Diabetic Complications

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					Diabetic Complications
Safia M Sherbeeni, MD, FRCPE
Consultant Endocrinologist
Director, Specialized Diabetes & Endocrine Center
King Fahd Medical City

Presented by; Badrudeen Mahmood Buhary
Asst. Consultant
Specialized Diabetes & Endocrine Center
King Fahd Medical City
“Persistent hyperglycemia is a Ticking Time Bomb”

                      Carl von Noorden. 1915
                      German diabetes specialist
Impact of DM

• The leading cause of adult blindness
• The leading cause of non-traumatic lower
  extremity amputation
• The leading cause of renal failure
• Results in 2-4 folds increased in CV risk
• The 4th leading cause of death globally
• Direct costs of treating diabetes: 2.5 %
  to 15 % of annual health budgets
• Cost is increased by 250 % in patients
  with complications compared to those
• Complications from diabetes result in
  – Disability
  – Reduced life expectancy
  – Huge health costs
Diabetic Complications
 • Acute:
    – DKA
    – HHS
 • Chronic:
    – Microangiopathic
       • Retinopathy
       • Nephropathy
       • neuropathy
    – Macroangiopathic
       • CVA
       • IHD
       • PVD
    – Others
       •   Diabetic Foot
       •   Infection
       •   Dermatologic
       •   musculoskeletal
Diabetes is:
 • The leading cause of blindness in people aged
   20-74 years
 • The leading cause of non-traumatic lower
   extremities amputation, accounting
   approximately for 50 % of cases. 5-15 % of
   people with diabetes require an amputation at
   some time in their lives and 15 % will develop
   foot ulcers.
 • The most common single cause of ESRD and
   accounting for 43 % of all new cases entering
   hemodialysis in USA.
 • Diabetic patients continue to have 3-5 folds
   greater risk of developing cardiovascular disease
   than do non diabetic persons
Chronic complications

    are extraordinarily high
    in the diabetic            50

    population                 45
o   Retinopathy 49 %           30

o   Neuropathy      40 %       20
o   Nephropathy 35 %            5
o   Macrovascular disease           DR   Neur   NP   CVD

         43 %
    In the UKPD study 50 % of the diabetic
    patients, at the time of diagnosis, already
    had evidence of tissue damage:
•   8% had CVD
•   37 % had microaneurysm or more severe
    retinopathy in one eye
•   18 % retinopathy in both eye
•   4 % clinical albuminuria

“Hyperglycemia is the primary initiating factor
  for damage of the target tissue”


    Aldose Reductase         AGEs            Reactive O Radicals   Protein Kinase C

                       Endothelial Dysfunction & Damage

        DR                   NP                     NP                CVD
Mechanism of tissue damage by

  Intracellular hyperglycemia damages cells by
  multiple mechanisms:
• Generation of reactive oxygen (Superoxide
  production by mitochondrial electron transport
  –   Diacylglycerol activation of PKC
  –   Advanced Glycation End product formation
  –   Aldose Reductase Activity and Redox changes
  –   Hexosamine pathway flux
• Derangement of NO bioavailability

• DR
• Retinal detachment
• Blindness

• Non-retinal:
  – Vitreous Hemorrhage
  – Glaucoma
  – Rubeosis iridis
  – Cataract
  – sty
Diabetic Retinopathy (DR)

• DR is the most frequent cause of new
  blindness among adults
• The prevalence of DR and vision-threatening
  retinopathy in know diabetic: 40.3 % and 8.2
• Poor glycemic control, duration of DM,
  presence of nephropathy and HTN are risk
Diabetic Retinopathy

• CSME (Clinically Significant Macular Edema)
• NPDR (Non-Proliferative DR)
  –   Mild
  –   Moderate
  –   Severe
  –   Very severe
• PDR (Proliferative DR)
  – Early
  – High risk
International Clinical Diabetic Retinopathy (DR) Disease Severity Scale

 Proposed Disease             Findings Observable With Dilated
 Severity Level               Ophthalmoscopy

 No apparent DR               No abnormalities
 Mild nonproliferative DR     Microaneurysms only
 Moderate nonproliferative    More than "mild" but less than "severe"
 Severe nonproliferative DR   Any of the following:
                              20 or more intraretinal hemorrhages in 4 quadrants
                              Definite venous beading in 2 or more quadrants
                              Prominent IRMA in 1 or more quadrants and no
 Proliferative DR             1or more of the following:
                              Definite neovascularization
                              Preretinal or vitreous hemorrhage

                                  IRMA = intraretinal microvascular abnormalities
Diabetic Retinopathy
 • The rate of progression to proliferative retinopathy 4 years
   after the initial evaluation was less than 1% for both young
   and older patients with diabetes and "no DR”
 • The risk in those with a "rare microaneurysm or
   hemorrhage" was 4.1 % in younger patients and
   considerably less in older patients
 • The risk of progression to proliferative DR in moderate
   non-proliferative DR with high-risk features after 1 year is
 • In eyes at the stage of severe non-proliferative DR, the
   rate of developing proliferative DR with high-risk
   characteristics within 1 year is approximately 17%, and
   within 3 years it is more than 40%
Diabetic Macular Edema

 •   Most frequent cause of decreased vision in patients with
     nonproliferative diabetes retinopathy.
 •   Clinical features:
      – Symptoms: decreased vision
      – May present as noncystoid or cystoid macular edema
      – In noncystoid edema, the retina at the posterior pole appears thickened
        and fluorescein angiography demonstrates intraretinal leakage during
        the late phase
      – In cystoid edema, diffuse retinal thickening at the foveal usually
        associated with microcysts and fluorescein angiography demonstrates
        flower-petal pattern of leakage at the fovea during the late phase
      – Resorption of the edema commonly results in precipitation of lipid
        residues beneath the sensory retinal which can be observed as white to
        yellow deposits of
        hard exudates
Diabetic Macular Edema

• Management:
  – Control diabetes, blood pressure and serum lipid profile.
  – Focal laser photocoagulation in a clinically significant macular edema
  – Consider vitrectomy if tractional component present or refractory to
    other treatment modalities.
  – Follow-up 2-4 months after treatment of the macular edema, if
    persists, consider re-treatment.
  – Recent advance: consider intravitreal or subtenon corticosteroid
    injections in refractory cases.
  Nonproliferative Diabetic Retinopathy

• Most common form of diabetic retinopathy.
• After 20 years of the disease, almost 100% of patients with
  type 1 and 60% of type 2 have some degree of retinopathy.
• Clinical features:
   – Signs:
      – Microaneurysm, intraretinal hemorrhages, cotton wool spots
        and hard exudates
      – Venous tortuosity or beading, capillary dropout and intraretinal
        microvascular abnormalities (IRMA)
      – Increasing formation of microaneurysm leads to increased
        vascular permeability of the retinal capillaries and result in
        retinal edema particularly in the macular area
Non-proliferative Diabetic Retinopathy

• Management:
   Improve patients education and understanding about the
    disease process.
   Control of blood glucose, cholesterol and blood
   Photocoagulation in severe non-proliferative retinopathy.
   Annual check-up 5 years after onset for patient aged
    less than 30 years old, and at time of diagnosis for
    patients aged 30 and older.
   Frequency of scheduled check-up depends on the status
    of the retinopathy
Proliferative Diabetic Retinopathy (PDR)

•   Characterized by growth of new vessels on the surface of the retina.
•   Clinical features:
      Symptoms: progressive loss of vision, particularly in those who are not
        properly followed or treated.
      Signs:
          • Fine to severe loops of new vessels that may grow on the optic disc:
             neovascularization of the disc (NVD) or elsewhere (NVE)
          • In the anterior segment, PDR is manifested by neovascularization of the
             iris (NVI), the angle (NVA) and may eventually complicated with
             neovascular glaucoma
          • These new vessels may leak and resulting in retinal edema. They are
             also fragile and prone to bleed
          • Opaque fibrovascular proliferation tissue often appears on the internal
             limiting membrane (adjacent to the new vessels) and becomes adherent
             to the vitreous
          • Contraction of this fibrovascular tissue may lead to:
                Distortion or dragging of the macula
                Mild to extensive retinal detachment
                Avulsion of retinal vessels and vitreous hemorrhages
Proliferative Diabetic Retinopathy (PDR)

 • Risk factors:
    – Duration of the diabetes
      30-34 years of diabetes increase the risk of
      retinopathy by 65%
    – Overt albuminuria
    – High level of blood total cholesterol and LDL
    – Others:
       • Race
       • cigarette smoking
       • alcohol
Proliferative Diabetic Retinopathy (PDR)

• Management:
   – Strict blood glucose, blood pressure and cholesterol control.
   – Photocoagulation for clinically significant macular edema prior to
     scatter (panretinal) photocoagulation (PRP).
   – Consider PRP in severe proliferative diabetic retinopathy.
   – Consider additional PRP if incomplete regression is observed,
     increasing of the extent of vitreous hemorrhage or worsening of
     overall vitreoretinal condition.
   – Vitrectomy.
   – Experimental treatments; Depo steroid injection for diabetic macular
     edema, systemic Protein kinase-C inhibitor and aldolase reductase
Diabetic Nephropathy

• DN
• Acute papillary necrosis
• Urinary Tract Infection
Diabetic Nephropathy

 • 20% to 40% of all diabetic have evidence of
   DN ( T1DM:30%-40%. T2DM: 5%-40%)
 • DM is the most common single cause of
   ESRD accounted for 43 % of all new cases
   of dialysis in USA, according to the US
   Renal Data System in 1999 (compared to
   33.8 % in 1988)
 • The annual cost is 18 billion US $
Diabetic Nephropathy

• In a hospital-based study from Dahran Health
  Center, DN was the cause in 60 % of ESRD
 Al-Khunaizi et al, SMJ 2003; 24 (7): 798-99

• Was 14.8 % in Al Hada Armed Forces
 Nephrol Dial Transplant 1994; 9 (8): 1072-6

• Prevalence of microalbuminuria was 41.3 %
 Al Zaid et al Diabetes Res Clin Prac 1994; 26 (2): 115-20
Diabetic Nephropathy

• DN is associated with increased mortality
• The 3 year mortality for patients with DN and
  on dialysis exceeds that of HTN by 26 % and
  that from GN by 72 %
DN and Mortality

    No nephropathy     1%

    microalbuminuria   3%
    macroalbuminuria   5%

         ESRD          19%
Natural History of DN

• The clinical course of DN is best defined in
  type 1 DM
• As first described by Mogensen
• 5 stages:
Natural History of DN

The clinical course of DN is best defined in type 1 DM
As first described by Mogensen there are 5 stages:
• Stage 1 glomerular hyperfiltration and renal enlargement:
   at onset of DM. The RBF and GFR increase. BP remains normal
• Stage 2 silent stage early glomerular lesion with normal albumin excretion and
   normal GFR; the pathological changes consist of glomerular basement
   membrane thickening, and mesangial matrix expansion. It appears 18 to 36
   months after onset. BP is normal
• Stage 3 incipient diabetic nephropathy or microalbuminuric stage. Occurs after
   5-10 years of DM the prevalence of microalbuminuria varies from 25 % to 40 %.
   Is higher in type 2. 80 % (and only 20%-40% of type 2) will develop overt
   nephropathy in 10-15 years with rate of 10% -20% increase in AER per year.
   GFR starts to fall and BP is usually elevated
• Stage 4 overt diabetic nephropathy proteinuria (detected by urine dipstick) and
   falling GFR by 2-20 ml/min/year. 50 % will go into ESRD in 10 years and 75 % in
   20 years. BP is elevated
• Stage 5 ESRD
Stage 1

•   At onset of DM.
•   Glomerular hyperfiltration
•   Renal enlargement
•   GFR increase.
•   BP remains normal
Stage 2

Silent Stage
• Appears 18 to 36 months after onset
• Early glomerular lesion with
  – glomerular basement membrane thickening, and
    mesangial matrix expansion
• Normal albumin excretion and
• Normal GFR.
• BP is normal
Stage 3

Incipient DN or Microalbuminuria Stage:
• Occurs after 5-10 years of DM
• Prevalence of microalbuminuria varies from 25 % to
  40 %.
• GFR starts to fall
• BP is usually elevated
• 80 % (20%-40% of type 2) will develop overt
  nephropathy in 10-15 years with rate of 10% -20%
  increase in AER per year.
Stage 4

Overt DN:
• Proteinuria (detected by urine dipstick)
• GFR falls by 2-20 ml/min/year.
• 50 % will go into ESRD in 10 years and 75 %
  in 20 years.
• BP is elevated
Stage 5


• Diabetic Neuropathy
• Stroke
• Demyelinating Disorders
Diabetic Neuropathy

• "The diabetic neuropathies are heterogeneous,
  affecting different parts of the nervous system
  that present with diverse clinical manifestations,"
• the presence of symptoms and/or signs of
  peripheral nerve dysfunction in people with
  diabetes after the exclusion of other causes,
• Quantitative electrophysiology, sensory, and
  autonomic function testing may help confirm the
Diabetic Neuropathy

 • The exact prevalence is difficult to
   determine due to the complex and varied
   clinical presentations and lack of a simple
   diagnostic test. Epidemiologic data suggest
   that approximately 30% to 40% of people
   with type 2 diabetes have a distal
   peripheral neuropathy
 Diabetic Neuropathy
• Distal symmetric polyneuropathy
  – Sensory
  – Motor
  – Sesorimotor
• Focal Neuropathies
  – Cranial mononeuropathy
  – Somatic
• Radiculopathy
• Autonomic
  –   Diabetic gastropathy
  –   Urinary bladder dysfunction
  –   ED
  –   Sweating abnormalities
  –   Diabetic diarrhea
Diabetic Neuropathy Classification and Staging

A.       Subclinical neuropathy
     –        Abnormal electrodiagnostic tests
          •      Decreased nerve conduction velocity
          •      Decreased amplitude of evoked muscle or nerve action
     –        Abnormal neurologic examination
          •      Vibratory and tactile tests
          •      Thermal warming and cooling tests
          •      Other
     –        Abnormal autonomic function tests
          •      Abnormal cardiovascular reflexes
          •      Altered cardiovascular reflexes
          •      Abnormal biochemical responses to hypoglycemia

         American Diabetes Association and American Academy of Neurology. Consensus statement report and
         recommendations of the San Antonio Conference on Diabetic Neuropathy. Diabetes Care. 1988; 11:592.
B.   Clinical neuropathy
     –   Diffuse Somatic Neuropathy
         •   Sensorimotor (Distal Symmetrical Sensorimotor Polyneuropathy)
             –   Primarily small-fiber neuropathy
             –   Primarily large-fiber neuropathy
             –   Mixed
     –   Autonomic Neuropathy
         •   Cardiovascular autonomic
         •   Abnormal pupillary function
         •   Gastrointestinal autonomic neuropathy
             –   Gastroparesis
             –   Constipation
             –   Diabetic diarrhea
             –   Anorectal incontinence
         •   Genitourinary autonomic neuropathy
             –   Bladder dysfunction
             –   Sexual dysfunction
     –   Focal Neuropathy
         •   Mononeuropathy
         •   Mononeuropathy multiplex
         •   Amyotrophy
Diabetic Autonomic Neuropathy (DAN)

 • Is a serious complication
 • Reported prevalence varies widely
 • Is the least recognized complication
 • Autonomic vasomotor, visceromotor, and
   sensory fibers innervate every organ
 • May affect many organs (cardiovascular,
   GIT, GU, Sudomotor, ocular)
• DAN manifests first in longer nerves
• May be either clinically evident or subclinical.
1.   Cardiovascular
2.   Gastrointestinal
3.   Genitourinary
4.   Metabolic
5.   Sudomotor
6.   Pupillary
Cardiovascular Autonomic Neuropathy

• Is the most studied
• Is serious and associated with increased
  mortality 5 times
Cardiovascular Autonomic Neuropathy

•   Resting tachycardia
•   Exercise intolerance
•   Orthostatic hypotension
•   Silent myocardial ischemia
CAN: Tests

• Valsalva maneuver
• Postural BP testing

• Esophageal dysmotility
• Gastroparesis (anorexia, nausea, vomiting,
  and early satiety)
• Enteropathy (constipation, diarrhea, fecal
• Gall bladder atony and enlargement

•   Neurogenic bladder (diabetic cystopathy)
•   Erectile Dysfunction
•   Retrograde Ejaculation
•   Dyspareunia

• Hypoglycemic unawareness
• Hypoglycemia-associated autonomic failure

•   Anhidrosis
•   Gustatory sweating
•   Heat intolerance
•   Dry skin

• Argyll-Robertson pupil
• Decreased diameter of dark-adapted pupil
Cerebrovascular Disease

• Diabetes is a major risk factor for stroke and
  is associated with an increase in overall
  stroke mortality
• hyperglycemia can adversely affect ischemic
Cerebrovascular Disease

• The etiology of stroke in diabetics is
  frequently microvascular disease from
  fibrinoid necrosis, which causes small
  subcortical infarcts designated as lacunar
• Diabetics also have an increased incidence of
  large vessel intracranial vascular disease.
Cerebrovascular Disease

• Although strict control of blood sugar has not
  been shown to reduce the overall incidence of
  stroke in diabetics
• Management of other associated risk factors
  (hypercholesterolemia, HTN, smoking) is
  important for the prevention of stroke in
  diabetic patients.
Cardiovascular Disease

•   IHD
•   CHF
•   Diabetic Cardiomyopathy
•   PVD
Cardiovascular Disease

• 2-4 fold ↑ risk of developing CVD
• CHD is one of the major causes of death
  – DM is associated with a 70% to 80% chance of
    premature death from cardiovascular disease
    and stroke
• Diabetes is a coronary heart disease
Cardiovascular Disease

• Cardiovascular diseases are a leading cause
  of diabetes-related morbidity and mortality
Cardiovascular Disease

• Long-term intensified management of multiple
  risk factors reduces cardiovascular disease
  by 50 %

 N Engl J Med 2003;348:383-93.
Diabetic Cardiomyopathy

 Accumulating data from experimental,
 pathological, epidemiological, and clinical
 studies have shown that diabetes mellitus
 results in cardiac functional and structural
 changes, independent of hypertension,
 coronary artery disease, age, dyslipidemia or
 any other known risk factor, which support the
 existence of diabetic cardiomyopathy.
• Refers to a disease process which affects the
  myocardium in diabetic patients causing a
  wide range of structural eventually leading to
  LVH, diastolic and systolic dysfunction or
  combination of these.
Stages of diabetic cardiomyopathy

       Stages        Characteristics          Functional features            Structural features             Study methods

Early stage     Depletion of GLUT4        No overt functional            Normal LV size, wall          Sensitive methods such as
                Increased FFA Carnitine   abnormalities or possible      thickness, and mass           strain, strain rate, and
                                          overt diastolic dysfunction                                  myocardial tissue velocity
                deficiency Ca2+
                                          but normal ejection fraction
                homeostasis changes
                Insulin resistance
Middle stage    Apoptosis and necrosis    Abnormal diastolic             Slightly increased LV mass,   Conventional
                Increased AT II Reduced   dysfunction and normal or      wall thickness, or size       echocardiography or
                                          slightly decreased ejection                                  sensitive methods such as
                IGF-I Increased TGF-ß1
                                          fraction                                                     strain, strain rate, and
                Mild CAN                                                                               myocardial tissue velocity
Late stage      Microvascular changes     Abnormal diastolic             Significantly increased LV    Conventional
                Hypertension CAD          dysfunction and ejection       size, wall thickness, and     echocardiography
                                          fraction                       mass
                Severe CAN
• Peripheral Arterial Disease is a major risk for
  lower limb amputation
• The true prevalence of PAD is difficult to
  determine for the following factors:
  – Most patients are asymptomatic
  – Many do not report their symptoms
  – Variation in tests used in diagnosis
  – Using ABI the prevalence: 20 % in patients aged
    >40 years and 29 % above 50 years of age
Diabetic Foot

 • Approximately 15% of persons with diabetes will
   have an ulcer in their lifetime
 • 0.5% to 29.0% will have neuropathic joint changes
 • The leading cause of non-traumatic lower
   extremities amputation, accounting approximately
   for 50 % of cases
 • One half to 80% of all amputations are diabetes-
 • 5-15 % of people with diabetes require an
   amputation at some time in their lives
Diabetic Foot

• Lower extremity amputation is associated with
  increased mortality
• 5% to 17% will die during the operation and
  2% to 23% will die within 30 days of surgery
• Five-year survival is 40% overall, but only
  25% in the very elderly (>80 years
Diabetic Foot

• The annual cost of diabetic foot ulcer care is
  $5 billion in direct cost and $400 million in
  indirect cost
• The direct cost of LEA ranges from $20,000
  to $60,000 per patient
Diabetic Foot Syndrome (DFS)

•   Skin
•   Joints
•   Vessels
•   Nerves
Pathogenesis of Diabetic Foot
                                                         Diabetes Mellitus

          Peripheral Arterial Disease                         Autonomic Neuropathy                       Peripheral Neuropathy

Arteriosclerosis   Cholesterol     ↓ Delivery of   O2,
                                                          ↓ Flare ↓ Perspiration   Autosympathectomy
                                                                                                          Sensory                      Motor
Oblitrans          Emboli          Nutrients and
                                                                                                                              Interosseous atrophy

                                                                      Dry Skin      ↑ Blood Flow                              Hammer Toes
                                                                                                                              Thinning of fat pad
                                                                                     ↑ Bone                                   over metatarsal heads
                                                                                                       Painless Trauma:

                                                                                     Joint Collapse    1. Mechanical
                                                                                                        - Foreign Body in
                                 Impaired Wound
                                                                                     Deformed Foot
                                                                                                        - Ill-fitting shoes
                                 Healing                                             (Charcot)
                                                                                                        - Home Surgery
                                                                                                        - Repetitive stress of
                                                                                     New Pressure
                                                                                                       2. Thermal
                                                                                                       3. Chemical

                   Blue Toe
                                                                      Infection                        Ulceration


  Major Gangrene                                                     Amputation
Diabetic Foot

• Risk Factors:
  – DM duration
  – Male sex
  – Smoking
  – Age
  – Presence of CVD, DR, nephropathy
  – Peripheral neuropathy
  – Bony deformity
  – PAD
  – History of ulcers or amputation
  – Severe nail pathology
Diabetic Foot

• Structural:
   –   Hammer Toes
   –   Pes Cavus
   –   Charcot’s Joint
   –   Hallux Valgus
• Skin:
  – Dry cracked skin
  – Callus
  – Bunion
  – Fungal Infection (athlete's foot)
  – Nail dystrophy
  – Ulcer
  – Gangrene
• Diabetic Ulcers:
  – Neuropathic
  – Ischemic
•   Xanthoma
•   Scleredema
•   Waxy skin
•   Diabetic dermopathy
•   Necrobiosis lipoidica diabetecorum
•   Granuloma annulare
•   Bullosis diabetecorum
•   Acanthosis Nigricans
•   Necrolytic migratory erythema
•   Skin infection
•   Candidiasis
•   Bacterial and fungal infection of nails
•   Necrotizing fasciitis
•   Malignant otitis externa
•   Mucormycosis
•   Lipatrophy
•   Lipohypertrophy
Screening & Prevention of Diabetic

• Type 1 DM:
  – 5 year after onset
  – At puberty whatever the duration
• Type 2 DM:
  – At diagnosis
• Re-screening:
  – Annually if no DR
  – Every 6 months or according to recommendation
Category           24-h Collection   Timed Collection   Spot Collection
                      (mg/24 h)         (µg/min)           (µg/mg

Normal                  <30                <20               <30

Microalbuminuria       30-299            20-190             30-299

Clinical                ≥300              ≥200               ≥300
• Two of three specimens collected within 3-6months
  should be abnormal to confirm microalbuminuria
• Obtain first morning void samples.
• Collect all samples at nearly the same time.
• Exclude conditions that may invalidate urine albumin
   –   Exercise within 24 hours
   –   Infection,
   –   Fever
   –   CHF
   –   Marked hypertension
   –   Pyuria
   –   Hematuria
   –   Ketosis
   –   Diyhdropyridine calcium channel blockers
   –   Day to day variation up to 40 %.
Screening & Prevention

• Tests:
• Urine Dipstick: each visit
• UMA:
   – Type 1 DM:
      • 5 year after onset
      • At puberty whatever the duration
   – Type 2 DM:
      • At diagnosis
   – Re-screening:
      • Annually
• S. Creatinine , BUN: initially then annually
Diabetic Neuropathy: screening

• Screening should include
  – Inquiring about neuropathic symptoms
  – Checking ankle reflexes
  – Examining sensory function in the feet (pinprick,
    temperature, vibration perception using a 128-Hz tuning
  – Examining pressure sensation using a 10-g
    monofilament pressure sensation
  – Examining the feet and lower limbs for
     • Calluses
     • Deformities
     • ulcers
Diabetic Neuropathy: screening

•   All patients should be screened for DPN
    1. When type 2 diabetes is diagnosed
    2. Five years after the diagnosis of type 1 diabetes
    3. At least annually thereafter.

 Cardiovascular Disease:
 – History including risk factors
 – Clinical examination
 – EKG at 40 years of age
 – ABI as indicated
• Diabetic foot:
  – Examination of foot each visit
  – Comprehensive Examination
    to R/O foot at risk annually
• Includes:
  – Biomechanical structure
  – Skin
  – Vascular status
  – Neurological
University of Texas Diabetic Wound Classification:

Stage   Grade 0                         Grade I                      Grade II                     Grade III

A       Pre or postulcerative lesion,   Superficial wound not        Wound penetrating to         Wound penetrating to bone
             completely epithelized         involving tendon,            tendon or capsule            or joint
                                            capsule or bone

B       Pre or postulcerative lesion,   Superficial wound not        Wound penetrating to         Wound penetrating to bone
             completely epithelized         involving tendon,            tendon or capsule with       or joint with infection
             with infection                 capsule or bone with         infection
C       Pre or postulcerative lesion,   Superficial wound not        Wound penetrating to         Wound penetrating to bone
             completely epithelized         involving tendon,            tendon or capsule with       or joint with ischemia
             with ischemia                  capsule or bone with         ischemia
D       Pre or postulcerative lesion,   Superficial wound not        Wound penetrating to         Wound penetrating to bone
             completely epithelized         involving tendon,            tendon or capsule with       or joint with infection
             with infection and             capsule or bone with         infection and ischemia       and ischemia
             ischemia                       infection and ischemia
International Consensus on the Diabetic Foot:
Risk Categorization
Category   Risk factors     Ulcer          Amputation     Prevention & Treatment
                                 Inciden      Incidence
1          No Sensory       2% - 6%        0%             Revaluation Once a Year
                Neuropath                                 Patient Education

2          Sensory          6% - 9%        0%             Podiatry every 6 months
                Neuropath                                 Over-The-Counter Shoes and
                y                                              Insoles
                                                          Evaluate the appropriate fit
                                                          Patient Education

3          Sensory          8% - 17%       1% - 3%        Podiatry every 2-3 months
                Neuropath                                 Professionally fit Therapeutic
                y                                              Shoes and Insoles
           +                                              Patient Education
           Foot Deformity
4          Previous Ulcer   26% - 79%      10% - 18%      Podiatry every 1-2 months
           Or                                             Professionally fit Therapeutic
           Amputation                                          Shoes and Insoles
                                                          Patient Education
Wagner Diabetic Ulcer Classification Scale
Grade   Wound Characteristics

0       Pre-ulceration lesion, healed ulcers, presence of bony deformity

1       Superficial ulcers without subcutaneous tissue involvement

2       Penetrating through the subcutaneous tissue; may expose bone, tendon, ligament, or joint capsule

3       Osteitis, abscess, or osteomyelitis

4       Gangrene of digit

5       Gangrene of foot

Glycemic Control:
• Blood glucose:
  – FBS and pre-meals: 80-120 mg/dl
  – 2-h PP: < 160-180 mg/dl
• HbA1C: < 7 %

• With no MAU:
  – ≤ 140/85
• With MAU:
  – ≤ 120/80

• No IHD:
  – < 2.5 mmol/l
• With IHD:
  – < 1 mmol/l

• < 1.6 mmol/l

• > 1.35 mmol/l
• D/C smoking
• DE

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