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    Complications of Diabetes Mellitus-Update

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    Anditha Namira RS
    The document discusses complications of diabetes mellitus, including both chronic and acute complications. Chronic complications involve microvascular changes like retinopathy, nephropathy, and neuropathy. Retinopathy can progress from nonproliferative to proliferative stages and potentially cause blindness. Nephropathy typically progresses through stages of hyperfiltration, microalbuminuria, proteinuria, and declining kidney function. Neuropathy commonly damages both sensory and motor nerves. Acute complications arise from hyperglycemia and include diabetic ketoacidosis, hyperglycemic hyperosmolar state, and lactic acidosis. The document also reviews macrovascular complications like coronary artery disease, cerebrovascular disease, and peripheral vascular disease.

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    © All Rights Reserved
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    Complications of Diabetes Mellitus-Update

    Uploaded by

    Anditha Namira RS
    356 views48 pages
    The document discusses complications of diabetes mellitus, including both chronic and acute complications. Chronic complications involve microvascular changes like retinopathy, nephropathy, and neuropathy. Retinopathy can progress from nonproliferative to proliferative stages and potentially cause blindness. Nephropathy typically progresses through stages of hyperfiltration, microalbuminuria, proteinuria, and declining kidney function. Neuropathy commonly damages both sensory and motor nerves. Acute complications arise from hyperglycemia and include diabetic ketoacidosis, hyperglycemic hyperosmolar state, and lactic acidosis. The document also reviews macrovascular complications like coronary artery disease, cerebrovascular disease, and peripheral vascular disease.

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    Complications of Diabetes Mellitus-update

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    The document discusses complications of diabetes mellitus, including both chronic and acute complications. Chronic complications involve microvascular changes like retinopathy, nephropathy, and neuropathy. Retinopathy can progress from nonproliferative to proliferative stages and potentially cause blindness. Nephropathy typically progresses through stages of hyperfiltration, microalbuminuria, proteinuria, and declining kidney function. Neuropathy commonly damages both sensory and motor nerves. Acute complications arise from hyperglycemia and include diabetic ketoacidosis, hyperglycemic hyperosmolar state, and lactic acidosis. The document also reviews macrovascular complications like coronary artery disease, cerebrovascular disease, and peripheral vascular disease.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    356 views48 pages

    Complications of Diabetes Mellitus-Update

    Uploaded by

    Anditha Namira RS
    The document discusses complications of diabetes mellitus, including both chronic and acute complications. Chronic complications involve microvascular changes like retinopathy, nephropathy, and neuropathy. Retinopathy can progress from nonproliferative to proliferative stages and potentially cause blindness. Nephropathy typically progresses through stages of hyperfiltration, microalbuminuria, proteinuria, and declining kidney function. Neuropathy commonly damages both sensory and motor nerves. Acute complications arise from hyperglycemia and include diabetic ketoacidosis, hyperglycemic hyperosmolar state, and lactic acidosis. The document also reviews macrovascular complications like coronary artery disease, cerebrovascular disease, and peripheral vascular disease.

    Copyright:

    © All Rights Reserved
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    Download as ppt, pdf, or txt
    of 48

    Complications of

    diabetes mellitus

    Complications of Diabetes
    Mellitus

    Chronic
    Complications of
    Diabetes Mellitus

    Microvascular

    Retinopathy
    (nonproliferative/proliferat
    ive)
    Nephropathy
    Neuropathy
    Sensory and motor (monoand polyneuropathy)
    Autonomic

    Macrovascular

    Coronary artery disease


    Peripheral vascular disease
    Cerebrovascular disease

    Acute
    Complications of
    Diabetes Mellitus

    Hyperglycemia
    crisis

    Diabetic
    ketoacidosis
    Hyperglycemia
    hyperosmolar State
    Lactic acidosis

    Hypoglycemia

    Microvascular
    Complications

    Increased Polyol Pathway Flux


    Aldose Reductase Function

    Advanced
    Glycation End-Product
    Formation

    Activation of Protein Kinase


    C

    Increased Hexosamine Pathway

    Diabetic retinopathy

    Pathophysiology of diabetic
    retinopathy
    Hyperglycemia
    Pericyte
    loss

    Hyperperfusion

    Capillary/
    Endothelial
    damage
    Capillary
    occlusion

    Loss of
    autoregulation
    Vasoactive
    factors

    Loss of tight
    junction

    Retinal
    ischemia
    Growth
    factors
    New vessels
    -Low resistance
    - No pericyte/autoregulation

    Macular
    oedema

    Advanced diabetic eye


    disease
    Retinal ischemia

    Neovascularitation

    Preretinal
    haemorrhage

    Pericyte
    loss

    Neovascular
    glaucoma

    Vitrous
    haemorrhage

    Blindness

    Retinal
    detachment

    Diabetic retinopathy

    Blindness is primarily the result of progressive diabetic


    retinopathy and clinically significant macular edema.
    Diabetic retinopathy is classified into two stages:
    nonproliferative and proliferative.
    Nonproliferative diabetic retinopathy : marked by retinal
    vascular microaneurysms, blot hemorrhages, and cotton
    wool spots
    The appearance of neovascularization in response to retinal
    hypoxia is the hallmark of proliferative diabetic
    retinopathy.
    Duration of DM and degree of glycemic control are the best
    predictors of the development of retinopathy; hypertension
    is also a risk factor
    The most effective therapy for diabetic retinopathy is
    prevention.

    Diabetic nephropathy

    Pathophysiology of diabetic
    nephropathy
    Hyperglycemia

    Renal
    vasodilatation
    Increased glomular
    filtration rate

    Protein glycation

    Increased
    intraglomerular
    capillary pressure
    Hypertension
    Increased
    protein excretion

    Microalbuminuria or
    macroalbuminuria

    Glomurular
    damage

    Nephropathy

    Diabetic nephropathy

    Diabetic nephropathy is the leading cause of ESRD in the US.


    Individuals with diabetic nephropathy almost always have diabetic
    retinopathy.
    The stages of diabetic nephropathy are :

    Hyperfiltration
    Microalbuminuria
    Overtproteinuria
    Declining GFR
    End stage renal failure

    Microalbuminuria is defined as 30 to 300 mg/d in a 24-h collection or


    30 to 300 g/mg creatinine in a spot collection (preferred method).
    The appearance of microalbuminuria (incipient nephropathy) in type
    1 DM is an important predictor of progression to overt proteinuria
    (300 mg/d) or overt nephropathy.
    Hypertension more commonly accompanies microalbuminuria or
    overt nephropathy in type 2 DM

    Diabetic nephropathy treatment

    The optimal therapy for diabetic nephropathy is


    prevention.
    Interventions effective in slowing progression from
    microalbuminuria to overt nephropathy include:

    near normalization of glycemia,


    strict blood pressure control, and
    administration of ACE inhibitors or ARBs, and
    treatment of dyslipidemia.

    Blood pressure should be maintained at 130/80 mmHg


    in diabetic individuals without proteinuria.
    A slightly lower blood pressure (125/75) should be
    considered for individuals with microalbuminuria or
    overt nephropathy
    A consensus panel of the ADA suggests modest
    restriction of protein intake in diabetic individuals with
    microalbuminuria (0.8 g/kg per day) or overt
    nephropathy (<0.8 g/kg per day)

    Diabetic neuropathy

    Mechanism of nerve damage in


    diabetes
    METABOLIC

    myoinositol

    VASCULAR

    glucose

    Altered membrane
    potensial

    Slow nerve
    conduction

    sorbitol

    nerve
    oedema

    AGE
    formation

    Arterial
    narrowing
    vasoconstriction

    NO
    production

    Impairing
    axonal transport

    Vessel
    occlusion

    H2O

    Diabetic neuropathy

    Diabetic neuropathy occurs in approximately 50% of


    individuals with long-standing type 1 and type 2 DM.
    The development of neuropathy correlates with the
    duration of diabetes and glycemic control; both
    myelinated and unmyelinated nerve fibers are lost.
    Several stage :
    Intraneural biochemical abnormalities; sorbitol
    accumulation, myoinositol depletion
    Impairement of electrophysiological measurement;
    decreased nerve conduction velocity; asymptomatic
    Clinical neuropathy; detectable using clinical
    methods; maybe symptomatic. Histological changes
    evident
    End stage complications. Exp are ulceration and
    Charcot neuroarthropathy; major derangements of
    neural structure and function.

    Clinical features
    symmetrical sensorimotor
    neuropathy
    Symptoms
    Loss of sensation ;

    Altered sensation:

    Anaesthesia;numbness
    Loss of pain perception
    Paraesthesiae
    Dysaesthesiae

    Pain

    Signs
    Sensory loss
    Diminished/absent
    tendon reflexs
    Muscle wasting and
    weakness
    Autonomic
    dysfunction
    Foot uleration

    Burning
    Hyperalgesia/allodynia
    Neuralgia lancinating pain
    Cramps ; restless leg

    Burning, feeling like the feet are on fire

    Stabbing, like sharp knives

    Freezing, like the feet are on ice,


    although they feel warm to touch

    Lancinating, like electric shocks

    Treatment of Symmetric
    Neuropathy

    Glucose control
    Pain control

    Tricyclic antidepressants

    Anticonvulsants

    Carbamazepine, gabapentin

    Topical creams

    Amitriptyline,desipramin, nortriptilin,
    trazodone

    capsaicin

    Foot care

    Autonomic Neuropathy

    DM-related autonomic neuropathy can involve multiple


    systems, including the cardiovascular, gastrointestinal,
    genitourinary, sudomotor, and metabolic systems.
    Autonomic neuropathies affecting the cardiovascular
    system cause a resting tachycardia and orthostatic
    hypotension.
    Gastroparesis and bladderemptying abnormalities are
    often caused by the autonomic neuropathy seen in DM
    (discussed below).
    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, leading to an inability to sense
    hypoglycemia appropriately ((hypoglycemia unawareness)

    Macrovascular
    complications

    Macrovascular
    complication

    Macrovascular complications of diabetes mellitus are


    condition characterized by atherosclerotic occlusive
    disease of cerebral, myocard and lower extremities.
    Atherothrombosis is the most common cause of
    macrovascular complications
    Atherothrombosis is characterized by a sudden
    (unpredictable) atherosclerotic plaque disruption
    (rupture or erosion) leading to platelet activation and
    thrombus formation
    Atherothrombosis is the underlying condition that
    results in events leading to myocardial infarction,
    ischemic stroke, amputation and vascular death

    Atherogenesis A Complex And Progressive


    Process1
    Pathology of Atherogenesis
    Initiation:
    Accumulation of lipids at
    vascular junctions
    experiencing high shear
    forces

    Inflammatory cytokines induce


    expression of adhesion molecules

    Macrophages
    bind to and enter
    intima wall

    Uptake of Lipids by
    Macrophages

    Macrophages
    become foam
    cells & fatty
    streak formed

    Chemo-attractants such as PDGF


    released from activated macrophages

    Smooth muscle
    cells (SMCs)
    migrate into the
    intima

    Result: Atherosclerotic
    plaque2

    Adapted from: P Libby, The Vascular Biology of Atherosclerosis, in: Braunwald


    E, Zipes DP & Libby P 6th Edition, Heart Disease: a Textbook of Cardiovascular
    Medicine 2001: London: WB Saunders. 2. Davies MJ. Heart 2000;83:361-66, with permission from the BMJ Publishing Group

    Atherothrombosis Has Multiple


    Manifestations
    Ischemic stroke

    Myocardial
    infarction

    Transient ischemic attack

    Angina:
    Stable
    Unstable

    Peripheral arterial disease:


    Intermittent claudication
    Rest pain
    Gangrene
    Necrosis
    Adapted from: Drouet L. Cerebrovasc Dis 2002;13(suppl 1):16

    Macrovascular disease in
    diabetes mellitus

    Cardiovascular and cerebrovascular disease account for


    up 70% of death in patients with type 2 DM
    All patients with type 2 diabetes have greater
    predipostition to macrovascular disease, often having a
    constellation of risk factors, which have been term
    insulin resistance.
    It has been hypotethesized that insulin resistance and
    hyperinsulinemia (environmental and genetic factors),
    are central to development :

    Glucose intolerance
    Hypertension
    Dyslipidemia
    Coagulopathy

    These factors promote accelerated atherosclerosis,


    explaining the increased risk of macrovascular disease.

    Diabetes and Macrovascular


    Disease

    Libby and Plutsky. Circulation. 2002.

    Strategies for reducing


    macrovascular complications

    Prevention proven intervention trials


    Hyperglycemia
    Dyslipidemia
    Hypertension
    Antiplatelet therapies

    Prevention suggested by epidemiologic


    analysis
    Disorders of thrombolysis
    Endothelial disorders

    The diabetic foot

    Diabetic foot disease

    Approximately 15% of individuals with DM develop a


    foot ulcer, and a significant subset will ultimately
    undergo amputation (14 to 24%risk with that ulcer or
    subsequent ulceration).
    Syndrome of diabetic foot disease
    Peripheral neuropathy, peripheral vascular disease
    and tissue infection
    Risk factors for foot ulcers or amputation include:
    male sex, diabetes 10 years duration, peripheral
    neuropathy, abnormal structure of foot (bony
    abnormalities,callus, thickened nails), peripheral
    arterial disease, smoking, history of previous ulcer or
    amputation, and poor glycemic control.
    The plantar surface of the foot is the most common
    site of ulceration.
    Ulcers may be primarily neuropathic (no
    accompanying infection) or may have surrounding
    cellulitis or osteomyelitis.

    Pathophysiology of diabetic
    foot
    Neuropathy

    Motor
    dysfunction

    Abnormal
    Foot posture

    Microvascular
    disease

    Neuropathy Neuropathy
    Reduced pain
    Sensation and
    proprioception

    Increased foot
    prssure

    Dry, cracked
    skin

    Poor tissue
    nutrition and
    oxygenation

    Cheiroarthropathy
    Arteriovenous
    shunting

    Callus

    Trauma

    Mechanical,
    thermal,
    chemical

    Ulcer
    Ischemia

    Macrovascular
    disease

    Acute Complication of
    Diabetes Mellitus

    Hyperglycemia crisis
    Diabetic

    ketoacidosis (DKA)
    Hyperglycemic Hyperosmolar State (HHS)

    Hypoglycemia

    Diabetic ketoacidosis
    (DKA)
    Hyperglycemic
    Hyperosmolar State (HHS)

    Pathophysiolgy of
    hyperglycemia crisis

    Diabetic ketoacidosis (DKA)

    DKA was formerly considered a hallmark of


    type 1 DM
    The symptoms and physical signs of DKA

    Symptoms : Nausea/vomiting, Thirst/polyuria,


    Abdominal pain, Shortness of breath
    Physical findings : Tachycardia, Dry mucous
    membranes/reduced skin turgor, Dehydration /
    hypotension, Tachypnea / Kussmaul,
    respirations/respiratory distress, Abdominal
    tenderness (may resemble acute pancreatitis or
    surgical abdomen), Lethargy /obtundation /
    cerebral edema / possibly coma

    Precipitating factors

    Inadequate insulin administration


    Infection (pneumonia/UTI/
    Gastroenteritis/sepsis
    Infarction (cerebral, coronary,
    mesenteric, peripheral)
    Drugs (cocaine)
    Pregnancy

    HHS: Differences from DKA


    Patients usually older- typically 60 or more
    Major pathophysiologic differences
    longer uncompensated osmotic diuresis
    greater volume depletion
    Acidemia (pH > 7.3) and ketosis are mild
    Higher mortality often 30-50%
    primarily due to underlying vascular or infectious
    event
    Occurs in Type 2 diabetics, often mild or unrecognized

    Definition of HHS

    Extreme hyperglycemia
    Increased serum osmolality
    Severe dehydration without
    significant ketosis or acidosis

    Joslins Diabetes Mellitus, 13th ed

    Clinical Findings of HHS

    HHS should be suspect : elderly patient with or without


    the preexisting diagnosis of diabetes who exhibits acute
    or subacute deterioration of CNS function and severely
    dehydrated
    Tachycardia
    Low grade fever
    Low or normal blood pressure
    Dehydration dry mucous membrane, absent axillary
    sweat, poor skin turgor.
    Nausea, vomiting, distension, and pain-gastroparesis is
    due to hypertonicity
    Lethargy, hallucinations, and psychosis

    Laboratory Findings
    DKA

    HHS

    Fluid Balance in Diabetic


    Hyperosmolarity
    ECF = 14 L

    ICF = 28 L

    ECF

    ICF
    H2O
    ECF hyperosmolar from ICF autotransfusion

    Osmotic Diuresis
    H2O

    Osmotic Diuresis

    ECF and ICF both hyperosmolar

    Priority in the
    Treatment of
    Hyperglycemia Crisis

    Replacing volume deficits normal saline


    according to BP, urine output and CVP value
    for old age, total deficits around 6-9 liters.

    Correcting hyperosmolarity to 300


    milliosmoles/L

    Managing any underlying illnesses

    Insulin ; RI 0.15u/kg bolus then 0.1/kg/hr


    infusion until blood sugar about 250mg/dl or
    osmo about 315

    Thank your for your


    attention

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