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PubMed2004

Transient diabetes insipidus after discontinuation of therapeutic vasopressin.

The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

Acute Disease↗
PubMed1978

Diabetes insipidus and pregnancy. Case report, incidence and review of literature.

The coexistence of diabetes insipidus (D.I.) and pregnancy is rare. Sixty-seven cases are reviewed, including one of our own. The condition tends to become worse in pregnancy, labor appears unaffected and lactation appears to lead to an improvement in D.I. Theories are discussed to account for the effect of pregnancy on D.I.

Adult↗
PubMed2002

[A case of central diabetes insipidus caused by metastatic small cell lung cancer].

A 58-year-old man was admitted to our hospital because of cough, polydipsia and polyuria. Chest CT films showed mediastinal lymphadenopathy, nodules in the lung fields, and pleural effusion. Histopathologic examination of transbronchial biopsy specimens showed oat cell carcinoma. MRI films revealed tumorous swelling of the pituitary stalk. Central diabetes insipidus caused by pituitary metastasis of small cell lung cancer was diagnosed. After treatment with whole-brain irradiation and chemotherapy, the size of the swollen pituitary stalk was reduced and his urine volume decreased. He died of respiratory insufficiency 15 months after the initial diagnosis. No recurrence of pituitary metastasis was apparent. This was a rare case of central diabetes insipidus caused by pituitary metastasis of small cell lung cancer successfully treated with radiotherapy and chemotherapy.

Carcinoma, Small Cell↗
PubMed1987

Central diabetes insipidus in children. Antidiuretic effect and pharmacokinetics of intranasal and peroral 1-deamino-8-D-arginine vasopressin.

The antidiuretic effect and pharmacokinetics of 10 to 20 micrograms of intranasal (IN) and 200 to 400 micrograms of oral (po) 1-deamino-8-D-arginine vasopressin (DDAVP) were studied in 10 paediatric diabetes insipidus patients. A significant increase in urine osmolality was obtained with all doses, maximum within 2 h and still present at 8 h. At 12 h after administration, the ratio urine osmolality/plasma osmolality was above 1 only after 20 micrograms intranasally and 400 micrograms perorally. The free water clearance decreased rapidly with all doses and was similar in magnitude and duration for both the intranasal and peroral routes of administration and remained negative for more than 8 h. The maximum plasma concentrations of DDAVP, measured with a specific and sensitive RIA method, was dose-dependent and there was not significant difference in time until maximum concentration was obtained or in plasma half-life between the two routes of administration. The ratio established, 1:20, by calculating the area under the curve showed a bio-equivalence between 10 micrograms IN and 200 micrograms po and between 20 micrograms IN and 400 micrograms po of DDAVP. This work further emphasized the effectiveness of the oral route and the rapidity of absorption. By continuous monitoring of DDAVP plasma values we have demonstrated that peak values were reached within one hour after administration. This study demonstrates that the doses needed to treat diabetes insipidus patients by the oral route will be approximately 20 times greater than by the nasal route.

Administration, Intranasal↗
PubMed1999

Ondine's curse in association with diabetes insipidus following transient vertebrobasilar ischemia.

Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine's curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial nerves' dysfunctions and a slight right-sided hemiparesis. An acute brainstem ischemia was diagnosed and treated immediately with high-dose heparin. Cerebral angiography revealed a proximal occlusion of the left vertebral artery but a normal right vertebral artery and a hyperplastic right posterior inferior cerebellar artery. Cranial Computed Tomography and MRI scan demonstrated multiple ischemic lesions in the posterior circulation. During a 4-week treatment course the patient underwent six episodes of acute severe hypoxia and hypercapnia requiring orotracheal intubation twice and manual ventilation by air mask over a few minutes for four times after a tracheostomy had been performed. Twice a short-term episode of hypothalamic Diabetes insipidus was observed following hypoventilation. We conclude that both Ondine's curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia.

Brain Stem Infarctions↗
PubMedDate not supplied

[Kluver Bucy syndrome and central diabetes insipidus: two uncommon complications of herpes simplex encephalitis].

Herpes Simplex Encephalitis (HSE) is an uncommon but severe disease with high mortality and morbidity. The major clinical manifestations are deteriorating consciousness with confusion, drowsiness or coma, altered behaviour, convulsions and a variety of neurological signs (hemiplegia, aphasia, ataxia, etc.). An uncommon complication of HSE is Kluver Bucy syndrome (KBS), characterized by hyperorality, bulimia and changes in emotional behaviour. Neuroimaging studies frequently show an involvement of the temporal lobes and limbic areas. Another uncommon complication of HSE is central diabetes insipidus as a result of herpes simplex infection of the hypothalamus. We report two pediatric cases of HSE complicated with Kluver Bucy syndrome and central diabetes insipidus.

Acyclovir↗
PubMed1989

Mammillary polydipsia and diabetes insipidus: a study of the rhythmicity of water intake.

Rats with polydipsia induced by electrolytic mammillary lesions show a normal daily rhythmicity of water intake compared with sham lesioned animals, when kept in a 12:12 hours light-dark cycle of illumination. Water is mainly consumed during the dark phase (approximately 80-90% of the total amount). On the other hand, rats with centrally induced diabetes insipidus by means of electrolytic lesions in the median eminence show a clear-cut alteration in this rhythmicity, drinking only 67% of the total amount during the dark phase. This effect could be due to the continuous necessity of these animals to drink water in order to maintain fluid homeostasis, and is not related to food rhythmicity alterations. Taken together, and on the basis of the daily rhythmicity of water intake, these results suggest that mammillary polydipsia may be different from that observed when diabetes insipidus is present.

Animals↗
PubMed1984

Involvement of vasopressin in brain edema formation: further evidence obtained from the Brattleboro diabetes insipidus rat with experimental subarachnoid hemorrhage.

Brain water accumulation (1.2%) with an accompanying increase in the sodium content was observed in Wistar rats as early as 1 hour after experimental subarachnoid hemorrhage (SAH). After 6 and 24 hours, the water content was 1.3 and 1.4%, respectively, higher than that of control animals. In contrast, in Brattleboro diabetes insipidus rats the content of brain water and electrolytes had not changed significantly 1 hour after the administration of blood into the subarachnoid space. Increased brain water and sodium and a normal potassium content, indicative of a vasogenic type of brain edema, were seen at 6 hours after SAH. In these animals, known to be devoid of vasopressin, the increase in brain water 24 hours after SAH was 2.6%, compared with 1.4% for Wistar rats with SAH. It is suggested that the lack of vasopressin could alter the course of brain edema formation after experimental SAH in Brattleboro diabetes insipidus rats. It is hypothesized that vasopressin, by regulating the water permeability of the brain capillaries, the choroid plexus, and the cerebrospinal fluid absorption structures, plays an important role in controlling the brain fluid and electrolyte balance during the course of SAH.

Animals↗
PubMed1983

[Therapy of endocrine diseases in childhood and adolescence. 2. Connatal athyreosis. 3. Diabetes insipidus neurohormonalis].

Congenital athyreosis may be due to different though mostly unknown factors. It should be diagnosed by TSH-screening. Immediate therapy consists of supplementation of thyroxin. The dose should be adjusted to the child's needs controlled by normal growth and bone age advance, normalization of TSH and thyroxin levels in serum. The goal must be to reach normal intelligence. Therapy should be continued during the entire life. Absence of adiuretin is the cause for diabetes insipidus neurohormonalis due to genetic disorders, tumor or infection of the hypothalamo-pituitary system. The disorder is best treated with synthetic desamino-8-vasopressin (minirin, alternatively with an oily suspension of pitressin). Diabetes insipidus renalis and psychogenic polydipsia should be ruled out before this therapy is started.

Adolescent↗