EMS Recap: Diabetic Ketoacidosis
In the United States, almost 6% of the population suffers from diabetes, but only 3% are ever diagnosed. A serious medical emergency that can arise from uncontrolled diabetes is diabetic ketoacidosis, or DKA. DKA shifts the body’s pH, interfering with many of its biochemical pathways.
The pancreas assists in maintaining serum blood glucose by producing the regulatory hormones glucagon and insulin. Glucagon stimulates the conversion of glycogen to glucose in the liver when serum blood glucose is low. Insulin facilitates cellular uptake of glucose when serum blood glucose is high. Glucose is the primary biochemical fuel for the body, and when there is not enough, the secondary source for fuel is fatty acids.
There are two types of diabetes. Diabetes type II is often the result of poor diet, genetic predisposition and glucose overload leading to insulin resistance. Glucose overload alters the insulin receptor sites, reducing the amount of glucose entering the cell. If left untreated, type II diabetes can eventually progress to diabetes type I, with decreased or nonexistent insulin production. A loss or reduction in insulin production results in an uncontrolled rise in serum blood glucose. Glucose is good for the body and necessary to begin cellular respiration; however, with no insulin to facilitate glucose entry, blood glucose levels will rise as well as glycogen levels, and the body has to look for an alternative energy source. That source is stored fatty acids. The stored fatty acids are converted into free fatty acids that are oxidized when they enter the liver. One of the byproducts is ketones. The abundance of ketones and associated pH reduction impair oxygen release from red blood cell hemoglobin. Less oxygen is available for cellular aerobic respiration. The result is tissue hypoxia, a shift toward anaerobic cellular respiration, and metabolic acidosis.
In summary, DKA is the result of a reduced supply of available glucose due to a decline in circulating insulin, an increase in circulating glucagon once the supply of glycogen is exhausted, a subsequent increase in fatty acid oxidation, and the production of ketones. DKA reduces the body pH. The drop in pH changes oxyhemoglobin bonding, causing limited oxygen release from hemoglobin for cellular respiration. With a reduction in available oxygen, aerobic cellular metabolism shifts to anaerobic metabolism, and the body pH continues to drop. Individuals with DKA need immediate definitive treatment most often accomplished in the hospital.
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Robert E. Sippel, Major, USAF (Ret.) MS, MAEd, NREMT-P, LP, is an assistant professor and clinical coordinator in the Emergency Health Science Department at the University of Texas Health Science Center, San Antonio, TX.
Michael R. Sippel, BS, NREMT-P, EMT-P, is a clinical adjunct faculty instructor in the Emergency Health Science Department and a first-year medical student at Texas Tech University Health Science Center, El Paso.