Diabetes insipidus in children with brain death

Fiser, Debra H.; Jimenez, Jorge F.; Wrape, Vicki; Woody, Robert C.

doi:10.1097/00003246-198706000-00002

Cited by 60 publications

(27 citation statements)

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“…In a study conducted on brain-dead children, Fiser et al 26 had already observed 38% diabetes insipidus. Other authors 7 also found DI in 14 out of 16 children who fulfilled the criteria for brain death, and inferred that the occurrence of DI after ischemic or hypoxic insult could represent the mesencephalic neuron cell death.…”

Section: Discussionmentioning

confidence: 96%

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Cintra

Maciel

Araújo

et al. 2004

Arq. Neuro-Psiquiatr.

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-Introduction: Patients with severe brain lesions (SBL) and brain-dead patients (BD) frequently present with vasopressin (AVP) secretion disorders. Objective: To evaluate AVP serum levels in SBL and BD patients. Design: Prospective, open label, observational trial. Setting: A general teaching hospital. Method:Three groups of adult subjects (age ≥ 18y) of both sexes were included in this study: control group: 29 healthy volunteers; SBL group: 17 patients with Glasgow Coma Scale (GCS) ≤8; and BD group: 11 brain-dead patients. Samples of venous blood were collected in the morning at rest from healthy volunteers and at 8 hourly intervals over a period of 24h from SBL and BD patients for AVP determinations. Concomitantly, some clinical and laboratorial variables were also recorded. Results: AVP serum levels (pg/ml) were [mean (SD); median]: control [2.2(1.1); 2.0]; SBL [5.7(6.3); 2.9]; and BD [2.6(1.0); 2.8]. AVP serum levels varied greatly in SBL patients, but without statistically significant difference in relation to the other groups (p=0.06). Hypotension (p=0.02), hypernatremia (p=0.0001), serum hyperosmolarity (p=0.0001) and urinary hypoosmolarity (p=0.003) were outstanding in BD patients when compared with SBL. Conclusions: The AVP serum levels did not demonstrate significant statistical difference between the groups, only showing a greater variability in SBL patients (manifested as serum spike levels). Hypernatremia and hyperosmolarity were present in BD patients, indicating a failure of the hypothalamic-pituitary system in AVP production and release.KEY WORDS: brain lesion, brain death, vasopressin. Níveis séricos de arginina vasopressina em pacientes com lesão cerebral grave e em pacientes com morte encefálicaRESUMO -Introdução: Pacientes com lesão cerebral grave (LCG) ou com morte encefálica (ME) freqüentemente apresentam alterações na secreção de vasopressina (AVP). Objetivo: Avaliar os níveis séricos de AVP em pacientes com LCG e ME. Desenho: Estudo prospectivo, aberto, observacional. Local: Um hospital geral universitário. Método: Sujeitos adultos (idade ≥18 anos), de ambos os sexos, foram divididos em três grupos: grupo controle: 29 voluntários sadios; grupo LCG: 17 pacientes com pontuação na Escala de Coma de Glasgow (ECG) ≤8; grupo ME: 11 pacientes com diagnóstico de ME.Amostras de sangue venoso foram colhidas pela manhã, em repouso, nos pacientes do grupo controle, e de 8/8h, por 24h, nos pacientes dos grupos LCG e ME, para dosagens de AVP. Variáveis clínicas e laboratoriais de interesse foram anotadas concomitantemente. Resultados: Os valores da AVP (pg/ml) foram [média (DP); mediana]: grupo controle [2,2(1,1); 2,0]; grupo LCG [5,7(6,3); 2,9] e grupo ME [2,6(1,0); 2,8]. Observouse maior variação dos níveis séricos de AVP no grupo LCG, mas sem diferença estatisticamente significativa em relação aos demais (p=0,06). Hipotensão (p=0,02), hipernatremia (p=0,0001), hiperosmolaridade sérica (p=0,0001) e hiposmolaridade urinária (p=0,003) foram proeminentes no grupo ME em relação ao grupo LCG. Con...

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Section: Discussionmentioning

confidence: 96%

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Cintra

Maciel

Araújo

et al. 2004

Arq. Neuro-Psiquiatr.

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“…The patients who had intracranial tumours, head injury, brain surgery, or DI before their hypoxic episodes were excluded. Crite-ria for the diagnosis of neurogenic DI in a child included: (1) urine output spontaneously exceeding an amount equal to 1.5 times the calculated maintenance fluid intake for 2 h (consecutive); (2) urine specific gravity not greater than 1.005 (and urine osmolality not more than 300 mOsm/kg H20 if measured); (3) a plasma sodium level greater than 150 mmol/1 (and serum osmolality greater than 310 mOsm/kg H20 if measured); (4) a concurrent low AVP level or observed response to exogenous AVP or desmopressin treatment; (5) no diuretics in use over the preceding 12 h, and (6) normal renal function and levels of potassium and calcium [3,7,16]. Plasma sodium levels were measured by the ion-selective electrode method.…”

Section: Methodsmentioning

confidence: 99%

“…Infrequently neurogenic DI may occur after severe hypoxic/ischaemic brain damage secondary to car-9 bon monoxide poisoning [11], respiratory failure [8], or cardiorespiratory arrest [1,13] and complicates the management of an already critically ill patient. Up to now there are only a few reports of children with neurogenic D] associated with hypoxic encephalopathy [1,7,13,16]. We report six children who developed neurogenic DI after severe hypoxia.…”

Section: Introductionmentioning

confidence: 90%

Neurogenic diabetes insipidus in children with hypoxic encephalopathy: Six new cases and a review of the literature

et al. 1996

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“…Because diabetes insipidus is the most common cause of hypernatremia in patients who have progressed to brain death, [20][21][22] the antidiuretic hormone analogues, vasopressin and desmopressin, have both been successfully used to prevent hypernatremia from excessive free water loss in potential organ donors. [23][24][25] Unfortunately, desmopressin has limited effectiveness in this setting because it can only be administered intranasally.…”

Section: Donor Hypernatremia In Liver Transplantationmentioning

confidence: 99%

Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: Effect of correction of donor hypernatremia

et al. 1999

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Donor hypernatremia was reported to cause postoperative graft dysfunction in human orthotopic liver transplantation (OLT). However, the effects of the correction of donor hypernatremia before organ procurement have not been confirmed. The aim of this study is to determine whether donor hypernatremia is associated with early graft dysfunction after OLT and to determine the effect of the correction of donor hypernatremia. One hundred eighty-one consecutive OLTs performed between May 1997 and July 1998 were entered onto this study. The cases were divided into three groups according to the donor serum sodium concentration: group A, serum sodium of 155 mEq/L or less before organ procurement (n ‫؍‬ 118); group B, peak sodium greater than 155 mEq/L and final sodium 155 mEq/L or less (n ‫؍‬ 36); and group C, final sodium greater than 155 mEq/L (n ‫؍‬ 27). Graft survival within 90 days after OLT and early postoperative graft function were analyzed. There were no significant differences in donor and recipient variables among the three groups. The frequencies of graft loss were 15 of 118 grafts (12.7%) in group A, 4 of 36 grafts (11.1%) in group B, and 9 of 27 grafts (33.3%; P F .05 v groups A and B) in group C. The liver enzyme values in groups B and C were significantly greater than those in group A postoperatively. The prothrombin times of group C were significantly longer than those of group A for the first 4 postoperative days. Recipients of hepatic allografts from donors with uncorrected hypernatremia had a significantly greater incidence of graft loss compared with recipients of hepatic allografts from normonatremic donors. However, the differences in graft survival were abrogated by the correction of donor hypernatremia before procurement. Copyright 1999 by the American Association for the Study of Liver DiseasesS everal retrospective analyses of donor and recipient variables have attempted to identify risk factors predictive of both patient and graft survival after orthotopic liver transplantation (OLT). To date, the following donor-associated risk factors have been shown to adversely affect patient or graft survival: donor age, 1,2 sex, 3,4 liver function test results, 5 cytotoxic cross-match, 6 length of intensive care unit (ICU) stay, 1 use of vasopressors, 7 and preservation time. 2,8,9 Previously, all these risk factors were considered static and not subject to manipulation by the procurement team, primarily because of time constraints. However, recent legislation requiring earlier notification of potential organ donors and earlier turnaround time for serum chemistries have provided additional time to manage brain-dead donors before organ procurement and correct such abnormalities as hypernatremia that may adversely impact on both graft and recipient survival.Uncorrected hypernatremia in organ donors has been associated with poor graft or patient survival in at least four studies. 7,9-11 These retrospective analyses suggested donor hypernatremia resulted in a greater incidence of early postoperative graft dys...

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Diabetes insipidus in children with brain death

Cited by 60 publications

References 0 publications

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Vasopressin serum levels in patients with severe brain lesions and in brain-dead patients

Neurogenic diabetes insipidus in children with hypoxic encephalopathy: Six new cases and a review of the literature

Influence of high donor serum sodium levels on early postoperative graft function in human liver transplantation: Effect of correction of donor hypernatremia

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