eMedicine Specialties > Endocrinology > Diabetes Mellitus

Diabetic Ketoacidosis: Treatment & Medication

Author: Osama Hamdy, MD, MB, BCh, PhD, Medical Director, Obesity Clinical Program, Joslin Diabetes Center, Assistant Professor of Medicine, Harvard Medical School, Boston, MA
Contributor Information and Disclosures

Updated: Sep 1, 2009

Treatment

Medical Care

Managing diabetic ketoacidosis (DKA) in an ICU during the first 24-48 hours is always advisable. When treating DKA, the points that must be considered and closely monitored include correction of fluid loss with IV fluids; correction of hyperglycemia with insulin; correction of electrolyte disturbances, particularly potassium loss; correction of acid-base balance; and treatment of concurrent infection if present.

Paying great attention to the correction of fluid and electrolyte loss during the first hour of treatment, followed by gradual correction of hyperglycemia and acidosis, always is advisable. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration means that at least 3 liters of fluid already have been lost.

  • Fluids: Initial correction of fluid loss is either by isotonic sodium chloride solution or by lactated Ringer solution.
    • Administer 1 liter over the first 30 minutes.
    • Administer 1 liter over the second hour.
    • Administer 1 liter over the following 2 hours.
    • Administer 1 liter every 4 hours, depending on the degree of dehydration and central venous pressure (CVP) readings.
    • When the patient becomes euvolemic, the physician may switch to half the isotonic sodium chloride solution, particularly if hypernatremia exists.
    • When blood sugar decreases to less than 180 mg/dL, isotonic sodium chloride solution is replaced with 5-10% dextrose with half isotonic sodium chloride solution.
  • Insulin8
    • When insulin treatment is started, several points must be considered.
      • A low-dose insulin regimen has the advantage of not inducing severe hypoglycemia or hypokalemia, as may be observed with a high-dose insulin regimen.
      • Only short-acting insulin is used for correction of hyperglycemia.
      • Subcutaneous absorption of insulin is reduced in DKA because of dehydration; therefore, using IV or IM routes is traditionally preferable. Subcutaneous use of the fast-acting insulin analog (lispro) has been tried in pediatric DKA (0.15 U/kg q2h). The results were shown to be comparable to IV insulin, but ketosis took 6 more hours to resolve. Such technically simplified methods may be cost-effective and may preclude ICU admissions in mild cases.
    • The initial insulin dose is a continuous IV insulin infusion using an infusion pump, if available, at a rate of 0.1 U/kg/h. A mix of 24 units of regular insulin in 60 mL of isotonic sodium chloride solution usually is infused at a rate of 15 mL/h (6 U/h) until the blood sugar drops to less than 180 mg/dL, then the rate of infusion decreases to 5-7.5 mL/h (2-3 U/h) until the ketoacidotic state abates. Larger volumes of an insulin and isotonic sodium chloride solution mixture can be used, providing that the infusion dose of insulin is similar. Larger volumes may be easier in the absence of an intravenous infusion pump (eg, 60 U of insulin in 500 mL of isotonic sodium chloride solution at a rate of 50 mL/h).
    • The optimal rate of glucose decline is 100 mg/dL/h.
    • Do not allow the blood glucose level to fall below 200 mg/dL during the first 4-5 hours of treatment.
    • Hypoglycemia may develop rapidly with correction of ketoacidosis.
    • A common mistake is to allow blood glucose to drop to hypoglycemic levels. This mistake usually results in a rebound ketosis derived by counter-regulatory hormones. Rebound ketosis requires a longer duration of treatment. The other hazard is that rapid correction of hyperglycemia and hyperosmolarity may shift water rapidly to the hyperosmolar intracellular space and may induce cerebral edema.
  • Electrolyte correction
    • Potassium
      • If the potassium level is greater than 6 mEq/L, do not administer potassium supplement.
      • If the potassium level is 4.5-6 mEq/L, administer 10 mEq/h of potassium chloride.
      • If the potassium level is 3-4.5 mEq/L, administer 20 mEq/h of potassium chloride.
      • Monitor serum potassium levels hourly, and the infusion must stop if the potassium level is greater than 5 mEq/L.
      • Monitoring of serum potassium must continue even after potassium infusion is stopped in the case of (expected) recurrence of hypokalemia.
      • In severe hypokalemia, not to starting insulin therapy is advisable unless potassium replacement is underway in order to avoid potentially serious cardiac dysrhythmia that may result from hypokalemia.
  • Correction of acid-base balance
    • Sodium bicarbonate only is infused if decompensated acidosis starts to threaten the patient's life, especially when associated with either sepsis or lactic acidosis.
    • If sodium bicarbonate is indicated, 100-150 mL of 1.4% concentration is infused initially. This may be repeated every half hour if necessary.
    • Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis.
  • Treatment of concurrent infection
    • In the presence of infection, administer proper antibiotics guided by the results of culture and sensitivity studies.
    • Starting empiric antibiotics on suspicion of infection until culture results are available may be advisable.

Medication

Regular and analog human insulins8  are used for correction of hyperglycemia, unless bovine or pork insulin is the only available insulin. Clinical considerations in treating diabetic ketoacidosis (DKA) include the following: (1) only short-acting insulin is used for correction of hyperglycemia in DKA, (2) the optimal rate of glucose decline is 100 mg/dL/h, (3) the blood glucose level should not be allowed to fall lower than 200 mg/dL during the first 4-5 hours of treatment, and (4) avoid induction of hypoglycemia because it may develop rapidly during correction of ketoacidosis and may not provide sufficient warning time.

Hypoglycemic agents

These agents reduce plasma glucose levels.


Regular insulin (Humulin, Novolin), Ultra–short-acting insulin analog (Humalog, NovoLog, Apidra)

Insulin suppresses hepatic glucose output and enhances glucose uptake by peripheral tissues. Insulin also suppresses ketogenesis and lipolysis, stimulates proper use of glucose by the cells, and reduces blood sugar levels.

Adult

0.1 U/kg/h IV infusion; lower to 0.05 U/kg/h when blood glucose level drops to <180 mg/dL

Pediatric

Administer as in adults

Medications that may decrease the hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase the hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone

Documented hypersensitivity; hypoglycemia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Not all ultra–short-acting analog insulins are tested in pregnancy; hyperthyroidism may increase renal clearance of insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction

More on Diabetic Ketoacidosis

Overview: Diabetic Ketoacidosis
Differential Diagnoses & Workup: Diabetic Ketoacidosis
Treatment & Medication: Diabetic Ketoacidosis
Follow-up: Diabetic Ketoacidosis
References
Further Reading
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References

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Further Reading

Related eMedicine topics:
Diabetes Mellitus, Type 1 [Endocrinology]
Diabetes Mellitus, Type 1 [Pediatrics: General Medicine]
Diabetes Mellitus, Type 1 - A Review
Diabetes Mellitus, Type 2 [Endocrinology]
Diabetes Mellitus, Type 2 [Pediatrics: General Medicine]
Diabetes Mellitus, Type 2 - A Review
Diabetic Ketoacidosis [Emergency Medicine]
Diabetic Ketoacidosis [Pediatrics: Cardiac Disease and Critical Care Medicine]
Disorders of Carbohydrate Metabolism
Metabolic Acidosis [Emergency Medicine]
Metabolic Acidosis [Nephrology]
Pediatrics, Diabetic Ketoacidosis

Clinical guidelines:
 Care of children and adolescents with type 1 diabetes: a statement of the American Diabetes Association. American Diabetes Association - Professional Association.  2005 Jan.  27 pages.  NGC:004193

Hyperglycemic crises in diabetes. American Diabetes Association - Professional Association.  2000 Oct (revised 2001; republished 2004 Jan).  9 pages.  NGC:003428

Clinical trials:
Cerebral Edema in Pediatric Diabetic Ketoacidosis

Ketosis Prone Diabetes in African-Americans

Use of Insulin Glargine to Treat Diabetic Ketoacidosis

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Keywords

diabetic ketoacidosis, ketoacidosis, acidosis, DKA, metabolic acidosis, diabetes, hyperglycemia, ketonuria, diabetes mellitus, type 1 diabetes, diabetes type 1, type 2 diabetes, diabetes type 2, insulin, human insulin, type 1 DM, type 2 DM,  ketogenesis, ketones, ketoacids, acetone, beta hydroxybutyrate, acetoacetate, Kussmaul respirations, increased thirst, polydipsia, increased urination, polyuria

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Contributor Information and Disclosures

Author

Osama Hamdy, MD, MB, BCh, PhD, Medical Director, Obesity Clinical Program, Joslin Diabetes Center, Assistant Professor of Medicine, Harvard Medical School, Boston, MA
Osama Hamdy, MD, MB, BCh, PhD is a member of the following medical societies: American Association of Clinical Endocrinologists and American Diabetes Association
Disclosure: Takeda phamaceutical North America Honoraria Speaking and teaching; Merck Inc Honoraria Speaking and teaching; Novo Nordisk Honoraria Speaking and teaching; Amylin Pharmaceutical Honoraria Speaking and teaching; Aventis Honoraria Speaking and teaching

Medical Editor

David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center
David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Don S Schalch, MD, Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics
Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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