Diabetic Diabetic Microvascular Microvascular Complications Complications Mathew John MD, DM, DNB Consultant Endocrinologist
Diabetic Diabetic Microvascular Microvascular ComplicationsComplications
Mathew John MD, DM, DNB
Consultant Endocrinologist
Microvascular complication
MICROVASCULAR COMPLICATIONS
Retinopathy
Neuropathy
NephropathyCardiomyopathy
Cheiroarhropathy
Dermopathy
Structure of talk
• Screening • Diagnosis • Treatment
Retinopathy Nephropathy
Neuropathy
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
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
UKPDS results of Intensive therapy
Risk reduction vs. conventional therapy
Risk factors for microvascular complications
• Degree of glycemic control• Duration of disease • Hypertension • Dyslipidemia • Smoking
Pathophysiology of complications
Diabetic Retinopathy
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
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
International Clinical Diabetic Retinopathy (DR) Disease Severity Scale
• No apparent DR
• Mild nonproliferative DR
• Moderate nonproliferative DR
• Severe nonproliferative DR
• Proliferative DR
Mild non proliferative retinopathy
Flame shaped hemorrhages
MicroaneursmsDot & Blot hemorrhages
Severe non proliferative retinopathy
Proliferative retinopathy
Clinically Significant Macular edema
www.retinalphysician.com/archive%5C2009%5CJan
Vitreous hemorrhage
Symptoms of diabetic retinopathy
NO SYMPTOMS
Even stages up to proliferative retinopathy can be asymptomatic
Visual loss : Macular edema Vitreous hemorrhage Retinal detachment
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 dilatationSlit lamp biomicroscopyIndirect ophthalmoscopy for retinal periphery Gonioscopy Flourescein Angiogram
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
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
Metabolic management
• Glycemic control • Intensive BP control : 34 % improvement in
retinopathy outcomes after intensive BP control
• Lipid management • Anemia correction
Diabetic Nephropathy
Nephropathy
• Leading cause of chronic renal failure in the developed world
• It is also one of the most significant long-term complications in terms of morbidity and mortality for individual patients with diabetes.
• Diabetes is responsible for 30-40% of all end-stage renal disease (ESRD)
• Microalbuminuria is a cardiovascular risk factor
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
Laboratory investigations
• Urine microalbumin • Serum creatinine • Serum potassium • Urine routine
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
Progression of nephropathy
Normal Microalbuminuria 2% per annum
Clinical Nephropathy> 300 mg/gm
2% per annum
< 30 mg/gm 30-300 mg/gm
If microalbumin is positive
• Do urine routine
• Urine microalbumin > 300 mg/gm : do 24 hour urine protein• Creatinine, serum potassium
• Consider ultrasound abdomen
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
Treatment
• Blockage of renin-angiotensin-aldosterone( RAAS) ACE inhibitor •Ramipril : 2.5 to 10 mg/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
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
Diabetic Neuropathy
WHO definition
A disease characterized by decline and damage of nerve function leading loss of sensation, ulceration and subsequent amputation.
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
Classification
• Symmetric polyneuropathy• Polyradiculopathy• Mononeuropathy• Autonomic neuropathy
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
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
Signs of sensory neuropathy
• Dystrophic nails• Callus • Dry skin/ cracked skin ( autonomic
neuropathy)• Charcot’s feet
Signs of motor neuropathy
• Muscle wasting • Muscle weakness
Claw toe
Diagnosis
• Clinical signs• Sensation: Vibration with tuning fork (128 Hz) Proprioception Touch/ pressure • Deep tendon reflexes : Ankle jerk Knee jerk
Simple tools
Monofilament: 5.07 Semmes-Weinstein (10-g) nylon filament test (10-g monofilament test)
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
Road to ulcer
Bunions Clawed toes Abnormal toe nails
Fissure Story –Origin: Dysautonomia Autonomic neuropathy
Dry Feet
Fissuring
Infection
Abscess
Ulcer
The Callus Story- Origin: Motor Motor Neuropathy
Deformity
Abnormal pressures
Callus
Callus haematoma
Abscess
Ulcer
The Extent of Diabetic Neuropathy
Carpal Tunnel Syndrome
• Most common entrapment neuropathy in type 2 DM
• Tingling, numbness, parasthesias• Women > men • Surgical release by severing the carpal ligament
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
Cranial Nerve Palsy
• 3 rd nerve palsy is the common
• Diplopia, eye pain, ptosis
• Usually pupillary sparing
• Spontaneous recovery present
Treatment
• Foot care education • Foot care education • Foot care education
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 amputationsDiabetic Medicine Volume 15 Issue S4, Pages S57 - S59
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.
Drugs for symptomatic relief
• Tricyclic antidepressants: amytryptline, imipramine
• Selective serotonin uptake inhibitors: Paroxetine, Escitalopram, Duloxetine
• Anticonvulsants : Carbamazepine, Gabapentin, Pregabalin
• Analgesics : Tramadol
Autonomic Neuropathy
• Cardiovascular • Gastrointestinal• Genitourinary • Erectile dysfunction
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
Thank you
• Nishanth S, Endocrinologist • Aniyan Poulose, Registrar • Pradeep R, Podiatrist • Vani KB, Diabetes Educator
The Endocrinology & Diabetes PracticeTrivandrum www.endocrinologydiabetes.com