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[IP] Current Standards for Managing Diabetic Ketoacidosis


I have recently been transferred to a new hospital where diabetic
ketoacidosis (DKA), even in its severe form (pH less than 7.1), is treated
by subcutaneous regular insulin given on a sliding scale. The interval
between doses is 4-6 hours. I have never seen or heard of subcutaneous (SC)
insulin treatment in severe DKA. Is such a treatment recommended?
from Zachary T. Bloomgarden, MD, 07/03/01
The physician asking the question clearly recognizes that the treatment
described represents inadequate management of DKA.
The current approach to treating DKA is clearly summarized in the American
Diabetes Association Clinical Practice Recommendations 2001 Position
Statement "Hyperglycemic Crises in Patients With Diabetes Mellitus."[1] The
diagnostic criteria for DKA are blood glucose over 250 mg/dL, arterial pH
below 7.3, bicarbonate concentration below 15 mEq/L, and moderate ketonuria
or ketonemia. DKA occurs with a frequency of 4-8 per 1000 patients with type
1 diabetes per year and at an average cost of $13,000 per episode, it
constitutes a substantial component of the overall expenditure for adults
with type 1 diabetes. Precipitating factors include acute illnesses such as
infection, pancreatitis, myocardial infarction, stroke, or trauma. Drugs
(steroids, thiazides, sympathomimetics, and alcohol), new-onset type 1
diabetes, or discontinuation of as well as inadequate dosages of insulin may
also lead to the development of DKA. Patients often stop using insulin for
economic reasons, whereas eating disorders may cause individuals to take
lower than recommended insulin dosages.
Although insulin administration is critically important in the treatment of
DKA, one must recognize that the management of dehydration and electrolyte
abnormalities is, in certain respects, even more crucial. Intravenous (IV)
fluid administration must be vigorous unless the patient has an underlying
fluid-retaining condition. For adults, this typically involves infusion of
approximately 1 liter of normal saline (NS) during the first hour, followed
by 250-500 mL/hour of half-NS (or NS if the sodium level remains < 135
mmol/L after being corrected for hyperglycemia by adding 1.6 mEq for each
100 mg/dL glucose > 100 mg/dL).
Correction of potassium (K+) deficiency is crucial, and on those infrequent
occasions with actual hypokalemia (< 3.3 mEq/L) initially, insulin should
not be administered until a sufficient amount of K+ has been given to bring
the level over 3.5 mEq/L. With normal renal function and K+ < 5.5 mEq/L,
20-30 mEq potassium is added, two thirds as the chloride and one third as
the phosphate salt, to each liter of IV fluid. With severe acidosis (pH <
6.9), 100 mM of sodium bicarbonate in 400 mL sterile water may be
administered over a 2-hour period. For a pH between 6.9 and 7.0, 50 mM of
sodium bicarbonate in 200 mL sterile water may be given over 1 hour, and if
the pH exceeds 7.0 there is no need for bicarbonate treatment.
Insulin, typically given in a 10-unit IV bolus followed by continuous
administration at a rate of 5 U/h, will decrease the blood glucose by 50-75
mg/dL/h. If the fall in glucose is lower and the patient is adequately
hydrated, the rate of insulin delivery should be doubled every hour until a
50-75 mg/h decrease in glucose is achieved.
To address what may be the basis for the aforementioned institution's
recommendation of SC insulin for severe DKA, consider that with mild DKA the
patient may be given insulin as 15 U IV, plus 15 U SC, plus 5 U SC on an
hourly basis. After the initial arterial blood pH measurement the anion gap
or venous pH should be monitored. However, it is important not to rely on
ketones as measured by the nitroprusside method, which only measures
acetoacetic acid and acetone, but not beta-hydroxybutyrate.
To avoid the very rare (particularly in adults) complication of
DKA-associated cerebral edema, which may result from the movement of water
into the brain when plasma osmolality declines rapidly, the serum osmolality
(calculated as: 2[Na (mEq/l)] + glucose (mg/dL)/18) should not be lowered by
more than 3mOsm/L per h; and the glucose should be allowed to stabilize at
250 mg/dL (250-300 mg/dL for hyperosmolar coma). Thus, when the blood
glucose reaches 250 mg/dL the rate of insulin administration should be
decreased to 3 U/h and 5%-10% dextrose should be added to fluids, continuing
until the acidosis and hyperosmolarity resolve. Other complications include
hypoglycemia from excess insulin, hypokalemia from insulin or from
bicarbonate, and hyperglycemia from premature interruption of IV insulin.
Hyperchloremia with non-anion gap metabolic acidosis is common as chloride
replaces ketoanions, but is not clinically significant in patients who do
not have renal failure.
Key measures in the prevention of DKA are ensuring better access to medical
care, education, and communication during intercurrent illness.
Sick-day management rules for patients with insulin-requiring diabetes
should include education on:
how and when to contact the healthcare provider
blood glucose goals and the use of supplemental short-acting insulin during
the importance of never discontinuing insulin
recommended approaches in cases of fever and infection
using an easily digestible liquid diet containing carbohydrates and salt if
the patient is anorexic
the need for accurate testing and recording of blood glucose levels and body
measurement of urine ketones when the blood glucose is unexpectedly and
persistently over 300 mg/dL.
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