Neuropathy Diabetik
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Transcript of Neuropathy Diabetik
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S. IRWANSYAH
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DEFINISI
GANGGUAN FUNGSIONAL ATAU ORGANIKDARI SARAF PERIFER
GANGGUAN INI DAPAT MENGENAI :SARAF SENSORIKSARAF MOTORIKSARAF OTONOMKOMBINASI
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KLASIFIKASI
BANYAK KLASIFIKASI DARI NEUROPATI.1.MENURUT ONSET SERANGAN:
NEUROPATI AKUT MIS : POLINEUROPATI IDIOPATIK AKUT NEUROPATI KRONIK
MIS : BERI BERIDIABETES MELLITUSLEPRA
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2.MENURUT DERAJATNYA
1. NEUROPATI RINGAN :SENSORIK SAJA
2. NEUROPATI SEDANG :
SENSORIK, MOTORIK,REFLEKS
3. NEUROPATI BERAT :
SENSORIK, MOTORIK,REFLEKS , ATROFI OTOT
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3. MENURUT JUMLAH SARAF YANGTERLIBAT
1. MONONEUROPATI SIMPLEKS :GANGGUAN PADA SATU SARAF PERIFER SAJA.
2. MONONEUROPATI MULTIPLEKS :MENGENAI BEBERAPA SARAF TEPI, BIASANYATIDAK BERDEKATAN DAN TIDAK SIMETRIS.
3. POLINEUROPATI :BBRP SARAF TEPI, SIMETRIS DAN SERENTAK,BIASANYA PREDOMINAN DI DAERAH DISTAL.
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4. MENURUT LETAK LESI
1 AKSONOPATI DISTAL :GANGGUAN PADA AKSON.
2. MIELINOPATI :GANGGUAN PADA SELUBUNG MIELIN.
3. NEURONOPATI : GANGGUAN PADA BADAN SEL SARAF DICORNU ANTERIOR, MEDULLA SPINALIS
ATAU PADA DORSAL ROOT GANGLION .
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ETIOLOGI
1. IDIOPATHIC INFLAMMATORY NEUROPATHIES - POLINEUROPATI IDIOPATIK AKUT
(GUILLAIN BARRE SYNDROME)- CHRONIC INFLAMMATORY DEMYELINATING
POLYNEUROPATHY
2. METABOLIC AND NUTRITIONAL NEUROPATHIES - DIABETES, HIPOTIROIDI, ACROMEGALI
- UREMIA- LIVER DISEASES- VIT B1, OR VIT B12 DEFICIENCY
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ETIOLOGI (lanjutan)
3. INFECTIVE AND GRANULOMATOUSNEUROPATHIES :
AIDS, LEPROSY. DIFTERI, SARCOIDOSIS
4. VASCULITIS NEUROPATHIES :- POLYARTERITIS NODOSA
- RHEUMATOID ARTHRITIS- SYSTEMIC LUPUS ERYTHEMATOSUS
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ETIOLOGI (lanjutan)
5. NEOPLASTIC AND PARAPROTEINEMICNEUROPATHIES :- COMPRESSION AND IRITATION BY TUMOR
- PARANEOPLASTIC SYNDROME- PARAPROTEINEMIAS- AMYLOIDOSIS
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ETIOLOGI (lanjutan)
6. DRUGS INDUCED AND TOXIC NEUROPATHIES - DAPSON, ISONIAZIDE, PHENYTOIN, PIRIDOKSIN
VINCRISTIN, HIDRALAZINE.
- ALKOHOL- TOKSIN: ORGANOPHOSPHAT
ARSENICLEAD
THALIUMGOLD
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ETIOLOGI (lanjutan)
7. HEREDITARY NEUROPATHIES - IDIOPATHIC
HEREDITARY MOTOR AND SENSORY NEUROPATHIES
HEREDITARY SENSORY NEUROPATHIESFAMILIAL AMYLOIDOSIS
- METABOLIC PORPHYRIA
METACHROMATIC LEUCODYSTROPHY ABETALIPOPROTEINEMIA
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ETIOLOGI
8. ENTRAPMENT NEUROPATHIES- UPPER LIMBS
MEDIAN NERVE (CARPAL TUNNEL SYNDROME)
ULNAR NERVERADIAL NERVE
- LOWER LIMBSPERONEAL NERVE
FEMORAL NERVEOBTURATOR NERVE
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MOST COMMON DISEASES AFFECTING THEPERIPHERAL NERVE
DANG THE RAPIST
Diabetes Trauma Rheumatic (collagen
vascular)Alcohol Hereditary Amyloid
Nutritional Environmental Paraneoplastic
Guillain Barre toxin and drugs Infections
Systemic diseases
Tumors
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PATOFISIOLOGI
ADA BEBERAPA PROSES PATOLOGI YANGMENGENAI SERABUT SARAF a.l.:
1. DEGENERASI WALLERIAN
TERJADI DEGENERASI AKSON DANSELUBUNG MIELIN KEARAH DISTAL DARILESI.
DEGENERASI BISA JUGA KE PROKSIMALSATU ATAU DUA SEGMEN .
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PATOFISIOLOGI
2. DEMIELINISASI SEGMENTAL TIMBUL BILA TERJADI LESI PADA SELSCHWANN
PROSES DIMULAI DI DAERAH NODUSRANVIER DAN MELUAS TAK TERATURMENGENAI SEGMEN-SEGMEN INTERNODUSLAIN.
AKSON DAPAT MENGALAMI DEGENERASI ATAU TIDAK TERGANGGU SAMA SEKALI.
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PATHOGENESIS
-Trauma-Entrapment-Tumor
-GBS-Metabolic-Nutritional
-Dying Back --Toxin--Nutritional
--Collagen
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PATOFISIOLOGI
3. DEGENERASI AKSON PRIMER
DISEBUT JUGA DENGAN AKSONOPATI .DEGENERASI AKSON INI BIASANYA DI IKUTIOLEH DEMIELINISASI SEGMENTAL YANGSEKUNDER.
SERING PADA UREMIA, KERACUNAN ALKOHOL, LEPRA, KARSINOMA.
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PATOFISIOLOGI
KERUSAKAN SARAF DIBAGI 3 TINGKAT PENTING UNTUK MENENTUKANPROGNOSE.
1. NEUROPRAKSIA :- KERUSAKAN PALING RINGAN- HANYA TERJADI GANGGUAN HANTARAN- TANPA GANGGUAN KONTINUITAS- PEMULIHAN TERJADI DALAM BEBERAPA MENIT
SAMPAI BEBERAPA MINGGU
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PATOFISIOLOGI
2. AKSONOTMESIS : - KERUSAKAN PADA AKSON DISERTAI
DEGENERASI- TANPA KERUSAKAN ENDONEURAL- REGENERASI KEMUNGKINAN DAPAT
TERJADI DENGAN HASIL YANG BAIK
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PATOFISIOLOGI
3. NEUROTMESIS :
- SARAF TERPUTUS TOTAL ATAUSEBAGIAN
- PENGOBATAN DGN PENYAMBUNGAN- KEMUNGKINAN PERBAIKAN 50%
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GEJALA KLINIK
1. GANGGUAN SENSORIK:Invo lvem ent o f sensory axons p rodu ces
imp airm ent o f sensa tion wi th dyses thes ias o r
paresthesias .
- RASA KAKU, DINGIN, PEDAS- GATAL DAN KEBAS-KEBAS- NYERI SEPERTI DITUSUK JARUM- RASA TERBAKAR- RASA BERJALAN DI ATAS KAPAS- RASA TERSANDUNG WAKTU BERJALAN- RASA TIDAK STABIL
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GEJALA KLINIK
2. GANGGUAN MOTORIK:Invo lvemen t o f mo to r axons p roduces m usc le
wast ing and w eakness fo l low ed by at roph y and
fasc icu la t ions - KELEMAHAN BERSIFAT LMN- SULIT MEMUTAR KUNCI PINTU- SULIT MEMBUKA KANCING BAJU- SULIT MEMUTAR TUTUP BOTOL- FOOT DROP- WRIST DROP- GANGGUAN GERAKAN TANGKAS
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GEJALA KLINIK
3. GANGUAN REFLEKS TENDON:The tend on r ef lexes su pp l ied b y th e affected n erve
are depressed o r absent .
Contoh :- REFLEKS TENDON BISEPS- REFLEKS TENDON TRISEPS
- KPR- APR
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GEJALA KLINIK
GANGGUAN OTONOMIK (lanjutan) :- GANGGUAN KANDUNG KEMIH :
ATONI KANDUNG KEMIH, RESIDU URINE
- IMPOTENSI- GANGGUAN KARDIOVASKULER:
HIPOTENSI ORTOSTATIK, SINKOP- GANGGUAN BERKERINGAT- CARDIO RESPIRATORY ARREST
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PREDOMINANTLY MOTOR NEUROPATHIES
Guillain-Barre Syndrome Diphtheric neuropathy
Dapsone-induced neuropathy Porphyria and multifocal motor neuropathy
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PREDOMINANTLY SENSORY NEUROPATHIES
Drug toxicity : pyridoxine, doxorubicine Autoimmune : paraneoplastic, Sjogren
syndrome, etc.
Infectious : diphtheria, HIV Deficiency : vit. E
Inherited : abetalipoproteninemia.
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DIAGNOSA
1. GEJALA KLINIK2. LABORATORIUM3. FOTO THORAKS
4. PUNKSI LUMBAL5. EKG6. BIOPSI : paling sering n. suralis atau n. cutaneus
radialis
7. ELEKTROFISIOLOGI: EMGNCV
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ELEKTRO MIOGRAFI
ELEKTRODA DITUSUKKAN KEDALAM SUATU OTOT SKELETUNTUK MEMPELAJARI PERUBAHAN POTENSIAL LISTRIKNYA .INDIKASI:GANGGUAN LOWER MOTOR NEURON , YANG LESINYA DI:
1. KORNU ANTERIOR2. RADIKS3. PLEKSUS4. SARAF PERIFER
5. NEUROMUSCULAR JUNCTION6. OTOT
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MANFAAT EMG
MEMBANTU DIAGNOSA SECARA DINI MENENTUKAN LETAK LESI MEMBEDAKAN LESI MIOGEN ATAU NEUROGEN
MENENTUKAN LESI PARSIAL ATAU TOTAL MEMBEDAKAN SENSORIK ATAU MOTORIK EVALUASI PENGOBATAN MEMBANTU MENENTUKAN PROGNOSE
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NERVE CONDUCTION VELOCITY( NCV)
NCV ATAU KHS NILAI NORMAL :
N. ULNARIS = 47 - 72 m / s
N. MEDIANUS = 46 - 72 m / sN. PERONEUS = 42 - 63 m / sN. TIBIALIS = 40 - 67 m / s
DISTAL LATENCY ( DL ) NILAI NORMAL N. MEDIANUS2,7 + 0,3 m/s
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MANFAAT PENGUKURAN KHS
MENGIKUTI PERJALANAN PENYAKIT MENGEVALUASI EFEK PENGOBATAN
MENENTUKAN PROGNOSE, APAKAHMASIH MUNGKIN DIPEROLEHPERBAIKAN LAGI.
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EMG DAN KHS PADA NEUROPATI
DIJUMPAI PENURUNAN KHS. PEMANJANGAN DISTAL LATENCY PENURUNAN AMPLITUDO GELOMBANG M DURASI YANG MEMANJANG POTENSIAL POLIFASIK FIBRILASI
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NEUROPATI DIABETIK
PREVALENSI : 10 - 20 % (SIMTOMATIK) KHS 80 % ABNORMAL KLINIS DAPAT MENGENAI:
SENSORIKMOTORIKOTONOMIK
KOMBINASI
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EPIDEMIOLOGY & ETIOLOGY
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
Mononeuropathy :Median nerve entrapment the most common
mononeuropathyCauses :
- repetitive motion injury duringmanual tasks
such as keyborad operation(entrapment)
- multifocl demyelination- ischemic injury- trauma
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Polyneuropathy : hundreds of potential etilogies DM is the most common cause in the US, affecting at
least 1-2% of the population Leprosy remains the most common cause of
neuropathy worldwide.
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
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DIABETIC NEUROPATHY
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Prevalence of Diabetes Mellitus
Worldwide: 194 million people USA: 18,2 million (18% of people > 65) About 40 % of U.S. adults ages 40- 74 (41 million
people) have abnormal blood glucose levels withouthaving DM.
Many will develop type 2 DM in the next 10 years. Total annual cost in 2002: $132 billion (one out of
every 10 health care dollars spent
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PATHOPHYSIOLOGY OFDIABETIC NEUROPATHY (Bird 2002 )
* Direct glucose neurotoxicityMetabolic derangements
Increased polyol pathway activity with accumulation of fructoseand sorbitol and reduced nerve inositol
Reduced Na+K+ ATPase Slowed axonal transport
Intracellular oxidative stress with premature apoptosisMicrovascular abnormalities Depressed prostaglandins Decreased nerve blood flow
Endoneurial ischemiaTrophic agent (nerve growth factor) deficiency
Abnormal glycation and glycosylation of proteins Altered nerve proteins Altered endothelial protein functions
Autoimmune-mediated neurotoxicity
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Types of DN
Focal (Mononeuritis) Entrapment Diffuse Proximal Distal Small- fiber (including
autonomic) Large-fiber
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DIABETIC NEUROPATHIC SYNDROMES
ISCHEMIC MONONEUROPATHY.- cranial (eg. CNs III, VI,VII)
diplopia, pupil-sparing third nerve palsy,hemifacial weakness- Radicular (thoracic, lumbosacral)
pain, followed by numbness or weakness in aradicular distribution
- Peripheral (eg. Femoral)pain, followed by numbness, weakness or
both in territory of a single nerve
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
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DIABETIC NEUROPATHIC SYNDROMES(cont.d)
SMALL FIBER NEUROPATHY:- pure small fiber neuropathy
numbness, paresthesias, painful dysesthesias,hyperesthesias.
- Diabetic neuropathy cachexiasubacute, severe neuropathic pain, rapid
weight loss- Autonomic neuropathy
erectile dysfunction, orthostasis, cardiacdysrhythmia, diarrhea, constipation
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
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DIABETIC NEUROPATHIC SYNDROMES (cont.d)
DISTAL SYMMETRIC NEUROPATHY:- large fiber sensory neuropathy
numbness, paresthesias, dysesthesias,hyperesthesias, ataxia.
- sensorimotor neuropathy
any of the above plus distal weakness
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
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DIABETIC NEUROPATHIC SYNDROMES (cont.d)
REGIONAL NEUROPATHIC SYNDROMES.- Diabetic amyotrophy
subacute weakness and atrophy of
proximal leg muscles- Diabetic thoracoabdominal neuropathy.
subacute weakness, numbness, and
atrophy in thorax and abdomen
CURRENT DIAGNOSIS & TREATMENT NEUROLOGY, 2007
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DIAGNOSIS
Status terkendalinya Baik Sedang Kurang Diabetus Mellitus terkendali
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Glukosa darah
Puasa mg/dl 80 - 120 < 140 > 140 mmol/l 4.4 - 6.7 < 7.8 > 7.8
2 jam pp mg/dl 80 - 160 < 180 > 180
mmol/l 4.4 - 8.9 < 10 > 10.0
Hb A1 % < 8.5 8.5 - 9.5 > 9.5
Glukosa Urine % 0 < 0.5 > 0.5
Kholesterol total mg/dl < 200 < 250 > 250
mmol/l < 5.2 < 6.5 > 6.5
Kholesterol HDL mg/dl > 40 > 35 < 35 mmol/l > 1.1 > 0.9 < 0.9
Trigliserid mg/dl < 150 < 200 > 200 mmol/l < 1.7 < 2.2 > 2.2
BMI kg/m 2 Pria < 25 < 27 > 27 Wanita < 24 < 26 > 26
Tekanan darah mm Hg < 140/90 < 160/95 > 160/95
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Treatment of Diabetic Neuropathy
Best Rx is prevention !!! Diabetics should do three things to
helpprevent the complications of diabetes:
1) Achieve ideal body weight2) Maintain regular exercise3) Maintain good control of
glucose level
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Treatment of Diabetic Neuropathy (cont.d)
Protect tissues from injury (check feet every day, good shoes, beware ofexcess heat or cold)
Medications can provide symptomaticrelief from pain
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Treatment of Diabetic Neuropathy (cont.d)
Pada DN demielinasi segmental Vit B12 menstimulasi sel-sel Schwann
memfasilitasi mielogenesis, meningkatkan sintesisprotein dan regenerasi syaraf
Vitamine B12- Cyanocobalamine- Mecobalamine - Hydroxycobalamine
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Pathogenesis of DN
Heterogenous with causative factors: Microvascular insufficiency oxidative stress nitrosative stress defective neurotrophism autoimmune mediated nerve destruction
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Treatment of Diabetic Neuropathy
Medications for Neuropathic Pain: Topical capsaicin Antidepressants (amitriptyline,
nortriptyline, imipramine) Anticonvulsants (gabapentin,
carbamazepine, clonazepam, phenytoin) Narcotics (avoid unless nothing else
works)
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PAINFUL DIABETIC NEUROPATHY
Cranial nerve neuropathy Acute thoracoabdominal neuropathy Acute distal sensory neuropathy Acute lumbar radiculoplexopathy Chronic distal small-fiber neuropathy
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TRAUMA SARAF PERIFER
Proksimal Regenerasi Sprouting * 1 - 5 mm / hari* Distal Degenerasi
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DERAJAT TRAUMA SARAF PERIFER
Regen. 1-5mm/hari AXONOTMESIS
Hantar saraf (-) Axon Putus Wallerian DegenMyelin utuhPerineurium utuhII
TrasientNEUROPRAXIAHantar saraf (-)
Axon utuhMyelin utuhPerineurium utuh
I
JELEKSeluruh jar.saraf putus +Jar.sekitarnya putusV
Hantar saraf (-) Axon PutusMyelin PutusPerineurium Putus
IV
JELEKNEUROTMESIS
Hantar saraf (-) Axon Putus Wallerian DegenMyelin menipisPerineurium Utuh
III
PrognoseSeddonSunderland
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