Cerebral edema complicating therapy for diabetic ketoacidosis

Duck, Stephen C.; Weldon, V. V.; Pagliara, A. S.; Haymond, M. W.

doi:10.2337/diabetes.25.2.111

Cited by 43 publications

(17 citation statements)

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“…It appears therefore that in diabetic ketoacidosis the osmotic diuresis overrides the antidiuretic effect of AVP. It has been suggested that inappropriate AVP secretion may contribute to the development of cerebral oedema in diabetic ketoacidosis [5]. However, in no patient in this study were features of fluid overload or cerebral oedema observed.…”

Section: Discussioncontrasting

confidence: 63%

“…There are a number of reasons for questioning whether impaired vasopressin secretion or activity occur in some patients with ketoacidosis: (1) infusions of hypertonic glucose have been shown to suppress plasma AVP [1]; (2) diabetes insipidus has been reported by some workers to have occurred in patients during the course of ketoacidosis [2,3]; (3) animal studies indicate that in states of acute metabolic acidosis, or potassium depletion, the antidiuretic activity of vasopressin becomes impaired [4]; and (4) it has been suggested that inappropriate AVP secretion may have contributed to the occurrence of cerebral oedema in a patient suffering from diabetic ketoacidosis [5].…”

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confidence: 99%

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Plasma Arginine Vasopressin in diabetic ketoacidosis

Walsh

Baylis

Malins³

1979

Diabetologia

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Summary. Plasma Arginine Vasopressin (AVP) was measured serially in 10 patients during the first 24 hours of treatment of diabetic ketoacidosis. AVP was elevated in all cases initially, ranging from 4.0-122.0 pmol/1, the basal level in healthy hydrated subjects being 1.57 _+ 0.59pmol/1 (_+ 1 SD). The levels fell progressively during the course of treatment. While there was no evidence that the massive increases in AVP noted in this study were associated with water overload it remains to be determined whether the high levels observed have any significant metabolic or haemodynamic role in this disorder.

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Section: Discussioncontrasting

confidence: 63%

mentioning

confidence: 99%

Plasma Arginine Vasopressin in diabetic ketoacidosis

Walsh

Baylis

Malins³

1979

Diabetologia

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“…A patient with diabetic ketoacidosis was reported [8] in whom right-sided focal seizures developed during therapy. At that time the serum sodium level had fallen to 120 mEq/liter although the blood glucose ievel was only 209 mgldl ( value on admission, 425 mg/dl).…”

Section: Chatrian Et A1 [4]mentioning

confidence: 99%

Epilepsia partialis continua associated with nonketotic hyperglycemia: Clinical and biochemical profile of 21 patients

Singh

Strobos

1980

Annals of Neurology

153

100

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In 21 patients, epilepsia partialis continua (EPC) was an early symptom of nonketotic hyperglycemia and occurred during an initial phase of hyponatremia and mild hyperosmolality. EPC persisted for an average of 8 days, and its duration correlated predominantly with the degree of hyponatremia. Depression of consciousness and cessation of seizures occurred with increasing severity of hyperglycemia and hyperosmolality. In 9 patients, EPC was the first symptom leading to the diagnosis of diabetes mellitus. Four patients died of serious associated illness. The majority of the patients had evidence of a localized structural cerebral lesion. Metabolic disturbances including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of EPC in areas of focal cerebral damage.

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“…2 " 6 In spite of a number of provocative theories concerning the fundamental mechanisms associated with the development of cerebral edema resulting from treatment for diabetes, many of the fundamental characteristics of this form of brain swelling remain to be determined.…”

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confidence: 99%

Regional Localization of Cerebral Edema Following Fluid and Insulin Therapy in Streptozotocin-Diabetic Rats

Tornheim

1981

Diabetes

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To evaluate the location and early time course for development of cerebra edema following therapy for diabetes, streptozotocin-diabetic rats were subjected to constant i.v. infusion with saline and regular insulin. At the end of 1, 2, and 5 h of therapy, these rats were killed and tested for density of the cerebral cortex, subcortical white matter, caudate-putamen, thalamus, and medulla. Density data from treated animals were compared with those from control animals. From these data, change in brain tissue volume as water was calculated. Diabetic animals killed after 1 h of fluid and insulin therapy demonstrated a modest increase in brain water content of all areas tested except white matter. Following 2 h of therapy, all regions tested were edematous, with a magnitude of edema that was similar to that seen at 1 h. After 5 h of therapy, there was further increase in water content of the cerebral cortex, but not the other regions examined. Treatment with saline alone did not result in central overhydration. The findings of this study suggest that aggressive therapy with fluids and insulin, but not fluid alone, results in global overhydration of the brains of diabetic animals. Prolonged fluid and insulin treatment with a return of blood glucose to normal values causes further and preferential accumulation of edema fluid in the cerebral cortex.

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Cerebral edema complicating therapy for diabetic ketoacidosis

Cited by 43 publications

References 0 publications

Plasma Arginine Vasopressin in diabetic ketoacidosis

Plasma Arginine Vasopressin in diabetic ketoacidosis

Epilepsia partialis continua associated with nonketotic hyperglycemia: Clinical and biochemical profile of 21 patients

Regional Localization of Cerebral Edema Following Fluid and Insulin Therapy in Streptozotocin-Diabetic Rats

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