diabetic neuropathy - 29 january 2014
TRANSCRIPT
Diabetic Neuropathy
Dr Muhammad Khurram
FCPS, FRCP
Diabetes Mellitus
• What is DM
• DM is an increasingly serious social, economicand medical threat that is not just a healthissue, but a development issue (as it hindersprogress).
DM Figure Wise
• World Total 366 + million
• Pakistan currently 7.1 + million
• % Population 7-9%
• By 2030 11.4 + million
• Death toll/year 88000
Diabetic Neuropathy
• The San Antonio Consensus Statement onDiabetic Neuropathy defined the condition asbeing a demonstrable disorder, eitherclinically evident or subclinical in the setting ofdiabetes without other causes of peripheralneuropathy.
• 50-90% of patients who have diabetes alsohas neuropathy
• 22.7% DM I, 32.1% DM II
• 11-32% of patients with Diabetic Neuropathyexperience painful symptoms
Risk Factors
• Glycaemic control• with age
– 5% 20-29 years 44.2% 70-79 years– 50% T2DM >60 years of age
• with duration of diabetes– 20.8% < 5years 36.8%>10 years
• Smoking• Microalbuminuria• Height• Nutritional factors, additional illnesses
Pathogenesis
• Increased aldose reductase activity.
• Auto oxidation of glucose
• Non enzymatic glycation of protein(AGE)
• Activation of protein kinase C
• Oxidative stress
• Decrease essential fatty acid
• Reduced serum levels of nerve growth factor
• Nerve ischemia/hypoxia.
• Axonal loss
• Focal demyelination & regeneration
• Intraneural capillary abnormalities
• conduction velocity and sensory thresholds
Classification
• Somatic
– Polyneuropathy
• Symmetrical, mainly sensory and distal
• Asymmetrical, mainly motor and proximal
– Mononeuropathy & MNM
• Visceral
– GIT, CVS, Genitourinary
– Vasomotor, sudomotor, pupillary
Clinical Features
• Alone or combination
• Occur as the disease duration increases and depend on glycemic control generally
• Acute and rapid
• Slow and progressive
Symmetrical Mainly Sensory DPN
• Asymptomatic
• Symptomatic– Paresthesia
– Pain
– Burning sensations
– Hyperaesthesia
– Gait
– Small muscle wasting
– Charcot Joint
Asymmetrical Motor DN
• Severe, progressive weakness of proximal muscles
• Predominant LL involvement
• Pain
• Neuropathic cahexia
• Upgoing planters and depressed refelexes
• Outcome
Mononeuropathy & MNM
• Peripheral/cranial nerve involvement
• Motor, sensory or both components
• Sudden and rapid onset
• Good recovery
• 3rd, 6th, Femoral/Sciatic nreves
• Truncal radiculopathies
• Entrapment neuropathies– Median, Ulnar, Lateral popliteal
– AGE of tissues and Neuropathy
Autonomic DNP
• Different- relation with glycemia control
• Sympathetic or parasympathetic predominance
• Poor outcome
• CVS– Postural hypotension, resting tachycardia, fixed heart
rate
• GIT– Dysphagia
– Nausea, vomiting, distension, bloating,
– Diarhea, incontinencnce
– Constipation
• Uinary
– Difficulty in micturation, incontinence, recurrent infection
• Sudomotor
– Sweating, Anhidrosis, Gustatory sweating
• Vasomotor
– Cold feet, Edema, Bullae
• Pupillary
– Meiosis, mydriatic resistance, reflex abnormality
• Erectile dysfunction
– Multifatorial
– Neuropathy, vascular, psychological, endocrine, Rx
How to diagnose
• History
• Clinical Examination
• Investigations
– General Investigations
– Imaging
– NCS
– Biopsy
AN Tests
• Resting heart rate
– >100/m is abnormal.
• Systolic BP response to standing
– BP measured supine. Patient stands, BP aft 2 m.
– Normal response- fall of <10 mmHg,
– Borderline - fall of 10–29 mmHg
– Abnormal - fall of >30 mmHg with symptoms
• Beat-to-beat HRV
– At rest and supine heart rate by ECG while patient
breathes at 6/m
– Difference of >15 bpm - normal, <10 bpm -
abnormal.
• Heart rate response to the Valsalva manoeuvre
– Exhales into manometer to 40 mmHg for 15 seconds
– Healthy subjects develop tachycardia & peripheral
vasoconstriction during strain & overshoot bradycardia,
rise in BP with release.
– The ratio of longest R-R to shortest R-R should be ≥1.2.
• Neurovascular flow
– Using noninvasive laser Doppler measures of
peripheral sympathetic responses to nociception.
• Radionuclide Cardiac Imaging
– MIBG
– 11-C-hydroxyephedrine
Tips
• Duration of illness
• Glycemia control
• Other complications
• Symptoms
• Clinical evaluation
Management
• Glycemia assessment and control
• Exclusion of other causes
• Risk factors modifications
• Specific measures
Exclusion of other causes/Risk factor modification
• Vitamin deficiencies
• Malignant disease (e.g., bronchogeniccarcinoma)
• Metabolic
• Toxic (e.g., alcohol)
• Infective/post infection
• Medications
Specific Measures
• Pain and paresthesias– Anticonvusants (gabapentin, pregabalin,
carbamezapine, phenytoin)
– TCA (amitryptaline, nortriptaline)
– Duloxetine
– Capsaicin
– Opiates
– Memrane stabilizers (mexilitine)
– Antioxidants
• Postural hypotension
– Compression stocking
– NSAIDS
– Fludrocortisone
• Gastroparesis
– Dopamine antagonisits
– Erythromycine
– Jejunal feeding, Pacing
• Diarrhea– Loperamide
– Abx
– Octreotide
– Clonidine
• Constipation– Laxative
• Bladder atony– Catheterisation
• Excessive sweating– Oxybutinin, propantheline
– Clonidine
– Glycopyrolate
• Erectile dysfunction– Sildenafil, verdenafil, tadalafil
– Dopamine agunsist- apomorphine SL
– PGE1- Alprostadil
– Vacuum devices, implants
– Psychosexual therapy
Take Home Message
• Diabetic neuropathy is common
• Metabolic & vascular factors cause it.
• Distal symmetrical sensorimotor polyneuropathy is commonest form
• Non DM aetiologies need exclusion
• Should be sought
• Optimal glycemic control is required
• Other DM issues should be managed
• Focused care and medications are required
THANX A LOT