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Diabetic neuropathy DR DINESH.pptx
- 1. Diabetic neuropathy DR A.DINESH 1ST YEAR PG, GEN MED
- 2. PREVALENCE: ~50% (18.8 – 61.9%) of indiviuals with long standing T1DM , T2DM develops diabetic neuropathy. Diabetic Neuropathy accounts a major contributor of all neuropathies (~27%) OTHERS HIV/AIDS CHEMO
- 7. Pathogenesis Increased aldose reductase activity Nerve ischemia /hypoxia Auto oxidation of glucose Non Enzymatic Glycation End products (AGE) Activation of protein kinase C Oxidative stress Reduced serum levels of nerve growth factors
- 12. classification SYMMETRIC / ASYMMETRIC NEUROPATHY AUTONOMIC NEUROPATHY MONONEUROPATHY AND ENTRAPMENT SYNDROME RADICULOPATHY/ POLYRADICULOPATHY SUPER IMPOSED CIDP TREATMENT INDUCED DIABETIC NEUROPATHY
- 15. SYMMETRIC NEUROPATHY: SENSORY/SENSORIMOTOR/MOTOR DSPN – DISTAL SYMMETRIC POLYNEUROPATHY SMALL FIBER NEUROPATHY LARGE FIBER NEUROPATH Y MIXED SMALL AND LARGE FIBER NEUROPATHY MOST COMMON
- 16. DSPN Most common form of diabetic neuropathy A mixed neuropathy with small, large fiber, autonomic, motor involvement( late stage). In a patient with DM if there are clinical signs of autonomic abnormalities , DSPN is invariably present. Insidious, progressive DSPN as “the presence of symptoms and signs of peripheral nerve dysfunction in people with diabetes after exclusion of other causes”
- 18. Symptoms: As small fibers are predominantly involved early the symptoms are related to damage of small fibers. Pain- dull constant pain/ sharp shooting or stabbing pain Hyperalgesia Allodynia Loss of thermal sensation Loss of pain(later stages) these symptoms are the main presentation in prediabetic individuals.
- 19. Symptoms worsens at night Manifested in the feet more than the hands Paresthesia or episodes of distorted sensation such as pins and needles, tingling, coldness, numbness-feeling like walking in cotton, burning sensation -hot foot. often accompany the pain. as a whole these are called“POSITIVE SYMPTOMS” DSPN WITH LARGE FIBER NEUROPATHY – presents with insensate foot, Poor balancing, Distal weakness of toes& ankles in later stages are called ”NEAGATIVE SYMPTOMS”
- 20. SIGNS: Sensory: loss or imapairment of sensation of toes and feet. Vibration sense often the first to go. as the sensory loss extends proximally from a sock to stocking distribution the finger tips become involved Autonomic: dry skin , fissures, callouses Motor: absent ankle reflex (large fibers), wasting of toe muscles
- 22. CARDIAC AUTONOMIC NEUROPATHY SIGNS/SYMPTOMS MECHANISM RESTING TACHYCARDIA VAGAL IMPAIRMENT & (sympathetic takeover) REDUCED HRV EARLY FINDING REDUCED RESPONSE TO HR, BP IN EXERCISE, STRESS, SLEEP ORTHOSTATIC HYPOTENSION DAMAGE TO EFFERENT SYMPATHETIC VASOMOTOR FIBERS SYMPTOMS: Lightheadedness, dizziness, weakness, fatigue, neck pain, blurring of vision SILENT MI ALTERED PAIN THRESHOLD/ SUBTHRESHOLD ISCHEMIS NOT SUFFICIENT TO INDUCE PAIN, DYSFUNCTION OF AFFRENT AUTONOMIC FIBERS CARDIOMYOPATHY LEFT VENTRICLE DIASTOLIC DYSFUNCTION, LOW PEAK DIASTOLIC
- 23. GI DIABETIC NEUROPATHY MECHANISM SIGNS/SYMPTOMS GASTROPARESIS DELAYED GASTRIC EMPTYING ( DUE TO HYPERGLYCEMIA OR HYPERGLYCEMIA INDUCED PARASYMPTHETIC DYSFUNCTION) BLOATING SENSATION EARLY SATIETY INDIGESTION NAUSEA, HEARTBURN ENTEROPATHY DIARRHEA ( NOCTURNAL DIARRHOEA) FECAL INCONTINENCE MAY ALTERNATE WITH CONSTIPATION COLONIC HYPOMOTILITY CONSTIPATION
- 24. UROGENITAL D.NEUROPATHY BLADDER DYSFUNCTION (INABILITY TO SENSE FULL BLADDER, FAILURE TO VOID COMPLETELY) INCREASED FREQUENCY URGENCY, NOCTURIA, WEAK STREAM, DRIBBLING, INCONTINENCE, URINARY RETENTION MALE SEXUAL DYSFUNCTION ERECTILE DYSFUNCTION DECREASED LIBIDO PREMATURE EJACULATION, RETROGRADE EJACULATION FEMALE SEXUAL DYSFUNCTION DECREASED SEXUAL DESIRE, DYSPAREUNIA INADEQUATE LUBRICATION DECREASED SEXUAL AROUSAL SUDOMOTOR ANHIDROSIS GUSTATORY SWEATING
- 25. OTHER AUTONOMIC NEUROPATHIC SYMPTOMS: ABNORMAL PUPILLARY FUNCTION- SMALL UNREACTIVE PUPIL HYPOGLYCMEIC UNAWARENESS SLEEP APNEA
- 26. MONO NEUROAPTHY CRANIAL NERVE INVOLVEMENT: Nerves of extra occular muscles are commonly affected. Occulomotor nerve palsy III: ( 42% microvascular causes) # Abrupt onset, # retro orbital pain, # ptosis, # ophthalmoplegia with sparing of pupilary fuction Muscles supplied by 3rd nr: SR, IR, MR, IO Other cranial nerves affected: 6, 7, 4(less common)
- 27. III NR PALSY:
- 28. MONO NEUROAPTHY Peripheral nerves – ulnar, median, radial, lateral popliteal nerve. Entrappment neuropathies are common. Carpel tunnel syndrome- median Nr Pathogenesis: swelling of synovial sheaths around carpal tunnel due to fluid accumulation, inflammation, injury, external compression increases intra tunnel pressure which damages myelin sheath,impairs axonal flow & blocks micro circulation of median nerve causes pain , tingling, numbness sensation Cubital tunnel syndrome- ulnar nerve at elbow common peroneal Nr: at head of fibula
- 29. Radiculopathy TRUNCAL RADICULOPATHY: Abrupt onset of pain pain over area of chest and abdomen which worsens at night. thoracic lumbar spinal nerve roots are commonly involved focal anterior abdominal wall weakness- pseudohernia
- 30. Lumbo sacral Radiculoplexopathy OTHER NAME: “BRUNS GARLAND SYNDROME” Diabetic amyotrophy, proximal motor neuropathy Male>female in T2 DM Pathogenesis : micro vasculitis leads to ischemeic nerve injury Severe pain in unilateral/bilateral thighs, lowerback Followed by lowerlimb muscle weakness often proximal & unilateral Knee jerk reduced or absent
- 31. SUPERIMPOSED CIDP A chronic condition >8 weeks A type of secondary CDIP Chronic hyperglycemic state impairs neuronal microcirculation leads to myelin damage. As a chronic insult spinal nerve roots release chemokines into CSF leads to increse TNF, IL production activates CD4 cells which targets myelin sheaths and destroys leads to nerve damage. Symptoms: presents with proximal muscle weakness and sensory involvement
- 32. HYPOGLYCEMIC NEUROPATHY It is treatment induced neuropathy where it probably due to microcirculation deficit in hyperglycemic period. As soon as the blood sugar levels was corrected microcirculation was not not restored as early because of endoneurial ischemia and the formation of axonal regeneration zonesupon attaining normoglycemic state producing ectopic depolarisations and pain starts 2-6 weeks after improvement of glycemic control
- 33. INVESTIGATIONS Blood glucose/ HbA1c Urine analysis for protein/glucose RFT/Electrolytes Vitamin B12 levels Serum protein Lipid profile CT/MRI brain (cranial nr palsy) CT Pelvis (motor neuropathy) NC study EMG study
- 34. Nerve conduction study It is a measure of how fast the nerve conduct the impulses Used in cases of paresthesia, weakness of arms or legs Procedure: 1.electrodes will be taped to skin along the nerves that are being studied
- 35. 2.Small stimulus is applied(electric current) that activate nerves 3.The electode will measure the current the current that travells down the nerve pathway If damaged? – the current will be slower/weaker Time of procedure- 30-90 min Complications- little discomfort from electric current, not painful Advantage: - non invasive, no anaesthesia needed - detect asymptomatic cases - monitering of progression/ remission of disease
- 36. INTERPRETATION: Speed of conduction depends on diameter of nerve and degree of myelination. In general , the range of normal conduction velocity will be approx 50-60 m/sec, however it vary from one nervr to another and and also individual variablility. Eg: Slow NCS Indicates damage to myelin Slowing across wrist jt for motor &sensory latancies of median nerve Indiacates compression of median nr – carpal tunnel synd Slowing of all nr conduction in >1limb Indicates polyneuropathy
- 37. Treatment
- 39. CORRECTION OF UNDERLYING PATHOGENEIC MECHANISM: NORMALISATION OF BLOOD GLUCOSE ANTIOXIDANT THERAPHY ALDOSE REDUCTASE INHIBITOR GROWTH FACTOR ANALOGUE PHYSICAL APPROACH PHARMACOLOGICAL APPROACH PROPER FOOT WEAR NSAIDS FOOT CARE ANTI DEPRESSANTS PHYSIOTHERAPHY ANTICONVULSANTS NOCTURNAL SPLINT ANTIOXIDANTS, AGE INHIBITORS
- 40. Anti convulsants: GABA ANALOGUES: Gabapentin, pregabalin (-) Ady cyclase, +k+ channels, (-)ca2+influx
- 41. pregabalin Gabapentin Initial dose 25-75mg 1-3*/day 100-300mg 1-3*/day Effective dose 300-600mg/day 900- 3,600mg/day Common Adverse effects Somnolence Dizziness Headache Ataxia Fatigue Weight gain xerostomia Somnolence Dizziness Headache Ataxia Fatigue Major adverse effects Hepatotoxic Angioedema Rhabdomyolysis Thrombocytopenia Suicidal thoughts Steven johnson syndrome Suicidal thoughts Seizure after discontinuation
- 42. Anti depressants: SNRI duloxetine venlafaxine Initial dose 20-30 mg/ day 37.5 mg/day Maximum dose 60-120 mg/day 75-225 mg/day Common adverse effects Dizziness, insomnia, somnolence, anorexia, fatigue, decreased libido same Major adverse effects SJS, HT crisis, GI bleed, Delirium, MI, arrythmia, heapatotoxic, glaucoma, seizure, hyponatremia Neuroleptic malignant syndrome same
- 43. Tricyclic anti-depressants Amitryptalline Nortyrptalline Desipramine Initial dose 10-25 mg/day Max dose 25-100 mg/day Adverse effects Dizziness, insomnia, somnolence, anorexia, fatigue, xerostommia, somnolence, urinary retention, , constipation, blurred vision, weight gain, mmydriasis Major adverse effects Same as duloxetine
- 44. ALPHA LIPOIC ACID Anti oxidant 600 mg/day iv for 5 -14 days Improves neuropathic symptoms including pain
- 45. Aldose reductase inhibitors Tolrestat, epalrestat, ranirestat, fidarestat Potentially slow or reverse the progression of neuropathy Under clinical trail
- 46. Refractory neuropathic pain Phenothiazines Opioids –Tramadol Lidocaine Mexiletine Local nerve blocks