Acute Cerebral Œdema During Treatment of Hyperglycæmia

Clements, Rex S.; Prockop, Leon D.; Winegrad, Albert I.

doi:10.1016/s0140-6736(68)90597-7

Cited by 68 publications

(31 citation statements)

References 15 publications

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“…The identity of the idiogenic solute is only speculative at the present time, although many investigators have suggested that it might consist of glucose metabolites (10)(11)(12)33). Our data does not support such a contention, since after 4 h of hyper glycemia, there was no change in the brain glucose total radioactivity (dpm per millimole glucose) ( Table IV).…”

Section: Discussionmentioning

confidence: 99%

“…The brain water content in the insulintreated animals was significantly greater than that of the peritoneal dialysis group (P < 0.05). Thus, although brain swelling may occur when plasma glucose is rapidly lowered without insulin (11,12), there is no increase in brain solute activity and the swelling is of a lesser magnitude.…”

Section: Discussionmentioning

confidence: 99%

“…If these sugar alcohols are generated in the brain during hyperglycemia and are unable to leave the central nervous system when the blood glucose is rapidly lowered, they might act as osmotically active particles, attracting water into the brain and leading to cerebral edema (11). During hyperglycemia, the concentration of sorbitol has been shown to increase in aorta (38), peripheral nerve (39,40), ocular lens (41), and in the CSF (11). When the plasma glucose in hyperglycemic dogs is rapidly lowered by intravenous infu sion of 0.9% NaCl, the CSF pressure increases concomitant with a further increase in CSF sorbitol (11).…”

Section: Discussionmentioning

confidence: 99%

“…During hyperglycemia, the concentration of sorbitol has been shown to increase in aorta (38), peripheral nerve (39,40), ocular lens (41), and in the CSF (11). When the plasma glucose in hyperglycemic dogs is rapidly lowered by intravenous infu sion of 0.9% NaCl, the CSF pressure increases concomitant with a further increase in CSF sorbitol (11). It has been sug gested that the elevated CSF sorbitol might be secondary to accumulation of osmotically significant quantities of sorbitol in brain (11,12,10).…”

Section: Discussionmentioning

confidence: 99%

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Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits

2000

Journal of the American Society of Nephrology

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with comments by ALLEN I. ARIEFF and RICHARD STERNS Reprinted from J. Clin. Invest. 52:571-583, 1973 abstract To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose = 61 mM), both brain (cerebral cortex) and muscle initially lost about 10% of water content. After 4 h of hyperglycemia, skeletal muscle water content remained low but that of brain was normal. Brain osmolality (Osm) (343 mosmol/kg H2O) was similar to that of cerebrospinal fluid (CSF) (340 mosmol/kg), but increases in the concentration of Na+, K+, Cl-, glucose, sorbitol, lactate, urea, myoinositol, and amino acids accounted for only about half of this increase. The unidentified solute was designated "idiogenic osmoles". When plasma glucose was rapidly lowered to normal with insulin, there was gross brain edema, increases in brain content of water, Na+, K+, Cl-and idiogenic osmoles, and a signifi cant osmotic gradient from brain (326 mosmol/kg H2O) to plas ma (287 mosmol/kg). By similarly lowering plasma glucose with peritoneal dialysis, increases in brain Na+, K+, C-, and water were significantly less, idiogenic osmoles were not pres ent, and brain and plasma Osm were not different. It is con cluded that during sustained hyperglycemia, the cerebral cortex adapts to extracellular hyperosmolality primarily by accumula tion of idogenic osmoles rather than loss of water or gain in solute. When plasma glucose is rapidly lowered with insulin, an osmotic gradient develops from brain to plasma. Despite the brain to plasma osmotic gradient, there is no net movement of water into brain until plasma glucose has fallen to at least 14 mM, at which time cerebral edema occurs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits

2000

Journal of the American Society of Nephrology

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“…Recent studies indicate its formation in nervous tissue [39,40], in blood vessels [41] and in the lens [42], particularly during hyperglycaemia. It may well play a pathophysiologic role in the development of diabetic neuropathy, angiopa~hy and cataract.…”

Section: Diabetotogiamentioning

confidence: 99%

Metabolism and oxidation of U-14C-glucose, xylitol, fructose and sorbitol in the fasted and in the streptozotocin-diabetic rat

Keller

Froesch

1971

Diabetologia

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Summary. 1. 24-h-fasted rats exhaled 35--37% of i.v. administered loads of labelled glucose, xylitol and fructose, and 20% of a sorbitol load as ir within a period of six hours. 2. Streptozotocin-diabetic rats exhaled under similar conditions only 11--18~ of these substrates as laCO 2. The rate of glucose oxidation was similar in both groups of animals when a correction for the different glucose pool size was applied, It is concluded that glucose oxidation to 14C0e takes place mainly in tissues which are not sensitive to insulin. 3. Urinary excretion of all substrates was 39--55% of the given dose in diabetic rats. The large difference of urinary carbon-14 between fasted and diabetic rats was due to the excretion of glucose-i~C by the diabetic rats. 4. Six hours after the administration of all four substrates, similar amounts of carbon-14 were recovered in serum, serum osazones, liver glycogen and total lipids and diaphragm glycogen within each group of animals. It is concluded that the similarities of the metabolism of all substrates is due to the rapid conversion of the substitute sugars to glucose.

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Cerebral oedema during treatment of diabetic ketoacidosis: are we any nearer finding a cause?

Edge

2000

Diabetes Metab. Res. Rev.

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Cerebral oedema remains the leading cause of death and morbidity in children with Type 1 diabetes mellitus. Around seven per thousand episodes of diabetic ketoacidosis (DKA) are complicated by cerebral oedema, and one-quarter of those children will die from it. The cause or causes of cerebral oedema are still very poorly understood, but lawyers are already keen to implicate various aspects of the management of DKA. There have been many theories as to the pathophysiology of cerebral oedema, and possible contributing factors may be excessive rate of rehydration, falling plasma osmolality (particularly that due to a reduction in plasma sodium concentration), hypoxia and insulin dosage. There is some supportive evidence for all of these factors in some cases, but there have been no sizeable case-control studies, in part because of the rarity of the condition. Furthermore, cerebral oedema can still occur even when the management of DKA follows current 'best practice' guidelines. As the mechanisms of cell volume regulation within the brain are increasingly understood, different questions may provide greater insights. For example, what is it about children that makes them so much more susceptible to cerebral oedema than adults? And why does one child treated in a certain way develop cerebral oedema whereas another does not? The anxiety over causing cerebral oedema has driven most of the changes in the management of DKA over recent decades, yet there is no evidence that the incidence has reduced. Until the causes are understood, we cannot be dogmatic about treatment recommendations.

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Acute Cerebral Œdema During Treatment of Hyperglycæmia

Cited by 68 publications

References 15 publications

Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits

Effects of Hyperglycemia and Rapid Lowering of Plasma Glucose in Normal Rabbits

Metabolism and oxidation of U-14C-glucose, xylitol, fructose and sorbitol in the fasted and in the streptozotocin-diabetic rat

Cerebral oedema during treatment of diabetic ketoacidosis: are we any nearer finding a cause?

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