Complications of Diabetes Mellitus Acute Complications of Diabetes Chronic complications of Diabetes

1. DR. RAHUL GARG
M.D. MEDICINE(Std)
SNMC Agra

2. Complications of diabetes mellitus
I. Acute complications:
 diabetic ketoacidosis
 hypoglycemia
 diabetic nonketotic hyperosmolar coma
II. Chronic complications:

a. Microvascular

retinopathy
nephropathy
neuropathy
diabetic foot
dermopathy
b. Macrovascular
Cerbrovascular.
Cardiovascular.
peripheral vascular disease.
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3. Diabetic ketoacidosis (DKA)
May be the 1st presentation of type 1 DM.
Result from absolute insulin deficiency or increase
requirement.
Mortality rate around 5%.
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4. Pathogenesis
 Insulin decrease ↓
 Counter-regulatory hormone increase: Glucagon,
catecholamines, cortisol & growth hormone ↑
 Hepatic glucose production increase ↑
 ↓glucose utilization of peripheral tissue
 => glycosuria, osmotic diuresis & dehydra-tion
 lead to the release of free fatty acid into circulation
from fatty tissue.
 Unrestrained hepatic fatty acid oxidation to ketone
bodies (β-hydroxybutyrate, acetone, acetoacetate)
 => resulting in ketonemia and metabolic acidosis.
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5. Diagnosis of DKA
Hyperglycemia
Ketonuria and ketonemia
Acidosis (PH< 7.3 )
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6. Predisposing factors for
DKA
Infection
Trauma
Myocardial Infarction
Stroke
Surgery
Emotional stress
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7. Clinical presentation of DKA
Polyuria and polydipsia.
Nausea and vomiting.
Anorexia and abdominal pain.
Tachycardia.
Fruity odor of the breath.
Hypotonia, stupor and coma.
Sign of dehydration.
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8. Treatment of DKA
Fluid replacement.
Insulin therapy for hyperglycemia.
Electrolyte correction.
Acidosis correction.
Treatment of precipitating cause.
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9. Complication of DKA
Cerebral edema
Vascular thrombosis
Infection
M I
Acute gastric dilatation
Respiratory distress syndrome
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10. Hypoglycemic coma
Hypoglycemia is the most frequent acute
complication in diabetes.
 Hypoglycemia is the level of blood glucose at
which autonomic and neurological dysfunction
begins
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11. Clinical manifestations of hypoglycemia:
 Autonomic dysfunctions:
1. Hunger
2. Tremor
3. Palpitation
4. Anxiety
5. Pallor
6. Sweating
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12. Neurologic dysfunctions:
1. Impaired thinking
2. Change of mood
3. Irritability
4. Headache
5. Convulsion
6. Coma
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13. Predisposing factors
Missed meal
Change in physical activity
Alterations or errors in insulin dosage
Alcohol ingestion
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14. Treatment of hypoglycemia
In mild cases oral rapidly absorbed carbohydrate
In sever cases (comatose patient) iv hypertonic
glucose 25% or 50% concentration
Glucagons injection
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15. Chronic Complications of DM
A. Macrovascular Complications:
B. Microvascular Complications:
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16. Macro-vascular Complications:
Ischemic heart diseases.
Cerebrovascular diseases.
Peripheral vascular diseases.
Diabetic patients have a 2 to 6 times higher risk
for development of these complications than the
general population
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17. Macro-vascular Complications:
 Accelerated atherosclerosis involving the aorta and large- and
medium-sized arteries.
 Myocardial infarction, caused by atherosclerosis of the
coronary arteries, is the most common cause of death in
diabetics.
 Gangrene of the lower extremities.
 Hypertension due to Hyaline arteriolosclerosis.
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18. Hypertension in DM
Type 2
Type 1
 present after several years of




DM
affects about 30% of patients.
Secondary to
nephropathy
Activation of the Renin
angiotensin system
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



Mostly present at diagnosis
Affects about 60% of patients
Secondary to insulin resistance
Activation of the sympathetic
nervous system

19. Dyslipidaemia in DM
Most common abnormality is ↓ HDL and ↑
Triglycerides
A low HDL is the most constant predictor of
Cardiovascular disease in DM.
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20. Screening for Macrovascular
Complications
1.
2.
3.
4.
Examine pulses for cardiovascular diseases.
lipid profile.
ECG.
Blood pressure.
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21. Microvascular Complications
Microvascular complications are specific to diabetes and
related to longstanding hyperglycaemia.
Both Type1 DM and Type2 DM are susceptible to
microvascular complications.
The duration of diabetes and the quality of diabetic control
are important determinants of microvascular abnormalities.
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22. Pathophysiology of microvascular disease
In diabetes, the microvasculature shows both functional
and structural abnormalities.
The structural hallmark of diabetic
microangiopathy is
thickening of the capillary basement membrane.
changes in basement membrane composition including
increased type IV collagen and its glycosylation (i.e
binding of glucose to wall of blood vessels).
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23. The main functional abnormalities include increased
capillary permeability, viscosity, and disturbed platelet
function.
These changes occur early in the course of diabetes
and precede organ failure by many years.
Increased capillary permeability is manifested in the
retina by leakage of fluorescein and in the kidney by
increased urinary losses of albumin which predict
eventual renal failure.
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24.  Platelets from diabetic patients show an exaggerated tendency to
aggregate, perhaps mediated by altered prostaglandin metabolism.
 Plasma and whole blood viscosity are increased in diabetes.
 These defects together with the platelet abnormalities may cause stasis
in the microvaculature, leading to increased intravascular pressure and
to tissue hypoxia.
 There is abnormal production of von Willebrand factor and endothelial
derived nitric oxide by endothelial cells which could contribute to tissue
damage.
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25. 1- Diabetic retinopathy
* Pathogenesis:
Histologically
the earliest lesion is thickening of the capillary basement
membrane.
On
fluorescein angiography the first abnormality is the capillary
dilatations (microaneurysms).

Microaneurysm may give rise to haemorrhage or exudate.
Vascular
occlusion, initially of capillaries and later of arteries and veins,
leads to large ischaemic areas (cotton-wool spots).
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26. DR. RAHUL GARG

27. Background Retinopathy
Micro aneurysms
Scattered exudates
Hemorrhages(flame
shaped, Dot and Blot)
Cotton wool spots (<5)
Venous dilatations
Background retinopathy
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28. Cotton wool spots
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29. Proliferative Retinopathy
New vessels (on disc,
elsewhere)
Fibrous proliferation
(on disc, elsewhere)
Hemorrhages
(preretinal, vitreous)
Panretinal photo-coagulation
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30. Other Eye Complications
- Cataracts.
- Glaucoma
- Macular edema.
-Ischaemic maculopathy.
-Proliferative retinopathy.
-Vitreous Bleeding.
-Rubeosis Iridis
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31. Vitreous Bleeding
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32. DR. RAHUL GARG

33. Proliferative retinopathy.
Note the abnormal
capillaries and
haemorrhages.
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34. 2- Diabetic Nephropathy (DN)
- Diabetic nephropathy is defined by persistent
albuminuria (>300 mg/day), decrease glomerular
filtration rate and rising blood pressure.
- About 20 – 30% of patients with diabetes develop
diabetic nephropathy
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35. Risk factors of DN
Duration of DM.
 Family History of hypertension. Cardiovascular
disease, nephropathy.
 Hyperglycemia.
 Hypertension.
 Microalbuminuria.
 Male gender.
 Cigarette smoking.

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36. Pathogenesis:
The glomerular and vascular lesions are linked to
hyperglycemia.
Nonenzymatic glycosylation to glomerular proteins
results in accumulation of irreversible advanced
glycosylation end products in the glomerular mesangium
and glomerular basement membrane.
This alteration leads to proteinuria and eventually
glomerulosclerosis
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37. Pathological pattern of DN
Diffuse form (more common): consist of thickining
of glomerular basement membrane with generalized
mesangial thickenings.
The nodular form (the Kimmelstiel-Wilson
lesion): (accumulation of periodic acid schiff positive
material are deposit in the periphery of glomerular tufts.
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38. Diabetic nephropathy
• The glomerulus shows sclerotic nodules in the center of the lobules
or segments.
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39. DR. RAHUL GARG

40. Stages of DN
Stage I
↑ glomerular filtration and kidney hypertrophy
Stage II
u-albumin excretion < 30mg/24h
Stage III
Microalbuminuria (30 – 300 mg/24h)
Stage IV
Overt nephropathy (> 300mg/24h, positive u dipstick)
Stage V
ESRD characterized by ↑ blood urea and creatinine levels,
hyperkalaemia and fluid overload
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41. Treatment to prevent progression to DN
Glycaemic control.
ACE inhibitor .
Blood pressure control.
Smoking cessation.
Proteins restriction.
Lipid reduction.
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42. 4. Diabetic Neuropathy
1. Sensorimotor neuropathy.
2. Autonomic neuropathy.
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43. Sensorimotor Neuropathy
Numbness, paresthesias.
Feet are mostly affected, hands are seldom affected.
Complicated by ulceration (painless), charcot
arthropathy.
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44. Complications of Sensorimotor neuropathy
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45. Autonomic Neuropathy
Symptomatic
Postural hypotension
Gastroparesis
Diabetic diarrhea
Neuropathic bladder
Erectile dysfunction
Neuropathic edema
Charcot arthropathy
Gustatatory sweating
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Subclinical abnormalities
Abnormal pupillary reflexes
Esophageal dysfunction
Abnormal cardiovascular
reflexes
Blunted counter-regulatory
responses to hypoglycemia
Increased peripheral blood
flow

46. Mononeuropathies
Cranial nerve palsies
(most common are n.
IV,VI,VII)
Truncal neuropathy
(rare)
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47. Entrapment Neuropathies
Carpal tunnel syndrome (median nerve)
Ulnar compression syndrome
Meralgia paresthetica (lat cut nerve to the thigh)
Lat Popliteal nerve compression (drop foot)
All the above are more common in diabetic patients
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49. DR. RAHUL GARG

50. 5. Infections
 Community acquired pneumonia
 Acute bacterial cystitis
 Acute pyelonephritis
 Pyelonephritis
 Perinephric abscess
 Fungal cystitis.
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51. foot care
Patient should
check feet daily
Wash feet daily
Keep toe nails short
Protect feet
Always wear shoes
Look inside shoes before
putting them on
Always wear socks
Break in new shoes gradually
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52. Foot ulcer
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54. Screening for Neuropathy
128 Hz tuning fork for
testing of vibration
perception
10g Semmers
monofilament
The main reason is to
identify patients at risk
for development of
diabetic foot
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55. Using of the Monofilament
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56. The end
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