Diabetic Ketoacidosis

DIABETIC ketoacidosis INTRODUCTION diabetic ketoacidosis (DKA) is a really real complication of diabetes mellitus, a metabolous rowdiness that is characterized by hyperglycemia, metabolic acidosis, and change magnitude consistence ketone concentrations. The well-nigh special K excites of DKA atomic number 18 contagion and poor compliance with medication regimens. opposite get tos include undiagnosed diabetes, alcohol abuse, and a multitude of aesculapian conditions such as cerebrovascular accident (CVA), obscure pregnancy, myocardial infarction, pancreatitis, and stress. diabetic ketoacidosis is a complicated pathology.Early recognition of DKA, a good pinch of the pathological processes of DKA, and aggressive manipulation argon the keys to successful treatment. With good cargon, DKA apprise be managed and the unhurried will survive. OBJECTIVES When the student has spot slight studying this module, he/she will be able to 1. secern the correct rendering of DKA. 2. discoer a basic portion of insulin. 3. come out(a) the insulin derangements of types I and II diabetes. 4. locate the basic cause of DKA. 5. Identify both specific causes of DKA. 6. Identify the cardinal unwellnessful mechanisms that produce the signs/symptoms of DKA. . Identify metabolic consequences of increased hormone concentrations in DKA. 8. Identify the criteria use to diagnose DKA. 9. Identify putting green signs and symptoms of DKA. 10. Identify science lab ab hauntities seen in DKA. 11. Identify complications of DKA. 12. Identify the three well-nigh alpha therapies for treating DKA. 13. Identify the correct roles of atomic number 11 hydrogen carbonate and ortho ortho ortho orthophosphate in treating DKA. 14. Identify an important recipe for using atomic number 19 electric switch in DKA. 15. Identify an important rule for displacement from IV to subcutaneous insulin.EPIDEMIOLOGY to the highest degree cases of DKA be seen in persevering roles with typ e I diabetes, still nigh 10%-30% of all cases of DKA march on in tolerant of roles with type II diabetes. 1 The relative incidence of DKA appears to be rising, and this whitethorn non be related to to the well air increase in the incidence of diabetes that has twist a serious public health problem. 2 diabetic ketoacidosis accounts for 50% of all diabetes-related admissions in young spate with the disease, and DKA is the most super C cause of diabetes-related demise in children and adolescents with type I diabetes. diabetic ketoacidosis is oft more familiar in children than in crowings, it is more common in women than in men, and it is more common in Caucasians. 4 The exact incidence of death from DKA is non ben, but it has been estimated to be amid 1%-10%. 5 endurance depends on the severity of the case, the age of the patient, the aim/absence of certain medical conditions, and how right away DKA is recognized and how effectively it is inured. If the condit ion is straightaway diagnosed and decently treated, the mortality invest send word be 250 mg/dL) metabolic acidosis ( broth pH ? . 30) and an high-minded aim of melodic line rip serum ketones ( 5 meq/L) and/or ketones in the urine. 11 Patients will in addition keep up an anion opening (Na+ Cl- + HCO3-), an high-minded store urea newton (BUN), hyponatremia, hyperkalemia, and the serum amylase whitethorn be elevated. The numerate personate phosphate level whitethorn be low but the serum level may be linguistic rule or elevated. At this time, there is no universally agreed upon consensus for the symptomatic criteria of DKA, and about sources feel that an anion gap 10-12 meq/L and serum bicarbonate (HCO3) ? 8 milliequivalent/L should be break apart of the criteria. learn break up Some authors feel that most important test for diagnosing DKA is sum blood ketone concentration. 12,13 The acidosis and hyperglycemia of DKA and the electrolyte changes that are s o commonly seen in DKA are well related. The commute in metabolism and the full(prenominal) concentration of acidic ketones seen in cases of DKA produces a metabolic acidosis. Acidosis and insulin deficiency causes special K to gaolbreak from the intracellular billet to the extracellular space and serum hyperkalemia is common.However, the osmotic diuresis that is characteristic of DKA causes grand to be excreted in the urine although the serum thou level may be high, the patient may be deeply depleted. Sodium and phosphate are excessively excreted by the osmotic diuresis, and hyponatremia is common. However, the serum phosphate level is ofttimes falsely normal or falsely elevated because phosphate, ilk super C, is excreted in the urine but acidosis induces phosphate to move from the intracellular space to the extracellular space.The serum level index be normal, but the actual total torso load is low. Learning Break The serum glucose merchantman be very elevated in seve re cases of DKA. However, serum glucose good deal be close to normal, and approximately 10% of patients with DKA will be euglycemic with a serum glucose ? 250 mg/dL. 14 COMPLICATIONS OF DIABETIC KETOACIDOSIS Patients who stupefy diabetic ketoacidosis that is instantly recognized and promptly and correctly treated should survive. The complications of DKA are complications of treatment and cerebral edema.Treatment complications are hypoglycemia, hyperkalemia, and occasionally pulmonary edema. These mess be avoided by using low-dose insulin therapy, monitoring blood glucose very closely, and by handlefully managing liquified renewal. Cerebral edema is a very serious complication of DKA. It occurs in approximately 1% of all children with DKA, but the mortality rate and the rate of neurological sequelae for these children perk up both been reported to be 21%, and the mortality rate and rate of sequelae contribute be as high as 24% and 26% respectively15,16 Adults with DKA rarely become cerebral edema. 7 Signs and symptoms include intellectual experimental condition changes, bradycardia, seizures, abnormal response to pain, and decorticate and decerebrate posturing. TREATMENT FOR DIABETIC KETOACIDOSIS The most important treatments for DKA are fluid replacement, insulin therapy, and correcting electrolyte balances. nurse baseline serum electrolytes, BUN, creatinine, serum glucose, an arterial or venous blood shoot a line (either one is admit), a complete blood count, an ECG, and a CXR. Consider different laboratory studies if DKA is thought to be caused by an vestigial disease. Fluid replacement Fluid replacement will replace the fluid deficit, assist simplification the blood glucose level, and maintain renal function. If the patient is severely hypovolemic, lend 1 litre of 0. 9% atomic number 11 chloride over 30 minutes. If the patient is mildly dehydrated, defend the serum atomic number 11. If it is normal or high, enforce 0. 45% sodium chlo ride IV at a rate of 250-500 mL/h. If the serum sodium is low, give 0. 9% sodium chloride IV at a rate of 15-20 mL/kg per minute of arc. formerly the blood glucose is approximately dickens hundred mg/dL, a solution of % dextrose with 0. 45% sodium chloride dismiss be used. 18Learning Break In the first minute of arc of treating a patient with DKA, fluid replacement is more important than insulin therapy and should take precedent. 19,20 Insulin therapy Insulin is a critical part perhaps the critical part of the treatment of DKA. It can be given as an IV infusion or frequent subcutaneous injections they are equally effective. Most clinicians prefer the IV route as the onset of put through is quicker and the half-life is shorter with the IV route than the onset of action of and half-life of insulin given subcutaneously because of that, therapy can be closely monitored.The American Diabetes stand recommends giving an initial IV bolus of unremitting insulin, 0. 1 U/kg. (Note If the serum thousand is 3. 3 milliequivalent/L insulin should not be given). Following the bolus dose, start a free burning IV infusion of uninterrupted insulin at a rate of 0. 1 U/kg/h. An alternative is to escape the bolus dose and start a continuous IV infusion of regular insulin at a rate of 0. 14 U/kg/h. If the serum glucose does not decrease by 10% within an hour of starting the insulin, give 0. 14 U/kg as a bolus dose, indeed continue the IV infusion.Once the serum glucose is 200 mg/dL, reduce the insulin dose to 0. 02-0. 05 U/kg/h or give subcutaneous doses of rapid-acting insulin, 0. 1 U/kg either two hours. The goal at this point is to keep the serum glucose in the midst of 150-200 mg/dL. 21 0. 1 U/kg IV bolus v 0. 1 U/kg/hr * v When serum glucose 200 mg/dL, decrease infusion to 0. 02-0. 05 U/kg/h v Keep serum glucose between 150-200 mg/dL until DKA resolves * If serum glucose doesnt v by at to the lowest degree 10% in the 1st hour of insulin therapy, give an IV bolus of 0. 14 U/kg and adjust the infusion. Correcting electrolyte imbalances If the serum super C is 3. 3 mEq/L, do not start insulin therapy and give 20-30 mEq of potassium per hour until the serum level is 3. 3 mEq/L. Fluid replacement and insulin therapy overturn blood sugar and correct acidosis and they also move potassium into the cells. If the serum potassium is 3. 3 mEq/L, serious arrhythmias could result. Once the hypokalemia has been corrected, insulin therapy can be started, and 20-30 mEq of potassium can be added to each liter of IV solution in enounce to maintain a serum potassium level between 4. -5. 0 mEq/L. Learning Break Serum glucose and serum potassium should be checked every hour until the patient is stable. Two other considerations for treatment are administering sodium bicarbonate to help correct the acidosis and replacing phosphate losses. Using sodium bicarbonate is controversial. sinful acidosis can decrease myocardial contractility, can cause and prolong coma, shifts the oxyhemoglobin dissociation curve to the right, and so forth , so correcting an acidosis would contain the appearance _or_ semblance important. However, there are risks involved (e. g. make tree trunk hypokalemia worse, cerebral edema), there are some(prenominal) clinical studies that indicate sodium bicarbonate therapy is not effective for patients with DKA, and for umteen patients the acidosis will correct with fluids and insulin and because they perplex suitable stores of bicarbonate. 22 The use of sodium bicarbonate should not be standard feel for for DKA. However, the American Diabetes Association does recommend that if a patient has a severe acidosis with a pH 6. 9, the patent should receive deoxycytidine monophosphate mEq of NaHCO3 in 400 mL IV fluid along with 20 mEq of potassium chloride this should be infused at 200 mL/h.Repeat this every two hours until the pH is ? 7. 0. 23 Low phosphate levels will usually correct as the hyperglycemia and acidosis are corrected, and phosphate replacement is not standard care for DKA. However, if the phosphate is very low 1. 0 mg/dL or the patient has anemia, cardiac disease, or hypoxia, 20-30 mEq of phosphate can be given. 24,25 SWITCHING TO SUBCUTANEOUS INSULIN diabetic ketoacidosis is considered to be resolved when the blood glucose is 200 mg/dL and at least two of these laboratory set are present a venous pH 7. 3, an anion gap 12 mEq/L, and a serum bicarbonate level 15. mEq/L. 26 If these laboratory value are present and the patient can eat, it is safe to start subcutaneous insulin. intravenous insulin should be continued for one to two hours after the first dose of subcutaneous insulin has been given. If this is not done, hyperglycemia and ketosis may recur. NURSING CARE, PREVENTION AND EDUCATION When providing care for a patient in the slap-up phase of DKA, the nurse should focus on hydration status/fluid replacement, monitoring of acid-base status, serum glucose, and serum electrolytes, close observation of the patients neurological status, and vital signs.Once a case of DKA has resolved it is important to know why it happened. Infections, medical conditions, and drugs are common causes of DKA. However, one of the most important causes of DKA is patient non-compliance with diabetic treatment regimens patients do not take their medication or do not take them properly, they erupt to observe their prescribed diet and lifestyle plans, and they do not or cannot understand the bedrock of self-care and prevention as they relate to diabetes.If non-compliance was the cause of a particular case of DKA, it is very important to determine why the non-compliance occurred, and there many possible reasons. Some of the more common ones are Poor introduction to medical care The patient may not have access to health care cultivation, may not have easy access to a physician, clinic, etc. , may not have or not know how to use society or public access hea lth care resources. The patient may not have money for medications. Lack of information The patient may have a poor brain of diabetes, and the patient may not understand the treatment regimens that have been prescribed. Lack of information can be damaging in many ways. If the patient doesnt understand the disease of diabetes, he/she might be less involuntary to comply with lifestyle and diet restrictions and less willing to take medications. The patient would not recognize possible warning signals of DKA. aroused issues For many people, diabetes requires lifestyle changes that they may not be willing to emotionally accept.Learning Break Although it may be said that non-compliance happens when the patient fails to provide good self-care, the word fail typically has a negative connotation. Also, when many people hear the term non-compliance, they imagine of a person willfully weakness to do what he/she knows is best. However, there are many cases of non-compliance that happen be cause the patient has not been properly educated, or doesnt have or doesnt know how to push the resources he/she needs.So when it has been determined that non-compliance was the cause of a particular case of DKA, interview the patient and find out a) the emotional uphold of diabetes on the patients life, b) how much he/she knows about the disease and the treatments, and c) what financial, medical, personal, and cordial resources the patient has available for self-treatment. Some of these issues moldiness be addressed by kindly workers, psychologists, or the patients physician. However, nurses have a primary role in supporting and educating patients who have had an incident of DKA related to on-compliance. The nurse will often be the first person to find out that the patient did not seek medical attention for an contagion because of financial concerns, or due to inability to each a physician, or because of a lack of understanding of the implications of infection in diabetes. The nurse must then discuss making the appropriate referrals and then set up a teaching plan. Some of the nursing diagnoses that might apply in theses situations would be disturbed nutrition, noncompliance, knowledge deficient, and risk for injury. SUMMARY diabetic ketoacidosis is a metabolic disturbance characterized by hyperglycemia, metabolic acidosis, and elevated body ketone concentrations. The basic cause of DKA is insulin deficiency, absolute or relative. The insulin deficiency most often occurs because of infection or non-compliance with diabetic treatment regimens. supererogatory hormone concentration and a metabolic shift are the pathogenic mechanisms that cause the signs and symptoms of DKA. The hormone concentrations cause hyperglycemia, and the metabolic shift causes acidosis and elevated body ketones. The basic diagnostic criteria for DKA are a blood glucose 250 mg/dL, a serum pH 7. 3, and elevated serum and/or urine ketone concentrations. separate important cri teria are an anion gap 10-12 mEq/L and serum bicarbonate (HCO3) ? 18 mEq/L. Hyperkalemia and hyponatremia are common in DKA. Hypophosphatemia can be seen. However, the total body load of potassium and phosphate is often low. Common signs and symptoms include dehydration, mental status changes, polydipsia, polyuria, vomiting, weakness, and weight loss. Complications of DKA include complications caused by treatment and cerebral edema. Treatment for DKA should focus on fluid replacement, insulin therapy, and correcting electrolyte abnormalities. Sodium bicarbonate is not standard care. If DKA if promptly recognized and properly an aggressively treated, patients should survive. REFERENCES 1. Wilson JF. In the clinic diabetic ketoacidosis. recital of internal Medicine. 2010 152ITC-1-ITC-16. 2. Kitabchi AE, Umpierrez GE, Miles JM, fisher cat JN. Hyperglycemic crises in boastful patients with diabetes. Diabetes Care. 2009321335-1343. 3. Wolfsdorf J, Glaser N, Sperling MA.diabetic ketoacidosis in infants, children, and adolescents a consensus pedagogy from the American Diabetes Association. Diabetes Care. 2006291150-1159. 4. Hamdy O. diabetic ketoacidosis. eMedicine. September 9, 2009. in stock(predicate) at http//emedicine. medscape. com/ denomination/118361. Accessed celestial latitude 24, 2010. 5. Hamdy O. Diabetic ketoacidosis. eMedicine. September 9, 2009. Available at http//emedicine. medscape. com/ article/118361. Accessed December 24, 2010, 6. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009321335-1343. . Rucker DW. Diabetic ketoacidosis. eMedicine. June 4, 2010. 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