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.

A Case of Cerebral Salt Wasting Syndrome in Neuromyelitis Optica Spectrum Disorder

Neuromyelitis optica spectrum disorder (NMOSD) may present with area postrema syndrome, which is characterized by intractable vomiting and hiccups. Hyponatremia is common in NMOSD and is mostly associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In contrast to SIADH, cerebral salt wasting syndrome (CSWS) causes hyponatremia, which is associated with severe natriuresis and extracellular volume depletion in patients with cerebral disease. To our knowledge, hyponatremia associated with CSWS has not been reported in a patient with NMOSD. Here, we describe a NMOSD presenting with hyponatremia, which may be caused by CSWS following area postrema syndrome.

The application of adrenal cortical hormone in the treatment of cerebral salt wasting syndrome / 中国医师进修杂志

Cerebral salt wasting syndrome (CSWS) is a common cause of refractory hyponatremia. Early diagnosis and treatment of CSWS can greatly improve the patient′s condition and improve the prognosis. Clinically by supplying sodium hydrate, most patients can resume normal serum sodium level, and get remission. But a few patients with low serum sodium, high urine sodium and low blood volume can not improve and even worse. Fludrocortisone and adrenal cortical hormone can rapidly and effectively reduce the urinary sodium level and urine volume, correct hyponatremia and low blood volume and improve the prognosis in such patients.

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.

Differentiation of the cerebral salt wasting syndrome and syndrome of inappropriate antidiuretic hormone secretion / 国际儿科学杂志

The cerebral salt wasting syndrome and syndrome of inappropriate antidiuretic hormone secretion are frequent in hyponatremia in patients with intracranial disorders.There is a major problem about the incidence,diagnosis,and differentiation of cerebral salt wasting syndrome and syndrome of inappropriate secretion of antidiuretic hormone in patients with acute central nervous system disorders.Clinical presentation of cerebral salt wasting syndrome is similar to syndrome of inappropriate antidiuretic hormone secretion,but the therapy is different.So differential diagnosis is essential for appropriate management.This paper differentiate two kinds of diseases from the pathogenesis,diagnosis and treatment.

Cerebral Salt Wasting Treated with Fludrocortisone in a 17-Year-Old Boy

Cerebral salt wasting is characterized by inappropriate natriuresis and volume contraction with associated cerebral pathology. It is distinct from the syndrome of inappropriate antidiuretic hormone secretion, which is characterized by inappropriate retention of free water. We report a patient with a porencephalic cyst who developed cerebral salt wasting. His initial treatment was supplementation of water and salt, which did not improve natriuresis or volume contraction. Fludrocortisone administration effectively managed the cerebral salt wasting.

Hyponatremia in Patients with Neurologic Disorders

The kidney and the brain play a major role in maintaining normal homeostasis of the extracellular fluid by neuroendocrine regulation of sodium and water balance. Therefore, disturbances of sodium balance are common in patients with central nervous system (CNS) disorders and clinicians should focus not only on the CNS lesion, but also on the potentially deleterious complications. Hyponatremia is the most common and important electrolyte disorder affecting patients with critical neurologic diseases. In these patients, the maladaptation to hyponatremia by impaired osmoregulation in pathologic lesions of brain may cause more aggressive cerebral edema and increased intracranial pressure due to hypoosmolality induced by hyponatremia. Furthermore, hyponatremia accompanied by CNS disorders has shown to increase delayed cerebral ischemia and mortality rates. Two main pathophysiologies of hyponatremia, excluding iatrogenic causes, are inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) syndrome. Differential diagnosis between these two entities can be difficult due to considerable overlap in the laboratory findings and clinical situations. SIADH is in a volume expanded status due to inappropriately secreted arginine vasopressin (AVP) and requires water restriction. However, CSW syndrome is characterized by renal sodium wasting mainly due to increased natriuretic peptides resulting in volume depletion and follows appropriate secretion of AVP. Therefore, maintenance of volume status and sodium replacement is the mainstay of treatment in CSW syndrome. In this review, we aimed to describe the regulation of sodium and water balance, and pathophysiology, diagnosis and treatment of hyponatremia in neurologic patients, especially focusing on SIADH and CSW syndrome.

Diagnosis and therapy of severe cerebral injured patients with hyponatremia / 中国基层医药

Objective To study the clinical features and therapeutic method of severe cerebral injured patients with hyponatremia.Methods The electrolyte and central venous pressure were examined on 45 cases of severe cerebral injured patients with hyponatremia every day.According to plasma sodium value and central venous pressure,we regulated treatment perscription daily.Results 45 patients occured hyponatremia in total 288 of severe cerebral injured patients.Hyponatremia was detected 5～13 days after operation or after injure.The morbility is usually the highest in the seventh day.Plasma sodium recovered to normal value in 14 days after operation.Conclusion Severe cerebral injured patients with hyponatremia should be diagnosed and treated as early as possible,then it will receive better prognosis.

Evaluating and Managing Hyponatremia / 대한구급학회지

Although hyponatremia is a common electrolyte disorder, its evaluation and management are not well defined. When diagnosed, hyponatremia should be categorized based on four criteria: volume status, urinary Na+, serum K+, and acid-base balance. This approach helps to determine what the cause of hyponatremia is and how it should be treated. Initially, hypovolemic hyponatremia, including cerebral salt wasting syndrome (CSWS), is treated by volume resuscitation and salt supplementation. Euvolemic hyponatremia, including the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), is treated by fluid restriction and salt supplementation, and hypervolemic hyponatremia is treated by fluid restriction and salt restriction. Hyponatremia can be managed well using these primary treatments and medications.

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.

Cerebral salt wasting following pituitary surgery for macroadenoma / 대한내과학회지

The central nervous system (CNS) has important roles in the regulation of sodium and water homeostasis, so the risk of hyponatremia is increased for patients with neurological disorders. Cerebral salt wasting (CSW) is a syndrome that is characterized by hyponatremia and extracellular volume contraction, and these problems are caused by natriuresis and the concomitant polyuria in patient with intracranial disease. It is critical to differentiate CSW from syndrome of inappropriate secretion of antidiuretic hormone (SIADH) for patients with hyponatremia and after they experience cerebral insults. This is because fluid restriction is the treatment of choice for SIADH and administration of isotonic or hypertonic saline is important for treating CSW. We report here on a case of CSW following trassphenoidal surgery for pituitary tumor in a 67-year-old man with nonfunctioning pituitary macroadenoma. Hyposmotic hyponatremia, increased urine output and signs of dehydration developed postoperatively, and the patient was managed by water and salt supplementation.

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.

A Case of Cerebral Salt Wasting Syndrome Associated with Tuberculous Meningitis / 결핵및호흡기질환

Hyponatremia which is due to excessive sodium loss in the urine and decrease in extracellular fluid volume following an acute or chronic central nervous system injury, has been conjunctively described as cerebral salt wasting syndrome (CSWS). This syndrome is often confused with dilutional hyponatremia due to inappropriate secretion of antidiuretic hormone. Accurate diagnosis and management are mandatory for improvement of the course of the disease. This report describes a case of a 31-year-old male patient with CSWS associated with tuberculous meningitis. The patient exhibited hyponatremia, polyuria, excessive natriuresis, volume depletion, and hypotension. He was diagnosed to manifest CSWS and was treated by administration of fluids, salt, and fludrocortisone. After the respective treatments, symptoms of polyuria and hypotension were gradually resolved and hyponatremia was corrected.

Two Cases of Cerebral Salt Wasting Syndrome Developing after Cranial Vault Remodeling in Craniosynostosis Children

Hyponatremia has been recognized as an important postoperative metabolic complication after central nervous system (CNS) operations in children. If not appropriately treated, the postoperative hyponatremia can cause several types of CNS and circulatory disorders such as cerebral edema, increased intracranial pressure. The postoperative hyponatremia after CNS surgery has been considered as one of the underlying causes of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). In some cases, however, the cerebral salt wasting (CSW) syndrome has been detected. CSW syndrome is far less well-known than SIADH and also different from SIADH in diagnosis and treatment. It causes an increase in urine output and urine sodium after a trauma of CNS and dehydration symptoms. The appropriate treatment of CSW syndrome is opposite the usual treatment of hyponatremia caused by SIADH. The latter is treated with fluid restriction because of the increased level of free water and its dilutional effect causing hyponatremia, whereas the former is treated with fluid and sodium resuscitation because of the unusual loss of high urinary sodium. Early diagnosis and treatment of CSW syndrome after CNS surgery are, therefore, essential. We made a diagnosis of CSW syndrome in two craniosynostosis children manifesting postoperative hyponatremia and supplied them an appropriate amount of water and sodium via intravenous route. The hyponatremia or natricuresis of the children improved and neurologic and circulatory sequelae could be prevented.

Diagnosis and treatment for the syndrome of inappropriate antidiuretic hormone secretion in neurosurgery / 临床外科杂志

Objective To study the diagnosis and treatment for the syndrome of inappropriate antidiuretic hormone secretion in neurosurgery.Methods Retrospective analyze clinical situation, treatment, and process of final diagnosis in 6 SIADH cases.Result Diagnosis of SIADH and differential diagnosis with CSWS is very difficult.In clinic the experimental therapy of restricting water and natrium is a important method of differential diagnosis,but also a effective therapy.Conclusion Speciality of SIADH is (1)hyponatremia(Na +≤128 mmol/L),natriuresis(Na +≥80 mmol/24h),(2)ADH assay is no significant for SIADH and CSWS,(3)no hypervolemia and edema exhibition,(4)restrict water is effective in treatment.

Cerebral Salt Wasting Syndrome Associated with Meningitis in a Child

Hyponatremia is commonly seen in those patients with central nervous system injury associated with infection or trauma. And decreasing intracranial pressure through restriction of maintenance fluid and salt is practiced as a routine therapeutic measure in the early stages of meningitis to prevent or ameliorate the syndrome of inappropriate secretion of antidiuretic hormone(SIADH). However, lots of patient do not show the typical symptoms of SIADH, instead they are dehydrated, have low plasma volume, increased urine sodium concentration and increased net sodium loss, which are the symptoms of cerebral salt wasting syndrome(CSW). Recent reports have prompted a reconsideration of CSW distinct from SIADH and moreover CSW has more proportion of hyponatremia associated with acute brain insult. CSW involves renal salt loss leading to hyponatremia and volume loss, whereas SIADH is a euvolemic or hypervolemic condition. While fluid restriction is the treatment of choice in SIADH, the treatment of CSW consists of vigorous sodium and volume replacement. And by correcting hyponatremic state as soon as possible, we can reduce mortality rate and improve neurologic sequelae. We report a case of CSW which was treated by replacement of vigorous sodium and volume replacement.

A Case of Cerebral Salt Wasting Syndrome associated with Tuberculous Meningitis / 대한내분비학회지

Hyponatremia in patients with central nervous system disorders is suggestive of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and volume restriction is recommended for its correction. However, if volume depletion is present in a situation otherwise compatible with SIADH, cerebral salt wasting syndrome (CSWS) should be considered as the cause of the hyponatremia to avoid hypovolemic shock that may be induced by the standard management of SIADH, i.e. volume restriction. We present a case of a 17-year-old male patient with CSWS associated with tuberculous meningitis. The clinical feature of the patient comprised hyponatremia, excessive natriuresis, polyuria, and hypovolemia. Following the administration of saline and fludrocortisone, natriuresis and polyuria were decreased, and the hyponatremia improved

A Study on Cerebral Salt Wasting Syndrome After Serious Cerebral Injury / 中国医师杂志

Objective To explore the pathogenesis, reason, diagnosis and treatment of cerebral salt wasting syndrome (CSWS) in the patients with serious cerebral injury. Methods The clinical data of 26 cases of CSWS after serious cerebral injury were analyzed retrospectively. Results The diagnosis of CSWS was confirmed by clinical symptoms of the patients and the results of laboratory examinations. After the effective treatment, the low plasma sodium level of 21 patients was corrected, and 5 patients died. Conclusion Hyponatremia,hypernatruria, hypovolemia, the increase of urinary amount and the elevation of plasma ANP and BNP level were main characteristics of CSWS.The supplement of water and salt was safe and effective in the treatment of CSWS.

Cerebral Salt Wasting Syndrome Associated with Pseudomonas Meningitis ccurred after Removal of Pituitary Adenoma: A Case Report

The authors report a case of cerebral salt wasting(CSW) syndrome followed by diabetes insipidus and meningitis after transsphenoidal approach for pituitary adenoma. Fluid and electrolyte imbalance occurs occasionally in neurosurgical patients due to DI or SIADH, however, CSW is different disease entity and the methods of treatment are different from those of DI or SIADH. A number of studies in recent years have shown that hyponatremia in many patients with intracranial disease might actually be caused by CSW in which a renal loss of sodium leads to hyponatremia and massive urinary water loss. CSW of this patient was resolved by fluid and salt replacement after 6 months.

A Case of Cerebral salt Wasting Syndrome with Pseudomonas Meningitis after Removal of Pituitary Adenoma / 대한내분비학회지

Hyponatremia is frequently seen in intracranial hemorrhagic patients and has been often attributed to inappropriate secretion of antidiuretic hormone. But in recent years, a number of studies have shown that hyponatremia in many patients with intracranial disease may actually be caused by cerebral salt wasting (CSW) syndrome and circulating Atrial natriuretic peptide (ANP) and Brain natriuretic peptide (BNP) are probably involved. This report describes a patient who developed bacterial meningites caused by pseudomonas aeruginosa and CSW syndrome after removal of pituitary adenoma. CSW syndrome resolved by fluid and salt replacement after 4 months.