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Diabetes Complications DG van Zyl. The Ticking Clock.

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Presentation on theme: "Diabetes Complications DG van Zyl. The Ticking Clock."— Presentation transcript:

1 Diabetes Complications DG van Zyl

2 The Ticking Clock

3 Different Diabetes Complications Macro vascular Micro vascular Neuropathy Infections

4 Mechanisms HyperglycemiaTissue damage *Repeated acute changes in cellular metabolism **Cumulative long term changes in stable macromolecules Genetic susceptibility Independent accelerating factors

5 Mechanisms of Hyperglycaemia Induced Damage Increased Polyol - sorbitol Pathway flux Increased AGES formation Activation of protein kinase C Increased Hexosamine pathway flux

6 Formation of AGEP

7 Macro vascular Complications

8 Macro-vascular Complications Ischemic heart disease Cerebrovascular disease Peripheral vascular disease Diabetic patients have a 2 to 6 times higher risk for development of these complications than the general population

9 Macro-vascular Complications The major cardiovascular risk factors in the non-diabetic population (smoking, hypertension and hyperlipidemia) also operate in diabetes, but the risks are enhanced in the presence of diabetes. Overall life expectancy in diabetic patients is 7 to 10 years shorter than non-diabetic people.

10 Macro-vascular Disease Once clinical macro-vascular disease develops in diabetic patients they have a poorer prognosis for survival than normoglycemic patients with macrovascular disease The protective effect females have for the development of vascular disease are lost in diabetic females

11 CAD Morbidity and Mortality in Type 2 DM Framingham Data: 20 year follow-up:Age 45-74: 2-3 fold increase in clinically evident atherosclerotic disease in diabetics women diabetics=male diabetics in terms of CAD mortality Multiple Risk Factor Intervention Trial (MRFIT) 5000 men with type 2 DM Followed for 12 years Men with type 2 DM had absolute risk of CAD-related death 3 times higher than non- diabetic cohort

12 Risk Factor Clustering in Diabetes Type 2 Diabetes at Diagnosis: 50% have hypertension 30% have dyslipidemia UKPDS: Prospective study Newly detected type 2 DM: 335 with CAD, 8 year follow-up Associated with elevated LDL-C, low levels of HDL-C, systolic hypertension

13 Cardiovascular Death Rates: MRFIT data Stamler J., et al Diabetes Care: 16:

14 Risk of MI in Diabetes Haffner, SM et al NEJM: 339:

15 Plasma Glucose as Independent Risk Factor Andersson, DK et al. Diabetes Care 18:

16 Glycemic Control to Reduce CAD DCCT trial: 1441 patients, type 1 diabetes Randomized to intensive glycemic control vs. conventional therapy Monitored prospectively for 6.5 years Results: Less retinopathy by 50% Macrovascular complications: 41% reduction (not statistically significant) -small number of events in young patient cohort UKPDS: 3867 patients with newly diagnosed type 2 DM Intensive vs. Conventional therapy 10 year follow-up Microvascular endpoints improved Trend only towards reduced incidence of MI ( p=0.052)

17 Effect of Hypertension

18 Why worry about Hypertension in Diabetic patients Treating hypertension can reduce the risk of: Death32% Microvascular disease 37% Stroke44% Heart failure56% UKPDS BMJ 1998;317:

19 Hypertension in Type 1 and 2 Diabetes Type 1 Develop after several years of DM Ultimately affects ~30% of patients Type 2 Mostly present at diagnosis Affects at least 60% of patients

20 Pathophysiology of hypertension Type 1 DM Secondary to nephropathy Activation of the RAAS Type 2 DM Hyperinsulinemia Secondary to insulin resistance Activation of the sympathetic nervous system

21 Goals of Treatment of Hypertension Lower target for diabetic patients than non- diabetic patients: 130/85 vs. 140/90 UKPDS 38. BMJ 1998;317: HOT. Lancet 1998;351:

22 Effect of Cholesterol

23 Dyslipidaemia in DM Most common abnormality is s HDL and s Triglyserides A low HDL is the most constant predictor of CV disease in DM Target lipid values: LDL 1.15 mmol/l, TG < 2.5 mmol/l

24 Micro vascular Complications

25 Eye Complications Cataracts Non enzymatic glycation of lens protein and subsequent cross linking Sorbitol accumulation could also lead to osmotic swelling of the lens but evidence of involvement in cataract formation is less strong

26 Eye Complications Retinopathy (stages) Background Pre-proliferative Proliferative Advanced diabetic eye disease Maculopathy Glaucoma

27 Diabetic Retinopathy (DR) DR is the leading cause of blindness in the working population of the Western world The prevalence increase with the duration of the disease (few within 5 years, 80 – 100% will have some form of DR after 20 years) Maculopathy is most common in type 2 patients and can cause severe visual loss

28 Background Retinopathy Micro aneurisms Scattered exudates Hemorrhages(flame shaped, Dot and Blot) Cotton wool spots (<5) Venous dilatations Background retinopathy

29

30 Pre-Proliferative Retinopathy Rapid increase in amount of micro aneurisms Multiple hemorrhages Cotton wool spots (>5) Venous beading, looping and duplication Proliferative retinopathy

31 Proliferative Retinopathy New vessels (on disc, elsewhere) Fibrous proliferation (on disc, elsewhere) Hemorrhages (preretinal, vitreous) Panretinal photo-coagulation

32 Proliferative retinopathy

33 Vitreous Bleeding

34 Rubeosis Iridis

35 Advanced Diabetic Eye Disease Retinal detachment with or without retinal tears Rubeosis iridis Neovascular glaucoma

36 Maculopathy Macular edema (focal or diffuse) Ischaemic maculopathy

37 Maculopathy

38 Diabetic Nephropathy (DN) Diabetes has become the most common cause of end stage renal failure in the US and Europe About 20 – 30% of patients with diabetes develop evidence of nephropathy The prevalence of DN is higher in Black Americans than in Whites (Figures for South Africa is not available)

39 Stages of Diabetic Nephropathy

40 Stages of DN Stage I glomerular filtration and kidney hypertrophy Stage II u-albumin excretion < 30mg/24h Stage III Microalbuminuria (30 – 300 mg/24h)

41 Stages of DN (cont) Stage IV Overt nephropathy (> 300mg/24h, positive u dipstick) Stage V ESRD characterized by blood urea and creatinine levels, hyperkalaemia and fluid overload

42 Diabetic Neuropathy Sensorimotor neuropathy (acute/chronic) Autonomic neuropathy Mononeuropathy Spontaneous Entrapment External pressure palsies Proximal motor neuropathy

43 Sensorimotor Neuropathy Patients may be asymptomatic / complain of numbness, paresthesias, allodynia or pain Feet are mostly affected, hands are seldom affected In Diabetic patients sensory neuropathy usually predominates

44 Complications of Sensorimotor neuropathy Ulceration (painless) Neuropathic edema Charcot arthropathy Callosities

45 Autonomic Neuropathy Symptomatic Postural hypotension Gastroparesis Diabetic diarrhea Neuropathic bladder Erectile dysfunction Neuropathic edema Charcot arthropathy Gustatatory sweating Subclinical abnormalities Abnormal pupillary reflexes Esophageal dysfunction Abnormal cardiovascular reflexes Blunted counter-regulatory responses to hypoglycemia Increased peripheral blood flow

46 Mononeuropathies Cranial nerve palsies (most common are n. IV,VI,VII) Truncal neuropathy (rare)

47 Entrapment Neuropathies Carpal tunnel syndrome (median nerve) Ulnar compression syndrome Meralgia paresthetica (lat cut nerve to the thigh) Lat Popliteal nerve compression (drop foot) All the above are more common in diabetic patients

48 Proximal Motor Neuropathy Amyotrophy – most common proximal neuropathy, affects the Quadriceps muscles with weakness and atrophy (synonym: Diabetic Femoral radiculo- neuropathy)

49 Diabetic Amyotrophy

50 Thoracoabdominal Radiculopathy

51 Sudomotor Dysautonomia

52 Summary Diabetic neuropathy is a common complication, and result in significant morbidity Diabetic neuropathy present in numerous ways Hyperglycemia is the cause of diabetic neuropathy

53 Summary (cont) Diabetic neuropathy have bad consequences Diabetic neuropathy can be prevented in only one way Once diabetic neuropathy is present it can only be managed symptomatically Early diagnosis and aggressive management can prevent progression

54 Infections The association between diabetes and increased susceptibility to infection in general is not supported by strong evidence However, many specific infections are more common in diabetic patients and some occur almost exclusively in them Other infections occur with increased severity and are associated with an increased risk of complications

55 Infections (cont) Several aspects of immunity are altered in patients with diabetes There is evidence that improving glycemic control patients improves immune function

56 Specific Infections Community acquired pneumonia Acute bacterial cystitis Acute pyelonephritis Emphysematous pyelonephritis Perinephric abscess Fungal cystitis Necrotizing fasciitis Invasive otitis externa Rhinocerebral mucormycosis Emphysematous cholecystitis

57 Rhino-Cerebral Mucormycosis

58 Screening and Management Strategy for Diabetes Complications

59 Screening for Macrovascular Complications 1.Examine pulses and for cardiovascular disease 2.Lipogram 3.ECG 4.Blood pressure 1-3 annually 4 every visit (quarterly)

60 Screening for Eye disease Annually Visual acuity (corrected with pinhole or lenses) Careful eye examination (noting the clarity of the lens and any retinal changes (Ophthalmoscopy through dilated pupils)

61 Screening for Eye disease When to refer? Severe non-proliferative/proliferative retinopathy Macular edema or exudates in close proximity to the macula Cataract Unexplained reduction in visual acuity

62 Screening for Nephropathy Annually Do one of the following: u Albumin:Creatinine ratio (spot sample) 24h u Albumin excretion rate Early morning Albumin concentration (spot sample) Dipstick for Microalbuminuria If positive the test must be repeated twice in the ensuing 3 months. Microalbuminuria with incipient nephropathy is diagnosed if 2 or more of the tests are within the microalbumin range

63 Microalbuminuria Increased risk for overt nephropathy Increased cardiovascular mortality Increased risk of Retinopathy Increased all-cause mortality Thus Microalbuminuria is an indication for screening for possible vascular disease and aggressive intervention to reduce all cardiovascular risk factors

64 Screening Tests for Microalbuminuria Category 24h u collection (mg/24h) Timed collection (mg/min) Spot collection (mg/mg creat) Normal Microalbumi nuria Albuminuria Overt

65 Who to Screen For Microalbuminuria Type 1 Diabetes Begin with puberty After 5 years duration of disease Should be done annually there after Type 2 Diabetes Start screening at the Diagnosis of diabetes Should be done annually there after

66 Management of Nephropathy Improvement of glycemic control Treatment of hypertension Treatment with angiotensin converting enzyme inhibitors Restriction of dietary intake of protein Once persistent elevation in u-Albumin is found refer to a Internist or Nephrologist

67 Screening for Neuropathy 128 Hz tuning fork for testing of vibration perception 10g Semmers monofilament The main reason is to identify patients at risk for development of diabetic foot

68 Using of the Monofilament

69 Management of Neuropathy Burning pain – TAD s / Capsaicin Lancinating pain – Anticonvulsants / TAD / Capsaicin Painful cramps – Quinidine sulphate Restless legs - Clonazepam

70 Dos and Don'ts of foot care Patient should check feet daily Wash feet daily Keep toenails short Protect feet Always wear shoes Look inside shoes before putting them on Always wear socks Break in new shoes gradually

71 Conclusion This is just an outline of the major diabetic complications, and doesn't aim to be comprehensive All complications are preventable with good glycaemic control The progression of most complications can be halted if detected early and appropriate therapy instituted


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