Tatalaksana Nyeri

Atikah binti su azmi Dr Rizqan sp an

Pain
- unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.’’

International Association for the Study of Pain, 1979

Definisi Nyeri (Pain) dari IASP
(International Association for the Study of Pain)

Pain (Nyeri) adalah suatu pengalaman sensorik dan emosional yang berkaitan dengan kerusakan jaringan atau diduga ada kerusakan jaringan

Nyeri adalah

pengalaman sensorik yang berkaitan dengan aktivasi nociceptor dan lintasan nyeri Nyeri adalah suatu pengalaman emosional Kerusakan jaringan tidak mesti ada

kehangatan .• Nyeri •  suatu yang berbahaya (noksius. epikritik) cnth sentuhan ringan. protofatik) •  suatu yang tidak berbahaya (nonnoksius.

PERCEPTION TRANSDUCTION TRANSMISSION MODULATION .

SENSATION  Dorsal root Peripheral nerve Spinal Cord C  A VI IX VII VIII I II III IV V X INPUT REFLEKS LAMINA REXED .

pressure Muscle tone Pain.Nerve Fibers Class A- A- A- A- Velocity Fast Fast Intermediate Intermediate Function Motor Touch. temperature B C Small Small Motor Pain .

pressure. lightly myelinated (Aδ) and unmyelinated (C) nerve fibers • Non-noxious (light touch. temperature) – Low threshold receptors.Sensation • Noxious (Pain) – High threshold receptors. conducted by smaller. conducted by large myelinated (Aβ) nerve fibers .

such as Bradykinin (redness & heat) o Substance P also proses degranulation of mast cells. which release histamine (swelling) .Peripheral sensitization Painful stimulus o Prostaglandins produced in Pain-sensitive tissue Prostaglandin Mast cell Histamine Bradykinin Substance P response to tissue injury. which dilates blood vessels and increases release of inflammatory mediators. increase sensitivity of nociceptor (pain) Blood vessel 1 Substance P 2 3 Nociceptor o Nociceptor then releases substance P.

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often burning pain Jenis C (0. sharp.5-2 meter/detik). more diffuse. slowconducting Mediate slow. fast conducting neurons  Mediate the feeling of initial fast. Rabaan Tekanan .Nyeri cepat (fast pain)  Thick. highly localized pain. myelinated. unmyelinated.  A-delta (kecepatan konduksi 12-30 detik) Nyeri lambat (slow pain)    Very thin. dull.

exercise injuries Neuropathic pain Pain related to disease or injury of the peripheral or central nervous system (extending to the spinal cord) Described as: burning. stabbing. Post herpetic neuralgia. ex: Neuropathic low back pain. Diabetic polyneuropathy . ex: Acute osteoarthritis. inflammation. Post operative pain. shooting. tingling. or like a vise or electric shock. or disease.Categorizing Pain Nociceptive pain Caused by activation or sensitization of peripheral nociceptors initiated by tissue injury. it can be secondary to an incision.

modulation . localize and limit tissue damage) – Easier to manage than chronic pain – Related to a form of tissue damage resulting in excitation of nociceptor nerve ending – involving four physical process ( transduction.Acute and Chronic pain: • Acute pain • caused by noxious stimulation – Trauma or surgery or disease process – Usually nociceptive ( serves to detect.

• Self limited / resolve with treatment in afew days or weeks .

PERCEPTION MODULATION TRANSMISSION TRANSDUCTION .

Two types of Nociceptive Pain • Somatic Pain • Visceral Pain Based on origin and features .

Somatic Pain • Superficial described as sharp. 2nd stage of labor. stabbing. and mucous membranes. subcutaneous tissues. • Deep described as dull. less well localized – Typically arises from skeletal muscles. joint or bones • Pain from surgical incision. well localized – Typically arises from the skin. peritoneal irritation . tendons. aching quality.

Visceral Pain • Due to a disease process or abnormal function of an internal organ or its covering (eg parietal pleura. pericardium or peritoneum) • Dull. Poorly localized • Associated with either abnormal sympathetic or parasympathetic activity causing nausea. vomiting. . sweating and changes in blood pressure and heart rate. Difuse.

• Parietal pain is typically sharp • Described as a stabbing sensation either localized to the area around the organ or referred to a distant site. .

gallbladder disease. ureteral obstruction. distension of uterus during 1st stage of labor .• Typically radiates with the same dermatome origin as the diseased viscus • Occurs as rhythmic contractions of smooth muscles • A cramping type accompanies gastroenteritis. menstruation.

• Chronic pain – may be due to nociception but in which psychological and behavioral factors often play a major role – Lasting ≥ 3 months .

consider the following: • Palliative factors: “What makes it better?” • Provocative factors: “What makes it worse?” • Quality: “What is it like?” • Radiation: “Where does it spread to?” • Severity: “How bad is it?” • Temporal factors: “Is it constant? Does it come and go?” .Assessing Pain “Tell me about any pain you have” For each pain.

Analgesic history: • • • • • “What has helped in the past?” “What has not helped in the past?” “Show me exactly what you are taking now” “How much and how often?” Does it help the pain? Does it relieve the pain or only reduce it?” • Does your medicine do anything that you don’t like?” .

Pain Assessment Self-Report: Visual Analog Scale Numeric Rating Scale Faces Pain Scale .

Numeric Rating Scale 0 1 2 No pain 3 4 5 6 7 8 9 10 Worst pain .

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Principal of pain management • Pain as the Fifth Vital Sign • Multimodal analgesic approach • “It is easier to keep pain at bay rather than trying to control it after it has resurfaced” .

3 step ladder for pain relief .

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Selective COX-2 Inhibitors Analgesia – Paracetamol – Opioid – NMDA Antagonist – Anticonvulsant Non-pharmacologic therapy – Psychological support – TENS (Transcutaneous Electric Nerve Stimulation) – Acupunture – Physiotherapy – Complementary therapies • .Multimodal Pain Control • • Inflammation – NSAID.

Adjuvant drugs: • Antidepressant • Alpha 2 Agonist • Steroids • Antiemetic Management of drug related side effects • Antacids • Laxatives/stool softeners .

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– Inhibits COX (prostaglandin synthetase) – Blocks response to inflammatory substances. acetylcholine.NSAID mechanism of Action – Inhibition of PG-mediated amplification of chemical and mechanical irritants on the sensory pathway. bradykinins. serotonin ═ mediation of peripheral inflammatory response .

dysphoria. respiratory depression.Opioid Receptors RECEPTOR RESPONSE ON ACTIVATION m (mu) k (kappa)  (delta) Analgesia. reduced GI motility Analgesia. miosis. miosis euphoria. facilitation of Mu receptor m1 k3 2 located supraspinally m2 k1 1 located at spinal level . psychotommetic effects Analgesia.

Undesirable Effects of Opioids Respiratory depression Sedation Nausea and Vomiting Suppression of cough reflex Psychic and Physical dependence Tolerance Constipation .

IV. sigma/ no activity on Mu. IV . IM.Agonists: Mu receptor – – – – Morphine: oral. IV. epidural Fentanyl: transdermal. transmucosal Agonist-antagonists: kappa. IV Tramadol: oral. potential to reverse effect of agonist – Nalbuphine: IM. intrathecal. epidural Meperidine: IV. transmucosal. IV – Butorphanol: IM. IM.

Ethical Consideration • Give regular analgesics of sufficient strength for continuous pain • Ensure pain control by titrating analgesic doses without overdosing • Recognize that analgesics are for pain control and aren’t to be used as sedatives • Recognize our own limitations and request advice from specialist pain relief services .

“Pain management is more of an art than a science” Thank you .

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