What is diabetic ketoacidosis?
Diabetic ketoacidosis, also known as DKA, is a buildup of acids in your blood. It can happen when your blood sugar is too high for too long. DKA is a serious complication of diabetes and could be life-threatening, but it usually takes many hours to become that serious. You can treat it and prevent it, too.
What are the symptoms of diabetic ketoacidosis?
The signs and symptoms of diabetic ketoacidosis often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first sign of diabetes. You may notice:
- Excessive thirst
- Frequent urination
- Nausea and vomiting
- Stomach pain
- Weakness or fatigue
- Shortness of breath
- Fruity-scented breath
The more specific signs of diabetic ketoacidosis, which can be detected through home blood and urine test kits, include:
- High blood sugar level (hyperglycemia).
- High levels of ketones in the urine.
What causes diabetic ketoacidosis?
In general, diabetic ketoacidosis occurs because there is not enough insulin to move sugar (glucose) into the cell, where it can be used for energy. In addition to a lack of insulin, certain body stressors combined with diabetes, such as an infection or illness, can trigger diabetic ketoacidosis.
Sometimes diabetic ketoacidosis is the first sign of diabetes in people who don’t know they have diabetes. (They have not previously diagnosed diabetes).
Diabetic ketoacidosis prevention
- If you have diabetes, take all of your medications as prescribed by your healthcare professional.
- Learn to recognize the symptoms of high blood glucose levels.
- Don’t skip insulin doses (an important factor in prevention).
- Check your glucose levels regularly as recommended by your doctor.
- Test your urine at home, especially when you feel sick. This will help detect ketones or elevated blood sugar levels, which should alert you to the possibility of diabetic ketoacidosis.
The risk of diabetic ketoacidosis is higher if:
- You have type 1 diabetes
- Often skips insulin doses
Infrequently, diabetic ketoacidosis can occur if you have type 2 diabetes. In some cases, diabetic ketoacidosis may be the sign that a person has diabetes.
Diabetic ketoacidosis is treated with fluids, electrolytes such as sodium, potassium and chloride and insulin. Perhaps surprisingly, the most common complications of diabetic ketoacidosis are related to this lifesaving treatment.
Diabetic ketoacidosis diagnosis
In general, DKA and HHS differ in presentation. If physical examination reveals dehydration along with a high capillary blood glucose level with or without urine or increased plasma ketone bodies, acute diabetic decompensation should be strongly suspected. A definitive diagnosis of DKA or HHS must be confirmed through laboratory investigation.
The clinical presentation can provide helpful information for the preliminary bedside diagnosis. DKA usually occurs in younger, lean patients with type 1 diabetes and develops within a day or so, whereas HHS is more likely to occur in older, obese patients with type 2 diabetes and can take days or weeks to fully develop. Also, HHS usually occurs in elderly diabetic patients, often those with decreased renal function who do not have access to water. Both DKA and HHS often present with polyuria and polydipsia, although polydipsia may be absent in elderly patients with HHS.
In both conditions, abdominal pain with nausea and vomiting can develop to decreased mesenteric perfusion and can be mistaken for an acute surgical abdomen. Kussmaul–Kien respiration (rapid and deep respiration) with breath acetone is typical of DKA but is absent in HHS. Although dehydration occurs in both conditions, it is often more pronounced in HHS. Because DKA and HHS are usually accompanied by hypothermia, a normal or elevated temperature may indicate an underlying infection.
Diabetic ketoacidosis treatment
The success of treatment of DKA and HHS depends on the adequate correction of dehydration, hyperglycemia, ketoacidosis and electrolyte deficits. Any comorbid precipitating event should be identified and treated appropriately. Both DKA and HHS are medical emergencies, and patients with these conditions must be admitted to the hospital.
The goal of initial fluid therapy is to expand extracellular volume (intravascular and extravascular) and restore renal perfusion. In the absence of significant cardiac problems, it is suggested that treatment begins with the infusion of isotonic saline (0.9% sodium chloride) at a rate of 15-20 ml/kg per hour for the first hour to rapidly expand the extracellular space. The subsequent choice of fluid replacement depends on hydration status, electrolyte levels, and urine output. In general, this can be an infusion of 0.45% sodium chloride at a rate of 4 to 14 ml/kg per hour if the serum sodium level is normal or elevated.
There is consensus that, in cases of DKA and HHS, regular insulin should be administered using continuous intravenous infusion in small doses through an infusion pump. Such low-dose insulin therapy provides insulin concentrations that are more physiologic and produce a more gradual and steady fall in plasma glucose levels, and it decreases the risk of hypoglycemia and hypokalemia. Although most of the protocols proposed suggest that a loading dose of insulin should be given at the initiation of insulin therapy, there are no data to support any advantage for such a recommendation.
Treatment of CAD and HHS with rehydration and insulin is typically associated with a rapid decrease in plasma potassium concentration, particularly during the first hours of therapy. This rapid decrease is due to several factors, the most significant being the insulin-mediated reentry of potassium into the intracellular compartment. Other factors include expansion of extracellular fluid volume, correction of acidosis, and ongoing loss of potassium due to osmotic diuresis and ketonuria.
The beneficial effect of phosphate therapy is purely theoretical. It would be expected to prevent possible complications associated with hypophosphatemia, such as respiratory depression, skeletal muscle weakness, hemolytic anaemia, and cardiac dysfunction. Furthermore, it would be expected to restore the level of diphosphoglycerate, which is decreased in CAD, shifting the oxygen dissociation curve to the right and improving oxygen delivery to the tissues. On the other hand, excessive phosphate administration can lead to hypocalcemia, tetanus, and soft tissue calcification. Finally, most randomized controlled trials have failed to demonstrate any clinical benefit from routine phosphate therapy.
Clinical and laboratory monitoring
Careful monitoring of vital signs, clinical conditions, and laboratory parameters of patients is important. Vital signs should be monitored every half hour for the first hour, every hour for the next 4 hours, and then every 2 to 4 hours until the resolution of the condition. An accurate record of hourly urine productivity is necessary to monitor kidney function.
On admission, a complete profile will include at least arterial or venous blood gas, plasma glucose, electrolyte, blood urea nitrogen and creatinine stages, serum or urine ketone levels, or both, and serum osmolality. Capillary blood glucose levels should be monitored hourly to allow adjustment of the insulin infusion dose. Electrolyte levels should be measured every 1 to 2 hours initially and every 4 hours thereafter. Venous pH measurement can replace arterial pH measurement and should be performed every 4 hours until CAD has been corrected.