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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyponatremia played an essential role in this case, determining the rapid transition from consciousness to a state of coma in female patient who had just come through the critical phase of intensive care. This circumstance underlines the importance of a correct water balance in patients undergoing neurosurgery, as well as a knowledge of the inappropriate antidiuretic hormone secretion (SIADH) syndrome responsible, either alone or in association, for the genesis of severe hyponatremia. In the differential diagnosis of hyponatremia, it is important to recall the role of an often mistaken syndrome (cerebral salt wasting syndrome) characterized by the secretion of a natriuretic factor that has still not been clearly identified.
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PMID:[Hyponatremia in neurosurgical patients]. 1063 54

Hyponatremia is a frequent event in neurosurgery practice and is usually associated with subarachnoid hemorrhage, head trauma, infections and neoplasms. The two common clinical manifestations are the inappropriate secretion of antidiuretic hormone (SIADH) and the cerebral salt wasting syndrome (CSWS), which were usually attributed to each other due to identical clinical presentation. In contrast to the better-recognized SIADH, there has not been a uniform consensus over the humoral and neural mechanisms of CSWS and functional aspects of renal response. In this article, we report on 2 cases of a primitive neuroectodermal tumor with prolonged CSWS manifested during the intraventricular dissemination of primary disease and the high catabolic stage.
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PMID:Prolonged cerebral salt wasting syndrome associated with the intraventricular dissemination of brain tumors. Report of two cases and review of the literature. 1102 17

Several authors described elevated natriuretic peptides, atrial natriuretic peptide(ANP) and brain natriuretic peptide (BNP), in patients with subarachnoid hemorrhage(SAH), which were account for inappropriate antidiuretic hormone(SIADH) or cerebral salt wasting syndrome(CSW). Although the secretion of natriuretic peptide depends on the total blood volume, central venous pressure, and cardiac output volume, the volume of fluid intake in patients with SAH had not been taken in consideration in previous report. We here examined the relationship between fluid intake and the natriuretic peptides in two cases without cardiac failure. ANP elevated 2 or 3 days after SAH and remained in normal range for 2 weeks. BNP elevated when the volume of fluid intake was increased, and BNP did not elevate during the periods with lower fluid intake. Several authors proposed the possibility of iatrogenic factor in natriuresis after SAH and these results supported this opinion.
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PMID:[Relationship between cardiac natriuretic peptide (ANP/BNP) and fluid intake in patients with subarachnoid hemorrhage]. 1121 65

Hyponatraemia in patients with an acute central nervous system disease can be caused by two different mechanisms: (1) retention [corrected] of free water, i.e. the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and (2) excessive sodium retention [corrected], i.e., the cerebral salt wasting syndrome (CSW). Although the concept of CSW is well known in adult medicine, it is still not established in child neurology. We conducted a retrospective analysis of electrolyte disturbances in 195 children with various acute CNS diseases. In 20 children (10.3%) hyponatraemia with plasma sodium below 130 mmol/l was identified. On the basis of clinical and laboratory data 7 of these 20 children were diagnosed as having SIADH, and the other 9 children, as having CSW. Our data suggest that hyponatraemia attributable to CSW is at least as frequent in children as SIADH. Because of their different pathophysiological mechanisms, which require diametrically opposed therapeutic regimens, early differential diagnosis is mandatory if the correct treatment is to be given.
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PMID:Hyponatraemia in children with acute CNS disease: SIADH or cerebral salt wasting? 1121 25

Hyponatremia is a common electrolyte disorder related to central nervous system diseases and is often attributed to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and on the other hand to the cerebral salt wasting syndrome (CSWS). This syndrome is characterized by hyponatremia due to excessive renal sodium excretion resulting from a centrally mediated process. Given the divergent nature of the treatment it is of paramount importance for a clinician to be able to recognize and differentiate between these two entities. Thus the monitoring of renal function tests, which are needed for earlier diagnosis of effective osmolality disorders, is important to do in intensive care units, which are caring for patients with central nervous system lesons. Two patients successfully treated for CSW due to ischemic stroke caused by arterial embolism from heart cavities are described.
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PMID:[Central salt-wasting diuresis syndrome as a cause of hyponatremia in patients at the internal medicine department]. 1150 21

Hyponatremia after cranial vault remodeling has been noted in a pediatric patient population. If left untreated, the patients may develop a clinical hypoosmotic condition that can lead to cerebral edema, increased intracranial pressure, and eventually, to central nervous system and circulatory compromise. The hyponatremia has traditionally been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH); however, in our patients the treatment has been resuscitation with normal saline as opposed to fluid restriction (the accepted treatment of SIADH), thus placing the diagnosis of SIADH in question. Patients who developed hyponatremia after intracranial injury or surgery were, until recently, grouped together as having SIADH. However, there are diagnosis and treatment differences between SIADH and another distinct but poorly understood disorder that is designated cerebral salt wasting syndrome (CSW). CSW is associated with increased urine output and increased urine sodium concentration and volume contraction, and it is frequently seen after a central nervous system trauma. We therefore developed a prospective study to evaluate the cause of the sodium imbalance.Ten consecutive pediatric patients who underwent intracranial surgery for various craniosynostotic disorders were postoperatively monitored in the pediatric intensive care unit for hemodynamic, respiratory, and fluid management. The first four patients were evaluated for electrolyte changes and overall fluid balance to determine the consistency with which these changes occurred. The remaining six patients had daily (including preoperative) measurement of serum electrolytes, urine electrolytes, urine osmolarity, serum antidiuretic hormone (ADH), aldosterone, and atrial natriuretic hormone (ANH). All patients received normal saline intravenous replacement fluid in the postoperative period. All of the patients developed a transient hyponatremia postoperatively, despite normal saline resuscitation. Serum sodium levels as low as 128 to 133 mEq per liter (normal, 137 to 145 mEq per liter) were documented in the patients. All patients had increased urine outputs through the fourth postoperative day (>1 cc/kg/h). The six patients who were measured had an increased ANH level, with a peak value as high as 277 pg/ml (normal, 25 to 77 pg/ml). ADH levels were low or normal in all but one patient, who had a marked increase in ADH and ANH. Aldosterone levels were variable. On the basis of these results, all but one patient showed evidence of CSW characterized by increased urine output, normal or increased urine sodium, low serum sodium, and increased ANH levels. The other patient had similar clinical findings consistent with CSW but also had an increase in ADH, thus giving a mixed laboratory picture of SIADH and CSW. The association of CSW to cranial vault remodeling has previously been ignored. This study should prompt reevaluation of the broad grouping of SIADH as the cause of all hyponatremic episodes in our postoperative patient population. An etiologic role has been given to ANH and to other, as yet undiscovered, central nervous system natriuretic factors. All of the patients studied required normal saline resuscitation, a treatment approach that is contrary to the usual management of SIADH. These findings should dictate a change in the postoperative care for these patients. After cranial vault remodeling, patients should prophylactically receive normal saline, rather than a more hypotonic solution, to avoid sodium balance problems.
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PMID:Hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder. 1171 18

Peters made the original description of the cerebral salt wasting syndrome (CSWS) in 1950 in three patients with hyponatremia that he assumed to be secondary to natriuresis of cerebral mechanism. Few years later, Schwartz describe the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in two patients with bronchial carcinoma, with characteristics similar to CSWS. Wijdicks gave clinical entity to CSWS when referring that it is the prevalent cause of hyponatremia in patients with subarachnoid hemorrhage, and stressed the risk of secondary cerebral infarction if restrictive plans of water and salt were used as a consequence of a miss diagnosis. However, CSWS has been recently questioned because of its atypical characteristics, not shared by other saline wasting syndromes. The volume status of patients with hyponatremia and natriuresis determines whether the cause of this disorder is SIADH or CSWS. Nevertheless the evidence are contradictory, the vasopressin level can be recognized only in relation to the tonicity of body fluids, and the natriuresis is a common final pathway for both syndromes. In this literature review, some issues of CSWS that are associated or opposed with SIADH and other saline wasting syndrome are discussed. We conclude that the reports that sustain CSWS are insufficient in their methodology and interpretation of the results. The absence of strict metabolic studies has been negatively replaced by the original information casually quoted, and the strength of tradition. Thereafter, the paradigm generates unfounded ethical dilemmas which render difficult any further investigations with appropriate controls.
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PMID:[Cerebral salt wasting. Half a century of a largely undefined syndrome]. 1180 34

The association between hyponatremia and intracranial pathology has been well described. When accompanied by natriuresis, hyponatremia has most commonly been attributed to inappropriate secretion of antidiuretic hormone. However, there is growing evidence to suggest that many of these patients may actually have cerebral mediated salt losses, a disorder referred to as the cerebral salt wasting syndrome (CSWS). While this syndrome has been reasonably well described in adults, data regarding CSWS in pediatric-aged patients remains sparse. Since fluid management of these disorders is different, it is important that the clinician be able to rapidly differentiate between them. We report three cases of CSWS in acutely brain-injured children and comment on the role that early quantitation of urine volume and urine sodium concentration had in rapidly establishing the correct diagnosis.
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PMID:Cerebral salt wasting syndrome following brain injury in three pediatric patients: suggestions for rapid diagnosis and therapy. 1189 88

Hyponatremia after chemotherapy is not an uncommon clinical syndrome. Both renal salt-wasting syndrome (RSWS) and syndrome of inappropriate antidiuretic hormone secretion (SIADH) have been reported as the underlying mechanisms for chemotherapy-induced hyponatremia. However, these two clinical syndromes have distinct clinical characteristics and managements. The key differential diagnostic feature for RSWS is the excessive urinary excretion of sodium, whereas the urinary excretion of sodium in SIADH is normal or decreased. The treatment for RSWS is supplement of salt, which is opposite to the treatment of SIADH. We report a case of a patient with hyponatremia and excessive urinary excretion of sodium after cisplatin-based chemotherapy. RSWS was diagnosed and the patient was treated with a sodium supplement. We also summarize the key diagnostic features and the most common differential diagnoses for hyponatremia syndrome.
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PMID:Renal salt-wasting syndrome in a patient with cisplatin-induced hyponatremia: case report. 1215 62

We report the case of a 56-year-old man with a frontal meningioma who underwent scheduled surgery under balanced general anesthesia without complications and was then transferred to the intensive care postoperative recovery unit for observation. On the day of admission he developed polyuria and a decrease in central venous pressure. Plasma sodium and osmolarity were in the normal ranges but urine analysis showed hyponatremia and hypo-osmolarity, suggesting cerebral salt wasting syndrome. Physiological saline solution was infused to maintain osmolarity and plasma concentrations of sodium within normal ranges. Diuresis peaked on the sixth day after surgery at 17,600 mL in 24 hours and decreased gradually to normal on the eleventh day after admission. Elevated plasma concentrations of atrial natriuretic peptides confirmed the diagnosis. Correct management is essential when neurosurgery patients develop altered plasma and urinary sodium concentrations and osmolarity. Differential diagnosis involves considering diabetes insipidus, inappropriate secretion of antidiuretic hormone and salt wasting syndrome. Transfer to an intensive care postoperative recovery unit and early treatment are important for lowering the risk of complications and death.
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PMID:[Polyuria as postoperative complication of frontal meningioma]. 1270 Dec 63


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