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

DefiniDefinissi i Nyeri (Nyeri (PainPain) dari ) dari IASPIASP

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 nyeriNyeri adalah suatu pengalaman emosionalKerusakan jaringan tidak mesti ada

(International Association for the Study of Pain)

• Nyeri suatu yang berbahaya (noksius,

protofatik) suatu yang tidak berbahaya

(nonnoksius, epikritik) cnth sentuhan ringan, kehangatan

TRANSDUCTION

TRANSMISSION

MODULATION

PERCEPTION

IIIIII

IV

V

VI X

IXVII

VIII

A

C

Peripheralnerve

Dorsal root

Spinal Cord

REFLEKS

SENSATION

INPUT

LAMINA REXED

Nerve FibersClass Velocity Function

A- Fast Motor

A- Fast Touch, pressure

A- Intermediate Muscle tone

A- Intermediate Pain, temperature

B Small Motor

C Small Pain

Sensation

• Noxious (Pain)– High threshold receptors, conducted by smaller,

lightly myelinated (Aδ) and unmyelinated (C) nerve fibers

• Non-noxious (light touch, pressure, temperature)– Low threshold receptors,

conducted by large myelinated (Aβ) nerve fibers

Peripheral sensitizationo Prostaglandins produced in response to tissue injury; increase sensitivity of nociceptor (pain)

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

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

Pain-sensitive tissue

Painful stimulus

Prostaglandin

Substance P

Histamine

Mast cellBlood vessel

Bradykinin

Nociceptor

Substance P

23

1

Thick, myelinated, fast conducting neurons

Mediate the feeling of initial fast, sharp, highly localized pain.

A-delta (kecepatan konduksi 12-30 detik)

Very thin, unmyelinated, slow-conducting

Mediate slow, dull, more diffuse, often burning pain

Jenis C (0,5-2 meter/detik).

RabaanTekanan

Nyeri cepat (fast pain) Nyeri lambat (slow pain)

Nociceptive painCaused by activation or sensitization of peripheral nociceptors initiated by tissue injury;

it can be secondary to an incision, inflammation, or disease.

ex: Acute osteoarthritis, Post operative pain, exercise injuries

Categorizing PainNeuropathic pain

Pain related to disease or injury of the peripheral or central nervous system (extending to the spinal cord)

Described as: burning, shooting, tingling, stabbing, or like a vise or electric shock.

ex: Neuropathic low back pain, Post herpetic neuralgia, Diabetic polyneuropathy

Acute and Chronic pain:

• Acute pain• caused by noxious stimulation

– Trauma or surgery or disease process– Usually nociceptive ( serves to detect, 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,

modulation

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

PERCEPTION

MODULATION

TRANSMISSION

TRANSDUCTION

• Somatic Pain

• Visceral Pain

Two types of Nociceptive Pain

Based on origin and features

Somatic Pain

• Superficial described as sharp, stabbing, well localized– Typically arises from the skin, subcutaneous tissues,

and mucous membranes.

• Deep described as dull, aching quality, less well localized– Typically arises from skeletal muscles, tendons, joint

or bones

• Pain from surgical incision, 2nd stage of labor, peritoneal irritation

Visceral Pain• Due to a disease process or abnormal function

of an internal organ or its covering (eg parietal pleura, pericardium or peritoneum)

• Dull, Difuse, Poorly localized• Associated with either abnormal sympathetic or

parasympathetic activity causing nausea, vomiting, sweating and changes in blood pressure and heart rate.

• Parietal pain is typically sharp • Described as a stabbing sensation either

localized to the area around the organ or referred to a distant site.

• Typically radiates with the same dermatome origin as the diseased viscus

• Occurs as rhythmic contractions of smooth muscles

• A cramping type accompanies gastroenteritis, gallbladder disease, ureteral obstruction, menstruation, distension of uterus during 1st stage of labor

• Chronic pain– may be due to nociception but in which

psychological and behavioral factors often play a major role

– Lasting ≥ 3 months

Assessing Pain“Tell me about any pain you have”

For each pain, 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?”

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 3 4 5 6 7 8 9 10No pain Worst

pain

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

Multimodal Pain Control• Inflammation

– NSAID, Selective COX-2 Inhibitors• Analgesia

– Paracetamol– Opioid– NMDA Antagonist– Anticonvulsant

• Non-pharmacologic therapy– Psychological support– TENS (Transcutaneous Electric Nerve Stimulation)– Acupunture– Physiotherapy– Complementary therapies

Adjuvant drugs: • Antidepressant• Alpha 2 Agonist• Steroids• Antiemetic

Management of drug related side effects• Antacids• Laxatives/stool softeners

NSAID mechanism of Action– Inhibition of PG-mediated amplification of

chemical and mechanical irritants on the sensory pathway.

– Inhibits COX (prostaglandin synthetase)– Blocks response to inflammatory substances,

bradykinins, acetylcholine, serotonin

═ mediation of peripheral inflammatory

response

Opioid ReceptorsOpioid Receptors

RECEPTOR RESPONSE ON ACTIVATION

(mu) Analgesia, respiratory depression, miosiseuphoria, reduced GI motility

(kappa) Analgesia, dysphoria, miosis, psychotommetic effects

(delta) Analgesia, facilitation of Mu receptor

located supraspinallylocated at spinal level

Undesirable Effects of Opioids

Respiratory depressionSedationNausea and VomitingSuppression of cough reflexPsychic and Physical dependenceToleranceConstipation

Agonists: Mu receptor– Morphine: oral, IV, IM, intrathecal, epidural

– Meperidine: IV, IM, epidural

– Fentanyl: transdermal, transmucosal, IV

– Tramadol: oral, IV, transmucosal

Agonist-antagonists: kappa, sigma/ no activity on Mu; potential to reverse effect of agonist– Nalbuphine: IM, IV– Butorphanol: IM, IV

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