2008 Clinical Practice Guidelines - Canadian Diabetes Association

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2008 CLINICAL PRACTICE GUIDELINES S64 RELATED WEBSITE Begg IS, Yale J-F, Houlden RL, et al. Canadian Diabetes Association’s clinical practice guidelines for diabetes and private and commercial driving. Can J Diabetes. 2003;27:128- 140. Available at: http://www.diabetes.ca/files/Driving GuidelinesBeggJune03.pdf. Accessed September 1, 2008. REFERENCES 1. Hepburn DA. Symptoms of hypoglycaemia. In: Frier BM, Fisher BM, eds. Hypoglycaemia and Diabetes: Clinical and Physiological Aspects. London, UK: Edward Arnold; 1993:93-103. 2. The Diabetes Control and Complications Trial Research Group. Effects of intensive diabetes therapy on neuropsychological function in adults in the Diabetes Control and Complications Trial. Ann Intern Med. 1996;124:379-388. 3. Reichard P, Pihl M. Mortality and treatment side-effects during long-term intensified conventional insulin treatment in the Stockholm Diabetes Intervention Study. Diabetes. 1994;43: 313-317. 4. Brands AM, Biessels GJ, de Haan EH, et al.The effects of type 1 diabetes on cognitive performance: a meta-analysis. Diabetes Care. 2005;28:726-735. 5. The Diabetes Control and Complications Trial Research Group. Adverse events and their association with treatment regimens in the Diabetes Control and Complications Trial. Diabetes Care. 1995;18:1415-1427. 6. The Diabetes Control and Complications Trial Research Group. Hypoglycemia in the Diabetes Control and Complications Trial. Diabetes. 1997;46:271-286. 7. Mühlhauser I, Overmann H, Bender R, et al. Risk factors of severe hypoglycaemia in adult patients with type I diabetes—a prospective population based study. Diabetologia. 1998;41: 1274-1282. 8. The DCCT Research Group. Epidemiology of severe hypoglycemia in the Diabetes Control and Complications Trial. Am J Med. 1991;90:450-459. 9. Davis EA, Keating B, Byrne GC, et al. Hypoglycemia: incidence and clinical predictors in a large population-based sample of children and adolescents with IDDM. Diabetes Care. 1997;20:22-25. 10. Egger M, Davey Smith G, Stettler C, et al. Risk of adverse effects of intensified treatment in insulin-dependent diabetes mellitus: a meta-analysis. Diabet Med. 1997;14:919-928. 11. Gold AE, MacLeod KM, Frier BM. Frequency of severe hypoglycemia in patients with type I diabetes with impaired awareness of hypoglycemia. Diabetes Care. 1994;17:697-703. 12. Mokan M, Mitrakou A, Veneman T, et al. Hypoglycemia unawareness in IDDM. Diabetes Care. 1994;17:1397-1403. 13. Meyer C, Grossmann R, Mitrakou A, et al. Effects of autonomic neuropathy on counterregulation and awareness of hypoglycemia in type 1 diabetic patients. Diabetes Care. 1998; 21:1960-1966. 14. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin-dependent diabetes mellitus: Diabetes Control and Complications Trial. J Pediatr. 1994;125:177-188. 15. Slama G, Traynard PY, Desplanque N, et al. The search for an optimized treatment of hypoglycemia. Carbohydrates in tablets, solution, or gel for the correction of insulin reactions. Arch Intern Med. 1990;150:589-593. 16. Wiethop BV, Cryer PE.Alanine and terbutaline in treatment of hypoglycemia in IDDM. Diabetes Care. 1993;16:1131-1136. 17. Brodows RG,Williams C, Amatruda JM. Treatment of insulin reactions in diabetics. JAMA. 1984;252:3378-3381. 18. Special problems. In: Skyler JS, ed. Medical Management of Type 1 Diabetes. 3rd ed. Alexandria, VA: American Diabetes Association; 1998:134-143. 19. Canadian Diabetes Association. The role of dietary sugars in diabetes mellitus. Beta Release. 1991;15:117-123. 20. Gunning RR, Garber AJ. Bioactivity of instant glucose. Failure of absorption through oral mucosa. JAMA. 1978;240:1611-1612. 21. Glucobay ® (acarbose) [product monograph]. Toronto, ON: Bayer Inc.; 2007. 22. Cryer PE, Fisher JN, Shamoon H. Hypoglycemia. Diabetes Care. 1994;17:734-755. 23. Glucagon [product monograph]. Toronto, ON: Eli Lilly Canada Inc.; 2007.
Hyperglycemic Emergencies in Adults Canadian Diabetes Association Clinical Practice Guidelines Expert Committee The initial draft of this chapter was prepared by Jeannette Goguen MD MEd FRCPC and Danièle Pacaud MD FRCPC KEY MESSAGES • Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. • DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. • Ketoacidosis requires insulin administration (0.1 U/kg/hour) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH ≤7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents.The specific issues related to treatment of DKA in children and adolescents are addressed in “Type 1 Diabetes in Children and Adolescents,” p. S150. INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarction, abdominal crisis, trauma and possibly treatment with insulin infusion pumps. HHS is much less common than DKA (1,2). In addition to the precipitating factors noted above for DKA, HHS has also been reported following cardiac surgery, and with the use of certain drugs, including diuretics, glucocorticoids, lithium and atypical antipsychotics. The clinical presentation of DKA includes symptoms of hyperglycemia, Kussmaul respiration, acetone-odoured breath, ECFV contraction, nausea, vomiting and abdominal pain. There may be a decreased level of consciousness. In HHS, there is often more profound ECFV contraction and decreased level of consciousness (proportional to the elevation in plasma osmolality). In addition, in HHS there can be a variety of neurological presentations, including seizures and a stroke-like state that can resolve once osmolality returns to normal (2-4). In both conditions, there may also be evidence of a precipitating condition. DIAGNOSIS DKA or HHS should be suspected whenever patients have significant hyperglycemia, especially if they are ill or highly symptomatic (see above). As outlined in Figure 1, to make the diagnosis and determine the severity of DKA or HHS, the following should be assessed: plasma levels of electrolytes (and anion gap), glucose, creatinine, osmolality and betahydroxybutyric acid (beta-OHB) (if available), blood gases, serum and urine ketones, fluid balance, level of consciousness, precipitating factors and complications (5). There are no definitive criteria for the diagnosis of DKA. Typically, the arterial pH is ≤7.3, serum bicarbonate is ≤15 mmol/L, and the anion gap is >12 mmol/L with positive serum and/or urine ketones (5-7). Plasma glucose is usually ≥14.0 mmol/L, but can be lower (8). DKA is more challenging to diagnose in the presence of the following conditions: 1) mixed acid-base disorders (such as associated vomiting, which will raise the bicarbonate level); 2) if there has been a shift in the redox potential favouring the presence of beta-OHB (rendering serum ketone testing negative); or 3) if the loss of ketoanions with sodium or potassium in osmotic diuresis has occurred, leading to a return of the plasma anion gap towards normal. It is therefore important to measure ketones in both the serum and urine. If there is an elevated anion gap, and serum ketones are negative, beta- OHB levels should be measured. Measurement of serum lactate should be considered in hypoxic states. In HHS, a more prolonged duration of relative insulin insufficiency and inadequate fluid intake (or high glucose intake) results in higher glucose levels (typically ≥34.0 mmol/L) and greater ECFV contraction, but minimal acid-base disturbance (5,6). S65 MANAGEMENT
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2008 Clinical Practice Guidelines - Canadian Diabetes Association

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