Cerebral salt wasting syndrome in brain injury patients: A potential cause of hyponatremia

doi:10.1016/S0003-9993(97)90173-8

Archives of Physical Medicine and Rehabilitation

Volume 78, Issue 5, May 1997, Pages 540-542

https://doi.org/10.1016/S0003-9993(97)90173-8 Get rights and content

Abstract

Hyponatremia is a common neuromedical problem seen in survivors of central nervous system injury. The etiology of this hyponatremia is often diagnosed as syndrome of inappropriate diuretic hormone (SIADH). Fluid restriction is usually the first line of treatment. However, this can exacerbate vasospasm and produce resultant ischemia. Cerebral salt wasting is a syndrome of renal sodium loss that may occur commonly after central nervous system injury, yet remains unrecognized. Treatment of cerebral salt wasting consists of hydration and salt replacement. This article uses a case report to discuss the importance of recognition of this syndrome, and treatment concerns are reviewed.

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Cited by (35)

Injury patterns in patients who "talk and die"
2013, Journal of Clinical Neuroscience
Citation Excerpt :
This result highlights the need for clinicians to use a low threshold for intensive monitoring of a young patient with a mild head injury who is confused and has a poor verbal GCS. Cerebral salt wasting and the syndrome of inappropriate antidiuretic hormone can be significant causes of hyponatremia in patients with head injuries,20 and seven of the 18 patients in the hematoma group developed hyponatremia, compared with one of the seven in the ICP group. The means of the lowest sodium level during the first 7 days for the hematoma and refractory ICP group were 135.27 and 136.43, respectively, and the difference was not statistically significant (p = 0.1).
Despite advances in the quality of and access to cerebral imaging, patients with mild head injuries still deteriorate and die in neurotrauma units. The term “talk and die” was first used by Reilly et al. to describe a subset of patients with head injuries who died following what was initially thought to be only a mild traumatic brain injury. A retrospective review of a database from a major Australian trauma center was performed to identify 25 patients who met the “talk and die” criteria between January 2000 and December 2009. The medical records of these patients and their imaging studies were analyzed to identify potentially preventable factors and injury patterns in this group of patients. The factors analyzed included age, modality of injury, therapeutic narcotic usage, seizures, and hyponatremia. Two groups of patients are described herein based on intracranial pathology, with statistically significant differences in age, mechanism, and coagulopathy identified.
Water and electrolytes disorders after brain injury: Mechanism and treatment
2012, Annales Francaises d'Anesthesie et de Reanimation
Les désordres hydroélectrolytiques sont fréquents au cours des agressions cérébrales, en particulier les dysnatrémies et les dyskaliémies. La séméiologie clinique habituelle des hyponatrémies est intriquée avec celle de la pathologie sous-jacente. La valeur absolue de la natrémie est moins importante que la vitesse d’installation du trouble. L’hyponatrémie vraie est hypotonique et correspond à une hyperhydratation intracellulaire, risquant d’aggraver un œdème cérébral. La distinction entre sécrétion inappropriée d’hormone antidiurétique et syndrome de perte de sel (CSWS) est difficile et repose sur l’évaluation de la volémie, abaissée en cas de CSWS et maintenue ou augmentée en cas de SIADH. Au cours de l’hémorragie sous-arachnoïdienne (HSA), la situation la plus commune est le CSWS. Dans ce cas, toute restriction hydrique est contre-indiquée. Le traitement du CSWS repose sur la compensation de la fuite urinaire en sodium et peut nécessiter le recours à un minéralocorticoïde. La correction d’une dysnatrémie ne doit pas excéder 0,5 mmol/L par heure soit 12 mmol/L par 24 heures. La surveillance de la natrémie doit être attentive dans les dix jours qui suivent une chirurgie hypophysaire. Tout traitement barbiturique peut être responsable de dyskaliémies menaçant le pronostic vital.
Electrolyte disturbances are frequent after brain injuries, especially dysnatremia and dyskalemia. In neurological patients, usual clinical signs of hyponatremia are frequently confounded with clinical signs of the underlying disease. Natremia absolute value is less important than speed of onset of the trouble. Most often, hyponatremia is associated with hypotonicity and intracellular hyperhydration, which may exacerbate a cerebral edema. Distinction between inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting syndrome (CSWS) may be difficult and is mainly based on assessment of patient's volemia, SIADH being associated with normal or hypervolemia and CSWS with hypovolemia. After subarachnoid haemorrhage, the most common disorder is CSWS. In this case, fluid restriction is strictly prohibited. Treatment of CSWS needs to compensate for the natriuresis and may justify the use of mineralocorticoid. It is important to avoid excessively rapid correction of hypernatremia, with a maximal speed of correction of 0.5 mmol/l/h. Serum sodium monitoring should be mandatory for the first ten postoperative days after pituitary adenoma surgery. Therapeutic barbiturate may be responsible for life threatening dyskalemia.
Head and spinal cord injury: Diagnosis and management
2012, Neurologic Clinics
Fluid and electrolyte disorders following surgery for brain tumors
2007, Anales de Pediatria
Entre las complicaciones que pueden aparecer en el postoperatorio inmediato de los tumores cerebrales destacan los trastornos hidroelectrolíticos (diabetes insípida, síndrome pierde sal y síndrome de secreción inadecuada de hormona antidiurética [SIADH]). Es importante su diagnóstico y tratamiento precoz de cara a prevenir los posibles efectos negativos que pueden tener sobre el propio sistema nervioso central (SNC).
Valorar la incidencia y características de los trastornos electrolíticos aparecidos en el postoperatorio inmediato de los niños intervenidos de tumores del SNC en nuestro centro.
Análisis retrospectivo de las historias clínicas de niños intervenidos de tumores del SNC en nuestro centro entre enero de 1998 y junio de 2005, que en el postoperatorio cumplieron criterios analíticos de diabetes insípida, síndrome pierde sal o SIADH.
Se detectaron 23 trastornos hidroelectrolíticos en 149 intervenciones (15,4 %). El 47,8 % fueron varones. La mediana de edad fue de 5 años y 3 meses (rango de 6 meses a 17 años). La alteración electrolítica más frecuente fue diabetes insípida (65,2 %). El trastorno apareció en una media de 19 h tras la cirugía. Se administró desmopresina en todos los casos, con resolución del cuadro en una media de 73 h tras el diagnóstico, excepto un caso de diabetes insípida permanente por lesión quirúrgica del eje hipotálamo-hipofisario. El síndrome pierde sal, con un 26,1 % de los casos, fue el segundo trastorno hidroelectrolítico en frecuencia. El tiempo medio de aparición tras la cirugía fue de 50,4 h. Se adecuó el aporte hidrosalino en todos los casos. El trastorno se resolvió en una media de 57,6 h tras su aparición. Sólo se detectaron 2 casos de SIADH que se trataron con restricción hídrica y adecuación de aportes de sodio. Ambos casos se resolvieron espontáneamente en las primeras 36 h tras el diagnóstico. Al alta ningún paciente presentaba alteraciones neurológicas secundarias al trastorno hidroelectrolítico.
El trastorno hidroelectrolítico más frecuente en post-operados de tumores cerebrales en nuestra serie ha sido la diabetes insípida. El tratamiento precoz con desmopresina evita en la mayor parte de los casos la aparición de hipernatremia. Si no existe lesión quirúrgica del eje hipotálamo hipofisario la resolución espontánea se produce en una media de 3 días. El manejo del síndrome pierde sal y el SIADH requiere una estrecha monitorización del sodio plasmático por la gran tendencia a la hiponatremia.
Fluid and electrolyte disorders such as diabetes insipidus, salt wasting syndrome (SWS) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) can appear in the immediate postoperative period after surgery for brain tumors. Early diagnosis and treatment are important to prevent the potential adverse effects of these disorders on the central nervous system (CNS).
To determine the incidence and characteristics of fluid and electrolyte disorders in the immediate postoperative period after surgery for CNS tumors in children treated in our hospital.
We retrospectively analyzed clinical and laboratory data in all infants and children who underwent surgery for CNS tumors in our hospital from January 1998 to June 2005 and who met the laboratory criteria for diabetes insipidus, SWS or SIADH.
Twenty-three electrolyte disorders were identified in 149 surgical patients (an incidence of 15.4 %). The median age was 5 years and 3 months (from 6 months to 17 years) and 48.7 % of the patients were male. The most frequent electrolyte disturbance was diabetes insipidus (65.2 % of all electrolyte disorders). On average, onset of diabetes insipidus occurred 19 hours after surgery. Treatment with desmopressin was administrated in all patients. On average, diabetes insipidus was resolved 73 hours after diagnosis, except in one patient with permanent diabetes insipidus due to a surgical lesion of the hypothalamic-pituitary axis. The second most frequent electrolyte disturbance was SWS (26.1 %) with a mean time of onset of 50.4 hours after surgery. On average, SWS was resolved 57.6 hours after administration of saline solutions. Only two patients developed SIADH, which was treated with water restriction and adequate sodium supply. Both cases of SIADH resolved spontaneously in the first 36 hours after diagnosis. At discharge, none of the patients showed neurological disturbances due to an electrolytic disorder.
In our series, the most frequent electrolyte disorder after surgery for CNS tumors was diabetes insipidus. Early treatment with desmopressin almost always prevents hypernatremia. Unless there is a surgical lesion of the hypothalamic-pituitary axis, spontaneous resolution will take place in 3 days on average. The management of SWS and SIADH requires close monitoring of plasma sodium due to the risk of hyponatremia.
Mechanisms counteracting swelling in brain cells during hyponatremia
2002, Archives of Medical Research
Water gain in the brain consequent to hyponatremia is counteracted by mechanisms that initially include a compensatory displacement of liquid from the interstitial space to cerebrospinal fluid and systemic circulation and subsequently an active reduction in cell water accomplished by extrusion of intracellular osmolytes to reach osmotic equilibrium. Potassium (K⁺), chloride (Cl⁻), amino acids, polyalcohols, and methylamines all contribute to volume regulation, with a major contribution of ions at the early phase and of organic osmolytes at the late phase of the regulatory process. Experimental models in vitro show that osmolyte fluxes occur via leak pathways for organic osmolytes and separate channels for Cl⁻ and K⁺. Osmotransduction signaling cascades for Cl⁻ and taurine efflux pathways involve tyrosine kinases and phosphoinositide kinases, while Ca²⁺ and serine-threonine kinases modulate K⁺ pathways. In-depth knowledge of the cellular and molecular adaptive mechanisms of brain cells during hyponatremia contributes to a better understanding of the associated complications, including the risks of inappropriate correction of the hyponatremic condition.
Hyponatremia in acute brain disease: The cerebral salt wasting syndrome
2002, European Journal of Internal Medicine
Hyponatremia in acute brain disease is a common occurrence, especially after an aneurysmal subarachnoid hemorrhage. Originally, excessive natriuresis, called cerebral salt wasting, and later the syndrome of inappropriate antidiuretic hormone secretion (SIADH), were considered to be the causes of hyponatremia. In recent years, it has become clear that most of these patients are volume-depleted and have a negative sodium balance, consistent with the original description of cerebral salt wasting. Elevated plasma concentrations of atrial or brain natriuretic peptide have been identified as the putative natriuretic factor. Hyponatremia and volume depletion may aggravate neurological symptoms, and timely treatment with adequate replacement of water and NaCl is essential. The use of fludrocortisone to increase sodium reabsorption by the renal tubules may be an alternative approach.

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Clinical noteCerebral salt wasting syndrome in brain injury patients: A potential cause of hyponatremia☆

Abstract

Am J Med

Am J Med

Lancet

Neurosurgical hyponatremia: the role of inappropriate diuresis

J Neurosurg

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after head injury

Neurosurgery

Hponatremia in acute brain disease

J Int Med

A salt wasting syndrome associated with cerebral disease

Trans Assoc Am Physiol

The physiopathology of ADH secretion

Hyponatremia in neurosurgery patients

Clin Neurosurg

Hypovolemia in patients with subarachnoid hemorrhage: therapeutic implications

Neurosurgery

Atrial natriuretic polypeptide in patients with subarachnoid hemorrhage due to aneurysmal rupture

Acta Neurochir (Wein)

Clinical note
Cerebral salt wasting syndrome in brain injury patients: A potential cause of hyponatremia☆