neurons. Critical care patients are at increased risk for disorders of extracellular sodium (dysnatremias), which endow increased morbidity and mortality. In the neurocritical care patient, specific causes of dysnatremia may exist, including hypernatremia caused by direct damage to the “posterior” hypothalamic-pituitary axis following trauma and/or in the hemorrhagic patient. This chapter illustrates aspects of physiopathology and management of these disorders from a neurocritical point of view. Disorders of plasma potassium, calcium, magnesium, and chloride are more rapidly reviewed with a focus on peculiar aspects concerning their management in neurocritical patients. When acute brain damage involves the “anterior” hypothalamic-pituitary-adrenal axis, acute pituitary failure may occur and put the patient at risk for cardiovascular instability caused by acute adrenal failure. Other endocrinologic disorders, such as hypothyroidism, hypogonadism, and growth hormone deficiency may appear after acute brain damage and impair recovery. This chapter reviews aspects of physiopathology and management of endocrinologic disorders with a neurocritical care specialist’s cut. Hyperglycemia is a constant element of disruption in the physiopathology of acute brain damage. Considerations on its management are briefly treated.
