Understanding the Presentation of Diabetic Ketoacidosis
Pathophysiology of DKA
The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA.
|Author's Note: Briefly review the typical presentation of a patient experiencing a hypoglycemic episode. See Mistovich’s January column Diabetic Emergencies: Understanding the Presentation of Hypoglycemia.|
Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are receiving more than an adequate amount of glucose. Basically, the general body tissue is starving while the brain has more than an adequate supply of glucose. Thus, the patient does not experience the sudden onset of signs and symptoms associated with hypoglycemia.
There are three major pathophysiologic syndromes associated with an excessively elevated blood glucose level in DKA: metabolic acidosis, osmotic diuresis and an electrolyte disturbance.
As acetoacetic acid is metabolized it produces acetone, which begins to accumulate in the blood. Small amounts of acetone are released in respiration and produce the characteristic “fruity breath” odor. In normal metabolism, ketones would be used as fuel in the peripheral tissue; however, due to the starvation state of the cells, the ketones are not used. An increase in ketone production and a decrease in peripheral cell use lead to metabolic acidosis – also called ketoacidosis. This is reflected in a decreasing pH value typically less than 7.40. The patient will also begin to eliminate large amounts of ketones through excretion in the urine.
Typically, when the blood glucose level reaches approximately 225 mg/dL a significant amount of glucose spills over into the urine. A glucose molecule produces an osmotic effect by drawing water across a semipermeable membrane. As an excessive amount of glucose enters the renal tubules, it draws a large amount of water that ends up producing a significant amount of urine. This is known as osmotic diuresis and leads to volume depletion and dehydration in the patient.
Large amounts of ketones also collect in the urine. Because ketones are strong organic acids, they must be buffered in order to be excreted. Sodium is typically used as the buffer. As we have been instructed, where sodium goes, water follows. Thus, the sodium used to buffer the ketones also draws a large amount of water into the renal tubules, which produces excessive urine and leads to further volume depletion and dehydration. The loss of large amounts of fluid also leads to the excretion of other electrolytes, such as potassium, calcium, magnesium and phosphorous. This produces electrolyte imbalance and disturbances.
Three Major Syndromes of DKA
The term diabetic ketoacidosis literally explains what the patient is experiencing. The term diabetes is often thought of as dealing with a glucose derangement or imbalance. However, this is not true. Diabetes simply means an increase in urine output. Thus, diabetic in DKA implies an increase in urine output that occurs from osmotic diuresis.
The term ketoacidosis is fairly self explanatory. It refers to the metabolic acidosis resulting from ketone production from fat metabolism. The DKA patient is therefore prone to metabolic acidosis from ketone production, severe dehydration from osmotic diuresis, and electrolyte disturbances. These pathophysiologic syndromes produce the signs and symptoms exhibited by the patient.
Unlike the hypoglycemic patient who experiences a sudden onset (minutes) of signs and symptoms when the supply of glucose to the brain is severely depleted, the DKA patient’s brain has a very large and abundant supply of glucose. The slow and gradual onset of signs and symptoms is related to the accumulating effect of the dehydration from osmotic diuresis and buildup of acid from ketone production. As the cells slowly become dehydrated and acidotic, the signs and symptoms begin to appear. And as the brain cells slowly dehydrate and are affected by the increasing acidic state over hours and days, the mental status slowly begins to alter.
Osmotic diuresis typically produces the classic signs and symptoms of hyperglycemia:
- Polyuria (excessive urination)
- Polydipsia (excessive drinking of fluids)
- Constant thirst
- Frequent urination at night
Osmotic diuresis leads to dehydration and a potential hypovolemic state from fluid loss, producing the following signs:
- Dry and warm skin
- Poor skin turgor
- Dry mucous membranes
- Decreased sweating
- Orthostatic vital signs
Other signs and symptoms include:
- Nausea and vomiting
- Abdominal pain (especially in children due to gastric distention or stretching of the liver capsule)
Kussmaul’s respirations are deep and rapid respirations that are an attempt to compensate for the increasing ketoacidosis. The deep and rapid respiratory rate blows off carbon dioxide, which is necessary for the production of carbonic acid. With the decreased availability of carbon dioxide, less carbonic acid is produced, thereby increasing the pH value and allowing more ketoacids to accumulate.
ECG changes and dysrhythmias may also result from the electrolyte disturbance.
Emergency Management of DKA
As with any patient in the prehospital environment, ensure an adequate airway, ventilation, oxygenation and circulation. Based on the physiologic syndromes of osmotic diuresis — leading to dehydration, ketoacidosis and electrolyte disturbances — the primary goal of prehospital treatment of a DKA patient is rehydration with isotonic fluids. Normal saline is an acceptable fluid. Administer the normal saline based on the blood pressure and other indicators of tissue perfusion. It would be acceptable to bolus the fluid in cases of severe hypovolemia and hypotension. Also be sure to place the patient on a continuous cardiac monitor and obtain and record the blood glucose level. Continuously reassess the patient for improvement or deterioration.
By understanding the pathophysiology of diabetic ketoacidosis, you should be better prepared to recognize the clinical presentation more promptly, differentiate the condition from other diabetic emergencies, and have a good foundation for understanding the emergency care necessary to manage the patient effectively.
- Dalton AL, Limmer D, Mistovich JJ, Werman HA. Advanced Medical Life Support: A Practical Approach to Adult Medical Emergencies, 3nd edition. Upper Saddle River, NJ: Prentice Hall, 2007.
- Guyton, A.C., and J.E. Hall. Textbook of Medical Physiology. 10th ed. Philadelphia: W.B. Sauders, 2001.
- Marx, J.A., R.S. Hockberger, R.M. Walls. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis: Mosby, Inc., 2002.
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