Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 12-year-old boy with tuberculous meningitis and hydrocephalous, after undergoing revision of ventriculo-peritoneal shunt had persistent impairment of sensorium and episodes of hyponatremia (serum sodium 104 to 125 mmol/l), accompanied by polyuria, signs of poor peripheral, perfusion hypotension and low CVP, and high urinary sodium excretion (114-60 mmol/l). A diagnosis of cerebral salt wasting syndrome (CSWS) was made and was treated with saline replacement and fludrocortisone (10 microg/kg/day). Within next 3 days the sensorium, signs of shock, urine output and serum and urinary sodium returned to normal. The case illustrates that life-threatening hyponatremia in a child with neurological illness could be caused by CSWS, which must be differentiated from Syndrome of inappropriate antidiuretic hormone secretion (SIADH), as CSWS requires rigorous salt and volume replacement in contrast to fluid restriction in SIADH.
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PMID:Hyponatraemia and hypovolemic shock with tuberculous meningitis. 1471 91

Hyponatremia is a frequent occurrence after pituitary surgery, having been described in 9% to 35% of the patients. It is produced by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or, more frequently, by the cerebral salt-wasting syndrome (CSWS). The clinical presentation of both syndromes is identical and the differential diagnosis can be difficult. The determination of the volemic state is essential for the diagnosis, since the patients with the SIADH are euvolemic or hypervolemic, while those with CSWS are hypovolemic. Several methods can be used to detect the volemic state in these patients and, among them, the furosemide test can best discriminate between SIADH and CSWS. A furosemide infusion (20 mg) normalizes sodium serum levels in SIADH patients, but not in CSWS patients who remain hyponatremic. The differentiation between the 2 syndromes is clinically relevant since their treatment is antithetical. SIADH patients need liquid restriction of liquids and/or furosemide to reduce the volume of extracellular water, while CSWS patients need volume replacement with sodium supplementation (or fludrocortisone can be a good alternative). The diagnosis and treatment of these syndromes are discussed on the basis of the literature reports.
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PMID:Differential diagnosis and treatment of hyponatremia following pituitary surgery. 1525 60

Virtually all hospitalized pediatric patients require some form of intravenous fluid administration. The foundation of current pediatric fluid therapy practice was formulated in the 1950s when pediatricians were dealing with relatively simple dehydration and normal homeostasis could largely be assumed. Recent advances in pediatric medicine have resulted in increased severity of illness and normal physiology can no longer be assumed. The traditional approach to pediatric fluid therapy has been recently challenged by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), cerebral salt wasting syndrome (CSWS), diabetic ketoacidosis (DKA) and hyponatremia caused by the inappropriate use of hypotonic solutions, all of which involve unusual sodium and serum osmolarity dynamics causing life threatening central nervous system (CNS) pathophysiology. In this review, we give an overview of the recent understanding of pediatric fluid therapy. The widespread use of acetate in place of lactate as a bicarbonate precursor and the expanding role of nonalbumin plasma expanders in pediatrics are also discussed as they will play a clinical role in the near future.
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PMID:Recent trends in pediatric fluid therapy. 1531 7

Cerebral salt wasting syndrome (CSWS) is a syndrome of hyponatremia and natriuresis described in patients with intracranial diseases. We describe a 3-year-old boy with tuberculous meningitis complicated by hydrocephalus and CSWS and emphasize the different clinical presentation and management of patients with CSWS and the syndrome of inappropriate secretion of antidiuretic hormone.
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PMID:Tuberculous meningitis complicated with hydrocephalus and cerebral salt wasting syndrome in a three-year-old boy. 1536 36

Hyponatremia and increased urine output after calvarial remodeling have been noted in pediatric patients with craniosynostosis. If not treated properly, patients develop hypoosmotic conditions that can lead to cerebral edema, increased intracranial pressure, and collapsed circulation. Postoperative hyponatremia after central nervous system surgery is considered as the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Recently, however, cerebral salt wasting syndrome (CSWS) instead of SIADH has been reported frequently. CSWS is associated with a decreased serum sodium level, increased urinary sodium level, increased urine output, decreased ECF volume, increased atrial natriuretic peptide (ANP) level, and increased brain natriuretic peptide (BNP) level. We experienced nine patients with craniosynostosis who underwent calvarial remodeling. By postoperative day 1, the ANP and BNP levels increased by 3-6 folds compared with the preoperative levels. They returned to the normal levels by postoperative day 5. The ADH level was within the normal range even after operation. The urinary sodium level increased in all patients by postoperative day 1 and 3. But the serum sodium level, and serum and urine osmolarity were normal due to appropriate replacement of sodium and fluid. After calvarial remodeling, the potential development of CSWS should be considered and distinguished from SIADH. The patients with CSWS require normal saline resuscitation and should prophylactically receive normal saline.
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PMID:Cerebral salt wasting syndrome after calvarial remodeling in craniosynostosis. 1622 64

Disorders of sodium and water balance are common in critically ill adult neurologic patients. Normal aspects of sodium and water regulation are reviewed. The etiology of possible causes of sodium disturbance is discussed in both the general inpatient and the neurologic populations. Areas of importance are highlighted with regard to the differential diagnosis of sodium disturbance in neurologic patients, and management strategies are discussed. Specific discussions of the etiology, diagnosis, and management of cerebral salt wasting syndrome, the syndrome of inappropriate antidiuretic hormone secretion, and central diabetes insipidus are presented, as well as the problems of overtreatment. The importance of diagnosis at an early stage of these diseases is stressed, with a recommendation for conservative management of milder cases.
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PMID:Disturbances of sodium in critically ill adult neurologic patients: a clinical review. 1636 41

A case of hyponatraemia associated with subarachnoid haemorrhage is presented. The provisional diagnosis of an inappropriate antidiuresis was made and treatment with fluid restriction was instituted. However the patient continued to deteriorate as the diuresis continued and the hyponatraemia worsened, resulting in hypovolaema. The salt wasting syndrome was subsequently diagnosed and saline and fludrocortisone (0.2 mg/day) was initiated, reducing the renal salt loss, increasing the plasma sodium and improving the neurological status of the patient. Cerebral salt wasting syndrome is an important and under-recognised cause of hyponatraemia in neurosurgical patients, particularly in patients with subarachnoid hemorrhage. It is essential to differentiate it from the syndrome of inappropriate antidiuretic hormone secretion to avoid complications of hypovolaemia and reduced cerebral perfusion as illustrated by this case. Brain natriuretic peptide may be responsible for this syndrome although this requires further investigation.
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PMID:Cerebral salt wasting syndrome: a case report. 1660 1

A 53-year-old male was admitted to our hospital for a high fever. He suffered a change in personality, memory loss and disorientation as well. The findings of cerebrospinal fluid showed monocytosis, but the titers of glucose, C1 and ADA were all normal. Although there was no bacterium in the CSF, the patient's electroencephalography finding was abnormal. We diagnosed his condition as viral meningoencephalitis and started treatment with antiviral agents. Blood chemistry showed serum sodium of 130 mEq/l and plasma osmolarity was reduced to 272 mOsm/kg, while urine osmolarity was high at 353 mOsm/kg. Two potential causes of hyponatremia in this patient were the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting syndrome (CSWS). Physical findings revealed a contracted extracellular fluid volume, strongly suggesting the presence of CSWS. The massive urine sodium loss overcoming sodium intake supported this diagnosis. After treatment with vigorous sodium and volume replacement for over 4 weeks, hyponatremia as well as meningoencephalitis were improved without any complication. To the best of our knowledge, this is the first report on CSWS in a patient with viral meningoencephalitis.
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PMID:[Cerebral salt wasting syndrome in a patient with viral meningoencephalitis]. 1712 84

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.
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PMID:[Case of cerebral salt wasting syndrome with difficulty in controling excessive urine volume]. 1736 22

Hyponatraemia is a common complication in patients undergoing neurosurgery. It can be caused either by the syndrome of inappropriate secretion of antidiuretic hormone or by the cerebral salt-wasting syndrome (CSWS). CSWS frequently occurs in patients suffering from subarachnoid haemorrhage and brain injury, but it is rare after pituitary tumour surgery. However, this diagnostic possibility should be considered as these disorders require specific treatment and have different prognoses. In this article, we present a case of acute and early hyponatraemia caused by CSWS after pituitary tumour surgery. We also revise the aetiology, mechanisms, differential diagnosis and treatment of hyponatraemia after pituitary surgery.
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PMID:Early hyponatraemia after pituitary surgery: cerebral salt-wasting syndrome. 1753 59


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