Uso de ibuprofeno en el tratamiento de pacientes pediátricos con poliuria y disnatremia. Reporte de una serie de casos / Ibuprofen use for the treatment of pediatric patients with polyuria and dysnatremia. A case series report

Los niños con lesiones selares y/o supraselares pueden presentar diabetes insípida central con posterior secreción inadecuada de hormona antidiurética. Nosotros observamos, en algunos casos, aumento de la incidencia de poliuria, natriuresis e hiponatremia, tríada diagnóstica del síndrome cerebral perdedor de sal. Aquí comunicamos la evolución de 7 pacientes con antecedentes de daño agudo del sistema nervioso central y diabetes insípida central seguida por síndrome cerebral perdedor de sal. Como tratamiento aportamos secuencialmente fluidos salinos parenterales, cloruro de sodio oral, desmopresina, mineralocorticoides e incluso tiazidas. Ante la persistencia de poliuria con hiponatremia, agregamos ibuprofeno. Como resultado de este esquema terapéutico secuencial, este grupo redujo significativamente los valores de diuresis diaria de 10 ml/kg/h a 2 ml/kg/h en un tiempo promedio de 5 días, normalizando también las natremias (de 161 mEq/L a 143 mEq/L) en un tiempo promedio de 9 días. En ningún caso observamos efectos adversos asociados al tratamiento.

Children with sellar and/or suprasellar lesions may develop central diabetes insipidus with subsequent inappropriate antidiuretic hormone secretion. An increased incidence of polyuria, natriuresis, and hyponatremia has been reported in some cases, which make up the diagnostic triad of cerebral salt wasting syndrome. Here we report the clinical course of 7 patients with a history of acute central nervous system injury and central diabetes insipidus followed by cerebral salt wasting syndrome. Treatment included the sequential use of parenteral saline solution, oral sodium chloride, desmopressin, mineralocorticoids, and even thiazides. Due to persistent polyuria and hyponatremia, ibuprofen was added. As a result of this sequential therapeutic regimen, daily urine output reduced significantly from 10 mL/ kg/h to 2 mL/kg/h over an average period of 5 days, together with a normalization of natremia (from 161 mEq/L to 143 mEq/L) over an average period of 9 days. No treatment-related adverse effects were observed in any case.

Ibuprofen use for the treatment of pediatric patients with polyuria and dysnatremia. A case series report. / Uso de ibuprofeno en el tratamiento de pacientes pediátricos con poliuria y disnatremia. Reporte de una serie de casos.

Children with sellar and/or suprasellar lesions may develop central diabetes insipidus with subsequent inappropriate antidiuretic hormone secretion. An increased incidence of polyuria, natriuresis, and hyponatremia has been reported in some cases, which make up the diagnostic triad of cerebral salt wasting syndrome. Here we report the clinical course of 7 patients with a history of acute central nervous system injury and central diabetes insipidus followed by cerebral salt wasting syndrome. Treatment included the sequential use of parenteral saline solution, oral sodium chloride, desmopressin, mineralocorticoids, and even thiazides. Due to persistent polyuria and hyponatremia, ibuprofen was added. As a result of this sequential therapeutic regimen, daily urine output reduced significantly from 10 mL/kg/h to 2 mL/kg/h over an average period of 5 days, together with a normalization of natremia (from 161 mEq/L to 143 mEq/L) over an average period of 9 days. No treatment-related adverse effects were observed in any case.

Los niños con lesiones selares y/o supraselares pueden presentar diabetes insípida central con posterior secreción inadecuada de hormona antidiurética. Nosotros observamos, en algunos casos, aumento de la incidencia de poliuria, natriuresis e hiponatremia, tríada diagnóstica del síndrome cerebral perdedor de sal. Aquí comunicamos la evolución de 7 pacientes con antecedentes de daño agudo del sistema nervioso central y diabetes insípida central seguida por síndrome cerebral perdedor de sal. Como tratamiento aportamos secuencialmente fluidos salinos parenterales, cloruro de sodio oral, desmopresina, mineralocorticoides e incluso tiazidas. Ante la persistencia de poliuria con hiponatremia, agregamos ibuprofeno. Como resultado de este esquema terapéutico secuencial, este grupo redujo significativamente los valores de diuresis diaria de 10 ml/kg/h a 2 ml/kg/h en un tiempo promedio de 5 días, normalizando también las natremias (de 161 mEq/L a 143 mEq/L) en un tiempo promedio de 9 días. En ningún caso observamos efectos adversos asociados al tratamiento.

Bases fisiopatológicas de los transtornos del sodio en pediatría / Pathophysiology of sodium disorders in children

Las disnatremias son el transtorno hidroelectrolítico prevalente en pacientes ambulatorios y hospitalizados. Su manejo inadecuado puede tener serias consecuencias, asociándose a un aumento en la morbimortalidad de los pacientes. El objetivo de este artículo es actualizar las bases fisiopatológicas de las disnatremias y revisar herramientas clínicas y de laboratorio que nos permitan realizar un enfrentamiento rápido y simple. Las disnatremias reflejan un transtorno del balance del agua, y el balance de agua tiene relación directa con la osmorregulación. Existen mecanismos para mantener el control de la osmolalidad plasmática, los cuales se gatillan con cambios de un 1-2 por ciento. A nivel hipotalámico existen osmorreceptores que censan cambios en la osmolalidad plasmática, regulando la secreción de Hormona Antidiurética (ADH), la que ejerce su acción a nivel renal, por lo cual el riñón es el principal regulador del balance hídrico. Cuando se está frente a una disnatremia, es fundamental evaluar cómo está funcionando este eje ADH-riñón. Dentro de las hiponatremias existen causas que son fáciles de identificar, sin embargo, diferenciar un síndrome de secreción inadecuada de ADH con un síndrome pierde sal cerebral suele ser más difícil. En el caso de las hipernatremias, sospechar una diabetes insípida y diferenciar su posible origen, central o nefrogénico, es fundamental para su manejo. En conclusión, el enfrentamiento de una disnatremia requiere conocer las bases fisiopatológicas de su desarrollo, para así poder realizar un diagnóstico certero y finalmente un tratamiento adecuado, evitando errores en su corrección que pueden poner en riesgo al paciente.

Dysnatremia is among the most common electrolyte disorders in clinical medicine and its improper management can have serious consequences associated with increased morbidity and mortality of patients. The aim of this study is to update the pathophysiology of dysnatremia and review some simple clinical and laboratory tools, easy to interpret, that allow us to make a quick and simple approach. Dysnatremia involves water balance disorders. Water balance is directly related to osmoregulation. There are mechanisms to maintain plasma osmolality control; which are triggered by 1-2 percent changes. Hypothalamic osmoreceptors detect changes in plasma osmolality, regulating the secretion of Antidiuretic Hormone (ADH), which travels to the kidneys resulting in more water being reabsorbed into the blood; therefore, the kidney is the main regulator of water balance. When a patient is suffering dysnatremia, it is important to assess how his ADH-renal axis is working. There are causes of this condition easy to identify, however, to differentiate a syndrome of inappropriate ADH secretion from cerebral salt-wasting syndrome is often more difficult. In the case of hypernatremia, to suspect insipidus diabetes and to differentiate its either central or nephrogenic origin is essential for its management. In conclusion, dysnatremia management requires pathophysiologic knowledge of its development in order to make an accurate diagnosis and appropriate treatment, avoiding errors that may endanger the health of our patients.

Syndromes related to sodium and arginine vasopressin alterations in post-operative neurosurgery

BACKGROUND: Cerebral salt wasting syndrome (CSWS), syndrome of inappropriate antidiuretic hormone secretion (SIADH) and diabetes insipidus (DI) are frequently found in postoperative neurosurgery. PURPOSE: To identify these syndromes following neurosurgery. METHOD: The study included 30 patients who had been submitted to tumor resection and cerebral aneurysm clipping. Sodium levels in serum and urine and urine volume were measured daily up to the 5th day following surgery. Plasma arginine vasopressin (AVP) was measured on the first, third and fifth days post-surgery. RESULTS: CSWS was found in 27/30 patients (90 percent), in 14 (46.7 percent) of whom it was associated with a reduction in the levels of plasma AVP (mix syndrome). SIADH was found in 3/30 patients (10 percent). There was no difference between the two groups of patients. CONCLUSION: CSWS was the most common syndrome found, and in half the cases it was associated with DI. SIADH was the least frequent syndrome found.

INTRODUÇÃO: A síndrome perdedora de sal (SPS), síndrome da secreção inapropriada do hormônio antidiurético (SIADH) e diabetes insipidus (DI) são freqüentemente encontradas no pós-operatório de neurocirurgia. OBJETIVO: Identificar essas síndromes relacionadas à neurocirurgia. MÉTODO: Foram estudados 30 pacientes submetidos à ressecção de tumor (n=19) e clipagem de aneurisma (n=11) cerebral durante os primeiros cinco dias do pós-operatório. Os pacientes foram submetidos a dosagens diárias de sódio sérico e urinário até o 5° dia pós-operatório, com controle de volume urinário neste período e dosagem de arginina-vasopressina (AVP) plasmática no 1°, 3° e 5° dias pós-operatórios. RESULTADOS: A SPS foi encontrada em 27/30 pacientes (90 por cento), em 14/27 (46,7 por cento) associada à diminuição dos níveis de AVP plasmática (síndrome mista). A SIADH foi encontrada em 3/30 pacientes (10 por cento). Não houve diferença entre os dois grupos de pacientes. CONCLUSÃO: A SPS foi a síndrome mais freqüente, em metade de casos associada ao DI. A SIADH foi a menos freqüente.

Hiponatremia prolongada após traumatismo cerebral, tratada com fludrocortisona / Prolonged hyponatremia after brain trauma treated with fludrocortisone

A hiponatremia é uma freqüente complicação do traumatismo craniano e surge, usualmente, nos primeiros dez dias depois do trauma e tem evolução limitada a poucos dias. Os autores apresentam um paciente que desenvolveu hiponatremia no nono dia após um acidente de motocicleta, a qual se prolongou por mais de vinte dias. Essa demorada hiponatremia pôde ocorrer porque o paciente foi tratado, inicialmente, com furosemida, como se tivesse a síndrome inapropriada da secreção do hormônio antidiurético, e com glicocorticóide, como se tivesse insuficiência glandular supra-renal. Contudo, o paciente teve síndrome cerebral perdedora de sal, que pode ocorrer após lesões do sistema nervoso central. Foi tratado com fludrocortisona (0,3 mg/dia) com reposição de sódio e de líquidos. Houve gradual desaparecimento da hiponatremia, e seu perfil físico e neural apresentou progressiva melhora. A fludrocortisona é um mineralocorticosteróide, e seu uso em pacientes com síndrome cerebral perdedora de sal é indicado pela ocorrência de secreção inapropriada do peptídeo natriurético cerebral, que inibe a secreção da aldosterona e, assim, provoca a perda renal de sódio.

Hyponatremia is a frequent complication following cranial traumatism and usually appears in the first ten days after the trauma, usually limited to a few days. The authors report a patient that developed hyponatremia on the 9th day after a motorcycle accident and it lasted twenty more days. The long period of hyponatremia could be explained by the treatment with furosemide, initially given with the assumption that he had inappropriate secretion of antidiuretic hormone syndrome, toghether with glucocorticoid, as if he had adrenal insufficiency. However, the patient had cerebral salt-wasting syndrome, which can happen after lesions of the central nervous system. Then, he was correctly treated with fludrocortisone (0.3 mg/day) and sodium plus fluid replacement. He gradually recovered from the hyponatremia and his physical and neural profile showed progressive improvement. Fludrocortisone is a mineralocorticosteroid and its use in a patient with cerebral salt-wasting syndrome is justified by its counter effect against the oversecretion of brain natriuretic peptide, which inhibits the aldosterone secretion, eventually leading to renal loss of sodium.