Increased Cerebrospinal-Fluid Pressure During Treatment of Diabetic Ketosis

Clements, Rex S.; Morrison, Anthony D.; Blumenthal, Stanley A.; Winegrad, AlbertI.

doi:10.1016/s0140-6736(71)92245-8

Cited by 111 publications

(34 citation statements)

References 17 publications

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“…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). The present study does not support these contentions.…”

Section: Discussioncontrasting

confidence: 80%

“…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: 98%

“…There have since been several similar reports (5-7) as well as two cases of cerebral edema associated with nonketotic hyperosmolar coma with hyperglycemia (nonketotic coma) (8,9). Recent evidence suggests that most patients being treated for diabetic ketoacidosis develop increased intracranial pres sure (10) and that rapid lowering of blood glucose in hyper glycemic dogs is often associated with increased cerebrospinal fluid (CSF) 1 pressure (11). The mortality among patients with such cerebral edema has been close to 100% (3,4), and treatment has generally been ineffectual.…”

Section: Introductionmentioning

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: Discussioncontrasting

confidence: 80%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

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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“…An asymptomatic increase in CSF pressure during treatment of DKA has been recognized for Ͼ25 years (195)(196)(197). Significant decreases in the size of the lateral ventricles, as determined by echoencephalogram, were noted in 9 out of 11 DKA patients during therapy (198,199).…”

Section: Cerebral Edemamentioning

confidence: 99%

Management of Hyperglycemic Crises in Patients With Diabetes

et al. 2001

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Abbreviations: AaO 2 , alveolar-to-arteriolar oxygen; AKA, alcoholic ketoacidosis; ARDS, adult respiratory distress syndrome; BUN, blood urea nitrogen; CPT, carnitine palmitoyl-transferase; CSF, cerebrospinal fluid; DKA, diabetic ketoacidosis; FFA, free fatty acid; HHS, hyperosmolar hyperglycemic state; IRI, immunoreactive insulin; PaO 2 , arteriolar partial pressure of oxygen; RDKA, recurrent DKA.A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances. Management of Hyperglycemic Crises in Patients With Diabetes T E C H N I C A L R E V I E R e v i e w s / C o m m e n t a r i e s / P o s i t i o n S t a t e m e n t s 132DIABETES CARE, VOLUME 24, NUMBER 1, JANUARY 2001Technical Review noted in newly diagnosed obese type 2 diabetic patients (5,26,31). Therefore, the concept that the presence of DKA in type 2 diabetes is a rare occurrence is incorrect.The most common types of infections are pneumonia and urinary tract infection, accounting for 30-50% of cases (Table 4). Other acute medical illnesses as precipitating causes include alcohol abuse, trauma, pulmonary embolism, and myocardial infarction, which can occur both in type 1 and 2 diabetes (6). Various drugs that alter carbohydrate metabolism, such as corticosteroids, pentamidine, sympathomimetic agents, and ␣-and ␤-adrenergic blockers, and excessive use of diuretics in the elderly may also precipitate the development of DKA and HHS.The recent increased use of continuous subcutaneous insulin infusion pumps that use small amounts of short-acting insulin has been associated with an incidence of DKA that is significantly increased over the incidence seen with conventional methods of multiple daily insulin injections, in spite of the fact that most of the mechanical problems with insulin pumps have been resolved (6,(32)(33)(34). In the Diabetes Control and Complications Trial, the incidence of DKA in patients on insulin pumps was about twofold higher than that in the multipleinjection group over a comparable time period (35). This may be due to the exclusive use of short-acting insulin in the pump, which if interrupted leaves no reservoir of insulin for blood glucose control.Psychological factors and poor compliance, leading to omission of insulin therapy, are important precipitating factors for recurrent ketoacidosis. In young female patients with type 1 diabetes, psychological problems complicated by eating disorders may be contributing factors in up to 20% of cases of recurrent ketoacidosis (36,37). Factors that may lead to insulin omission in younger patients include fear of weight gain with good metabolic control, fear of hypoglycemia, rebellion against authority, and stress related to chronic disease (36). Noncompliance with insulin therapy has been found to be the leading precipitating cause for DKA in urban African-Americans and medically indigent patients (5,26). In addition, a recent study showed that diabetic patients without health insurance or with Medicaid alone had hospitali...

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“…Recent evidence suggests that most patients being treated for diabetic ketoacidosis develop increased intracranial pressure (10) and that rapid lowering of blood glucose in hyperglycemic dogs is often associated with increased cerebrospinal fluid (CSF) 1 pressure (11).…”

Section: The Journal Of Clinical Investigation Volume 52 March 1973mentioning

confidence: 99%

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Arieff¹,

Kleeman²

1973

J. Clin. Invest.

182

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A B S T R A C T 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 H20) 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 significant osmotic gradient from brain (326 mosmol/ kg H20) to plasma (287 mosmol/kg). By similarly lowering plasma glucose with peritoneal dialysis, increases in brain Na+, K+, Cl-, and water were significantly less, idiogenic osmoles were not present, and brain and plasma Osm were not different. It is concluded that during sustained hyperglycemia, the cerebral cortex adapts to extracellular hyperosmolality This work was presented in part at International Symposium on the

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Increased Cerebrospinal-Fluid Pressure During Treatment of Diabetic Ketosis

Cited by 111 publications

References 17 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

Management of Hyperglycemic Crises in Patients With Diabetes

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

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