neuropathy diabetik

7/28/2019 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.



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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



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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



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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



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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



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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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Terima kasih

neuropathy diabetik

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