Metabolic complications of Diabetes Mellitus

1. Metabolic complications of Diabetes Mellitus Dr. Essam H. Jiffri

2. Introduction • - Metabolic complications, particularly diabetic ketoacidosis and hypoglycaemia, • are life-threatening and can cause permanent neurological damages. • -Diabetic patients present with impaired consciousness may be caused by other conditions

4. Diabetic Ketoacidosis • -Diabetic ketoacidosis (DKA) was responsible for 70% of diabetic deaths before the advent of insulin therapy and mortality rates are still up to 7%. • -It is mainly a recognized complication of IDDM, DKA can also occur in NIDDM.

5. Diabetic Ketoacidosis • -The clinical features of DKA result from: • insulin deficiency • increases in counter-regulatory hormones, produce major changes in: • fuel, water and electrolyte metabolism • glycogenolysis and gluconeogenesis occur.

6. Diabetic Ketoacidosis • Increased secretion • of counter-regulatory hormones leading to increased hepatic • glucose output

7. Diabetic Ketoacidosis • -Tissue uptake of glucose is reduced, contributing to the hyperglycaemia. • -As glucose does not enter cells, the extracellular osmotic pressure tends to rise, causing water to transfer from the intracellular to extracellular compartment. • - The renal threshold for glucose is exceeded and glycosuria occurs.

8. Diabetic Ketoacidosis • - The presence of excess non-absorbed solute in the glomerular filtrate causes an osmotic diuresis which interferes with tubular reabsorptive function, leading to: • water • sodium and • potassium depletion

9. Diabetic Ketoacidosis • - Lipolysis results from insulin deficiency • - NEFAs are released and transported to liver(reduced insulin and increased glucagon) leading to: • greater amount of fatty acids being metabolized by beta-oxidation • Acetyl CoA is exceeded and increased amount of ketone bodies

10. Diabetic Ketoacidosis • Acetoacetate and β-hydroxybutyrate are week acids and increase H+ conc in the blood, exceeding the buffering capacity and causing acidosis • - The H+ ions exchange with potassium across cell membranes, causing hyperkalaemia in some patients.

11. Diabetic Ketoacidosis • The effect of acidosis • is direct stimulation • of respiratory centre • by H+, causing deep hyperventilation (Kussmaul breathing)

12. Diabetic Ketoacidosis • - A history of polyuria, polydipsia, fatigue and vomiting. • - Physical signs include: • dehydration • tachycardia, • warm skin • Kussmaul respiration • Odour of acetone on the breath

14. Diabetic KetoacidosisManagement • - Diabetic ketoacidosis is a medical emergency. • - The aim of treatment is to replace fluids and electrolytes, and restore metabolic control. • - Patients require several liters of isotonic solution of saline to be infused, because of • loss of sodium.

15. Diabetic KetoacidosisManagement • -Intravenous insulin infusion is required, initially 6 units h-1. • - Intravenous potassium may be required, the rate depending on the plasma potassium • level. • - Bicarbonate is sometimes infused to correct the metabolic acidosis in severely affected patients (pH 7.0).

16. Diabetic KetoacidosisMonitoring • Blood glucose should be monitoring hourly using test strip. • Laboratory analysis of glucose and electrolytes should be done after 2h, and four hourly until the patient is stable. • - Blood gases should be monitored periodaclly.

17. Hyperosmolar Non-ketotic Coma • - Occurs mainly in elderly patient with NIDDM • - Some degree of ketosis • Hyperglycaemia is more severe than in DKA • The condition has a high mortality rate over 50%

18. Lactic Acidosis • Lactic acidosis is usually associated with renal failure

19. Principal features of three forms of metabolic decompensation in diabetes

20. Long-term complication • long-term complications may result from : • Microvascular changes • Macrovascular disease

21. KEY POINTS Diabetic Ketoacidosis (DKA) is a medical emergency Patients with DKA are dehydrated, sodium depleted and acidotic Plasma potassium levels should be monitored during treatment