A Rare Lesion in the Anterior Region of the Third Ventricle: Rosette-Forming Glioneuronal Tumor.

Rosette-forming glioneuronal tumor (RGNT) is a rare and indolent mixed glioneuronal tumor involving primarily the fourth ventricular region and occurring predominantly in young adults. We present a case of a 44-year-old woman presented with progressive headaches, vomiting, and a sudden decreasing level of consciousness. The magnetic resonance imaging showed a regular lesion within the anterior portion of the third ventricle and the patient underwent an endoscopic approach to remove the tumor that was exclusively within the anterior portion of the third ventricle. Histopathology showed an RGNT that was totally removed. We also report some unusual complications that are described in the literature and are related to ventricular endoscopy such as seizures and hydroelectrolyte disorders. With two years of follow-up, the patient had no complaints and no tumor progression was observed.

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.

Pituitary Apoplexy-associated Cerebral Salt Wasting Syndrome: A Case Report and Literature Review.

PURPOSE: This is a case report of a patient experiencing hyponatremia who was ultimately diagnosed with pituitary apoplexy-associated cerebral salt wasting syndrome (CSWS). METHODS: Laboratory tests, clinical evaluations, and magnetic resonance imaging were performed by specialists. FINDINGS: The patient presented with severe headache, thirst, and polyuria. Results of laboratory tests indicated hyponatremia, decreased plasma osmolality, and elevated urine osmolality. Fluid restriction worsened the situation, and normal saline treatment helped return serum sodium and chloride levels to normal. Pituitary apoplexy-associated CSWS was finally considered. IMPLICATIONS: Pituitary apoplexy is a rare but reasonable etiology for CSWS with hyponatremia. Saline therapy is usually effective.

A Probable Association of Aseptic Meningoencephalitis, Complicated With Cerebral Salt Wasting Syndrome Following COVID-19 Vaccination: A Case Report.

Coronavirus disease-19 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) occurred worldwide, and it affected millions of people around the world and killed millions of lives without a definitive treatment. During this challenging time, vaccine production has been hugely carried out leading to the invention of many vaccines against COVID-19. As any vaccine can have some side effects, COVID-19 vaccines also need surveillance and reporting side effects worldwide. Currently, more than 10 vaccines are available against SARS-CoV-2 infection globally. There are many neurological complications reported by SARS-CoV-2 vaccines. There are some reported neurological complications, such as ischemic stroke, Guillain-Barré syndrome, transverse myelitis, Bell's palsy, cerebral venous sinus thrombosis, optic neuritis, meningoencephalitis, small fiber neuropathy, and Tolosa-Hunt syndrome. We present a case of an elderly man who presented with fever, fits, hyponatremia, and polyuria following COVID-19 vaccination and was found to have cerebral salt wasting (CSW) with the exclusion of other causes.

Cerebral Salt Wasting Syndrome Following Right Occipital Craniotomy in a Patient With Metastatic Lung Adenocarcinoma.

Cerebral salt wasting syndrome (CSW) is characterized by excessive natriuresis leading to hyponatremia and hypovolemia. It is commonly encountered among patients who have undergone brain trauma or subarachnoid hemorrhage. The occurrence of CSW after neurosurgical procedures has been frequently reported in the pediatric age group; however, it is a rare phenomenon in adults. We describe the case of a 59-year-old female who developed symptoms of polyuria and polydipsia after a right occipital craniotomy.

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.

Late-Onset Intracranial Hemorrhage Presenting as Refractory Hyponatremia: A Case Report.

Here, we report a case of refractory hyponatremia and delayed intracranial hemorrhage following a head injury. A 70-year-old male patient was admitted with complaints of left chest pain and light-headedness after a fall. Hyponatremia recurred despite the correction with intravenous saline. Head computed tomography revealed a chronic subdural hematoma. The subsequent introduction of tolvaptan improved hyponatremia and disorientation. Delayed intracranial hemorrhage is a differential cause of refractory hyponatremia after head contusion. This case is clinically relevant because (i) the diagnostic delay of late-onset intracranial hemorrhage is common but fatal, and (ii) refractory hyponatremia can be a hint of late-onset intracranial hemorrhage.

Suspected Cerebral Salt Wasting Syndrome with Cervical Spinal Lesion in a Domestic Shorthair Cat.

A 12-year-old spayed female domestic short cat was presented with tetraplegia. The cat also showed signs of hyponatremia and dehydration, which were rapidly corrected by intravenous fluid infusion. Based on thorough physical and neurological examinations, the patient was suspected of having an intracranial disease. MRI revealed a high-signal T2 image of the bilateral parietal cerebral cortical gray matter junction, which is associated with fast electrolyte calibration, and a high-signal T2 image of the C2 spinal cord ventral area, which is associated with ischemic myelopathy. The cat reappeared three days later due to anorexia. Laboratory examinations revealed that the cat was clinically dehydrated and exhibited hyponatremia. Other causes of hyponatremia were excluded through history-taking, laboratory examination, imaging, and therapeutic response to fluid therapy, except for cerebral salt-wasting syndrome (CSWS). The cat was discharged 3 days after the start of fludrocortisone therapy with electrolytes within the normal range. Magnetic resonance imaging (MRI) was performed again 1 month after hospitalization, and the cerebral lesion disappeared, but the spinal cord lesion worsened compared to the previous image. The patient was euthanized due to the progression of the spinal lesion, with a poor prognosis and poor quality of life. This is the first case of suspected CSWS with a cervical spinal lesion in a cat.

Cerebral Salt Wasting Syndrome in the Setting of Hypovolemic Isotonic Hyponatremia: A Case Report.

Cerebral salt wasting syndrome (CSWS) is a condition characterized as the loss of sodium secondarily due to an intracranial process, commonly following the neurosurgical resection of mass lesions. This condition leads to a hypovolemic hypotonic hyponatremia. The identification of this syndrome is often mistaken for syndrome of inappropriate anti-diuretic hormone (SIADH). The treatment for both conditions is vastly different. Given the risk of mortality when balancing sensitivities in hyponatremia and its commonality in clinical scenarios, a distinction is crucial. In this case report, we discuss a patient who presented with CSWS following the surgical resection of a pituitary adenoma. She subsequently developed hypernatremia, treated with DDAVP for the suspicion of diabetes insipidus. Once this was discontinued, she further presented with worsening hyponatremia. This hyponatremia persisted even after the discontinuation of DDAVP, with no significant intervention leading to hypovolemic isotonic hyponatremia, supporting a diagnosis of CSWS. Our findings stress the importance of the proper identification of hyponatremia with guided treatment following neurosurgical intervention and give physicians an insight into the anomalies of hyponatremia that should be further discussed.

Hiccup: The Striking Manifestation of Hyponatremia Due to Ischemic Stroke-Induced Cerebral Salt Wasting Syndrome (CSWS).

Among many clinical symptoms, hiccups are an infrequent presentation of hyponatremia. Hyponatremia indicates a serum sodium level of less than 135 mmol/l, the most common reported electrolyte abnormality. Cerebral salt wasting syndrome is a less common cause of hyponatremia, which can arise from a spectrum of brain pathology. This case report brings attention to a case of hyponatremia due to cerebral salt wasting syndrome in a 76-year-old man who suffered from an ischemic stroke. The hyponatremia appeared vaguely, with only a hiccup as a symptom.

Cerebral Salt-Wasting Syndrome in a Patient With Active Pulmonary Tuberculosis.

A 37-year-old female with a medical history of recently diagnosed active pulmonary tuberculosis and a new intracranial lesion presented with altered mental status, nausea, and vomiting for two days. An initial physical examination revealed that the patient was euvolemic. Laboratory findings revealed a serum sodium concentration of 105 mEq/L. During her admission, she was initially managed with lactated ringer solution in the emergency department, followed by 3% normal saline in the intensive care unit, and, eventually, on oral sodium chloride and fluid restriction on discharge. Once she was stabilized, she had episodes of dizziness, and concerns were raised about the salt-wasting syndrome.

Cerebral Salt Wasting Syndrome (CSW): An unusual cause of hypovolemia after spontaneous cerebral hemorrhage successfully treated with fludrocortisone.

Our objective is to demonstrate the interest of thinking about Cerebral salt wasting syndrome (CSW) in front of hyponatremia with severe hypovolemia after a brain injury, and at the same time the interest to differentiate between Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) and Cerebral salt wasting syndrome (CSW) as two etiologies to be evoked in front of a hyponatremia with brain injury. Case report: We report the case of a 63-year-old patient with a recent history of hemorrhagic stroke admitted for severe hypovolemic shock in whom the investigations find a very deep hypotonic hyponatremia secondary to a cerebral salt wasting syndrome successfully treated with fludrocortisone. Discussion: CWS is characterized by hypotonic hyponatremia associated with cerebral associated with hypovolemia, the difficulty of the diagnosis is explained by the points of convergences with SIADH which is also presented with hyponatremia. The treatment is based on filling with saline, if the symptoms are severe, hypertonic saline has its place. Fludrocortisone has proven its effectiveness in the correction of refractory hyponatremia in CWS. Conclusion: It is essential to differentiate between hyponatremia in CWS and hyponatremia in SIADH because the medical care is categorically different.

A multi-parameter study of the etiological diagnosis of hyponatremia after hypothalamic tumor surgery.

OBJECTIVES: This study aimed to analyze the difference between cerebral salt-wasting syndrome (CSWS) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in patients with hyponatremia after hypothalamic tumor surgery, and to explore a convenient and effective way to identify CSWS and SIADH. METHODS: Patients undergoing craniotomy of hypothalamic tumor admitted to the Department of The Affiliated Hospital of Qingdao University from December 2018 to May 2020 were enrolled in this study. Plasma brain natriuretic peptide (BNP), 24-h urine sodium, 24-h urine volume, and the diameter of the inferior vena cava (IVCD) were measured daily before operation and 1-7 days after operation, to analyze differences in plasma BNP, 24-h urinary sodium excretion, 24-h urine volume, and IVCD between the CSWS and SIADH. RESULTS: The medical data of 31 patients with hypothalamic tumors were collected. Fifteen of these patients (48%) had postoperative hyponatremia, nine patients (29%) had CSWS, and six patients (19%) had SIADH. Plasma BNP, 24-h urinary sodium excretion, and 24-h urine volume in the CSWS group were significantly higher than those in the SIADH group. IVCD decreased in the CSWS group and increased in the SIADH group. CONCLUSIONS: When hyponatremia occurs after hypothalamic tumor surgery, plasma BNP, 24-h urinary sodium excretion, 24-h urine volume, and IVCD are of great help in identifying CSWS and SIADH.

Coexistence of Triphasic Diabetes Insipidus and Cerebral Salt Wasting Syndrome Following Extraction of Sellar/Suprasellar Grade I Pilocytic Astrocytoma.

Water homeostasis disorders, such as syndrome of inappropriate antidiuretic hormone secretion (SIADH), diabetes insipidus (DI), and cerebral salt-wasting syndrome (CSWS), can develop after neurosurgery. Additionally, DI, SIADH, and CSWS have been reported concurrently in association with some neurosurgical conditions, in particular after pituitary gland surgery or as sequelae of post-traumatic brain injury. Therefore, neurosurgeons should expect water homeostasis disorders after the removal of tumors of the sellar/suprasellar region and be prepared to aggressively manage them.

Acute hyponatremia after aneurysmal subarachnoid hemorrhage: Frequency, treatment, and outcome.

We retrospectively examined the course of serum sodium levels in 180 patients with acute aneurysmal subarachnoid hemorrhage (SAH) who had been admitted to the anesthesiologic-neurosurgical intensive care unit of the University Medical Center Regensburg, Germany, between January 2014 and December 2018. Each patient file was analyzed regarding the frequency and intensity of hyponatremic episodes and the administered medication. At admission to the intensive care unit (ICU), 18patients had shown initial hyponatremia (<135 mmol/L) and 4 patients hypernatremia (greater than145 mmol/L). 88(48.9%) of the 158 patients with normal serum sodium levels developed at least one hyponatremic episode during ICU treatment. The number of hyponatremic episodes was similar between patients with higher-grade and lower-grade aneurysmal SAH (P = 0.848). At the end of ICU treatment, outcome did not differ between patients with and without hyponatremia (40/88, 45.5% vs. 38/70, 54.3%, P = 0.270). At 6 months after SAH, however, good outcome (Glasgow outcome scale, GOS 4-5) was more frequently observed in patients with hyponatremia (26/88, 29.5% vs. 32/70, 45.7%, P = 0.036). Medication with sodium chloride, fludrocortisone, or tolvaptan was initiated in 75.4% patients with mild hyponatremia (130-134 mmol/L) and in 92.9% with moderate hyponatremia (125-129 mmol/L). At 6 months after SAH, patients treated with tolvaptan had a lower rate of poor outcome than patients who had not received tolvaptan (1/14, 7.1% vs. 25/74, 33.8%, P = 0.045). In patients with acute aneurysmal SAH and hyponatremic episodes, consequent treatment of hyponatremia prevented impaired outcome. Because administration of tolvaptan rapidly normalized serum sodium levels, this therapy seems to be a promising treatment approach.

Frequency of Hyponatremia in Patients of Tuberculosis Bacterial Meningitis in a Tertiary Care Hospital.

Introduction Tuberculous meningitis (TBM) brings significant morbidity and mortality worldwide. Hyponatremia has long been documented as a potentially grave metabolic result of TBM. The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has been supposed to be accountable for the majority of cases of hyponatremia in TBM. Cerebral salt wasting syndrome (CSWS) is being progressively reported as a basis of hyponatremia in some of these cases. Differentiating CSWS from SIADH can be challenging but is vital because treatment of these two conditions is profoundly different. Objective The rationale of our study is to determine the frequency of hyponatremia and etiology in patients presenting with TBM in a tertiary care hospital in order to establish the local perspective as there is paucity of local data. Methods A total of 160 hospitalized patients at a tertiary care hospital in Pakistan who fulfilled the inclusion criteria were enrolled in this study after informed consent. The study was conducted for six months at the department of neurology, Jinnah Postgraduate Medical Centre (JPMC), Karachi, Pakistan. Brief history was taken and demographic information was entered in the performa by researchers. The data was collected and analyzed on Statistical Package for Social Sciences (SPSS) version 18.0 (IBM Corp., Armonk NY, USA). Demographic data were presented as simple descriptive statistics giving mean and standard deviation for age, height, weight, GCS (Glasgow Coma Scale), serum sodium and duration of symptoms. Frequencies and percentages were calculated for categorical variables like gender, hypertension, smoking status, T2DM (Type 2 Diabetes Mellitus), BMRC (British Medical Research Council Contemporary Clinical Criteria for TBM) stage, hyponatremia, SIADH and CSWS. Effect modifiers were controlled through stratification of age, gender, hypertension, smoking status, T2DM, BMRC stage and duration of symptoms to see the effect of these on the outcome variable (hyponatremia). Quantitative data were presented as simple descriptive statistics giving mean and standard deviation and qualitative variables were presented as frequency and percentages. Post stratification chi-square test was applied with a p-value of ≤0.05 taken as significant. Results In our study, out of 160 patients with TBM, 40% (64) had hyponatremia. Moreover, 14.4% and 25.6% had SIADH and CSWS, respectively with 60% (96) of patients were male and 40% (64) were female. Mean age of patients in our study was 46.78±2.81 years. Whereas, mean duration of symptoms, serum sodium, GCS, height and weight in our study was 1.2±0.78 weeks, 128.65±7.52 mmol/L and 11.21±3.14%, 158±7.28 cm and 78.7±9.87 kg, respectively. Conclusion This study concluded that the frequency of hyponatremia among patients of TBM was significant, consistent with previous studies. Privation of proper assessment and management can lead to grave and permanent neurological consequences, as well as death. Healthcare providers should be aware of the implication of sodium deregulation among patients of TBM and differentiate between the numerous therapeutic preferences in order to advocate safe and effective treatment.

Tuberculous Meningitis Presenting as Cerebral Salt Wasting Syndrome: A Review of Literature with Clinical Approach to Hyponatremia.

Hyponatremia in the neurocritical care patients is commonly encountered in the setting of either syndrome of inappropriate ADH secretion or cerebral salt wasting. However, differentiation of SIADH and CSW is paramount in view of their divergent treatment strategies.

Tubercular meningitis presenting as cerebral salt wasting syndrome in an adult: A case report.

INTRODUCTION: Cerebral salt wasting syndrome (CSWS) is a cause of hyponatremia in the setting of intracranial pathologies such as Central Nervous System (CNS) trauma, infections, and tumors. It is important to differentiate CSWS from the syndrome of inappropriate antidiuretic hormone secretion (SIADH) as their management differs. CSWS leads to hypovolemia as opposed to euvolemia or hypervolemia in SIADH. SIADH is managed with fluid restriction and this could worsen CSWS which is managed with adminstration of intravenous crystalloids to correct hyponatremia. CASE SUMMARY: A 42-year-old male was admitted after a week of low-grade fever with easy fatigability, hypersomnolence, and excessive thirst. He had polyuria which started 5 days before presentation, and unintentionally lost 3 kg of weight in the past month. He had orthostatic hypotension, and was dehydrated, but vital signs were normal with the exception of his temperature. Cerebrospinal fluid (CSF) analysis revealed a glucose of 42 mg/dl, protein 170 mg/dl, cell count 28/mm3 with 65% lymphocytes which was consistant with tubercular meningitis. CSF AFB culture was positive in addition to a positive CSF PCR for M. tuberculosis. DISCUSSION: Presentation of CNS infection with tuberculosis may be non-specific and its insidious onset could lead to delayed or missed diagnosis; however persistent constitutional symptoms and signs with history of weight loss and a close contact with tuberculosis may raise the possibility of tuberculosis. Early diagnosis and treatment has an excellent prognosis, but any delay contributes to death and disability despite anti-tubercular drug therapy.CSWS should be managed with salt and volume replacement, but more importantly, the causative CNS insult should also be confirmed and addressed.