Psychosomatics 45:82-83, February 2004
© 2004 The Academy of Psychosomatic Medicine
Lithium-Induced Nephrogenic Diabetes Insipidus in a Surgical Patient
François Sirois, M.D.
Received May 6, 2003; revision received June 11, 2003; accepted June 19, 2003. From the Department of Psychiatry, Laval Hospital. Address reprint requests to Dr. Sirois, Department of Psychiatry, Laval Hospital, 2725, chemin Sainte-Foy, Sainte-Foy, Quebec, Canada G1V 4G5; fsir{at}globetrotter.net (e-mail).
Nephrogenic diabetes insipidus is a well-established complication of long-term lithium therapy. It may affect about 10%–15%1 of patients treated 15 years or more. It is known that long-term administration of lithium induces an irreversible reduction of urinary-concentrating capacity and a partly reversible reduction in the glomerular filtration rate.2 Such complications are usually heralded either by clinical symptoms of polydipsia, polyuria, and nocturia or by abnormal laboratory values of serum creatinine or urinary density. The onset of nephrogenic diabetes insipidus can be associated with a surgical episode in which it presents a challenge for fluid management. A previous report3 indicated that such an occurrence could have been suspected on clinical grounds had a exhaustive history been possible. The current report also emphasizes that a symptom of polydipsia was present; it does not stress the medical management of nephrogenic diabetes insipidus but opens the question of setting long-term lithium treatment short of significant renal impairment.
Case Report
Ms. A, a 47-year-old woman, was admitted for an acute abdominal syndrome. A toxic megacolon was suspected, since a radiographic investigation showed a distended but unobstructed large intestine. Surgery followed within 48 hours, with local resection of the affected necrotic part of the transverse colon and a temporary colostomy. At her admission, Ms. A had hypernatremia (levels of 142, 145, and 152 mmol/liter) and a serum creatinine level elevated to 155 µmol.
Ms. A had been hospitalized six times previously for bipolar I disorder within a 6-year span, ending 18 years ago; she had not been hospitalized since and had been taking lithium for the last 23 years. Her current lithium dose at the time of hospitalization was 300 mg t.i.d. and 150 mg at bedtime; her serum level was 0.7 meq/liter at admission. Her psychiatric condition had been stable for at least the last 10 years. Three weeks before hospitalization, her serum lithium level was 0.7 meq/liter, her serum creatinine level was 114 µmol/liter (upper normal=115), her urinary density level was equal or less than 1.005 (normal=1.003–1030). When questioned before surgery, she admitted drinking about 4 liters a day of fluid.
In the immediate postoperative period, full-blown nephrogenic diabetes insipidus appeared. Two days after surgery, the in-and-out balance of fluids was 19 liters given and 15 liters excreted; in the next 10 days, diuresis was reduced to about 8 liters a day. An additional week was needed to achieve a better control of her nephrogenic diabetes insipidus. During the early phase of postoperative management, Ms. A was administered haloperidol up to 6 mg over 24 hours intravenously for mild agitation and a slight hypomanic mood; the drug was tapered rapidly. Her hospital course was uneventful, and Ms. A was discharged within a month. During the later part of her hospitalization, valproic acid was prescribed at 250 mg b.i.d., with methotrimeprazine, 25 mg at bedtime, since she was anxious about her condition, appeared fidgety, and complained of disturbed sleep. Her mood remained well controlled, without psychomotor instability or alteration of speech.
Discussion
A number of issues relevant to lithium management are raised here. The first question is whether any significant physiological stress can trigger nephrogenic diabetes insipidus in people receiving lithium treatment for over 10 years. Nephrogenic diabetes insipidus is known to occur after surgery,3,4 after brain injury,5 during pregnancy,6 or while fasting.7 The implication is that any long-term user of lithium should be monitored for such complication in case of any serious health problem.
The second question is the issue of reversibility. During the first 25 years of lithium use, it was thought that nephrogenic diabetes insipidus was reversible with an off-lithium period;2 reports about patients with nephrogenic diabetes insipidus persisting or recurring many years after lithium discontinuation5,8,9 have blurred that notion. Short-term studies of lithium withdrawal1,9 suggested a partly reversible reduction of its urinary-concentrating capacity. While only 12% of long-term lithium users might develop nephrogenic diabetes insipidus, Boton et al.10 found that 50% of such users might have a lessened ability to concentrate urine. Bendz et al.1 also showed that both the glomerular filtration rate and the urinary-concentration capacity were lessened. A reduced urinary-concentration capacity was found by Bendz et al.2 to be associated with treatment duration rather than with age, with no difference between high and low serum levels. By contrast, a reduction in the glomerular filtration rate was associated both with age and treatment duration.
The next question is, therefore, how long should patients be maintained on lithium? Previously, it was thought for life. Now, should a 10-year or a 15-year period be a cut-off point for the maximum duration of treatment? Any stable bipolar patient should probably be switched to anticonvulsant medication to prevent irreversible kidney damage. A further question is about the optimal lithium serum level. Lower levels around 0.4 to 0.6 mmol/liter are advocated. Although Schou and Vestergaard11 suggested that such a regimen might eliminate the risk of renal impairment, Bendz et al.2 produced data to the contrary.
REFERENCES
- Bendz H, Aurell M: Drug-induced diabetes insipidus. Drug Safety 1999; 21:449–456[CrossRef][Medline]
- Bendz H, Aurell M, Lanke J: A historical cohort study of kidney damage in long-term lithium patients: continued surveillance needed. Eur Psychiatry 2001; 16:199–206[CrossRef][Medline]
- Johnson M, Ogorman J, Golembiewski GH, Paluzzi MW: Nephrogenic diabetes insipidus secondary to lithium therapy in the postoperative patient—a case report. Am Surg 1994; 60:836–839[Medline]
- Gray EJ, Dierks EJ: Lithium-induced diabetes insipidus in a surgical patient: report of a case and review of the literature. J Oral Maxillofac Surg 1996; 54:909–912[Medline]
- Thompson CJ, France AJ, Baylis PH: Persistent nephrogenic diabetes insipidus following lithium therapy. Scott Med J 1997; 42:16–17[Medline]
- Yingling DR, Utter G, Vengalil S, Mason B: Calcium channel blocker, nimodipine, for the treatment of bipolar disorder during pregnancy. Am J Obstet Gynecol 2002; 187:1711–1712[Medline]
- Lam SS, Kjellstrand C: Emergency treatment of lithium-induced diabetes insipidus with nonsteroidal anti-inflammatory drugs. Ren Fail 1997; 19:183–188[Medline]
- Stone KA: Lithium-induced nephrogenic diabetes insipidus. J Am Board Fam Pract 1999; 12:43–47[Abstract]
- Bucht G, Wahlin A: Renal concentrating capacity in long-term lithium treatment and after withdrawal of lithium. Acta Med Scand 1980; 207:309–314[Medline]
- Boton R, Gaviria M, Battle DC: Prevalence, pathogenesis, and treatment of renal dysfunction associated with chronic lithium therapy. Am J Kidney Dis 1987; 10:329–345[Medline]
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