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A Valid Physiological Approach, Not a Panacea

Robert S. Sherwin, MD

Arch Intern Med. 1977;137(10):1361-1362.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Diabetic ketoacidosis is the result of increased hepatic production of glucose and ketones as well as reduced catabolism of these substrates, primarily by muscle. From a theoretical standpoint, optimal insulin therapy in this disorder would deliver maximally effective concentrations of insulin to target tissues (principally the liver, muscle, and fat) and at the same time minimize complications accompanying insulin treatment, for example, hypokalemia, hypoglycemia, and cerebral edema. The accepted method of treatment for diabetic ketoacidosis has been to inject intermittently high doses (100 to 200 units) of insulin every few hours. To the surprise of many clinicians, recent reports have documented the efficacy of a low-dose continuous infusion method using only 4 to 8 units per hour.^1-3 These new observations have raised the following questions: Why should low doses given continuously be as effective as large doses given by intermittent injection? Are there any significant benefits to be derived . . . [Full Text PDF of this Article]

Author Affiliations
New Haven, Conn

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