Transient hypothalamic hypothyroidism and diabetes insipidus after electrical injury.

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.

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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)

CASE REPORT

A 29-year-old woman referred to our hospital after an electric shock injury had an electricity entrance hole in the left hand and exit sites in both feet. Mild sinusoidal tachycardia and dry mouth were found on physical examination. Thirty-six hours after hospitalization, diluted polyuria (urine output [greater than or equal to] 1 L/hr) was noticed. Serum electrolyte, glucose, calcium, serum urea nitrogen, and creatinine levels were normal. Creatine kinase (CK) and lactate dehydrogenase (LDH) levels were moderately elevated. No osmotic agent or diuretic intake was present. A hyposthenuric (density 1,005), clear diuresis of about 1,200 to 1,400 mL/hr was detected, while serum osmolality was 297 mOsm/kg and urine osmolality was 194 mOsm/kg. Central venous pressure was low (-4 cm [H.sub.2]O). In addition to parenteral fluid replacement, 2 [micro]g desmopressin acetate (dDAVP) was given subcutaneously. Afterward, the diuresis rate decreased to 500 to 700 mL/hr. However, 12 hours after dDAVP injection, the diuresi s rate increased to 1,200 to 1,300 mL/hr. The dose was gradually increased to 4 [micro]g twice daily, and diuresis continued in the range of 4,000 to 7,000 mL/24 hours.

The dDAVP was discontinued after 3 weeks. After this point, there was no increase in diuresis rate, and urine density had increased to 1,016. The patient had a history of goiter and had not used any medication for this problem. Hormonal research revealed a severely decreased thyrotropin level, whereas total and free triiodothyronine and thyroxine levels were normal. Thyrotropin-releasing hormone (TRH) testing was done, and the thyrotropin level increased mildly after 40 minutes. During 3 months of follow-up, thyroid hormone and thyrotropin levels were normal. Cranial magnetic resonance imaging and abdominal ultrasonography revealed no disease.

DISCUSSION

A diagnosis of DI is suspected in patients who have sudden onset of polyuria associated with polydipsia. The three primary characteristics of central DI are a diluted urine excretion in the presence of strong osmotic and nonosmotic stimuli for vasopressin secretion, absence of an intrinsic renal disease, and an increase in urine osmolality after dDAVP injection.1'2 The basic criteria for DI diagnosis are persistence of urine specific density levels (1,005) and urine osmolality levels <200 mOsm/kg. (2) Mild DI cases show a higher urine osmolality of 200 to 600 mOsm/kg. Plasma osmolality in central DI is above the normal value of 287 mOsm/kg. (1,3) Vasopressin is the specific drug for such cases. (4,5) Currently, the synthetic long-acting vasopressin analogue dDAVP, which has high antidiuretic but low vasopressor action, is preferred. (4,5) However, use of vasopressin preparations carries the risk of serious complications, including coronary artery spasm, arrhythmias, and water intoxication. (4,5)

On admission, our patient with an electric shock injury had only moderately elevated CK and LDH levels. Sudden onset of diluted polyuria began after 36 hours, and dehydration signs appeared, including sinusoidal tachycardia, dry mouth, low central venous pressure, and slightly elevated serum osmolality in contrast with low urine density and osmolality. These findings are consistent with hyposthenuric polyuria syndrome, which may be seen in central DI. Positive response to dDAVP supported our diagnosis. Dehydration and other tests that may cause a negative effect on wound healing and a delay in recovery were not used in this dehydrated patient. Because of excessive fluid loss (urine output >300 to 500 mL/hr), dDAVP therapy was appropriate to prevent hypoperfusion of damaged tissues and to maintain intravascular fluid support.

Two cases of DI caused by electric shock have previously been reported (3) Besides hypothalamic hypothyroidism, a subnormal or flat response to TRH can occur in many conditions, especially hyperfunctioning thyroid adenomas. (6,7) Three months of follow-up without any medication revealed a spontaneous normalization of thyroid hormones and thyrotropin, showing that thyrotropin deficiency depended on a reversible lesion on TRH synthesizing anterior hypothalamic regions.

The mechanism causing abnormal vasopressin and TRH deficiency in our patient is not known. The patient did not define a fall, strike, or convulsion due to electric shock. Theoretically, giant cells, just like muscle and nerve cells, are more sensitive to lysis, and most signs of electrical damage are related to neuromuscular injury (3,8) Central, peripheral, and autonomous nerve systems may be affected. (8,9) Most of the neurologic deficits occur early in the course and recover spontaneously, while permanent deficits may appear within days to months. (9)

CONCLUSION

We report a case of transient hypothalamic hypothyroidism and transient DI due to electrical injury. The clinical syndrome in this case was probably due to nonthermal injury. However, the exact mechanism through which both vasopressin-producing supraoptic and paraventricular nuclei and TRH-synthesizing anterior hypothalamus are affected and the reversibility of these lesions are not known.

References

(1.) Reeves WB, Andreoli TE: The posterior pituitary and water metabolism. Textbook of Endocrinology. Wilson JD, Foster DW (eds). Philadelphia, WB Saunders co, 8th Ed, 1992, pp 311-348

(2.) Lee RC, Kolodney MS: Electrical injury mechanisms: electrical breakdown of cell membranes. Plast Reconstr Surg 1987; 80:672-681

(3.) Urquart CK, craft PD, Nehlawi MM: Transient diabetes insipidus following electrical burns in two patients. South Med J 1994; 87:412-413

(4.) Cobb WE, Spare S, Reichlin S: Neurogenic diabetes insipidus: management with dDAVP, Ann Intern med 1978; 88:183-188

(5.) Richardson DW, Robinson AG: Desmopressin. Ann Intern Med 1985; 103:228-239

(6.) Larsen PR, Ingbar SH: The thyroid gland. Textbook of Endocrinology. Wilson JD, Foster DW (eds). Philadelphia, WB Saunders Co, 8th Ed, 1992, pp 357-480

(7.) Snyder PJ, Jacobs LS, Rabello MM, et al: Diagnostic value of thyrotropin-releasing hormone in pituitary and hypothalamic disease. Ann Intern Med 1974; 81:751-757

(8.) Dimick AR: Electrical injuries. Principles of Internal Medicine. Isselbacher KJ, Braunwald E, Wilson JD, et al (eds). New York, McGraw-Hill Inc. 13th Ed, 1994, pp 2480-2482

(9.) Grube BJ, Heimbach DM, Engrav LH, et al: Neurologic consequences of electrical burns. J Trauma 1990; 30:254

RELATED ARTICLE: KEY POINTS

* We report a patient with transient hypothalamic hypothyroidism and transient diabetes insipidus due to electrical injury.

* For diabetes insipidus, dDAVP was given to the patient for a short time.

* Hypothyroidism spontaneously improved without any medication

* The mechanism of vasopressin and thyrotropin releasing hormone deficiencies due to electrical injuries is not exactly known as of now.

From the Department of Internal Medicine, Haydarpasa State Hospital, Istanbul, Turkey.

Reprint requests to Ali Ozdemir, MD, Barbaros Mah, Sirma Perde cad, Barinak Sitesi A-2 D:8 Uskudar, Istanbul, Turkey.