Transient Hypothalamic Hypothyroidism and Diabetes Insipidus After Electrical Injury

Ali Özdemir, MD, Pinar Seymen, MD, Ömer Atalay Yürekli, MD, Muazzez Caymaz, MD, Yildiz Barut, MD, Meltem Eres, MD


South Med J. 2002;95(4) 

In This Article

Abstract and Introduction

Transient or permanent diabetes insipidus (DI) due to damage in vasopressinergic neurons -- which may be hereditary or caused by head injury, brain surgery, tumors, granulomatous disorders, infections, vascular disorders, autoimmunity, and idiopathic causes -- is not rare. Hypothalamic hypothyroidism is due to decreased thyrotropin-releasing hormone secretion and is seen rarely. We report a case of transient hypothalamic hypothyroidism and transient DI due to electrical injury.

Hypotonic polyuria syndromes are neurogenic diabetes insipidus (DI), nephrogenic DI, and primary polydipsia. In the neurogenic or central form, the primary defect is decreased or absent secretion of vasopressin. The syndrome of central DI must be differentiated from other types of polyuria, including primary polydipsia, nephrogenic DI, certain osmotic diuretic states, and that caused by the administration of loop diuretics.[1]

Electrical fields damage the cells by both thermal and nonthermal mechanisms. The role of thermal effect of electrical energy on tissue damage and the irreversibility of this damage are well known, but it is obvious that all of the clinical signs cannot be explained in this way. Another important damage mechanism is cell lysis as a result of cell membrane destruction, disturbed electrochemical equilibrium inside and outside the cell, and additional effects of cytokines freed from the damaged cells.[2]