Management of DM and its complications

1. Management of DM and itscomplications

2. Complications are either… • Acute---DKA ---hyperosmolor non ketotic coma ---hypoglycemia ---lactic acidosis • Chronic ---macrovascular ---microvascular

3. Prevalance of complications at the time of diagnosis { UKPDS }

5. Chronic complications • Macrovascular • microvascular

6. Macrovascular complication • 40-50 % of people with DM die from these complications • Factors that contribute to the ↑ risk include 1-↑ prevalance of hypertension in diabetics 2--↑ lipid profile 3—abnoramlity in clotting system 4—effect of hyperglycemia on progression of atherosclerotic lesions

7. Macrovascular complications • Stroke • MI • Peripheral vascular disease • Foot problems

8. Microvascular complications • Retinopathy • Nephropathy • Neuropathy • Foot problems

9. Coronary artery disease • Coronary artery disease accounts for the majority of diabetic deaths • Certain features of CAD in diabetics include: • Adjusted for age MI is 2-5 times more frequent in patients with diabetes • Pts with DM who have MI have a lower survival rate compared to pts without DM • ↑ incidence of silent MI –40% • Silent MI may present as new onset of CCF • Small vessel disease with relatively patent coronary arteries are more common

10. Peripheral vascular disease {PVD} Special characteristics of PVD • Location—tibial + popliteal arteries are common----aorta ,ileal, femoral –rare • Extend—multi segmental occlusion • Progression—accelerated progression compared to non diabetics • Gangrene---risk ↑ more than non diabetics over 40 yrs of age

11. Retinopathy • Background—this is the most common type of retinopathy --not usually seen untill after 10 yrs of DM ---may be found in 30 % of pts with type 2 DM • Proliferative • maculopathy

12. Nephropathy Consists of the following clinical stages: • ↑ GFR > 150 mls /min • Microalbuminurea 30-300 mg /24 hrs • Clinical albuminuria also called macroalbuminuria > 300 mg/ 24 hrs • Worsening of proteinuria , hypertension and ↓GFR • Kidney failure occurs when GFR ↓ to ≤ 10mls/min

13. Factors influencing renal function in DM • Glomerular basement membrane damage → diabetic nephropathy • Renal artery stenosis and ischaemia due to atherosclerosis • Ascending infection • Renal papillary necrosis

14. Neuropathy Different clinical presentations • Symmetrical sensory polyneuropathy • Mononeuritis multilplex • Autonomic neuropathy

15. Sensory neuropathy • Insidious onset of loss of sensation in feet and hands—gloves and stockings • Loss of vibration sense and reduced or absent ankle or knee jerk • Loss of peripheral nerve function results in wasting of small muscles of feet and hands

16. Mononeuritis multiplex • Nerves commonly affected are 3rd and 6th • Amyotrophic motor neuropathy characterized by unilateral or bilateral pain and weakness of the quadriceps—they often recover spontanously • Median nerve palsy leeds to carpal tunnel syndrome • Peroneal nerve palsy leeds to foot drop

17. Autonomic neuropathy • CVS—loss of vagal { parasympathetic tone} produces --resting tachycardia --loss of sinus rhythm –change in heart rate with respiration---sinus arrythmia • Loss of sympathetic activity in arterioles results in peripheral vasodilatation and postural hypotension • Rx—support stockings • --fludrocortisone • -alfa blockers

18. GIT • Gastroparesis--Delayed gastric emptying results in early statiety or recurrent vomiting • --treated with –dopamine agonist • metochlorpramide • domperidone • erythromycin • Nocturnal diarrhea • loperamide • Constipation due to colonic atony • laxatives

19. Autonomic bladder • Loss of bladder smooth muscle tone results in incomplete emptying , stasis , and ↑ risk of infection • In severe cases the bladder is persistantly distended—atonic which results in over flow incontinance • sympathomimetics—carbachol • antichilinesterase drugs

20. Gustatory sweating • Eating cause excessive facial sweating • Anticholinergic drugs--probantheline Erectile dysfunction • impotence

21. Foot disease • Neuropathic foot ulcer • Ischaemic foot ulcer • Charcots arthropathy

22. Can we prevent type 2 DM • Before pts develop DM ,they almost always have “ pre diabetes” • Clinical trails have documented that dietary changes and regular exercise prevent or delay the development of overt DM in individuals at high risk

23. Risk factors for type 2 DM • Age > 45 • 1st degree relative with type 2 DM • History of gestational diabetes or delivery of infant >9 lbs • PCO • Abdominal obesity • CVD, hypertension ,dyslipidemia ,other metabolic syndrome features

24. Prediabetes Defined as- • IFG—FBS =100 -125 mg/dl…5.6 - 6.9 mmol / l • Impaired glucose tolerance---plasma glucose level 140 – 199 mg/dl …7,8 – 11.0 mmol / l, 2 hrs after 75 gms of glucose

25. Evaluation and treatment • FBG • HbA1c • Serum electrolytes • Urine for protein and microalbuminuria • ECG • Fasting lipid profile

26. Treatment • Diet • Exercise • Stop smoking • Treat hyperlipidemia ---statin group • Treat hypertension—mainly ACEI • Prevent proteinuria by prescribing ACEI • Start ASA as prophylaxis for IHD • OHG • Insulin

27. ADA Rx goals for glycemic control

30. OHG • Biguanides— • Suppress hepatic glucose production • Decrease intestinal glucose absorption • Improve insulin sensitivity • metformin • Sulphonylurea • Increase pancreatic insulin secretion • —glimepiride • ---glipizide • ---glyburide • ---chlorpropamide

31. Thiazolidinediones— • ↓ post prandial hyperglycemia • ---Rosiglitazone • ---poglitazone

32. Cont.. • Alfa glucosidase inhibitors— • ↓post prandial hyperglycemia by decreasing GIT carbohydrate absorption • arcabose • Meglitinides--- • Increase pancreatic insulin secretion through different glucose binding sites than used by sulphonylureas • repaglinide

33. Type 2 diabetes is a progressive disease • Over time most pts will need insulin to control glucose

34. Insulin therapy in type 2 diabetes • Don,t wait forever • Don,t be afraid of hypoglycemia • Consider combination therapy • Don,t under insulinize • Consider insulin pump therapy

40. DIABETIC KETOACIDOSIS Leading cause of death in pts with type 1 diabetes under the age of 20 yrs

41. Risk factors for DKA • Results from absolute or relative insulin deffeciency • Missing the dose of insulin • Infection • Increase food intake • Stress like MI or surgery

42. Diagnosis Triad of. • Hyperglycemia—glucose more than 15mmol /l • Metabolic acidosis—PH < 7.2 ---HCO3 <17 mmol /l • Ketones in the urine

43. Principles of management • Rehydration • Insulin • Correction of K+ • Correction of acidosis • + / - antibiotics

44. Rehydration • 1 litre NS over 30 min • 1 litre over 1 hr • 1 litre over 1 hr • 1 litre over 2 hrs • 1 litre over 4 hrs • I litre over 6 hrs Change ½ saline once BS reaches 13 mmol / l

45. Insulin therapy • 10 -20 units of RI is given IM stat • 4 - 6 units / hr by IV infusion untill BS ↓ to 10 – 15 mmol/l then ↓ to 1 - 4 units / hr • Aim to ↓ BS 3 – 6 mmol / hr • Change to SC once BS ↓13 mmol / l

46. Potassium replacement • 1st 30 min if K+ > 5.5 mmol/l– no K+ • If 3.5 5.5 --give 20 meq in the 1st litre • If < 3.5 --give 40 meq in the 1st litre • Continue K+ infusion 20 meq in each litre to maintain K+ at the level of 3.5 – 4. 5

47. Bicarbonte replacement Bicarbonate is replaced when the PH is between 7.0 – 7.1 Antibiotics These are used when there is strong suspicion of infection

48. HYPOGLYCEMIA Causes • Missed delayed or inadequate meal • Unaccustomed exercise • Alcohol • Increase dose of drugs ..insulin or OHG • Gastroparesis • Malabsorption • factitious

49. NON KETOTIC HYPEROSMOLARDIABETIC COMA Characterized by • Severe hyperglycemia--> 50 mmol / l • No ketones in the urine • Severe dehydration • Occurs in the elderly • Risk of thrombosis is high • Mortality is high

50. Management Differs from DKA in the following • Very sensitive to insulin so very small dose should be started • Calculate osmolality and start either ½ or ¼ saline Plasma osmolality =2Na + 2K + glu + urea=280 - 295