Adipsia increases risk of death in patients with central diabetes insipidus.

Central diabetes insipidus (CDI) is caused by deficiency of arginine vasopressin, an antidiuretic hormone. Patients with CDI manifest polyuria which is usually compensated for by increases in water intake. However, some patients are not able to sense thirst due to the destruction of osmoreceptors in the hypothalamus. These adipsic CDI patients are easily dehydrated and the consequent dehydration could be life-threatening. The objective of this study was to investigate the prognosis of adipsic CDI patients. We have reviewed 149 patients with CDI in three hospitals using databases of the electronic medical recording systems, and examined whether adipsia could affect the morbidity and mortality in CDI patients with multivariable analyses. Twenty-three patients with CDI were adipsic while the remaining 126 patients were non-adipsic. The multivariate analyses showed that the incidence of serious infections which required hospitalization was significantly higher in the adipsic CDI patients compared to that in non-adipsic CDI patients (p <0.001). A total of 6 patients with CDI died during the follow-up (median duration; 60 months, range 1 to 132 months). Four of them were adipsic, three of whom died of infection. The statistical analyses revealed that the risk of death in adipsic CDI patients was significantly higher than in non-adipsic patients (p =0.007). It is thus suggested that adipsic CDI patients were susceptible to serious infections which could be the causes of death.

Central diabetes insipidus in pediatric severe traumatic brain injury.

OBJECTIVES: To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality. DESIGN: Retrospective chart and imaging review. SETTING: Children's Hospital, level 1 trauma center. PATIENTS: Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011. MEASUREMENTS AND MAIN RESULTS: Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04). CONCLUSIONS: The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.

Evaluation of patients with intracranial tumors and central diabetes insipidus.

The aim of the study is to evaluate the etiologic and clinical characteristics, treatment regimens, and outcome of the patients with intracranial tumors presenting with central diabetes insipidus (DI). Sixty-nine patients with intracranial tumors presenting with central DI between 1972 and 2012 were retrospectively evaluated. Fifty-three out of 69 patients were included in the analysis. Male/female ratio was 1.52, median age was 7.6 years. Of 53 patients, 37 patients (69.8%) were diagnosed with Langerhans cell histiocytosis, 14 patients (26.4%) with germinoma, 1 (1.9%) with astrocytoma, and 1 (1.9%) with optic glioma. 10-year overall survival (OS) rate and disease-free survival rate for all patients were 91.7% and 52%. 10-year OS rate according to diagnostic criteria was 91% for Langerhans cell histiocytosis (LCH) cases, 79% for intracranial germinoma, which was statistically significant (P = .0001). Central DI may be very important clinical presentation of serious underlying disease in children. Intracranial tumors are the most frequent cause of DI. Most frequent diagnosis were LCH and germ cell tumors in our series.

Combined central diabetes insipidus and cerebral salt wasting syndrome in children.

Central diabetes insipidus, a common consequence of acute central nervous system injury, causes hypernatremia; cerebral salt wasting syndrome can cause hyponatremia. The two conditions occurring simultaneous are rarely described in pediatric patients. Pediatric cases of combined diabetes insipidus and cerebral salt wasting after acute central nervous system injury between January 2000 and December 2007 were retrospectively reviewed, and clinical characteristics were systemically assessed. Sixteen patients, aged 3 months to 18 years, met study criteria: 11 girls and 5 boys. The most common etiologies were severe central nervous system infection (n = 7, 44%) and hypoxic-ischemic event (n = 4, 25%). In 15 patients, diabetes insipidus was diagnosed during the first 3 days after acute central nervous system injury. Onset of cerebral salt wasting syndrome occurred 2-8 days after the onset of diabetes insipidus. In terms of outcome, 13 patients died (81%) and 3 survived under vegetative status (19%). Central diabetes insipidus and cerebral salt wasting syndrome may occur after acute central nervous system injury. A combination of both may impede accurate diagnosis. Proper differential diagnoses are critical, because the treatment strategy for each entity is different.

Early central diabetes insipidus: An ominous sign in post-cardiac arrest patients.

PURPOSE: Central diabetes insipidus (CDI) after cardiac arrest is not well described. Thus, we aim to study the occurrences, outcomes, and risk factors of CDI of survivors after out-of-hospital cardiac arrest (OHCA). MATERIALS AND METHODS: We retrospectively analyzed post-OHCA patients treated at a single center. Central diabetes insipidus was retrospectively defined by diagnostic criteria. One-month cerebral performance category (CPC) scores were collected for outcomes. RESULTS: Of the 169 patients evaluated, 36 patients (21.3%) were diagnosed with CDI. All CDI patients had a poor neurologic outcome of either CPC 4 (13.9%) or CPC 5 (86.1%), and CDI was strongly associated with mortality. Age (odds ratio [OR], 0.96; 95% confidence interval [CI], 0.93-0.99), respiratory arrest (OR, 6.62; 95% CI, 1.23-35.44), asphyxia (OR, 9.26; 95% CI, 2.17-34.61), and gray to white matter ratio on brain computed tomogram (OR, 0.88; 95% CI, 0.81-0.95) were associated with the development of CDI. The onset of CDI was earlier (P < .001) and the maximum 24-hour urine output was larger (P = .03) in patients with worst outcomes. CONCLUSIONS: All patients diagnosed with CDI had poor neurologic outcomes, and occurrence of CDI was associated with mortality. Central diabetes insipidus patients with death or brain death had earlier occurrence of CDI and more maximum urine output.

Central diabetes insipidus in children with acute brain insult.

Central diabetes insipidus occurs in patients with overwhelming central nervous system injuries, and may be associated with brain death. The clinical picture of children with acquired central diabetes insipidus after acute brain insult is seldom reported. We retrospectively reviewed cases dating from January 2000-February 2008 at a tertiary pediatric intensive care unit. Fifty-four patients (28 girls, 26 boys), aged 3 months to 18 years, were enrolled. Etiologies included severe central nervous system infection (35.2%), hypoxic-ischemic events (31.5%), head injury (18.5%), and vascular lesions (14.8%). In 39 (72.2%) patients, diabetes insipidus was diagnosed during the first 2 days after acute central nervous system injury, and 40 (74.0%) developed maximum serum sodium concentrations of >160 mEq/L. In 16, sequential cerebral salt wasting syndrome developed after their initial diabetes insipidus presentation. Overall mortality at 2 months after admission was 77.8%. Our results demonstrate that patients who develop central diabetes insipidus after acute central nervous system injury manifest high mortality. Development of central diabetes insipidus within the first 2 days and a maximum plasma sodium >160 mEq/L were significant predictors of outcomes.

Central nervous system-related permanent consequences in patients with Langerhans cell histiocytosis.

BACKGROUND: Permanent consequences in Langerhans cell histiocytosis (LCH) are irreversible late sequelae related to the disease that may severely impair the quality of life of survivors. The frequency and pattern of permanent consequences affecting the central nervous system (CNS) remains to be determined. PROCEDURE: In this single center study, 25 LCH patients observed for a median time of 10 years 3 months underwent a uniform thorough follow-up program including neuropsychological testing and electrophysiological evaluation. RESULTS: Overall permanent consequences were seen in 9 of 25 patients. Intracranial abnormalities were the most frequent including diabetes insipidus (DI) in seven patients, anterior pituitary deficiencies in five patients, and neurodegenerative CNS disease in five patients. No patient had overt neurological symptoms upon neurological evaluation, but psychological testing revealed subtle deficits in short-term auditory memory (STAM) in 14 patients. Brain stem evoked potentials showed abnormalities in four of nine tested patients, all of these four had neurodegeneration on MRI. CONCLUSION: Psychoneuroendocrine sequelae were found in an unexpectedly high number of patients in this single center study. Long-term follow-up focusing on such sequelae are important in LCH survivors, in order to detect early deficits, to monitor the evolution of the disease, and to provide specific support.