Musculoskeletal Injuries, Diseases, and Disorders – Learning Objectives

Pictures coming soon!

Zoë Soon

Learning Outcomes and Specific Learning Objectives Study Guide

Learning Outcomes:

By the end of this section you will be able to:

Describe key aspects of Musculoskeletal Disorders including:

  1. Bone fractures, healing, exuberant callus formation, and compartment (acute, chronic and crush) syndromes
  2. Aspects of trauma including nerve damage, fat emboli, DIC, rhabdomyolysis, shock
  3. Dislocation and subluxations, sprains and strains, tendinitis, bursitis, and meniscus tears
  4. Osteoporosis, Osteomalacia, and Rickets
  5. Muscular Dystrophy and Fibromyalgia
  6. Rheumatoid Arthritis, Osteoarthritis, and Gout

Specific Learning Objectives Study Guide:

By the end of this section you will be able to:

Describe and explain the following terms and facts associated with Trauma:

  • Leading cause of death in people aged 1-44.
  • Due to sports, automobile accidents, falls, workplace accidents, assault, child abuse, etc.

Trauma always involves inflammation – usually in proportion to the amount of cellular damage.

Trauma can possibly involve:
  • Contusions – bruise under closed skin involving:
    • microscopic rupture of blood vessels; Swelling & inflammation
    • Possibly includes damage to underlying muscle cells;
    • Ecchymotic (black & blue) due to local hemorrhage → changing to yellow
    • RICE Treatment; Usually full recovery
    • Contusions – can affect any tissue: e.g. brain, lungs, muscle, bones
    • Bone bruise:  microscopic damage of bone blood vessels, and possibly some trabeculae; will not be visible in MRI or other imaging
    • Pain due to irritation of nociceptors by chemicals released from damaged cells, by swelling, and be chemicals released by WBCs.
  • Bone Fractures:  will be visible with x-ray and MRI;  Most Common Fractures:
    a) Males 15-24yrs (tibia, clavicle, lower humerus) – clavicle most common childhood fracture
    b) Elderly 65+yrs (hip)
    c) Workplace (hands and feet)

    d) Osteoporosis (upper femur, upper humerus,  vertebrae, & pelvis)

Describe different types of Bone Fractures:

  • Simple – bone ends maintain their alignment & position
  • Oblique – break at an angle to the shaft of a long bone
  • Comminuted – many fracture lines and many fragments involved in bone break
  • Open – bone end penetrates the skin to be exposed to the outside environment; is a risk factor for osteomyelitis and osteonecrosis; classified Type I to Type IIIC increasing in terms of severity; Type I opening is smaller than 1cm;
  • Segmented – 2 or more breaks in the same bone – one bone fractured into 3 or more parts
  • Spiral – spiral direction of fracture in a long bone
  • Transverse – fracture is perpendicular to the length of long bone
  • Impacted – bone telescoped into itself.
  • Compression fracture of vertebrae
  • Colle’s fracture = fracture of distal radius (& possibly ulna) from falling forward
  • Pott’s fracture = fracture of distal fibula (possibly tibia) from excess stress on ankle
  • Pathologic – infection, cyst, tumor, osteoporosis, Paget disease
  • Greenstick/Incomplete – until age 10 bones are more resilient than adult’s
  • Avulsion – fragment of bone connected to a ligament or tendon detaches from main bone
  • Stress fracture – usually incomplete
  • Fracture through growth/epiphyseal plate – may result in premature bone fusion and growth cessation; usually an incomplete fracture with proper reduction and fixation will offset any chance of premature fusion;  crush injuries are more likely to lead to stoppage of bone growth.
  • Transchondral fractures – frequent in teens; separation of cartilaginous joint surface (articular cartilage) from main shaft of bone– may not be painful except during movement; may hear clicking (crepitus).

 

Describe possible signs & symptoms of Bone Fractures:

  • Nerve damage – pain, numbness, surrounding muscles become flaccid (may be temporary or take time to subside) = phenomenon called local shock
  • Muscle spasms – due to irritating chemicals

Describe shin splints (Medial Tibial Stress Syndrome, MTSS):

  • Pain along the shinbone associated with repeated trauma (excessive running or walking) that has damaged Sharpey’s (collagen) fibers that connect fascia to the periosteum of the tibia (where it inserts into the tibia bone).
  • Risk factors include: improper footwear, overdoing it without proper conditioning or training

Signs & Symptoms of Bone Fractures:

  • Pain
  • Numbness
  • Deformity
  • Swelling
  • Muscle spasms
  • Tenderness
  • Crepitus = grating sound if bone ends move over each other
  • Decreased mobility
  • Bleeding (if open fracture)
  • Shock (low blood pressure) = pallor, diaphoresis tachycardia, nausea/vomiting

Emergency Treatment of Bone Fractures in the Field:

  • Cover open wound with sterile dressing material.
  • Splint for support, & immobilize for transport including joint above & below fracture.
  • Elevate limb slightly; Apply cold compress.
  • Keep patient warm; check for signs of shock.

Describe Fracture Healing of Cortical/Compact and Cancellous/Trabecular/Spongy Bone – 5 Stages

  • Stage 1: Hematoma Formation – collection of blood & subsequent clot and inflammation zone forms at fracture line; stage lasts 1-3 days; macrophages begin removing dead osteocytes and debris
  • Stage 2: Hematoma Organization – fibrin (ropy protein) in blood clot (thrombocytes & RBCs) strengthens, organizes into mesh and contracts – granulation tissue in that zone fills with chondroblasts as mesenchymal stem cells within the periosteum produce more and more daughter chondroblasts and osteoblasts, capillary buds form and neovascularization begins; stage lasts 3 days – 2 weeks
  • Stage 3: Pro-callus Formation – chondroblasts are producing fibrocartilage-like extracellular matrix as they mature to chondrocytes, creating an external and internal pro-callus;  this replaces the hematoma which is degraded by phagocytes (e.g. macrophages)  and fibrin which is dissolved by plasmin; the pro-callus is full of collagen and joining the two bone ends and forming a bulge (collar) around the fracture
  • Stage 4: Bony Callus Formation – daughter osteoblasts being to produce more and more osteoid (extracellular matrix glycoprotein material) containing calcium phosphate hydroxyapatite minerals which turn the cartilage pro-callus into a bony callus which is stronger; the bone matrix in this zone is not organized and is termed woven bone
  • Stage 5: Remodeling – as the osteoblasts mature into osteocytes, the collagen matrix becomes more organized, the compact bone of the diaphysis becomes more apparent; the osteoclasts assist in remodeling the bone to form a medullary cavity as well as trabecular bone.  Bone transitions from woven bone to lamellar bone to becoming fully regenerated and can support weight.

Discuss Healing and Factors that Affect Healing:

  • Healing Time – is usually 4 months to a year;  healing time is affected by age:  Children healing fastest, and older adults healing more slowly.
  • Amount of local damage
  • Proximity of bone ends to each other
  • Presence of foreign material or infection & acceptance of bone graft (if required)
  • Blood supply to fracture site; amount of hypoxia
  • Osteonecrosis (ischemic death of bone cells) can occur – usually due ischemia of bone tissue for many reasons including:  trauma, thrombosis, embolism, radiation therapy for cancer, blood vessel injury – perhaps due to vasculitis or long-term glucocorticoid use)
  • Systemic factors – age (older people take longer to heal), nutrition, circulatory problems (e.g. diabetes), anemia, RA (rheumatoid arthritis), glucocorticoid use, etc.
  • Low blood pressure (due to excessive bleeding or widespread inflammation)

 

Discuss Possible Complications of Bone Fractures: 

  • Muscle spasms – triggered by pain/irritation can pull bones out of alignment & damage soft tissue
  • Neurovascular damage: due to:
    • a) damage during fracture (from force, fracture fragments, joint dislocation, or hemorrhage)  or
    • b) during treatment of fracture (moving/splinting fracture)
  • Infections – osteomyelitis; bacterial toxins (tetanus), risk factors: open fracture, surgery
  • Septic = infected by harmful microbes
  • Aseptic = free from harmful microbes
  • Ischemia – ↑edema in 1st 48hr tightens cast
  • Be careful that cast not become too loose later as edema decreases & muscle atrophies
  • Fat emboli – fat marrow escapes into vein
  • Fracture blisters (edema between epidermis & dermis)
  • Failure to heal (non-union) due to infection, or gap, or repetive stress, poor circulation
  • Deformity (mal-union) during healing due to improper alignment
  • Residual effects such as osteoarthritis or stunted growth
  • Exuberant Callus formation

 

Compartment Syndrome (acute, chronic, or crush) = high pressure in muscle compartment that is enclosed in fascia reduces blood flow leading to hypoxia (& therefore damage).

  • a) Plasma protein & fluid leak into tissue causing more swelling.
    • Exudate = fluid that leaks from blood vessels
    • Edema = fluid accumulating beneath skin or in a cavity, due to increased interstial fluid (during inflammation) and/or impaired fluid removal by lymph/capillary vessels
  • b) Necrosis of muscle & nerves can occur (within 4-8hr).
  • c) Symptoms: 5Ps (Severe Pain, Paralysis, Paresthesia, Pallor & Pulselessness).
  • d) Monitor:  Used tonometer (>30mmHg = bad);  Capillary refill time of less than 2sec (hold hand higher than heart and press fingernail until white then watch for return to colour)
  • e) Acute Compartment Syndrome requires immediate surgery (Fasciotomy) to reduce pressure accompanied by skin grafts.

If not treated = Compartment Tamponade

  • 1. muscle ischemia (hypoxia) → muscle infarction and leads to Crush Injury:
    • Rhabdomyolysis = muscle cell lysis ↑ potassium, phosphate, creatine, myoglobin in ECM which draws in fluid (ECF shift) and myoglobinemia  → kidney damage (→Renal Failure)
    • and (lactic) acidosis/hyperkalemia →  Cardiac Dysrhythmia (→Shock)
    • and permanent skeletal muscle damage
    • muscle necrosis/damage fibrosis & shortening of muscle, if in forearm, leads to → Volkmann’s ischemic contracture (permanently flexed wrist  and finger joints into claw)
  • 2. neural injury → if permanent → loss of function (muscle weakness and/or loss of sensations)
  • *Need to watch out for Reperfusion Injury = sudden restoration of blood flow introduces a lot of Reactive Oxidative Species (ROS) which can induce apoptosis and more cell damage
  • **must prevent by releasing pressure slowly and treating with bicarbonate.
  • *Need to watch out for Disseminated Intravascular Coagulation (DIC) – which may occur due to necrotic muscle tissue.
  • Acute Compartment Syndrome -requires immediate fasciotomy – causes include: bone fracture, burn, drug overdose, thrombosis, reperfusion injury, vascular damage.
  • Crush Syndrome – worsening of untreated acute compartment syndrome, often due to crush injury
  • Chronic Compartment Syndrome – usually caused by repetitive activities (e.g. running) – characterized by pain that doesn’t go away even with ibuprofen, decreased sensation, paleness of skin, weakness, swollen shiny skin, pain on movement, .

 

Shock = not enough blood flow to tissues

Signs of Shock = pallor, diaphoresis, hypotension, reflex tachycardia, nausea/vomiting

 

Rhabdomyolysis = Rapid breakdown of muscle, releasing myoglobin into extracellular space & bloodstream, which travels to kidney & is excreted in urine.

  • Causes: crush, burn, compression injury, drug overdoses, earthquake victims, serious infections, toxins, diabetic ketoacidosis, extreme hypothermia/heatstroke
  • Signs & Symptoms: muscle pain, weakness, swelling, & dark urine; oliguria; hyperkalemia may trigger cardiac dysrhythmias; low BP; electrolyte imbalance can cause nausea, vomiting, confusion, coma
  • Urinalysis:  reveals brown urine, due to myoglobinuria
  • Evaluation: ↑ serum CK, K+, PO4 levels
  • Treatment: rapid IV hydration to maintain adequate urinary flow (with bicarbonate if metabolic acidosis is occurring); & possibly hemodialysis
  • Potential Complications of Rhabdomyolysis:
    • myoglobin breakdown products damage kidney Renal Failure
    • Disseminated Intravascular Coagulation (DIC, formation of small blood clots in bloodstream) initiated by released components of necrotic muscle… which can lead to organ failure & uncontrolled bleeding.

Disseminated Intravascular Coagulation (DIC) = results from an imbalance of clotting/hemostasis factors.

  • Causes: serious infections (e.g. sepsis), trauma, burn, placental abruption, pre-eclampsia, toxins, snake bites
  • Pathogenesis:
    • Severe endothelial damage
    • leads to release of large amounts of pro-inflammatory cytokines
    • stimulate too much thrombin lead to too many fibrin/platelet clots
    • leads to clot obstructions of capillaries throughout the body leads to ischemia/hypoxia/damage of tissues and multiple organ failure and
    • risk of bleeding out (as platelets are all “used up”).
  • Signs & Symptoms: purpura (blood-spotted skin), pain
  • Diagnostic Test: measure of coagulant (e.g. fibrin, platelets) and anti-coagulant factors

 

Methods to Reduce Chances of Complications of Bone Fractures:

  • Wound debridement
  • Windowed cast
  • Realign and Reduction using: intramedullary nails, pins, plates, wire meshes, casts, and/or traction
  • Tetanus booster
  • Antibiotics
  • Monitor for signs of fat emboli – may travel to:
    • lungs, causing ARDS (pallor, diaphoresis, chest pain, dyspnea, tachycardia, cyanosis)
    • brain, causing CVA
  • Bone graft (taken from iliac crest, fibula, or rib)
  • Bone cement
  • Exercise – maintain muscle function

 

Joints – Dislocation & Subluxation:

  • Dislocation: bones in joint lose contact with each other due to tearing of surrounding tissue (e.g. joint capsule, ligament(s), and or muscles/tendons)
  • Subluxation: partial loss of contact between bone in a joint – often self-resolves
  • Risk Factors: joint diseases (e.g. rheumatic arthritis)
  • Symptoms: pain, muscle atrophy, swelling
  • Diagnostic Tools: imaging (e.g. x-ray, MRI, arthroscopy)
  • Treatment: PRICE, anti-inflammatories, analgesics, surgical repair, physiotherapy
  • Adhesive capsulitis:  scarring and adhesions forming in connective tissue surrounding the glenohumeral joint – causing stiffness and loss of range of motion.  Prevent this from occurring by following prescribed stretching and exercise regime

 

Differentiate between Sprains and Strains and describe features of each:

  • Sprain: ligament tear
  • Strain: muscle or tendon tear (tendonitis)
    • Grade 1 or 1st degree: mild, fibers are stretched but stable; will slowly self repair
    • Grade 2 or 2nd degree: moderate, some fibers are torn; will slowly self repair, follow prescribed stretching/exercise regime to avoid scarring/shortening and to increase muscle strength surrounding joint to provide more stability and make joint more resilient against future injuries
    • Grade 3 or 3rd degree: severe, fibers are completely torn; surgical repair is required, if possible (dependent on age, co-morbidities etc.)
    • Grade 4 tear of ligament involves avulsion as well (complete tear plus bone fracture)
  • Rotator Cuff tear:  tear to one of the 4 muscles that stabilize the glenohumeral shoulder joint
  • Ligaments and Tendons – consists of dense regular connective tissue (e.g. organized collagen)
  • Signs & Symptoms:  pain, swelling, dislocation, weakness of joint, less mobility.  Sprains tend to heal more slowly than strains
  • Risk Factors: Sports; Overweight, Age – collagen fibers have decrease elasticity & are more susceptible to injury
  • Diagnostic Tools: MRI, radiography, arthroscopy, or arthrography
  • Prevention:  Proper warm-up; appropriate sport wear; avoid over-use; ramp up exercise slowly over months when first starting
  • Treatment:  PRICE for first 48-72hrs (possibly alternate heat & cold)
    • Protection; Rest; Ice; Compression; Elevation
    • Compression bracing to provide support while healing
    • Gradual, Prolonged Rehabilitation Exercises (first without weight & only if no pain)
    • Gradual exercise & blood flow help with healing
    • Occupational Therapy – identify ergonomic problems

Describe Meniscus Tears = tears to white or red zone in knee cartilages

  • Terrible Triad:  Knee injury involving tear to MCL, ACL & medial meniscus (frequent soccer injury)
    • Prevent by strengthening surrounding muscles, using proper footwear

Discuss Overuse Injuries = damage to muscles/tendons/nerves due to repetitive movements, perhaps with no warm-up, with inappropriate equipment/training/technique – can lead to fibrous scar tissue & loss of range of motion, & is a risk factor for osteoarthritis

  • Repetitive Strain Injuries: e.g. carpal tunnel syndrome
  • Tendinitis: caused by tennis, golf, painting, keyboard use, running, massage
  • Epicondylopathy = most often tendinopathy = microtears in tendon inflammation & pain (e.g. tennis/golfer’s elbow)
  • Bursitis = inflammation due to kneeling or gout or infection
  • Treat with PRICE, surgery, physiotherapy, massage, antibiotics as appropriate

Discuss Diagnostic Tools and Treatments

  • Arthroscopy = use of arthroscope (camera on thin bendy wire) to view inside joint through small incision
  • Arthrography = injection of MRI or x-ray contrast dye (e.g. gadolinium or iodine respectfully) to better visualize joint in MRI or CT scan
  • Prolotherapy = Proliferation Therapy = injections of dextrose, thought to cause local inflammation, which stimulates increased blood flow and supply of nutrients; possibly speeding up tissue repair
  • Extracorporeal Shockwave Therapy = use of shockwaves; thought to cause local inflammation, which stimulates increased blood flow and supply of nutrients; possibly speeding up tissue repair

 

Osteoporosis =  reduced bone volume due to:  loss of osteoid & CaPO4

chronic disease of many older adults, where old cortical & trabecular bone is being resorbed faster than new bones is being made; most severe in femoral neck, vertebrae & wrist; impacted by levels of TH, cortisol, GH, estrogen & testosterone.

Risk factors:  age, biological (XX) female due to lower estrogen levels post-menopause, sedentary, smoker, use of corticosteroids, early menopause, low dietary Ca++ & vitamin D, genetics, excessive alcohol or caffeine, smoking, rheumatic arthritis, diabetes, genetics

1st Degree Osteoporosis = age-related

2nd Degree Osteoporosis = due to underlying disease (e.g. celiac disease, hyperthyroidism, hyperparathyroidism)

Signs & Symptoms: fractures (1.5million/yr US), e.g. hip fractures; height reduction, kyphosis, vertebral compression fractures
Check-ups: regular bone mass density scan test >50yrs
Evaluation: DXA, CT, MRI, serum/urine Ca++/PO4 tests
Prevention: through avoidance of risk factors

Treatment with Bisphosphonates ( ↓ osteoclast activity) & Weight-bearing exercises

Physiotherapy to alleviate pain & maintain function to muscles/tendons/nerves due to repetitive movements, perhaps with no warm-up, with inappropriate equipment/training/technique – can lead to fibrous scar tissue & loss of range of motion, & is a risk factor for osteoarthritis

 

Osteomalacia =  reduced mineralization of bone in adults due to:  reduced CaPO4 within osteoid; bones become soft.

and

 

Rickets =  reduced mineralization of bone in children due to:  reduced CaPO4 within osteoid; bones become soft; most often due to low levels of Vitamin D3 and/or calcium & causes bow-legging.

Risk factors: age, vegetarians, malnourishment, vitamin D deficiency (caused by diet, different drugs or diseases – renal)

Signs & Symptoms: skeletal pain, “knock-knees”, “bow legs”, easy fractures

Evaluation: serum levels of Ca++, PO4, PTH, bone deformities, bone biopsy; Treatment: calcium carbonate, vitamin D

 

Muscular Dystrophy = A group of autosomal recessive/dominant disorders that causes degeneration of skeletal muscle over time

Risk factors: inherited genetic diseases

Duchenne’s MD is most common type of MD and it affects young biological (XY) males as it is an X-linked recessive disease; biological (XX) females are carriers

Signs & Symptoms: ascending weakness of muscles starting at age 2-3yrs affecting legs, hips shoulders etc. progresses rapidly

  • Waddling gait, Gower Maneuver (pushing to get up),
  • Pseudohypertrophy of calf muscles, reduced tendon reflexes
  • Kyphoscoliosis
  • Frequent respiratory infections
  • Cardiac myopathy
  • Respiratory or heart failure by age 20
Diagnostic tests:
  • Genetic Tests
  • Prenatal screening – chorionic villus (placenta) testing and amniocentesis is avail.
  • Elevated serum creatine kinase levels
  • Electromyography
  • Muscle biopsy to check dystrophin levels
  • Blood test shows abnormal dystrophin levels
  • Abnormal ECG and echocardiograph

Treatment:

  • moderate exercise
  • mobility devices
  • physiotherapy & massage
  • ventilator
  • possible future genetic therapies 

Fibromyalgia = syndrome characterized by idiopathic chronic pain, numbness, tingling, stiffness, cognitive and memory problems; fatigue and sleep disturbances, anxiety, depression, possible irritable bowel syndrome and possible jaw pain;  with no obvious inflammation or atrophy.

Risk factors:

  • biological females; 20-50yrs;
  • history of auto-immune disease (e.g. Rheumatoid Arthritis, Lupus, Ankylosing Spondylitis)
  • physical/psychological trauma, or chronic pain
Treatment
  • Stress avoidance or reduction
  • Regular exercise in the morning
  • Pace activity & rest as needed
  • Applications of heat or massage
  • Analgesic drugs, NSAIDs, new drugs
  • Low doses of antidepressants (SSNRIs)
  • Serotonin Norepinephrine Reuptake Inhibitors
  • Massage therapy

 

Osteoarthritis = inflammatory joint disease due to “wear and tear”, most often affecting hips and knees

Risk factors:

  • obesity
  • biological males; 40+yrs; biological females 55+yrs
  • history of auto-immune disease (e.g. Rheumatoid Arthritis, Lupus, Ankylosing Spondylitis)
  • physical/psychological trauma, or chronic pain
Signs & Symptoms:
  • Joint pain that is relieved when joint is rested
  • Heberden nodes in distal finger joints = thickening of subchondral bones (sclerosis = ↑ bone density)
  • Bouchard nodes in middle joints of fingers = ditto
Pathophysiology:
  • articular cartilage degenerates, and fibrillation (deep long fissures in articular cartilage occur),
  • joint capsule thickens, becomes fibrotic and sticks to deformed underlying bone narrowing joint space, limiting ROM, causing:
  • pain & stiffness, swelling, paresthesia (e.g. numbness), stiffness, creaking, limp, predisposition to falls.
  • irritation of many sensory nerve endings in joint capsule
  • Bone spurs (osteophytes) form & can break off (“joint mice”) into synovial cavity & irritate synovial membrane causing synovitis; subchondral cysts form; exudate buildup
Evaluation:  clinical assessment, X-ray

Treatment: rest, orthotics, ROM exercises, physio & massage therapy, loss of body fat, pain & anti-inflammatory meds, possible surgery if deformation (hip & knee replacements are common), acupuncture, canes, hand braces.

Rheumatoid Arthritis:  Chronic, systemic, inflammatory auto-immune disease causing joint swelling, tenderness, destruction of synovial joints leading to disability & premature death.

Pathophysiology: Inflammation spreads to articular cartilage, fibrous joint capsule, surrounding ligaments & tendons

Most common in fingers, feet, wrists, elbows, ankles, knees; also shoulders, hips, cervical spine (lungs, heart, kidneys, & skin).

  • Synovitis – marked inflammation, cell proliferation
  • Pannus – made of granulation tissue = new connective tissue with tiny blood vessel that typically forms in a wound during the healing process; but in this case healing doesn’t occur and it spreads
  • Cartilage erosion – creates unstable joint
  • Fibrosis (scar tissue) – calcifies and obliterates joint space

Possible Complications:

  • Ankylosis – joint fixation and deformity develop if untreated
  • Atrophy of muscles
  • Bone alignment shifts (Ulnar drift, deformation and swanning of fingers); Boutonniere deformity
  • Muscle spasms due to inflammation/pain
  • Contractures and deformity develop.
  • Flare-ups associated with anemia (e.g. iron-deficiency)
  • More prone to lung fibrosis, atherosclerosis, MI, and stroke
  • Chronic anti-inflammatory use can cause bleeds

Risks: age, genetics, female, smoking, possible T cell defect in telomere repair, imbalance of chemokines involved in triggering an immune response, long-term exposure to antibodies.

Diagnostic Tests:  Appearance of auto-antibodies (Rheumatoid Factors, RF)

Gouty Arthritis:  Chronic, systemic, inflammatory auto-immune disease causing joint swelling, tenderness, destruction of synovial joints leading to disability & premature death.

Risk factors: men >40yrs, low fluid, high meat diet, alcohol, obesity, family history (“rich man’s disease”)

Pathophysiology:

  • Results from deposits of uric acid and crystals in the joint, causing inflammation
  • Formation of tophus – large, hard nodule of urate crystals
  • Tophi cause local painful inflammation and occur after the first attack of gout.
  • Uric acid & crystal formation resulting from inadequate renal excretion, chemotherapy, and/or genetic factors
Treated by reducing uric acid levels by drugs & dietary changes
Diagnosed by examination of synovial fluid and blood tests

 

 

 

 


About the Author

Zoë Soon, MSc, PhD, B.Ed.
Associate Professor of Teaching,
IKB Faculty of Science | Department of Biology
The University of British Columbia | Okanagan Campus | Syilx Okanagan Nation Territory