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NYERI Dr. fajar as sp.AS Sp.An .MSc

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NYERIDr. fajar as sp.AS Sp.An .MSc

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DEFINISI dan KLAsIFIKASI NYERI• SENSASI

PROTOPATIK (NOXIOUS) EPIKRITIK (NON NOXIOUS)

•SENSASI EPIKRITIK SENTUHAN, TEKANAN, PROPRIOSEPSI, TEMPERATUR RESEPTOR AMBANG RENDAH ( LOW THRESHLOD ) DIHANTARKAN SERABUT SYARAF BESAR BERMYELIN

•SENSASI PROTOPATIK RESEPTOR AMBANG TINGGI (HIGH THRESHOLD) DIHANTARKAN SERABUT SYARAF KECIL, MYELIN

( A DELTA ) & SERABUT SYARAF TIDAK BERMYELIN ( C )

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• IASP ( The International Association For Study Of Pain )

→ PENGALAMAN & EMOSI SENSORI YANG TIDAK MENYENANGKAN DIHUBUNGKAN

DENGAN KERUSAKAN JARINGAN ATAU POTENSIAL RUSAK

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KLASIFIKASI NYERI - PATOFISIOLOGI

NYERI NOSISEPSI NYERI NEUROPATIK

- ETIOLOGI NYERI POST OPERATIF NYERI KANKER

- LOKASI NYERI KEPALA NYERI PUNGGUNG BAWAH ( NPB )

- KLINIS NYERI AKUT NYERI KRONIS

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NYERI NOSISEPSI AKTIFASI ATAU SENSITISASI NOSISEPTOR PERIFER RESEPTOR KHUSUS YANG MENGHANTARKAN STIMULUS NOXIOUS

NYERI NEROPATIK AKIBAT INJURI ATAU ABNORMAL STRUKTUR SYARAF PERIFER ATAU SENTRAL

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NYERI AKUT AKIBAT STIMULASI NOKSIUS KARENA INJURI, PRO SES PENYAKIT ATAU FUNGSI OTOT dan VISERA ABNORMAL HAMPIR SELALU NOSISEPSI PROSES FISIOLOGI

1. TRANSDUKSI 2. TRANSMISI 3. MODULASI 4. PERSEPSI

DIHUBUNGKAN DENGAN STRESS NEURO ENDOKRIN

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NYERI POSTOPERATIF, NYERI OBSTETRI, PENYAKIT MEDIKAL AKUT (AMI,PANCR.AKUT, Batu ginjal)“SELF LIMITED” ATAU SEMBUH DALAM BEBERAPA HARI ATAU BEBERAPA MINGGU DAPAT MENJADI NYERI KRONIS ADA 2 TYPE :

SOMATIK VISERAL

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• NYERI SOMATIK - SUPERFISIAL : KULIT, SUBKUTIS, MEMBRAN MUKUS - DEEP : OTOT, TENDON, JOINT, TULANG

• NYERI VISERAL - PROSES PENYAKIT ATAU FUNGSI ABNORMAL ORGAN INTERNAL (LEURA, PERICARD, PERITONIUM) - TYPE :

1. NYERI VISERAL TERLOKALISIR 2. NYERI PARIETAL TERLOKALISIR 3. NYERI PARIETAL REFERAL 4. NYERI VISERAL REFERAL

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• NYERI KRONIS - NYERI PERSISTEN SETELAH AKUT ATAU PENYEMBUH AN NYERI AKUT TIDAK TERJADI, DALAM WAKTU 1 - 6 BULAN - NOSISEPSI NEROPATIK ATAU KOMBINASI - FAKTOR PSIKOLOGIS DAN LINGKUNGAN SANGAT BERPERAN - NEUROENDOKRIN ( - )

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Activation of the Central Nervous System

at the Spinal Cord Level

Tissue Damage Activation of the Peripheral Nervous

System

Transmission of the Pain Signal to the Brain

Pain

.The Pain Response

Samad TA et al. Nature. 2001;410:471-5.

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Nociceptive afferent fiber

Normal Nerve Impulses Leading to Pain

Noxiousstimuli

Descendingmodulation

Ascendinginput

Spinal cord

Perceived pain

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Activation

External

Stimuli

Heat

Mechanical

Chemical

VR1Ca2+

mDEG

P2X3

Generator potentialsaction potentials

Voltage gated sodium channels

Pain and auto-sensitization

Woolf & Mitchel, 2001

Transduction

ATP

Na+

Modifikasi Meliala, 2003

ACTION POTENTIALACTION POTENTIAL

KERUSAKAN JARINGAN

INFLAMASI

SSA MI NOSSENSITISASI

AKTIFASIECT. DISC.

Si-Na+

KORNU DORSALIS

PgB5HTAdenosin

PengalamanKognitifBehaviourPsikologik

Inhibisi desenden

OTAK

PAIN – NO PAIN

R-NE

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Nociception

Spinothalamictract Peripheral

nerve

Dorsal Horn

Dorsal root ganglion

Pain

Modulation

Transduction

Ascendinginput

Descendingmodulation

Peripheralnociceptors

Trauma

Adapted from Gottschalk A et al. Am Fam Physician. 2001;63:1981, and Kehlet H et al. Anesth Analg. 1993;77:1049.

Perception

Transmission

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Dorsal HornDorsal root

ganglion

Peripheral sensoryNerve fibers

A

A

C

Largefibers

Smallfibers

There are Two Sensory Afferent Neurons1. Large myelinated A fibers

• Very fast conduction velocity • Respond to innocuous stimuli

2. Small myelinated A & C unmyelinated fibers• Slow conduction velocity • Respond to noxious stimuli

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PAIN PATHWAYSADA 3 NEURON

1. FIRST ORDER NEURON2. SECOND ORDER NEURON3. THIRD ORDER NEURON

FISIOLOGI NOSISEPSI

1. NOSISEPTOR FREE NERVE ENDING ( SUHU, MEKANIK DAN KIMIA JARINGAN RUSAK ) TYPE :

1. MEKANO NOSISEPTOR 2. SILENT NOSISEPTOR 3. POLIMODAL MEKANO HEAT NOSISEPTOR

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1. MEKANO NOSISEPTOR : → SENTUHAN , TUSUKAN 2. SILENT NOSISEPTOR : → INFLAMASI 3. POLIMODAL MEKANOHEAT NOSISEPTOR : - TEKANAN KUAT

- SUHU ↑ ( > 42º C dan < 18º C ) - ALLOGENS ( PAIN PRODUCING SUBSTANCE ) SEPERTI : BRADIKININ, HISTAMIN, SEROTONIN, H+, K+, PROSTAGLANDIN dan ATP

2. MEDIATOR KIMIA / NYERI → SUBSTANS P ( SP ) dan CALCITONIN GENE RELATED PEPTIDE ( CERP ) → GLUTAMAT

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3. MODULASI NYERI → MODULASI PERIFER :

1. HIPERALGESIA PRIMER 2. HIPERALGESIA SEKUNDER

→ MODULASI SENTRAL A. FASILITAS B. INHIBISI

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4. ANALGESI PREEMPTIF → ANALGESI EFEKTIF SEBELUM TRAUMA PEMBEDAHAN → INFILTRASI DENGAN ANESTESI LOKAL → BLOKADE NEURAL SENTRAL → PENGGUNAAN OPIOID DOSIS EFEKTIF → PENGGUNAAN KETAMIN → EFEKTIF MELEMAHKAN SENSITISASI PERIFER dan SENTRAL

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PATOFISIOLOGI NYERI KRONIS• MEKANISME PERIFER, SENTRAL dan PSIKOLOGIS• SENSITISASI NOSISEPTOR MEMEGANG PERANAN BESAR • MEKANISme PERIFER SENTRAL dan SENTRAL KOMPLEK → LESI NERVUS PERIFER, GANGLION, RADIX DORSA LIS, RADIX NERVUS dan STRUKTUR SENTRAL

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NYERI KRONIK- NEUROENDOKRIN STRESS RESPON (-)-- NYERI DIHUBUNGKAN DG PARAPLEGIA- GANGGUAN TIDUR- DEPRESI-GANGGUAN NAFSU MAKAN

EVALUASI PASIEN DENGAN NYERI- BEDAKAN NYERI AKUT dan KRONIS- NYERI AKUT →TERAPEUTIK- NYERI KRONIK → INVESTIGATIVE MEASURE

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RESPON SISTEMIK TERHADAP NYERINYERI AKUT :• EFEK KARDIOVASKULER :

- TAKHIKARDI - HIPERTENSI - PENINGKATAN IRITABILITAS JANTUNG - PENINGKATAN RESISTENSI VASKULER SISTEMIK - CARDIAC OUTPUT MENINGKAT

• EFEK RESPIRASI - KONSUMSI OKSIGEN TUBUH TOTAL MENINGKAT - PRODUKSI KARBONDIOKSIDA MENINGKAT - MINUTE VENTILATION MENINGKAT

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• EFEK GASTROINTERSTINAL dan URINARY : - TONUS SPINKTER ↑ - ↓ MOTILITAS INTERSTINAL dan URINARY

- ↑ ILLEUS - RETENSI URIN - STRESS ULCER - ASPIRASI - MUAL MUNTAH

• EFEK ENDOKRIN - ↑ HORMON KATABOLIK (KATEKOLAMIN, KORTISOL,GLUKAGON) - ↓ HORMON ANABOLIK ( INSULIN dan TESTOSTERON)

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• EFEK IMUN - LEKOSITOS - LYMPHOPENIA - MUDAH INFEKSI

• LAIN – LAIN - ANSIETAS - GANGGUAN TIDUR

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Terapi

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Prostaglandin produced in response to tissue injury; increase sensitivity of nociceptor (pain)

Nociceptor then releases substance P, which dilates blood vessels and increases release of inflammatory mediators, such as Bradykinin (redness & heat)

Substance P also promotes degranulation of mast cells, which release histamine (swelling)

1

2

3

Pain-sensitive tissue

Painful stimulus

Prostaglandin

Substance P

Histamine

Mast cellBlood vessel

Bradykinin

Nociceptor

Substance P

23

1

Inflammation Tissue

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TreatmentMethods

Drug therapyRemove the causeof pain

Regionalanalgesia

Physicalmethods

Psychologicalapproaches

• Surgery• Splinting

Non-opioid• Aspirin & other NSAIDs• Paracetamol• Combinations

Opioid• Morphine• Others

High-tech• Epidural infusion• Local anaesthetic + opioid

Low-tech• Nerve bloks• Local anesthetic + opioid

• Physiotherapy• Manipulation• TENS• Acupunture• Ice

• Psychoprophylaxis• Relaxation• Hypnosis

Acute pain interventions

McQuary, 2000 An evidence-based resource for pain relief,

Multimodal Pain ManagementCoordinated use of medication & non medication to control the painConsider the psycho-socio-cultural-spiritual aspects

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