title: Clinical analysis of hyponatremia in acute craniocerebral injury.
abstract: OBJECTIVE
  To explore pathological mechanisms of central hyponatremia and its treatment.
  
  
  METHODS
  Synchronous assay was made for changes of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endogenous digitalis-like substance (EDLS), antidiuretic hormone (ADH) in blood, and Na(+) concentrations in blood and urine, and plasma- and urine-osmolality in 68 patients with acute craniocerebral injury (ACI).
  
  
  RESULTS
  Of the 68 patients with ACI, 27 were found to have hyponatremia, and such illness was mostly concentrated on severe cases.
  
  
  CONCLUSIONS
  The central hyponatremia in patients with ACI may be related to the increase in the secretion of EDLS and ADH as the result of damaged functions of the hypothalamic-hypophysial system, and it seems that the decrease in blood ANP and BNP has no direct effect on Na(+) concentrations in blood. Inappropriate secretion of antidiuretic hormone syndrome and cerebral salt-wasting syndrome are the two main reasons for hyponatremia in patients with craniocerebral injury. The pathological mechanism, diagnostic standards, as well as treatment methods for the two, however, are not just the same. Intravenous injection of extrinsic thyrotropin-releasing hormone might inhibit dilutional hyponatremia arising from the increase in ADH secretion by patients with ACI.
authors: Department of Neurosurgery, Xinhua Hospital, Jiaotong University School of Medicine, Shanghai, China.
authors: Wenchuan
authors: W
authors: Zhang
authors: Shiting
authors: S
authors: Li
authors: Massimiliano
authors: M
authors: Visocchi
authors: Xuhui
authors: X
authors: Wang
authors: Jiyao
authors: J
authors: Jiang
mesh_terms: D000293:Adolescent; D000328:Adult; D009320:Atrial Natriuretic Factor / Q000097:blood; D002298:Cardenolides / Q000097:blood / Q000378:metabolism*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D006259:Craniocerebral Trauma / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D007010:Hyponatremia / Q000209:etiology / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009481:Neurophysins / Q000097:blood / Q000378:metabolism*; D011498:Protein Precursors / Q000097:blood / Q000378:metabolism*; D012503:Saponins / Q000097:blood / Q000378:metabolism*; D014667:Vasopressins / Q000097:blood / Q000378:metabolism*; D055815:Young Adult
chemical_list: C438657:AVP protein, human; D002298:Cardenolides; D009481:Neurophysins; D011498:Protein Precursors; D012503:Saponins; C034504:digoxin-like factors; D014667:Vasopressins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor