Letter: Manifestations of Water and Sodium Disorders Following Surgery for Sellar Lesions

To the Editor: It is widely known that magnocellular neurons in the hypothalamic supraoptic and paraventricular nuclei are capable of synthesizing antidiuretic hormone (ADH), which is subsequently transported along the hypothalamic-neurohypophyseal tract to the posterior pituitary, where it is secreted into the circulatory system.1 As ADH regulates the body's water and sodium balance, any damage to the hypothalamic-neurohypophyseal system caused by surgery for sellar lesions will lead to disordered water and electrolyte balance. The main manifestations of postoperative water and sodium disorders after surgery for sellar lesions include diabetes insipidus (DI), cerebral salt-wasting syndrome, and syndrome of inappropriate antidiuretic hormone secretion (SIADH).2-4 Clinicians often get confused when these manifestations occur after surgery in the sellar region, and they may not be able to effectively treat these disorders if the underlying pathological mechanisms are not understood. Here, we will review the characteristics of postoperative water and sodium imbalances associated with surgery for sellar lesions, and propose the concept of “relative DI” that may arise during SIADH. The main manifestations of DI following trans-sphenoidal surgery for pituitary adenoma include polydipsia and polyuria, the incidences of which vary between 1% and 67%.5 According to our clinical observations, the probability of hypernatremia occurring after trans-sphenoidal surgery for sellar lesions is low, whereas patients with craniopharyngioma who opt for craniotomy are highly likely to develop postoperative hypernatremia. This may be due to the tight adhesion of the craniopharyngioma to the surrounding tissues, and the extensive intraoperative damage inflicted on the hypothalamic-neurohypophyseal system, resulting in extremely low postoperative ADH levels and further hypertonic dehydration. In contrast, the occurrence of DI following trans-sphenoidal surgery for pituitary adenomas is generally transient and often resolves spontaneously within 3 to 5 d.6 Transient DI immediately after surgery occurs due to the damage or partial resection of the neurohypophysis, causing reduced release of ADH into the blood. This condition persists for several months only in few cases, and permanent DI is rare. Among those with permanent DI, a very small number of cases present with “triphasic DI.” “Triphasic DI” is seen in cases where 85% or more of the hypothalamic magnocellular neurons are damaged and polyuria occurs 2 to 4 d after surgery. This is followed by an excessive release of ADH for about a week, during which the patient has reduced urine output and may even develop hyponatremia. After the residual ADH is released, the patient develops permanent DI.5 We have observed that some patients present with hyponatremia combined with recurrent polyuria following surgery for sellar lesions. One of the presumed causes is cerebral salt-wasting syndrome. When the hypothalamic-pituitary axis is damaged by intraoperative procedures, subsequent elevation of levels of atrial natriuretic peptide and brain natriuretic peptide may inhibit the release of ADH and aldosterone, which can promote renal drainage and sodium excretion, thereby decreasing blood volume. Another possible cause may be a severe decline in the function of the hypothalamic-pituitary-adrenal axis; this further leads to a sharp decrease in aldosterone. As aldosterone promotes sodium retention and potassium excretion, inadequate aldosterone levels will reduce renal reabsorption of sodium and water, leading to a further decrease in blood sodium levels. SIADH is one of the main causes of readmission due to hyponatremia following trans-sphenoidal surgery for pituitary adenomas.7,8 Hyponatremia generally appears 5 to 7 d after surgery, lasts for about 1 wk, and is subsequently corrected when the posterior pituitary re-establishes an intact ADH secretory pathway. The delay in onset can be attributed to the fact that the stretching and deformation of the pituitary stalk, partial axonal damage and transection, and damage to the blood supply of the pituitary stalk are gradual processes and do not manifest immediately during surgery. In addition, intraoperative damage to the neurohypophysis, peripheral vascular bed, and mechanism of ADH secretion into the bloodstream also takes several days to repair. Patients who develop SIADH often do not have a large urine output. However, we have found that some patients with delayed hyponatremia may present with transient polyuria (more than 3000 mL of urine per day), lasting from about 1 to 3 d, in the later stages of hyponatremia after which the patient's blood sodium levels return to normal. This phase has not been previously reported in the literature and often goes unnoticed. Therefore, we divided hyponatremia into early and late stages. The early stage involves low urine output and hyponatremia due to excessive ADH secretion and the late stage involves a relative decrease in ADH secretion, which manifests as a transient increase in urine output and a gradual rise in blood sodium level. We call this transient presence of polyuria “relative DI,” which spontaneously corrects the hyponatremia after excreting the excess water accumulated during the early stage of hyponatremia. In conclusion, this paper summarized and analyzed the manifestations of water and sodium imbalances in patients who undergo surgery for sellar lesions. It is worth mentioning that the concept of “relative DI” in the clinical course of SIADH was introduced for the first time in this paper. It is important to note that polyuria in the late stage of hyponatremia cannot be treated simply with antidiuretic therapy as such a treatment strategy may exacerbate the hyponatremia. Funding This work was financially supported by the Innovation Joint Fund Project of Fujian Province, China (No. 2019Y9045); Leading Project of Fujian Province, China (No. 2018Y0067); and Qihang Fund of Fujian Medical University (No. 2018QH1244). Disclosures The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.