Diabetic Ketoacidosis

OBJECTIVES: After the session the students will be able to: 1. Know Diabetic Ketoacidosis 2. Apply proper nursing care when this kind of situation happens 3. Help in the prevention of DKA by giving education to those patients with DM.

Definition: is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Causes This condition is known as ketoacidosis. First sign of type 1 diabetes in people who do not yet have other symptoms. Diagnosed with type 1 diabetes. Infection, injury, a serious illness, missing doses of insulin shots, or surgery can lead to diabetic ketoacidosis in people with type 1 diabetes. People with type 2 diabetes can also develop ketoacidosis, but it is less common. It is usually triggered by uncontrolled blood sugar or a severe illness Risk Factors : have type 1 diabetes are under the age of 19 have had some form of trauma, whether emotional or physical have a high fever have had a heart attack or stroke smokers abuse drugs or alcohol Although DKA is rare in people who have type 2 diabetes, those who have type 2 diabetes and are of African-American or Hispanic descent are more likely to develop it than those who arent. Signs and Symptoms: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue

Shortness of breath Fruity-scented breath Confusion Dry skin and mouth

More-specific signs of diabetic ketoacidosis which can be detected through home blood and urine testing kits include: High blood sugar level (hyperglycemia) High ketone levels in your urine Laboratory Tests Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: Blood sugar level. If there isn't enough insulin in the body to allow sugar to enter cells, blood sugar level will rise (hyperglycemia). As the body breaks down fat and protein for energy, the blood sugar level will continue to rise. Ketone level When the body breaks down fat and protein for energy, toxic acids known as ketones enter the bloodstream. Blood acidity If the patient has excess ketones in the blood, the blood will become acidic (acidosis). This can alter the normal function of various organs throughout the body. Serum electrolyte levels. Serum potassium levels initially are high or within the reference range in patients with DKA. This is due to the extracellular shift of potassium in exchange of hydrogen, which is accumulated in acidosis, in spite of severely depleted total body potassium. This needs to be checked frequently, as values drop very rapidly with treatment. An ECG may be used to assess the cardiac effects of extremes in potassium levels. The serum sodium level usually is low in affected patients. The osmotic effect of hyperglycemia moves extravascular water to the intravascular space. For each 100 mg/dL of glucose over 100 mg/dL, the serum sodium level is lowered by approximately 1.6 mEq/L. When glucose levels fall, the serum sodium level rises by a corresponding amount.Additionally, serum chloride levels and phosphorus levels always are low in these patients. Amylase levels Hyperamylasemia may be seen in patients with diabetic ketoacidosis, even in the absence of pancreatitis. Urine dipstick The urine dipstick test is highly positive for glucose and ketones. Rarely, urine is negative for ketones, due to the fact that most available laboratory tests can detect only acetoacetate, while the predominant ketone in severe untreated DKA is beta-hydroxybutyrate.When the clinical condition improves with treatment, the urine test result becomes positive due to the returning predominance of acetoacetate. Serum or capillary beta-hydroxybutyrate levels can be used to follow response to treatment in patients with DKA. levels greater than 0.5 mmol/L are considered abnormal, and levels of 3 mmol/L correlate with the need for treatment for DKA. Bicarbonate levels Use bicarbonate levels in conjunction with the anion gap to assess the degree of acidosis that is present.

CBC count Even in the absence of infection, the CBC count shows an increased white blood cell (WBC) count in patients with diabetic ketoacidosis. High WBC counts (>15 X 109/L) or marked left shift may suggest underlying infection. BUN level BUN frequently is increased in patients with diabetic ketoacidosis. Urine and blood cultures Urine and blood culture findings help to identify any possible infecting organisms in patients with diabetic ketoacidosis. ECG DKA may be precipitated by a cardiac event, and the physiological disturbances of DKA may cause cardiac complications. An ECG should be performed every 6 hours during the first day, unless the patient is monitored. An ECG may reveal signs of acute myocardial infarction that could be painless in patients with diabetes, particularly in those with autonomic neuropathy. An ECG is also a rapid way to assess significant hypokalemia or hyperkalemia. T-wave changes may produce the first warning sign of disturbed serum potassium levels. Low T wave and apparent U wave always signify hypokalemia, while peaked T wave is observed in hyperkalemia. Note that high serum glucose levels may lead to delusional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. LABORATORY FINDINGS Glycosuria of 4+ and strong ketonuria with hyperglycemia, ketonemia, low arterial blood pH, and low plasma bicarbonate are typical of diabetic ketoacidosis. Serum potassium is often elevated despite total body potassium depletion resulting from protracted polyuria or vomiting. Elevation of serum amylase is common but often represents salivary as well as pancreatic amylase. Thus, in this setting, an elevated serum amylase is not specific for acute pancreatitis. Serum lipase may be useful if the diagnosis of acute pancreatitis is being seriously considered. Azotemia (medical condition characterized by abnormally high levels of nitrogen-containing compounds, such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds in the blood) may be a better indicator of renal status than serum creatinine, since multichannel chemical analysis of serum creatinine (SMA-6) is falsely elevated by nonspecific chromogenicity of keto acids and glucose. Most laboratories, however, now routinely eliminate this interference. Leukocytosis as high as 25,000/mcL with a left shift may occur with or without associated infection. The presence of an elevated or even a normal temperature would suggest the presence of an infection, since patients with diabetic ketoacidosis are generally hypothermic if uninfected. Imaging tests Radiologic studies that may be helpful in patients with DKA include the following: Chest radiography: To rule out pulmonary infection such as pneumonia

Head CT scanning: To detect early cerebral edema; use low threshold in children with DKA and altered mental status Head MRI: To detect early cerebral edema (order only if altered consciousness is present

Do not delay administration of hypertonic saline or mannitol in those pediatric cases where cerebral edema is suspected, as many changes may be seen late on head imaging.

Treatment Fluid replacement. Patient will receive fluids either orally or through a vein (intravenously) until rehydrated. The fluids will replace those who are lost through excessive urination, as well as help dilute the excess sugar in the blood. Electrolyte replacement. Electrolytes are minerals in the blood that carry an electric charge, such as sodium, potassium and chloride. The absence of insulin can lower the level of several electrolytes in the blood. Patient may receive electrolytes through IV to help keep heart, muscles and nerve cells functioning normally. Insulin therapy. Insulin reverses the processes that cause diabetic ketoacidosis. Along with fluids and electrolytes, the patient will receive insulin therapy usually through a vein. When the blood sugar level falls below 240 mg/dL and the blood is no longer acidic, The doctor might order to stop the intravenous insulin therapy and resume to the normal subcutaneous insulin therapy. NURSING IMPLICATIONS Dehydration: The patient in DKA is treated initially with intravenous fluids, progressing to oral fluids as the patient's condition improves. Urinary output, vital signs and specific gravity are monitored closely in order to evaluate the effectiveness of fluid replacement. Normal saline is usually the IV solution of choice. The adult fluid deficit is approximately 6-12 liters. Insulin: Patients in DKA require rapid-acting insulin. Regular insulin U-100 is administered IVP, or in severe cases of DKA, an insulin drip is started. Insulin is given until the blood sugar reaches about 250mg/ml. An insulin drip consists of placing 100 units of regular insulin in 500cc's of D5W solution. The drip is then titrated according to the desired dosage per hour. Electrolytes: Electrolyte replacement is managed based on laboratory results. As hydration progresses, laboratory values will change as the electrolytes move from compartment to fluid compartment. Potassium replacement becomes more crucial with the administration of insulin. Insulin causes potassium to move into the intracellular compartment at the time acidosis is corrected. Potassium chloride is given IV up to 10 mEq/hour or 100 -200 mEq/day. Magnesium sulfate is administered up to 2 mEq/kg every four hours. Sodium and phosphate are given as required by laboratory findings. NURSING DIAGNOSIS AND INTERVENTIONS: Nursing Diagnosis: Deficient fluid volume r/t osmotic diuresis associated with hyperglycemia.

Interventions: Administer IV fluids and increase fluid intake. Measure blood glucose levels every hour and administer insulin per sliding scale orders. Blood glucose levels are at crisis level, and close monitoring prevents further complications of DKA. Monitor VS especially cardiac output with lab tests and or ECG. Close cardiac monitoring is necessary for the patients critical condition. Assess hydration status every hour by monitoring: urine specific gravity, I&O, skin turgor and vital signs. Detects subtle changes in the hydration status of the patient. Nursing Diagnosis: Ineffective breathing pattern of Kussmaul respirations r/t metabolic acidosis associated with DKA. Interventions: Monitor O2 sat levels and Respiratory rate, rhythm and depth every hour. Detects respiratory compensation. Assess LOC with GCS monitoring. Provides constant monitoring of neurological status. Ask patient questions about the level of her energy and ask patient to quantify from 1-10 the level of her fatigue every hour. Evaluate fatigue levels on constant basis. Possible Complications Fluid buildup in the brain (cerebral edema) Heart attack and death of bowel tissue due to low blood pressure Kidney failure Treatment complications include: Low blood sugar (hypoglycemia). Low potassium (hypokalemia). Swelling in the brain (cerebral edema). If Left untreated, the risks are much greater. Diabetic ketoacidosis can lead to loss of consciousness. Eventually, diabetic ketoacidosis can be fatal. PREVENTION
Make a commitment to managing diabetes.Make healthy eating and physical activity part of the

daily routine. Take oral diabetes medications or insulin as directed.

Monitoring blood sugar levels. Careful monitoring is the only way to make sure that the blood sugar

level remains within target range.

Adjust insulin dosage as needed. Check ketone level. When ill or under stress, test the urine for excess ketones with an over-the-

counter urine ketones test kit. If the ketone level is moderate or high, contact the doctor right away or seek emergency care.
Be prepared to act quickly. If you suspect that the patient has diabetic ketoacidosis blood sugar

level is high and excess ketones in the urine seek emergency care.