Diabetic neuropathy by Dr Shahjada Selim

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selimshahjda@gmail.com

Diabetic Neuropathy

Dr Shahjada SelimAssistant Professor

Department of Endocrinology

Bangabandhu Sheikh Mujib Medical University

Dhaka, Bangladesh

selimshahjada@gmail.com

Global Situation Prevalence: 22.7% T1DM, 32.1% T2DM USA: 17% of costs of treating diabetic

complications (approx $300 per patient per year)

UK: £13 million p.a on diabetic foot complications

1. Young MJ, Boulton AJ, MacLeod AF, Williams DR, Sonksen PH. Diabetologia 1993;36(2):150-4.

2. Caro, J. J., A. J. Ward, et al. (2002). Diabetes Care 25(3): 476-81.

HISTORY• 1864-Marchal de calve -DM affects nervous sys

• 1890-Buzzard -motor weakness

• 1893-Leyden -classification

• 1936-Jordan -autonomic neuropathy

• 1947-1973 Pirart -25 yr prospective study

• Dyck & co -Rochester diabetic neuropathy study

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Pathology

Axonal loss, focal demyelination & regeneration

↓ conduction velocity and ↑ sensory thresholds

www.plymouthdiabetes.org.uk/

Pathophysiology-biochemical and vascular factors

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Risk Factors

Glycaemic control-DCCT ↑ 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

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Presentations

3 types of neuropathy:

1. Progress steadily with increasing duration of diabetes and associated with other diabetic complications-common

2. Acute onset with resolution over period of months-rare

3. Pressure palsies

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Presentations

Diffuse symmetrical sensorimotor polyneuropathy

Predominantly sensory Predominantly feet ↓ pain and temperature sensation Parasthesiae and numbness Neurogenic pain/allodynia Neuropathic oedema Wasting occurs only if severe

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Diffuse symmetrical sensorimotor polyneuropathy

Problems: Pain and oedema Diabetic foot ulceration

Present in 80% of foot ulcers Principle cause in 39% of ulcers Partly responsible in 36% of ulcers

www.plymouthdiabetes.org.uk/

www.plymouthdiabetes.org.uk/

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Autonomic Neuropathy Closely associated with sensorimotor

neuropathy Signs are common if looked for (40%

subjects have abnormal CVS tests) but symptoms are rare (<1%)

Affects the response to hypos but not awareness

If symptoms: mortality=30-50% over 10 years

www.plymouthdiabetes.org.uk/

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Diffuse Small Fibre Neuropathy

T1DM Young, ♀ > ♂ Selective damage to small nerve fibres Pain and temp lost but LT retained Symptomatic autonomic neuropathy,

Charcot arthropathy and foot ulcers ? autoimmune

www.plymouthdiabetes.org.uk/

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Mononeuropathies

Acute ? Secondary to ischaemia Pain and weakness (severe) Resolve over months

Amyotrophy (Older > )♂ ♀ 3rd nerve 6th nerve Truncal radiculopathies

Diabetic Amyotrophy

www.plymouthdiabetes.org.uk/

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Insulin Neuritis

Acute & diffuse May be painful Follows improvement of blood

glucose control ?steal phenomenon

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Acute diffuse painful neuropathy Not related to duration of diabetes or

complications Association with marked weight loss severe burning/shooting pain, “electric

shocks”, allodynia Resolve spontaneously, usually with weight

gain, 6-8 months. Some 2 years. Does not relapse Signs may be lacking and dissociated from

symptoms

www.plymouthdiabetes.org.uk/

Pressure Palsies

↑ susceptibility to pressure damage

Limited joint mobility (soft tissue)

Carpal tunnel Ulnar nerve Lateral popliteal nerve

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DiagnosisAnnual review Enquire annually for:· Painful neuropathy· Loss of sensation· Erectile impotence Note duration of DM, treatment,

complications & weight Ask about other manifestations of

autonomic neuropathy if:· Other complications are present· Anaesthesia is contemplated· Blood glucose control is erratic

DiagnosisExamine: For evidence of peripheral neuropathy

annually LT

OR if new symptoms Vibration LT ?Thermal thresholds ?Pain For postural hypotension if symptoms

of autonomic neuropathy

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Examination-ANS

Ewing’s batteryAbnormal results common Valsalva-expiration for 15 secs against 40

mmHg. Rest 1 min then repeatx2. Avoid in proliferative retinopathy. RR max : RR min>1.21 =Normal, <1.20 = abnormal.

HR increase on standing RR 30:15 ratio > 1.04 HR↑ at max overshoot or 15 seconds ≥ 15bpm

(abnormal if<12)

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Ewing’s battery

HR variation during deep breathing (6 breaths per minute) Max-min > 15bpm (<10 is abnormal)

Postural BP-2 mins after standing Fall< 10mmHg normal >30 mmHg abnormal

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Diagnosis

Consider differential diagnoses HSMN Ethanol B12/folate Malignancy Renal failure Drugs AI disease Cord problems Leprosy

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Prevention

Control DCCT (1995)

Tight control-3% neuropathy at 5 years Conventional-10%

UKPDS (1998) Tight control (HbA1c 7%)-31.2% neuropathy

at 15 years Conventional (HbA1c 7.9%)-51.7% P=0.005 No protective effect seen for BP control

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Prevention

Aldose reductase inhibitors Gamma Linoleic Acid Vasodilators-ACE? AGE inhibitors Antioxidants NGFs ? Smoking cessation, ? BP reduction

Treatment-Painful neuropathyGeneral Measures

Improve glycaemic controlExclude or treat other contributory factors•Alcohol excess•Vitamin B12 deficiency/Folate•UraemiaSimple analgesia-NSAID/ParacetamolExplanation, empathy and reassurance

Choose drugs according to dominant symptoms

Burning pain

Tricyclics

Anticonvulsants

Duloxetine

Lancinating pain

Tricyclics

Anticonvulsants

Duloxetine

Other symptomsAllodynia•Plastic film•Leg cradle at nightRestless legs•RopinirolePainful Cramps•Quinine sulphate

NICE CG 87

May 2009

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Treatment -ANS

Postural hypotension Fludrocortisone NSAIDs Compression stockings Elevate the head of the bed

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Treatment -ANS

Bladder Manual SP pressure ISC ? Anticholinesterase Cyclical antibiotics if recurrent infections

Sweating ?clonidine

Erectile dysfunction

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Treatment -ANS

Gastroparesis Improve glycaemic control Prokinetic drugs

Metoclopramide, domperidone, cisapride, erythromycin (250 mg tds) Octreotide? If severe→admit for IV fluids, IV drugs ± NG tube ± IV/jejunal

feedingDiarrhoea Codeine/loperamide/diphenoxylate Clonidine or octreotide Treat bacterial overgrowth (oxytet/erythromycin) if

suspected/present

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Thanks

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