Orthopedic (Final)

ORTHOPEDIC NOTE

Orthopedic Special Thanks to

Hussain Al-Hamza Hassan Ibrahim Al-Hammadi

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[ORTHOPEDIC]

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) 2) 3) 4)

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Fracture of Shoulder and Upper limb Fracture of pelvis and Lower Limb Disorder of Upper Limb Disorder of Lower Limb

Orthopedic Note

ORTHOPEDIC NOTE

Metabolic Disorders (Osteoporosis, Osteomalacia & Rickets) Ali Al-Saeed Hussain Al-Hamza

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

Introduction to Bones -

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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 -

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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). -

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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. Orthopedic Note

[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

208 Clinical presentation -

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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 -

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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 -

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When only particular bone or group of bone affected. It is due to immobilization or inflammation. It is usually reversible after managing the cause.

Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

Causes of osteoporosis

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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

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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 Orthopedic Note

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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%)

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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.

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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.

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Signs of severe postmenopausal osteoporosis: 1- Compression fractures of vertebra. 2- Wedging at multiple levels. 3- Biconcave distortion of end-plates.

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Before diagnosing that osteoporosis is postmenopausal you have to exclude other causes.

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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. Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS] 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 -

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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. Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS] Involutional (type II) osteoporosis

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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.

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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.

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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 -

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Most commonly affect middle age men, sometimes seen in pregnant female in 3 rd trimester. Usually affect the left hip (1/3 bilaterally) Self-limiting condition (recovery occur within 6 months)

Orthopedic Note

[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

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Hypercortisonism -

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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 -

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Will cause hypercalcaemia and hypercalciuria.

Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

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). Osteomalacia = soft bone (occur at any age) Rickets= osteomalacia + bone deformity (occur only in children)

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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 (‫ )تتكدس‬irregularly 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

Orthopedic Note

[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

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mild osteomalacia can cause fracture if it is superimposed on postmenopausal or senile osteoporosis.

Clinical feature -

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Craniotabes is may the first manifestation of rickets in infants. Rickets in infants: o Tetany DDX of Craniotabes: o Convulsions 1- Rickets 2- Thalassemia 3- Syphylsis 4-normal premature infant o Failure to thrive 5- osteogenesis imperfecta 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

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Usually wrist X-ray is used for diagnosis. Active rickets shows:  Thickening and widening of growth plate.  widening of the physis and flaring of the metaphysic.  Cupping of metaphysis Metaphysis widening may remain after healing.  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.

Orthopedic Note

[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

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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 Slow fading of skeletal  lateral indentation of the acetabula (‘trefoil’ champagne glass structure, resulting in 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 -

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Normal/Low serum calcium level o If the serum calcium remains persistently low after treatment there may be signs of secondary hyperparathyroidism. DDx Normal Ca+2 with phosphate Nutritional Low serum phosphate level Rickets, familial hypophystemia, Fanconi syndrome Increase alkaline phosphatase +2 Ca with phosphate Renal dystrophy +2 Decrease calcium in urine Ca with normal phosphate Celiac disease 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 -

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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 Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS] 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

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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 -

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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) Orthopedic Note

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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

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.

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 03

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. Orthopedic Note

[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

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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 -

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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 -

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It rare metabolic bone disease, inherited as Autosomal recessive characterized by low alkaline phosphatase It cause severe rickets.

Orthopedic Note

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[OSTEOPOROSIS, OSTEOMALACIA, & RICKETS]

Q/Compare between osteoporosis and osteomalacia?

Comparsion between osteoporosis and osteomalacia Similarity

Differences

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Common in ageing women Prone to pathological fracture Decreased bone density 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

ORTHOPEDIC NOTE

Infection of bone and Joint Burair Al Jassas Mohammed Al_Shaikh

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[INFECTION OF BONE AND JOINT]

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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.

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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 2

Orthopedic Note

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[INFECTION OF BONE AND JOINT]

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).

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Orthopedic Note

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 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.

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Orthopedic Note

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 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 “Flareup” 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. 5

Orthopedic Note

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 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.

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Orthopedic Note

[INFECTION OF BONE AND JOINT]

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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 infant Congenital syphilis Affect epiphysis and metaphysis

Syphilitic osteo-periostitis Infant, older children, or adult Congenital or acquired syphilis 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. 7

Orthopedic Note

Arthritis

Septic arthritis

Tuberculous arthritis

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:

[INFECTION OF JOINT]

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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 a) Complete resolution,b)partial loss of cartilage,c)fibrous ankylosis,d)bony ankylosis. 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.

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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.

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Investigation:

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 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 2

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[INFECTION OF JOINT]

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.

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ORTHOPEDIC NOTE

RHEUMATOID ARTHRITIS Ali Zaki

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[RHEUMATOID ARTHRITIS]

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. 2

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[RHEUMATOID ARTHRITIS]

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. 3

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[RHEUMATOID ARTHRITIS]

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.

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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 softtissue 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.

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[RHEUMATOID ARTHRITIS]

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 Arthritis

for

Diagnosis

of

Rheumatoid

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 6

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[RHEUMATOID ARTHRITIS]

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.

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[RHEUMATOID ARTHRITIS]

Control of pain and stiffness with nonsteroidal 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.

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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

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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. 8

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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, periarticular 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.

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ORTHOPEDIC NOTE

OSTEOARTHRITIS Husain AlShulah Hasan AlSaihati

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[LECTURE TITLE]

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 synovialderivedinterleukin-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

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[LECTURE TITLE]

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 deeper layers there is patchy loss of metachromasia. Most striking, however, is increased cellularity, and the appearance of clusters of chondrocytes. In later stages, clefts become more extensive and in some areas cartilage is lost to the point where underlying bone is completely denuded.

the the the the

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. 3

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[LECTURE TITLE]

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. 4

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[LECTURE TITLE]

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

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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.

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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.

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ORTHOPEDIC NOTE

za

Bone Tumors Zaid Al-Helal Issac Al-Mughaizel

208 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

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Introduction and Classification Growth of Bone

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.

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 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

Bone Histology 1) Bone Matrix (Osteoid) 2) Bone Cells a. Osteocyte b. Osteoblast c. Osteoclast 2

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 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

Incidence Growth Margin Metastasis Suffix Notice

Benign (noncarcenous) More Common Slow Well defined edges and sometime sclerotic Does Not - Oma May relapse the bone tissue which make it weaker and result in pathological fracture

Malignant (Carcenous) Less Common Rapid ill-defined edges Does - Sarcoma May relapse the bone tissue which make it weaker and result in pathological fracture (it is more with malignant)

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

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C) According to Cell Type: Benign Bone (Osteoid)

Cartilage

Osteoma Osteoid Osteoma Osteblastoma Chondroma Osteochondroma Chondromyxoid Fibroma Chondroblastoma

Malignant Osteosrcoma

Chondrosarcoma Fibrosarcoma (Malignant fibrous histocytoma- FMH) Ewing Sarcoma Lymphoma

Fibrous Tissue

Fibroma

Marrow

Eosinophilic Grannuloma

Vascular

Hemangioma

Angiosarcoma

Uncertain

Giant Cell Tumor Cyst (tumor like lesion)

Malignant GCT Adamantioma

Anatomical Location of the bone Tumor:

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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

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Tumors Work up 1) Lab investigation: 1. 2. 3. 4. 5. 6. 7.

CBC: Anemia Inflammatory Markers (CRP,ESR) Urine Examination: important in multiple myeloma Bone Profile Renal Profile Liver Profile 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)

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)

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.

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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 7

Sunburst

Codman's

Onion Peel

Complex

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Staging and Spread of Bone Tumor Staging of benign bone tumors as described by Enneking: Latent

Active Agressive

Well-defined margin. Grows slowly and then stops Remains static/heals spontaneously E.g. Osteoid osteoma Progressive growth limited by natural barriers Not self-limiting. Tendency to recur E.g. Aneurysmal bone cyst 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 1A 1B 2A 2B

Grade Low Low High High

3A

Low

3B

High

Site Intracompartmental Extracompartmental Intracompartmental Extracompartmental Intra or Extracompartmental Intra or Extracompartmental

Metastasis No No No No Yes 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. 8

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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.

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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 darkbrown 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.

Enchondroma Incidences Growth

Site Size Malignant changes Presentation

More common Within the bone Expand the bone and thins its cortex Long bones But over 50% in small bone of hands and feet

Ecchondroma

(Periosteal Chondroma)

Less common Outward from bone Hands, feet, flat bones (e.g.: scapula and ilium)

Less

Large More

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.

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

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.

1) Incidence: age: 15 – 50 age group 2) Pathology: there are 2 forms of chondroma 01

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[BONE TUMORS]

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

00

2) Pathology: a. Sites: ends of long bone at which most growth occur:  Lower end of femur  Lower end of radius  Upper of humerus  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

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[BONE TUMORS]

Malignant Bone Tumor 1)

2)

2)

3)

4) 5)

6)

Osteosarcoma (Osteogenic Sarcoma) Incidence: Age : Childhood and adolescence 10 – 30 Old age as a complication of Paget's disease 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 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 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 Classification: primary and secondary (following Paget's disease, x-ray therapy) Differential Diagnosis:  Subacute osteomyelitis  Giant cell tumor  Ewing tumor  Chondrosarcoma  Metastatic  MFH Treatment: limb sparing resection followed by chemotherapy.

02

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 preArise from malignant existing lesion or transformation of from malignant osteochondroma transformation of especially diphysial enchondroma especially aclasis or multible ollier disease 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.

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1) 2)

3)

4)

5)

6) 7)

[BONE TUMORS]

Ewing's Sarcoma (Endothelial Sarcoma of Bone) Incidence: ages of 5 and 20 years, 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. 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. Imaging:  X-ray: ‘onion-peel’ effect.  CT and MRI: large extraosseous component.  Radioisotope scans: multiple areas of activity in the skeleton. Differential Diagnosis: subacute osteomyelitis and metastasis from suprarenal neuroblastoma (Histologically) Diagnosis: Biopsy is essential 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 03

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Age

Sites

Clinical Features

Imaging

Benign Bone Tumors Osteoma

Chondroblastoma

Chondroma

Osteochondroma

Giant Cell Tumor

Pain worse at night and relieved by NSAID

10 - 35

5 - 25

Knee Hip Shoulder

 Plain x-ray: sclerotic thickening of shaft  CT: Nidus

Pain

15 - 50

 Enchondroma: Long bones  Ecchondroma: Hands, feet, flat bones

Asymptomatic Pathological fracture

Bone cortex thinning but no erosion.

10 - 20

Growing epiphyseal cartilage plate

Circumscribed hard swelling usually not painful

Mashroom like stalk

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

Chondrosarcoma

Ewing's Sarcoma

Myeloma

04

10 – 30 Old ages

30 - 60

5- 20

45 - 70

Metaphysis of long

 Central: Femur, tibia, humerus  Peripheral: Flat bone Tibia, Fibula Humerus Clavicle

local pain swelling

Plain radiograph irregular medullary and cortical destruction of metaphysic and aggressive periosteal reactions

Dull ache Enlarging lump Pathological fracture Pain in the middle of the bone Swelling backache, bone pain or a pathological fracture

Osteoporosis, and lytic lesions.

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[BONE TUMORS]

Cyst (Tumor Like lesions) 1) 2)

3)

4)

Simple bone Cyst (Solitary Bone Cyst - Umicameral Bone Cyst) Incidence: Childhood, seldom in adult. 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. 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. 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.

05

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-aulait 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

ORTHOPEDIC NOTE

Back Pain Hassan Al-Ahmadi Bandar Al-Rasheedi Fawaz Al-Khaldi

208

PRAY

FOR

US

[BACK PAIN]

208

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.

 

2

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[BACK PAIN]

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

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Investigations: Plain X-ray: 1. 2.

To roll-out other possible causes like trauma or fracture. 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. 2.

•

•

If there is no red flag signs the disc prolapse can be treated conservatively like : bed rest analgesia, physiotherapy, muscle relaxants. 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.

4

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208

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.

5

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208

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).  

6

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.

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[BACK PAIN]

208

 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, longterm 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 Gramnegative 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).

7

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208

[BACK PAIN]

- 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 !!

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

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. 8

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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 9

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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. b. c. d. e.

Thyroid Breast Prostate Kidney 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.

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•

Surgical: Excision, Fusion ,Instrumentation.

•

Non surgical: if the stability is not compromised like lymphoma treated with chemotherapy , or like multiple myeloma by radiotherapy.

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208

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 flulike 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 broadspectrum 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.

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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 ( retrospondylolysthesis) - 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. 02

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[BACK PAIN]

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 % . 03

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[BACK PAIN]

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 )

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[BACK PAIN]

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.

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ORTHOPEDIC NOTE

Ligamentous Injury

Jehad Abdullah AL-Saihati Louai Hassan AL-Khalaf

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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)

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[LIGAMENTOUS INJURY]

Type

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Complete

Features

   

Instability of the joint. More than 50% of the joint is damaged. Clinical findings & MRI findings. (High signal intensity) Surgically corrected

partial   



Stable joint. Damage is less than 50%. There are Clinical findings & MRI findings (High signal intensity). Does not need any surgical intervention

sprain     

strain

Stable joint.  While he is  going down stairs. Swelling only.  No radiological findings. Soft tissue injury.

Stable joint. There is high signal intensity on MRI. No disruption of fibers.

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.

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 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

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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

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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.

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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.

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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%)

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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.

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ORTHOPEDIC NOTE

Arthroscopy & Arthrocentesis Hassan Ibrahim Al-Hammadi Ahmed Maitham Al-Nasser

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Introduction: -

[ARTHROSCOPY & ARTHROCENTESIS] ARTHRO-SCOPY

Definition: 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 Patient is in lateral position 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 2

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[ARTHROSCOPY & ARTHROCENTESIS]

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3) 4) -

Wrist: useful in: triangular fibro-cartilage tear & inter-osseous ligament ruptures 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: o o o o o

Safe But Not entirely free of complications e.g.: Thrombo-phlebitis (DVT 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

Orthopedic Note

[PROSTHESIS AND AMPUTATION]

208 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  

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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

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[PROSTHESIS AND AMPUTATION]

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

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

8

•

suction socket : it has to be a regular smooth stamp.

•

suspension belts

•

elastic stocking : if there is an irregularity of the stamp.

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[PROSTHESIS AND AMPUTATION]

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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: Return Patient to maximum level of independent function. Ablation of diseased tissue. Reduce morbidity & mortality. Considered first part of a Reconstruction to produce a physiological end organ. o Requires a Multidisciplinary approach. o o o o

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[PROSTHESIS AND AMPUTATION]

 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.

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[PROSTHESIS AND AMPUTATION]

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.

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ORTHOPEDIC NOTE

Principle of Fracture Management Mohammed Al-Marhoon Mansour Moayed Al-Jishi

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[PRINCIPLE OF FRACTURE MANAGEMENT ]

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.

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[PRINCIPLE OF FRACTURE MANAGEMENT ]

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 threefold 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

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[PRINCIPLE OF FRACTURE MANAGEMENT ]

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

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[PRINCIPLE OF FRACTURE MANAGEMENT ]

208

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

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Orthopedic Note

ORTHOPEDIC NOTE

Spine Fracture Ahmed Abdul-Rauf Al-Jishi Abdullah Sami Al-Elaiw Husain Ali Al-Subai’e

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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           

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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 • Falls 25% • Gunshot 15% • Sport 10% •

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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 Orthopedic Note

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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 1 st 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% 3

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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 4

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• 1. 2. 3. 4.

Cervical collar removed carefully Tenderness Interspinous widening Malialignement of spinouse process 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 injuryhigher 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

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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

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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 • • • • • •

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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

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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

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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.

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(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.

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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 01

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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. 00

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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.

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