UNIT – 4
CHRONIC COMPLICATIONS OF
• Discuss Follow up care of DM for early
identification and management of complications
• Describe the most common chronic
complications of Type 1 & Type 2 DM
• Discuss Common presentations of the common
• List Screening recommendations(who, when and
• Explain how to manage common complications
• Expedite patient referral for further Management
What are the Aims of Monitoring
in DM Care?
– Glycemic control
– Identification and control of associated risk
– Assessment of adherence
– Psychosocial assessment
– Prevention, Identification and treatment of
– Diabetes education history
– DKA frequency, severity, and cause
– Hypoglycemic episodes
– Current treatment
• Medications, meal plan, physical activity patterns and results of glucose monitoring
– Adherence to treatment
• Weight, BMI, waist circumference
• B/P including orthostatic measurement, when
• Fundoscopic examination
• Comprehensive foot examination
– Palpation of dorsalis pedis and posterior tibial pulses
– Presence/absence of patellar and Achilles reflexes
– Determination of proprioception, vibration, and
– 2hr Postprandial
– Urine Ketone
– Urine Glucose
Self Monitoring of Blood Glucose
• Ideally the Standard Of Care in DM management
• Frequency and targets dictated by particular needs and goals of patient
• Very important for patients treated with insulin,
Type 1 patients and pregnant women
• Helps prevent asymptomatic hypoglycemia and
• Recommendation is > 3X a day in Type 1 and 2 on multiple Insulin injection
• No consensus on frequency for type 2 patients
– Tells about the glucose level over months (2-3
– Has similar relation with chronic complications
with FPG and 2h postprandial glucose
– At least 2x a year for patients who meet
– Quarterly in patients whose therapy has
changed or who are not meeting glycemic goals
Fasting Blood glucose
• Fasting Blood glucose
– Tells short term glucose level
– When combined with postprandial plasma it is
best alternative to HB A1C
– Poor means of assessment
– May be the only tool available in some setups
Urine Ketone/Serum Ketone
• Early indicators of DKA
• Should be measured when plasma glucose is
persistently above 300mg/dl,
• during concurrent illnesses, or
• Patients with symptoms such as nausea,
Vomiting, or abdominal pain
• Glycemic controls
– HB A1c <7%
– Pre-prandial (capillary plasma) 80-130mg/dl
– Postprandial G (capillary plasma) <180mg/dl
Chronic Complications of DM
• Diabetes-related complications affect many organ systems and are responsible for the majority of morbidity and mortality associated with the disease.
• Diabetes-related complications usually do not appear until the second decade of hyperglycemia. However it can be seen at diagnosis in many Type 2 DM .
• Diabetes-related complications can be divided into vascular and nonvascular complications and are similar for type 1 and type 2 DM.
• The vascular complications of DM can be:
– microvascular (retinopathy, neuropathy, nephropathy), or
– macrovascular complications (coronary heart disease [CHD], peripheral
arterial disease [PAD], cerebrovascular disease).
• Nonvascular complications include gastroparesis, infections (PTB and UTI), skin changes, Periodontal disease and hearing loss.
• 35yrs old female known type 1 diabetic on
NPH 40/28 came for regular follow up – (old
chart was lost)
• FBS – 220mg/dl & HgA1c – 8.5%
• What further history do you wish to know?
• Duration of DM, home blood glucose profile
• History of polySx, hypoglycemic episodes
• Any hx suggestive of infection at any site
• Hx of visual disturbance, foot ulcer, Sx of
• Insulin injection techniques, sites, & place of
• Any other known chronic illness like HTN,
Case 1 cont’d….
• Patient is diabetic for the last 30 years
• Takes her medication regularly as prescribed
• FBS usually >200mg/dl for the past 05 years
& post prandial glucose is between 250 &
• Complains of dysuria, & urgency – no poly
symptoms & no hypoglycemic episodes.
Case 1 cont’d….
• No visual complaints – but was told to have
some changes on routine retinal screening
• No foot ulcer & no symptoms of peripheral
• Rotates injection site, has no induration, &
stores insulin in the refrigerator
• How would you investigate this patient?
Case 1 cont’d
– +/- Urine culture
• CBC – Normal
• U/A –
Glucose – ++
Protein – +++
Ketone – negative
Leukocyte & nitrite –both positive
WBC – 10-15/ HPF
Epithelial cells – Many/LPF
• What is your final diagnosis?
• How would you treat this patient?
Case 1 cont’d
• Management of Patient
✓ Ciprofloxacin 500mg PO BID for 7 – 10 days
✓ Titrate insulin dose & start regular insulin
✓ Advise on continuing retinal follow up
✓ Advise on diet and exercise
✓ Appoint after 02 weeks
Case 1 cont’d
• 2 weeks later
✓ Proteinuria – ++
✓ No WBC & RBC
✓ Leukocytes & Nitrites – both negative.
• How would you like to proceed?
Case 1 cont’d
• Discuss on Diagnosis of proteinuria – needs to
be repeated and confirmed 3-6months later
• Discuss on causes that transiently increase
• UTI, hematuria, heart failure, fever, severe
hyperglycemia, severe HTN and vigorous
• Diabetic nephropathy is the leading cause of Chronic Kidney Disease(CKD) and End Stage Renal
• Albuminuria in individuals with DM is associated with an increased risk of CVD
• Patients with nephropathy commonly have retinopathy
• An important marker of increased cardiovascular risk. It carries a mortality rate ~50% from Cardio Vascular causes.
• Its pathogenesis is related to chronic hyperglycemia
• Occurs in 20-40% of diabetic patients
• Type 1: 10-20 years after initial diagnosis
• Type 2: May even be present at time of
diagnosis (long pre-clinical period)
• Usually progresses from albuminuria to
• Intervention at the stage of Microalbuminuria can retard the progression to end-stage renal disease
• Hyperglycemia is necessary for the development of the lesions of diabetic nephropathy and also to
sustain the lesions.
• Hemodynamic mechanisms may also be involved. Hyper filtration modulates the rate of progression of diabetic lesions. Systemic BP levels are also implicated in progression.
• Genetic predisposition to or protection from
diabetic nephropathy appears to be the most
important determinant of diabetic nephropathy risk.
• Screen for albuminuria
✓ Type 1: 5 years after diagnosis
✓ Type 2: At the time of diagnosis
✓ In every pregnant lady
✓ Thereafter, screening should be done yearly
• Measure serum creatinine at least yearly
• Refer to Internist / Nephrologist patients
with persistent proteuinuria and deranged
Prevention of Diabetic Nephropathy
• Intensive glycemic control shown to prevent
microvascualr complications including Diabetic
Nephropathy in both type 1&2 diabetes.
• The lowest possible HbA1c is the target.
• Treatment of hypertension is of paramount
importance in the prevention of Diabetic Nephropathy.
• Life style modifications particularly cessation of
smoking must be encouraged.
• The above measures also reduce CV morbidity and mortality substantially.
Treatment: Diabetic Nephropathy
• Improved Glycemic control.
• strict blood pressure control is effective in
reducing albumin excretion and slowing the
decline in renal function.
• Blood pressure should be maintained at
<140/90 mmHg in diabetic individuals.
• Administration of an ACE inhibitor or ARB.
• Dyslipidemia should also be treated.
• Cessation of smoking
• 60yrs old male presented to ER with history of
Rt. toe ulceration of 15days duration
• Was on treatment (cloxacillin & wound care) at
nearby clinic but no change
• Complains of numbness of lower limbs with
burning & tingling sensation
• History of HTN diagnosed 5yrs back – not on
What additional information do you like to
• Patient claims he had mild trauma to the
feet while walking with sandals
• But wound was noticed by child as he has
difficulty of vision
• He has mild pain and there is a pussy
discharge from the wound
• No past history of diabetes
• He did not take antihypertensives as he did
not want his body to “adapt” to the
• He has no Shortness Of Breath on exertion
What are the possible diagnosis and how do
• Physical Exam
–BP – 150/95mmHg
–Bilateral cataract & loose upper front incisors
–Shiny, dry, cracked, lower limbs with loss of
–Rt. 1st digit well circumscribed 2x2cm
ulceration & whitish discharge, tenderness
not as marked as size of wound
–All peripheral pulses are palpable
–Decreased sensation & +ve monofilament
• Investigation results
–WBC- 14,000 N-85%, L-15%
–Platelet – 250,000
–U/A – protein 1+ and glucose 2+
–FBS – 180mg/dl repeat
–BUN – 30 & Creat. – 1.4mg/dl
Retinal screening – Background
• ECG – non revealing
• X-ray of the foot: Non-revealing
• Lipid profile
– Total Cholesterol – 270mg/dl
– LDL – 150mg/dl
– HDL – 35mg/dl
– Triglyceride – 172mg/dl
• Type 2 DM with chronic complications
– Diabetic foot ulcer – Wagner Stage 2
– Diabetic neuropathy
– Diabetic retinopathy
– Diabetic nephropathy
• Stage I hypertension
• Most common of the chronic DM complications
• Occurs in ~50% of individuals with long-standing type 1 & type 2 DM
• Impairs quality of life
• As with other complications, development of neuropathy correlates with duration of DM & glycemic control.
• Other risk factors are obesity, hypertension, smoking, alcohol use and dyslipidemia.
• Most important risk factor for foot ulcer and amputation
• May manifest as polyneuropathy, mononeuropathy, and/or autonomic neuropathy
Pathogenesis of Diabetic Neuropathy
• Metabolic factors
– High blood glucose
– Advanced glycation end products
– Abnormal blood fat levels
• Nerve fiber repair mechanisms
• Symptoms of gastro paresis
– Examination of feet- sensory tests using 128 Hz tuning fork or cotton wool, 10-g monofilament pressure sensation at the distal plantar aspect of both great toes and metatarsal joints,
pin prick sensation and assessment of ankle reflexes
– Blood pressure and pulse on
Classification of Diabetes Neuropathy
– Distal Symmetric Polyneuropathy
– Autonomic neuropathy
– Mononeuropathy (focal and multifocal)
Distal symmetric polyneuropathy
• Commonest type of diabetic neuropathy.
• Distal symmetric sensory or sensorimotor neuropathy
– ↓ pain sensation and vasculopathy ulcer risk
• Patients complain of numbness, tingling, sharpness, or burning that begins in the feet / hands & spreads proximally
• Pain is present at rest and worsens at night.
• Physical examination reveals sensory loss, loss of ankle deep-tendon reflexes, and abnormal position sense
• It is a diagnosis of exclusion
• Individuals with long-standing type 1 or 2 DM may develop signs of autonomic dysfunction
• DM-related autonomic neuropathy can involve the cardiovascular, gastrointestinal, genitourinary, sudomotor, and metabolic systems.
– cardiovascular system cause a resting tachycardia and orthostatic hypotension. Sudden death have also been attributed to autonomic
– Gastroparesis and bladder emptying abnormalities are often caused by
the autonomic neuropathy seen in DM.
–Hyperhidrosis of the upper extremities and anhidrosis of the lower extremities result from sympathetic nervous system dysfunction.
Anhidrosis of the feet can promote dry skin with cracking, which increases the risk of foot ulcers.
– Autonomic neuropathy may reduce counterregulatory hormone release
(especially catecholamines), leading to an inability to sense hypoglycemia appropriately
• It is a syndrome characterized by severe disabling pain in the distribution of one or more nerve roots. It may be accompanied by motor weakness.
– Intercostal or truncal radiculopathy causes pain
over the thorax or abdomen.
– Involvement of the lumbar plexus or femoral nerve may cause severe pain in the thigh or hip and may be associated with muscle weakness in the hip flexors or extensors (diabetic amyotrophy).
• Fortunately, diabetic polyradiculopathies are
usually self-limited and resolve over 6–12 months.
• It is dysfunction of isolated cranial or peripheral
• It is less common than polyneuropathy in DM
• It presents with pain and motor weakness in the
distribution of a single nerve.
– Carpal tunnel syndrome….
– Involvement of the third cranial nerve is most common and is heralded by diplopia. Physical examination reveals ptosis and ophthalmoplegia with normal pupillary constriction to light.
– Sometimes other cranial nerves, such as IV, VI, or VII (Bell’s palsy), are affected.
Treatment of Diabetic neuropathy
• Improve glycemic profile
• Foot care
• May use analgesics initially
• Tricyclic antidepressants – amitriptyline
25mg po nocte – may increase dose gradually
• Carbamazepine 200mg po nocte & increased
• Refer to neurologist
Diabetic foot ulcer
• Major Cause of Hospital Admission in diabetes
• Leading cause of non traumatic lower extremity amputation
• Major Causes of foot ulcer–
– Trauma in Neuropathy &/or
– Peripheral Arterial Disease
– Infection – Not Primary Cause
• Infection is Secondary to Ulceration of Protective Epidermis
• 15% of Diabetics Develop it at Some Time
• Typical Places:
– Plantar Surface of the Great Toe
– Heads of Metatarsals
– Lateral margins due to ill fitting shoe
Risks For Foot Ulceration
• Poor diabetes control
• Long duration of diabetes
• Peripheral Neuropathy: Somatic & Autonomic
• Peripheral Vascular Disease
• Foot Deformity – Claw Toes, Hammer Toes
• Presence of Callus
• Previous Foot Ulcers
• Poor Sight
• Male sex
• Old age
Evaluation for the foot at risk
• Look for Peripheral Arterial Disease
– Symptoms :Intermittent Claudication, Cold Feet, Nocturnal Pain, Rest Pain, Pain Relieved with Dependency or rest,
– Signs: Absent Pulses, Blanching On Elevation, Delayed Venous Filling After Elevation, Loss Of Hair On Foot & Toes, Gangrene
– Doppler studies
• Look for Neuropathy
– Tuning Fork
• Anatomic Deformities
Prevention Diabetic foot disease
Patient education should emphasize
(1) careful selection of footwear,
(2) daily inspection of the feet to detect early signs of poor-fitting footwear or minor trauma,
(3) daily foot hygiene to keep the skin clean and moist,
(4) avoidance of self-treatment of foot abnormalities and high-risk behavior (e.g., walking barefoot), and
(5) prompt consultation with a health care provider if an abnormality arises.
The 6 Ps for Prevention of Foot Ulcer
1. Podiatric Care
2. Pulse Examination
3. Protective Shoes
4. Pressure Reduction
5. Prophylactic Surgery
6. Preventive Education
• Common microvascular complication:
– Type 1: Mostly occurs after 15-20 years
– Type 2: Often present at diagnosis (long preclinical period)
– The leading cause of adult-onset blindness
• Diabetes also ↑ risk of glaucoma &
• Fundamental defects in retinopathy:
– Vascular leakage & neovascularization
• Non (pre-)proliferative retinopathy
– Abnormal vessels within retina
• Basement membrane thickening
• Macular edema, lipid exudates
– Intraretinal angiogenesis
• Proliferative retinopathy
– Vitreous/preretinal hemorrhage
– Retinal detachment
– Type 1: After 5 years of diagnosis
– Type 2: At time of diagnosis
– Pregnant ladies
– Thereafter, screen annually
• Positive findings should be referred to
ophthalmologists for follow up and
END OF UNIT – 4