ORTHOPEDIC NOTE
208
Orthopedic
P R A Y F O R U S
Special Thanks to Hussain Al-Hamza Hassan Ibrahim Al-Hammadi
208 [ORTHOPEDIC]
2 Orthopedic Note
Index
1) Metabolic Disorders:(Osteoporosis, Osteomalacia & Rickets)
2) Infection Of Bone and Joint
3) Rheumatoid Arthritis
4) Osteoarthritis
5) Bone Tumors
6) Back Pain
7) Ligamentous Injury
8) Arthroscopy and Arthrocentesis
9) Arthroplasty
10) Prosthesis and Amputation
11) Principle of Fracture Management
12) Spine Fracture
This note is missing the following topics
1) Fracture of Shoulder and Upper limb
2) Fracture of pelvis and Lower Limb
3) Disorder of Upper Limb
4) Disorder of Lower Limb
ORTHOPEDIC NOTE
208
Metabolic Disorders
(Osteoporosis, Osteomalacia & Rickets)
P R A Y F O R U S
Ali Al-Saeed Hussain Al-Hamza
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
2 Orthopedic Note
Introduction to Bones
- Bone classified into
o Cancellous bone = trabecular bone = spongy bone (15% of skeleton)
o Cortical bone =compact bone (85% of skeleton)
- Biochemical tests:
o Serum bone alkaline phosphatase
It is index for osteoblastic activity (bone formation)
o Osteocalcin (Gla protein)
More Specific marker for bone formation
If raised, suggest increase bone turnover
o Urinary hydroxyproline excretion
Indicate bone resorption (not much sensitive), increased in high
turnover
o Excretion of pyridinium compounds and telopeptides
More sensitive for bone resorption
Osteoporosis
- Osteoporosis is the commonest metabolic bone disorder.
- WHO operationally define osteoporosis as a bone density that falls 2.5 standard
deviations (SD) below the mean. (T-score less than -2.5= osteoporosis).
(notice: T-score = - 1 to - 2.5 = osteopenia)
- Osteoporosis characterized by
o Abnormally low bone mass.
o Defect in bone structure (abnormal microarchitectural)
o Increase fragility of bone increase risk of fracture
- Bone in Osteoporosis
o Fully mineralized.
o Its Cortex is thin.
o Its Cancellous region is porous.
- In osteoporosis there is a Quantitative defect
o There is decrease in bone per unit area brittle bone.
- Mechanism of osteoporosis
o Predominant bone resorption
o Decrease bone formation
o Or both
Q/ is the loss of bone strength proportional to the reduction of bone mass in osteoporosis?
No, reduction of strength is out of proportion to diminished bone mass because there is
alteration in mechanical properties of bone (du e to loss of structural connectivity between bone plates).
- Osteoporotic fracture
o In tubular bone (long bone), it is common in diaphyseo-metaphyseal junctions.
o In Cancellous bone, it is common in Vertebral bodies.
o Cancellous bones are more prone to osteoporotic fracture than cortical bone.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
3 Orthopedic Note
Clinical presentation
- Back pain
- Decrease height
- Kyphosis (dowager’s hump)
- Low energy fractures
o Women who have had one low-energy fracture have twice the normal risk of
developing another.
- Transverse abdominal creases
Diagnosis of Osteoporosis
- X-ray shows (only if at least 30% of bone mass have been lost)
o Osteopaenia (decrease bone density) (less characteristic, seen with osteomalacia)
o loss of trabecular definition
o thinning of the cortices
o insufficiency fractures
o ballooning of the disc spaces.
- DXA (Dual-energy X-ray absorptiometry)
o It measure the BMD (bone mineral density)
o It is the golden standard test.
o DXA is performed on the spine and hips.
o More than 2 SD (standard deviations) below the average is indicative of
osteoporosis.
- Quantitative Ultrasound
o Advantage: no radiation exposure
- Biochemical tests
o Usually normal, unless osteoporosis is secondary to metabolic disease.
Regional osteoporosis
- When only particular bone or group of bone affected.
- It is due to immobilization or inflammation.
- It is usually reversible after managing the cause.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
4 Orthopedic Note
Causes of osteoporosis
- Primary osteoporosis
o Involutional osteoporosis
Type I osteoporosis: Postmenopausal (Post-Climacteric Osteoporosis)
Type II osteoporosis: Senile Osteoporosis
o Idiopathic osteoporosis
Juvenile type
Adult type
Idiopathic transient osteoporosis
- Secondary osteoporosis:
o Nutritional
Malabsorption
Malnutrition
Scurvy
o Inflammatory disorders
Rheumatoid disease
Ankylosing spondylitis
Tuberculosis
o Drug induced
Corticosteroids
Excessive alcohol consumption (ethanol)
Anticonvulsants
Heparin
Chemotherapy & Immunosuppressives (Methotrexate)
o Endocrine disorders
Gonadal insufficiency
Turner’s syndrome
Oophorectomy
Amenorrhea (in athletes or anorexia nervosa)
hypogonadism
Hyperparathyroidism
Thyrotoxicosis
Cushing’s disease
Diabetes mellitus
o Malignant disease
Carcinomatosis & Multiple myeloma
Leukaemia
o Hematological disorder
Sickle cell anemia
Thalassemia
o Other
Smoking
Chronic obstructive pulmonary disease (COPD)
Osteogenesis imperfect
Homocystinuria
Chronic renal/liver disease
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
5 Orthopedic Note
Postmenopausal osteoporosis
- postmenopausal osteoporosis is an exaggerated form of physiological bone depletion
that normally occur with aging and loss of gonadal activity.
- Normally after menopause bone resorption accelerate by 3% per year.(before menopause
it is 0.3%)
- Postmenopausal osteoporosis is the most common form of osteoporosis.
- Two overlapping phases of Postmenopausal osteoporosis:
o high-turnover osteoporosis
early postmenopausal syndrome.
characterized by rapid bone loss due predominantly to increased
osteoclastic resorption.
Measurement of excreted collagen cross-link products and telopeptides
may suggest a high-turnover type of bone loss.
o low-turnover osteoporosis
It is due to a combination of gradual slow-down in osteoblastic activity,
dietary insufficiencies, chronic illness and reduced mobility.
- Pathophysiology:
o Estrogen deficiency RANKL & osteoprotegerin increases
osteoclast proliferation, differentiation, activation and survival.
- Risk Factors of Postmenopausal osteoporosis
o Genetic predisposition “family history” (most important)
o Caucasian (white) or Asiatic ethnicity
o Early-onset menopause and oophorectomy (ovariectomy)
o Smoking
o Alcohol
o Early hysterectomy
o Nutritional insufficiency & lack of exercise
- Patient most commonly present with vertebrae fracture that
o Mostly associated with aortic calcification
o The second common feature is fracture of proximal end of femur.
- The most common fracture is vertebrae, then hip, followed by colles’ fracture
- X-ray of spine may show wedging or compression of vertebral bodies and lateral view
show calcification of aorta.
- Before diagnosing that osteoporosis is postmenopausal you have to exclude other
causes.
- Prevention:
o By routine DXA screening and giving prophylactic treatment.
o Maintain adequate dietary/supplement intake of calcium and vitamin D.
o Regular physical activity with avoiding of smoking and alcohol.
Signs of severe postmenopausal osteoporosis:
1- Compression fractures of vertebra.
2- Wedging at multiple levels.
3- Biconcave distortion of end-plates.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
6 Orthopedic Note
- Treatment:
o supplement of calcium (1200 mg/d) and vitamin D (800 IU/d)
o HRT (hormonal replacement therapy)
Estrogen or combine estrogen-progesterone.
HRT is rarely used nowadays.
Continuous use is required to maintain the effect.
S/E: thromboembolism, stroke, breast cancer, endometrial cancer.
o Bisphosphonates
They are first-line therapy for treatment and prevention.
They reduce osteoclastic bone resorption and bone turnover.
Examples: Alendronate (once weakly) , pamidronate (once every 3
months)
S/E: stomach upset and erosion of esophagus
o Parathyroid hormone (Teriparatide)
Added to Bisphosphonates (if there is no improvement)
Can be used alone as second line therapy
o Denosumab
Anti-RANKL antibody
- Treatment of femoral bone (and other long bone) fracture
o May need operative treatment
- Management of Vertebral fractures:
o Analgesia
o Partial rest
o Physiotherapy
o Spinal orthoses (for support and pain relieve)
o Operation for severe cases
Post-Climacteric Osteoporosis in men
- With the gradual depletion in androgenic hormone, men eventually suffer the same bone
changes as postmenopausal women.
- This occur 15 year later than female (age of 65 y), unless there is specific cause of
testicular atrophy.
- Osteoporotic fractures in men under 60 years of age should arouse the suspicion of
some underlying disorder
o Hypogonadism (treatment will be administration of testosterone)
o anti-gonadal hormone (which used to treat prostate cancer)
o metastatic bone disease
o multiple myeloma
o liver disease
o renal hypercalciuria
o alcohol abuse
o malabsorption disorder and Malnutrition
o glucocorticoid medication
- Treatment:
o As postmenopausal osteoporosis
Alendronate + calcium & Vitamin D supplement
o If testosterone is very low, consider hormonal therapy.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
7 Orthopedic Note
Involutional (type II) osteoporosis
- It is age-related osteoporosis
- 1/3 of white women will have at least vertebral fracture after age of 75 year.
- Age-related fractures are much less common in black population.
- In advance age :
o Rate of bone loss slowly decrease
o There is qualitative changes contribute to increase of bone fragility in old age.
- Causes:
o Increase incidence of chronic illness
o Mild urinary insufficiency
o Dietary deficiency
o Lack of exposure to sunlight
o Muscular atrophy
o Loss of balance & increase tendency to fall
- Many old people suffer from vitamin D deficiency and develop some degree of
osteomalacia on top of the postmenopausal osteoporosis.
- Treatment
o Initially treatment is directed at management of fracture
o Managing the causes
o Vitamin D and calcium supplement
o Antiresorptive medication
Idiopathic transient osteoporosis
- Most commonly affect middle age men, sometimes seen in pregnant female in 3rd
trimester.
- Usually affect the left hip (1/3 bilaterally)
- Self-limiting condition (recovery occur within 6 months)
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
8 Orthopedic Note
Hypercortisonism
- Causes:
o Cushing’s disease (pituitary adenoma or adrenal hyperplasia)
o corticosteroids long-term therapy
- Corticosteroids therapy if administered to condition associated with bone loss (such
as rheumatoid arthritis), patient will suffer from sever osteoporosis.
- Effect of steroid on bone:
o Steroid suppress osteoblast function (the main effect)
o Reduce calcium absorption
o Increase calcium excretion
o Stimulate PTH secretion
o Depress OPG expression increase osteoclastogensis and bone resorption
Hyperthyroidism
- Thyroxin speed up bone turnover Resorption rate exceed formation rate.
- Fracture seen mainly in older patient.
- Treatment: treat both hyperthyroidism and osteoporosis
Multiple myeloma and carcinomatosis
- myelomatosis and metastatic bone disease are characterized by 3 things
o Generalized osteoporosis + anemia + a high ESR
- Bone loss is due to overproduction of local osteoclast-activating factors
- Treatment: bisphosphonates
Alcohol abuse
- Bone changes due to
o decreased calcium absorption
o liver failure
o Direct depression on osteoblast function.
o tendency to falls & injuries
o Alcohol also has a mild glucocorticoid effect.
Sever osteoporosis
- Will cause hypercalcaemia and hypercalciuria.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
9 Orthopedic Note
RICKETS AND OSTEOMALACIA
- Rickets and osteomalacia are different expressions of the same disease: that is
inadequate mineralization of bone.
- Osteoid throughout the skeleton is incompletely calcified, and the bone is therefore
‘softened’ (osteomalacia).
- In children there are additional effects on physeal growth and ossification, resulting
in deformities of the endochondral skeleton (rickets).
- Etiology:
o Nutritional lack of Vitamin D
o underexposure to sunlight (due to sun-blocking lotions, or overall cover by
clothing)
o intestinal malabsorption (crohn’s, whipple’s,celiac diseases)
o decreased 25-hydroxylation
liver disease
anticonvulsants
o reduced 1-alpha -hydroxylation
renal disease (such as Fanconi’s syndrome)
nephrectomy
1-alpha -hydroxylase deficiency
- The pathological changes may also be caused by calcium deficiency or
hypophosphataemia.
- Pathology of rickets:
o Inability to calcify intracellular matrix of deep layers of physis.
o Cells in proliferative zone bile up (تتكدس) irregularly instead of been in columns.
o Increase thickness of physeal palate
o Poor mineralization in the zone of calcification.
o bone formation is sparse in the zone of ossification.
o All of this will result in
Thin and weak trabeculae
Broad cup-shaped joint
- Pathology of osteomalcaia :
o Sparse islands of bone are lined by wide osteoid seams, producing
unmineralized ghost trabeculae that are not very strong.
o The cortices also are thinner than normal and may show signs of new or
older stress fractures.
o stress deformities of the bones
indentation of the pelvis
coxa vara (bending of the femoral neck)
bowing of the femora and tibiae
Osteomalacia = soft bone (occur at any age)
Rickets= osteomalacia + bone deformity (occur only in children)
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
01 Orthopedic Note
- mild osteomalacia can cause fracture if it is superimposed on postmenopausal or
senile osteoporosis.
Clinical feature
- Rickets in infants:
o Tetany
o Convulsions
o Failure to thrive
o Listlessness (Lacking energy)
o Muscle flaccidity
o Craniotabes ( soft or thinned skull that collapse underneath when pressure
applied, recoil when pressure released)
o frontal bossing and caput quadratum (square head)
o hot-cross-bun skull (prominence of suture lines )
o Thickening of the knees, ankles and wrists (from physeal overgrowth).
o rickety rosary (Enlargement of the costochondral junctions)
o Harrison’s sulcus (lateral indentation of the chest)
o Pigeon chest (Pectus carinatum)
o protuberant abdomen
o cross-legged (due to distal tibial bowing)
o in severe cases: spinal curvature, coxa vara and bending or
fractures of the long bones occurs.
- Osteomalacia in adult
o Bone pain
o Backache
o Muscle weakness
o Vertebral collapse with loss of height.
o Mild kyphosis
o Knock knee (genu valgum)
o Stress fractures
X-ray Findings
o Active rickets shows:
Thickening and widening of growth plate.
widening of the physis and flaring of the metaphysic.
Cupping of metaphysis
Bowing of diaphysis (sometimes)
sub-periosteal erosions ( seen at the sites of maximal remodeling)
medial borders of the proximal humerus, femoral neck, distal femur
and proximal tibia.
lateral borders of the distal radius and ulna.
Craniotabes is may the first manifestation of rickets in infants.
DDX of Craniotabes:
1- Rickets 2- Thalassemia
3- Syphylsis 4-normal premature infant
5- osteogenesis imperfecta
Metaphysis widening may remain after healing.
Usually wrist X-ray is used for diagnosis.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
00 Orthopedic Note
Slow fading of skeletal
structure, resulting in
o Healing rickets
Sclerotic line in metaphyseal region.
o Osteomalacia
Looser zone (thin transverse band of refraction in normal-looking
bone)
It is the classical lesion of osteomalacia.
Commonly seen in shaft of long bones and axillary edge of
scapula.
It is due to incomplete stress fracture which heal with callus
lacking in calcium.
Biconcave vertebrae (from disc pressure) , called codfish vertebrae
lateral indentation of the acetabula (‘trefoil’ champagne glass
pelvis)
spontaneous fractures of the ribs, pubic rami, femoral neck or the
metaphyses above and below the knee.
o features of secondary hyperparathyroidism
characteristically appear in the middle phalanges of the fingers
in severe cases so-called ‘brown tumours’ are seen in the long
bones.
Biochemistry Finding
- Normal/Low serum calcium level
o If the serum calcium remains persistently low after treatment there may be
signs of secondary hyperparathyroidism.
- Low serum phosphate level
- Increase alkaline phosphatase
- Decrease calcium in urine
- In vitamin D deficiency 25-OH D levels also are low.
- calcium phosphate product = Calcium serum level X phosphorus serum level
o normally = 3 mmol/L
o if it is less than 2.4 mmol/L is diagnostic for rickets/osteomalacia.
Bone biopsy
- it is not used regularly, it is used for atypical causes when diagnosis difficult to reach.
- It will shows:
o Osteoid seams are both wider and more extensive.
o tetracycline labelling shows that mineralization is defective.
Nutritional Rickets
- In the past the vast majority of cases of rickets and osteomalacia were due to dietary
vitamin D deficiency and/or insufficient exposure to sunlight. These now less
common especially in developed world.
- Dietary lack of vitamin D (less than 100 IU per day) is common in
o strict vegetarians
Normal Ca+2 with phosphate DDx
Nutritional
Rickets, familial hypophystemia, Fanconi syndrome
Ca+2 with phosphate Renal dystrophy
Ca+2 with normal phosphate Celiac disease
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
02 Orthopedic Note
o in old people who often eat very little
o even in entire populations whose traditional foods contain very little vitamin D
- treatment :
o Vitamin D supplement (400-1000 IU/d) (for elderly up to 2000 IU/d)
o Calcium supplement
Intestinal malabsorption
- Intestinal malabsorption (especially fat malabsorption; steatorrhea) can cause
vitamin D deficiency.
- Treatment:
o Large dose of vitamin D supplement (50 000 IU/d)
Vitamin D resistant rickets and osteomalacia
- There are several types don’t respond to physiological doses of vitamin D.
- Tackle deformity (bow leg in one side, knock knee in other side) is the hallmark of
this disease.
- Examples:
o Inadequacy of hepatic 25-OHD
o Abnormalities of 1,25-(OH)2D metabolism
o Hypophosphataemic rickets and osteomalacia (most important one)
Inadequacy of hepatic 25-OHD
- Either there is defective conversion to 25-OHD or rapid breakdown of 25-OHD
- Causes: drugs (anticonvulsant, rifampicin), liver failure
- Treatment: very large dose of Vitamin D
Abnormalities of 1,25-(OH)2D metabolism
- Causes:
o Renal failure reduced 1α-hydroxylase activity deficiency of
1,25-(OH)2D
Treatment: 1,25-(OH)2D (calcitriol) supplement or very large dose of
vitamin D.
o renal osteodystrophy (advance renal failure on haemodialysis)
o Vitamin D dependent rickets type I (pseudo vitamin D deficient rickets)
Autosomal recessive
It is due to deficiency of 1α-hydroxylase
Children develop severe rickets, secondary hyperparathyroidism,
multiple fractures, generalized myopathy, and dental enamel
hypoplasia
Treatment: life-long calcitriol supplement (1,25-(OH)2D)
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
03 Orthopedic Note
o Type II vitamin D dependent rickets and osteomalacia
Autosomal recessive
It is due defective vitamin D receptor at target organs (intestine and
bone)
Plasma 1,25-(OH)2D level is elevated
It resistant to treatment with both vitamin D and calcitriol.
Children/adult will develop hypocalcaemia with secondary
hyperparathyroidism
Treatment: life-long parenteral calcium
Hypophosphataemic rickets and osteomalacia
- Number of conditions impair tubular reabsorption of phosphate chronic
hypophosphatemia.
- chronic hypophosphatemia cause defective bone mineralization (even with normal
calcium level, and absence of hyperparathyroidism).
- Causes:
o Familial hypophosphatemic rickets
o Adult-onset hypophosphataemia
o renal tubular defects
o Oncogenic osteomalacia
Familial hypophosphatemic rickets
- X-linked dominant disorder
- In some countries, it is the commonest cause of rickets.
- starting in infancy and causing bony deformity of the lower limbs if it is not
recognized and treated.
- Lower limbs deformity (genu valgum or genu varum) develop in age of walking .
- Growth is below normal.
- Epiphyseal changes on X-ray.
Calcitriol toxicity
Patients treated with supra-physiological doses of calcitriol run the risk of developing:
- Hypercalcaemia
- hypercalciuria
- nephrocalcinosis
To avoid these adverse effects plasma calcium level should be monitored.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
04 Orthopedic Note
- Normal calcium level, no hyperparathyroidism, no myopathy.
- Neurological symptoms in adulthood due to heterotopic bone formation in the
longitudinal ligaments of the spinal canal.
- Treatment:
o Phosphate supplement (up to 3 g/d)
o Vitamin D or calcitriol (to prevent hyperparathyroidism that is secondary to
phosphate administration)
o Treatment is continued until growth ceases.
o If the child needs to be immobilized, vitamin D must be stopped temporarily
to prevent hypercalcaemia from the combined effects of treatment and
disuse bone resorption.
o Bony deformities may require bracing or osteotomy.
Adult-onset hypophosphataemia
- Rare condition.
- Characterized by unexplained bone loss and joint pains in adults.
- Treatment:
o Phosphate supplement
o Vitamin D supplement
o Calcium supplement
Oncogenic osteomalacia
- Induced by certain tumors, particularly
o vascular tumors (haemangiopericytomas)
o fibrohistiocytic lesions ( giant cell tumors and pigmented villonodular
synovitis)
- Usually osteomalacia appears in adulthood, before the tumor is discovered.
- the condition is believed to be mediated by phosphatonin
- Treatment:
o Surgical removal of tumor (Removal of the tumour will reverse the bone
changes)
o If can’t remove tumor, give phosphate, vitamin D and calcium supplement.
Hypophosphatasia
- It rare metabolic bone disease, inherited as Autosomal recessive characterized by
low alkaline phosphatase
- It cause severe rickets.
208 [OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]
05 Orthopedic Note
Q/Compare between osteoporosis and osteomalacia?
Comparsion between osteoporosis and osteomalacia
Similarity
Common in ageing women Prone to pathological fracture
Decreased bone density Differences
Osteoporosis osteomalacia Well unwell Pain only with fracture Generalized chronic ache Muscle normal Muscle weakness No looser’s zones Looser’s zones Normal Alkaline phosphate Increased Alkaline
phosphate Normal serum phosphorus Decrease serum
phosphorus Ca X P >2.4 mmol/L Ca X P < 2.4 mmol/L
ORTHOPEDIC NOTE
208
Infection of bone and Joint
P R A Y F O R U S
Burair Al Jassas Mohammed Al_Shaikh
208 [INFECTION OF BONE AND JOINT]
2 Orthopedic Note
Osteomyelitis
Infection of bone by pyogenic organisms. Either acute or chronic.
Acute osteomyelitis
Acute pyogenic infection of bone, also called acute osteitis. Two types:
1- Acute hematogenous osteomyelitis: occur mainly in childhood, organism reach
the bone through blood stream. 2- Osteomyelitis complicating open fracture or surgical operation. Organisms
reach the bone through a wound.
Acute hematogenous osteomyelitis
Mainly in childhood.
Early diagnosis is important because satisfactory outcome depend on early and
sufficient treatment.
Cause: mainly staphylococcus aureus, occasionally salmonella.
Pathology: organism reaches bone from blood stream through septic focus
elsewhere in the body like boil in skin.
Infection occurs in metaphysis of long bone. Pus is formed, because of the acute
inflammatory reaction induced by the organism, and escape to the surface causing
sub periosteal abscess. The abscess burst into soft tissue forming a sinus.
The blood supply to the bone is cut off by septic thrombosis. The ischemic bone
die and separate as a sequestrum. New bone is laid down beneath periosteum,
forming involucrum.
The epiphyseal cartilage plate prevent the spread of infection, but if the affected
metaphysis lies partly in joint cavity e.g. the upper metaphysis of the humerus, all
208 [INFECTION OF BONE AND JOINT]
3 Orthopedic Note
the metaphyses at the elbow and upper and lower metaphyses of the femur, the
joint is become liable to be infected causing acute pyogenic arthritis. Even when
the joint isn’t infected it may swell from an effusion of clear fluid (sympathetic
effusion).
Clinical features: tibia, femur and humerus are mostly affected. Severe pain over the
affected bone with a history of recent boil or minor injury.
Constitutional illness with pyrexia.
Bone tenderness.
Warm skin.
Indurated soft tissue.
Fluctuant abscess may be present.
Good range of movement unless infection spread to joint (septic arthritis).
208 [INFECTION OF BONE AND JOINT]
4 Orthopedic Note
Imaging: radiographic: normal in the early stage. Two or three weeks later
rarefaction of the metaphyseal area and new bone outlining raised periosteum.
Radioisotope scanning: reserved for the diagnosis of less accessible sites such as
pelvis and spine.
Investigation:
1- positive blood culture in early stage.
2- increased polymorphonuclear leukocytosis.
3- C- reactive protein and ESR are raised.
Diagnosis: differentiate acute osteomyelitis from pyogenic arthritis by:
1- Greatest tenderness over the bone rather than the joint.
2- Good range of movement in acute osteomyelitis.
3- Fluid but no pus in pyogenic arthritis.
Blood culture should be taken before antibiotic is recommended.
Complications:
1- Septicemia or pyemia
2- Pyogenic arthritis ( spread of infection to adjacent joints)
3- Growth retardation (epiphyseal plate damage).
Note: acute osteomyelitis often progress to chronic osteomyelitis.
Treatment:
General: bed rest and systemic intravenous antibiotics.
Third generation cephalosporin (broad-spectrum) and penicillin (anti- staph.) given
initially before organism being identified.
In case of MRSA replace penicillin with vancomycin.
Continue treatment for at least 4 weeks.
Local: operation is controversial. Operation in order to 1) release pus and 2) relieve
pain if there isn’t marked improvement in the antibiotic treatment within 24 hours.
Osteomyelitis complicating open fracture or surgical operation
Site of entry of the organism is the wound. Any part of the bone may be affected;
also suppuration and necrosis may occur, but pus discharge through the primary
wound not collecting under periosteum.
Clinical features: children and adult, pain isn’t the predominant feature, purulent
discharge in the wound.
Radiographic features: rarefaction and sequestrum in late stage. Not helpful in early
stage.
Treatment: drainage, removal of any sequestrum (bone fragment) and Anti-bacterial.
Chronic osteomyelitis (chronic pyogenic osteomyelitis)
It occurs as a complication of acute stage.
Cause: staph., strep., pneumo., typhoid.
208 [INFECTION OF BONE AND JOINT]
5 Orthopedic Note
Pathology: common in long bone confined to one end of the bone. Pus, fibrous
tissue, granulation tissue, sequestra and sinus present. Sinus tends to break down and
heal while sequestrum never healed.
Clinical features: main symptom is purulent discharge from the sinus or pain in
other cases.
Reappearance of healed sinus with local pain, pyrexia and abscess is called “Flare-
up” of infection.
Imaging: thickened and dense bone with patchy necrosis giving a honeycombed
appearance.
Complications: pathological fracture, Amyloid disease, persistence discharge of pus,
squamous cell carcinoma.
Treatment:
1) Remove dead and foreign material.
2) Obliterate dead space.
3) Stabilize the skeleton.
4) Soft tissue cover.
5) Reconstruction of bone defect.
6) Antibiotics.
Brodie’s abscess
Special form of chronic osteomyelitis.
Abscess near metaphysic.
Boring pain is the main symptom.
On imaging: circular or oval cavity surrounded by sclerosis and rest of bone is
normal.
Treatment: operation. Pus evacuation and muscle flap to obliterate dead space.
TB
Occur in vertebral body, occasionally in long bone or bone of hand and foot.
Pathology: tubercle bacilli reach the bone through blood stream or by direct
extension from focus of infection in soft tissue or joint. The bone is destroyed and
replaced by granulation tissue. A tuberculous abscess is commonly formed. With
treatment there is healing with fibrosis.
Tuberculous vertebral body collapse anteriorly, but retain normal behind giving
wedge-shaped.
The articular end of bone is frequently eroded by TB beginning primarily in the
joint.
TB in the hand or foot.
The metacarpals or phalanges are most commonly affected bones (tuberculous
dactylitis). Fusiform swelling represents thickened and raised periosteum. Later,
bone destroyed and new bone formed giving distended appearance.
208 [INFECTION OF BONE AND JOINT]
6 Orthopedic Note
Clinical features: pain is the initial symptom, swelling and formation of “cold”
abscess.
Radiographic features:
1. Diffused rarefaction around the site of infection.
2. Erosion or “eating away “of the bone without surrounding sclerosis.
3. Shadow in the soft tissue denoting abscess.
Investigation: ESR raised, +ve Mantoux test, yellow and creamy pus, culture to
identify the organism and biopsy will show the histological features of TB.
Diagnosis: history of contact with TB patient, raised ESR, +ve Mantoux test and
evidence of tuberculous lesion elsewhere.
Diagnosis is proved by:
1) Identifying the causative organism
2) Demonstration of typical histological features.
Treatment: anti-TB for 6 months and pus aspiration.
Spirochaetal infection
Now a day seen only rarely.
Two conditions which are likely to be encountered by the orthopedic surgeon are dealt with here: syphilis and yaws.
Syphilis
Causative organism is treponema pallidum.
Types of syphilis: congenital syphilis and acquired syphilis.
Types of syphilitic bone:
Syphilis of bone can take many forms, but the commonest types
are syphilitic metaphysitis, and syphilitic osteo-periostitis.
208 [INFECTION OF BONE AND JOINT]
7 Orthopedic Note
Syphilitic metaphysitis
Clinical features: present as sever local limb pain in young infants in the first six
months of life with congenital syphilis. It can affect several
epiphyses, with replacement of the adjacent metaphysic by
granulation tissue.
Radiographic features: these appear as a zone of seclerosis (The
surrounding bone is thick and sclerotic). When this process occurs in
the tibia it is called "sabre shin" or "sabre tibia".
Investigation: Wasserman reaction is positive (is an antibody test for syphilis).
Treatment: by intensive antisyphilitic drugs like benzylpenicillin, penicillin, or third generation cephalosporins.
Syphilitic osteo-periostitis
Occurs when diaphysis or body of a bone is infected by syphilis.
Clinical features: occurs in infant with congenital syphilis, or in older children or adult with acquired syphilis. They present with deep boring pain, worse at night, and swelling are the predominant symptoms. On examination either a localized fusiform swelling over the shaft of the bone or a diffuse thickening of the whole length of the bone.
Radiographic features: ranging from sever osteoporosis to dense sclerosis and may be easily confused with a malignant bone tumor. Occasionally the predominant change is bone destruction without new bone formation.
Investigation: Wassermann reaction is positive. Treatment: intensive antisyphilitic drugs.
Syphilitic metaphysitis Syphilitic osteo-periostitis
infant Infant, older children, or adult
Congenital syphilis Congenital or acquired syphilis
Affect epiphysis and metaphysis Affect diaphysis or body of bone
Yaws
Causative organism is treponema pertenue.
Clinical features: Children under 10 years old are the usual victims. skeletal changes
similar to those of syphilis develop – periosteal new bone formation, cortical
destruction and osteochondritis.
Radiographic features: X-rays show features such as cortical erosion, joint destruction and periosteal new bone formation; occasionally thickening of a long
bone may be so marked as to resemble the ‘sabre tibia’ of late congenital
syphilis.
Investigation: serological tests and dark-field examination of scrapings from one of the skin lesions.
Treatment: benzylpenicillin, penicillin, or erythromycin.
Septic arthritis
Also called pyogenic arthritis or infective arthritis.
Types: acute, subacute, or chronic.
When pus is formed within the joint the condition is sometimes termed suppurative
arthritis.
Causative organism:
Arthritis
Septic arthritis Tuberculous
arthritis
208 [INFECTION OF JOINT]
2 Orthopedic Note
a) Complete resolution,b)partial loss of cartilage,c)fibrous
ankylosis,d)bony ankylosis.
Route of Infection:
1. Haematogenous.
2. Direct invasion.
Penetrating wound.
intra articular injection.
arthroscopy.
3. Eruption of bone abscess.
4. Extension from adjacent focus of osteomyelitis.
Pathology:
infection causes an acut, or subacute synovitis
with purulent exudate.
Outcome (Sequelae): varies from complete
resolution, total destruction of the joint and
fibrous, or bony ankylosis.
Clinical features:
the onset is acute or subacute, with pain and swelling of the joint. There is
constitutional illness, with pyrexia.
On examination the joint is swollen( due to fluid effusion and thickening of
synovial membrane), skin is warm, and it is often red. Reluctant to move the joint
and muscle spasm.
Radiographic features: in early stages radiographs do not show any alteration from the
normal, though ultrasound scan may reveal the presence of an effusion. Later, there may
be diffuse rarefaction of bone, loss of cartilage space, and possibly destruction of bone.
Radioisotope bone scanning shows increased uptake of the isotope.
Investigation:
Blood Work-up:
CBC: WBC, C-reactive protein, and ESR are raised.
Strongly suspected if the WBC is >50,000mm (with 90% PMN, even
if the cultures are negative).
Bacteriological examination of aspirated joint fluid usually identifies the
causative organism.
Treatment:
Bed rest.
I.V broad-spectrum antibiotics until the result of culture appear.
The joint is rested, usually in a plaster splint.
The fluid exudate is removed by aspiration or incision.
Arthrotomy and Joint Debridement.
Tuberculous arthritis
Pathology:
joint most affected are the intervertebral joint of the thoracic or lumbar spine, and
next in frequency the hip and knee. The synovial membrane is much thickened by
inflammatory reaction and giant-cell systems. Articular cartilage is soon
208 [INFECTION OF JOINT]
3 Orthopedic Note
destroyed and underlying bone is eroded. Cold abscess is a common feature.
Abscess may eventually rupture, giving rise to a chronic tuberculous sinus. This
may provide a route for the entry of secondary infecting organism.
Outcome: varies from complete resolution, total destruction of the joint and
fibrous, or bony ankylosis.
Route of Infection:
Haematogenous from a focus elsewhere.
Direct continuity from adjacent bone.
Clinical features: children and young adults are most commonly affected. In general the
predominant symptoms are pain, swelling, and impairment of function. On examination
there are signs of inflammation in addition to painful restriction of movement in all
direction due to protective muscle spasm. In addition to general symptom of TB.
Radiographic features: in early stages radiographs show diffuse rarefaction of bone
adjacent to the joint. Later, cartilage space is narrowed and the underlying bone is eroded.
Radioisotope bone scanning shows increased uptake of the isotope.
Investigations:
ESR is raised in active stage. Its gradual decrease is an indication of healing.
Positive Mantoux test (also called PPD test (purified protein derivative).
Aspiration of the joint may yield a little turbid fluid.
Culture.
Biopsy shows caseous granulation and acid-fast bacilli.
Treatment:
Antibiotic (Rifampicin, Isoniazid, Pyrazinamide, Streptomycin, and Ethambutol).
Bed rest.
The joint is rested, usually in a plaster splint.
The fluid exudate is removed by aspiration or incision.
ORTHOPEDIC NOTE
208
RHEUMATOID
ARTHRITIS
P R A Y F O R U S
Ali Zaki
208 [RHEUMATOID ARTHRITIS]
2 Orthopedic Note
Rheumatoid arthritis (RA) is the most common cause of chronic inflammatory joint
disease. The most typical features are a symmetrical polyarthritis and tenosynovitis,
morning stiffness, elevation of the erythrocyte sedimentation rate (ESR) and the
appearance of autoantibodies that target immunoglobulins (rheumatoid factors) in the
serum.
Epidemiology
The reported prevalence of RA in most populations is 1–3 per cent, with a peak
incidence in the fourth or fifth decades. Women are affected 3 or 4 times more
commonly than men.
Risk Factors
Important factors in the evolution of RA are:
(1) genetic susceptibility.
(2) an immunological reaction, possibly involving a foreign antigen, preferentially
focussed on synovial tissue.
(3) an inflammatory reaction in joints and tendon sheaths.
(4) the appearance of rheumatoid factors (RF) in the blood and synovium.
(5) perpetuation of the inflammatory process.
(6) articular cartilage destruction.
Pathology
Rheumatoid arthritis is a systemic disease but the most characteristic lesions are seen in
the synovium or within rheumatoid nodules. The synovium is engorged with new
blood vessels and packed full of inflammatory cells.
JOINTS AND TENDONS
The pathological changes, if unchecked, proceed in four stages:
Stage 1 – pre-clinical: Well before RA becomes clinically apparent the immune
pathology is already beginning. Raised ESR, C-reactive protein (CRP) and RF may be
detectable years before the first diagnosis.
Stage 2 – synovitis: There is thickening of the capsular structures, villous formation of
the synovium and a cell-rich effusion into the joints and tendon sheaths. Although
painful, swollen and tender, these structures are still intact and mobile, and the disorder is
potentially reversible.
208 [RHEUMATOID ARTHRITIS]
3 Orthopedic Note
Stage 3 – destruction: Persistent inflammation causes joint and tendon destruction.
Stage 4 – deformity: The
combination of articular
destruction, capsular stretching
and tendon rupture leads to
progressive instability and
deformity of the joints. The
inflammatory process usually
continues but the mechanical
and functional effects of joint
and tendon disruption now
become vital.
EXTRA-ARTICULAR TISSUES
Rheumatoid nodules: The rheumatoid nodule is a small granulomatous lesion occur
under the skin (especially over bony prominences), in the synovium, on tendons, in the
sclera and in many of the viscera.
Lymphadenopathy: Not only the nodes draining inflamed joints, but also those at a
distance such as the mediastinal nodes, can be affected. This, as well as a mild
splenomegaly, is due to hyperactivity of the reticuloendothelial system. More severe
splenomegaly can also be associated with neutropaenia as part of Felty’s syndrome.
Vasculitis: This can be a serious and life-threatening complication of RA. Involvement
of the skin, including nailfold infarcts, is common but organ infarction can occur.
Muscle weakness: Muscle weakness is common. It may be due to a generalized
myopathy or neuropathy, but it is important to exclude spinal cord disease or cord
compression due to vertebral displacement (atlantoaxial subluxation). Sensory
changes may be part of a neuropathy, but localized sensory and motor symptoms can
also result from nerve compression by thickened synovium (e.g. carpal tunnel
syndrome).
Visceral disease: The lungs, heart, kidneys, gastrointestinal tract and brain are
sometimes affected. Ischaemic heart disease and osteoporosis are common
complications.
Clinical features
The onset of RA is usually insidious, with symptoms emerging over a period of
months. Occasionally the disease starts quite suddenly.
In the early stages the picture is mainly that of a polysynovitis, with soft-tissue
swelling and stiffness.
208 [RHEUMATOID ARTHRITIS]
4 Orthopedic Note
Typically, a woman of 30–40 years complains of pain, swelling and loss of mobility in
the proximal joints of the fingers. There may be a previous history of ‘muscle pain’,
tiredness, loss of weight and a general lack of well-being. As time passes, the symptoms
‘spread’ to other joints – the wrists, feet, knees and shoulders in order of frequency.
Another classic feature is generalized stiffness after periods of inactivity, and especially
after rising from bed in the early morning. This early morning stiffness typically lasts
longer than 30 minutes.
Physical signs may be minimal, but usually there is symmetrically distributed swelling and
tenderness of the metacarpophalangeal joints, the proximal interphalangeal joints
and the wrists. Tenosynovitis is common in the extensor compartments of the wrist
and the flexor sheaths of the fingers; it is diagnosed by feeling thickening, tenderness and
crepitation over the back of the wrist or the palm while passively moving the fingers. If
the larger joints are involved, local warmth, synovial hypertrophy and intra-articular
effusion may be more obvious. Movements are often limited but the joints are still stable
and deformity is unusual.
In the later stages joint deformity becomes increasingly apparent and the acute pain of
synovitis is replaced by the more constant ache of progressive joint destruction. The
combination of joint instability and tendon rupture produces the typical ‘rheumatoid’
deformities: ulnar deviation of the fingers, radial and volar displacement of the wrists,
valgus knees, valgus feet and clawed toes. Joint movements are restricted and often very
painful. About a third of all patients develop pain and stiffness in the cervical spine.
Function is increasingly disturbed and patients may need help with grooming, dressing
and eating.
Extra-articular features: These often appear in patients with severe disease. The most
characteristic is the appearance of nodules. They are usually found as small
subcutaneous lumps, rubbery in consistency, at the back of the elbows, but they also
develop in tendons (where they may cause ‘triggering’ or rupture), in the viscera and the
eye. They are pathognomonic of RA, but occur in only 25% of patients.
Less specific features include muscle wasting, lymphadenopathy, scleritis, nerve
entrapment syndromes, skin atrophy or ulceration, vasculitis and peripheral sensory
neuropathy. Marked visceral disease, such as pulmonary fibrosis, is rare.
208 [RHEUMATOID ARTHRITIS]
5 Orthopedic Note
Imaging
X-rays: Early on, x-rays show only the features of synovitis: soft-tissue swelling and
peri-articular osteoporosis. The later stages are marked by the appearance of marginal
bony erosions and narrowing of the articular space, especially in the proximal joints of
the hands and feet. Flexion and extension views of the cervical spine often show
subluxation at the atlanto-axial or mid-cervical levels; surprisingly, this causes few
symptoms in the majority of cases.
Ultrasound scanning and MRI The use of other imaging techniques to look at soft-
tissue changes and early erosions within joints has become more common. Ultrasound
can be particularly useful in defining the presence of synovitis and early erosions.
Additional information on vascularity can be obtained if Doppler techniques are used.
208 [RHEUMATOID ARTHRITIS]
6 Orthopedic Note
Blood investigations
Normocytic, hypochromic anaemia is common and is a reflection of abnormal
erythropoiesis due to disease activity. It may be aggravated by chronic gastrointestinal
blood loss caused by non-steroidal anti-inflammatory drugs. In active phases the ESR
and CRP concentration are usually raised.
Serological tests for rheumatoid factor are positive in about 80 per cent of patients and
antinuclear factors are present in 30 per cent. Neither of these tests is specific and
neither is required for a diagnosis of rheumatoid arthritis. Newer tests such as those for
anti-CCP antibodies have added much greater specificity but at the expense of
sensitivity.
Synovial biopsy
Synovial tissue may be obtained by needle biopsy, via the arthroscope, or by open
operation. Unfortunately, most of the histological features of rheumatoid arthritis are
non-specific.
ACR criteria for Diagnosis of Rheumatoid
Arthritis
1. RA Diagnosis requires four of the following 2. Symptoms that must be present for at least 6 weeks
1. Morning stiffness in and around joints for >= 1 hour 1. Most common presenting symptom
2. Symmetric joint involvement 1. Most common presenting sign
3. Soft tissue swelling of at least three joint areas
208 [RHEUMATOID ARTHRITIS]
7 Orthopedic Note
1. PIP joint 2. MCP joint 3. Wrist joint 4. Elbow joint 5. Knee joint 6. Ankle joint 7. MTP joint
4. Swelling of mcp, pip or wrist joints 3. Signs that may be present at any time
1. Rheumatoid Nodules (Subcutaneous Nodules) present 2. Rheumatoid Factor positive 3. X-ray changes
1. See XRay Changes in Rheumatic Conditions 2. Bone Erosions 3. Periarticular Osteopenia (bone decalcification)
1. Especially involving the hands and wrists
Treatment
There is no cure for rheumatoid arthritis. A multidisciplinary approach is needed from
the beginning: ideally the therapeutic team should include a rheumatologist, orthopaedic
surgeon, physiotherapist, occupational therapist, orthotist and social worker.
PRINCIPLES OF MEDICAL MANAGEMENT
Treatment should be aimed at controlling inflammation as rapidly as possible. This is
likely to require the use of corticosteroids for their rapid onset. Steroids should be
rapidly tapered to prevent significant side effects.
In addition, disease-modifying antirheumatic drugs (DMARDs) should be started at this
time. The first choice is now methotrexate. This may be used initially alone or in
combination with sulfasalazine and hydroxychloroquine. Leflunomide can also be
considered if methotrexate is not tolerated. Gold and penicillamine are now used rarely.
208 [RHEUMATOID ARTHRITIS]
8 Orthopedic Note
Control of pain and stiffness with non-
steroidal anti-inflammatory drugs (NSAIDs)
may be needed, maintaining muscle tone
and joint mobility by a balanced programme
of exercise, and general advice on coping
with the activities of daily living.
If there is no satisfactory response to
DMARDs, it is wise to progress rapidly to
biological therapies such as the TNF
inhibitors infliximab, etanercept and
adalimumab.
Additional measures include the injection of
long acting corticosteroid preparations into
inflamed joints and tendon sheaths.
Prolonged rest and immobility is likely to
weaken muscles and lead to a worse prognosis. However, some splinting can be helpful
at any stage of the disease.
PHYSIOTHERAPY AND OCCUPATIONAL THERAPY
If these fail to restore and maintain function, operative treatment is indicated.
SURGICAL MANAGEMENT
At first this consists mainly of soft-tissue procedures (synovectomy, tendon repair or
replacement and joint stabilization); in some cases osteotomy may be more
appropriate.
In late rheumatoid disease, severe joint destruction, fixed deformity and loss of function
are clear indications for reconstructive surgery. Arthrodesis, osteotomy and
arthroplasty all have their place and are considered in the appropriate chapters. It
appears safe to continue methotrexate during elective orthopaedic surgery. However,
doses of corticosteroids should be as low as possible and biological therapies such as the
TNF inhibitors should be stopped prior to surgery where possible.
Complications
Fixed deformities
Muscle weakness Even mild degrees of myopathy or neuropathy, when combined with
prolonged inactivity, may lead to profound muscle wasting and weakness. This should be
prevented by control of inflammation, physiotherapy and pain control.
Joint rupture Occasionally the joint lining ruptures and synovial contents spill into the
soft tissues.
● ● ●
KEY ELEMENTS IN MEDICAL TREATMENT
Identify patients with RA as early as
possible
Start disease-modifying
antirheumatic drugs (DMARDs)
immediately
Consider combination therapy with
multiple DMARDs
If DMARDs fail, progress rapidly to
biological therapies such as the TNF
inhibitors infliximab, etanercept and
adalimumab
● ● ●
208 [RHEUMATOID ARTHRITIS]
9 Orthopedic Note
Infection Patients with rheumatoid arthritis – and even more so those on corticosteroid
therapy – are susceptible to infection.
Spinal cord compression This is a rare complication of cervical spine (atlanto-axial)
instability.
Systemic vasculitis
Amyloidosis
Prognosis
Rheumatoid arthritis runs a variable course. When the patient is first seen it is
difficult to predict the outcome, but high titres of rheumatoid factor, peri-
articular erosions, rheumatoid nodules, severe muscle wasting, joint
contractures and evidence of vasculitis are bad prognostic signs. Women, on
the whole, fare somewhat worse than men. Without effective treatment about 10
per cent of patients improve steadily after the first attack of active synovitis; 60 per
cent have intermittent phases of disease activity and remission, but with a slow
downhill course over many years; 20 per cent have severe joint erosion, which is
usually evident within the first 5 years; and 10 per cent end up completely disabled.
In addition, a reduction in life expectancy by 5–10 years is common and is often due
to premature ischaemic heart disease. However, early aggressive medical treatment
appears to reduce the morbidity and mortality.
ORTHOPEDIC NOTE
208
OSTEOARTHRITIS
P R A Y F O R U S
Husain AlShulah Hasan AlSaihati
208 [LECTURE TITLE]
2 Orthopedic Note
Definition
a chronic disorder of synovial joints in which there is progressive softening and disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes), cyst formation and sclerosis in the subchondral bone, mild synovitis and capsular fibrosis. In its most common form, it is unaccompanied by any systemic illness and, although there are sometimes local signs of inflammation, it is not primarily an inflammatory disorder. It is also not a purely degenerative disorder, and the term ‘degenerative arthritis’ – which is often used as a synonym for OA – is a misnomer. Osteoarthritis is a dynamic phenomenon; it shows features of both destruction and repair. Cartilage softening and disintegration are accompanied from the very outset by hyperactive new bone formation, osteophytosis and remodelling. The final picture is determined by the relative vigour of these opposing processes.
Aetiology
The most obvious thing about OA is that it increases in frequency with age. Cartilage does ‘age’, showing diminished cellularity, reduced proteoglycan concentration, loss of elasticity and a decrease in breaking strength with advancing years deterioration are restricted to certain joints, and to specific areas of those joints, ‘Inheritance’ has for many years been thought to play a role in the development of OA. one should bear in mind that OA of large ,joints is often attributable to anatomical variations, e.g. acetabular dysplasia and other forms of epiphyseal ,dysplasia, and it is these that are inherited rather than any tendency to develop OA as a primary abnormality, Articular cartilage may be damaged by trauma or previous inflammatory disorders. Enzymes released by synovial cells and leucocytes can cause leaching of proteoglycans from the matrix, and synovial-derivedinterleukin-1 (IL-1) may suppress proteoglycan synthesis. In most cases the precipitating cause of OA is increased mechanical stress in some part of the articular surface. This may be due to increased load (e.g. in deformities that affect the lever system around a joint)or to a reduction of the articular contact area (e.g.with joint incongruity or instability)
Pathogenesis
The earliest changes are an increase in water content of the cartilage and easier extractability of the matrix proteoglycans. At a slightly later stage there is loss of proteoglycans and defects appear in the cartilage. As the cartilage becomes less stiff, secondary damage to chondrocytes may cause release of cell enzymes and further matrix breakdown. Cartilage deformation may also add to the stress on the collagen network, thus amplifying the changes in a cycle that leads to tissue breakdown. Articular cartilage has an important role in distributing and dissipating the forces associated with joint loading. When it loses its integrity these forces are increasingly concentrated in the subchondral bone. The result: focal trabecular degeneration and cyst
208 [LECTURE TITLE]
3 Orthopedic Note
formation, as well as increased vascularity and reactive sclerosis in the zone of maximal loading. What cartilage remains is still capable of regeneration, repair and remodelling. As the articular surfaces become increasingly malapposed and the joint unstable, cartilage at the edges of the joint reverts to the more youthful activities of growth and endochondral ossification, giving rise to the bony excrescences, or osteophytes, that so clearly distinguish osteoarthritis from ‘atrophic’ disorders such as rheumatoid disease.
Pathology The cardinal features are: (1) progressive cartilage destruction (2) subarticular cyst formation (3) sclerosis of the surrounding bone (4) osteophyte formation (5) capsular fibrosis
The histological appearances vary considerably, according to the degree of destruction. Early on, the cartilage shows small irregularities or splits in the surface, while in the deeper layers there is patchy loss of metachromasia. Most striking, however, is the increased cellularity, and the appearance of clusters of chondrocytes. In later stages, the clefts become more extensive and in some areas cartilage is lost to the point where the underlying bone is completely denuded. The subchondral bone shows marked osteoblastic activity. The capsule and synovium are often thickened but cellular activity is slight; however, sometimes there is marked inflammation or fibrosis of the capsular tissues. Marked vascularity and venous congestion of the subchondral bone.
Prevalence Osteoarthritis is the commonest of all joint diseases, affecting both sexes and all races; Autopsy studies show OA changes in everyone over the age of 65 years. Radiographic ,surveys suggest that the prevalence rises from 1 per cent below the age of 30 years to over 50per cent in people above the age of 60. Osteoarthritis of the finger joints is particularly common in elderly women, affecting more than 70 per cent of those over70 years.
Risk factors
1. Joint dysplasia Disorders such as congenital acetabular dysplasia and Perthes’ disease presage a greater than normal risk of OA in later life
2. Trauma Fractures involving the articular surface areobvious precursors of secondary OA
3. Occupation There is good evidence of an association between OA and certain occupations which cause repetitive stress,
4. Bone density It has long been known that women with femoral neck fractures seldom have OA of the hip.
208 [LECTURE TITLE]
4 Orthopedic Note
5. Family history 6. Obesity The simple idea that obesity causes increased joint loading The
association is closer in women than in men
Symptoms 1)Patients usually present after middle age. symptoms centre either on one or two of the weight bearing joints(hip or knee), on the interphalangeal joints (especially in women) or on any joint that has suffered a previous affliction 2)Pain is the usual presenting symptom. it may be referred to a distant site– for example, pain in the knee from OA of the hip . It starts insidiously and increases slowly over months or years. It is aggravated by exertion and relieved by rest, although with time relief is less and less complete the late stage the patient may have pain in bed at night. 3)Stiffness is common; characteristically it occurs after periods of inactivity, but with time it becomes constant and progressive 4)Deformity may result from capsular contracture or joint instability, but be aware that the deformity may actually have preceded and contributed to the onset of OA. 5)Loss of function, though not the most dramatic, is often the most distressing symptom. A limp, difficulty in climbing stairs, restriction of walking distance Typically, the symptoms of OA follow an intermittent course, with periods of remission sometimes lasting for months.
Signs 1)Joint swelling may be the first thing one notices in peripheral joints (especially the fingers, wrists, knees and toes). This may be due to an effusion. 2)Tell-tale scars denote previous abnormalities, and muscle wasting suggests longstanding dysfunction. 3)Deformity is easily spotted in exposed joints (the knee or the large-toe metatarsophalangeal joint). 4)Local tenderness is common, and in superficial joints fluid, synovial thickening or osteophytes may be felt. 5)Limited movement in some directions but not others is usually a feature, and is sometimes associated with pain at the extremes of motion. 6)Crepitus may be felt over the joint (most obvious in the knee) during passive movements. 7)Instability is common in the late stages of articular destruction, but it may be detected much earlier by special testing. Instability can be due to loss of cartilage and bone, asymmetrical capsular contracture and/or muscle weakness.
208 [LECTURE TITLE]
5 Orthopedic Note
Other joints should always be examined; they may show signs of a more generalized disorder. Function in everyday activities must be assessed.
Imaging 1)X-rays :X-ray appearances are so characteristic that other forms of imaging are seldom necessary for ordinary clinical assessment. The cardinal signs are asymmetrical loss of cartilage (narrowing of the ‘joint space’), sclerosis of the subchondral bone under the area of cartilage loss, cysts close to the articular surface, osteophytes at the margins of the joint and remodelling of the bone ends on either side of the joint. Late features may include joint displacement and bone destruction THE CARDINAL SIGNS OF OSTEOARTHRITIS
1. Narrowing of the ‘joint space’ 2. Subchondral sclerosis 3. Marginal osteophytes 4. Subchondral cysts 5. Bone remodelling
2)Radionuclide scanning: Scanning with 99mTc-HDPshows increased activity during the bone phase in the subchondral regions of affected joints. This is due to increased vascularity and new bone formation 3)CT and MRI Advanced imaging is sometimes needed to elucidate a specific problem, e.g. early detection of an osteocartilaginous fracture, bone oedema or avascular necrosis. These methods are also used for severity grading in clinical trials.
Arthroscopy Arthroscopy may show cartilage damage before x-ray changes appear. The problem is that it reveals too much, and the patient’s symptoms may be ascribed to chondromalacia or OA when they are, in fact, due to some other disorder
Complications 1)Capsular herniation Osteoarthritis of the knee is sometimes associated with a marked effusion and herniation of the posterior capsule (Baker’s cyst). 2)Loose bodies Cartilage and bone fragments may give rise to loose bodies, resulting in episodes of locking. Rotator cuff dysfunction Osteoarthritis of the acromioclavicular joint may cause rotator cuff impingement, tendinitis or cuff tears. Spinal stenosis Longstanding hypertrophic OA of the lumbar apophyseal joints may give rise to acquired spinal stenosis. The abnormality is best demonstrated by CT and MRI. 3)Spondylolisthesis In patients over 60 years of age, destructive OA of the apophyseal joints may result in severe segmental instability and spondylolisthesis
208 [LECTURE TITLE]
6 Orthopedic Note
Clinical variants of osteoarthritis MONARTICULAR AND PAUCIARTICULAR OSTEOARTHRITIS In its ‘classic’ form, OA presents with pain and dysfunction in one or two of the large weightbearing joints. POLYARTICULAR (GENERALIZED) OSTEOARTHRITIS This is by far the most common form of OA, though most of the patients never consult an orthopaedic surgeon. The patient is usually a middle-aged woman who presents with pain, swelling and stiffness of the finger joints. The first carpometacarpal and the big toe metatarsophalangeal joints, the knees and the lumbar facet joints may be affected at more or less the same time. OSTEOARTHRITIS IN UNUSUAL SITES Osteoarthritis is uncommon in the shoulder, elbow, wrist and ankle. If any of these joints is affected one should suspect a previous abnormality – congenital or traumatic – or an associated generalized disease such as a crystal arthropathy. RAPIDLY DESTRUCTIVE OSTEOARTHRITIS (see also page 84) Every so often a patient with apparently straightforward OA shows rapid and startling progression of bone destruction. The condition was at one time thought to be due to the dampening of pain impulses by powerful anti-inflammatory drugs –
Differential diagnosis of osteoarthritis 1)Avascular necrosis ‘Idiopathic’ osteonecrosis causes joint pain and local effusion. Early on the diagnosis is made by MRI. Later x-ray appearances are usually pathognomonic The cardinal distinguishing feature is that in osteonecrosis the ‘joint space’ (articular cartilage) is preserved in the face of progressive bone collapse and deformity. 2)Inflammatory arthropathies Rheumatoid arthritis, ankylosing spondylitis and Reiter’s disease may start in one or two large joints. The history is short and there are local signs of inflammation. X-rays show a predominantly atrophic or erosive arthritis. Sooner or later other joints are affected and systemic features appear. 3)Polyarthritis of the fingers Polyarticular OA may be confused with other disorders which affect the finger joints Nodal OA affects predominantly the distal joints, rheumatoid arthritis the proximal joints. Psoriatic arthritis is a purely destructive arthropathy and there are no interphalangeal ‘nodes’. Tophaceous gout may cause knobbly fingers, but the knobs are tophi, not osteophytes. X-rays will show the difference. 4)Diffuse idiopathic skeletal hyperostosis (DISH) This is a fairly common disorder of middle-aged people, characterized by bone proliferation at the ligament and tendon insertions around peripheral joints and the intervertebral discs (Resnick et al., 1975). On x-ray examination the large bony spurs are easily mistaken for osteophytes. Multiple diagnosis Osteoarthritis is so common after middle age that it is often found in patients with other conditions that cause pain in or around a joint.
208 [LECTURE TITLE]
7 Orthopedic Note
Management The management of OA depends on the joint involved, the stage of the disorder, the severity of the symptoms, the age of the patient and his or her functional needs. EARLY TREATMENT Treatment is symptomatic. The principles are: (1) maintain movement and muscle strength by Physical therapy (2) protect the joint from‘overload’(Load reduction) (3)relieve pain by Analgesic medication (4) modify daily activities INTERMEDIATE TREATMENT Joint debridement may be done either by arthroscopy or by open operation.In localized articular overload arising from joint malalignment or incongruity , a corrective osteotomy may prevent or delay progression of the cartilage damage. LATE TREATMENT Progressive joint destruction, with increasing pain, instability and deformity (particularly of one of the weightbearing joints), usually requires reconstructive surgery. Three types of operation have, at different times, held the field: Realignment osteotomy, arthroplasty and Arthrodesis.
za
ORTHOPEDIC NOTE
208
Bone Tumors
P R A Y F O R U S
Zaid Al-Helal Issac Al-Mughaizel
Lecture Index
Introduction and Classification
How to Diagnose Bone Tumor
Staging and spread of Bone Tumor
General Principle of Bone Tumor Management
Benign Bone tumor
Malignant Bone Tumor
Tumor Like lesion
208 [BONE TUMORS]
2 Orthopedic Note
Introduction and Classification
Parts of long Bones
Metaphysis: Part of the bone between the epiphysis and the diaphysis; it contains the connecting cartilage enabling the bone to grow.
Diaphysis (shaft): Elongated hollow central portion of the bone located between the methaphyses and encloses the medullary cavity.
Distal epiphysis: Enlarged terminal part of the bone, farthest from the center of the body.
Proximal epiphysis: Enlarged terminal part of the bone, nearest the center of the body.
Bone Structure
Epiphyseal plate is a hyaline cartilage plate in the
metaphysic at each end of a long bone
Cortical bone (compact bone): It gives strength to the
hollow part of the bone.
medullary cavity :is the central cavity of bone shafts where
red bone marrow and/or yellow bone marrow (adipose
tissue) is stored
Periosteum: is an envelope of fibrous connective tissue
that is wrapped around diaphyses
Cancellous bone - spongy bone that stores the red bone
marrow; where blood cells are made
Types of bone
Growth of Bone
The bones of embryos are made largely of cartilage. They
are soft. The process of ossification uses calcium to
create bone as the child grows and matures. Bones
gradually become hard and strong
Body Bones
Bone Histology
1) Bone Matrix (Osteoid)
2) Bone Cells
a. Osteocyte
b. Osteoblast
c. Osteoclast
208 [BONE TUMORS]
3 Orthopedic Note
Bone Tumors are abnormal and uncontrollable growth of cell within the bone
Classification:
A) According to Type of Growth:
Benign and malignant are relatively uncommon in comparison with malignancies
arising in other tissues of the body
B) According to Site of Origin:
1) Primary Bone Tumors:
Originate from the bone tissues.
Usually single lesion.
2) Secondary Bone Tumors:
Originate from other body tissues and metastasis to bone
Multiple lesions
More common than primary
Method of spread to bone: blood vessels (e.g.: prostate) locally (e.g.: breast)
Common sites that metastasize to bone:
o Thyroid (Most common to give bone metastasis)
o Breast
o Lung
o Kidney
o Prostate (least common)
Common bone sites of secondary metastasis: in skeleton contain vascular
marrow:
o Vertebral bodies
o Ribs
o Pelvic
o Upper ends of femur and humerus
Clinical features(from most common to least common):
Bone pain, pathological fracture, neurological symptoms, and local swelling
Benign (noncarcenous) Malignant (Carcenous)
Incidence More Common Less Common Growth Slow Rapid Margin Well defined edges and sometime
sclerotic ill-defined edges
Metastasis Does Not Does Suffix - Oma - Sarcoma Notice May relapse the bone tissue which
make it weaker and result in pathological fracture
May relapse the bone tissue which make it weaker and result in
pathological fracture (it is more with malignant)
208 [BONE TUMORS]
4 Orthopedic Note
C) According to Cell Type:
Benign Malignant
Bone (Osteoid) Osteoma
Osteoid Osteoma Osteblastoma
Osteosrcoma
Cartilage
Chondroma Osteochondroma
Chondromyxoid Fibroma Chondroblastoma
Chondrosarcoma
Fibrous Tissue Fibroma Fibrosarcoma
(Malignant fibrous histocytoma- FMH)
Marrow Eosinophilic Grannuloma Ewing Sarcoma
Lymphoma
Vascular Hemangioma Angiosarcoma
Uncertain Giant Cell Tumor
Cyst (tumor like lesion) Malignant GCT Adamantioma
Anatomical Location of the bone Tumor:
208 [BONE TUMORS]
5 Orthopedic Note
How to Diagnose Bone Tumor
History: 1) Age: the age of the patient with the site of the tumor are the most helpful
tools in narrowing the differential diagnosis Primary Bone Tumor: each primary tumor is more common in specific age
interval
Multible myloma in old (over 60 years old)
Chondrosarcoma in old (over 40 years old )
Giant after closer of epiphysis (20 -40 years)
Ostesarcoma 2 periods: (10 – 30) and (over 60 years old)
Ewing sarcoma and simple bone cyst more common in children and teen ages
(15- 20 years old)
Secondary Bone tumors: In patients over 70 years of age, metastatic bone lesions
are more common than all primary tumors together.
2) Pain: it is due to tumor itself, pressure of tumor on the nerve, or pathological
fracture. Benign tumor usually painless and malignant usually painful after swelling
appearance.
3) Swelling: due to the tumor itself or due to the growth of soft tissue.
4) Pathological fracture : Sometimes it is the first symptom
5) Neurological symptoms: it is caused either by local invasion of the nerve or
by pressure symptoms.
6) Constitutional symptoms (e.g.: weight loss)
7) Accidental findings: Patient may be completely asymptomatic and the tumor
discovered accidently
Clinical Examination: 1) General appearance
2) Local: Tenderness and Swelling
3) Other systems: Chest, Abdomen, Pelvis, Lymph nodes
208 [BONE TUMORS]
6 Orthopedic Note
Tumors Work up
1) Lab investigation: 1. CBC: Anemia
2. Inflammatory Markers (CRP,ESR)
3. Urine Examination: important in multiple myeloma
4. Bone Profile
5. Renal Profile
6. Liver Profile
7. Others
a. Prostate Specific Agent and acid phosphatase for prostatic cancer
b. Benes jones protein
All previous investigation may appear in normal range in benign bone tumor.
All previous investigation should be done in suspicion of malignant bone tumor
2) Radiological investigation:
1. Plain Radiography: looking for
A) Type of Bone lesion
Ostolytic: indicate there is resorption of the bone
Osteosclerotic: the bone appear more whiter (but not stronger) as in prostatic
metastasis and osteoma
B) Presence of pathological fracture
2. CT scan: done to know exact size of lesion, view Bone destruction, and to
confirm pathological fracture.
3. MRI: done to view Soft tissue extension
(cannot be viewed in plain x-ray) and
Bone tumor necrosis (e.g.: spinal cord
extension in vertebral tumor)
4. Bone Scan (scintigraphy): small bone lesions or skip lesion as multiple myloma
or multiple metastasis
3) Biopsy: it is the only instigation tool that can give definitive diagnosis
1. Open Biopsy: if there is suspicion of spreading or benign tumor
2. Needle (Gore) Biopsy : in inaccessible area or in spine
Differential Diagnosis Number of conditions may mimic the tumor: Soft tissue hematoma, myoscitis ossificans,
stress fracture, bone infection and gout.
Soft Tissue Extension Usually implies
malignancy (More likely to form discrete soft
tissue mass)
Benign conditions with soft tissue extension
(e.g.: Osteomyelitis: Usually infiltration of fat)
208 [BONE TUMORS]
7 Orthopedic Note
Aim of radiographical investigation
1) Localize Bone lesion: Central Vs peripheral
2) Describe the lesion:
a. Pattern: due to pattern of growing (slow or rapid)
Geographic: well circumscribed bone lesion. It usually implies
benign lesion.
Moth-Eaten: usually due to osteolytic lesion
Premative: long transition between normal and abnormal bone.
Usually implies malignant lesion
b. Marginal definition
c. Periosteal reaction
i. Benign: None or solid (only thickening)
ii. Aggressive (as in malignant): in that type of reaction the lesion growing fast so the
periosteum fails to form a new bone tissue rapidly:
1. Sunburst: lesion grows rapidly but steadily and the periosteum does not have
enough time to lay down even a thin shell of bone. So, the tiny fibers that connect
the periosteum to the bone (Sharpey's fibers) become stretched out perpendicular
to the bone
2. Codman's triangle: the periosteum does not have time to ossify with shells of new
bone, so only the edge of the raised periosteum will ossify.
3. Onion Peel: multilayered periosteal reaction demonstrates multiple concentric
parallel layers of new bone adjacent to the cortex. (E.g.: Ewing Sarcoma)
Solid Sunburst Codman's Onion Peel Complex
208 [BONE TUMORS]
8 Orthopedic Note
Staging and Spread of Bone Tumor
Staging of benign bone tumors as described by Enneking: Latent Well-defined margin.
Grows slowly and then stops Remains static/heals spontaneously E.g. Osteoid osteoma
Active
Progressive growth limited by natural barriers Not self-limiting. Tendency to recur E.g. Aneurysmal bone cyst
Agressive Growth not limited by natural barriers E.g. giant cell tumor
Surgical Stage: Staging’ the tumor is an important step towards selecting the operation best suited to that
particular patient, and carrying a low risk of recurrence.
Bone sarcomas are broadly divided as follows:
•Stage I: All low-grade sarcomas.
•Stage II: Histological high-grade lesions.
• Stage III: Sarcomas which have metastasized.
Stage Grade Site Metastasis
1A Low Intracompartmental No 1B Low Extracompartmental No 2A High Intracompartmental No 2B High Extracompartmental No
3A Low Intra or
Extracompartmental Yes
3B High Intra or
Extracompartmental Yes
*intracompartmental: Lesions that are confined to an enclosed tissue space (e.g. a bone, a joint
cavity or a muscle group within its fascial envelope) are called
*extracompartmental: Those that extend into interfascial or extrafascial planes with no natural
barrier to proximal or distal spread
Staging of soft tissue tumors: According to their histological grade (G), size (T), lymph node involvement (N) and
whether they have metastasized (M).
Aggressiveness Tumors are graded not only on their cytological characteristics but also on their clinical
behavior i.e.: the likelihood of recurrence and spread after surgical removal.
208 [BONE TUMORS]
9 Orthopedic Note
General Principle of Bone Tumor Treatment
Tumor Excision: we go from least invasion to most radical 1) Intracapsular excision or curettage : subtotal removal
Done for benign tumor which have good sclerotic edges or
pseudocapsule
2) Marginal excision goes beyond the capsule
3) Wide local excision : removal of the Tm with wide margin of
normal tissue (IA)
For local malignant
4) Radical excision: removal of the entire bone or Muscle
compartment in which the tumor lies (IIA_ IIB ) with or
without amputation.
Reconstruction Surgery (limb salvage) Arthroplasty, allograft,
Arthrodesis. Amputation.
Chemotherapy
Radiotherapy: may be employed postoperatively when a marginal or Intralesional
excision has occurred, so as to ‘sterilize’ the tumor bed.
The main complications of this treatment are the occurrence of post-irradiation
spindle-cell sarcoma and pathological fracture in weight bearing bones, particularly in
the proximal half of the femur.
208 [BONE TUMORS]
01 Orthopedic Note
Benign Bone Tumors
Osteoid Osteoma 1) Incidence:
Age: 10 -35
Male to female ratio: 3/1
Site: cortex of long bone or cancellous bone
of spine
2) Pathology: The excised lesion appears as a dark-
brown or reddish ‘nucleus’ surrounded by dense
bone; the central area consists of unorganized
sheets of osteoid and bone cells.
There is no risk of malignant transformation.
3) Clinical features: Increasingly severe, well
localized, deep aching pain which worse at night
and eased by aspirin or NSAID (diagnostic)
On examination: Local bone tenderness
4) Imaging: sclerotic lesion in x-ray and
nidus(structure that resembles a nest - عش- ) in CT
5) Treatment: Complete removal or destruction of
the nidus.
Osteoblastoma This tumor is characterized by immature osteoid and
is more commonly located in the posterior elements
of the spine and occasionally the skull. They are
larger than osteoid osteoma. These can be aggressive
and have higher recurrence rate following curettage.
Chondroblastoma This tumoris rare tumor occurs between 5-25 years of
age, more commonly in the knee,hip and shoulder area.
The tumor usually involve physis and patient tend to
present with pain. The lesion is lytic with calcification
occuring in aproximately 50% of cases. Secaondary
aneurysmal bone may occure. They are aggressive benign
tumor but metastsis can occure (as giant cell tumor)
Chomdromyxoid Fibroma It occurs eccentrically in the metaphysic of proximal tibia.
Treatment includes curettage and bone grafting
Chondroma 1) Incidence: age: 15 – 50 age group
2) Pathology: there are 2 forms of chondroma
Enchondroma Ecchondroma (Periosteal Chondroma)
Incidences More common Less common
Growth Within the bone Expand the bone
and thins its cortex Outward from bone
Site
Long bones But over 50% in
small bone of hands and feet
Hands, feet, flat bones (e.g.: scapula
and ilium)
Size Large Malignant changes
Less More
Presentation Pathological fracture
Asymptomatic
1) Imaging: bone cortex thinning but no erosion
Multible enchondromata is rare and called
dyschondroplasia (ollier diseas), occurs in children
2) Treatment: often left alone. If it causes a fracture
or is unsightly it should be removed by curettage
and the defect filled with bone graft.
Osteochondroma 1) Incidence: commonest benign tumor of bone
Age: 10 – 20 age groups
2) Pathology: At operation the cartilage cap is seen
surmounting a narrow base or pedicle of bone. Large
lesions may have a ‘cauliflower’ appearance, with
degeneration and calcification in the centre of the
cartilage cap.
3) Clinical Features: circumscribed painless (usually)
hard swelling near the joint. It may become painful due
to pressure effect or formation of overlying
pseudobursa.
4) Imaging: mashroom like stalk of bony tumor
5) Treatment: the tumor should be excised if it causes
pain or enlarges after puberty and must be sent for
routine histological examination to exclude any
malignant change.
208 [BONE TUMORS]
00 Orthopedic Note
Hemangioma 1) Types:
a. Capillary Hemangioma: dark red, irregular,
slightly raised blotch on skin (port wine stain)
b. Cavernous Hemangioma (widely dilated vascular
channel with intervening connective tissue):
localize or diffuse tumor within the skin,
subcutaneous tissue or muscle
2) Clinical Features:
a. Symptom:
i. Cosmotic
ii. Symptom of thrombosis (pain and swelling)
iii. Elephantiasis: massive hemangioma in legs
b. Characteristic feature: compressible and vary
in size from day to day
c. Imagining: Variegated serpiginous appearance in
MRI . The x-ray shows coarse vertical
trabeculation (the so-called ‘corduroy
appearance’)
3) Treatment:
If operation is needed there is a risk of profuse
bleeding, and embolization may be useful.
Giant Cell Tumor 1) Incidence: Age: 20 – 40
About 10% of cases behave as malignant tumor
and metastasis occur through blood to lung
2) Pathology:
a. Sites: ends of long bone at which most growth
occur:
Lower end of femur
Upper end of tibia
It may occurs in the spine and sacrum
b. Growth: occupying epiphyseal region extending
to the joint surface. It destroy the bone
substance, but new bones forms beneath the
raised periosteum and pathological fracture
occur
c. Histology: mononuclear oval or spindle
shaped stromal cell interseprated with giant
cell (may contain as fifty nuclei which represent
fused conglomeration of oval or spindle shape
stromal cellm, which frequently show mitotic
figures)
3) Clinical Features:
a. Pain at tumor site
b. Tender firm swelling
c. Pathological fracture
4) Imaging: radiograph show lytic destruction of
bone substance, but no sclerotic rim or periosteal
reaction. The tumor tends to extend eccentrically
and as far as the articular surface of the bone.
5) Treatment:
Well-confined, slow-growing: treated by thorough
curettage and ‘stripping’ of the cavity with burrs and
gouges, followed by swabbing with hydrogen
peroxide or by the application of liquid nitrogen;
the cavity is then packed with bone chips.
Aggressive tumours: excision followed, if necessary,
by bone grafting or prosthetic replacement.
Tumours in awkward sites (e.g. the spine) :
supplementary radiotherapy
Lower end of radius
Upper of humerus
208 [BONE TUMORS]
02 Orthopedic Note
Malignant Bone Tumor
Osteosarcoma
(Osteogenic Sarcoma)
1) Incidence: Age :
Childhood and adolescence 10 – 30
Old age as a complication of Paget's disease
2) Pathology: Affects metaphysis of long bones, and
shows alternate areas of cavitations and dense areas.
Origin: primitive forming cell in the metaphysis
Sites: area where most active growth occurs in
long bones:
Lower end of femur
Upper end of tibia
Upper end of humerus
Growth: the tumor begins in the metaphysis and
destroys the bone structure and brusts into the
surrounding soft tissue. It is seldom cross the
epiphyseal cartilage into epiphysis.
Histology: it varies widely but there always will be
found areas of neoplastic new bone or osteoid
tissue that indicate the true nature of the lesion.
Characteristic spindle cells with a pink-staining
osteoid matrix; others may contain cartilage cells
or fibroblastic tissue with little or no osteoid.
Metastasis: early by blood, especially to the lung
2) Clinical Feature: local pain and swelling (With
minimal trauma). The overlying skin is warmer than
normal due to vascularity of tumor and the part may
be so distended by tumor appear starched and shiny
3) Imaging:
Plain radiograph irregular medullary and cortical
destruction of metaphysis. Later on cortex appear
to have been burst open. Periosteal reaction
(Codman triangle, sunray) maybe present.
Page 114
MRI: soft tissue extension
Radioisotope (technetium) scanning: skip lesion
CT chest: for lung metastasis
4) Classification: primary and secondary (following
Paget's disease, x-ray therapy)
5) Differential Diagnosis:
Subacute osteomyelitis
Chondrosarcoma
MFH
6) Treatment: limb sparing resection followed by
chemotherapy.
Chondrosarcoma
1) Incidence: Ages: 30 – 60 years old fourth and fifth decades male > female.
2) Pathology: A biopsy is essential to confirm the diagnosis.
Central Peripheral
Femur, tibia, humerus Flat bone
Arise without pre-existing lesion or from malignant
transformation of enchondroma especially
ollier disease
Arise from malignant transformation of osteochondroma
especially diphysial aclasis or multible
exostoses
Low-grade chondrosarcoma may show histological features no different from those of an aggressive benign cartilaginous lesion.
High-grade tumours are more cellular, and there may be obvious abnormal features of the cells, such as plumpness, hyperchromasia and mitoses.
3) Clinical features: Patients may complain of a dull ache or a gradually enlarging lump. Medullary lesions may present as a pathological fracture.
4) Imaging: X-ray changes comprise features of both a chondrosarcoma and a periosteal osteosarcoma: an outgrowth from the bone surface, often containing flecks of calcification, as well as ‘sunray’ streaks and new-bone formation at the margins of the stripped periosteum. The dominant cell type is chondroblastic.
5) Treatment: Surgical removal. Chemotherapy and Radiotherapy are not useful.
Giant cell tumor
Ewing tumor
Metastatic
208 [BONE TUMORS]
03 Orthopedic Note
Ewing's Sarcoma
(Endothelial Sarcoma of Bone)
1) Incidence: ages of 5 and 20 years,
2) Pathology:
Origin: endothelial element in diaphysis
Site: Usually in a tubular bone and especially in
the tibia, fibula, humerus or clavicle.
Metastasis: by blood to lungs and other bones
Macroscopically the tumor is lobulated and
often fairly large. It may look grey or red if
haemorrhage has occurred into it.
Microscopically, sheets of small dark
polyhedral cells with no regular arrangement
and no ground substance are seen.
3) Clinical Feature: pain in the middle of the bone
(often throbbing in character) and swelling. The
overlying skin is stretched and wormer
Generalized illness and pyrexia, together with a
warm, tender swelling and a raised ESR, may
suggest a diagnosis of osteomyelitis.
4) Imaging:
X-ray: ‘onion-peel’ effect.
CT and MRI: large extraosseous
component.
Radioisotope scans: multiple areas of
activity in the skeleton.
5) Differential Diagnosis: subacute osteomyelitis
and metastasis from suprarenal neuroblastoma
(Histologically)
6) Diagnosis: Biopsy is essential
7) Treatment: Surgery, radiotherapy and
multichemotherapy.
Myeloma
(Myelomatosis – Plastocytoma) 1) Incidence: aged 45–70 years old
2) Clinical features:
Symptoms: backache, bone pain or a
pathological fracture.
Hypercalcaemia may cause symptoms such as
thirst, polyuria and abdominal pain.
Clinical signs (apart from a pathological
fracture): are often unremarkable.
o Pale due to anemia
o Localized tenderness (no swelling) and
restricted hip movements could be due to a
plasmacytoma in the proximal femur.
o In late cases there may be signs of cord or
nerve root compression, chronic nephritis
and recurrent infection.
3) Investigation:
a. Lab investigation:
1. CBC: Mild anemia is common,
2. ESR: almost constant feature is a high
3. Blood chemistry: raised creatinine level and
hypercalcaemia.
4. Bence Jones protein in urine,
5. Serum protein electrophoresis: characteristic
abnormal band.
6. proteinurea
b. Imaging: x rays shows osteoporosis, and lytic
lesions.
c. A sternal marrow puncture may show
plasmacytosis, with typical ‘myeloma’ cells.
4) Pathology:
Origin: plasma cell of bone marrow
At operation the affected bone is soft and crumbly.
The typical microscopic picture is of sheets of
plasma-cytes with a large eccentric nucleus
containing a spoke-like arrangement of chromatin.
5) Bauer's Positive criteria for survival:
A solitary metastasis
No pathological fracture
No visceral metastases
Renal or breast primary
No lung cancer
208 [BONE TUMORS]
04 Orthopedic Note
Age Sites Clinical Features Imaging
Benign Bone Tumors
Osteoma 10 - 35 Pain worse at night and
relieved by NSAID
Plain x-ray: sclerotic thickening of shaft
CT: Nidus
Chondroblastoma 5 - 25 Knee Hip
Shoulder
Pain
Chondroma 15 - 50
Enchondroma: Long bones
Ecchondroma: Hands, feet, flat bones
Asymptomatic Pathological fracture
Bone cortex thinning but no erosion.
Osteochondroma 10 - 20 Growing epiphyseal
cartilage plate
Circumscribed hard swelling usually not
painful Mashroom like stalk
Giant Cell Tumor
20 – 40
Lower end of femur, Lower end of radius, Upper of humerus Upper end of tibia
Pain at tumor site Tender firm swelling Pathological fracture
lytic destruction of bone substance, but no sclerotic rim or periosteal reactio
Malignant Bone Tumors
Osteosarcoma
10 – 30 Old ages
Metaphysis of long local pain swelling
Plain radiograph irregular medullary and cortical destruction of
metaphysic and aggressive periosteal
reactions
Chondrosarcoma
30 - 60
Central: Femur, tibia, humerus
Peripheral: Flat bone
Dull ache Enlarging lump
Pathological fracture
Ewing's Sarcoma
5- 20
Tibia, Fibula
Humerus Clavicle
Pain in the middle of the bone Swelling
Myeloma
45 - 70 backache, bone pain or a pathological fracture
Osteoporosis, and lytic lesions.
208 [BONE TUMORS]
05 Orthopedic Note
Cyst (Tumor Like lesions)
Simple bone Cyst
(Solitary Bone Cyst - Umicameral Bone Cyst)
1) Incidence: Childhood, seldom in adult.
2) Pathology: The lining membrane consists of
flimsy fibrous tissue, often containing giant cells.
In an actively growing cyst, there is osteoclastic
resorption of the adjacent bone.
3) Imaging: X-rays show a well-demarcated
radiolucent area in the metaphysis, often extending
up to the physeal plate; the cortex may be thinned
and the bone expanded.
4) Treatment: Asymptomatic lesions in older
children can be left alone but the patient should be
cautioned to avoid injury. ‘Active’ cysts, those in
young children should be treated, in the first
instance, by aspiration of fluid and injection of
80–160 mg of methylprednisolone or autogenous
bone marrow.
Aneurysmal Bone Cyst 1) Incidence: At any age, more in young adults.
2) Pathology: When the cyst is opened it is found to
contain clotted blood, and during curettage there
may be considerable bleeding from the fleshy
lining membrane.
3) Histologically: the lining consists of fibrous
tissue with vascular spaces, deposits of
haemosiderin and multinucleated giant cells. The
appearances resemble those of giant-cell tumour.
Malignant transformation does not occurs
4) Imaging: X-rays show a well-defined radiolucent
cyst, often trabeculated and eccentrically placed.
5) Treatment: The cyst should be carefully opened,
thoroughly curetted and then packed with bone
grafts.Sometimes the graft is resorbed and the cyst
recurs, necessitating a second or third operation.
In these cases, packing with methylmethacrylate
cement may be necessary.
Localised Fibrous Dysplasia of Bone
(Monostotic Fibrous Dysplasia)
1) Introduction: Fibrous dysplasia is a developmental
disorder in which areas of trabecular bone are replaced
by cellular fibrous tissue containing flecks of osteoid
and woven bone. The most common sites of
occurrence are the proximal femur, tibia, humerus, ribs
and cranio-facial bones. It is associated with café-au-
lait patches on the skin and (in girls) precocious sexual
development (Albright’s syndrome)
2) Pathology: At operation the lesional tissue has a
coarse, gritty feel. The histological picture is of loose,
cellular fibrous tissue with widespread patches of
woven bone and scattered giant cells.
3) Imaging: radiolucent ‘cystic’ areas in the metaphysis
or shaft. The weightbearing bones may be bent,and
one of the classic features is the ‘shepherd’s crook’
deformity of the proximal femur.
4) Treatment: Small lesions need no treatment. Those
that are large and painful or threatening to fracture (or
have fractured) can be curetted and grafted.
Metaphysial Fibrous Defect
(Fibrous Cortical Defect)
(Non Ossifying Fibroma)
1) Incidence:
It is the commonest benign lesion of bone
Age group: Children.
2) Clinical features: Asymptomatic
3) Pathology: solid lesion consisting of unremarkable
fibrous tissue with a few scattered giant cells.
4) Imaging: oval radiolucent area surrounded by a thin
margin of dense bone. Views in different planes may
show that a lesion that appears to be ‘central’ is actually
adjacent to or within the cortex, hence the alternative
name ‘fibrous cortical defect’.
5) Treatment: Treatment is usually unnecessary. If the
defect is very large or has led to repeated fractures, it
can be treated by curettage and bone grafting
ORTHOPEDIC NOTE
208
Back Pain
P R A Y F O R U S
Hassan Al-Ahmadi Bandar Al-Rasheedi Fawaz Al-Khaldi
208 [BACK PAIN]
2 Orthopedic Note
Back Pain :
1. people have 80% chance to have back pain in their life at least one, 30% of the will
referred to orthopedics and only 0.5% will operated. That means the majority of back
pain does not mean serious problem and we can treat it with conservative management
2. 90% of back pain cases will resolved within 6 weeks.
3. We do not go for surgery unless the patient develop certain warning signs
4. It is very common problem.
5. Some patients go for chronic state where they became ??????(2:40)
6. Etiologies:
Idiopathic.
Disc pathology.
Trauma.
Degeneration (aging).
Infections.
Tumors.
And so many.
Disc Prolapse:
Very common.
Account for 1-3% as cause of back pain.
Peak incidence : 30-50 years.
Heavy weight lifting is associated with disc prolapse.
More common in smokers.
Anatomy:
most common site of disc prolapse is postro-lateral because
it is the weakest point.
If the prolapse in the postro-lateral position it will press on the
disc below and its nerve root( red circles)
But if the prolapse in far lateral the compression will be on the
same nerve root( black arrow and black circle).
Sometimes a local inflammatory response with edema
aggravates the symptoms.
208 [BACK PAIN]
3 Orthopedic Note
CLINICAL PRESENTATION:
1) The initial clinical presentation is pain due to tear in the
annulus.
2) The only outer part of the disc is innervated .
3) No innervation to the nucleus.
4) The pain will radiate to lower limbs.( the classical sign of a
disc prolapse.)
5) The patient may complains of sensory or motor deficient.
6) A large central rupture may cause compression of the cauda
equine and the symptom are loss of control of bowls and
urinary system (this case must not wait more than 24h for
surgery otherwise the availability to retain their urinary and bowl control will be lost).
7) The patient usually in pain and tenderness on the spin.
8) You must do sensory and motor evaluation in the lower limbs.
9) Special tests:
a) Straight leg raising test: for sciatic nerve.
b) Femoral stretch test: for femoral nerve.
10) Reflexes: deep tendon reflexes:
a) Patellar tendon reflex L4
b) Achills tendon reflex S1
208 [BACK PAIN]
4 Orthopedic Note
Investigations:
Plain X-ray:
1. To roll-out other possible causes like trauma or fracture.
2. See the secondary effect of disc prolapse like scoliosis or loss of
lordosis.
MRI: the gold standard for diagnosis disc prolapse.
1. To see if the prolapse affect the nerve root or not.
Treatment:
1. If there is no red flag signs the disc prolapse can be treated conservatively like : bed rest
analgesia, physiotherapy, muscle relaxants.
2. Surgery if there is red flag signs like: cauda equine syndrome, motor deficient, not
responding for conservative treatment more than 6 weeks, frequent attacks of sciatica.
Types of surgery:
• Discectomy:
1. Open.
2. Microscopic.
3. Endoscopic.
• Percutanouse:
1. Disc ablation.
The second common cause of back pain is Degerative etiologies:
• OA
• RA
• AS
These patients will present as:
1. Spinal canal stenosis.
2. Facet arthritis.
3. Deformity.
208 [BACK PAIN]
5 Orthopedic Note
Spinal canal stenosis:
You must know is the stenosis central or peripheral because the symptoms and
treatment will differ.
Etiology: 1.Congenital
1.Developmental
2.Achondroplasia
2.Acquired
a. Degenerative: Spondylolisthetic worse
if imposed on a developmental narrowing.
b. Disc Herniation.
c. Degenerative & Disc Herniation.
d. Degenerative & congenital.
3.Others:
a. Paget's.
b. Spinal tumor.
c. Infection (TB).
d .Post-surgery.
e .Trauma.
1. Central stenosis:
neurogenic claudication. (from compression on the cauda equina).
Feel heaviness start from proximal to distal and relief by sitting.
increased unsteadiness or loss of balance.
feeling better if they walk stooped forward because the spinal canal get widened.
Rarely - urinary incontinence & cauda equina syndrome.
2. Foramina stenosis:
Radicular signs from narrowing of the lateral recess or the neural foramen. (like sciatica
nerve pain).
Physical examination can be unimpressive in patients with central stenosis.( you find nothing).
Some time you need to do Stress Test = walk until symptoms occur or ask the patient to come if
he has the symptoms.
Check distal pulses to screen for vascular causes of claudication.
208 [BACK PAIN]
6 Orthopedic Note
Investigation:
1. X-ray: bone spurs, decreased disc height and facet hypertrophy in older patients.
2. CT: (gold standard for evaluating degenerative diseases):
It gives the relationship between the bone and spinal cord.
The spinal canal normally 15mm in the lumber spine.
anything less than 10 mm AP diameter = absolute spinal stenosis and need
surgery.
3. MRI: to see the tissues around the disc.
4. Myelogram: inject the dye inside spinal canal like in the LP(it is dynamic processes).
Treatment:
Non-Operative:
• NSAIDs
• Muscle relaxants
• Antidepressants for chronic radicular pain.
• Epidural & nerve root block steroid injections - good long-term relief in patients with
foramenal or lateral recess stenosis
• Physiotherapy
• (with massage, ultrasound, TENS, braces or supports, acupuncture,
biofeedback, hot or cold packs, traction, or manipulation) can offer
symptomatic calcitonin.
Operative:
Indications:
1. Severe neurological symptoms.
2. Failed conservative treatment + impaired ADL (activities of daily living).
Depend on the cause is it central or peripheral stenosis.
In central stenosis we can do laminectomy and in foramina stenosis we remove the
articular surface.
208 [BACK PAIN]
7 Orthopedic Note
SPINAL INFECTION :- - The axial skeleton accounts for 2–7 per cent of all cases of osteomyelitis. - Predisposing factors include : DM , malnutrition, substance abuse, (HIV),malignancy, long-term use of steroids, renal failure , septicaemia and in IV drug addicts (pseudomonas) .
PYOGENIC OSTEOMYELITIS
- Acute pyogenic infection of the spine is uncommon. - it may resemble tuberculous spondylitis clinically and radiographicall ,but in OSTEOMYELITIS runs a more acute course
- 70 % arise from UTI, chronically ill, elderly. Due to Batson's venous plexus = communication between. pelvic & vertebral plexus.
Pathology :-
- Staphylococcus aureus is most common cause , but in immunosuppressed patients Gram-negative organisms such as E. coli and Pseudomonas are the most common( Also > candida and coccidiomycosis ) . - The usual sources of infection are: (1) haematogenous spread from a distant focus of infection or (2) inoculation during invasive procedures - there is destruction of the intervertebral disc and erosion of adjacent bone .It may also spread along the anterior longitudinal ligament to an adjacent vertebra, or into the paravertebral soft tissue ( from the thoracic spine along the psoas to the groin / and from the lumbar region to the buttock, the sacroiliac joint or the hip. ) - The spinal canal is rarely involved ( epidural abscess ), which is a surgical emergency! - Commonest site : T10
Clinical features:-
- Often there is a significant delay in diagnosis (6-12 weeks).
- The predominant findings are local pain with restriction of all movement by muscle spasm .
- Triad = fever + back pain + tenderness
- There may also be point tenderness over the affected vertebra. - A careful history and general examination are essential to exclude a focus of infection (skin, ENT, chest, pelvis).
208 [BACK PAIN]
8 Orthopedic Note
- lumbar spine is the area most often affected - uncommonly cause paralysis . while thoracic & cervical regions , are affected less often but have a higher incidence of paralysis.
- Systemic signs such as pyrexia and tachycardia are often present but not marked.
Diagnosis :-
- Has to be mainly differentiated from tuborculous spondylitis ( relative acute onset , history of pre-existing infection or septic focus, pyrexia , leukocytosis and identification of the organism ) are the main diagnostic criteria of PYOGENIC OSTEOMYELITIS
Investigation :- 1) X-rays may show no change for several weeks. Early signs are :
loss of disc height
diminution of disc space
local erosion of bone
Reactive new bone formation.
Soft-tissue swelling may be visible.
The early loss of disc height distinguishes vertebral osteomyelitis from metastatic disease, where the disc can remain intact despite advanced bony destruction.
Well …. the this box from dr. slide !!
2) Percutaneous CT guided needle biopsy - positive in 68-86% of cases; ( infections of
upper cervical spine & sacrum are not safely accessible to needle aspiration; do stains for AFB & fungi )
3) MRI : Very sensitive & specific (for differentiating from tumour). Can detect it early [however , in Apley it was highly sensitive but not specific ]
Similar features may be seen in discitis. Needle biopsy may help with diagnosis, but
often no organism is found. Other investigations : A- The white cell count is usually elevated B- C-reactive protein (CRP) level usually elevated C- ESR : usually elevated .Also used to follow treatment ( gallium scans can also be used ) D- Antistaphylococcal antibodies may be present in high titres.
A. 2 weeks - disc space narrowing (infections involving vertebral bodies frequently extend into & destroy adjacent Intervertebral discs; usually two vertebral bodies and a disc space affected)
B. 6 weeks - erosion vertebral body endplate; osteolysis
C. 8 weeks - reactive screrosis due to trabecular collapse
D. 12 weeks - new bone formation is noted
E. 6-12months - intervertebral fusion - usually signifies a resolution of process
208 [BACK PAIN]
9 Orthopedic Note
E- Blood culture is essential in patients who are febrile and If the result is negative a closed needle biopsy is performed for bacteriological culture and tests for antibiotic sensitivity F- Serological studies for Salmonella and Brucella should be performed, especially in endemic regions and in patients who have recently visited these areas.
Treatment :-
- Treatment is started on the basis of a clinical diagnosis of infection and includes : bed rest, pain relief , intravenous antibiotic for 2 weeks ; - if there is a good response (clinical improvement, a falling CRP and ESR. and a normal white cell count), oral antibiotics are then used for a further 3 months - Operative treatment is seldom needed. The indications for surgery :
Failure to obtain a positive yield from a closed needle biopsy and a poor response to conservative treatment;
Need for open biopsy
If neurology is not settling
Paraspinal or epidural abscess
Instability due to vertebral collapse
Prognosis :-
- The outcome is usually favourable. Spontaneous fusion of infected vertebrae is a common radiological feature of healed staphylococcal osteomyelitis. - Good Prognostic signs:-
1. age less than 60 years 2. normal immune status 3. decreasing ESR 4. Staph aureus infection
208 [BACK PAIN]
01 Orthopedic Note
Tumors:
Tumors is the 4th common cause of back pain.
Classification:
Primary: primary tumors and are rare. They can either be benign or malignant .
Secondary: secondary or metastatic tumor results from spine cancer originating in another part
of the body. This is a malignant tumor and is classified by its location in the spine (cervical,
thoracic, lumbar or sacrum). The types of cancer that most frequently lead to a spine tumor
include:
a. Thyroid
b. Breast
c. Prostate
d. Kidney
e. Bowel
Clinical Presentation
• Age :specially old ages
• Night pain : The most common symptom of a spine tumor .
• Weight loss
• Neurological signs
Investigation: X-ray : shows tumor that arise from the bones of the spine or eroding the bone from outside.
CTscan : show small tumors and bone destruction
MRI : for soft tissues involvement and if the is any compression
Treatment:
Depending of the type of tumor.
• Surgical: Excision, Fusion ,Instrumentation.
• Non surgical: if the stability is not compromised like lymphoma treated with
chemotherapy , or like multiple myeloma by radiotherapy.
208 [BACK PAIN]
00 Orthopedic Note
DISCITIS
is an infection in the intervertebral disc space that affects different age groups, but usually spontaneously affects children under 8 years of age
Infection limited to the intervertebral disc is rare and when it does occur it is usually due to direct inoculation .
More common in children
Clinical features:- With direct infection there is always a history of some invasive procedure. Acute back
pain and muscle spasm . Systemic features are usually mild
In children the infection is assumed to be blood-borne. There may be a history of a flu-like illness followed by back pain, muscle spasm and severe limitation of movement.
Investigations :- CRP , ESR are elevated.
WBC sometimes normal and the patient is apyrexic
X-rays, radioscintigraphy and MRI show the same features as in pyogenic spondylitis.
Treatment :-
Prevention is always better than cure. Following an injection into the disc, a broad-spectrum antibiotic should be administered intravenously.
Non-iatrogenic discitis is usually self-limiting.
During the acute stage : bed rest , analgesics and IV antibiotic are essential. If symptoms do not resolve rapidly, a needle biopsy is advisable.
Surgical evacuation or decompression indicated Only if there are signs of abscess formation ,cord or nerve root pressure ( rarely )
Spondylolysis :- ( briefly )
it is defined as a defect in the pars interarticularis of the vertebral arch (the pars interarticularis is detached and there is a separation of the joints. )
It may be caused by stress fracture or injury
Clinically , spondylolysis usually symptomless ( without displacement ) but may cause back pain .
If displacement occur , this will lead to spondylolisthesis.
208 [BACK PAIN]
02 Orthopedic Note
SPONDYLOLISTHESIS - Spondylolisthesis is the anterior or posterior displacement of a vertebra or the vertebral column in relation to the vertebrae below . - The shift is almost always between L4 and L5, or between L5 and the sacrum. Displacement usually forwards , and it is rarely occurring backwards ( retro-spondylolysthesis) - Normal discs, laminae and facets constitute a locking mechanism that prevents each vertebra from moving forwards on the one below. Forward shift (or slip) occurs only when this mechanism has failed.
Classification :-
1- Dysplastic :
- The superior sacral facets are congenitally defective; slow forward slip leads to severe displacement and is often associated with more severe neurological deficits. It is difficult to treat because the posterior elements and transverse processes tend to be poorly developed, leaving little surface area for a posterolateral fusion.
Associated anomalies (usually spina bifida occulta) are common. 2- Lytic or isthmic [ commonest ] :- - In this, there are defects in the pars interarticularis as in ununited fracture (spondylolysis), or repeated breaking and healing may lead to elongation of the pars. This causes the body and the superior articular process ( and the whole spinal column above it ) to slip forwards leaving behind the laminae and the inferior articular process in normal relation with the sacrum .
The defect is usually present by the age of 7, but the slip may appear some years later.
Often runs in families, and is more common in certain races, notably Eskimos; and the incidence increases with age . The condition is more common in those whose spines are subjected to extraordinary stresses (e.g. competitive gymnasts and weight-lifters).
3- Degenerative [ pseudo SPONDYLOLISTHESIS ] : - Degenerative changes in the ( posterior ) facet joints & the discs and osteophyte formation permit forward slip despite intact laminae (it can occur at any level but almost always at L4/5 and mainly in middle age women ) .
In this type displacement is occasionally backwards rather than forwards but in either case displacement is not severe and so the neurological disturbance
Many of these patients have generalized osteoarthritis and pyrophosphate crystal arthropathy.
208 [BACK PAIN]
03 Orthopedic Note
4- Post-traumatic : Unusual fractures may result in destabilization of the lumbar spine. 5- Pathological : Bone destruction (e.g. due to tuberculosis , neoplasm , Paget's or metabolic diseases ) may lead to vertebral slipping. 6- Postoperative (iatropathic) : Occasionally, excessive operative removal of bone in decompression operations results in progressive spondylolisthesis.
Clinical features :- 1) Spondylolysis , and even spondylolisthesis, may be discovered incidentally during routine
x-ray examination.
2) With slipping there may be pressure on the dura mater and cauda equine , or on the nerve roots; these roots may also be compressed in the narrowed intervertebral foramina.
3) Disc prolapse is liable to occur and Sciatica may occur in one or both legs.
4) In children the condition is usually painless. In adolescents and adults backache is the
usual presenting symptom; it is often intermittent, coming on after exercise or strain. coughing and sneezing can intensify this pain .
5) Patients aged over 50 are usually with degenerative spondylolisthesis. They always have
backache, some have sciatica and some present because of claudication due to spinal stenosis.
6) the buttocks look curiously flat, and transverse loin creases are seen.
7) A ‘step’ can often be felt when the fingers are run down the spine.
8) Movements are usually normal in the younger patients but there may be ‘hamstring
tightness’; in the degenerative group the spine is often stiff.
Radiological studies :- - X-ray : Lateral / oblique views show the forward shift of the upper part of the spinal column on the stable vertebra below; elongation of the arch or defective facets may be seen. - However , CT scan is better .
Prognosis :- - Dysplastic spondylolisthesis appears at an early age, often goes to a severe slip and carries a significant risk of neurological complications. - Lytic (isthmic) spondylolisthesis with less than 10% displacement does not progress after adulthood, but may predispose the patient to later back problems. It is not a contraindication to strenuous work unless severe pain supervenes . With slips of more than 25 % there is an increased risk of backache in later life. - Degenerative spondylolisthesis progresses slowly and seldom exceeds 30 % .
208 [BACK PAIN]
04 Orthopedic Note
Treatment :-
- If there are no symptoms , no treatment is required . - Moderate symptoms are often relieved with Conservative treatment, similar to that for other types of back pain ( physiotherapy / NSAID / ……) - Operative treatment is indicated: (1) if the symptoms are disabling and interfere with work and recreational activities; (2) if the slip is more than 50 per cent and progressing; (3) if neurological compression is significant.
For children, posterior intertransverse fusion in situ is almost always successful; if neurological signs appear, decompression can be carried out later.
For adults, either posterior or anterior fusion is suitable.
However, in the ‘degenerative’ group, where neurological symptoms predominate, decompression without fusion may suffice.
Fusion of the spine is normally done by bridging the vertebrae with Bone graft ( usually abtained from ilium )
208 [BACK PAIN]
05 Orthopedic Note
Red flags for possible serious spinal pathology :-
• Presentation under age 20 or onset over 55
• Thoracic pain • Past hx of carcinoma, steroids • Unwell, weight loss • Widespread neurology • Structural deformity • Abnormal blood parameters.
APPROACH TO DIAGNOSIS IN PATIENTS WITH LOW BACK PAIN The following is a suggested approach to more specific diagnosis.: Careful history taking and examination will uncover one of five pain patterns: 1. Transient backache following muscular activity : This suggests a simple back strain that will respond to a short period of rest followed by gradually increasing exercise. People with thoracic kyphosis or fixed flexion of the hip, are particularly prone to back strain because they tend to compensate for the deformity by holding the lumbosacral spine in hyperlordosis. 2. Sudden, acute pain and sciatica :
A. In young people (those under the age of 20) it is important to exclude infection and spondylolisthesis; both produce recognizable x-ray changes.
B. Patients aged 20–40 years are more likely to have an acute disc prolapse: diagnostic
features are: (1) a history of a lifting strain, (2) unequivocal sciatic tension; (3) neurological symptoms and signs.
C. Elderly patients may have osteoporotic compression fractures, but metastatic disease and
myeloma must be excluded. 3. Intermittent low back pain after exertion: Patients of almost any age may complain of recurrent backache following exertion or lifting activities and this is relieved by rest. In early cases x-rays usually show no abnormality; later there may be signs of lumbar spondylosis osteoarthritis of the facet joints. 4. Back pain plus pseudoclaudication : These patients are usually aged over 50 and may give a history of previous, longstanding back trouble. The diagnosis of spinal stenosis should be confirmed by CT and/or MRI. 5. Severe and constant pain localized to a particular site : This suggests local bone pathology, such as a compression fracture, Paget’s disease, a tumour or infection.
ORTHOPEDIC NOTE
208
Ligamentous Injury
P R A Y F O R U S
Jehad Abdullah AL-Saihati Louai Hassan AL-Khalaf
208 [LIGAMENTOUS INJURY]
2 Orthopedic Note
Definition of Ligament:
Ligaments link bones to other bones and provide supports to joints.
Ligaments are classified as dense connective tissue, and they consist of a
protein substance called collagen.
Normal collagen consists of:
- 90% type 1 collagen.
- 9% type 3 collagen.
- 1% fibroblast cells (the cells that produce collagen).
Patella
Patellar tendon connects quadriceps muscle to the fibula.
Patellar tendon is connective tissue
(sometimes they call it as a ligament) in which
it connects 2 bones and it is 99% consists of
type 1 collagen.
The patella is a sesamoid bone that is located
within the tendon (the largest sesamoid bone
in the body)
Function of the patella is protection of the
quadriceps tendon.
Absence of the patella will lead to a friction
between the bone (femur and fibula) and the
tendons (patellar & quadriceps)
208 [LIGAMENTOUS INJURY]
3 Orthopedic Note
strain sprain partial Complete Type
Stable joint.
There is high signal intensity on MRI.
No disruption of fibers.
Stable joint.
While he is going down stairs.
Swelling only.
No radiological findings.
Soft tissue injury.
Stable joint.
Damage is less than 50%.
There are Clinical findings & MRI findings (High signal intensity).
Does not need any surgical intervention
Instability of the joint.
More than 50% of the joint is damaged.
Clinical findings & MRI findings. (High signal intensity)
Surgically corrected
Fea
tures
Grading of sprain:
Grade 1 sprain: there is damage to a few collagen fibers, producing a
local inflammatory response. This is characterized by pain over the
affected ligament.
Grade 2 sprain: there is damage to a more extensive number of collagen
fibers. This produces a more marked inflammatory response
characterized by intense pain ant joint effusion (swelling).
Grade 3 sprain: the damage to collagen fibers is such that there is a
complete rupture of the ligament. This produces intense pain, joint
effusion and marked joint Instability. Surgery may be necessary to restore
joint stability.
The Repair Process
Inflammatory Phase:
The inflammatory phase follows trauma to collagen fibers and lasts for 3-5 days
Repair Phase:
The repair phase is mediated by blood clotting over the damaged tissue.
Blood platelets from a mesh to initiate healing. Also present in the blood
clot are fibroblast cells, which proliferate and begin to lay down type 3
(immature) collagen tissue, between 3-21 days after the injury.
208 [LIGAMENTOUS INJURY]
4 Orthopedic Note
Remodeling phase:
The remodeling phase follows the repair phase and can last for up to a year.
It involves maturation of collagen tissue from type 3 to type 1 and
realignment of collagen tissue.
Knee
208 [LIGAMENTOUS INJURY]
5 Orthopedic Note
Anterior Cruciate ligament:
Most crucial ligament injuries occur without contact (twisting injury). The
foot is fixed with internal rotation while the rest of the body is externally
rotated which will lead to complete rupture of the ligament.
Clinical presentation:
Severe swelling
Severe pain
Limitation of movement
Special test:
Lachmann Test of the Knee:
It is for anterior translation of the tibia.
Flexion of the knee at 90 degree, then anterior
withdrawal test of both right and left sides and
we check for any asymmetry.
The teared ligament will show prominent
anterior translation.
Management:
Surgical reconstruction of the ligament maintains stability to prevent further
damage of other:
Ligaments
Meniscus
Cartilage
If not treated, it may cause repeated twisting of the ligament, which will lead to:
severe osteoarthritis after 5 years
complete damage to the knee joint after 30 years
208 [LIGAMENTOUS INJURY]
6 Orthopedic Note
The surgical intervention for ACL is done only by the replacement of the
ligament by:
Allograft: (No risk of rejection.) OR
Autograft:
Mid third of the patellar tendon + bones from
both patella and tibia. (bone- tendon- bone )
Semi tedinosis and gracilis tendon
Advantages of Autograft (semi tedinosis and gracilis tendon):
Stronger.
Small incision.
Less bleeding.
Less complication.
Less than 1% risk of getting HIV or Hepatitis.
N.B. slow healing process and needs longer time for rehabilitation.
Posterior Cruciate Ligament: PCL
It is caused by Dash board injury in which the "Tibia" goes back.
Management:
Mainly conservative.
Surgical intervention is needed in:
o Avulsion: intact tendon with broken bone at the
end of the tendon.
o Clear instability: (usually identified by the
patient).
o Multiple ligament injury.
208 [LIGAMENTOUS INJURY]
7 Orthopedic Note
Medial Collateral Ligament: MCL
Isolated injury commonly happens when the there is a direct injury from
the lateral side.
Special test:
Valgus stress test.
Can be done at 0° or 30°.
30° is more specific, because at 0° the knee joint
is locked by the capsule and ACL.
Management:
Mainly conservative.
Needs surgical intervention if there is avulsion.
Lateral Collateral Ligament: LCL
Special test is by varus stress test.
Management::
Surgical intervention:
Repair.
Reconstruction.
208 [LIGAMENTOUS INJURY]
8 Orthopedic Note
SHOULDER
Anterior shoulder dislocation
Most common injury in handball players.
Most commonly affect: Anterior Inferior
Glenu-Humeral Ligament (AIGHL).
Clinical Presentation:
Severe pain.
Can't move his hand.
Holding his arm near his chest.
Management:
Younger age group(20-25 years) :
o We prefer to treat him surgically because if we try to do a
close reduction of the joint there will be high rate of
recurrence (80%) (because young patients are very active)
N.B 2nd injury usually happens with minimal injury than the 1st one
Elderly patients ( >50 years)
o Usually treated with close reduction due to low recurrence
rate (about 20%)
208 [LIGAMENTOUS INJURY]
9 Orthopedic Note
Ankle Joint
The most common injury occurs at the
Inversion & Planter flexion.
The stress will be on
Anterior Talofibular ligament.
Management:
The first thing is to do X-ray to the foot.
Then RICE:
o Rest.
o Ice.
o Compression.
o Elevation.
99% of cases are managed
conservatively.
ORTHOPEDIC NOTE
208
Arthroscopy &
Arthrocentesis
P R A Y F O R U S
Hassan Ibrahim Al-Hammadi Ahmed Maitham Al-Nasser
208 [ARTHROSCOPY & ARTHROCENTESIS]
2 Orthopedic Note
Introduction:
- DDeeffiinniittiioonn: endoscopic procedure for: visualization & operating
on intra-articualr structures of different joints
- performed for: diagnostic & therapeutic reasons
- Almost all joints can be reached (but most useful in: hip, ankle, wrist, knee, shoulder)
- it's invasive procedure (→ shouldn't be used as alternative to: examination & imaging)
Technique:
instrument:
- Arthroscope= rigid telescope, fitted with fibreoptic illumination
- Tube diameter= [2mm (for small joints) – 5mm (for knee)]
- it carries lens system → magnified image
- eyepiece: for direct viewing
procedure:
- best carried out under General Anesthesia→ muscle relaxation → better manipulation
- joint is distended, with fluids & arthroscope is introduced, per-cutaneously
- various instruments (e.g. probes, forceps, curettes) can be inserted through skin portals;
to expose less accessible joint parts or to obtain biopsy
- it's guided by image, on monitoring
- at the end: joint is washed out & small skin wounds are sutured
Note: patient can go home late the same day
Advantages:
- small: incision & scars - ↓complication rate
- Rapid recovery - improved Dx
Disadvantages: few e.g.
- need experience - equipments - expensive
Diagnosis:
1) Knee:
- Most accessible joint
- Appearance of synovium & articular surfaces will differentiate between:
inflammatory (& non-inflammatory), destructive (& non-destructive) lesions
- Uses: meniscal tears, cruciate ligament deficiency,
osteo-cartilaginous fractures, cartilaginous loose bodies & synovial tumors
2) Shoulder:
- More difficult
- But can explore: articular surfaces & glenoid labrum
- Uses: rotator cuff lesions
lateral position atient is inP
SCOPY-ARTHRO
208 [ARTHROSCOPY & ARTHROCENTESIS]
3 Orthopedic Note
3) Wrist:
- useful in: triangular fibro-cartilage tear & inter-osseous ligament ruptures
4) Hip:
- Less widely used
- But useful in diagnosing un-explained hip pain
- Examples: labral tears, synovial lesions, loose bodies & articular surface damage
(accuracy >50%)
Contra-indications:
- few
- e.g. :
o joint Ankylosis
o skin infection
o joint Deformity
Complications:
- Safe
- But Not entirely free of complications e.g.:
o Thrombo-phlebitis (DVT <1%)
o Hemo-arthrosis
o Infection (<1%)
o joint Stiffness
o Algo-dystrophy (following arthroscopy)
in selected cases exceptindication (to avoid compartment syndrome) -is a contra Trauma
208 [ARTHROSCOPY & ARTHROCENTESIS]
4 Orthopedic Note
Definition:
= needle insertion, into joint (for: aspiration or injection)
#It's Aseptic procedure
Indications: Diagnostic & Therapeutic
Contra-indications:
- Skin: infections, lesions & cellulitis
- Bacteremia & Osteomyelitis
- Coagulopathy
Complications: .
- Injury - skin Infection
- Hemoarthrosis
CENTESIS-ARTHRO
.tttSeptic Arthritis
*Antibiotics (for 6weeks)
*Debridement (don't await
culture & sensitivity)
Notes about needle used
is best)gauge=18 : use the largest (Size*
(5mm thickness)patellar -lateral mid: Site*
*Debridement (don't await culture & sensitivity)
small are for
Local Anesthesia
208 [ARTHROSCOPY & ARTHROCENTESIS]
5 Orthopedic Note
Synovial Fluid Analysis:
Types:
- Normal
- Inflammatory (RA) - Non-inflammatory (OA)
- Septic
- Blood
Basic Tests:
- e.g. Septic Arthritis: ↓Glucose & ↑Protein, ↑LDH
#even –ve culture & sensitivity
Characteristics:
- Normal: ↑viscosity
- RA: ↓viscosity & ↑volume
ORTHOPEDIC NOTE
208
Arthroplasty
P R A Y F O R U S
Alawi M. Al-Khadrawi Mouayd M. Al-Shakhal
208 [ARTHROPLASTY]
2 Orthopedic Note
Arthroplasty
What is it?
Arthroplasty is the surgical refashioning by realigning or reconstructing a dysfunctional joint., aims to relieve pain and to retain or restore functional range of motion (F.R.O.M) .
What joints?
Hip (intracapsular fracture)
Shoulder (in multi-fragmentary fracture of proximal humorous and unsalvageable by internal fixation; can be treated by hemi-arthroplasty)
Elbow
Knee
Spine (disk replacement)
IPJ (Interphalangeal Joints)
What are the types of arthroplasty?
Arthroplasty The main
varieties as applied to the hip
joint: (a) excision
arthroplasty (Girdlestone);
(b) partial replacement – an
Austin Moore prosthesis has
been inserted after removing
the femoral head; (c) total
replacement – both articular
surfaces are replaced.
• Excision arthroplasty – Sufficient bone is excised from the articulating parts of the joint to
create a gap at which movement can occur (e.g. Girdle- stone’s hip arthroplasty). This movement
is limited and occurs through intervening fibrous tissue, which forms in the gap. In some
situations, e.g. after excising the trapezium, a shaped ‘spacer’ can be inserted; this is often tendon
harvested from nearby.
• Partial replacement – One articulating part only is replaced (e.g. a femoral prosthesis for a
fractured femoral neck, without an acetabular component); or one compartment of a joint is
replaced (e.g. the medial or lateral half of the tibiofemoral joint). The prosthesis is kept in
position either by acrylic cement or by a press-fit between implant and bone.
• Replacement – Both the articulating parts are replaced by prosthetic implants; for
biomechanical reasons, the convex component is usually metal and the concave high-density
polyethylene. Metal-on- metal replacements are also becoming more common. Irrespective of
type, these components are fixed to the host bone, either with acrylic cement or by a cementless
press-fit technique.
(a) (b) (c)
208 [ARTHROPLASTY]
3 Orthopedic Note
The advantages of prosthetic replacement over internal fixation:
Earlier full weight-bearing
Prevention of non-union
Avoiding avascular necrosis
Elimination of failure of fixation.
The disadvantages:
More extensive procedure.
Increased blood loss.
Increase the risk of prosthetic dislocation.
Indications
Painful disabling arthritic joint no longer responsive to adequate conservative
management .
1. Relieve pain
2. Restore f.r.o.m (Functional Range of Motion) => ( motion with stability )
3. Correct deformity .
Conditions indicating arthroplasty:
Severe OA (Osteoarthritis; in which conservative management is not enough)
Inflammatory Arthritis (e.g. SLE, R.A ..)
AVN (Avascular Necrosis of the femoral head)
Fracture
Failed reconstruction
Tumor
failed Arthrodesis
What are the causes of Avascular necrosis of the femoral head?
1- Idiopathic
2- Trauma (fractures)
3- Hip dislocation
4- Alcoholism
5- Cushing's syndrome (Fat infiltration fat embolization)
6- Fat embolization (e.g. Fractures)
7- Sickle cell disease (in middle east), Perthes disease (in Caucasians)
8- SLE , RA (Systemic Lupus Erythmatosous ; Rheumatoid arthritis)
9- Caisson disease (Decompression disease or Divers' disease)
208 [ARTHROPLASTY]
4 Orthopedic Note
Contraindications
1. Recent or current sepsis (Infection) -Most Important-
2. Age (relative) . Skeletal immaturity (absolute).
3. Muscle or neurological weakness (abductor, extensor)
4. General condition
5. stable arthrodesis- prospects of a successful arthroplasty are not good, a constrained
prosthesis is usually required, in the event of failure rearthrodesis may not succeed
6. Non ambulators
7. Neuropathic joint (controversial)
Preoperative preparation & assessment
I. History :
- Pain from involved joint!
- Is it indicated for Arthroplasty?
- Hx of other diseases (DM/HTN/MI/Hematological Disorders/Prostate disease)
- Past history (Medical & Surgical)
II. Physical Examination & evaluation; especially general and local joint examination
III. Investigations : "Memorize it like your name"
-CBC, ESR, CRP, UA/C, RBS
-CxR, ECG, PT, PTT, RFT, LFT
-RADIOLOGICAL: AP pelvis
AP hip centered (rotation) & lateral
IV. Templating & planning
V. Cross-match blood ( consider autologous)
VI. Prophylactic Antibiotic (given before inflating the tourniquet)
VII. Prophylactic Antithrombotic + mechanical.
VIII. Informed consent
IX. Preparation of surgical Site (mark / wash chlorhexidine / shaving)
Aims & Technical goals
1. Restore Mechanical Alignment
2. Maintain Good Soft Tissue Balance
3. Maintain Joint Line Level
208 [ARTHROPLASTY]
5 Orthopedic Note
Fixation Types "Very Important "
How to fix the implant to the bone ?
1. Cement (PMMA; Polymethyl methacrylate acid) => Total knee Replacement
2. Biological (Hydroxyapatite; stimulate bone on-growth) => Femur , acetabulum
3. Press fit => for acetabulum fixation
4. Screws => Hold: Acetabulum-hip , Knee
Commonest Fixation method is : Cement
Commonest fixation method of total knee replacement is: PMMA Cement
Commonest fixation method of Acetabulum are: Biological & Press fit
COMPLICATIONS
Intraoperative Complications
Nerve Injury
Vascular injury
Postoperative Complications
Infection
** Infection: commonest cause of hip replacement failure in sickle cell
disease**
Wound healing problem
DVT (deep venous thrombosis)
Pulmonary embolism
Urinary tract infection
Urinary retention
Dislocation (commoner in the hip more than the knee).
Lower Limb discrepancy (Associated with Hip replacement, not with knee r.)
**lower limb discrepancy is NOT a complication of total knee
replacement**
Decrease Quadriceps Power (in total knee replacement)
Decrease R.O.M (Range of Motion)
Periprosthetic fracture: (e.g. patellar problem: patellar maltracking, patellar
fracture, patellar loosening
Loosening
**Loosening (commonest cause of hip replacement failure)**
References:
1. Dr. Al-Omran A.S. lecture. (31/3/2012)
2. Apley's system of orthopaedics and fractures 9th edition 2010.
3. Bailey's and love's short practice of surgery 25th edition.
ORTHOPEDIC NOTE
208
Prosthesis And
Amputation
P R A Y F O R U S
Ali H Buzaid Ahmed Al-Khalifah.
208 [PROSTHESIS AND AMPUTATION]
2 Orthopedic Note
Implants
Known problem of implantation:
Stress riser: a focus point of stress on an implanted orthosis is very likely to be its point
of failure [Fracture]
o Upper and lower limits of internal Fixation device.
o Lower limit of hip prosthesis.
o Tumor
o Above or below a united fracture.
The problem was due the difference between the material and the bone elasticity . so
they develop ‘isoelastic’ implant.
Holes: drilling the hole produce Stress riser . but with screw it weakens it much less .
Materials:
The ideal material would be : Insoluble,Strong, non-toxic, non-carcinogenic , non-
irritant.
1. Metals
2. Plastic: High density plyethylene [HPD]
3. ceramics
Fixation:
Bone turn over regularly [ so after a year the implant is attached to a different bone]
leading to :
1. Loosening
2. Wear particles.
3. Foerign body reaction
The implants are Fixed to the skeleton in 4 ways:
1. Tight fit.
2. Mechanically with screws.
3. Bone cement.
4. Bone ingrowth.
208 [PROSTHESIS AND AMPUTATION]
3 Orthopedic Note
Introduction:
Orthotic:
A device applied directly and externally to the patient’s body [normal or diseased] for support.
Like brace or splint while prosthesis is a device to replace an amputated part of the body.
• used to control motion & function of body segments : CAN reconstruction , Fixation
of the spine to support the fixation or prevent stiffness to preserve the functionality by
placing a functional brace providing movement and stability [ex: knee in cemen]
• Compensate for a disorder & reduce handicap for biomechanical (& psychological)
reasons. (ACL):
• Preserve good range of motion.
• Prevent later deformity while the nerve regenerate.
• Orthoses rely on 3 point fixation .
• Named according to the joints over which they pass (eg. Knee Ankle Foot Orthotses)
depend upon the joint it crossover.
Materials used:
Cloth material
Fiproplast material.
Types:
Thermoplastic : if you want made a custom brace [modeling]
Thermoforming plastics - soften when reheated & rigid when cooled
Thermosetting:
Thermosetting plastics - mix liquid + catalysts to form model . it going to be
hard all the time no matter heat or cold.
TREATMENT OBJECTIVES:
FUNCTIONAL + BIOMECHANICAL
• To rest a joint or fracture in a chosen position.
• To correct, prevent or support a fixed deformity. [In case of wrist drop .. use splint]
• Control ROM of joints and direction during activity. Mostly knee or elbow to Lock
the joint
208 [PROSTHESIS AND AMPUTATION]
4 Orthopedic Note
ORTHOTIC PRESCRIPTION:
a). Extent : Knee-ankle-foot orthoses etc
b). Control : Free knee, Lock knee etc.
COMMON ORTHOTICS:
1. INSOLES:
Panter fasciitis or flat foot
2. ORTHOPEDIC SHOES.
3. THORACO-LUMBAR-SACRAL-HIP-KNEE-ANKLE-FOOT ORTHOSES.
4. UNILATERAL HIP ABDUCTION ORTHOSES.
5. LUMBOSACRAL SUPPORT WITH THORACIC EXTENSION.
6. LUMBAR ORTHOSES (BOSTON BRACE).
7. THE HALO-SPINAL IMMOBILIZATION SYSTEM.
8. MCP ORTHOSES.
9. RADIAL PALSY SPLINT.DYNAMIC ELBOW BRACE
208 [PROSTHESIS AND AMPUTATION]
5 Orthopedic Note
Orthopaedic Implants:
Screws:
cortical screws
cancellous screws
locking screws
Plates
Concave plates
placing a concave bend on a plate is useful in transverse fractures to ensure compressive forces occur on both the far and near cortices of the fracture
Compression plates: compression plates work by placing a cortical screw eccentrically into an oval hole in the plate.
Locking plates
o advantages of locking plates locked plate/screw constructs compared to non-
locked plate/screw constructs result in less angulation in comminuted metaphyseal fractures
o indications for locking plate technology indirect fracture reduction diaphyseal/metaphyseal fractures in osteoporotic bone bridging severely comminuted fractures plating of fractures where anatomical constraints prevent
plating on the tension side of the bone (e.g. short segment fixation).
o locking plate screw biomechanics bicortical locking screws have significantly more
resistance to all applied forces, with resistance to torsion increased the most (versus unicortical)
unicortical locking screws have less torsion fixation strength than non-locking bicortical constructs
o percutaneous locking plates: application has less soft-tissue stripping but higher chance malunion
o hybrid locked plates: utilize locking and nonlocking screws in order to assist with fracture reduction (nonlocking screws) as well as provide a fixed angle construct (locking screws).
o locking plate construct stability increases with: bicortical locking screws increased number of screws screw divergence from screw hole < 5 degrees longer plate
o Bridging plates
distal-femoral-plate
208 [PROSTHESIS AND AMPUTATION]
6 Orthopedic Note
provides relative stability, relative length and alignment preserves the blood supply to the fracture fragments as the fracture site
is undisturbed during the operative procedure this theoretically improves secondary bone healing
allows some motion at fracture site; relative stability leads to callus formation
Intramedullary nails
Overview o a load-sharing device
Material Properties o stiffness
torsional rigidity defined as amount of torque needed to produce torsional
(rotational) defomation depends on
shear modulus polar moment of inertia
increased by reaming decreased by slotting of nail
bending rigidity depends on
material properties Young modulus of elasticity of material
structural properties area moment of inertia length
Radius of curvature o intramedullary nail radius of curvature is greater (straighter) than the radius
of curvature of the femur
Interlocking o dynamic locking-->axially and rotationally stable fractures o static locking-->axially and rotationally unstable fractures o secondary dynamization for nonunion
remove proximal interlocking screw or move proximal interlocking screw from the static to dynamic slot
208 [PROSTHESIS AND AMPUTATION]
7 Orthopedic Note
External fixators
Factors that increase stability of conventional external fixators o contact of ends of fracture (most important) o larger diameter pins (second most important) o additional pins o decreased bone to rod distance o pins in different planes o increasing size or stacking rods o rods in different planes o increased spacing between pins
Factors that increase stability of circular (Ilizarov) external fixators o larger diameter wires o decreased ring diameter o olive wires o extra wires o wires cross perpendicular to each other o increased wire tension o placement of two central rings close to fracture o increased number of rings
Total Hip Implants
Material Properties o rigidity depends on length and radius of femoral stem
Biomechanics o place femoral component in neutral or slight valgus to reduce moment
arm and stress on cement o increasing femoral offset does the following
advantages moves abductor moment away from center of rotation increase abductor moment arm reduces abductor force required for normal gait
disadvantages increased strain on implant increases strain on medial cement mantle
208 [PROSTHESIS AND AMPUTATION]
8 Orthopedic Note
PROSTHESIS :
Are functional , cosmetic orboth replacements of the missing parts of the limbs.
ELEMENTS OF A PROSTHESIS:
1. Socket
• transmits forces between the stump[is the part remnant of the amputated part-> and
most be computable with it] & the prosthesis in all planes
• may be proximal, distal or total bearing
2. Means of Suspension
• suction socket : it has to be a regular smooth stamp.
• suspension belts
• elastic stocking : if there is an irregularity of the stamp.
208 [PROSTHESIS AND AMPUTATION]
9 Orthopedic Note
AMPUTATION
DEFINITION: Amputation is a removal of a whole or part of a limb.
Indications for Amputation: Three Ds: (1) Dead. (2) Dangerous. (3) Damned nuisance.
1. Dead:
o Peripheral vascular disease (90% from all indications)
o Severe trauma, burns and frostbite.
(Trauma scoring system: MESS score. (Mangled Extremity Severity
Score) doctor said: no need to know about this.
2. Dangerous Disorders: (Life Saving)
o Malignant tumors.
Ex: Extra compartmental tumor and need for radical excision.
o Potentially lethal sepsis due to infection.
o Crush injury. In crush injury, releasing the compression may result in
renal failure (Crush Syndrome).
3. Damned nuisance: (Bothering symptoms, sign or even Shape)
Retaining the limb may be worse than having no limb at all. This may be
because of :
o Pain.
o Gross malformation.
Ex: Congenital anomalies (Useless limb need to be amputated to
be suitable for prosthesis).
o Recurrent sepsis.
o Severe loss of function.
The combination of deformity and loss of sensation is particularly trying,
and in the lower limb is likely to result in pressure ulceration.
Aims of Amputation: o Return Patient to maximum level of independent function.
o Ablation of diseased tissue.
o Reduce morbidity & mortality.
o Considered first part of a Reconstruction to produce a physiological end
organ.
o Requires a Multidisciplinary approach.
208 [PROSTHESIS AND AMPUTATION]
01 Orthopedic Note
Pre-operative Evaluation: o Peripheral circulation:
o Clinical: feel pulses, skin temperature.
o Doppler: Ankle/ Brachial index more than .45 = 90% healing;
inaccurate with calcified vessels.
o Toe systolic BP - 55 mm Hg min for distal healing.
More than 55 to asses healing after amputation.
o Transcutaneous PO2 min 35 for assured healing.
o Arteriogram: to assess obstruction or sever stenosis in the vessels.
o Immune Competence:
o Serum albumin at least 3g/dl.
o WBC more than 1500/ml.
o Systemic:
o Control diabetes.
o Evaluate cardiac, renal + cerebral circulation.
o Correction of malnutrition.
o Psychological:
o Early plan for return to function.
o Pre-op. Counseling.
o Pre-op. Pain Control:
o Pain clinic review.
o Spinal anesthesia.
Complications:
o IMMEDIATE COMPLICATIONS:
Hemorrhage.
o EARLY COMPLICATIONS:
In addition to the complications of any operation (especially secondary
hemorrhage), there are two special hazards:
Breakdown of skin flaps: This may be due to ischemia, suturing under
excess tension or (in below-knee amputations) an unduly long tibia
pressing against the flap.
Gas gangrene Clostridia and spores from the perineum may infect a
high above-knee amputation (or re-amputation), especially if performed
through ischemic tissue.
208 [PROSTHESIS AND AMPUTATION]
00 Orthopedic Note
o LATE COMPLICATIONS:
Skin Eczema is common, and tender purulent lumps may develop in
the groin.
Ulceration is usually due to poor circulation, and re-amputation at a
higher level is then necessary.
Muscle if too much muscle is left at the end of the stump, the resulting
unstable ‘cushion’ induces a feeling of insecurity that may prevent proper
use of prosthesis; if so, the excess soft tissue must be excised.
Blood supply: Poor circulation gives a cold, blue stump that is liable to
ulcerate.
Neuroma: due to regeneration of nerve and cause proliferation in soft
tissue and cause pain if exposed under skin.
Phantom limb: This term is used to describe the feeling that the
amputated limb is still present. In contrast, residual limb pain exists in
the area of the stump. More in patients with depressive symptoms.
Difficult to treat and need long term medications.
Joint stiff or deformed: Fixed flexion and fixed abduction at the hip in
above-knee stumps. It should be prevented by exercises. If it becomes
established, sub trochanteric osteotomy may be necessary.
Bone spur often forms at the end of the bone, usually painless. If there
has been infection, the spur may be large and painful and it may need to
be excised.
ORTHOPEDIC NOTE
208
Principle of Fracture
Management
P R A Y F O R U S
Mohammed Al-Marhoon Mansour Moayed Al-Jishi
208 [PRINCIPLE OF FRACTURE MANAGEMENT ]
2 Orthopedic Note
Principles of Fracture Management
Management at the scene of an accident As casualties with airway obstruction succumb within minutes, securing a patent airway
is always a priority. Once the airway is open, the casualty must be oxygenated and
ventilated if breathing is not adequate. circulatory compromise is addressed primarily
by control of external hemorrhage; an intravenous cannula should be placed. During this
immediate management phase, the assumption is always made that damage to the
cervical and thoraco-lumbar spine may have occurred. The stability of the cervical
spine must be protected at all times until the neck can be cleared from the risk of injury
by manual immobilization or a rigid cervical collar. Limb fractures and dislocations
should be reduced and the limb returned, if possible, to its anatomical position with
gentle traction and straightening. This may require analgesia, the limb should then be
splinted with traction this reduces pain and hemorrhage, and minimizes neurovascular
damage.
Transfer to hospital since any delayed or prolonged transfer to hospital is associated
with poor outcomes, during the transfer, the casualty’s vital signs and ECG should be
continuously monitored clinically and with available equipment.
Management at the hospital (ATLS)
A: Airway with cervical spine protection. B: Breathing. C: Circulation with hemorrhage control. D: Disability or neurological status. E: Exposure and Environment – remove clothing, keep warm.
Fracture
A fracture is a break in the structural continuity of bone. If the overlying skin remains intact it is a closed (or simple fracture); if the skin or one of the body cavities is breached it is an open (or compound) fracture, liable to contamination and infection.
208 [PRINCIPLE OF FRACTURE MANAGEMENT ]
3 Orthopedic Note
Types of Fracture COMPLETE FRACTURES:
The bone is split into two or more fragments. The fracture pattern on x-ray can help
predict behavior after reduction: in a transverse fracture the fragments usually remain in
place after reduction; if it is oblique or spiral, they tend to shorten and re-displace even if
the bone is splinted. In an impacted fracture the fragments are jammed tightly together
and the fracture line is indistinct. A comminuted fracture is one in which there are more
than two fragments; because there is poor interlocking of the fracture surfaces, these
are often unstable.
INCOMPLETE FRACTURES
Here the bone is incompletely divided and the periosteum remains in continuity. In a
greenstick fracture the bone is buckled or bent this is seen in children, In contrast,
compression fractures occur when cancellous bone is crumpled. This happens in adults and
typically where this type of bone structure is present, e.g. in the vertebral bodies,
calcaneum and tibial plateau.
Management
1) Reduction
2) Immobilization(hold)
3) Rehabilitation(exercise)
REDUCTION
Reduction should aim for adequate apposition and normal alignment of the bone fragments. The greater the contact surface area between fragments the more likely healing is to occur. There are two methods of reduction:
CLOSED REDUCTION
Under appropriate anaesthesia and muscle relaxation, the fracture is reduced by a three-fold manoeuvre:
(1) the distal part of the limb is pulled in the line of the bone; (2) repositioned (3) alignment is adjusted in each plane.
OPEN REDUCTION
Operative reduction of the fracture under direct vision Which is indicated: (1) when closed reduction fails (2)when there is a large articular fragment that needs accurate positioning or (3) for traction fractures in which the fragments are held apart
208 [PRINCIPLE OF FRACTURE MANAGEMENT ]
4 Orthopedic Note
Immobilization (hold reduction) CAST SPLINTAGE for distal limb fractures and for most children’s fractures. It is safe enough, so long as the practitioner is alert to the danger of a tight cast and provided pressure sores are prevented INTERNAL FIXATION
Bone fragments may be fixed with screws, a metal plate held by screws, k-wires, a long intramedullary rod or nail (with or without locking screws), circumferential bands or a combination of these methods. Properly applied, internal fixation holds a fracture securely so that movement can begin at once;and with early movement the ‘fracture disease’ (stiffness and oedema) is abolished.
EXTERNAL FIXATION
A fracture may be held by transfixing screws or tensioned wires that pass through the bone above and below the fracture and are attached to an external frame. This is especially applicable to the tibia and pelvis, but the method is also used for fractures of the femur, humerus, lower radius and even bones of the hand.
Rehabilitatoin (EXERCISE) More correctly, restore function – not only to the injured parts but also to the patient as a whole. The objectives are to reduce oedema, preserve joint movement, restore muscle power and guide the patient back to normal activity
208 [PRINCIPLE OF FRACTURE MANAGEMENT ]
5 Orthopedic Note
Complications of fractures EARLY COMPLICATIONS
VISCERAL INJURY Fractures around the trunk are often complicated by injuries to underlying viscera, the most important Being penetration of the lung with life-threatening pneumothorax following rib fractures.
VASCULAR INJURY
The fractures most often associated with damage to a major artery are those around the knee and elbow, humeral and femoral shafts. The artery may be cut, torn, compressed or contused, either by the initial injury or subsequently by jagged bone fragments. The effects vary from transient diminution of blood flow to profound ischemia, tissue death and peripheral gangrene.
COMPARTMENT SYNDROME
Fractures of the arm or leg can give rise to severe ischaemia, even if there is no damage to a major vessel. Bleeding, oedema or inflammation (infection) may increase the pressure within one of the osseofascial compartments; there is reduced capillary flow, which results in muscle ischaemia, further oedema, still greater pressure and yet more profound ischaemia – a vicious circle that ends, after 12 hours or less, in necrosis of nerve and muscle within the compartment.
HAEMARTHROSIS
The joint is swollen and tense and the patient resists any attempt at moving it. The blood should be aspirated before dealing with the fracture
others Gas gangrene and tetanus in open fracture Hypovolemia Fat embolism ARDS
LATE COMPLICATIONS Non-union
Malunion Delayed Union 2ry osteoarthritis in articular fracture
ORTHOPEDIC NOTE
208
Spine Fracture
P R A Y F O R U S
Ahmed Abdul-Rauf Al-Jishi Abdullah Sami Al-Elaiw Husain Ali Al-Subai’e
208 [SPINE FRACTURE]
2 Orthopedic Note
PATHOPHYSIOLOGY OF SPINE INJURIES Stable and unstable injuries A stable injury is one in which the vertebral components will not be displaced by normal movements; in a stable injury, if the neural elements are undamaged there is little risk of them becoming damaged. An unstable injury is one in which there is a significant risk of displacement and consequent damage – or further damage – to the neural tissues.
Thoraco-lumbar fracture
Neurological deficit may occur in 10–25% of patients with spinal trauma
Incidence of spinal injury in the US is between 4 and 5.3 per hundred thousand of population
The common causes of spinal trauma include
Road traffic accidents - 45% (most common)
Falls - 20%
Sports -15%
The male to female ratio is 4:1.
The overall survival rate for patients with spinal injuries is 86% at 10 years so, we have to know that this patient can be treated.
Incidence of noncontiguous, multilevel vertebral injuries is approximately 20%
Most injuries of the thoracolumbar spine occur in the transitional area – T11 to L2 – between the somewhat rigid upper and middle thoracic column and the flexible lumbar spine.
The upper three-quarters of the thoracic segments are also protected to some extent by the rib-cage and fractures in this region tend to be mechanically stable. However, the spinal canal in that area is relatively narrow so cord damage is not uncommon and when it does occur it is usually complete (Bohlman, 1985).
The spinal cord actually ends at L1 and below that level it is the lower nerve roots that are at risk.
Mechanism of injury
• Motor vehicle accidents 50%
• Falls 25%
• Gunshot 15%
• Sport 10%
• Most of patient with spine injury have an associated injuries
• 80% multiple injuries
• 26% head & face injury
• 16% major chest injury
• 10% major abdominal injury
• 8% long bone/ pelvic fractures
208 [SPINE FRACTURE]
3 Orthopedic Note
Incidence of missed spinal fracture
• The prevalence of delay in diagnosis of trauma
• cervical spine is 22-33%
• doctor said: (20%) of patients misdiagnosed as spinal fracture so x-ray should be taken .
• thoracolumbar spine is 5%.
• 22% in tertiary centre.
• The main causes are :-
• a low level of suspicion or incoopeartive (main cause)
• failure to take proper radiographs
• poly trauma
• failure to interpret the x ray
• intoxication
• decrease level of consciousness Multiple Spinal Fracture
• Calenoff, Chessare,& Rogers reported an incidence of 4.5%
Demographics
• SCI is predominantly a disease of young men.
• Average age at injury is 29.7 years.
• Median age is 25 years
• 82% male.
• Occurrence increase with increase daylight. Medical problems in Spinal cord injury
• The leading cause of death in acute phase is respiratory failure & pneumonia.
• Pulmonary problems also the leading cause of readmission in the 1st year. Leading cause of death in Spinal cord injury
• Respiratory disease (main cause) 20.5%
• Accident, poisoning, violence 9.7%
• Circulatory disease 8.8%
• Infections 8.8%
• Genitourinary disease 4.0%
• Neoplasm 3.9%
208 [SPINE FRACTURE]
4 Orthopedic Note
Approach to Spine Trauma
• Pre Hospital Care
• The aim is to retrieve the patient from the site of injury safely and rapidly
• Transfer to a suitable facility.
• spinal trauma should be suspected in 1. all unconscious patients 2. High energy trauma 3. Evidence of neurological deficit (i.e, can,t move even 1mm) 4. Multiple injuries
• Proper extraction
• Intubation
• Immobilization
• Cervical collar, sand bag, tape,
• ? Neck position
• ?pediatrics Emergency Assessment
• ATLS
• Evaluating spinal injury begins in the secondary survey
• History is taken & head to toe examination
• Obtain history from
• Patient
• Family members
• Paramedical personnel History
• Mechanism of injury
• Position of the patient when found
• Transient motor or sensory loss
• Paradoxical breathing
• Seat belt Physical Examination Patients complaining of back pain following an injury or showing signs of bruising and tenderness over the spine, as well as those suffering head or neck injuries, chest injuries, pelvic fractures or multiple injuries elsewhere, should undergo a careful examination of the spine and a full neurological examination, including rectal examination to assess sphincter tone. Inspection
• All clothing should be carefully removed
• Any bleeding , abrasion or lacerations
• Limb asymmetry
• Voluntary limb movement
• Chest expansion Palpation
208 [SPINE FRACTURE]
5 Orthopedic Note
• Cervical collar removed carefully 1. Tenderness 2. Interspinous widening 3. Malialignement of spinouse process 4. Step off
Neurological Evaluation
1. Sensory evaluation 2. Motor evaluation 3. Reflexes
Spinal reflexes: bcz , it help in prognosis of patient. Cresmatic reflex
• Stocking inner thigh & observing the scrotum movement
• Absence means UMNL
• Unilateral absence suggest LMNL Sacral Sparing When we have somebody with spinal cord injury, it is ether complete or incomplete, because if it is incomplete we want to treat them for give chance for recovery, so sacral sparing consist of three tests:
1. Perianal/perineal sensation 2. Rectal tone 3. Big toe flexion
• Implies partial structural continuity of white matter long tracts
• May be only evidence of incomplete injuryhigher chance of recovery
• Essential to check and document Bulbocavernosus reflex
• Pull glans or press clitoris do PR anal contraction (int. sphincter) around gloved finger
• Absence is indicator of spinal shock
• If female pull her catheter. RADIOLOGICAL ASSESMENT
• PLAIN FILM
• AP & LATERAL
208 [SPINE FRACTURE]
6 Orthopedic Note
X-rays The anteroposterior x-ray may show loss of height or splaying of the vertebral body with a crush fracture.
Widening of the distance between the pedicles at one level, or an increased distance between two adjacent spinous processes, is associated with posterior column damage.
The lateral view is examined for alignment, bone outline, structural integrity, disc space defects and soft-tissue shadow abnormalities. Always look carefully for evidence of fragment retropulsion towards the spinal canal.
CT
• Injury suspected on plain films
• Better visualize fracture (specificity and sensitivity)
• Unable to adequately assess on plain films
• Fracture or soft tissue injury in the plane of the CT can be missed
Plain x-rays, while showing the lower thoracic and lumbar spine quite clearly, are less revealing of the upper thoracic vertebrae because the scapulae and shoulders get in the way CT and MRI Rapid screening CT scans are now routine in many accident units. Not only are they more reliable than x-rays in showing bone injuries throughout the spine, and indispensable if axial views are necessary, but they also eliminate the delay, discomfort and anxiety so often associated with multiple attempts at ‘getting the right views’ with plain x-rays.
MRI
• Invaluable for assessing cord and soft tissues
• R/O associated disc herniation ( facet dislocations)
• Hemorrhage vs edema in soft tissues ????
• Ligamentous tears and facet capsule disruptions visualized with fat suppression
• May allow prognostic assessment of final motor function
• Intrasubstance hematoma
208 [SPINE FRACTURE]
7 Orthopedic Note
The common mechanisms of injury are: • Flexion–compression – failure of the anterior column and wedge-compression of the vertebral body. Usually stable, but greater than 50 per cent loss of anterior height suggests some disruption of the posterior ligamentous structures. • Lateral compression – lateral wedging of the vertebral body resulting in a localized ‘scoliotic’ deformity. • Axial compression – failure of anterior and middle columns causing a ‘burst’ fracture and the danger of retropulsion of a posterior fragment into the spinal canal. Often unstable. • Flexion–rotation – failure of all three columns and a risk of displacement or dislocation. Usually unstable. • Flexion–distraction – the so-called ‘jack-knife’ injury causing failure of the posterior and middle columns and sometimes also anterior compression. • Extension – tensile failure of the anterior column and compression failure of the posterior column. Unstable. Classification of ThoracoLumbar spine Fracture Read: http://orthoinfo.aaos.org/topic.cfm?topic=a00368 1-Compression Fracture
208 [SPINE FRACTURE]
8 Orthopedic Note
This is by far the most common vertebral fracture and is due to severe spinal flexion, though in osteoporotic individuals fracture may occur with minimal trauma. The posterior ligaments usually remain intact, although if anterior collapse is marked they may be damaged by distraction. CT shows that the posterior part of the vertebral body (middle column) is unbroken. Pain may be quite severe but the fracture is usually stable. Neurological injury is extremely rare. Management: Patients with minimal wedging and a stable fracture pattern are kept in bed for a week or two until pain subsides and are then mobilized; no support is needed. Those with moderate wedging (loss of 20–40 per cent of anterior vertebral height) and a stable injury can be allowed up after a week, wearing a thoracolumbar brace or a body cast applied with the back in extension. At 3 months, flexion–extension x-rays are obtained with the patient out of the orthosis; if there is no instability, the brace is gradually discarded. If the deformity increases and neurological signs appear, or if the patient cannot tolerate the orthosis, surgical stabilization is indicated. If loss of anterior vertebral height is greater than 40 per cent, it is likely that the posterior ligaments have been damaged by distraction and will be unable to resist further collapse and deformity. If the patient is neurologically intact, surgical correction and internal fixation is the preferred treatment, though if necessary even these patients can be treated conservatively with vigilant monitoring of their neurological status. In the rare cases of patients with a wedge compression fracture and neurological impairment treatment will depend on the degree of dysfunction and the risk of progression. If nerve loss is incomplete there is the potential for further recovery; any increase in kyphotic deformity or MRI signs of impending cord neurological compression would be an indication for operative decompression and stabilization through a trans-thoracic approach. If there is complete paraplegia with no improvement after 48 hours, conservative management is adequate; the patient can be rested in bed for 5–6 weeks, then gradually mobilized in a brace. With severe bony injury, however, increasing kyphosis may occur and internal fixation should be considered.
208 [SPINE FRACTURE]
9 Orthopedic Note
(a) Central compression fracture of the vertebral body and (b) anterior wedge-compression fracture with less than 20 per cent loss of vertebral body height. In both cases the middle and posterior columns are intact; further collapse can be prevented by immobilization for 8–12 weeks in (c) a plaster ‘jacket’
More severe and potentially unstable compression fractures may need posterior internal fixation.
2- Burst Fracture
Severe axial compression may ‘explode’ the vertebral body, causing failure of both the anterior and the middle columns. The posterior column is usually, but not always, undamaged. The posterior part of the vertebral body is shattered and fragments of bone and disc may be displaced into the spinal canal. The injury is usually unstable. Anteroposterior x-rays may show spreading of the vertebral body with an increase of the interpedicular distance. Posterior displacement of bone into the spinal canal (retropulsion) is difficult to see on the plain lateral radiograph; a CT is essential. Management: If there is minimal anterior wedging and the fracture is stable with no neurological damage, the patient is kept in bed until the acute symptoms settle (usually under a week) and is then mobilized in a thoracolumbar brace or body cast which is worn for about 12 weeks. Wood et al. (2003) carried out a prospective randomized trial comparing operative and non-operative treatment of stable thoracolumbar burst fractures with no neurological impairment; they found no difference in the long-term results in the two groups, but complications were more frequent in the surgical group.
208 [SPINE FRACTURE]
01 Orthopedic Note
Severe compression may shatter the middle column and cause retropulsion of the vertebral body (a). The extent of spinal canal encroachment is best shown by CT (b).
Burst fracture – treatment (a) Burst fracture in a 44-year-old man who fell from his horse; 3 months later he developed paraesthesia in both legs. (b–e) Internal fixation and grafting through a transthoracic transdiaphragmatic approach provided total stability (the Kaneda method).
3- Fracture Dislocation
Segmental displacement may occur with various combinations of flexion, compression, rotation and shear. All three columns are disrupted and the spine is grossly unstable. These are the most dangerous injuries and are often associated with neurological damage to the lowermost part of the cord or the cauda equina. The injury most commonly occurs at the thoracolumbar junction. X-rays may show fractures through the vertebral body, pedicles, articular processes and laminae; there may be varying degrees of subluxation or even bilateral facet dislocation. Often there are associated fractures of transverse processes or ribs. CT is helpful in demonstrating the degree of spinal canal occlusion. Management: In neurologically intact patients, most fracturedislocations will benefit from early surgery. In fracture-dislocation with paraplegia, there is no convincing evidence that surgery will facilitate nursing, shorten the hospital stay, help the patient’s rehabilitation or reduce the chance of painful deformity. In fracture-dislocation with a partial neuro - logical deficit, there is also no evidence that surgical stabilization and decompression provides a better
208 [SPINE FRACTURE]
00 Orthopedic Note
neurological outcome than conservative treatment. If surgical decompression and stabilization are performed, this may require a combined posterior and anterior approach. In fracture-dislocation without neurological deficit, surgical stabilization will prevent future neurological complications and allow earlier rehabilitation. When specialized surgery cannot be performed, these injuries can be managed non-operatively with postural reduction, bed rest and bracing. For patients with neurological impairment who have the benefit of being treated in a specialized spinal injuries unit, a strong case can be made for managing them also by non-operative methods.
Thoracolumbar fracture-dislocation (a) Fracture-dislocation at T11/12 in a 32-year-old woman who was a passenger in a truck that overturned. She was completely paraplegic and operation was not thought worthwhile. (b) Four weeks later the deformity has increased, leaving her with a marked gibbus. (c,d) A similar injury in a 17-year-old man, treated by open reduction and internal fixation.
4- Flexion Distraction or Jack-knife injury
Combined flexion and posterior distraction may cause the mid-lumbar spine to jack-knife around an axis that is placed anterior to the vertebral column. This is seen most typically in lap seat-belt injuries, where the body is thrown forward against the restraining strap. There is little or no crushing of the vertebral body, but the posterior and middle columns fail in distraction; thus these fractures are unstable in flexion. The tear passes transversely through the bones or the ligament structures, or both. The most perfect example of tensile failure is the injury described by Chance in 1948, in which the split runs through the spinous process, the transverse processes, pedicles and the vertebral body. Neurological damage is uncommon, though the injury is (by definition) unstable. Xrays may show horizontal fractures in the pedicles or transverse processes, and in the anteroposterior view the apparent height of the vertebral body may be increased. In the lateral view there may be opening up of the disc space posteriorly.
208 [SPINE FRACTURE]
02 Orthopedic Note
Management: The Chance fracture (being an ‘all bone’ injury) heals rapidly and requires 3 months in a body cast or well-fitting brace. Flexion–extension lateral views should then be taken to ensure that there is no unstable deformity. Severe ligamentous injuries are less predictable and posterior spinal fusion is advisable.
Jack-knife injuries (a) Whereas flexion usually crushes the vertebral body and leaves the posterior ligaments intact, the jack-knife injury disrupts the posterior ligaments causing only slight anterior compression. (b) The rare Chance fracture.
Complications of spine fracture • Neurological injury
• Instability ( pain & deformity)
• Complication of surgery
Sources: Apleys System of Orthopaedics and Fractures 9 ed + Dr. Dakheel lecture. Black font color : Apleys System of Orthopaedics and Fractures. Blue font color : doctors slides. Red font color : doctors note.
208 [SPINE FRACTURE]
03 Orthopedic Note
Top Related