eMedicine Specialties > Pediatrics: General Medicine > Endocrinology
Diabetes Insipidus: Follow-up
Updated: Feb 6, 2009
Follow-up
Further Inpatient Care
- Subsequent admissions are determined by the need for intravenous rehydration, especially during intercurrent GI illnesses.
Further Outpatient Care
- Regular follow-up visits with an endocrinologist (for central diabetes insipidus [CDI]) or a nephrologist (for nephrogenic diabetes insipidus [NDI]) are necessary for dosage adjustment.
- When indomethacin is used in long-term therapy, carefully observe renal function for any signs of toxicity.
Inpatient & Outpatient Medications
- In addition to the medications already listed, aqueous vasopressin (Pitressin) and desmopressin (DDAVP) preparations are available for intravenous use in emergency circumstances.
Transfer
- Transfer to an academic center is highly advised for initial diagnosis and treatment, especially because central diabetes insipidus may require involved diagnostic studies and neurosurgical or oncologic treatment.
- Subsequent episodes requiring intravenous rehydration can be treated by routine admission.
Deterrence/Prevention
- Reduce or eliminate activities resulting in increased insensible fluid losses.
- Avoid creating barriers to drinking water.
Complications
- Growth failure
- Nocturia and enuresis
- Hypernatremic dehydration
- Seizures
- Mental retardation
Prognosis
- Long-term survival in cases of central diabetes insipidus depends on the precipitating cause. In primary central diabetes insipidus, the prognosis is excellent with early recognition and appropriate DDAVP therapy.
- The earlier onset of nephrogenic diabetes insipidus and the reduced ability to treat this variety of the disease renders the child more prone to attention deficits, hyperactivity, learning disorders, and psychomotor delay.
- As long as water remains available at all times to replace the massive losses, long-term survival is not in question.
Patient Education
- Parents must replace water in infants and young children who cannot express thirst or access fluids without assistance.
- GI illnesses that cause decreased intake, increased stool losses, or both must receive early and serious attention to prevent life-threatening electrolyte and fluid balance abnormalities.
Miscellaneous
Medicolegal Pitfalls
- Failure to recognize excessive fluid losses
- Failure to diagnose an underlying condition causing secondary central diabetes insipidus (CDI)
- Overtreatment with desmopressin (DDAVP) resulting in hyponatremia and seizures
Special Concerns
- Surgical procedures of any kind require replacement of fluids at a much higher rate than normal maintenance; inattention to this may result in serious consequences.
More on Diabetes Insipidus |
| Overview: Diabetes Insipidus |
| Differential Diagnoses & Workup: Diabetes Insipidus |
| Treatment & Medication: Diabetes Insipidus |
Follow-up: Diabetes Insipidus |
| Multimedia: Diabetes Insipidus |
| References |
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References
Bichet DG, Arthus MF, Lonergan M, et al. X-linked nephrogenic diabetes insipidus mutations in North America and the Hopewell hypothesis. J Clin Invest. Sep 1993;92(3):1262-8. [Medline]. [Full Text].
Friedman E, Bale AE, Carson E, et al. Nephrogenic diabetes insipidus: an X chromosome-linked dominant inheritance pattern with a vasopressin type 2 receptor gene that is structurally normal. Proc Natl Acad Sci U S A. Aug 30 1994;91(18):8457-61. [Medline]. [Full Text].
Wildin RS, Antush MJ, Bennett RL. Heterogeneous AVPR2 gene mutations in congenital nephrogenic diabetes insipidus. Am J Hum Genet. Aug 1994;55(2):266-77. [Medline].
Faerch M, Christensen JH, Corydon TJ, et al. Partial nephrogenic diabetes insipidus caused by a novel mutation in the AVPR2 gene. Clin Endocrinol (Oxf). Mar 2008;68(3):395-403. [Medline].
Alon U, Chan JC. Hydrochlorothiazide-amiloride in the treatment of congenital nephrogenic diabetes insipidus. Am J Nephrol. 1985;5(1):9-13. [Medline].
Blackett PR, Seif SM, Altmiller DH, Robinson AG. Familial central diabetes insipidus: vasopressin and nicotine stimulated neurophysin deficiency with subnormal oxytocin and estrogen stimulated neurophysin. Am J Med Sci. Nov-Dec 1983;286(3):42-6. [Medline].
Davies JH, Penney M, Abbes AP, et al. Clinical features, diagnosis and molecular studies of familial central diabetes insipidus. Horm Res. 2005;64(5):231-7. [Medline].
Garofeanu CG, Weir M, Rosas-Arellano MP, et al. Causes of reversible nephrogenic diabetes insipidus: a systematic review. Am J Kidney Dis. Apr 2005;45(4):626-37.
Leung AK, Robson WL, Halperin ML. Polyuria in childhood. Clin Pediatr (Phila). Nov 1991;30(11):634-40. [Medline].
Libber S, Harrison H, Spector D. Treatment of nephrogenic diabetes insipidus with prostaglandin synthesis inhibitors. J Pediatr. Feb 1986;108(2):305-11. [Medline].
Mulders SM, Bichet DG, Rijss JP, et al. An aquaporin-2 water channel mutant which causes autosomal dominant nephrogenic diabetes insipidus is retained in the Golgi complex. J Clin Invest. Jul 1 1998;102(1):57-66. [Medline]. [Full Text].
Pivonello R, Colao A, DiSomma C, et al. Impairment of bone status in patients with central diabetes insipidus. J Clin Endocrinol Metab. Jul 1998;83(7):2275-80. [Medline]. [Full Text].
Saborio P, Tipton GA, Chan JC. Diabetes insipidus. Pediatr Rev. Apr 2000;21(4):122-9; quiz 129. [Medline].
Soylu A, Kasap B, Ogun N, et al. Efficacy of COX-2 inhibitors in a case of congenital nephrogenic diabetes insipidus. Pediatr Nephrol. Dec 2005;20(12):1814-7. [Medline].
Further Reading
Keywords
diabetes insipidus, DI, hypernatremia, thirst, polydipsia, dehydration, central diabetes insipidus, CDI, nephrogenic diabetes insipidus, NDI, failure to thrive, nocturia, fecalith, Wolfram syndrome, diabetes mellitus, optic atrophy, mental retardation, hypokalemia, hypercalcemia
Follow-up: Diabetes Insipidus