Mechanisms of hyponatremia and diabetes insipidus after acute spinal cord injury: a critical review

Abstract The incidence of hyponatremia after spinal cord injury was reported to be between 25 and 80%. Hyponatremia can lead to a variety of clinical symptoms, from mild to severe and even life-threatening. Hyponatremia is often associated with diabetes insipidus, which refers to insufficient arginine vasopressin (AVP) secretion or defective renal response to AVP, with clinical manifestations of syndromes such as hypoosmolality, polydipsia, and polydipsia. Recent mechanistic studies on hyponatremia and diabetes insipidus after acute spinal cord injury have been performed in isolation, without integrating the above two symptoms into different pathological manifestations that occur in the same injury state and without considering the acute spinal cord injury patient’s condition as a whole. The therapeutic principles of CSWS and SIADH are in opposition to one another. It is not easy to identify the mechanism of hyponatremia in clinical practice, which makes selecting the treatment difficult. According to the existing theories, treatments for hyponatremia and diabetes insipidus together are contraindicated, whether the mechanism of hyponatremia is thought to be CSWS or SIADH. In this paper, we review the mechanism of these two pathological manifestations and suggest that our current understanding of the mechanisms of hyponatremia and diabetes insipidus after high acute cervical SCI is insufficient, and it is likely that there are other undetected pathogenetic mechanisms.