Musculoskeletal Disorders and pain

Inflammation
What is inflammation ?

Response of a living tissue to a harmful stimuli May be Mechanical, Chemical, Physical, Thermal, Microbial or any other.

Primary objectives of inflammation.

Remove unwanted stimulus.

Hasten recovery. Provide defence.

Minimize damage.

Inflammation
Cardinal Symptoms

Heat (Calor) Redness (Rubor) Pain (Dolor) Swelling (Tumor) Loss of function (Functio Laesa)

Physiology of Inflammation
Occurs in 3 phases

Acute transient phase (vasodilation & permeability).

capillary

Delayed sub-acute phase (infiltration of WBCs & phagocytic cells). Chronic proliferative phase (tissue degeneration & fibrosis).
Inflammation is essential but at times gets exaggerated & sustained with no apparent benefit.

Physiology of Inflammation
Chemical mediators released

Prostaglandins Thromboxanes (TXA2)

Histamine
Kinins Leukotrienes Complements Platelet activating factor (PAF)

Cytokines

 Prostaglandins intensify effect of Bradykinin & Histamine Stimulate migration of phagocytes through capillary walls
Mast cell Capillary

Inflammatory Response

Monocyte

Free nerve ending (senses pain)

Mechanical, Chemical injury, Microbes, Antigens. triggers inflammatory response

Macrophage Neutrophil Inflammatory mediators Prostaglandins Histamine Bradykinin

Physiology of Inflammation
Arachidonic Acid Metabolism
Chemical & Mechanical stimuli activates Phospholipase A

Harmful Stimulus

Cell Perturbation (agitation or disturbance)

Liberates Membrane Phospholipids
Release

ARACHIDONIC ACID (AA)

Lipoxygenase

Cyclo-oxygenase Endoperoxides PGG2 LEUKOTRIENES PROSTAGLANDINS PGE2 PGD2 PGF2a PROSTACYCLINS PGI2 THROMBOXANE TXA2 PGH2

Hydroperoxides

STOMACH, KIDNEYS

BLOOD VESSEL WALL

PLATELETS

Pain

"An unpleasant sensory and emotional experience

associated with actual or potential tissue damage, or

described in terms of such damage.

Pain that accompanies tissue injury and inflammation

results from local stimulation and enhances sensitivity of pain fibres which in turn leads to excitation of neurons in spinal cord. Prostaglandins, bradykinin, sub P causes pain.

Characteristics of Pain
Acute Chronic

1. Limited to days or weeks 2. Well defined 3. Involves anxiety

4. Useful physiological signal 5. Expect cure of pain

Duration unpredictable Poorly defined Involves depression & frustration Has no useful function Only can hope to control pain

Brain

Central & Peripheral Receptors

Spinal cord

Peripheral receptors

PERCEPTION OF PAIN
Injury
Nociceptors

Signals
Sensory neuron

Spinal cord
Nerve Pathways

Hypothalamus Initiation of pain signals Pain

Musculoskeletal Disorders

Illness resulting from cumulative trauma to the muscles, nerves, tendons, ligaments, joints, bones, cartilage, or spine discs Musculoskeletal disorders have high impact on* The patient Society The primary care physician

* Glazier, et al. J Rheum. 1996;23:351356

OA

In India 7.35 % of the total population suffering from Osteoarthritis Degenerative arthritis rises steeply with age. Less than 1% have it between the ages of 25 and 34, >30% after the age of 70 As with many other forms of arthritis, women are disproportionately affected, especially with hand and knee (OA)

What is Osteoarthritis ?

Affects the joint, commonly occurs in the hands, hips, knees, neck & lower back.

What is Osteoarthritis ?
Tendon

Ligament Muscle Knee Joint (Side view)

Synovium

Cartilage

Joint is surrounded by a fibrous envelope or capsule called synovium which produce fluid to reduce friction & wear in a joint. Muscles & tendons power the joint.

How does OA develop ?

Cartilage destruction

Breakdown of cartilage results in joint pain.

It becomes pitted & weak.

Knee (Front View)

Loses elasticity leading to damage by excess use or injury.

How does OA develop ?

Bony spurs

Cartilage breaks down, joint lose normal shape. Bone ends thicken, bone at the edge of joint may grow outward & form bony spurs.

Knee (Front View)

How does OA develop ?

Loose bone pieces

Fluid-filled cysts may form in the bone near the joint. Bits of bone or cartilage may float loosely in the joint space.

Fluid-filled cysts

Loose cartilage particles

How does OA develop ?

In OA joints become swollen & damage. Can be painful & difficult to move due to inflammation.

OSTEOARTHRITIS
Exposed Bone Eroding cartilage

Bone Spurs

Eroding Meniscus

Progressive Disease

OA Management
Non pharmacological methods

Social support
Weight loss, if the patient is overweight Physiotherapy and exercise

Occupational therapy
Bracing

OA Management
Pharmacological management

Symptom modifying drugs

Analgesics
Nonsteroidal anti-inflammatory drugs Visco-supplementation (Sodium Hyaluronate inj. (Hyaluronic

Acid) - an important component of synovial fluid, provides

lubricating properties)

Corticosteroids Glucosamine sulfate Chondroitin sulfate

Other Nutraceuticals

RA & AS

Approximately 1% of Caucasian adults is affected by rheumatoid arthritis (RA). It is two to three times more frequent among women and its prevalence also increases with age Ankylosing spondylitis affects between 0.5-1% of the population and has a male predominance

What is Rheumatoid Arthritis ?

Is a chronic, inflammatory disorder wherein bodys immune system attacks its own tissues (autoimmune disorder) leading to inflammatory disease of joints. Affects both sides of the body eg. hand, knuckles, knee etc.

Rheumatoid Arthritis of the hand

Affects finger joints closest to the body.

How does RA develop ?

Healthy joint cartilage covers & cushions bones for smooth movement. In RA cells of synovium grow & divide abnormally leading to thickening & swelling.

How does RA develop ?

Bone loss/ erosion

Inflammation causes warmth, redness, swelling & pain. Abnormal synovial cells begin to invade & destroy cartilage & bone within the joint.

Cartilage loss

RA of the finger

Surrounding muscles, ligaments & tendons that support & stabilize joint become weak & unable to work normally leading to pain & deformities.

RA of the Knee
Destruction of cartilage
Bone Inflamed joint capsule Inflamed synovium Synovial fluid Joint pain occurring in various joints

Enlarge view of a joint

Rheumatoid Arthritis

Comparison of OA & RA
Osteoarthritis

Rheumatoid Arthritis

Begins after age 40 or as a result of direct joint injury.

Begins between the ages of 25 & 50.

Is caused due to breakdown of cartilage because of wear & tear. Common in both men & women.
Develops gradually over several years.

Is an auto-immune disorder.

3 times more common in women.

Unpredictable course with occasional spontaneous remission.

Comparison of OA & RA
Osteoarthritis

Rheumatoid Arthritis

Usually begins in joints on one side of the body. Primarily affects joints of knees, hands, hips, feet & spine. Rarely affects knuckles, wrist, elbows, or shoulders Morning stiffness lasts usually less than 30 mins.

Strikes joints on both sides of the body at the same time. Affects most joints symmetrically knuckles, wrist, elbows, or shoulders.

Morning stiffness lasts longer than 2 hrs.

Physical therapy & exercise improves out come.

Gentle exercise & rest is the best course of action.

Ankylosing Spondylitis

Systemic manifestation decreased chest expansion, iritis, fever, fatigue, anaemia, anorexia, weight loss, aortic insufficiency. Synovitis followed by pannus formation (new bone) Erosion of cartilage. Ossification of the cartilage and obliteration of the entire joint. Bony extensions formed in the intervertebral discs connecting the vertebral bodies.

Pathology

Ankylosing Spondylitis

Course of disease is highly variable ranging from mild stiffness with radiographic feature of sacroilitis to patient with fused spine and bilateral hip arthritis.

Diagnosis- Modified New York criteria

History of back pain

Limitation of lumbar spine mobility

Limited chest expansion for age and sex

Radiographic sacroilitis
Presence of any of criteria with X ray positive finding

Ankylosing Spondylitis Management

No definite treatment for AS

Exercise is one of the most important activities to maintain

restore spinal mobility, maintain posture, chest expansion. NSAIDs Indomethacin is particularly effective. Intraarticular injection of steroids only in severe unresponsive to NSAIDs.

Pain and Fever in URTI & Viral Fever Acute painful conditions & Infections like Pharyngitis, Sinusitis & Tonsilitis are always accompanied by inflammation of the surrounding tissues and pain in that region (Localized). In addition, the patient also experiences generalized fever, bodyache and malaise. Viral fever characterized by high grade fever and severe bodyache, malaise.

Radiofrequency : frequency of electrical signals Radiofrequency : a development of heat based radiofrequency denervation, procedures used in medicine to treat especially chronic pain.
Heat may be applied to the body's surface or to deep tissues. Hot packs, infrared heat, paraffin (heated wax) baths, and hydrotherapy (agitated warm water) provide surface heat. Heat may be generated in deep tissues by electric currents (diathermy) or high-frequency sound waves (ultrasound).

Current Treatment Options

Patient Education Physiotherapy Medications Analgesics & anti-inflammatory form the important component of medications which includes paracetamol, NSAIDs, Coxibs

Postoperative Pain

An unpleasant sensory & emotional experience associated with actual or potential tissue damage. Complex process influenced by both physiological & psychological factors 77% patients experience pain after surgery Among them 80% experience moderate to severe pain

Postoperative Pain

Postoperative pain can be divided into acute pain and chronic pain:

Acute pain is experienced immediately after surgery (up to 7 days) Chronic pain which lasts more than 3 months after the injury

Recent suggested criteria pain more than 2 month post-surgery Joshi GP. Anesth Clin North Am 2005; 23; 21-36

Goals of Post Operative Pain Management

Improve quality of life for patient Facilitate rapid recovery & return to full function Reduce mortality Allow early discharge from hospital

MOA of Conventional NSAIDs

Harmful Stimulus Cell Perturbation Liberates Chemical & Mechanical stimuli activates Phospholipase A Membrane Phospholipids Release ARACHIDONIC ACID (AA)

Lipoxygenase Hydroperoxides LEUKOTRIENES

Cyclo-oxygenase Non-Selective NSAIDs

Cyclo-oxygenase-1 (COX-1) Protective Prostaglandins & Thromboxane

Cyclo-oxygenase-2 (COX-2) Inflammatory Prostaglandins

MOA of Conventional NSAIDs

Arachidonic acid

7
COX-1

Conventional NSAIDs

COX-2
Inducible Bad Prostaglandins Inflammation Pain, & Fever

Constitutive Good Prostaglandins Gastrointestinal toxicity

Thromboxane A2 Impaired platelet function

Limitations of Conventional NSAIDs

GI distress, ulceration/bleeding Renal impairment or failure Increase in incidence and severity of cardiovascular side effects Platelet inhibition may cause bleeding

Limitations of COXIBs

Cardiovascular morbidity & mortality has back lifted coxibs