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Diabetes Insipidus and Epidural Analgesia for Labor

Passannante, Anthony N. MD; Kopp, Vincent J. MD; Mayer, David C. MD

Case Reports

Department of Anesthesiology, University of North Carolina Hospitals, Chapel Hill, North Carolina.

Accepted for publication November 30, 1994.

Address correspondence and reprint requests to Anthony N. Passannante, MD, Department of Anesthesiology CB 7010, 223 Burnett-Womack, Chapel Hill, NC 27599-7010.

Diabetes insipidus (DI) is a complication of pregnancy with an incidence of 2-4 cases per 100,000 pregnancies [1]. Patients with DI complain of unremitting thirst, a symptom which should raise suspicion of hypovolemia. Peripartum DI can occur in combination with hypertension and abnormalities in liver and kidney function, making differentiation from preeclampsia difficult [2,3]. Because urinary output does not decrease with mild hypovolemia in patients with DI, dehydration is likely if fluid intake is not adequate. When regional anesthetic techniques for labor are used, attention to the potential hazard of hypovolemia is mandatory. Although epidural analgesia is used routinely at many centers, it is rare that central venous pressure (CVP) monitoring is required to ensure its safety. This case illustrates the utility of CVP monitoring when noninvasive assessment of volume status is difficult. It also shows that thirst does not necessarily imply volume depletion.

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Case Report

A 20-yr-old female, gravida 2, para 1, presented with twin pregnancy at 32 3/7 wk gestation, after suffering a tonicclonic seizure. Her first pregnancy was uncomplicated. The patient had received regular prenatal care, and this pregnancy previously was uncomplicated. There was no history of hypertension, peripartum hemorrhage, or hypotension. Physical examination revealed an arterial blood pressure of 169/79 mm Hg, very dry mucous membranes, 2+ pitting edema of the lower extremities, and 2+ deep tendon reflexes. Laboratory analysis revealed serum sodium of 143 mmol/L, potassium of 3.8 mmol/L, blood urea nitrogen of 9 mg/dL, albumin of 3.1 mg/dL, and glucose of 143 mg/dL. Results of dipstick urinalysis were negative for glucose. Coagulation studies and liver function tests were normal. Infant heart rates were 140-160 bpm with reduced variability. A diagnosis of eclampsia was made. Lactated Ringer's solution with 5% dextrose (D5LR) at 125 mL/h, and magnesium sulfate were started. Induction of labor with oxytocin was also begun.

Over the next 6 h, urine output was 5 L, while fluid input was less than 1 L. Evaluation for DI ensued. Measured plasma osmolality was 297 mosm/kg, and urine osmolality was 207 mosm/kg. Therapy with 1-deamino, 8-D-arginine vasopressin (dDAVP) 10 micro gram intranasally twice daily was started. Concomitant with initiation of dDAVP therapy, epidural analgesia was requested.

The patient continued to complain of extreme thirst and dry mouth. Arterial blood pressure was 180/98 mm Hg, and heart rate was 118 bpm. Urine output was 750 mL/h. Serum sodium was 148 mmol/L. Lactate dehydrogenase was now increased at 330 U/L (normal 134-261), while the platelet count and coagulation studies remained normal. Fluid balance in the 12 h since hospital admission showed an output 5 L more than fluid input. To better assess intravascular volume, a central venous catheter was inserted which showed CVP to be 14 mm Hg. With this information, no fluid bolus was given before epidural placement or dosing. A lumbar epidural catheter was inserted, and analgesia for labor was achieved with 0.25% bupivacaine.

With the onset of epidural block, CVP decreased to 5 mm Hg with a sensory level at the eighth thoracic dermatome (T-8) and decreased to 2 mm Hg as the sensory level moved cephalad to T-6. Maternal blood pressure never decreased to less than 130/75 mm Hg. The infant heart rates were unaffected. Healthy male twins were delivered. Therapy with dDAVP continued for 2 days. The patient's thirst abated, urine osmolality increased to 350 mOsm/kg, and serum electrolytes returned to normal. After delivery, free access to oral fluids was allowed. Intravenous (IV) fluid therapy was continued with D5LR at 125 mL/h for 24 h, and she received magnesium sulfate until 48 h postpartum. After dDAVP was initiated the obligate excretion of large amounts of water stopped, and she regained the ability to correctly regulate her electrolytes. The patient was discharged home on the fourth postpartum day with no signs of symptoms of DI.

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This case illustrates several important points about DI in pregnancy. Of primary importance, DI can occur in the peripartum period without any previous history, and this can represent latent central or nephrogenic DI, or DI secondary to excessive placental secretion of vasopressinase [4,5]. The placenta normally secretes small amounts of vasopressinase with serum levels peaking at term. Factors predisposing some patients to placentally derived vasopressinase levels high enough to induce DI are unknown. Because placentally secreted vasopressinase does not degrade dDAVP, dDAVP effectively reverses DI, even when vasopressinase levels are high. The clinical setting, abrupt presentation, and rapid recovery strongly suggest DI induced by placentally secreted vasopressinase. Because vasopressinase levels decline by 25% a day after delivery, quick postpartum recovery is normal [6]. The risk of recurrence in a subsequent pregnancy is unknown.

The second point is that DI in pregnancy makes noninvasive volume assessment difficult. The initial CVP of 14 mm Hg was unexpected, given documented urine output in excess of IV fluid input. While CVP is a pressure reading, and not an actual measurement of circulating blood volume, its increase argues against serious intravascular volume depletion. For comparison, Benedetti et al. [7] studied 10 women with severe preeclampsia and found the average CVP to be 3 mm Hg during early labor. It is plausible that eclamptic vasoconstriction could force blood volume into the central compartment, leading to increased CVP readings in the presence of actual hypovolemia. Alternatively, vasoconstriction on top of a normal circulating volume could lead to an increased CVP, a phenomenon we believe we observed. Because there is a paucity of literature concerning CVP changes on establishment of an epidural block for labor, it is unclear whether the decrease in CVP we observed is normal, or the result of the epidural anesthetic unmasking clinically inapparent hypovolemia.

Thirdly, extreme thirst in pregnancy should suggest DI. The patient had dry mucous membranes and remarkable thirst. She was thirsty because her serum osmolarity was increased. Increased serum osmolality is the most potent stimulus for thirst. A normal thirst threshold for nonpregnant humans is 298 mOsm/kg, but in pregnancy it is reduced to 287 mOsm/kg [8]. Pregnancy causes a resetting of the body's "osmostat" so that normal serum osmolality in pregnancy declines from 280 to 270 mOsm/kg [9]. On presentation to the hospital, her "normal" serum electrolytes gave an estimated serum osmolality of 297 mOsm/kg (using 2[sodium] + blood urea nitrogen/2.8 + glucose/18 to estimate osmolality) [10], which is distinctly increased for a pregnant female. Although hypovolemia can be a stimulus for thirst, the evidence here supports pure hyperosmolarity as the thirst stimulus.

Fourth, epidural placement in the face of peripartum DI should be performed cautiously. The clinical picture at the time of epidural placement in our patient was ambiguous. The patient was mildly tachycardic, had a large, documented negative fluid balance, and had dry oral mucous membranes. Because urine output could not be used as a measure ofadequate intravascular volume, we were not comfortable establishing a major conduction block without CVP monitoring.

Finally, patients with DI need access to liquids containing free water. On presentation to most delivery suites, maternal oral intake is restricted, making IV fluid management more important. This patient's serum sodium increased from 143 to 148 mmol/L while she was receiving D5LR at 125 mL/h. In response to thirst, small quantities of ice chips and slightly hypertonic (the osmolarity of D5LR is 525 mOsm/L) [11] fluids were given. Unable to concentrate her urine, the patient could not combat hyperosmolality without large amounts of free water. Whether hyperosmolality contributed to the presentation of eclampsia is conjectural, but it is safe to say that metabolic disturbances do not decrease the risk of seizures.

In summary, this report shows that DI can present during late pregnancy, and that unremitting thirst and dry mucous membranes can occur without serious hypovolemia. Epidural analgesia is well tolerated if intravascular volume is adequate. The CVP changes illustrate the effects of decreased sympathetic tone on venous capacitance, venous return, and right heart filling pressures. Although DI in pregnancy is rare, its hallmarks remain the same: unremitting thirst, increased serum osmolarity, and hyposthenuria. Due to massive output of dilute urine, access to free water is important to these patients and can be provided either orally or with properly selected IV fluids.

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1. Hime MC, Richardson JA. Diabetes insipidus and pregnancy. Case report, incidence, and review of literature. Obstet Gynecol Surv 1978;33:375-9.
2. Ferrara JM, Malatesta R, Kemman E. Transient nephrogenic diabetes insipidus during toxemia in pregnancy. Diagnost Gynecol Obstet 1980;2:227-30.
3. Goodman H, Sachs BP, Phillipe M, et al. Transient, recurrent nephrogenic diabetes insipidus. Am J Obstet Gynecol 1984;149:910-2.
4. Iwasaki Y, Oiso Y, Kondo K, et al. Aggravation of subclinical diabetes insipidus during pregnancy. N Engl J Med 1991;324:522-6.
5. Durr JA, Hoggard JD, Hunt JM, Schrier RW. Diabetes insipidus in pregnancy associated with abnormally high circulating vaso-pressinase activity. N Engl J Med 1987;316:1070-4.
6. Page EW. The value of plasma pitocinase determinations in obstetrics. Am J Obstet Gynecol 1986;68:288-9.
7. Benedetti TJ, Cotton DB, Miller FC, et al. Hemodynamic observations in severe pre-eclampsia with a flow-directed pulmonary artery catheter. Am J Obstet Gynecol 1980;136:465-70.
8. Davison JM, Gilmore EA, Durr J, et al. Altered osmotic thresholds for vasopressin secretion and thirst in human pregnancy. Am J Physiol 1984;246:F105-9.
9. Hayslett JP. Renal disease in pregnancy. In: Wyngaarden JB, Smith LH, Bennett JC, eds. Cecil textbook of medicine. Philadelphia: WB Saunders, 1992:599-602.
10. Andreoli TE. Disorders of fluid volume, electrolyte, and acidbase balance. In: Wyngaarden JB, Smith LH, Bennett JC, eds. Cecil textbook of medicine. Philadelphia: WB Saunders, 1992:528-40.
11. Sendak MJ. Monitoring and management of perioperative fluid and electrolyte therapy. In: Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and practice of anesthesiology. St Louis: Mosby Year Book, 1993;921.
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