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Complications of
fractures
CLASSIFICATION
1)Immediate: (Occur atthetimeofinjury)
Systemic:
Local :
Hypovolaemic shock
Injury to major vessels, peripheral nerves, muscles and
tendons,, joints and viscera.
2)Early:
Systemic:
(occur on initial few days (1-2
days) after injury)
Hypovolaemic shock
ARDS and Fat embolism
syndrome.
DVT and pulmonary embolism
Crush syndrome
Aseptic traumatic fever
Septicaemia ( in open fractures)
Local: infection
Compartment syndrome
3) Late : (Occur long time after injury)(1-2 weeks)
Delayed union
non union
Malunion
cross union
Others :
Avascular necrosis
Shortening
joint stiffness
Reflex sympathetic dystrophy (sudeck dystrophy)
myositis ossificans
Osteomyelitis
osteoarthritis
. Ischemic contrature
Sourceofhaemorrhage:
HYPOVOLEMIC SHOCK
a) External: In compound fractures, c or s injury to
major vessel
b) Internal: In blunt injury abdomen,&chest and
pelvic fractures etc.
Blood loss :
• Femoral shaft fractures range 1000 – 1500 ml.
• Pelvic fractures range 1500– 2000 ml.
• Tibial shaft fractures range 500 – 1500 ml.
Grading of blood loss
Clinical features :
•Hypotension, Tachycardia
•Oliguria, Clouded sensorium
•Cool, clammy, moist skin.
•Increased respiratory rate, Low volume rapid / thready pulse.
•Sweating, Sunken eyeballs, Tongue – pale and dry
•Patient gradually becomes drowsy, BP falls and renal output
decreases ; patient may become unconscious and die.
management
Starts even before the cause is established
• Two large bore iv cannulas put
• Infuse 2000 ml of crystalloids (ringer lactate) followed by
colloid (haemaccel) and blood if needed
• Venous cut down & central line if peripheral
vasoconstriction is present
• Localise the site of bleed- if in body cavities, perform
chest aspiration or diagnostic peritoneal lavage.
Sometimes a simple x ray is enough.
• Chest bleeding----chest tube
• Abdominal bleeding---- laparotomy
• Blood loss from # ---- immobilisation
• Pelvis stabilisation c external fixator
• Advanced---- emergency angiography & embolisation of
vessel
Injury to major vessels
c/f of ischemic limb
Pain palor
Paraesthesia pulseless
Paralysis
Diagnosis
Clinical
Doppler study
Angiogram (ischemia)
Consequences
No effect ( good collateral circulation)
Exercise ischemia
Ischaemic contracture
gangrene
Injury to nerves
How damaged?
# fragments
Entrapment btw # fragment during reduction
Entrapment in callus /fibrous tissue
Sharp object direct injury
Consequences:
Neuropraxia ( compression) --- physiological disruption of
conduction. local myelin damage with nerve still intact
Axonotmesis (crush) --- discontinuity of axons
Neurotmesis – complete rupture of nerve
c/f:
neuropraxia: numbness & tingling sensation (
dermatomes)
axonotmesis: dec sensation & motor weakness
neurotmesis: complete loss of sensation & no power
Dx: clinical
Electromyography ( EMG)
nerve conduction study
MRI
Rx: neuropraxia : splint & vit B1/B6/B12
axonotmesis: exploration
end to end anast
nerve grafting
physiotherapy
ARDS (Acute Respiratory Distress Syndrome)
Respiratory distress following a trauma
release of Inflammatory cells and proteinaceous fluid
that accumulate in the alveolar spaces
Disruption of microvasculature of pulm system
decrease in diffusing capacity and hypoxemia.
Onset- 24 hours after injury
c/f:
1)Dyspnoea
2)Tachypnoea
Diagnosis:
1)Spo2 <50%
2)Xray – diffuse pulm
Infiltrates
Management:
1)100% oxygen
2)Assisted ventilation
Fat embolism syndrome
One of the most serious comp
Seen in fracture of long bone ( # shaft femur)
Pathogenesis ( 2 theories)
# bone
Hormonal changes thrombosis
FAT
Lipase
FREE FATTY ACID plt & firbin agg
Release into circulation vasculitis
Attack wall of vessels
2)Disrupted bone marrow /adipose tissue
fat globules forced into torn venules
lung capillaries
c/f
made clinically ( 24 to 72 hrs)
Pulm: tachypnoea
spo2 < 50%
resp distress
Cerebral: drowsy
restlessness
disoriented
coma
Others: petechial rash
conjunctival petechia
retinopathy
tachycardia
Diagnosis
Clinically
tachycardia
Spo2<50%
Petechial rash
Fever
Esr inc
Hb & plt dec
Fat globule in urine and sputum
Fundoscopy : retinal petechia
Xray: patchy pulmonary infiltrates( snow storm appearance )
treatment
Respiratory support
Iv dextran
Anticoagulants – LMWH
Corticosteroids
Iv 5% dextrose with 5% alcohol – causes emulsification
of fat globules
DEEP VEIN THRMBOSIS AND
PULMONARY EMBOLISM
Is common in lower limb injuries, pelvic fractures and
spinal injury.
Commonly occurs in leg veins (calf)/ but may also
involve thigh.
Pulmonary embolism is a complication of DVT where
clot is detached from its site of formation and passes
via I.V.C. and right heart to pulmonary arteries
which may lead to collapse and sudden death.
PATHOLOGY
Virchow'striad
1. decreased flow rate
of the blood
2. damage to the blood
vessel wall
3. hypercoagulability
trauma
immobilisation
Venousstasis
thrombosis
Risk factors
1)Immobilisation
2)Surgery
3)Cast
4)Smoking
5)Obesity
6)Ocp
7)pregnancy
DVT can be recognized as early as 48 hours of
injury. Pulmonary embolism usually develops 4-
5days after injury.
C/F (PE)
Dyspnoea
Tachypnoea
Tachycardia
Hypotension
hemoptysis
c/f ( DVT)
oedema
Erythema
dilated veins of the leg
Dull aching or nagging pain in calf muscles.
Superficial blebs in the skin, skin red and warm.
Low grade fever with increased pulse rate is characteristic.
Patient complains of swelling, difficulty in standing, walking and cramps
in the leg.
Diagnosis
Dvt:
Homans test : Forcible dorsiflexion at foot ----- calf or
popliteal region pain.
Constrast venography
Doppler ultrasound
D-dimers
Pulmonary embolism
D-dimer
Blood gas- resp alkalosis
Ecg- S1Q3T3
CXray
CT pulm angiography (gold standard test)
V/Q Scan
treatment
DVT
Prophylaxis
1)Active/ passive calf pump and toe
movement
2)Elevation
3)Deep breathing exercise
4)Elastic TED stockings
5)Early internal fixation to provide
early mobility.
Management
1)Bed rest
2)Elevation
3)Inj LMWH
4)Warfarin
5)Venous bypass
6)IVC filters
PE
Management
1)Pulm support
2)Anticoagulant
OR thrombolysis
3)Surgical embolectomy
4)IVC filter
Crush syndrome
RTA
High energy trauma
Crush muscles
Myohemoglobin into circ
Ppt in renal tubules
Acute tubular necrosis
c/f ( ARF) appear within 2 -3 days
1)Oliguria
2)Hyperkalemia & m/b acidosis
3)Dec urine output
4) Restlessness
5) Delirium
Treatment
Prophylaxis
Application of tourniquet and gradual release to slowly
allow the myoglobin to reach the kidneys
Management
rx as acute renal failure – aggressive fluid resuscitation
maintenance of electrolyte
imbalance
• What is Compartment syndrome?
An elevation of the interstitial pressure in a closed
osteofascial compartment that results in
microvascular compromise.
Compartment syndrome
• Compartments are groups of
muscles surrounded by
inelastic fascia.
• Increased pressure within a
muscle compartment causes
decreased blood supply to
affected muscles.
• Any swelling of muscles leaves
no room for expansion and
blood supply is progressively
shut off.
• If affected muscles are
deprived of blood supply for
> 6 hours, nerve and muscle
tissue can be permanently
damaged.
etiology
1) Decrease compartment size
-Tight dressings/closure of fascial defect
-External pressures : casts, splints ,lying on limb for long
period,
2)Increase compartment contents
Hemorrhage -- vascular injury, coagulopathy
Muscle edema -- severe exercise , crush injury
Burn -- increase capillary permeability
Pathophysiology
This vicious cycle continues
until total vascularity of mm
& nerves within compartment
is compromised
Leading to mm necrosis & nerve
damage
Necrotic mm undergo healing
with fibrosis
contactures
Clinical Presentation:
• Swelling/ Tightness of compartment
• pain out of proportion
• decrease power in mm within affected comp
• Pallor/Cyanosis
• Hyperesthesia/Paresthesia
• Paralysis : full recovery is rare
diagnosis
1) Stretch test ( earliest sign)
Pain on passive stretching of mmm
Ex: passive extension of fingers --- pain flexor comp of
forearm
2) Measure pressure in each compartment
>40mm h2o
treatment
Limb elevation & active movement as prevention
Remove any bandage /slab /cast then readjust
Early surgical decompression within 6hrs
Like fasciotomy & fibulectomy(middle 3rd of fibula is
excised to decompress all comp of legs)
Delayed & non union
Delayed union : When a fracture takes more than the
usual time to unite
Non union : When the process of healing stops before
completion. To diagnose non union the fracture has
to be minimum 6 months old & progressive
evaluation of xray done.
TYPES
1. Atrophic: no or minimal callus formation
2. Hypertrophic: callus is present but it does not
bridge the fracture site.
COMMON SITES
Neck of femur
Scaphoid
Lower third of tibia
Lower third of ulna
Lateral condyle of humerus
C/F
Persistent Pain
Increase deformity @ fracture site ( non union)
Abnormal mobility(non union)
Refracture
Radiological findings
Delayed union: inadequate callus, visible fracture
line
Non union: ends are rounded, smooth sclerotic.
Medullary cavity may be obliterated. visible fracture
line.
treatment
1)Asymptomatic – no Rx ( scaphoid)
2)ORIF & bone grafting
3)Excision & replacement by prothesis ( THR)
4) ILIZAROV’s mtd:
MALUNION
MALUNION : When a fracture does not unite in
proper position
Causes:
1.Improper reduction
2.Unchecked muscle pull ( # clavicle)
3.Excessive comminution ( colle’s #)
Common sites: supracondylar # of humerus
colle’s #
olecranon #
# both forearm bone
C/F
Deformity
Shortening of limb
Limitation of movements
Treatment
1.osteoclasis:
2.Redoing the fracture surgically: most common. ORIF
is generally done along with bone grafting.
3.Corrective osteotomy:
4.Excision of protruding bone.
Cross union : 2 bones unites with each other
common in # forearm
shortening
Common comp of malunion, crushing, growth defect
Treatment:
<2cm : not noticeable
shoe raise
>2cm : elderly: shoe raise
young: limb length equalisation procedure
Avascular necrosis
# blood supply to a part of bone
necrosis of that part
Common sites:
Site
-head of the femur
-Proximal pole of scaphoid
-Body of talus
Cause
-fracture neck of femur
-post disclocation of hip
-# thru waist of scaphoid
- # thru neck of talus
c/f
1)Early stage – asymptomatic
2)Later stage – 2* osteoarthristis
Painful limitation of joint movement
Stiffness
Diagnosis:
Suspected in # where it is known to occur because pain and
stiffness appear late
Xray changes
1)Sclerosis of necrotic area; with revascularisation, new bone is
deposited around dead bone resulting in increase bone density
2)Subchondral cysts
3) deformity of bone because of collapse of necrotic bone
4)Osteoarthritis: dec joint space, osteophytes
treatment
Prevented by early, energetic reduction
Rx:
1)Delay weight bearing for revascularisation
2)Revascularisation procedure by vascularised bone
graft
3)Excision of avascular segment not hampering
functions
4)Excision & prosthesis
5)Total joint rep or arthrodesis
Myositis ossificans
Ossification of hematoma around joint
formation of mass of bone
Restricting joint mvnts
Causes
1)Severe injury to a joint when capsule & periosteum
stripped from bone by violent disp of the fragments
2)Common in children: periosteum is loosely attached to
bone
3)Common arnd elbow jt
4)Massage foll trauma aggr myositis
Consequences / clinical features
1)Stiffness of jt
2)Restriction of jt
3)Complete loss of mvnt
Xray:
Active myositis: fluffy margins of bone mass
Mature myositis : trabeculated with well defined margins
Rx
Active: early ; rest, NSAIDS, physiotherapy
late: physiotherapy & french osteotomy
Sudeck’s dystrophy
Is a group of disorder where there is dysfunction in
the normal “ injury and repair process” leading to an
exaggerated response to anoxious stimulus.
Trauma is relatively minor and hence symptoms and
signs are out of proportion to the trauma
c/f
Pain
Hyperaesthesia
Tenderness
Swelling
Skin: red shiny warm ( early stage)
Late: prog atrophy of skin mm & nails
Joint deformities & stiffness
Xray: characteristics spotty rarefaction
Rx.
Physiotherapy
Betablocker
Sympathetic blocks

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complication of fractures.ppt

  • 2. CLASSIFICATION 1)Immediate: (Occur atthetimeofinjury) Systemic: Local : Hypovolaemic shock Injury to major vessels, peripheral nerves, muscles and tendons,, joints and viscera. 2)Early: Systemic: (occur on initial few days (1-2 days) after injury) Hypovolaemic shock ARDS and Fat embolism syndrome. DVT and pulmonary embolism Crush syndrome Aseptic traumatic fever Septicaemia ( in open fractures) Local: infection Compartment syndrome
  • 3. 3) Late : (Occur long time after injury)(1-2 weeks) Delayed union non union Malunion cross union Others : Avascular necrosis Shortening joint stiffness Reflex sympathetic dystrophy (sudeck dystrophy) myositis ossificans Osteomyelitis osteoarthritis . Ischemic contrature
  • 4. Sourceofhaemorrhage: HYPOVOLEMIC SHOCK a) External: In compound fractures, c or s injury to major vessel b) Internal: In blunt injury abdomen,&chest and pelvic fractures etc. Blood loss : • Femoral shaft fractures range 1000 – 1500 ml. • Pelvic fractures range 1500– 2000 ml. • Tibial shaft fractures range 500 – 1500 ml.
  • 6. Clinical features : •Hypotension, Tachycardia •Oliguria, Clouded sensorium •Cool, clammy, moist skin. •Increased respiratory rate, Low volume rapid / thready pulse. •Sweating, Sunken eyeballs, Tongue – pale and dry •Patient gradually becomes drowsy, BP falls and renal output decreases ; patient may become unconscious and die.
  • 7. management Starts even before the cause is established • Two large bore iv cannulas put • Infuse 2000 ml of crystalloids (ringer lactate) followed by colloid (haemaccel) and blood if needed • Venous cut down & central line if peripheral vasoconstriction is present • Localise the site of bleed- if in body cavities, perform chest aspiration or diagnostic peritoneal lavage. Sometimes a simple x ray is enough. • Chest bleeding----chest tube • Abdominal bleeding---- laparotomy • Blood loss from # ---- immobilisation • Pelvis stabilisation c external fixator • Advanced---- emergency angiography & embolisation of vessel
  • 8. Injury to major vessels
  • 9. c/f of ischemic limb Pain palor Paraesthesia pulseless Paralysis Diagnosis Clinical Doppler study Angiogram (ischemia) Consequences No effect ( good collateral circulation) Exercise ischemia Ischaemic contracture gangrene
  • 10.
  • 11. Injury to nerves How damaged? # fragments Entrapment btw # fragment during reduction Entrapment in callus /fibrous tissue Sharp object direct injury Consequences: Neuropraxia ( compression) --- physiological disruption of conduction. local myelin damage with nerve still intact Axonotmesis (crush) --- discontinuity of axons Neurotmesis – complete rupture of nerve
  • 12. c/f: neuropraxia: numbness & tingling sensation ( dermatomes) axonotmesis: dec sensation & motor weakness neurotmesis: complete loss of sensation & no power
  • 13. Dx: clinical Electromyography ( EMG) nerve conduction study MRI Rx: neuropraxia : splint & vit B1/B6/B12 axonotmesis: exploration end to end anast nerve grafting physiotherapy
  • 14. ARDS (Acute Respiratory Distress Syndrome) Respiratory distress following a trauma release of Inflammatory cells and proteinaceous fluid that accumulate in the alveolar spaces Disruption of microvasculature of pulm system decrease in diffusing capacity and hypoxemia. Onset- 24 hours after injury
  • 15. c/f: 1)Dyspnoea 2)Tachypnoea Diagnosis: 1)Spo2 <50% 2)Xray – diffuse pulm Infiltrates Management: 1)100% oxygen 2)Assisted ventilation
  • 16. Fat embolism syndrome One of the most serious comp Seen in fracture of long bone ( # shaft femur) Pathogenesis ( 2 theories) # bone Hormonal changes thrombosis FAT Lipase FREE FATTY ACID plt & firbin agg Release into circulation vasculitis Attack wall of vessels
  • 17. 2)Disrupted bone marrow /adipose tissue fat globules forced into torn venules lung capillaries
  • 18. c/f made clinically ( 24 to 72 hrs) Pulm: tachypnoea spo2 < 50% resp distress Cerebral: drowsy restlessness disoriented coma Others: petechial rash conjunctival petechia retinopathy tachycardia
  • 19. Diagnosis Clinically tachycardia Spo2<50% Petechial rash Fever Esr inc Hb & plt dec Fat globule in urine and sputum Fundoscopy : retinal petechia Xray: patchy pulmonary infiltrates( snow storm appearance )
  • 20.
  • 21. treatment Respiratory support Iv dextran Anticoagulants – LMWH Corticosteroids Iv 5% dextrose with 5% alcohol – causes emulsification of fat globules
  • 22. DEEP VEIN THRMBOSIS AND PULMONARY EMBOLISM Is common in lower limb injuries, pelvic fractures and spinal injury. Commonly occurs in leg veins (calf)/ but may also involve thigh. Pulmonary embolism is a complication of DVT where clot is detached from its site of formation and passes via I.V.C. and right heart to pulmonary arteries which may lead to collapse and sudden death.
  • 23. PATHOLOGY Virchow'striad 1. decreased flow rate of the blood 2. damage to the blood vessel wall 3. hypercoagulability trauma immobilisation Venousstasis thrombosis
  • 24. Risk factors 1)Immobilisation 2)Surgery 3)Cast 4)Smoking 5)Obesity 6)Ocp 7)pregnancy DVT can be recognized as early as 48 hours of injury. Pulmonary embolism usually develops 4- 5days after injury. C/F (PE) Dyspnoea Tachypnoea Tachycardia Hypotension hemoptysis
  • 25. c/f ( DVT) oedema Erythema dilated veins of the leg Dull aching or nagging pain in calf muscles. Superficial blebs in the skin, skin red and warm. Low grade fever with increased pulse rate is characteristic. Patient complains of swelling, difficulty in standing, walking and cramps in the leg.
  • 26. Diagnosis Dvt: Homans test : Forcible dorsiflexion at foot ----- calf or popliteal region pain. Constrast venography Doppler ultrasound D-dimers Pulmonary embolism D-dimer Blood gas- resp alkalosis Ecg- S1Q3T3 CXray CT pulm angiography (gold standard test) V/Q Scan
  • 27. treatment DVT Prophylaxis 1)Active/ passive calf pump and toe movement 2)Elevation 3)Deep breathing exercise 4)Elastic TED stockings 5)Early internal fixation to provide early mobility. Management 1)Bed rest 2)Elevation 3)Inj LMWH 4)Warfarin 5)Venous bypass 6)IVC filters PE Management 1)Pulm support 2)Anticoagulant OR thrombolysis 3)Surgical embolectomy 4)IVC filter
  • 28. Crush syndrome RTA High energy trauma Crush muscles Myohemoglobin into circ Ppt in renal tubules Acute tubular necrosis
  • 29. c/f ( ARF) appear within 2 -3 days 1)Oliguria 2)Hyperkalemia & m/b acidosis 3)Dec urine output 4) Restlessness 5) Delirium Treatment Prophylaxis Application of tourniquet and gradual release to slowly allow the myoglobin to reach the kidneys Management rx as acute renal failure – aggressive fluid resuscitation maintenance of electrolyte imbalance
  • 30. • What is Compartment syndrome? An elevation of the interstitial pressure in a closed osteofascial compartment that results in microvascular compromise. Compartment syndrome
  • 31. • Compartments are groups of muscles surrounded by inelastic fascia. • Increased pressure within a muscle compartment causes decreased blood supply to affected muscles. • Any swelling of muscles leaves no room for expansion and blood supply is progressively shut off. • If affected muscles are deprived of blood supply for > 6 hours, nerve and muscle tissue can be permanently damaged.
  • 32. etiology 1) Decrease compartment size -Tight dressings/closure of fascial defect -External pressures : casts, splints ,lying on limb for long period, 2)Increase compartment contents Hemorrhage -- vascular injury, coagulopathy Muscle edema -- severe exercise , crush injury Burn -- increase capillary permeability
  • 33. Pathophysiology This vicious cycle continues until total vascularity of mm & nerves within compartment is compromised Leading to mm necrosis & nerve damage Necrotic mm undergo healing with fibrosis contactures
  • 34. Clinical Presentation: • Swelling/ Tightness of compartment • pain out of proportion • decrease power in mm within affected comp • Pallor/Cyanosis • Hyperesthesia/Paresthesia • Paralysis : full recovery is rare
  • 35. diagnosis 1) Stretch test ( earliest sign) Pain on passive stretching of mmm Ex: passive extension of fingers --- pain flexor comp of forearm 2) Measure pressure in each compartment >40mm h2o
  • 36.
  • 37. treatment Limb elevation & active movement as prevention Remove any bandage /slab /cast then readjust Early surgical decompression within 6hrs Like fasciotomy & fibulectomy(middle 3rd of fibula is excised to decompress all comp of legs)
  • 38. Delayed & non union Delayed union : When a fracture takes more than the usual time to unite Non union : When the process of healing stops before completion. To diagnose non union the fracture has to be minimum 6 months old & progressive evaluation of xray done.
  • 39.
  • 40. TYPES 1. Atrophic: no or minimal callus formation 2. Hypertrophic: callus is present but it does not bridge the fracture site. COMMON SITES Neck of femur Scaphoid Lower third of tibia Lower third of ulna Lateral condyle of humerus
  • 41. C/F Persistent Pain Increase deformity @ fracture site ( non union) Abnormal mobility(non union) Refracture Radiological findings Delayed union: inadequate callus, visible fracture line Non union: ends are rounded, smooth sclerotic. Medullary cavity may be obliterated. visible fracture line.
  • 42.
  • 43. treatment 1)Asymptomatic – no Rx ( scaphoid) 2)ORIF & bone grafting 3)Excision & replacement by prothesis ( THR) 4) ILIZAROV’s mtd:
  • 44. MALUNION MALUNION : When a fracture does not unite in proper position Causes: 1.Improper reduction 2.Unchecked muscle pull ( # clavicle) 3.Excessive comminution ( colle’s #) Common sites: supracondylar # of humerus colle’s # olecranon # # both forearm bone
  • 45. C/F Deformity Shortening of limb Limitation of movements Treatment 1.osteoclasis: 2.Redoing the fracture surgically: most common. ORIF is generally done along with bone grafting. 3.Corrective osteotomy: 4.Excision of protruding bone.
  • 46. Cross union : 2 bones unites with each other common in # forearm
  • 47. shortening Common comp of malunion, crushing, growth defect Treatment: <2cm : not noticeable shoe raise >2cm : elderly: shoe raise young: limb length equalisation procedure
  • 48. Avascular necrosis # blood supply to a part of bone necrosis of that part Common sites: Site -head of the femur -Proximal pole of scaphoid -Body of talus Cause -fracture neck of femur -post disclocation of hip -# thru waist of scaphoid - # thru neck of talus
  • 49.
  • 50. c/f 1)Early stage – asymptomatic 2)Later stage – 2* osteoarthristis Painful limitation of joint movement Stiffness Diagnosis: Suspected in # where it is known to occur because pain and stiffness appear late
  • 51. Xray changes 1)Sclerosis of necrotic area; with revascularisation, new bone is deposited around dead bone resulting in increase bone density 2)Subchondral cysts 3) deformity of bone because of collapse of necrotic bone 4)Osteoarthritis: dec joint space, osteophytes
  • 52.
  • 53. treatment Prevented by early, energetic reduction Rx: 1)Delay weight bearing for revascularisation 2)Revascularisation procedure by vascularised bone graft 3)Excision of avascular segment not hampering functions 4)Excision & prosthesis 5)Total joint rep or arthrodesis
  • 54. Myositis ossificans Ossification of hematoma around joint formation of mass of bone Restricting joint mvnts
  • 55. Causes 1)Severe injury to a joint when capsule & periosteum stripped from bone by violent disp of the fragments 2)Common in children: periosteum is loosely attached to bone 3)Common arnd elbow jt 4)Massage foll trauma aggr myositis Consequences / clinical features 1)Stiffness of jt 2)Restriction of jt 3)Complete loss of mvnt
  • 56. Xray: Active myositis: fluffy margins of bone mass Mature myositis : trabeculated with well defined margins Rx Active: early ; rest, NSAIDS, physiotherapy late: physiotherapy & french osteotomy
  • 57. Sudeck’s dystrophy Is a group of disorder where there is dysfunction in the normal “ injury and repair process” leading to an exaggerated response to anoxious stimulus. Trauma is relatively minor and hence symptoms and signs are out of proportion to the trauma c/f Pain Hyperaesthesia Tenderness Swelling Skin: red shiny warm ( early stage) Late: prog atrophy of skin mm & nails Joint deformities & stiffness
  • 58. Xray: characteristics spotty rarefaction Rx. Physiotherapy Betablocker Sympathetic blocks