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Diabetic Ketoacidosis. A Review

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  1. 1. JOURNAL CLUB BRITISH MEDICAL JOURNAL: DIABETIC KETOACIDOSIS Dr. Sujay Iyer
  2. 2. TABLE OF CONTENT Introduction Definition Diagnosis Epidemiology Pathophysiology Etiology Clinical Presentation Laboratory Evaluation Management Complications Topics of discussion References
  3. 3. INTRODUCTION Diabetic Ketoacidosis is an acute, major, life- threatening complication of Diabetes. It mainly occurs in patients with Type 1 Diabetes but it is not uncommon in some patients with type 2 diabetes. The overall mortality rate for DKA is 0.2-2%, being at the highest in developing countries.
  4. 4. DEFINITION DKA is an extreme metabolic state caused by insulin deficiency. It is defined as an acute state of severe uncontrolled diabetes associated with ketoacidosis that requires emergency treatment. It is a state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration and acidosis-producing derangements in intermediary metabolism.
  5. 5. DIAGNOSIS Triad of hyperglycemia, anion gap metabolic acidosis and ketonemia. ADA (2009) Glucose> 13.9 mmol/L (250 mg/dl). Bicarbonate< 18mmol/L; pH< 7.3. Ketones positive result for urine or serum ketones by nitroprusside reaction. JBDS (2013) Glucose> 11 mmol/L (200 mg/dl) or known Diabestes. Bicarbonate< 15mmol/L or pH< 7.3 or both. Ketones> 3mmol/L or (++) in urine dipstick.
  6. 6. EPIDEMIOLOGY DKA accounts for 14% of all hospital admissions of patients with diabetes and 16% of all diabeties- related fatalities. DKA is frequently observed in diagnosis of type 1 diabetes and often indicates this diagnosis (3%). It occurs primarily in patients with type 1 diabetes, but can also occur in type 2 patients. The incidence of DKA in developing countries is higher. It is far more common in young patients.
  7. 7. PATHOPHYSIOLOGY DKA is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis and ketonuria. It usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (i.e, glucagon, cortisol, growth hormone, epinephrine). This imbalance enhances hepatic gluconeogenesis, glycogenolysis, lipolysis and ketogenesis.
  8. 8. PATHOGENESIS ALGORITHM
  9. 9. ETIOLOGY Inadequate insulin treatment or noncompliance. New onset diabetes (20-25%) Acute illness - Infection (30 to 40%) - CVA - Acute MI - Acute pancreatitis Drugs - Clozapine or olanzapine - Cocaine - Lithium - SGLT2 inhibitors - Terbutaline
  10. 10. CLINICAL PRESENTATION: SYMPTOMS DKA usually evolves rapidly, over a 24 hour period. Earliest symptoms are polyuria, polydipsia and weight loss. Nausea, vomiting and abdominal pain are usually present. Malaise, generalized weakness and fatigability. As the duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation can develop. Frank coma is uncommon in DKA.
  11. 11. CLINICAL PRESENTATION: SIGNS Ill appearance. Labored respiration (Kussumaul). Dry mucous membranes, dry skin and decreased skin turgor. Decreased reflexes. Characterstic ketotic breath odor. Tachycardia Hypotension Tachypnea Hypothermia/ Fever (if infection is present) Confusion Coma Abdominal tenderness.
  12. 12. LABORATORY EVALUATION Blood test for glucose every 1-2 hour. ABG/ VBG. Serum electrolyes (includes phosphate) Renal function test. Urine dipstick test (acetoacetate). Serum ketones (3-hydroxybetabutyrate). CBC. Anion gap. Osmolarity. Cultures. Amylase. Repeat lab investigations are key!
  13. 13. MANAGEMENT Correction of fluid loss with intravenous fluids. Correction of hyperglycemia with insulin. Correction of electrolyte disturbances, particularly potassium loss. Correction of acid-base balance. Treatment of concurrent infection, if present.
  14. 14. MANAGEMENT ALGORITHM
  15. 15. CORRECTION OF FLUID LOSS It is a critical part of treating patients with DKA. Use of isotonic saline. 15-20mL/kg/hour for the first few hours. Recommended schedule: - Administer 1-3 L during first hour. - Administer 1 L during second hour. - Administer 1 L during the following 2 hours. - Administer 1 L every 4 hours, depending on the degree of dehydration and CVP. When patient becomes euvolemic, switch to 0.45% saline is recommended, particularly if hypernatremia exists.
  16. 16. INSULIN THERAPY Insulin therapy to be initiated only if potassium levels are above 3.3 mEq/L. Intravenous regular insulin preferred. Initiated with IV blous of regular insulin (0.1 units/kg) followed by continuous infusion of regular insulin of 0.1 units/kg/hour. SC route may be taken in uncomplicated DKA (0.3 U/kg then 0.2 U/kg one hour later). When serum glucose reaches 200 mg/dl, reduce insulin infusion to 0.02-0.03 U/kg/hour and switch the IV saline solution to dextrose in saline. Revert to SC insulin, after patient begins to eat (continue IV infusion simultaneously for 1 to 2 hours).
  17. 17. POTASSIUM REPLACEMENT If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride is started with saline (20 to 40 mEq/hour). If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCl (20 to 30 mEq) is added to each liter of IV replacement fluid and continued until the serum potassium concentration has increased to the 4.0 to 5.0 mEq/L range. If the serum potassium is initially greater than 5.3 mEq/L, then potassium replacement should be delayed.
  18. 18. CORRECTION OF ACIDOSIS Bicarbonate therapy is a bone of contention among physicians and still remains a controversial subject, as clear evidence of benefit is lacking. Bicarbonate therapy is only administered if the arterial pH is less than 6.9. 100 mEq of sodium bicarbonate in 400 mL sterile water is administered over two hours. Repeat doses until pH rises above 7.0. Bicarbonate therapy has several potential harmful effects.
  19. 19. COMPLICATIONS CVT Myocardial Infarction DVT Acute gastric dilatation Erosive gastritis Late hypoglycemia Respiratory distress Infection (UTI) Hypophosphatemia Mucormycosis CVA Cerebral edema (rare in adults)
  20. 20. TOPICS OF DISCUSSION ABG or VBG (Kelly Am et al. & Ma OJ et al.) Insulin when? (S Arora et al.) Bicarbonate therapy: to use or not to use? (Chua et al. & Duhon et al.) Utility of insulin bolus (Goyal et al.) Euglycemic DKA: Its not a myth (Peters et al.) Which fluid? (3 Studies) Insulin How? (4 Studies) Transition from IV to SC insulin (O Malley et al. & Avanzini et al.).
  21. 21. ABG OR VBG? Study #1: Kelly AM et al. Review Article Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care (2010) For pH, mean difference was found to be 0.02. For bicarbonate, mean difference was found to be -1.41 mmol/L. Study #2: Ma OJ et al. - Arterial Blood Gas Results Rarely Influence Emergency Physician Management of Patients with Suspected Diabetic Ketoacidosis ABG analysis changed ED physicians diagnosis in 1% of patients. ABG analysis changed ED physicians treatment in 3.5% of patients (Change from SQ to IV insulin or vice versa). ABG analysis changed patient disposition in 2.5% of patients. Venous pH correlated well with arterial pH with difference of - 0.015 +/- 0.006 pH units.
  22. 22. ABG OR VBG Other Reasons ABGs can cause radial artery spasm, infarct, and/or aneurysms ABGs are painful to patients, even more so than IV access By the way, when is the last time you checked a Modified Allens Test before doing a radial ABG? The VBG-electrolytes were 97.8% sensitive and 100% specific for the diagnosis of DKA in hyperglycemic patients (Menchine M et al., 2011).
  23. 23. INSULIN WHEN? Study: S. Arora et al - Prevalence of hypokalemia in ED patients with diabetic ketoacidosis (2012) Hypokalemia was observed in 5.6% of patients with DKA. These findings support the ADA recommendation to obtain a serum potassium before initiating intravenous insulin therapy in a patient with DKA.
  24. 24. BICARBONATE THERAPY Study #1: Chua et al. - Bicarbonate in Diabetic Ketoacidosis A Systematic Review (2011). Transient improvement in metabolic acidosis. No improved glycemic control. Risk of cerebral edema in pediatric patients. No studies with pH