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Objective: To describe a dog with suspected cerebral salt wasting syndrome (CSWS) secondary to traumatic brain injury (TBI). Case Summary: A 2‐month‐old intact male Chihuahua‐American Pitbull Terrier mix weighing 1.94 kg presented to a veterinary teaching emergency room after suffering bite wound‐penetrating trauma to the head. Treatment was initiated with hyperosmotic agents, fluid resuscitation, and analgesia. The dog's neurologic dysfunction warranted hospitalization and continuous monitoring. Within 24 hours, the dog developed hyponatremia (133 mmol/L compared to 143 mmol/L on presentation [reference interval 142–149 mmol/L]). As the dog had concurrent tachycardia, increase in urine sodium concentration, polyuria, and weight loss, a diagnosis of cerebral salt wasting was suspected. A 2% hypertonic saline constant rate infusion was administered for volume replacement, and the patient showed improvement in clinical signs and blood sodium concentration. The dog was discharged on Day 5. Recheck examination showed significant neurologic improvement with sodium just below the low end of the reference range (141 mmol/L [reference interval 142–149 mmol/L]). New or Unique Information Provided: This is the first description of suspected CSWS in veterinary medicine. Hyponatremia is a common finding in critically ill neurologic people, including those with TBI, and is typically associated with either syndrome of inappropriate antidiuretic hormone or CSWS. As treatment recommendations for syndrome of inappropriate antidiuretic hormone and CSWS are diametrically opposed, identifying the presence of hyponatremia and distinguishing between these 2 clinical entities is critical for improving patient care for those with TBI. This case highlights the characteristics and clinical progression regarding the diagnosis and management of suspected CSWS. [ABSTRACT FROM AUTHOR]

The subject of hyponatremia is undergoing significant changes after developing a more pathophysiologic approach that is superior to the ineffective volume approach and can more effectively identify the different causes of hyponatremia. This new approach identified cerebral salt wasting (CSW) in 24 (38%) of 62 hyponatremic patients from the medical wards of the hospital with 21 showing no evidence of cerebral disease to support our proposal to change CSW to renal salt wasting (RSW). RSW had to be differentiated from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) because of diametrically opposite therapeutic goals of water-restricting water-logged patients with SIADH or administering salt water to volume-depleted patients with RSW. Both syndromes present with identical clinical parameters that require a difficult protocol to make such a differentiation possible. We describe rat clearance studies demonstrating natriuretic activity in the plasma of patients with neurosurgical and Alzheimer diseases (AD) and eventually identify the protein as haptoglobin-related protein without signal peptide, which can serve as a biomarker to simplify diagnosis of RSW and delivery of the proper management to improve clinical outcomes. We also discuss the introduction of a new syndrome of RSW in AD and its implications. The high prevalence of RSW and identification of the natriuretic factor have created debates over the existence of RSW with none questioning or addressing the pathophysiologic data that identified patients with RSW. We also discuss the potentially large group of patients with RSW who are normonatremic.

Abstract Background Delayed cerebral ischemia is a clinical entity commonly encountered in patients presenting with acute neurological injury and is often complicated by dysnatremias, such as the cerebral salt wasting syndrome. In this case report, we described an exceptional case of polyuria attributed to an initial cerebral salt wasting phenomenon and iatrogenic-induced medullary washout. Case presentation A 53-year-old woman was admitted to our hospital for the management of a Modified Fisher scale grade 4 subarachnoid hemorrhage due to a ruptured posterior communicating aneurysm. She was initially managed with coil embolization and external ventricular drain due to secondary hydrocephalus. Throughout the course of her hospitalization, she developed severe polyuria reaching up to 40L per day. To keep up with the excessive urinary losses and maintain appropriate cerebral perfusion, fluid replacement therapy was adjusted every hour, reaching up to 1.3 L of crystalloid per hour in addition to aminergic support. An initial diagnosis of partial diabetes insipidus, followed by a cerebral salt wasting syndrome was suspected. While the urine output continued to increase, her serum urea concentration progressively decreased to a point of almost being undetectable on day 9. At that time, the presence of an interstitial medulla washout was hypothesized. Various pharmacological and non-pharmacological interventions were progressively introduced to regain normal renal homeostasis, including non-steroidal anti-inflammatory drugs, fludrocortisone, oral urea and high-protein intake. Medications were progressively weaned, and the patient was successfully discharged from the ICU. Conclusions Cerebral salt wasting should be considered in the initial differential diagnosis of a patient presenting with polyuria in the context of acute neurological injury. Early recognition of this entity is critical to quickly implement proper management. However, as shown in this case report, the concomitance of delayed cerebral ischemia may complexify that management.

Background: Delayed cerebral ischemia is a clinical entity commonly encountered in patients presenting with acute neurological injury and is often complicated by dysnatremias, such as the cerebral salt wasting syndrome. In this case report, we described an exceptional case of polyuria attributed to an initial cerebral salt wasting phenomenon and iatrogenic-induced medullary washout. Case presentation: A 53-year-old woman was admitted to our hospital for the management of a Modified Fisher scale grade 4 subarachnoid hemorrhage due to a ruptured posterior communicating aneurysm. She was initially managed with coil embolization and external ventricular drain due to secondary hydrocephalus. Throughout the course of her hospitalization, she developed severe polyuria reaching up to 40L per day. To keep up with the excessive urinary losses and maintain appropriate cerebral perfusion, fluid replacement therapy was adjusted every hour, reaching up to 1.3 L of crystalloid per hour in addition to aminergic support. An initial diagnosis of partial diabetes insipidus, followed by a cerebral salt wasting syndrome was suspected. While the urine output continued to increase, her serum urea concentration progressively decreased to a point of almost being undetectable on day 9. At that time, the presence of an interstitial medulla washout was hypothesized. Various pharmacological and non-pharmacological interventions were progressively introduced to regain normal renal homeostasis, including non-steroidal anti-inflammatory drugs, fludrocortisone, oral urea and high-protein intake. Medications were progressively weaned, and the patient was successfully discharged from the ICU. Conclusions: Cerebral salt wasting should be considered in the initial differential diagnosis of a patient presenting with polyuria in the context of acute neurological injury. Early recognition of this entity is critical to quickly implement proper management. However, as shown in this case report, the concomitance of delayed cerebral ischemia may complexify that management. [ABSTRACT FROM AUTHOR]

The application of pathophysiologic tenets has created significant changes in our approach to hyponatremia and hyponatremia-related conditions. This new approach incorporated the determination of fractional excretion (FE) of urate before and after the correction of hyponatremia and the response to isotonic saline infusion to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from renal salt wasting (RSW). FEurate simplified the identification of the different causes of hyponatremia, especially the diagnosis of a reset osmostat and Addison's disease. Differentiating SIADH from RSW has been extremely difficult because both syndromes present with identical clinical parameters, which could be overcome by successfully carrying out the difficult protocol of this new approach. A study of 62 hyponatremic patients from the general medical wards of the hospital identified 17 (27%) to have SIADH, 19 (31%) with reset osmostat, and 24 (38%) with RSW with 21 of these RSW patients presenting without clinical evidence of cerebral disease to warrant changing the nomenclature from cerebral to renal salt wasting. The natriuretic activity found in the plasma of 21 and 18 patients with neurosurgical and Alzheimer's disease, respectively, was later identified as haptoglobin-related protein without signal peptide (HPRWSP). The high prevalence of RSW creates a therapeutic dilemma of deciding whether to water-restrict water-logged patients with SIADH as compared to administering saline to volume-depleted patients with RSW. Future studies will hopefully achieve the following: 1. Abandon the ineffective volume approach; 2. Develop HPRWSP as a biomarker to identify hyponatremic and a projected large number of normonatremic patients at risk of developing RSW, including Alzheimer's disease; 3. Facilitate differentiating SIADH from RSW on the first encounter and improve clinical outcomes. [ABSTRACT FROM AUTHOR]

Background: Hyponatremia is common in patients with central nervous system disease. It may prolong hospitalization and increase morbidity and mortality. However, the incidence and risks factors remain largely unknown in traumatic brain injury (TBI). The objectives of this study are to characterize hyponatremia in TBI patients and find its main risk factors.Methods: All patients admitted with a diagnosis of acute TBI over a 1-year period were included, except patients with known chronic hyponatremia, those who died within 72 h, and those receiving hyperosmolar therapy to treat their intracranial hypertension. Sodium levels throughout hospitalization were collected. Post-traumatic hyponatremia was defined as follows: borderline (1-2 points below normal and 1-2 days duration) and significant (more than 2 points below normal and/or more than 2 days duration). Demographic data, GCS, mechanism of injury, and CT findings were collected. These factors were correlated to the incidence of hyponatremia.Results: Hyponatremia was found in 29% of the 283 included patients and was significant in 2/3 of the cases. Significant hyponatremia had a narrower peak, between 7 and 11 days, while borderline hyponatremia started earlier and was more distributed in time. Factors associated with hyponatremia were greater age (p = 0.004), worse ISS (p = 0.017), worse Marshall Grade on CT (p = 0.007), and a diffuse pattern of injury on CT (p < 0.001). Significant hyponatremia was associated with: a diffuse pattern of injury on CT (p = 0.032), the presence of intracerebral hemorrhage (p = 0.027), and multiple lesions on CT (p = 0.043).Conclusions: Post-traumatic hyponatremia is common and can lead to serious consequences in TBI patients. Adequate monitoring and treatment are therefore important. Older patients and those with more significant injury on CT are more at risk. [ABSTRACT FROM AUTHOR]

The application of pathophysiologic tenets has created significant changes in our approach to hyponatremia and hyponatremia-related conditions. This new approach incorporated the determination of fractional excretion (FE) of urate before and after the correction of hyponatremia and the response to isotonic saline infusion to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from renal salt wasting (RSW). FEurate simplified the identification of the different causes of hyponatremia, especially the diagnosis of a reset osmostat and Addison’s disease. Differentiating SIADH from RSW has been extremely difficult because both syndromes present with identical clinical parameters, which could be overcome by successfully carrying out the difficult protocol of this new approach. A study of 62 hyponatremic patients from the general medical wards of the hospital identified 17 (27%) to have SIADH, 19 (31%) with reset osmostat, and 24 (38%) with RSW with 21 of these RSW patients presenting without clinical evidence of cerebral disease to warrant changing the nomenclature from cerebral to renal salt wasting. The natriuretic activity found in the plasma of 21 and 18 patients with neurosurgical and Alzheimer’s disease, respectively, was later identified as haptoglobin-related protein without signal peptide (HPRWSP). The high prevalence of RSW creates a therapeutic dilemma of deciding whether to water-restrict water-logged patients with SIADH as compared to administering saline to volume-depleted patients with RSW. Future studies will hopefully achieve the following: 1. Abandon the ineffective volume approach; 2. Develop HPRWSP as a biomarker to identify hyponatremic and a projected large number of normonatremic patients at risk of developing RSW, including Alzheimer’s disease; 3. Facilitate differentiating SIADH from RSW on the first encounter and improve clinical outcomes.

Background: To evaluate serum antidiuretic hormone (ADH), its receptors, and renin levels in cerebral salt wasting (CSW) in tuberculous meningitis (TBM).Methods: Patients diagnosed with definite (n = 30) or probable TBM (n = 47) who developed hyponatremia (CSW, SIADH, or miscellaneous causes) were included. Sequential measurement of serum ADH, ADH-R, and renin activity by enzyme-linked immunosorbent assay was done and correlated with serum sodium level, urinary output, and fluid balance.Results: Out of 79 TBM patients, CSW was observed in 36, SIADH in four, and miscellaneous hyponatremia in eight patients. CSW patients had a longer hospital stay (P < 0.001), lower GCS score (P < 0.007), higher MRC grade (P < 0.007), and a lower serum Na (P < 0.001) compared to non-CSW TBM patients. In severe CSW patients, serum ADH and ADH-R were correlated with hyponatremia and returned to baseline on correction; however, serum renin levels remained elevated. Serum ADH was related to hyponatremia but ADH-R and renin were not. ADH-R and renin levels did not significantly differ in CSW and SIADH.Conclusion: CSW is the commonest cause of hyponatremia in TBM and correlates with disease severity. ADH is related to hyponatremia, but ADH receptor and renin are not. [ABSTRACT FROM AUTHOR]

Objective: Tuberculous meningitis (TBM) is a common infection of the central nervous system. TBM with hyponatremia is very common. If hyponatremia is not treated properly, it might affect the outcome of TBM patients. Methods: We included 226 patients diagnosed with TBM who were admitted from August 2010 to August 2015 and retrospectively analyzed the clinical data of patients with and without hyponatremia. Results: In total, 45.6% (103/226) patients had hyponatremia and 54.4% (123/226) patients did not have hyponatremia. Serum sodium and severity of TBM were independent prediction factors of poor outcomes in TBM. The prognosis of patients with hyponatremia was worse than that of patients without hyponatremia. The mortality was 3.9% (4/103) in the hyponatremia group, while 0% (0/123) in the non-hyponatremia group. The degree of hyponatremia was related to imaging, cerebrospinal fluid (CSF) cell count and protein, severity of TBM, time to correct hyponatremia, and prognosis. We analyzed the causes of hyponatremia and found syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was the most common cause (77.7%, 80/103), followed by cerebral salt wasting (CSW) (17.5%, 18/103). Comparing SIADH and CSW, there was a significant difference in mean blood pressure, albumin, and hematocrit, and no significant difference in demographic characteristics, imaging, CSF cell count and protein, severity, occurrence and correction time of hyponatremia, or prognosis. Conclusion: TBM with hyponatremia was dominated by moderate hyponatremia, which often manifested as SIADH. The more severe hyponatremia was, the longer the correction time of hyponatremia, which will affect the prognosis of TBM patients. [ABSTRACT FROM AUTHOR]

Abstract Background Disorders of water and sodium balance can occur after brain injury. Prolonged polyuria resulting from central diabetes insipidus and cerebral salt wasting complicated by gradient washout and a type of secondary nephrogenic diabetes insipidus, however, has not been described previously, to the best of our knowledge. We report an unusual case of an infant with glioblastoma who, after tumor resection, was treated for concurrent central diabetes insipidus and cerebral salt wasting complicated by secondary nephrogenic diabetes insipidus. Case presentation A 5-month-old Hispanic girl was found to have a large, hemorrhagic, suprasellar glioblastoma causing obstructive hydrocephalus. Prior to mass resection, she developed central diabetes insipidus. Postoperatively, she continued to have central diabetes insipidus and concurrent cerebral salt wasting soon after. She was managed with a vasopressin infusion, sodium supplementation, fludrocortisone, and urine output replacements. Despite resolution of her other major medical issues, she remained in the pediatric intensive care unit for continual and aggressive management of water and sodium derangements. Starting on postoperative day 18, her polyuria began increasing dramatically and did not abate with increasing vasopressin. Nephrology was consulted. Her blood urea nitrogen was undetectable during this time, and it was thought that she may have developed a depletion of inner medullary urea and osmotic gradient: a “gradient washout.” Supplemental dietary protein was added to her enteral nutrition, and her fluid intake was decreased. Within 4 days, her blood urea nitrogen increased, and her vasopressin and fluid replacement requirements significantly decreased. She was transitioned soon thereafter to subcutaneous desmopressin and transferred out of the pediatric intensive care unit. Conclusions Gradient washout has not been widely reported in humans, although it has been observed in the mammalian kidneys after prolonged polyuria. Although not a problem with aquaporin protein expression or production, gradient washout causes a different type of secondary nephrogenic diabetes insipidus because the absence of a medullary gradient impairs water reabsorption. We report a case of an infant who developed complex water and sodium imbalances after brain injury. Prolonged polyuria resulting from both water and solute diuresis with low enteral protein intake was thought to cause a urea gradient washout and secondary nephrogenic diabetes insipidus. The restriction of fluid replacements and supplementation of enteral protein appeared adequate to restore the renal osmotic gradient and efficacy of vasopressin.

Disturbances in water and salt balances are relatively common in children after brain tumor surgery. However, the coexistence of different diseases of water and sodium homeostasis is challenging to diagnose and treat. The coexistence of combined central diabetes insipidus (CDI) and cerebral salt wasting syndrome (CSWS) is rare and may impede accurate diagnosis. Herein, we report the case of an 18-year-old girl who underwent surgery for a germinoma and who presented prolonged coexistence of CDI and CSWS. The patient was diagnosed with panhypopituitarism with CDI at presentation and was treated with hydrocortisone, levothyroxine, and desmopressin. Postoperatively, she developed polyuria of more than 3L/day, with a maximum daily urine output of 7.2 L/day. Her serum sodium level decreased from 148 to 131 mEq/L. Polyuria was treated with desmopressin at incremental doses, and hyponatremia was managed with fluid replacement. At 2 months after surgery, she presented with hyponatremia-induced seizure. Polyuria and hyponatremia combined with natriuresis indicated CSWS. Treatment with fludrocortisone were initiated; then, her electrolyte level gradually normalized. CSWS is self-limiting and generally resolves within 2 weeks. However, the patient in this study still required treatment with vasopressin and fludrocortisone at 16-months after surgery. Hyponatremia in a patient with CDI may be erroneously interpreted as inadequate CDI control or syndrome of inappropriate antidiuretic hormone secretion, leading to inappropriate treatment. The identification of the potential combination of CDI and CSWS is important for early diagnosis and treatment.

Disorders of tonicity, hyponatraemia and hypernatraemia, are common in neurosurgical patients. Tonicity is sensed by the circumventricular organs while the volume state is sensed by the kidney and peripheral baroreceptors; these two signals are integrated in the hypothalamus. Volume is maintained through the renin-angiotensin-aldosterone axis, while tonicity is defended by arginine vasopressin (antidiuretic hormone) and the thirst response. Edelman found that plasma sodium is dependent on the exchangeable sodium, potassium and free-water in the body. Thus, changes in tonicity must be due to disproportionate flux of these species in and out of the body. Sodium concentration may be measured by flame photometry and indirect, or direct, ion-sensitive electrodes. Only the latter method is not affected by changes in plasma composition. Classification of hyponatraemia by the volume state is imprecise. We compare the tonicity of the urine, given by the sodium potassium sum, to that of the plasma to determine the renal response to the dysnatraemia. We may then assess the activity of the renin-angiotensin-aldosterone axis using urinary sodium and fractional excretion of sodium, urate or urea. Together, with clinical context, these help us determine the aetiology of the dysnatraemia. Symptomatic individuals and those with intracranial catastrophes require prompt treatment and vigilant monitoring. Otherwise, in the absence of hypovolaemia, free-water restriction and correction of any reversible causes should be the mainstay of treatment for hyponatraemia. Hypernatraemia should be corrected with free-water, and concurrent disorders of volume should be addressed. Monitoring for overcorrection of hyponatraemia is necessary to avoid osmotic demyelination. [ABSTRACT FROM AUTHOR]

Background: Cerebral salt wasting (CSW) is a complication in patients with aneurysmal subarachnoid hemorrhage (aSAH) and other neurological conditions. It results in hyponatremia and hypovolemia due to unregulated natriuresis and loss of extracellular fluid volume. A lesser recognized mechanism of dysregulation of volume and sodium in aSAH patients is due to varying levels of antidiuretic hormone (ADH) following the injury to the anterior communicating artery and/or internal carotid arteries. Dysregulation of ADH can make the degree of sodium and volume changes even more difficult to treat in aSAH patients with CSW. Case description: A 55-year-old presented to an emergency department with headache and nausea for 5 days. She was found to have aSAH due to a ruptured anterior communicating artery aneurysm (ACOM). Hospital course was complicated by refractory polyuria from CSW and likely dysregulation of ADH secretion managed with intravenous 1-deamino-8-D-arginine vasopressin (DDAVP) concordantly with hypertonic saline. This combination maintained euvolemia and her serum sodium level. Follow up imaging showed pituitary stalk hyperintensity in the magnetic resonance imaging secondary to ischemic insult. Conclusion: Transient ADH deficiency may occur in patients with aSAH from ruptured ACOM aneurysm. ADH deficiency if coexistent with CSW, can result in hyponatremia and refractory polyuria. It is possibly due to vasospasm of anteromedial central and hypophyseal arteries or hypothalamic ischemia. DDAVP in combination with hypertonic saline can be safely used to treat polyuria in this setting.

Background: Craniopharyngioma (CP), despite being a malformational tumor of low histological grade, causes considerable morbidity and mortality mostly due to hypothalamo-pituitary dysfunction that is created by tumor itself or its treatment. Summary: Fluid-electrolyte disturbances which range from dehydration to fluid overload and from hypernatremia to hyponatremia are frequently encountered during the acute postoperative period and should be carefully managed to avoid permanent neurological sequelae. Hypopituitarism, increased cardiovascular risk, hypothalamic damage, hypothalamic obesity, visual and neurological deficits, and impaired bone health and cognitive function are the morbidities affecting the well-being of these patients in the long term. Key Messages: Timely and optimal treatment of early postoperative and long-term complications of CP is crucial for preserving quality of life of these patients. [ABSTRACT FROM AUTHOR]

Cerebral salt wasting (CSW) is an important cause of hyponatraemia in the background of a central nervous system disease. It causes hypovolaemic hyponatraemia and is associated with polyuria and high urine sodium levels. It is important to distinguish it from the more common syndrome of inappropriate antidiuretic hormone and this is primarily based on the volume status. Although CSW has been known to present with confusion, stupor, abnormal behaviour and seizures, its association with catatonia is yet to be reported. We report a case in which the patient developed CSW and hyponatraemia as a sequela of tuberculous meningitis and presented with catatonia. Prompt correction of hyponatraemia resulted in complete reversal of catatonia. This highlights the importance of evaluating all patients with catatonia for electrolyte abnormalities, especially hyponatraemia as its correction leads to excellent outcomes. [ABSTRACT FROM AUTHOR]

Background: Disorders of water and sodium balance can occur after brain injury. Prolonged polyuria resulting from central diabetes insipidus and cerebral salt wasting complicated by gradient washout and a type of secondary nephrogenic diabetes insipidus, however, has not been described previously, to the best of our knowledge. We report an unusual case of an infant with glioblastoma who, after tumor resection, was treated for concurrent central diabetes insipidus and cerebral salt wasting complicated by secondary nephrogenic diabetes insipidus.Case Presentation: A 5-month-old Hispanic girl was found to have a large, hemorrhagic, suprasellar glioblastoma causing obstructive hydrocephalus. Prior to mass resection, she developed central diabetes insipidus. Postoperatively, she continued to have central diabetes insipidus and concurrent cerebral salt wasting soon after. She was managed with a vasopressin infusion, sodium supplementation, fludrocortisone, and urine output replacements. Despite resolution of her other major medical issues, she remained in the pediatric intensive care unit for continual and aggressive management of water and sodium derangements. Starting on postoperative day 18, her polyuria began increasing dramatically and did not abate with increasing vasopressin. Nephrology was consulted. Her blood urea nitrogen was undetectable during this time, and it was thought that she may have developed a depletion of inner medullary urea and osmotic gradient: a "gradient washout." Supplemental dietary protein was added to her enteral nutrition, and her fluid intake was decreased. Within 4 days, her blood urea nitrogen increased, and her vasopressin and fluid replacement requirements significantly decreased. She was transitioned soon thereafter to subcutaneous desmopressin and transferred out of the pediatric intensive care unit.Conclusions: Gradient washout has not been widely reported in humans, although it has been observed in the mammalian kidneys after prolonged polyuria. Although not a problem with aquaporin protein expression or production, gradient washout causes a different type of secondary nephrogenic diabetes insipidus because the absence of a medullary gradient impairs water reabsorption. We report a case of an infant who developed complex water and sodium imbalances after brain injury. Prolonged polyuria resulting from both water and solute diuresis with low enteral protein intake was thought to cause a urea gradient washout and secondary nephrogenic diabetes insipidus. The restriction of fluid replacements and supplementation of enteral protein appeared adequate to restore the renal osmotic gradient and efficacy of vasopressin. [ABSTRACT FROM AUTHOR]

Background: Delayed hyponatremia is a serious complication seen after pituitary surgery. We document the incidence, presentation, outcome and risk factors for this condition.Materials and Methods: This was a retrospective study involving 222 patients operated for nonfunctioning pituitary macroadenomas between 2007-2016. Delayed hyponatremia was defined as serum sodium <135 mmol/L, occurring after the third post-operative day. Hyponatremia was categorized as mild (134-130 mmol/L), moderate (129-125 mmol/L) and severe (<125 mmol/L). All patients received intravenous (0.9%) saline, intravenous hydrocortisone and 12g oral salt over 24 hours. Patients with severe hyponatremia were given 3% saline.Results: Fifty eight patients (26%) developed delayed hyponatremia; thirty (13.5%) had severe hyponatremia. Delayed hyponatremia usually (43.1%) occurred on the seventh post-operative day (range, 3-15 days). Most patients (81%) remained asymptomatic; 11 patients developed vomiting (5), seizures (3), lethargy (1), fever (1) and paralytic ileus (1). One patient developed status epilepticus. Patients who manifest symptoms had lower sodium levels as compared to those who did not have symptoms (mean 117.7 mmol/L vs. 123 mmol/L; P < 0.01). Male gender (P = 0.002) and intra-operative CSF leak (P = 0.003) were risk factors for developing delayed hyponatremia. Other factors like, age, pre-operative cortisol levels, extent of resection and post-operative diabetes insipidus did not correlate with the occurrence of delayed hyponatremia. Patients who maintained their mean serum sodium levels >138 mmol/L (day 1-day 3) were unlikely to develop delayed hyponatremia (sensitivity, 55.2% and specificity, 83.9%), positive predictive value, 63.2% [confidence interval (CI) 48, 76.7%] and negative predictive value, 78.8% (CI 70.6, 85.5%). In most patients (57%) hyponatremia was corrected within 48 hours (h).Conclusions: We recommend routine serum sodium testing on the seventh post-operative day for all patients undergoing pituitary surgery. Most patients remain asymptomatic and unless they are detected early they can go on to develop serious complications. [ABSTRACT FROM AUTHOR]

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Guillain-Barre syndrome (GBS) is the commonest cause of acute polyradiculoneuropathy that requires hospitalization. Many of these patients experience systemic and disease-related complications during its course. Notable among them is hyponatremia. Though recognized for decades, the precise incidence, prevalence, and mechanism of hyponatremia in GBS are not well known. Hyponatremia in GBS patients is associated with more severe in-hospital disease course, prolonged hospitalization, higher mortality, increased costs, and a greater number of other complications in the hospital and worse functional status at 6 months and at 1 year. Though there are several reports of low sodium associated with GBS, many have not included the exact temporal relationship of sodium or its serial values during GBS thereby underestimating the exact incidence, prevalence, and magnitude of the problem. Early detection, close monitoring, and better understanding of the pathophysiology of hyponatremia have therapeutic implications. We review the complexities of the relationship between hyponatremia and GBS with regard to its pathophysiology and treatment.

The subject of hyponatremia is undergoing significant changes after developing a more pathophysiologic approach that is superior to the ineffective volume approach and can more effectively identify the different causes of hyponatremia. This new approach identified cerebral salt wasting (CSW) in 24 (38%) of 62 hyponatremic patients from the medical wards of the hospital with 21 showing no evidence of cerebral disease to support our proposal to change CSW to renal salt wasting (RSW). RSW had to be differentiated from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) because of diametrically opposite therapeutic goals of water-restricting water-logged patients with SIADH or administering salt water to volume-depleted patients with RSW. Both syndromes present with identical clinical parameters that require a difficult protocol to make such a differentiation possible. We describe rat clearance studies demonstrating natriuretic activity in the plasma of patients with neurosurgical and Alzheimer diseases (AD) and eventually identify the protein as haptoglobin-related protein without signal peptide, which can serve as a biomarker to simplify diagnosis of RSW and delivery of the proper management to improve clinical outcomes. We also discuss the introduction of a new syndrome of RSW in AD and its implications. The high prevalence of RSW and identification of the natriuretic factor have created debates over the existence of RSW with none questioning or addressing the pathophysiologic data that identified patients with RSW. We also discuss the potentially large group of patients with RSW who are normonatremic.

Purpose: To evaluate the frequency and causes of hyponatremia in acute encephalitis syndrome (AES) and its effect on outcome. Patients and Methods: Consecutive patients with AES were subjected to neurological evaluation including Glasgow Coma Scale, focal weakness, movement disorder, and reflex changes. The etiology of AES was based on blood and cerebrospinal fluid enzyme-linked immunosorbent assay and polymerase chain reaction. We have categorized patients into neurological or systemic AES. Hyponatremia was diagnosed if 2 consecutive serum sodium levels were below 135 mEq/L, 24 hours apart. Serum and urinary osmolality and electrolytes were measured on alternate days. Fluid intake, output, and body weight were measured daily. The hyponatremia was categorized into syndrome of inappropriate secretion of antidiuretic hormone (SIADH), cerebral salt wasting (CSW), or miscellaneous group. Outcome at 1 month was assessed by modified Rankin scale. Results: Of 79 patients, 34 had neurologic AES and 45 had systemic AES; 22 (27.8%) patients had hyponatremia. The neurologic AES as compared to systemic AES was more commonly associated with hyponatremia (38.2% vs 20%, P = .07), need longer hospitalization (25.0 vs 12.5 days, P = .003), and longer time for sodium correction (13.3 vs 8.2 days, P = .05). The hyponatremia was due to CSW in 12 patients, SIADH in 2 patients, and indeterminate in 8 patients. Thirty-six patients had poor outcome (15 died) and 43 had good outcome which was not related to hyponatremia. Conclusion: Hyponatremia occurs in one-third of patients with AES, being commoner in neurologic AES, and CSW is the commonest cause. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is on the rise, especially in today’s fast-paced world. TBI requires not only neurosurgical expertise but also neurointensivist involvement for a better outcome. Disturbances of sodium balance are common in patients with brain injury, as the central nervous system plays a major role in sodium regulation. Hyponatraemia, defined as serum sodium

Objective: The study aimed to evaluate the frequency, severity, and causes of hyponatremia in stroke and its influence on outcome.Materials and Methods: Consecutive computed tomography- or magnetic resonance imaging-proven stroke patients within 7 days of stroke were included. Severity of stroke was assessed using the National Institute of Health Stroke Scale and consciousness using the Glasgow Coma Scale. Hyponatremia was defined if 2 consecutive serum sodium levels were <135 mEq/L and hypernatremia if >145 mEq/L. Causes of hyponatremia, such as cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH), were based on predefined criteria. Patients with CSW were managed by salt supplementation and normal saline, and fludrocortisone was used in refractory cases. In SIADH, fluid was restricted. Outcome on discharge was defined using the modified Rankin Scale (mRS).Results: One hundred patients with stroke were included: 47% had ischemic stroke and 53% had intracerebral hemorrhage. Forty-three percent of the patients had hyponatremia, 6% had hypernatremia, and 4% had both. Hyponatremia was due to CSW in 19 (44.2%), SIADH in 3 (7%), miscellaneous causes in 14 (32.6%), and indeterminate in 7 (16.3%) patients. Duration of hospitalization was the independent predictor of hyponatremia and CSW. Fourteen patients died, whereas 15 had good outcome (mRS score of ≤2) and 71 had poor outcome (mRS score of 3-5). Hypernatremia was associated with high mortality compared with eunatremia and hyponatremia.Conclusion: Hyponatremia occurred in 43% of stroke patients. CSW was the most common cause of hyponatremia. Hyponatremia, however, was not related to death or disability. [ABSTRACT FROM AUTHOR]

Many systemic complications follow aneurysmal subarachnoid hemorrhage and are primarily due to sympathetic nervous system activation. These complications play an important role in the overall outcome of patients. The purpose of this review is to provide an update on the diagnosis, pathophysiology, and management of systemic complications specifically associated with aneurysmal subarachnoid hemorrhage. Special focus has been made on systemic complications that occur more frequently in patients with aneurysmal subarachnoid hemorrhage compared to other stroke subtypes and in the neurocritical care patient population. These complications include neurogenic pulmonary edema, electrocardiographic changes, troponin elevation, neurogenic stunned myocardium, hyponatremia, and anemia. [ABSTRACT FROM AUTHOR]

Hyponatremia occurs in about 30% of hospitalized patients and syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common cause of hyponatremia. SIADH should be differentiated from other causes of hyponatremia like diuretic therapy, hypothyroidism and hypocortisolism. Where possible, all attempts should be made to identify and rectify the cause of SIADH. The main problem in SIADH is fluid excess, and hyponatremia is dilutional in nature. Fluid restriction is the main stay in the treatment of SIADH; however, cerebral salt wasting should be excluded in the clinical setting of brain surgeries, subarachnoid hemorrhage, etc. Fluid restriction in cerebral salt wasting can be hazardous. Sodium correction in chronic hyponatremia (onset >48 hours) should be done slowly to avoid deleterious effects in brain.