RT 208 Pathology Flashcards
Vitamin D
Absorption of calcium in the intestine. Activated by ultraviolet radiation
Vitamin A
Needed for bone resorption that occurs during normal development. Retarded development of bone occurs without it.
Vitamin C
needed for synthesis of collagen which is used by osteoblasts to make osteoid.
Pituitary Gland
Human Growth Hormone
Stimulates reproduction of cartilage cells in epiphyseal plates
Thyroid Hormone
Thyroid Gland -T3 and T4 stimulates the replacement of cartilage in epiphyseal plates. Excessive secretion halts bone growth. A deficiency causes stunted growth.
Calcitonin
calcium storage in bone
Sex hormones
Androgens (testosterone), and Estrogens . Testes, ovaries and adrenal gland (zona reticularis of adrenal cortex).
Parathyroid Gland
parathormone. Stimulates osteoclasts to release calcium into the blood stream.
Minerals
Calcium 25% Phosphorus 12% Magnesium 0.37% Potassium 0.7% Zinc .009% Copper .0009%
Protein
for Osteoid production
Etiology:
Vitamin C deficiency leading to inadequate production of collagen
S/S
Internal bleeding into joints, periosteum and mucus membranes, petechiae, ecchymoses, anemia, pallor, bleeding gums and loose teeth.
Tx
Restore vitamin C intake. 100-200 mg p.o. daily
Etiology:
Rate of bone resorption increases while rate of bone formation slows down causing loss of bone mass.
Lack of estrogens and androgens in post-menopausal women
and androgens in post-menopausal women
Nutritional disorders
not enough protein or calcium in diet
Disuse
Lack of exercise which is necessary for osteoid formation. “Atrophy”of disuse.
Example: patient’s whose extremities have been in a cast for six weeks.
Osteoporosis Treatment
Basically symptomatic and try to prevent additional fractures Estrogens to decrease bone resorption Fluoride to stimulate bone formation Calcium and Vitamin D Teach patient good body mechanics
Symptoms of Osteomalacia - Rickets
Etiology:
Sunlight stimulates ergosterol
Renal Rickets
Etiology
Vitamin D deficiency either due to inadequate dietary intake, malabsorption in gastrointestinal tract or too little sunlight.
Sunlight stimulates ergosterol in the skin and makes vitamin D active.
Vitamin D is necessary for the absorption of calcium and phosphorus in the GI tract.
Renal Rickets
kidney injury causes retention of phosphorus in the body which stimulates the parathyroid gland to release parathormone and increase calcium levels in the blood by removing calcium from the bone.
Osteomalacia
There is plenty of osteoid but no calcium to provide strength. Bow legs, knock knees result
Hyperparathyroidism - Primary
is where one or more of the parathyroid glands enlarge and increase the secretion of PTH (parathormone). Parathyroid adenoma accounts for 80% of this problem
Hyperparathyroidism - Secondary
Excessive compensatory production of PTH because of high levels of phosphorus in the blood due to renal problems. Hypocalcemia from inadequate dietary calcium can cause it too.
S/S
Kidney stones, chronic back pain from fx, neuromuscular and CNS (personality disturbances, depression, psychosis, and coma)
Osteitis DeformansPaget’s Disease
a slowly progressive metabolic disorder characterized by an initial phase of bone resorption (osteoclastic phase), followed by a reactive phase of abnormal bone formation (osteoblastic phase).
Osteitis DeformansPaget’s Disease - Etiology
exact cause is unknown but it is thought that viral infection (mumps) may trigger it years after the exposure. 5% of patient’s with Paget’s disease develop osteosarcoma.
Paget’s Disease
Paget’s disease occurs worldwide but is rare in Asia, Middle East, Africa and Scandinavia.
In United States approximately 2.5 million people over the age of 40, mostly men have the disease
.
S/S: Early stages patient may be asymptomatic. Pain may occur from impingement of abnormal bone on spinal cord. Cranial enlargement (frontal and occipital bones) involved.
Pagetic sites are warm, tender and susceptible to pathologic fracture.
Treatment - Paget’s Disease
Drug therapy: Calcitonin given sc or IM or etidronate given p.o. to retard bone resorption
Mithramycin (cytoxic antibiotic) to decrease calcium loss, urinary hydroxypoline and serum alkaline phosphatase
Surgery: to repair fracture sites or correct deformities
Other tx: aspirin, ibuprofen for pain (symptomatic)
Tumors of the Bone -Primary
originate in bone or bone components
Tumors of the Bone - Secondary
metastatic tumors from other cancers (breast, prostate, etc.) that spread to the bone via the blood stream (nutrient artery and branches) or by direct invasion (proximity). The cancer usually will appear in the metaphysis (area between diaphysis and epiphysis) where the nutrient artery enters the bone. Cancer cells get trapped in the capillary beds of the bone and start growing.
Primary tumor of the bone - Osteoma
Benign Age of patient - any Common site -Skull, ear, sinuses Etiology -Bony outgrowth in EAM. Bilateral, multiple lesions Tx: Surgical Excision
Primary tumor of the bone - Fibroma
Benign
Age of patient - any
Common site -Fibrous bone tissues
Etiology -Displaces bone cells
Primary tumor of the bone - Osteochondroma
Benign
Age of patient - Age 15 to 25
Common site Lower femur
Etiology -Most common benign tumor
Primary tumor of the bone - Chondroma
Benign
Age of patient - any
Common site = Phalanges of hands and feet
Etiology = Develops from cartilage
Primary Malignant Bone Tumors -Osteosarcoma
Age of patient - 10-25 Location - Metaphysis of long bones Femur Tibia Humerus
Comments - Most common
15% 5 year survival rate
Treatment - 1. Surgery:
(a) resection
(b) Amputation
2. XRT
3. Chemo
Primary Malignant Bone Tumors -Fibrosarcoma
Age of patient -Males
30 to 40
Location - Fibrous tissue surrounding bone
1. Flat bones
Comments - Vary rare tumor
Nonosseous origin
Treatment -
- Surgery:
a. Amputation - XRT
- Chemo
Primary Malignant Bone Tumors -Chondrosarcoma
Age of patient -Males
30 to 50
Location - Pelvis Femur Ribs Shoulder
Comments - Develops From cartilage Painless, slow growing
Treatment -
Surgery
XRT for palliation
Chemo
Primary Malignant Bone Tumors -Ewings Sarcoma
Age of patient -Males 10 to 20
Location - Lower ext. Femur Pelvis Tib/Fib Vertebrae
Comments -Bone marrow Poor Px Mets to lung
Treatment -
Surgery
XRT
Chemo
Primary Malignant Bone Tumors -Giant Cell Tumor
Age of patient - Females 18-50
Location -
Long bones
Knee area
Comments -Benign tumor that becomes malignant
Treatment -
Surgery
Curettage
Scraping away material from cavity or surface
Inflammatory Lesions of the Bone - Osteomyelitis
a pyogenic infection of bone that may be acute or chronic.
Etiology:
(a) Complication of an acute localized infection
(b) Hematogenous dissemination- bacteremia
(c) Traumatic implantation: GSW, compound fx
Most common bacteria is Staph Aureus, E. Coli, Proteus vulagaris Pseudomonas Aeruginosa
Terms:
(a) Sequestrum: dead bone that collects and drains
its way out through an abscess or sinus tract
(b) Involucrum: Necrotic bone stimulates periosteum to create new
bone at the site of the infection.
S/S: Patient may have pain, tenderness, heat, swelling and restricted movement in the infected bone.
Dx: History of injury
Blood Tests: leukocytosis, elevated Erythrocyte Sedimentation Rate (ESR)
Blood cultures:
Hematogenous dissemination
bacteremia
Traumatic implantation
GSW, compound fx
Osteomyelitis -Most common bacteria
Staph Aureus, E. Coli, Proteus vulagaris Pseudomonas Aeruginosa
Sequestrum
dead bone that collects and drains its way out through an abscess or sinus tract
Involucrum
Necrotic bone stimulates periosteum to create new
bone at the site of the infection.
Osteomyelitis: S/S
Patient may have pain, tenderness, heat, swelling and restricted movement in the infected bone.
Osteomyelitis: Dx:
History of injury
Legg-Calve Perthes – Coxa Plana
Etiology: Spontaneous vascular interuption causes necrosis of femoral head in 1-3 weeks
New blood supply causes bone resorption and deposition of new bone cells. Deformity may result from pressure on weakened area (6 mo)
New bone replaces necrotic bone (2-3 years)
S/S: Persistent limp that becomes more severe especially during second stage of disease.
Mild pain (hip, thigh or knee) that is aggravated by activity and relieved by rest. Severely restricted abduction and rotation of hip.
Osteomyelitis: Blood Tests
leukocytosis, elevated Erythrocyte Sedimentation Rate (ESR) Blood cultures:
Inflammatory Lesions of the Bone - Legg-Calve Perthes Disease (Coxa Plana)
It is a disease where vascular interruption of the blood supply to a bone causes ischemic necrosis of the head of the femur. This causes the femoral head to flatten. It occurs most frequently in boys aged 4 to 10. The disease runs it’s course in 3 to 4 years. It may lead to premature osteoarthritis in later life due to misalignment of the acetabulum and flattened femoral head.
Legg-Calve Perthes – Coxa Plana Etiology
Spontaneous vascular interuption causes necrosis of femoral head in 1-3 weeks
Legg-Calve Perthes S/S
Persistent limp that becomes more severe especially during second stage of disease. Mild pain (hip, thigh or knee) that is aggravated by activity and relieved by rest. Severely restricted abduction and rotation of hip.
Legg-Calve Perthes – Coxa Plana - DX
- Physical exam and history
- Hip x-ray taken every 3-4 months
- Aspiration and culture of synovial fluid
to rule out joint sepsis
Tx: Protect femoral head from further damage by containing it within the acetabulum.
3 months of bed rest with reduced weight traction then hip abduction splint or cast
Inflammatory Lesions of the Bone - Osgood-Schalatter Disease
Is a painful, incomplete separation of the epiphysis of the tibial tubercle from the tibial shaft. It is most common in adolescent boys and affects both knees.
Osgood-Schalatter Disease - Etiology
Trauma before the complete fusion of the epiphysis to the main bone. It may be a single violent trauma or repeated knee flexion against a tight quadraceps muscle or a deficient blood supply and or caused by genetic factors.
It occurs between the ages of 10 to 15 years old.
Osgood Schlatter Disease - S/S
Constant aching, pain and tenderness below the knee cap which worsens during any activity that causes forceful contraction of the patellar tendon on the tubercle.
Soft tissue swelling, heat and tenderness may be present
Osgood Schlatter Disease - DX
Physical exam: examiner forces the tibia into internal rotation while slowly extending the patient’s knee from a 90 degree flexion. At about 30 degrees flexion there is pain that subsides immediately with external rotation of the tibia
X-rays may be normal or show epiphyseal separation and soft tissue swelling for up to six months after onset.
TX: 6 to 8 weeks of immobilization through reinforced elastic knee support, plaster cast or splint. This allows revascularization and
re-ossification of the tubercle and minimizes the pull of the quadriceps muscle.
(2) Supportive treatment may include activity restrictions and cortisone injections into the joint to relieve tenderness.
(3) Surgery in extreme cases. It may be necessary to remove or “fix” the epiphysis or drill holes through the tubercle of the main bone for form vascular channels
Inflammatory Lesions of the Bone -Aseptic Necrosis
Etiology: Death of bone with secondary irritation and low grade inflammation
(a) Idiopathic: no known cause
(b) Associated trauma
S/S: The age group is between 5 to 15 years old.
Symptoms: pain, muscle spasm, and postural disorders. It is usually self limited and spontaneously regenerates. It is a slow process.
Common sites: Small bones of the wrist and ankle
NOTE: Scaphoid bone of the wrist is most common which is why we do a PA wrist with ulna deviation.
Treatment: Immobilization
Treatment: Immobilization and analgesics
Aseptic Necrosis - Etiology
Death of bone with secondary irritation and low grade inflammation
(a) Idiopathic: no known cause
(b) Associated trauma
Aseptic Necrosis - S/S
The age group is between 5 to 15 years old.
Symptoms: pain, muscle spasm, and postural disorders. It is usually self limited and spontaneously regenerates. It is a slow process.
Aseptic Necrosis - common sites
Small bones of the wrist and ankle
NOTE: Scaphoid bone of the wrist is most common which is why we do a PA wrist with ulna deviation.
Aseptic Necrosis - Treatment
Treatment: Immobilization
Treatment: Immobilization and analgesics
Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis)
The most common form of arthritis. It is a chronic condition causing deterioration of the joint cartilage and formation of reactive bone at the margins and subchondral areas of the joint.
Generally it begins at age 40 and progresses through middle age. Disability depends on the site and severity of involvement. It can range from minor limitations of the fingers to severe disability in persons with knee or hip involvement.
Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - Etiology
(1) Primary: A normal part of aging from metabolic, genetic, chemical and mechanical factors (wear and tear).
(2) Secondary: develops following a predisposing event such as trauma (sprain, fracture or congenital deformity)
Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - S/S
- Joint pain after exercise or weight bearing that is relieved by rest. Stiffness in the morning
(2) Grating of the joint during motion and limited movement
(3) Osteoarthritis of the interphalangeal joints produces irreversible changes in the distal joints (Heberden’s nodes) and proximal joints (Bouchard’s nodes). These may be painless at first but eventually become red, swollen and tender
Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - DX
Thorough physical exam will confirm symptoms, and a lack of systemic symptoms rules out inflammatory joint disorders such as rheumatoid arthritis.
X-rays: PA, Lateral and oblique views confirm:
(1) Narrowing of joint space
(2) Joint deformity due to degeneration or articular damage
(3) Bony growths at weight-bearing areas
(hips and knees)
Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - TX
Pallative through medication and therapy
(1) Analgesics: aspirin, phenylbutazone, ibuprofen
(2) Intraarticular injections of corticosteroids
(3) Reduce joint stress by immobilization
(4) Surgery:
(a) Arthroplasty: joint replacement
(b) Arthrodesis: Surgical fusion (laminectomy)
(c) Osteoplasty: Scraping deteriorated bone from joint
(d) Osteotomy: change alignment of bone to relieve
stress by excision of wedge of bone or cutting of bone
Arthroplasty
joint replacement
Arthrodesis
Surgical fusion (laminectomy)
Osteoplasty
Scraping deteriorated bone from joint
Osteotomy:
change alignment of bone to relieve stress by excision of wedge of bone or cutting of bone
Inflammatory Lesions of the Bone Septic Arthritis
A medical emergency. Septic arthritis is caused by a bacterial invasion of the joint with inflammation of the synovial lining. If the organism enters the joint cavity then effusion and pyogenesis follow with eventual destruction of the bone and cartilage. Septic arthritis can lead to ankylosis and fatal septicemia.
Inflammatory Lesions of the Bone Septic Arthritis Etiology
Bacteria spread from a primary site through blood or contiguous extension to the joint.
Common organisms: Gram positive: Staph Aureous, Strep Pyogenes, Strep peumoniae, and Strep Viridans.
Gram Negative: Neiserria gonorrhea and Hemophilus influenzae
Other: E. Coli, Salmonella, and Pseudomonas
Note: Gram Positive usually infect Adults
H. Influenzae infect children
Inflammatory Lesions of the Bone Septic Arthritis DX
Laboratory: Gram stain or culture of synovial fluid. Joint fluid analysis shows gross pus or watery, cloudy fluid, decreased viscosity and WBC count of 50,000 per cubic mm.
X-ray: Distension of joint capsule followed by narrowing of the joint space (indicating damage) and erosion of the bone.
Nuclear medicine: 3 phase bone scan
Inflammatory Lesions of the Bone Septic Arthritis TX
Antibiotic Therapy Culture and Sensitivity
(1) Penicillin G: Staph Aureous, Staph Pyogenes
Staph Pneumoniae, Staph Viridens, and
N. Gonorrhea
(2) Nafcillin: for Penicillin resistant bacteria
(3) Ampicillin: for H. Influenzae
(4) Gentamicin: for Gram negative bacilli
Inflammatory Lesions of the Bone Septic Arthritis TX (1) Penicillin
G: Staph Aureous, Staph Pyogenes Staph Pneumoniae, Staph Viridens, and N. Gonorrhea
Inflammatory Lesions of the Bone Septic Arthritis TX (2) Nafcillin
for Penicillin resistant bacteria
Inflammatory Lesions of the Bone Septic Arthritis TX (3) Ampicillin
for H. Influenzae
Inflammatory Lesions of the Bone Septic Arthritis
TX(4) Gentamicin
for Gram negative bacilli
Inflammatory Lesions of the Bone Gouty Arthritis
Gout is a metabolic disease (an error in Purine metabolism) marked by urate deposits in the joint. It mainly occurs in the joints of the lower extremities.
Primary Gout
Purine is an amino acid which causes an over production of uric acid with retention in the blood (hyperuricemia).
Secondary Gout
Develops during the course of other diseases (obesity, diabetes mellitus, hypertension, sickle cell anemia and renal disease
Gouty Arthritis - DX
Presence of monosodium urate monohydrate crystals in the synovial fluid (arthrocentesis) or tophaceous material reveals intracellular crystals of sodium urate.
Increased serum uric acid in primary gout
Increased urinary uric acid in secondary gout
TX: Immobilization of joint
Analgesics: Acetaminophen
Corticosteroids or Corticotropin (IV or IM) Joint Aspiraton
Gout Treatment
TX: Reduce hyperuricemia
Allopurinol = reduces uric acid formation
Colchicine = prevents recurrent attacks
Probenecid and Sulfinpyrazone = promote uric acid excretion
NOTE: These drugs should not be given to patients with uric acid kidney stones.
Allopurinol
reduces uric acid formation
Colchicine
prevents recurrent attacks
Probenecid and Sulfinpyrazone
promote uric acid excretion
Inflammatory Lesions of the Bone Rheumatoid ArthritisAutoimmune Disorder
A chronic, systemic, inflammatory disease that primarily attacks peripheral joints (MCP) and surrounding muscles, tendons, ligaments and blood vessels.
Pathogenic Process: It believed that altered IgG antibodies are not recognized by the body so the body creates antibodies against itself (called RF antibodies).
Rheumatoid ArthritisAutoimmune Disorder Pathogenic Process
It believed that altered IgG antibodies are not recognized by the body so the body creates antibodies against itself (called RF antibodies).
Rheumatoid Arthritis -Pathogenic Process
Synovitis develops from congestion and edema of the synovial capsule.
Formation of pannus (thickened layers of granulation tissue antigen/antibody) marks the second stage of the disease. Pannus covers and invades the cartilage causing damage
Fibrous ankylosis (fibrous invasion of the pannus and scar formation occludes the joint space) characterized by the third stage of the disease
Rheumatoid Arthritis - S/S
RA develops insidiously and produces non-specific symptoms such as fatigue, malaise, anorexia and persistent low-grade fever, and weight loss. Later more specific localized articular symptoms develop at the following joints: PIP, MCP, and metarsophalangeal joints.
Rheumatoid Arthritis - DX
X-ray shows demineralization of bone and soft and soft tissue swelling. Later loss of cartilage and narrowing of joint spaces. Finally, bone and cartilage destruction, subluxations and deformities.
Lab: Rheumatoid Factor (RF) positive with a titer of 1:160 or higher
Erythrocyte Sedimentation Rate: elevated
Synovial fluid analysis: increased volume and turbidity but decreased viscosity and C3 & C4 complement. WBC count more than 10,000 per cubic cm.
Rheumatoid Arthritis Treatment TX
Salicylates (aspirin) decrease pain and inflammation
Non-Steroid Anti-inflamatory agents (NSAID)
such as Indomethacin, Fenoprofen and
Ibuprofen) are used
Immunosuppressive drugs such as
Cyclophsphamide and Azathioprin are used
* Supportive measures include 8 to 10 hours of sleep, splinting of joints and physical therapy that includes Range of Motion (ROM) exercises
Muscle and Connective Tissue Disorders
- Tendonitis: is an inflammation of the tendons and muscle attachments to bone.
Typical sites include: Rotator cuff, Hip, Achilles tendon and Hamstring
Etiology: Trauma. Strain during sports activity and musculoskeletal disorders such as Rheumatic disease, congenital defects, postural misalignments or hypermobility and abnormal body development - Bursitis: usually occurs at middle age from recurring trauma that stresses a joint or from an inflammatory joint disease such as rheumatoid arthritis or gout. Septic bursitis may result from wound infection or bacterial invasion of the skin covering the bursa.
Tendonitis:
Tendonitis: is an inflammation of the tendons and muscle attachments to bone.
.
Tendonitis:
Typical sites include:
Typical sites include: Rotator cuff, Hip, Achilles tendon and Hamstring
Tendonitis: Etiology
Trauma. Strain during sports activity and musculoskeletal disorders such as Rheumatic disease, congenital defects, postural misalignments or hypermobility and abnormal body development
Tendonitis: Bursitis:
usually occurs at middle age from recurring trauma that stresses a joint or from an inflammatory joint disease such as rheumatoid arthritis or gout. Septic bursitis may result from wound infection or bacterial invasion of the skin covering the bursa.
Muscle and Connective Tissue Disorders -Tendonitis - S/S
restricted movement of joint and localized pain that occurs mainly at night. Fluid accumulation causes swelling.
Calcific tendonitis: calcium deposits in the tendon cause proximal weakness and erosion into the adjacent bursa
Muscle and Connective Tissue Disorders -Bursitis - S/S
Fluid accumulation in the bursa causes irritation, inflammation, and sudden or gradual pain with limited movement.
Tendonitis- Diagnosis: X-rays
Diagnosis: X-rays: with tendonitis x-rays will be normal at first but may later show bone fragments, osteophyte formation, sclerosis, or calcium deposits.
Bursitis- Diagnosis: X-rays
Localized pain and inflammation and a history of unusual strain or injury 2 to 3 days before the onset of pain. During early stages the x-rays are normal except in situations of calicific bursitis.
Treatment – Bursitis and Tendonitis
- Rest the joint. Use immobilization with splint, cast or sling
- Analgesics
- Application of cold and warm compresses
- Ultrasound (diathermy)
- Injections of corticosteroids/lidocaine
Epicondylitis (tennis elbow)Epitrochlear Bursitis
Inflamation of the forearm extensor, supinator tendon.
Epicondylitis (tennis elbow)Epitrochlear Bursitis -Etiology
Partial tear of the tendon. It is a common injury in persons whose activities require a forceful grasp, wrist extension against resistance and frequent forearm rotation.
Epicondylitis (tennis elbow)Epitrochlear Bursitis - S/S
Elbow pain that worsens and radiates to forearm and hand.
Epicondylitis DX
Patient history. Doctor may reproduce pain by wrist extension and supination with lateral movement.
X-rays are negative
TX: Injections of corticosteroids and lidocaine
Aspirin
Supportive treatment includes: immobilization with a splint, heat therapy and short wave diathermy or ultrasound and physical therapy such as manipulation and massage to detach the tendon from the chronically inflammed periosteum.
Carpal Tunnel Syndrome
The most common nerve entrapment syndrome.
It involves entrapment and compression of the median nerve at the wrist, within the carpal tunnel.
Other structures passing through the carpal tunnel are: flexor tendons to the fingers and thumb and blood vessels.
Carpal Tunnel Syndrome -Etiology
The carpal tunnel is formed by the carpal bones and the transverse carpal ligament. Inflammation or fibrosis of the tendon sheaths that pass through the carpal tunnel cause edema and compression of the median nerve.
Carpal Tunnel Syndrome -Causes
may include: rheumatoid arthritis, flexor tenosynovitis, nerve compression, pregnancy, renal failure, menopause, diabetes mellatus, acromegaly, edema following a Colles fracture, hypothyroidism, benign tumors, tuberculosis and other granulomatous disease.
Repetitive motion syndromes have been identified as a causative agent too
Hallux Valgus - Bunion
lateral deviation of the great toe at the metarsophalangeal joint. It occurs with medial enlargement of the first metatarsal head and bunion formation (bursa and callus formation at the bony prominency)
Hallux Valgus - Bunion - Etiology
It may be congenital or familial but it is most often acquired from degenerative arthritis or prolonged pressure on the foot by shoes that compress the foot.
Congenital hallux valgus occurs as a result of abnormal bone alignment
Hallux Valgus - Bunion - S/S
Tender bunion covered by a deformed, hard, erythematous skin and palpable bursa. Pain from pressure caused by shoes is an indication too.
Hallux Valgus - Bunion - Traetment
Good footcare and proper shoes. Foam pads to separate first and second toes at night. Severe disease is treated by bunionectomy with corrective immobilization.
Congenital Disorders
Tailipes: Clubfoot
Most common congenital disorder of the lower extremities. It is marked by a deformed talus bone and shortened Achilles tendon.
1:1000 births
Talipes equinovarus: foot points downward
Talipes Treatment
- Correct deformity
- Maintain correction until foot regains normal muscle balance
- Observe foot for evidence of deformity recurrence
Deformity is corrected in sequential order with: - forefoot adduction then varus (inversion) and finally equinus (plantar flexion)
Congenital Hip Dysplasia
Abnormality of hip joint that is present at birth and is the most common disorder that affects hip joints of children under 3 years old.
Congenital Hip Dysplasia- Etiology:
Unproven theories suggest:
(1) Maternal hormones relax ligaments for preparation of labor
(2) Breech delivery rather than normal cephalic delivery
Congenital Hip Dysplasia - DX
1) check skin folds at hip area. Should be equal bilaterally
(2) Place child prone and observe buttock fold. Affected side will be higher
(3) Move patient into positions that would dislocate hip
(4) x-rays show the location of the femur in relation to the shallow acetabulum
Spinal Disorders
Kyphosis
Lordosis
Scoliosis
Herniated Nucleus Pulposes
Scoliosis
is a lateral curvature of the spine that may be found in the thoracic, lumbar, or thoracolumbar spinal segments. The curve may be convex to the right (most common in T-spine) or to the left (lumbar). Rotation of the vertebral column around it’s axis occurs and may cause rib cage deformity. Scoliosis is most often associated with kyphosis and lordosis.
Scoliosis -Causes
(1) Functional (postural) = poor posture
(2) Structural (deformity of vertebral bodies)
(a) Congenital: Wedge vertebra
(b) Paralytic or musculoskeletal due to asymmetric paralysis from polio or cerebral palsy
(c) Idiopathic (most common): may be transmitted as an autosomal dominant or multifactorial trait. Classified as infantile, juvenile or adolescent which generally affects girls between the ages of 10 to skeletal maturity.
Scoliosis - Diagnosis
Look at persons back
- Is one shoulder higher than the other?
- When child’s arms hang loosely at their side does one arm swing away from the body more than the other?
- Is one hip higher or more prominent than the other?
- Does child tend to tilt to one side?
Scoliosis - Diagnosis
X-rays in the AP and lateral projections taken with the patient standing upright and bending.
Measuring the degree of curvature using the Cobb Method
Note:
(1) Curve of 25 degrees or less = Monitor every three months
(2) Curve 30-50 degrees = spinal exercise and brace
(3) Curve of 40 degrees or more may require spinal fusion
Scoliosis - Diagnosis
Measuring the degree of curvature using the Cobb Method
Measuring the degree of curvature using the Cobb Method - Curve of 25 degrees or less
Monitor every three months
Measuring the degree of curvature using the Cobb Method - Curve 30-50 degrees
spinal exercise and brace
Measuring the degree of curvature using the Cobb Method - Curve of 40 degrees or more
may require spinal fusion
Herniated Nucleus Pulposes
This problem occurs when all or part of the nucleus pulposes (the soft gelatinous central portion of the intervertebral disk) is forced through the disk’s weakened or torn outer ring (annulus fibrosis)
HNP
The extruded disk may impinge on spinal nerve roots as the exit from the spinal canal or the spinal cord itself. This will result in back pain and other signs of nerve root irritation (tingling, shooting pains etc.).
HNP Etiology
- Severe trauma or strain to the back
- Intervertebral disk degeneration due to age
(a) 90% occurs in lumber or Lumbar sacral region
(b) 8% in the cervical region
(c) 2% in the thoracic region
HNP - Signs/Symptoms
Severe low back pain which radiates to the buttocks, legs and feet, usually unilaterally. Pain may be sudden following the injury and may go away but recur at intervals.
Sciatic pain follows beginning as a dull pain in the buttocks. Valsalva maneuver, coughing, sneezing or bending intensifies the pain.
Sensory and motor loss in the affected nerve root may result in atrophy of leg muscles and weakness
HNP Diagnosis
(1) X-rays to R/O other abnormalities of spine
(2) Check of extremity pulses including posterior tibial and dorsalis pedis pulses, skin temperature to R/O ischemic disease
(3) Myelography: contrast injection into the subarachnoid space of spinal canal between 3rd and 4th lumbar vertebrae
(4) Computed Tomography
(5) MRI – shows soft tissue swelling and herniation
HNP Treatment: Usually conservative
(1) Bed rest with pelvic traction, heat, and an exercise program
(2) Aspirin to reduce inflammation and edema
(3) Epidural injections of steroids (cortisone or dexamethasone) and lidocaine as well as muscle relaxants (diazepam or methocarbamol)
(4) Surgery: laminectomy: excision of a portion of the lamina and remove protruding disk. Spinal fusion may be necessary to overcome segmental instability.
(5) Chemonucleolysis: injection of the enzyme Chymopapain to dissolve the disk
(6) Microdiskectomy (laser) removal of fragments of the disk
Fractures and Dislocations
Fracture: Loss of integrity of the bone structure
(1) Causes: trauma, child abuse, pathologic (metabolic or nutritional), tumors (primary or metastatic), and stress fractures (prolonged standing, walking or running)
S/S: the “5 P’s” for arm and leg fractures:
(1) Pain and point tenderness
(2) Pallor
(3) Pulse loss
(4) Paresthesia
(5) Paralysis
Fracture
Loss of integrity of the bone structure
Fractures and Dislocations S/S
the “5 P’s” for arm and leg fractures:
(1) Pain and point tenderness
(2) Pallor
(3) Pulse loss
(4) Paresthesia
(5) Paralysis
Fracture Incomplete:
break partially extends through bone (Greenstick)
Fracture Complete:
Bone breaks into two or more pieces
Fracture Simple (closed):
overlying skin is not broken
Fracture Compound (open):
overlying skin is broken with risk of infection
Fracture Non-displaced:
fractured bones remain in alignment
Fracture Displaced:
Bone ends are not in alignment creating risk of muscle contractures and deformity
Fracture Transverse:
break runs transversely across bone
Fracture Oblique:
break runs at an angle across the bone
Fracture Spiral
break winds around bone like a coil
Fracture Linear:
Break runs the length of the bone
Fracture Comminuted:
bone is shattered or compressed in fragment
Fracture Impacted:
Bone ends are driven into each other
Fracture Compression:
Bone collapses (vertebrae) under pressure
Fracture Avulsion:
overexertion tears a muscle or ligament away from bone with pulling away a piece of the bone
Fracture Depression:
Trauma drives bone fragments inward
Dislocation
the bones of the joint totally lose contact with their articulating surfaces
Subluxation
the bones of the joint partially lose contact with their articulating surfaces
Disolocation and Subluxations Etiology
May be congenital or occur as a result of trauma
