If you have diabetes, learn to recognize the signs and symptoms of DKA. Know when to test for ketones, such as when you are sick. If you use an insulin pump, check often to see that insulin is flowing through the tubing. Make sure the tube is not blocked, kinked or disconnected from the pump.

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Classification and diagnosis of diabetes: standards of care in diabetes Diabetes Care. PMID: pubmed. Maloney GE, Glauser JM. Diabetes mellitus and disorders of glucose homeostasis.

In: Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Updated by: Sandeep K. Dhaliwal, MD, board-certified in Diabetes, Endocrinology, and Metabolism, Springfield, VA. Also reviewed by David C.

Dugdale, MD, Medical Director, Brenda Conaway, Editorial Director, and the A. Editorial team. Diabetic ketoacidosis. DKA happens when the signal from insulin in the body is so low that: Blood sugar glucose can't go into cells to be used as a fuel source. The liver makes a large amount of glucose.

Fat is broken down too rapidly for the body to process. Common symptoms of DKA can include: Decreased alertness Deep, rapid breathing Dehydration Dry skin and mouth Flushed face Frequent urination or thirst that lasts for a day or more Fruity-smelling breath Headache Muscle stiffness or aches Nausea and vomiting Stomach pain.

Exams and Tests. Ketone testing is usually done when DKA is suspected: Most often, urine testing is done first. If the urine is positive for ketones, most often a ketone called beta-hydroxybutyrate is measured in the blood.

This is the most common ketone measured. The other main ketone is acetoacetate. Other tests for ketoacidosis include: Arterial blood gas Basic metabolic panel , a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions, including the anion gap Blood glucose test Blood pressure measurement Osmolality blood test.

Outlook Prognosis. Most people respond to treatment within 24 hours. Sometimes, it takes longer to recover. If DKA is not treated, it can lead to severe illness or death. Possible Complications. Health problems that may result from DKA include any of the following: Fluid buildup in the brain cerebral edema Heart stops working cardiac arrest Kidney failure.

When to Contact a Medical Professional. In the absence of timely treatment, DKA progresses to coma and death. Headache and fluctuating level of consciousness herald this complication in some patients, but respiratory arrest is the initial manifestation in others. The cause is not well understood but may be related to too-rapid reductions in serum osmolality or to brain ischemia.

It is most likely to occur in children 5 years when DKA is the initial manifestation of diabetes mellitus Diabetes Mellitus DM Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia.

Children with the highest BUN blood urea nitrogen levels and lowest PaCO2 at presentation appear to be at greatest risk. Delays in correction of hyponatremia and the use of bicarbonate during DKA treatment are additional risk factors.

In patients suspected of having diabetic ketoacidosis, serum electrolytes, blood urea nitrogen BUN and creatinine, glucose, ketones, and osmolarity should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas measurement.

DKA is diagnosed by an arterial pH 7. Guidelines differ on specific levels of hyperglycemia to be included in the diagnostic criteria for DKA. Hyperglycemia causes an osmotic diuresis with A presumptive diagnosis may be made when urine glucose and ketones are positive on urinalysis.

Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic acid and not beta-hydroxybutyric acid, which is usually the predominant ketoacid. Blood beta-hydroxybutyrate can be measured, or treatment can be initiated based on clinical suspicion and the presence of anion gap acidosis if serum or urine ketones are low.

Symptoms and signs of a triggering illness should be pursued with appropriate studies eg, cultures, imaging studies. Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium.

Common causes include diuretic use, diarrhea, heart failure Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.

As acidosis is corrected, serum potassium drops. An initial potassium level 4. read more which may be present in patients with alcoholic ketoacidosis Alcoholic Ketoacidosis Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia.

read more and in those with coexisting hypertriglyceridemia. Buse JB, Wexler DJ, Tsapas A, et al : Update to: Management of Hyperglycemia in Type 2 Diabetes, A Consensus Report by the American Diabetes Association ADA and the European Association for the Study of Diabetes EASD.

Diabetes Care 43 2 —, doi: Garber AJ, Handelsman Y, Grunberger G, et al : Consensus statement by the American Association of Clinical Endocrinologists and American College of Endocrinology on the comprehensive type 2 diabetes management algorithm executive summary.

Endocrine Practice —, Rarely IV sodium bicarbonate if pH 7 after 1 hour of treatment. The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia 1, 2 Treatment references Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.

Identification of precipitating factors is also important. Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment. Intravascular volume should be restored rapidly to raise blood pressure and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 hours.

Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 1. Additional boluses or a faster rate of infusion may be needed to raise the blood pressure.

Slower rates of infusion may be needed in patients with heart failure or in those at risk for volume overload.

If the serum sodium level is normal or high, the normal saline is replaced by 0. Pediatric maintenance fluids Maintenance requirements Dehydration is significant depletion of body water and, to varying degrees, electrolytes. Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree read more for ongoing losses must also be provided.

Initial fluid therapy should be 0. Hyperglycemia is corrected by giving regular insulin 0. Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by preflushing the IV tubing with insulin solution.

Children should be given a continuous IV insulin infusion of 0. Ketones should begin to clear within hours if insulin is given in sufficient doses. Serum pH and bicarbonate levels should also quickly improve, but restoration of a normal serum bicarbonate level may take 24 hours.

Bicarbonate should not be given routinely because it can lead to development of acute cerebral edema primarily in children. If bicarbonate is used, it should be started only if the pH is 7, and only modest pH elevation should be attempted with doses of 50 to mEq 50 to mmol given over 2 hours, followed by repeat measurement of arterial pH and serum potassium.

A longer duration of treatment with insulin and dextrose may be required in DKA associated with SGLT-2 inhibitor use. When the patient is stable and able to eat, a typical basal-bolus insulin regimen Insulin regimens for type 1 diabetes General treatment of diabetes mellitus for all patients involves lifestyle changes, including diet and exercise.

Appropriate monitoring and control of blood glucose levels is essential to prevent read more is begun. IV insulin should be continued for 2 hours after the initial dose of basal subcutaneous insulin is given.

Children should continue to receive 0. If serum potassium is 3. Initially normal or elevated serum potassium measurements may reflect shifts from intracellular stores in response to acidemia and belie the true potassium deficits that almost all patients with DKA have.

Insulin replacement rapidly shifts potassium into cells, so levels should be checked hourly or every other hour in the initial stages of treatment. Causes include alcohol use disorder, burns, starvation, and diuretic use. Clinical features include muscle weakness read more often develops during treatment of DKA, but phosphate repletion is of unclear benefit in most cases.

If potassium phosphate is given, the serum calcium level usually decreases and should be monitored. Treatment of suspected cerebral edema is hyperventilation, corticosteroids, and mannitol , but these measures are often ineffective after the onset of respiratory arrest.

Gosmanov AR, Gosmanova EO, Dillard-Cannon E : Management of adult diabetic ketoacidosis. Diabetes Metab Syndr Obes —, French EK, Donihi AC, Korytkowski MT : Diabetic ketoacidosis and hyperosmolar hyperglycemic syndrome: review of acute decompensated diabetes in adult patients.

BMJ l, Overall mortality rates for diabetic ketoacidosis are 1, 2, 3 Prognosis references Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Another study had lower rates of persistent neurologic sequelae and death 4 Prognosis references Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis.

Edge JA, Hawkins MM, Winter DL, Dunger DB : The risk and outcome of cerebral oedema developing during diabetic ketoacidosis. Arch Dis Child 85 1 , Marcin JP, Glaser N, Barnett P, et al : Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema.

J Pediatr 6 , Glaser N. Cerebral edema in children with diabetic ketoacidosis. Curr Diab Rep ;1 1 Kuppermann N, Ghetti S, Schunk JE, et al.