Pain and Musculo Skeletal Disorders

8/13/2019 Pain and Musculo Skeletal Disorders

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Musculoskeletal Disorders

and pain


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Inflammation

What is inflammation ?

Response of a living tissue to a harmful stimuli

May be Mechanical, Chemical, Physical, Thermal, Microbialor any other.

Primary objectives of inflammation.

Remove unwanted

stimulus.

Minimize damage.

Hasten recovery.

Provide defence.


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Inflammation

Cardinal Symptoms

Heat (Calor)

Redness(Rubor)

Pain(Dolor)

Swelling(Tumor)

Loss of function(Functio Laesa)


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Physiology of Inflammation

Occurs in 3 phases Acute transient phase (vasodilation & capillary

permeability).

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.


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Chemical mediators released

Prostaglandins

Thromboxanes (TXA2)

Histamine

Kinins

Leukotrienes Complements

Platelet activating factor (PAF)

Cytokines


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

Free nerve

ending

(senses pain)

Capillary

Mast cell

Mechanical,Chemicalinjury,Microbes,Antigens.triggersinflammatory

response

Monocyte

Macrophage

Neutrophil Inflammatory mediators

Prostaglandins

Histamine

Bradykinin

Inflammatory

Response


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ArachidonicAcid Metabolism

Harmful Stimulus

Cell Perturbation (agitation or disturbance)

Liberates

Membrane PhospholipidsChemical & Mechanical stimuli

activates Phospholipase A

Lipoxygenase

Endoperoxides

PGG2 PGH2

PROSTAGLANDINS PROSTACYCLINS THROMBOXANE

PGE2 PGD2 PGF2 PGI2 TXA2

ARACHIDONIC ACID (AA)

STOMACH, KIDNEYS BLOOD VESSEL WALL PLATELETS

Release

Hydroperoxides

LEUKOTRIENES

Cyclo-oxygenase


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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.


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Characteristics of Pain

Acute Chronic

1. Limited to days or weeks Duration unpredictable

2. Well defined Poorly defined

3. Involves anxiety Involves depression &

frustration

4. Useful physiological signal Has no useful function

5. Expect cure of pain Only can hope to controlpain


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Central &

Peripheral

ReceptorsBrain

Spinal cord

Peripheral

receptors


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PERCEPTION OF PAIN

Injury

Signals

Spinal cord

Hypothalamus

Initiation of pain signals

Pain

Nociceptors

Sensory neuron

Nerve Pathways


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Musculoskeletal Disorders

Illness resulting from cumulative trauma to themuscles, 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


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OA

In India 7.35 % of the total population suffering fromOsteoarthritis

Degenerative arthritis rises steeply with age. Less than 1% haveit between the ages of 25 and 34, >30% after the age of 70

As with many other forms of arthritis, women aredisproportionately affected, especially with hand and knee (OA)


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What is

Osteoarthritis ?

Affects the joint, commonlyoccurs in the hands, hips,

knees, neck & lower back.


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Tendon

Ligament

Synovium

Muscle

Knee Joint(Side view)

Cartilage

What is

Osteoarthritis ?

Joint is surrounded by

a fibrous envelope or

capsule called -

synovium whichproduce fluid to

reduce friction & wear

in a joint. Muscles &

tendons power the

joint.


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How does OA

develop ?

Breakdown ofcartilage results in

joint pain.

It becomes pitted &

weak.

Loses elasticity

leading to damage by

excess use or injury.

Cartilage destruction

Knee(Front View)


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Loose bone pieces

Fluid-filled cystsLoosecartilageparticles

How does OA

develop ?

Fluid-filled cysts

may form in the

bone near the joint.

Bits of bone or

cartilage may float

loosely in the jointspace.


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How does OA

develop ?

In OA joints become

swollen & damage.

Can be painful & difficult to

move due to inflammation.


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OSTEO RTHRITIS

Progressive Disease

Exposed Bone

Eroding Meniscus

Eroding cartilage

Bone Spurs


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O ManagementNon pharmacological methods

Social support

Weight loss, if the patient is overweight

Physiotherapy and exercise Occupational therapy

Bracing


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O ManagementPharmacological management

Symptom modifying drugs

Analgesics

Nonsteroidal anti-inflammatory drugs

Visco-supplementation (Sodium Hyaluronate inj. (HyaluronicAcid) - an important component of synovial fluid, provides

lubricating properties)

Corticosteroids

Other Nutraceuticals

Glucosamine sulfate

Chondroitin sulfate


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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


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What is

Rheumatoid Arthritis ?

Is a chronic, inflammatory

disorder wherein bodys

immune system attacks its

own tissues (autoimmunedisorder) leading to

inflammatory disease of joints.

Affects both sides of the bodyeg. hand, knuckles, knee etc.


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Rheumatoid Arthritis

of the hand

Affects finger joints

closest to the body.

H d RA


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How does RA

develop ?

Healthy joint cartilagecovers & cushions

bones for smooth

movement.

In RA cells of

synovium grow &

divide abnormallyleading to thickening

& swelling.


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How does RA

develop ?

Inflammation causes

warmth, redness,

swelling & pain.

Abnormal synovial

cells begin to invade

& destroy cartilage &

bone within the joint.

Bone loss/erosion

Cartilage loss


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RA of the

finger

Surrounding

muscles, ligaments &

tendons that support

& stabilize jointbecome weak &

unable to work

normally leading to

pain & deformities.


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Bone

Inflamed joint capsule

Inflamed

synovium

Synovial

fluid

Destruction ofcartilage

Joint pain

occurring in

various jointsEnlarge view of a joint

RA of the Knee


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Rheumatoid Arthritis


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Comparison of OA & RA

Osteoarthritis Rheumatoid Arthritis

Begins after age 40 or as a Begins between the ages of

result of direct joint injury. 25 & 50.

Is caused due to breakdown of Is an auto-immune disorder.cartilage because of wear &

tear.

Common in both men & women. 3 times more common in women.

Develops gradually over several Unpredictable course with

years. occasional spontaneous remission.


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Comparison of OA & RA

Osteoarthritis Rheumatoid Arthritis

Usually begins in joints on Strikes joints on both sides of

one side of the body. the body at the same time.

Primarily affects joints of knees,

Affects most joints symmetrically -hands, hips, feet & spine. knuckles, wrist, elbows, or shoulders.

Rarely affects knuckles, wrist,

elbows, or shoulders

Morning stiffness lasts usually Morning stiffness lasts longerless than 30 mins. than 2 hrs.

Physical therapy & exercise Gentle exercise & rest is the

improves out come. best course of action.


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Systemic manifestationdecreased 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.

Ankylosing Spondylitis


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Pathology


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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


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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.

NSAIDsIndomethacin is particularly effective.

Intraarticular injection of steroids only in severe

unresponsive to NSAIDs.


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Acute painful conditions & Infections like Pharyngitis,

Sinusitis & Tonsilitisare 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 fevercharacterized by high grade fever and severebodyache, malaise.

Pain and Fever in URTI & Viral Fever


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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).


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Current Treatment Options

Patient Education

Physiotherapy

Medications

Analgesics & anti-inflammatory form the important

component of medications which includes

paracetamol, NSAIDs, Coxibs


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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


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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-surgeryJoshi GP. Anesth Clin North Am 2005; 23; 21-36


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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


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MOA of Conventional NSAIDs

Harmful Stimulus

Cell Perturbation

Liberates

Membrane PhospholipidsChemical & Mechanical stimuli

activates Phospholipase A

Lipoxygenase

ARACHIDONIC ACID (AA)

Release

Hydroperoxides

LEUKOTRIENES

Non-Selective NSAIDs

Cyclo-oxygenase

Cyclo-oxygenase-1

(COX-1)

Cyclo-oxygenase-2

(COX-2)

Protective Prostaglandins &

Thromboxane

Inflammatory

Prostaglandins


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MOA of Conventional NSAIDs

Arachidonic acid

COX-1 COX-2

Conventional NSAIDs

Constitutive

Good Prostaglandins

Thromboxane A2

Inducible

Bad Prostaglandins

Gastrointestinal

toxicity

Impaired

platelet function

Inflammation

Pain, & Fever

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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


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Pain and Musculo Skeletal Disorders

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