Common complications of DKA include hypoglycemia, hypokalemia, and recurrent hyperglycemia. These may be minimized by careful monitoring. Hyperchloremia is a common but transient finding that usually requires no special treatment. Cerebral edema is a rare but important complication of DKA. Although it can affect adults, it is more common in young patients, occurring in 0.
Papilledema, hypertension, hyperpyrexia, and diabetes insipidus also may occur. Patients typically improve mentally with initial treatment of DKA, but then suddenly worsen. Dilated ventricles may be found on CT or magnetic resonance imaging. Treatment of suspected cerebral edema should not be delayed for these tests to be completed. In more severe cases, seizures, pupillary changes, and respiratory arrest with brain-stem herniation may occur.
Once severe symptoms occur, the mortality rate is greater than 70 percent, and only about 10 percent of patients recover without sequelae. Avoiding overhydration and limiting the rate at which the blood glucose level drops may reduce the chance of cerebral edema. About 10 percent of the patients initially diagnosed with cerebral edema have other intracranial pathology such as subarachnoid hemorrhage. The main differences in the management of children and adolescents compared with adults are the greater care in administering electrolytes, fluids, and insulin based on the weight of the patient and increased concern about high fluid rates inducing cerebral edema.
Although DKA is less common in these patients than among those with type 1 diabetes, it does occur. C-peptide levels may be helpful for determining the type of diabetes and guiding subsequent treatment. Risk factors for adolescent type 2 diabetes are hypertension and acanthosis nigricans.
Older patients are less likely to be on insulin before developing DKA, less likely to have had a previous episode of DKA, typically require more insulin to treat the DKA, have a longer length of hospital stay, and have a higher mortality rate 22 percent for those 65 years and older versus 2 percent for those younger than 65 years.
A blood glucose concentration of less than mg per dL, a bicarbonate level of 18 mEq per L or greater, and a venous pH level of greater than 7. Intravenous insulin should continue for one to two hours after initiation of subcutaneous insulin. For patients who are unable to eat, intravenous insulin may be continued to maintain the blood glucose in a target range i. Prevention of another episode should be part of the treatment of DKA.
Most patients with DKA will need lifetime insulin therapy after discharge from the hospital. Education about diabetes is a cornerstone of prevention that also has been found to reduce length of stay. Information from references 49 through Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. Address correspondence to David E. Trachtenbarg, M. Reprints are not available from the author. Guest editor of the series is Eric Henley, M. Ketoacidosis in Apache Indians with non—insulin-dependent diabetes mellitus.
Arch Intern Med. Impact of a critical pathway on inpatient management of diabetic ketoacidosis. Diabetes Res Clin Pract. Diabetes Care. Management of hyperglycemic crises in patients with diabetes. Deaths associated with diabetic ketoacidosis and hyperosmolar coma. Med J Aust. Diabetic ketoacidosis in a patient with acromegaly. Med Sci Monit. Pasternak DP. Hemochromatosis presenting as diabetic ketoacidosis with extreme hyperglycemia. West J Med. Cooppan R, Kozak GP. Hyperthyroidism and diabetes mellitus.
An analysis of 70 patients. Association of diabetic ketoacidosis and acute pancreatitis: observations in consecutive episodes of DKA. Am J Gastroenterol. Fulminant diabetes mellitus associated with pregnancy: case reports and literature review.
Endocr J. New-onset diabetes and ketoacidosis with atypical antipsychotics. Schizophr Res. Steroid-induced diabetic ketoacidosis. Am J Med Sci. Diabetic ketoacidosis following glucagon therapy in acute pancreatitis. A case report. Ir Med J. Diabetes mellitus during interferon therapy for chronic viral hepatitis. Dig Dis Sci. Diabetic ketoacidosis and insulin resistance with subcutaneous terbutaline infusion: a case report.
Am J Obstet Gynecol. Fetal death associated with severe ritodrine induced ketoacidosis. Pickup J, Keen H. Continuous subcutaneous insulin infusion at 25 years: evidence base for the expanding use of insulin pump therapy in type 1 diabetes.
A case of diabetic non-ketotic hyperosmolar coma with an increase with plasma 3-hydroxybutyrate. Endocrinol Jpn. Stoner GD.
Hyperosmolar hyperglycemic state Am Fam Physician. Cessation of insulin infusion at night-time during CSII-therapy: comparison of regular human insulin and insulin lispro. Exp Clin Endocrinol Diabetes. Siperstein MD. Diabetic ketoacidosis and hyperosmolar coma. Endocrinol Metab Clin North Am.
Samuelsson U, Ludvigsson J. When should determination of ketonemia be recommended? Diabetes Technol Ther. The direct measurement of 3-beta-hydroxy butyrate enhances the management of diabetic ketoacidosis in children and reduces time and costs of treatment.
Diabetes Nutr Metab. Transient elevation of liver transaminase after starting insulin therapy for diabetic ketosis or ketoacidosis in newly diagnosed type 1 diabetes mellitus.
American Diabetes Association. Hospital admission guidelines for diabetes. Diabetic ketoacidosis—pathogenesis, prevention and therapy. Clin Endocrinol Metab. Efficacy of subcutaneous insulin lispro versus continuous intravenous regular insulin for the treatment of patients with diabetic ketoacidosis.
Am J Med. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Current perspectives on the use of continuous subcutaneous insulin infusion in the acute care setting and overview of therapy. Crit Care Nurs Q. Comparison of the effectiveness of various routes of insulin injection: insulin levels and glucose response in normal subjects.
J Clin Endocrin Metab. Comparative study of different insulin regimens in management of diabetic ketoacidosis. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis?
Prompt institution of dialysis is important as the diabetic patient may tolerate uraemia less well. Uncontrolled ketosis may worsen hyperkaliemia and metabolic acidosis.
Insulin requirements may be increased due to insulin resistance, or decreased due to impaired clearance of circulating insulin [ 38 , 56 ]. The vast majority of patients require intermittent haemodialysis. Patients with cardiac dysfunction or autonomic neuropathy tend to develop hypotension during treatment.
Also, anticoagulation with heparin may increase the risk of hemorrhage from proliferative retinopathy, therefore prostacyclin may be a safer alternative [ 52 ]. Peritoneal dialysis may be complicated by peritonitis and chest infections.
Also, haemodialysis allows greater fluid removal and remove restrictions for administration of drugs and nutrition [ 56 ]. Despite the strong prevalence of compromised immune status, constant state of protein malnutrition, frequent vascular accessing with a predisposition to significant infections, increased incidence of cardiovascular diseases, the occurrence of DKA in patients with chronic renal failure is quite rare.
Kidneys play a major role in insulin breakdown [ 38 ]; advanced chronic renal failure is associated with both insulin resistance and decreased insulin degradation. The latter may lead to a marked decrease in insulin requirement. Therefore, many patients see an improvement in glycemic control when they progress to haemodialysis. Furthermore, in hyperglycemic dialysis-dependent patients volume contraction due to osmotic diuresis is not encountered. Since glycosuria and osmotic diuresis account for most of the fluid and electrolyte losses seen in DKA, anuric patients may be somewhat protected from dehydration.
However they may still be prone to development of hyperkalemia and metabolic acidosis [ 37 ]. In persistent and long-lasting DKA, a substantial volume loss can still occur due to a prolonged decrease in oral intake or increased insensible water losses related to tachypnea and fever.
The uremic environment can affect methods used to assess glycemic control. Changes in dietary intake and exercise ie, reduced intake due to anorexia prior to starting dialysis can also affect the response to administered insulin.
In patients treated with peritoneal dialysis, glucose contained in peritoneal dialysate will tend to increase the need for hypoglycemic therapy. Therefore, the treatment of oliguric patient certainly differs from the wide accepted DKA treatment guidelines. First of all, end-stage-renal-disease patients with DKA may be less likely volume depleted; in most cases the extracellular volume is expanded from its baseline secondary to hyperglycemia.
The volume expansion may cause dyspnea, nausea, vomiting, seizures and coma [ 54 ]. In oliguric patient, fluid hydration in amounts usually administered in the DKA treatment may precipitate severe pulmonary edema. Therefore, the need for fluid resuscitation in these patients must be justified clinically or by laboratory testing and potential volume resuscitation should be performed carefully, using central venous access for continuous monitoring. When volume overload is apparent, immediate haemodialysis is the therapy of choice.
Metabolic control can be difficult to achieve. Insulin is normally metabolized by kidneys and in chronic renal failure insulin degradation is much slower. Furthermore, insulin is not excreted either by haemodialysis or peritoneal dialysis.
Hyperinsulinemia resulting from aggressive glucose — lowering therapies may easily lead to severe and prolonged hypoglycemia. One cannot readily predict insulin requirements in this setting and careful individualized therapy is essential.
As already emphasized, kidneys in end-stage renal disease are not able to contribute to the overall acid-base balance. Therefore, DKA in these patients may be both profound and prolonged. In addition, pulmonary dysfunction related to volume overload and sometimes underlying pulmonary infections can impair respiratory compensation to metabolic acidosis. Bicarbonate administration is rarely of value in DKA [ 55 ] and the associated volume, sodium and osmotic overload may be particularly problematic for anuric patients.
In this situation, significant metabolic acidosis will only be correctable by haemodialysis [ 53 ]. Total body concentration of potassium is unchanged, and patients with DKA and end stage renal failure frequently have a high serum potassium level.
Lack of insulin causes translocation of intracellular potassium to the extracellular compartment. Hyperglycemia causes hypertonicity of extracellular fluids, which also leads to shift of potassium from the cells to the extracellular compartment.
The important potassium — lowering effect of osmotic diuresis is missing. Even when testing reveals hypokalemia, total body potassium stores may be high, and these patients are unable to excrete a potassium load. Consequently, hypokalemia must be documented and acidosis corrected before potassium supplementation is initiated.
All dialysis patients presenting with significant symptoms should undergo immediate cardiac monitoring. If there is clinical suspicion or electrocardiographic evidence of hyperkalemia, they should receive immediate potassium lowering therapies, including emergent haemodialysis. In a study performed in USA in [ 1 ] the occurrence of diabetic ketoacidosis after renal transplantation was followed.
A female sex, recipients of cadaver kidneys, patients age 33—44 vs. However, the rate of diabetic ketoacidosis decreased more over time in tacrolimus users. Diabetic ketoacidosis was independently associated with increased mortality. In summary, acute renal failure rarely develops in patients with diabetic ketoacidosis, but it can be life-threatening. Insulin requirements may be increased due to insulin resistance, or decreased due to impaired clearance of circulating insulin.
Patients with uncontrolled diabetes may already be predisposed to hypophosphatemia. In the presence of metabolic acidosis, proximal tubular reabsorption of phosphate is inhibited, and the overall level of the extracellular phosphate is further reduced.
In cases of severe acidosis, phosphate replacement is of paramount importance. Indications for haemodialysis in patients with acute renal failure and DKA include oliguria, persistent metabolic acidosis resistant to standard therapy, fluid overload and hypertension. Early initiation of haemodialysis is not only effective against uremia and hypervolemia but also contribute to rapid correction of metabolic acidosis and hypophosphatemia.
The occurrence of DKA in patients with advanced chronic renal failure is quite rare. Chronic renal failure is associated both with insulin resistance and decreased insulin degradation. In oliguric patients, fluid hydration in amounts usually administered in DKA treatment may precipitate severe pulmonary edema. Sodium and osmotic overload may be particularly problematic for anuric patients. Pulmonary dysfunction due to frequent pulmonary infections can impair ventilatory compensation to metabolic acidosis.
Bicarbonate administration is rarely of value in DKA. In this situation, significant metabolic acidosis will only be correctable by haemodialysis. Most DKA patients on both peritoneal and haemodialysis are hyperkalemic and the potassium replacement in DKA is usually not necessary. Diabetic ketoacidosis is serious metabolic complication in diabetic patients with acute myocardial infarction, stroke and renal insufficiency.
Conversely, severe diabetic ketoacidosis is an important risk factor for acute myocardial infarction, stroke and acute renal failure. Acidosis in these patients is usually deeper, prolonged and resistant to therapy.
In all of the three conditions a fluid resuscitation in quantities commonly used in the treatment of DKA can not be performed. In addition, in many cases there is more or less marked insulin resistance. In chronic renal insufficiency, on the contrary, intensive insulin therapy usual for the treatment of ketoacidosis may carry a risk of hyperinsulinemia and prolonged hypoglycemia.
Electrolyte imbalance, especially potassium deficiency or excess can have serious consequences, especially in patients with myocardial infarction, and special care should be given to electrolyte monitoring. Finally, we believe that more attention should be paid to the possible acid-base disorders in diabetic patients suffering cerebrovascular insults. Clinical assesment in these cases is not sufficient because the significant overlapping of the signs and symptoms, therefore DKA symptoms may be attributed to cerebrovascular pathology.
The conclusions based on blood glucose levels would not be appropriate, since glycemia tends to be high in distressed patients. Acid-base status should be determined routinely, along with glycemia and HbA1c in all diabetics affected by stroke in order to prevent misdiagnosis. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers.
Login to your personal dashboard for more detailed statistics on your publications. Edited by Alan Escher. Edited by Oluwafemi Oguntibeju. We are IntechOpen, the world's leading publisher of Open Access books. Built by scientists, for scientists. Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Introduction Diabetic ketoacidosis DKA is considered a predominantly acute type 1 diabetic complication, although it may occur in type 2 diabetes as well, particularly in patients who already have a decreased insulin secretion capacity.
Acute MI is seen with higher frequency in patients with diabetes and is associated with greater morbidity and mortality than in patients without diabetes. During DKA events, the myocardium is denied glucose uptake because of high levels of ketones and free fatty acids, leading to myocardial ischemia. This can further exacerbate the cardiovascular damage that has already occurred from acute MI.
Additional tissue damage occurs in the heart due to increased levels of free radicals. As previously mentioned, during states of acidosis there is an increase in catecholamine release. This increase prevents any reserve insulin secretion, exacerbating lipolysis and cardiac tissue uptake of free fatty acids, thereby further injuring the myocardium with toxic fatty acids.
The cardiac muscle is susceptible to minor changes in the pH of extracellular fluid in regard to ion exchange with intracellular fluid. In states of acidosis, there is an increase in hydrogen ions, and this increase affects multiple organelles within the myocardium. Low pH reduces the calcium concentration, resulting in less tension generated by myofibrils.
In fact, tissue acidosis in myocardial ischemia develops just before or at the onset of contractility failure. In cases of extreme acidosis, necrosis can occur in the myocardium. The treatment for ketoacidosis involves insulin and potassium replacement, which are both considered high-alert medications per the Institute for Safe Medication Practices ISMP.
Extra precautions to help reduce medication errors are necessary for these drugs, such as high-alert auxiliary labels placed by the pharmacist and automated alerts. Administering these medications in a timely manner is important to prevent patient complications. Pharmacists should be directly involved in the standardized process for ordering, storing, and preparing the drugs administered for ketoacidosis to ensure accuracy and help prevent medication errors.
A pharmacist can also be a valuable source of drug information for these medications when questions arise among medical staff. In the community and ambulatory care settings, pharmacists can also be valuable assets to educate patients on prevention of DKA and AKA. These pharmacists often see patients on a more frequent basis and can play a pivotal role in educating patients on the signs and symptoms of acidosis, and when to seek urgent medical care.
Furthermore, these pharmacists have access to important information about patient medication compliance, and when an intervention may be necessary to prevent the development of ketoacidosis. Patients with diabetes should be educated to not stop their insulin abruptly without consulting their physician and to monitor for signs and symptoms of ketoacidosis in times of acute illness.
Alcoholics should be educated on their risk of complications such as ketoacidosis and referred for alcohol abuse counseling. DKA and AKA are serious metabolic emergencies that can result in cardiovascular complications due to electrolyte disturbances with potassium, magnesium, and phosphorus.
Acute cardiovascular changes can also occur due to catecholamine release. Pulmonary edema and respiratory failure are secondary conditions that can occur as a result of ketoacidosis, and myocardium ischemia can be further exacerbated by ketoacidosis during acute MI. It is important to immediately start treatment for patients with ketoacidosis because successful management can prevent potentially life-threatening cardiovascular complications.
DuBose TD Jr. Acidosis and alkalosis. Accessed October 6, Acid-base balance. Principles of Critical Care. Letter to the editor: measured values incompatible with human life. Kishore P. Diabetic ketoacidosis. Merck Manual Professional Version. June 1, Accessed January 20, Respiratory failure in diabetic ketoacidosis.
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