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. 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. UKPDS results of Intensive therapy
Risk reduction vs. conventional therapy
7. Risk factors for microvascular
complications
• Degree of glycemic control
• Duration of disease
• Hypertension
• Dyslipidemia
• Smoking
• Genetic factors
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. 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. Symptoms of diabetic retinopathy
NO SYMPTOMS
Even stages up to proliferative retinopathy can be
asymptomatic
Visual loss : Macular edema
Vitreous hemorrhage
Retinal detachment
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. International Clinical Diabetic
Retinopathy (DR) Disease Severity Scale
• No apparent DR
• Mild nonproliferative DR
• Moderate nonproliferative DR
• Severe nonproliferative DR
• Proliferative DR
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. 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. Metabolic management
• Glycemic control
• Intensive BP control : 34 % improvement in
retinopathy outcomes after intensive BP control
• Lipid management
• Anemia correction
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. 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
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. Progression of nephropathy
Normal Microalbuminuria
2% per
annum
Clinical
Nephropathy
> 300 mg/gm
2% per
annum
< 30 mg/gm 30-300 mg/gm
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. 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. 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. 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
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. 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
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. 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. Cranial Nerve Palsy
• 3 rd nerve palsy is
the common
• Diplopia, eye pain,
ptosis
• Usually pupillary
sparing
• Spontaneous
recovery present
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. 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.
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. Thank you
• Nishanth S, Endocrinologist
• Aniyan Poulose, Registrar
• Pradeep R, Podiatrist
• Vani KB, Diabetes Educator
The Endocrinology & Diabetes Practice
Trivandrum
www.endocrinologydiabetes.com
Editor's Notes
50 % of all patients with type 1 DM and PDR and &gt; 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.