Diabetic Microvascular Complications

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A basic presentation of diabetic microvascular complication highlighting the importance of screening

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  • 50 % of all patients with type 1 DM and PDR and > 10 years duration have concomitant proteinuria
  • Measurement of the albumin-to-creatinine ratio in a random spot collection
    OR
    2) 24-h collection with creatinine, allowing the simultaneous measurement of creatinine clearance; and
    OR
    3) timed (e.g., 4-h or overnight) collection.
  • In the Kumamoto Study, a reduction in the conversion from micro- to macroalbuminuria was observed with intensive treatment
  • It often is considered that the clinical expression of diabetic neuropathy is the tip of the iceberg. Patients presenting with symptoms, particularly numbness and pain, represent only a small percentage of patients with neuropathy. Clinical examination may detect asymptomatic neuropathy in another 30% of patients. Further sophisticated testing, including quantitative sensory testing and electrophysiologic testing, such as nerve conduction velocity, might pick up abnormalities in another 30% to 40% of patients who cannot be detected on clinical examination, but such testing is rarely, if ever, done in clinical practice on asymptomatic patients.
    The clinician usually can differentiate the symptoms of neuropathy from other symptoms based on the pattern of complaints and physical findings. Occasionally, electrophysiologic testing may be required.
  • Diabetic Microvascular Complications

    1. 1. Diabetic MicrovascularDiabetic Microvascular ComplicationsComplications Mathew John MD, DM, DNB Consultant Endocrinologist
    2. 2. Microvascular complication MICROVASCULAR COMPLICATIONS Retinopathy Neuropathy Nephropathy Cardiomyopathy Cheiroarthropathy Dermopathy
    3. 3. Structure of talk • Screening • Diagnosis • Treatment Retinopathy Nephropathy Neuropathy
    4. 4. Therapeutic failures in diabetes • When a patient reaches end stage renal failure • When a patient becomes blind or severely visually impaired • When a patient has a leg or foot amputated • When a patient suffers from MI or stroke
    5. 5. Magnitude of the problem • Somewhere in the world a leg is lost to diabetes every thirty seconds • Leading cause of new onset blindness • 10% to 20% of people with diabetes die of renal failure • Diabetes is the leading cause of end stage renal disease requiring dialysis • Every 10 seconds a person dies from diabetes-related causes
    6. 6. UKPDS results of Intensive therapy Risk reduction vs. conventional therapy
    7. 7. Risk factors for microvascular complications • Degree of glycemic control • Duration of disease • Hypertension • Dyslipidemia • Smoking • Genetic factors
    8. 8. Pathophysiology of complications
    9. 9. Diabetic Retinopathy
    10. 10. Retinopathy • Sight threatening microvascular complication • Changes in retinal microvascular architecture • Leading cause of new onset blindness in the developed world • > 90 % of vision loss resulting from proliferative retinopathy can be prevented
    11. 11. How common is retinopathy ? • Type 1 diabetes : 25 % of type 1 diabetes after 5 years : 60-80 % after 10-15 years • Type 2 diabetes : PDR present in 25 % after 15 years
    12. 12. Symptoms of diabetic retinopathy NO SYMPTOMS Even stages up to proliferative retinopathy can be asymptomatic Visual loss : Macular edema Vitreous hemorrhage Retinal detachment
    13. 13. Screening & Diagnosis • Dilated fundus evaluation : annually / 6 monthly • Ophthalmologist Only 50 % of the eyes are correctly classified as to the presence of retinopathy through undilated eye examinations Appropriate eye evaluation Pupillary dilatation Slit lamp biomicroscopy Indirect ophthalmoscopy for retinal periphery Gonioscopy Flourescein Angiogram
    14. 14. International Clinical Diabetic Retinopathy (DR) Disease Severity Scale • No apparent DR • Mild nonproliferative DR • Moderate nonproliferative DR • Severe nonproliferative DR • Proliferative DR
    15. 15. Mild non proliferative retinopathy Flame shaped hemorrhages Microaneursms Dot & Blot hemorrhages
    16. 16. Severe non proliferative retinopathy
    17. 17. Proliferative retinopathy
    18. 18. Clinically Significant Macular edema www.retinalphysician.com/archive%5C2009%5CJan
    19. 19. Vitreous hemorrhage
    20. 20. Prognosis • High risk PDR : 28 % risk of severe vision loss within 2 years • Untreated CSME is associated with a 25 % moderate visual loss after 3 years PDR : Proliferative diabetic retinopathy CSME : Clinically significant Macular edema ETDRS study, 1991
    21. 21. Effective LASER treatment HIGH RISK PDR • This risk is reduced to < 4 % by panretinal photocoagulation • Reduced need for pars plana vitrectomy(PPV) by 50 % CLINICALLY SIGNIFICANT MACULAR EDEMA Loss of vision in CSME reduced by 50 % after focal laser photocoagulation
    22. 22. Metabolic management • Glycemic control • Intensive BP control : 34 % improvement in retinopathy outcomes after intensive BP control • Lipid management • Anemia correction
    23. 23. Diabetic Nephropathy
    24. 24. Nephropathy • Leading cause of chronic renal failure in the developed world  • Diabetes is responsible for 30-40% of all end-stage renal disease (ESRD) • Microalbuminuria is a cardiovascular risk factor
    25. 25. Signs & Symptoms • None • None • None • New onset hypertension/ resistant hypertension • Edema • Reducing insulin requirements As diabetic nephropathy is asymptomatic, we need to screen for nephropathy in all our patients with diabetes mellitus
    26. 26. Laboratory investigations • Urine microalbumin • Serum creatinine • Serum potassium • Urine routine
    27. 27. Urine microalbumin Measurement of the albumin-to-creatinine ratio in a random spot collection Preferable : early morning urine Short-term hyperglycemia, exercise, urinary tract infections, marked hypertension, heart failure, and acute febrile illness can cause transient elevations in urinary albumin excretion Repeat urine sample to confirm microalbuminuria
    28. 28. Progression of nephropathy Normal Microalbuminuria 2% per annum Clinical Nephropathy > 300 mg/gm 2% per annum < 30 mg/gm 30-300 mg/gm
    29. 29. If microalbumin is positive • Do urine routine • Urine microalbumin > 300 mg/gm : do 24 hour urine protein• Creatinine, serum potassium • Consider ultrasound abdomen
    30. 30. Treatment • Intensive glycemic control 25% risk reduction (P = .0099) in microvascular end points in UKPDS trial 33 % in RR reduction after microalbuminuria or clinical grade nephropathy after 12 years • Hypertension control Risk reduction in diabetic nephropathy progression with the use of antihypertensive therapy : 29 % in UKPDS study
    31. 31. Treatment • Blockage of renin-angiotensin- aldosterone( RAAS) ACE inhibitor •Ramipril :2.5 to 10mg/day •Perindopril :4-8 mg/day •Enalapril : 2.5 –20mg/day •Lisinopril : 2.5-20 mg/day Agents that block the RAAS provide additional benefit on reduction of microalbumin independent of blood pressure reduction Angiotensin Receptor Blocker Irbesartan 150-300 mg/day Telmisartan 40-80 mg/day Losartan 50-100 mg/day
    32. 32. Prevention of nephropathy progression • Dietary protein restriction • Blood pressure : < 130/80 mm Hg < 120/75 mm Hg if proteinuria or renal insufficiency is present • Blood sugars HbA1c < 7 % • ACE inhibitor/ Angiotensin receptor blocker • Statins for CV risk
    33. 33. Diabetic Neuropathy
    34. 34. WHO definition A disease characterized by decline and damage of nerve function leading loss of sensation, ulceration and subsequent amputation.
    35. 35. Why is neuropathy important ? • Neuropathy increases risk of amputation 1.7 fold • Neuropathy + deformity: increases risk of amputation 12 fold • Neuropathy + deformity + previous ulceration: increases risk by 36 fold • Autonomic neuropathy: 25-50 % , 5 –10 year mortality
    36. 36. Classification • Symmetric polyneuropathy • Polyradiculopathy • Mononeuropathy • Autonomic neuropathy
    37. 37. Symmetric polyneuropathy • Most common form of diabetic neuropathy • Affects distal lower extremities and hands (“stocking- glove” sensory loss) • Symptoms/Signs – Pain – Paresthesia/dysesthesia – Loss of vibratory sensation
    38. 38. Symmetric neuropathy Small fiber neuropathy • Involves A delta and C fibres • Painful paraesthesias that are burning, stabbing, crushing, aching, or cramp like, with increased severity at night • Loss or pain & temperature sensation • Preserved reflexes Large fiber neuropathy • Large fiber sensory nerves • Electric tingling or a snug bandlike sensation around ankles and feet • Prominent ataxia • Absent ankle jerk reflexes, prominent proprioceptive sensory impairment • Gait instability with eyes closed
    39. 39. Signs of sensory neuropathy • Dystrophic nails • Callus • Dry skin/ cracked skin ( autonomic neuropathy) • Charcot’s feet
    40. 40. Signs of motor neuropathy • Muscle wasting • Muscle weakness Claw toe
    41. 41. Diagnosis • Clinical signs • Sensation: Vibration with tuning fork (128 Hz) Proprioception Touch/ pressure • Deep tendon reflexes : Ankle jerk Knee jerk
    42. 42. Simple tools Monofilament: 5.07 Semmes-Weinstein (10-g) nylon filament test (10-g monofilament test)
    43. 43. Biothesiometer • Basically an electronic tuning fork • To detect the vibration perception threshold Picture courtesy: http://www.diabetes.usyd.edu.au/foot/Fexam1.html >25 volts: suggestive of neuropathy
    44. 44. Road to ulcer Bunions Clawed toes Abnormal toe nails Picture courtesy: http://www.diabetes.usyd.edu.au/foot/Fexam1.html
    45. 45. Fissure Story –Origin: DysautonomiaAutonomic neuropathy Dry Feet Fissuring Infection Abscess Ulcer
    46. 46. The Callus Story- Origin: Motor Motor Neuropathy Deformity Abnormal pressures Callus Callus haematoma Abscess Ulcer
    47. 47. The Extent of Diabetic Neuropathy
    48. 48. Carpal Tunnel Syndrome • Most common entrapment neuropathy in type 2 DM • Tingling, numbness, parasthesias • Women > men • Surgical release by severing the carpal ligament
    49. 49. Diabetic Amyotrophy • Acute or subacute pain, weakness, and atrophy of the pelvic girdle and thigh musculature. • Weak hip flexion • Absent knee jerk • Initially unilateral • Weight loss
    50. 50. Cranial Nerve Palsy • 3 rd nerve palsy is the common • Diplopia, eye pain, ptosis • Usually pupillary sparing • Spontaneous recovery present
    51. 51. Treatment • Foot care education • Foot care education • Foot care education • Metabolic management • Symptomatic treatment Effective patient education can reduce the incidence of foot ulceration and amputation by over 50 % Boulton AJM. Lowering the risk of neuropathy, foot ulcers and amputations Diabetic Medicine Volume 15 Issue S4, Pages S57 - S59
    52. 52. Basic foot care education  Washing and inspecting feet on a daily basis  Selecting and using appropriate and properly fitted footwear  Using slippers indoors (i.e., no bare feet).  Providing proper nail and callus care (e.g., no bathroom surgery)  Avoiding extreme temperatures  Avoiding soaking feet for > 10 min  Promptly reporting problems, such as infections, ulcers, and cuts that do not heal.
    53. 53. Drugs for symptomatic relief • Tricyclic antidepressants: amytryptline, imipramine • Selective serotonin uptake inhibitors: Paroxetine, Escitalopram, Duloxetine • Anticonvulsants : Carbamazepine, Gabapentin, Pregabalin • Analgesics : Tramadol
    54. 54. Autonomic Neuropathy • Cardiovascular • Gastrointestinal • Genitourinary • Erectile dysfunction
    55. 55. Key messages • Diabetic microvascular complications are preventable • SCREEN 1. Microalbumin to detect nephropathy 2. Neurological exam for neuropathy 3. Retina evaluation for retinopathy • TREAT 1. ACEI/ ARB for nephropathy 2. Foot care education for neuropathy 3. Good metabolic control for all microvascular complications
    56. 56. Thank you • Nishanth S, Endocrinologist • Aniyan Poulose, Registrar • Pradeep R, Podiatrist • Vani KB, Diabetes Educator The Endocrinology & Diabetes Practice Trivandrum www.endocrinologydiabetes.com

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