Archive for the ‘Diabetic Ketoacidosis’ Category
When the individual’s blood sugar gets very high and they are profoundly deficient in insulin, the body becomes unable to utilize blood sugar efficiently. The body then begins to burn fat stores for food. As these fat stores are burned, a by product is released called Ketones. It is ketones that are responsible for lowering the body’s pH level below 7.35. Metabolic acidosis occurs when the pH of the body drops below 7.35. The body attempts to excrete the ketones via the kidneys, causing ketones to be released in the urine, a term called ketonuria. However along with the negative ketones, the body’s positively charged electrolytes are also excreted. This leads to an electrolyte imbalance. The body continues to burn other glucose stores in the body such as proteins, causing nitrogen losses.
Now the body has depletion in electrolytes. This can cause nausea and vomiting, depleting more electrolytes. The individual is now in a severe hyperglycemic state and is hypovolemic as well. If these conditions are left untreated, the person can go into hypovolemic shock, become comatose and die.
Outward signs and symptoms of DKA include the following; eyeballs are soft and appear sunken, skin turgor is poor, (Dehydration of tissues can be tested by pinching the skin fold on the sternum. If the skin stays in one place or does not loose its shape rapidly, then dehydration can be assumed.), the person is very pale, cold, clammy, and exhibits deep rapid respirations, an effort the body makes to eliminate excess carbon dioxide. The individual may also exhibit severe abdominal pain and tachycardia, (heart rate greater than 100 beats per minute.) Diagnostic laboratory findings from arterial blood gases would indicate a pH less than 7.35, blood glucose level greater than 250 mg/dL, serum bicarbonate level less than 15 mEq/L, as well as ketones in the urine.
Interventions must be immediate to prevent irreversible destruction to the body’s organs and prevent coma or death. Ensure a patent airway, and begin to administer oxygen via nasal cannula or mask. Establish an intravenous access with a large bore needle (18 to 20 gauge). Begin fluid stabilization with 0.9 Normal Saline. This is an isotonic fluid, compatible with the body’s pH. The purpose of using an isotonic infusion initially is to re-establish blood pressure which was low and to increase urinary out put to 30-60ml/hr. When urinary output is less than 30 ml/hr, kidney failure can rapidly occur. Fluids should continue for one hour or until stabilization occurs. Next begin insulin infusion with a drip rate or 0.1U/kg/hr. During this time it is important to monitor the person’s vital signs every fifteen minutes until stable or for at least one hours after treatment begins. If necessary, potassium should be administered to correct for hypokalemia, and sodium bicarbonate to correct for metabolic acidosis, if the pH is less than 7.0. The person should also have electrocardiogram leads placed on chest to monitor heart rhythms.
When the diabetic is at home and feels these bodily signs and symptoms beginning to occur, they should take the following steps; call 911, check their blood sugar, administer insulin per sliding scale, drink an electrolytic fluid, (i.e., sports fluids), breath into a paper bag, use oxygen if available, lie down, raise feet level with the heart and wait for the ambulance.
Preventative measures to avoid DKA include consistent control of blood sugar with administration of insulin per protocol. The diabetic should avoid too much food intake, and avoid taking too much or too little insulin. Stressful life situations can also cause elevations in glucose levels. Therefore the diabetic should prepare to check their blood sugar more often during times of stress and administer insulin as prescribed.
Understanding the complications of diabetes can help the diabetic take the necessary actions to prevent DKA from occurring and help them live a healthy life.
- Lewis, Heiitkemper, Dirkesen, Medical Surgical Nursing 6th ed., Copyright 2006, Mosby, St. Louis., pages 1273 -1278.
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