5. Introduction
• Structural break in continuity of the bone
• Complete/ incomplete break in continuity of the
cortex of the bone
Causes:
• Traumatic (in normal bones) or pathological (in
diseased bones)
• Green stick (in immaturity)
• <fall/ accident/ tumors/ immaturity/ drugs>
6. Classification
• Based on etiology
• Traumatic
• Fatigue/ stress
• Pathological
• Clinical basis
• Closed
• Open
• Based on involvement of joint
• Extra capsular / articular
• Intracapsular/ articular
• Based on number of
fragments
• Simple
• Comminuted
• Involvement of vital structures
• Simple
• Complicated
• Pattern
• Linear
• Transverse
• Oblique
• Spiral
• Comminuted
• Compacted
• Compression
• Greenstick
• Impacted
7. Pathophysiology
• Injury/ stress periosteum and blood vessels in
cortex, marrow and surrounding soft tissue
disturbed hematoma formation replaced by
granulation tissue
• Pathophysiology is d/t inflammatory response
• Osteoblasts produce callus (osteoid)
• Osteoclasts remodelling and resorption
• Osteoblasts mature into osteocytes
8. Clinical Features
• Pain
• Deformity, swelling, tenderness
• Muscular spasm
• Broken skin with bone protruding outside
• Limited range of motion
• Ecchymosis, DNVS altered/ intact
• Crepitus/ clicking sound on movement
12. Introduction
• Myelo – marrow
• Infection/inflammation of bone + marrow
• Usu. By pyogenic organisms
• Pathologically significant types:
• Pyogenic osteomyelitis
• Tuberculous osteomyelitis
13. Classification
Based on origin:
• Primary
• Secondary
Based on cause/ duration:
• Acute (7 days) – Staph., Streptococcus, Pneumococcus,
Salmonella
• Sub acute – over 21 days
• Chronic – discharging sinus e.g. tuberculous
14. ETIOLOGY
Age group Most common organisms
Newborns (< 4 months) S. aureus, Enterobacter spp.,Gp.A
beta hemolytic Streptococcus
Children (4 months – 4 years) S. aureus, Gp.A beta hemolytic
Streptococcus, Haemophilus
influenzae, Enterobacter spp.
Children/ adolescents (4 yrs+) S. aureus, Gp.A beta hemolytic
Streptococcus, H. influenzae,
Enterobacter spp.
Adult (18+) S. aureus, occasionally
Enterobacter or Streptococcus
spp.
15. Pathogenesis
• Pathogen grows in a hematoma or in weakened area or
site of infection travels through blood to metaphysea
end of marrow cavity pus formed pressure built
spread along marrow cavity (leads to periosteitis)
• Infection may form subperiosteal abscess or drain via
sinuses.
• Combination of suppuration and impaired blood supply
erosion, infarction and necrosis of cortex
(sequestrum).
• New bone formed beneath periosteum over infected
bone (involucrum)
16. Pathogenesis (cntd….)
• Acute osteomyelitis may be contained to a
localized area and sealed by fibrous tissues and
granulation tissue BRODIE’s Abscess
• After involucrum formation; resolution may occur
or complications may occur
• Basic pattern:
• Suppuration ischemic necrosis healing by
fibrosis/ bony repair
18. Clinical features
• Pain
• History of or current infection source
• Restricted movement
• Local rise of temperature
• Tenderness over affected area
• Swelling and redness
• In infants, continuous crying, fever, malaise, ill and toxic
look.
• Discharging pus from sinus
19. Investigations
• Blood –TC, DC, ESR, Hb% WBC and ESR
elevated
• Blood C/S
• Imaging – X ray, CT scan, MRI
• Bone scan
20. Treatment
• Immobilization, traction, bed rest
• Supportive measures (analgesic, fluid support)
• I & D, C/S of pus.
• Acute osteomyelitis
• Systemic antibiotic, intracavitary instillation via closed system,
continuous irrigation with low intermittent suction
• Limited irrigation
• Packed wet antibiotic soaked dressing
• Chronic osteomyelitis (poor prognosis)
• Surgery for removal of dead bone and abscess
• Hyperbaric O2
• Skin, bone and muscle grafts
22. Introduction
• Group of congenital primary muscular diseases
• Progressive, symmetrical wasting of skeletal
muscles without neural or sensory deficits.
• Major forms:
• Duchenne’s
• Becker’s
• Myotonic
• Facio- scapulo-humeral
• Limb girdle
• occulopharyngeal
23. Common to all forms of muscular dystrophies
are muscle fiber necrosis, regenerative activity,
replacement by interstitial fibrosis and adipose
tissue.
24. Pathophysiology
• Metabolic changes that causes the muscles to die are
present from foetal life itself.
• Abnormally permeable cell membrane leakage of a
variety of muscle enzymes (esp. creatinine kinase).
• Phagocytosis of muscle cells by inflammatory cells may
cause scarring and loss of muscle function.
• Skeletal muscles replaced by fat and connective tissues
deformed bones progressive immobility.
• Fibrosis of cardiac and smooth muscles.
25. Clinical features
• Weakness on site of dystrophy
• Enlarged firm calf muscles, toe walking and lumbar
lordosis
• Difficulty in climbing stairs, inability to raise arms
above head
• Winging of scapula, abnormal movement
27. Treatment
Supportive care only
• Breathing exercise
• Awareness of early signs / symptoms
• Orthopedic appliances, physiotherapy
• Surgery to correct deformity (contractures)
• Dietary regulation - Low calorie, high protein, high
fiber diet
• Genetic counseling
29. Introduction
Disorder of purine metabolism with one or more of the
following:
1. Increased sr. uric acid concentration (hyperuricemia)
2. Recurrent attacks of characteristic type of acute
arthritis (with monosodium urate monohydrate <tophi>
crystals seen inWBCs of synovial fluid)
3. Aggregated deposits of tophi in and around the joints
4. Renal diseases
5. Uric acid nephrolithisasis.
37. Rheumatoid Arthritis
• Chronic, multisystem disease
• Symetrical, destructive, deforming poly arthritis of
small and large synovial joints with associated systemic
disturbances.
• 80% cases are seropositive for RF (also elevated in
hepatitis, cirrhosis, sarcoidosis and leprosy)
• Other lab findings:
• Normocytic normochromic RBC
• Elevated ESR
• Leucocytosis
• Hypergamma globulinaemia
38. Etiopathogenesis
Occurs in immunologically predisposed individuals to
the effect of microbial agents acting as triggers.
• Immunological derangements
• Trigger events:
• Infectious agents – mycoplasma, EBV, CMV,
rubella.
• Male: female = 3:1
• Common between 3rd and 5th decades
39. Antigenic exposure CD4+T cells activated
Cytokine secretion activate endothelial
cells, B lymphocytes and macrophages
IgM against IgG (anti-IgG)/ Rheumatoid
factor damage to synovium, small blood
vessel and collagen.
Inflammatory cell collection stimulated
macrophages cytokines pannus
formation
Damage & destruction of bone and cartilage
fibrosis and ankylosis JOINT
DEFORMITIES
40. Diagnosis criteria
1. Morning stiffness (>1 hr)
2. Arthritis of >3 joint areas
3. Arthritis of hand joints
4. Symmetrical arthritis
5. Rheumatoid nodules
6. Rheumatoid factor
7. Radiological changes
Duration > 6 weeks
Diagnosis – if 4 or more criteria (+)
41.
42. Clinical features
• Onset is gradual
• Joint pain, stiffness and symmetrical swelling of a
number of peripheral joints
• Initially – pain only on movement of joints
• Later – pain at rest & early morning stiffness
• First affects small joints of fingers and toes wrist,
elbows, shoulder, knees and ankle, subtalar and mid
tarsal joints.
• PIP swelling spindle appearance of fingers
• MTP swelling broad forefoot
43. Investigations
• Blood picture – anaemia, ESR elevated
• Serology – RA factor (+)
• X ray of affected joint – periartcular osteoporosis,
loss of articular space, erosions, subluxation and
ankylosis
• Synovial fluid analysis/ arthroscopy
44.
45. Microscopic appearance
Articular lesions:
• Diffuse synovitis with pannus formation
• Foci of fibrinoid necrosis and fibrin deposition
• Intense inflammatory infiltration
Extra articular lesions:
• Non specific inflammatory changes seen
• Rheumatoid nodules in SC tissues over pressure
points (elbows, occiput and sacrum)
46. Variants
• Juvenile RA
• <16 yrs of age with fever and predominant involvement of
ankle and knee.
• Felty’s syndrome
• Polyarticular RA + splenomegaly/ hypersplenism
• Ankylosing spondylitis
• Rheumatoid involvement of spine, esp SI joints in young males
with HLA B27 association
47. Treatment
• General supportive care – rest, nutrition,
physiotherapy
• Local measures – splints, intra articular steroid
injection
• NSAIDS
• IMMUNOMODULATION – azathioprine,
cyclophospamide, cyclosporine.
• Medical synovectomy
• Surgical correction and rehabilitation
52. Introduction
• Myasthenia – muscular weakness
• Gravis – serious
• Neuromuscular disorder of autoimmune origin in which
AchReceptors in motor end plates are damaged.
• Adult women: adult men = 3:2 (15-50 yrs)
• Descending polyneuropathy
• In late cases, muscle fatigue and respiratory paralysis death
• c/f aggravate on use and relieved on rest
53.
54.
55. Investigations
• Tensilon test :
• Injection of endrophonium or neostigmine
temporarily improves muscle function within 30-60
secs to 30 mins.
• Sr. Ach receptor antibody titer – increased
• EMG – electromyelography
58. Introduction
• Clinical syndrome involving multiple bones
• Quantitative reduction of otherwise normal bone
tissue mass
• Results in fragile skeleton which is a/w increased
risk of fractures and consequent pain n deformity.
• Common in elderly and post menopausal women.
• Radiologically evident after >30% of bone mass
has been lost
• Sr. calcium, phosphorus, ALP usu. Normal
60. Primary osteoporosis
Cause: osteopenia without underlying disease or medication
• Idiopathic – in young and juveniles
• Involutinoal – postmenopausal women, ageing individuals
Risk factors
• Genetics – more in whites and asians
• Sex – females> males
• Reduced physical activities (old age)
• Deficiency of sex hormones – oestrogen (post menopausal), androgen
(in male)
• Combined deficiency of calcitonin and oestrogen
• Hyperparathyroidism
• Deficiency ofVit D
61. Secondary osteoporosis
• Immobilization
• Chronic anaemia
• Acromegaly
• Hepatic diseases
• Hyperparathyroidism
• Hypogonadism
• Thyrotoxicosis
• Starvation
• Effect of medications – hypercortisonism,
adminsitration of anticonvulsants, large dose of
heparin.
