CORRELATES OF BRAIN EDEMA IN UNCONTROLLED IDDM

被引:95
作者
DURR, JA
HOFFMAN, WH
SKLAR, AH
ELGAMMAL, T
STEINHART, CM
机构
[1] MED COLL GEORGIA,DEPT PEDIAT,PEDIAT ENDOCRINOL SECT,AUGUSTA,GA 30912
[2] UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262
[3] MED COLL GEORGIA,DEPT MED,AUGUSTA,GA 30912
关键词
D O I
10.2337/diabetes.41.5.627
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Blood glucose, plasma sodium, bicarbonate (HCO3-) vasopressin, and hematocrit were monitored before and during treatment in patients with uncontrolled insulin-dependent diabetes mellitus (IDDM). These parameters were correlated with simultaneous serial cranial computed tomography readings of brain edema. Six of seven patients had positive computed tomography readings for brain edema on admission. Initial brain edema correlated directly with blood glucose (r = 0.79, P = 0.033) and inversely with HCO3-(r = -0.76, P = 0.047). At 6 h, brain edema still correlated with acidosis (HCO3-; r = -0.79, P = 0.033) but no longer with blood glucose. At that time, however, brain edema correlated with the rate of change in blood glucose (r = 0.915, P = 0.005). Results of interactive stepwise regression analysis suggest that the change in the calculated effective plasma osmolality plays a predominant role in the progression of brain edema during therapy (r = 0.995, P < 0.001). Thus, although hyperglycemia and acidosis probably predispose to diabetic brain edema, osmotic factors may be major predictors of its evolution. No relationships were detected between brain edema and initiation of insulin therapy, plasma vasopressin, or changes in hematocrit. The factors responsible for initial brain edema and its progression, statistically identified in this study, require reassessment of common theories that attribute brain edema exclusively to therapy.
引用
收藏
页码:627 / 632
页数:6
相关论文
共 43 条
[31]   RECEPTOR-MEDIATED PEPTIDE-TRANSPORT THROUGH THE BLOOD-BRAIN-BARRIER [J].
PARDRIDGE, WM .
ENDOCRINE REVIEWS, 1986, 7 (03) :314-330
[32]   HYPERGLYCEMIA, POLYOL ACCUMULATION, AND INCREASED INTRACRANIAL PRESSURE [J].
PROCKOP, LD .
ARCHIVES OF NEUROLOGY, 1971, 25 (02) :126-+
[33]   OSMOTIC OPENING OF BLOOD-BRAIN BARRIER IN MONKEY WITHOUT ASSOCIATED NEUROLOGICAL DEFICITS [J].
RAPOPORT, SI ;
THOMPSON, HK .
SCIENCE, 1973, 180 (4089) :971-971
[34]  
ROSENBLOOM AL, 1990, J PEDIATR-US, V117, P1009, DOI 10.1016/S0022-3476(05)80167-2
[35]   INTRACEREBRAL CRISES DURING TREATMENT OF DIABETIC-KETOACIDOSIS [J].
ROSENBLOOM, AL .
DIABETES CARE, 1990, 13 (01) :22-33
[37]  
VANDERMEULEN JA, 1987, LANCET, V2, P306
[38]   INCREASED INTRACRANIAL-PRESSURE IN GALACTOSEMIA - CONSIDER THIS DIAGNOSIS WITH A BULGING FONTANEL, HEPATOMEGALY, AND FAILURE TO THRIVE [J].
VOGEL, R ;
GAIFMAN, M ;
NITZAN, M .
CLINICAL PEDIATRICS, 1976, 15 (04) :386-388
[39]   CEREBRAL EDEMA IN DIABETIC-KETOACIDOSIS [J].
WINEGRAD, AI ;
KERN, EFO ;
SIMMONS, DA .
NEW ENGLAND JOURNAL OF MEDICINE, 1985, 312 (18) :1184-1185
[40]   PLASMA VASOPRESSIN IN UNCONTROLLED DIABETES-MELLITUS [J].
ZERBE, RL ;
VINICOR, F ;
ROBERTSON, GL .
DIABETES, 1979, 28 (05) :503-508