The document discusses various early complications that can arise from fractures and injuries. It covers local complications like visceral injuries, vascular injuries, nerve injuries, compartment syndrome and infection. It also discusses general complications like shock, fat embolism and pulmonary embolism. For each complication, it provides details on symptoms, risk factors, diagnostic steps and emergency treatment approaches.

1. Dr. Praveen Mehar . J
(DNB ORTHO)

2.  Diaphysis
 Shaft of a long bone
 Epiphysis
 Ends of the bone
 Metaphysis
 Area between the diaphysis and epiphyses
 Hyaline cartilage
 Found at the ends of the bone
 Periostium
 Membrane covering the bone
 Marrow cavity
 Space in the diaphysis
 Endosteum
 Lining of the medullary cavity

4.  Bone Consists
 Organic component (%40)
 Collagen
 Proteoglycans
 Matrix proteins
 İnorganic component (%60)
 Calcium hydroxyapatite [Ca10(PO4)6(OH)2]
 Osteocalcium Phosphate

5. Types of Fracture Healing
1. Primary Healing
2. Secondary Healing
3. Distraction Osteogenesis

6.  Primary fracture healing
 Involves direct attempt by the cortex to reestablish
itself
 Occurs only with anatomic reduction & rigid
fixation
 Gaps in reduction heal by vessel ingrowth-
mesenchymal cells- osteoblasts-osteoclast cutting
cones
 Direct contact areas heal by cutting cones allowing
passage of vessels

7.  Secondary fracture healing
 Response of periosteum/ external soft tissues
 Recapitulation of embryonic intramembranous
ossification and endochondral bone formation
 Intramembraneous= peripheral to fracture
 Endochondral= adjacent to fracture
 Motion enhances periosteal response
 External soft tissue forms bridging calus
(endochondral)

8.  Stages of Healing
Hematoma Formation 1-2 Days
Inflammation 2-7 Days
Soft Callus Formation 1-3 Weeks
Hard Callus Formation 3-6 Weeks
Remodelling Phase >8. Weeks

9. Hematoma Formation
 Hematoma forms in
medullary canal and
surrounding soft tissue in
first 24-48 hours

10. Inflammation
 Hematoma in fracture site brings hematopoietic cells
secreting growth factor
 Growth factors
 Insulin-like growth factor (IGF-1)
 Transforming growth factor (TGF)
 Vascular endothelial growth factor (VEGF)
 Fibroblast growth factor (FGF)
 Fibroblasts, osteoprogenitor cells produce granulation
tissue around fracture ends
 Osteoblasts proliferate
 By 1st-2nd week, abundant cartilage over fracture site
ready for calcification (occurs identical to growth
plate)

11. Inflammation
Periost
Devitalized marrowEndosteum
Hematoma
Dead osteocytes/empty lacunae
WBC
AngiogenesisGranulation
tissue

12. Soft Callus ( Fibrous Callus) Formation
 Fibrous tissue forms at periphery where blood
supply is abundant
 Fibrocartilage forms at center where blood supply
is limited
 Increased instability results in increased callus
size
 Tissues bridge fracture and decrease
interfragmentary strain

13. Soft Callus ( Fibrous Callus) Formation
Granulation tissue
Fibrous tissue
Fibrocartilage

14. Hard Callus Formation
 Intramembranous
ossification
 bone from fibrous tissue
 Endochondral ossification
 bone from cartilage

15. Hard Callus Formation
Fibrous tissueIntramembranous
ossification
FibrocartilageEndochondral
ossification

16. Remodelling Phase
 Begins in middle of repair phase, continues until fx
clinically healed
 Osteoclastic tunneling (cutting cones) in concert with
osteoblast deposition
 Can continue up to 7 years
 Remodeling based on stresses (Wolff’s law)
 Bone formed in response to mechanical load

17. 

20. Distraction Osteogenesis
 Gradual traction applied to cortical osteotomy
 Bone forms under the law of tension stress
 Wolff’s Law occurs even with tension
 Typically intramembranous ossification
 Used in limb lengthening
 Treatment of limb deformities
 Transportation of cortical bone

21. Conditions that interfere with fracture healing
 High energy traumas brings soft tissue problems that
lead non unioun
 Poor blood supply to the fractured area; could lead to
avascular or aseptic necrosis
 Poor immobilization of fracture site may cause
misalignment, nonunion or deformity
 Infection – more common with open fractures
 Cortisone= negative effect, decreased callus
formation

23. General Local
Early Late

24.  General complications
 Shock
 Hypovolemic or hemorrhagic shock.
 Septic shock.
 Neurogenic shock.
 Fat embolism.
 Pulmonary embolism.
 Crush syndrome.
 Multiple organs failure syndrome (MOFS).
 Thrombo-embolism.
 Tetanus.
 Gas gangrene.

25.  Local complications
 Early
1. Visceral injury (the lung, the bladder, the urethra,
and the rectum).
2. Vascular injury.
3. Nerve injury.
4. Compartment syndrome.
5. Haemoarthrosis.
6. Infection.
7. Gas gangrene.
8. Fracture blisters.
9. Plaster and pressure sores.

26. 1. Delayed union.
2. Non-union.
3. Malunion.
4. Avascular necrosis.
5. Growth disturbance.
6. Bed sore.
7. Myositis ossificans.
8. Muscle contracture.
9. Tendon lesions.
10. Nerve compression and entrapment.
11. Joint instability.
12. Joint stiffness.
13. Complex regional pain syndrome.
( algodystrophy).
14. Osteoarthritis.

28.  Shock
 Three types of shock may complicate fractures
 Hypovolemic or hemorrhagic shock
 This type of shock is due to blood loss due to
vascular injury. The vessels may be injured by
the fracture pieces or in open fractures the
vessels are injured by the same cause like in
missile or bullet

29.  injury.In hypovolemic shock there will be
reduction in the circulating volume causing
reduction in venous return and cardiac output.
 The patient usually; severely pallor, shivering,
rigor, hypotensive and sometimes comatose.
 Treatment by 1) control of hemorrhage (may
require surgery).
 restoration of circulating volume (fluid and
blood products).

30.  Occur in
 Large bulk of muscle crushed
 Tourniquet left for TOO long
 What happened?
 1st
theory =Compression releasedacid
myohaematin enter the
circulationkidneyblocks the tubules Renal
failure and death.

31.  Limb
 Pulseless
 Red
 Swollen
 Renal
 Secretion diminished
 Low output uraemia
 Acidosis
 Neurologically
 Drowsynot treated  DEATH

32.  1st
rule = Limb crushed severely(>6hrs)
 How the amputation done?
 Above the compression or crushed injury
 Before compression is released

33.  CommonestCommonest Complications of Trauma &
Surgery
 Most frequently
 Calf
 Less frequent in proximal of thigh & pelvis
 Pulmonary Embolism
 From Proximal of thigh & pelvis
 Incidence=5% & Fatal = 0.5%

34.  The primary cause in surgical
 HYPERCOAGULABILITYHYPERCOAGULABILITY of the Blood
 due to activation of Factor XFactor X by ThromboplastinThromboplastin from
damaged tissues
 Thrombosis occurssecondary factors are
 Stasis
 Pressure
 Prolonged immobility
 Endothelial damage
 Increase in no & stickiness of platelet

35.  Old people
 Cardiovascular Disease
 Bedridden patient
 Patients undergoing hip arthroplasty

36.  Pain the calf or thigh
 Soft tissue tenderness
 Sudden slight increase in temperature
 Sudden increase in pulse rate
 Homann’s Sign positiveHomann’s Sign positive

37.  Ascending venography (bilaterally)
 US scanning (detecting prox DVT)
 Radioactive iodine labelled fibrinogen(clot)
 Doppler technique (measure blood flow)

38.  Difficult to diagnose =only minority have
symptoms (chest pain, dyspnoe, heamoptysis)
 So high risk patients should be examine for
pulmonary consolidation
 X-ray
 Pulmonary angiography

39.  Prophylactic treatment
 Foot elevation
 Graduated compression stockings
 Exercise
 Anticoagulant treatment
 Subcut low dose heparin 5000 units preops & 3/7
postops (but CI in older patientbleeding)
 Change to low molecular weight heparin (less likely to
cause bleeding)

40.  Localized DVT
 Elastic stockings
 Low dose subcut heparin (5000 unit)
 More extensive DVT
 Bed rest
 Elastic stockings
 Full anticoagulation
 Heparin IV (10000 units 6 hourly)
 Continue for 5-7/7 with last 2/7 warfarin introduce

41.  Cardiorespiratory resuscitation
 Oxygen
 Large dose heparin (15 000 units)
 Streptokinase (dissolve clot)
 Antibiotics (prevent lung infection)

42.  What is Tetanus?
 Tetanus organism live only in dead tissueexotoxin
blood & lymph to CNS anterior horn cell
 Will develop
 Tonic clonic contraction
 Jaw and face (trismus and risus sardonicus)
 Neck and trunk
 Diaphragm and Intercostal muscle spasmASPHYXIA

43.  Active immunization (tetanus toxoid)
 Booster doses (immunized patients)
 Non Immunized patients
 Wound toilet & antibiotics
 If wound contaminated antitoxin

44.  IV antitoxin
 Heavy Sedation
 Muscle Relaxant drug
 Tracheal Intubation
 Controlled respiration

45.  By clostridial infection (esp C.welchii)
 Anaerobic with low oxygen tension
 Produce toxinsdestroy cell walltissue
necrosis Spreading

46.  Within 24 hours
 Intense pain
 Swelling
 Brownish discharge
 Pulse rate increased
 Charasteristis smell
 Little or no pyrexia
 Gas formation not marked
 ToxaemiccomaDEATH

47.  Deep penetrating wound should be
EXPLORED
 ALL dead tissue completely EXCISED
 Doubt about tissue viabilityleft it OPEN
 No antitoxin

48.  The key = EARLY DIAGNOSIS
 General measures (fluid, IV antibiotics)
 Hyperbaric oxygen (limiting spread)
 Decompression of wound
 Removal of all dead tissue
 Amputation (advanced case)

49.  Only minority patients with circulating fat
globules will develop POST TRAUMATIC
RESPIRATORY DYSFUNCTION
 Source of fat emboli=bone marrow
 Usually in MULTIPLE CLOSED FRACTURE
 But other condition also reported (burns, renal
infarction, cardiopulmonary operation)

50.  Usually young adults with LL fracture
 Early warning signs (72 hrs. of injury)
 Rise in temperature and pulse rate
 More pronounced case
 Breathlessness
 Mild mental confusion
 Petechia (chest & conjuntival fold)
 Most severe case
 Marked respiratory distress coma ARDS

51.  Mild case
 Monitoring of blood PO2
 Signs of hypoxia
 Oxygen
 If severe
 Intensive care with sedation and assisted ventilation
 Swan ganz Catheterization (monitor cardiac Fx)
 Fluid balance
 Supportive
 Heparin-thromboembolism
 Steroids-pulmonary oedema
 Aprotinin-prevent aggregation of chylomicrons

52. General Local
Early Late
* Early complication : those that arise during the first few weeks
following injury.

53.  Local Visceral Injury
 Vascular Injury
 Nerve Injury
 Compartment Syndrome
 Haemarthrosis
 Infection
 Gas gangrene

54.  Fracture around the trunk are often Cx by injury
to the adjacent viscera :
 Pelvic fracture
 Rib fracture penetration to the lungs
Pneumothorax
Bladder and urethral
rupture

55.  Most commonly – knee, femoral shaft, elbow,
and humerus.
 Artery may be cut, torn, compressed or
contused.
 Intima may be detached, thrombus block,
artery spasm
 Effect ?? ↓↓ bld flow coz Ischemia leads to
tissue death & peripheral gangrene

56.  Common vascular injuries may associate with the
following fractures.
1. First rib or clavicle fracture (subclavian artery).
2. Shoulder dislocation (Axillary artery).
3. Humeral supracondylar fracture (brachial artery).
4. Elbow dislocation (Brachial artery).

57. 5. Pelvic fracture (presacral and internal iliac).
6. Femoral supracondylar fracture (Femoral artery).
7. Knee dislocation (Popliteal artery).
8. Proximal tibia (popliteal or its branches).

58.  .

59.  Pt with ischemia may have 5 P’s:
- paraesthesia/numbness
- pain
- pallor
- pulselessness
- paralysis
 Investigate if suspect vascular injury :
Angiogram

60.  Emergency treatment
 All bandages/splints removed
 The fracture X-Ray again
 Circulation reassessed for next half hour
 If no improvement, do vessels exploration
 Suture torn vessels, vein grafting, if
thrombosed do endarterectomy
 Aim: to restore bld flow

61.  Variable degree of motor and sensory loss
along the distribution of the nerve
 May be neurapraxia, axonotmesis or
neurotmesis
 Radial nerve is most frequently damaged
nerves.

62. NerveNerve TraumaTrauma EffectEffect
AxillaryAxillary Dislocation ofDislocation of
shouldershoulder
Deltoid paralysisDeltoid paralysis
RadialRadial # of humerus# of humerus Wrist dropWrist drop
MedianMedian Supracondylar # ofSupracondylar # of
humerushumerus
Pointing indexPointing index
UlnarUlnar # medial epicondyl# medial epicondyl
humerushumerus
Claw handClaw hand
SciaticSciatic Post dislocation of hipPost dislocation of hip Foot dropFoot drop
CommonCommon
peronealperoneal
Knee dislocation #Knee dislocation #
neck of fibulaneck of fibula
Foot dropFoot drop

63.  In closed injuries – nerve is seldom severed and
spontaneous recovery should be awaited.
 In open fractures – complete
lesion(neurotmesis) : the nerve is explored
during wound debridement and repaired.

64.  Definition
Compartment syndrome involves the compression of
nerves and blood vessels within an enclosed space,
leading to impaired blood flow and nerve damage.
 Fascia separate groups of muscles in the arms and legs
from each other. Inside each layer of fascia is a confined
space, called a compartment, that includes the muscle
tissue, nerves, bones and blood vessels.
 A rise in pressure within these compartments may
jeopardize the blood supply to the muscles & nerves
within the compartment.

65.  Causes:
-any injury/infection leading to edema of muscle
-fracture haematoma within the compartment
-ischemia to the compartment leading to muscle
oedema
-Due to tight bandages or casts
 Hallmark Symptoms:
- severe pain that does not respond to elevation
or pain medication.
- In more advanced cases, there may be
decreased sensation, weakness, and paleness
of the skin.

66.  Injuries with a high risk of developing
Compartments synd:
 # of the elbow
 # of the forearm bone
 # of the proximal third of the tibia

67. Arterial ischaemia blood flow
Damage
Direct
injury
oedema
Compartment
pressure
5P’s
Pain
Pallor
Paraesthesi
a
Pulseless
Paralysis
………….....
.
…………….
Fasciotomy

68.  A vicious cycle cont. until the total vascularity
of the muscles and nerves is jeopardized.
 This result in ischaemic muscle necrosis and
nerve damage. (within 12 hours)
 The necrotic muscle undergo healing with
fibrosis, leading to Volkmann’s contracture.
 Nerve damage may result in motor and
sensory loss. In extreme case  gangrene

69.  clinically:
- should be tested by stretching the
muscles  when the toes or fingers are
passively hyperextended there is ↑ pain
in the calf or forearm.
 Early preventing : limb elevation
 Dx : confirmed by direct intracompartmental
pressure measuring > 40mmHg is an indication
of compartment decompression and
fasciotomy.

70. 

71. Treatment
 First removed all the bandages & dressing.
Fasciotomy is performed.
 The wound should be left open and
inspected 2 days later.
 If there is muscle necrosis  debridement
 If muscle is healthy suture (w/o tension)/
skin grafted / simply heal by 2˚ intention.

72. 

73. 

74.  Fractures involve joints, leads to acc. of blood
within the joints.
 C/Feature :The joint is swollen and tense and
patient will resists any movement.
 Tx : the blood should be aspirated before
dealing with the fracture.

75.  Causes:
 Open fracture (common)
 Use of operative method in the Tx of #
 Wound becomes inflamed and starts draining
seropurulent fluid.
 Infection may be superficial, moderate
(osteomyelitis), severe (gas gangrene).
 Post-traumatic wound infx is most common
cause of chronic osteomyelitis union will be
slow and ↑ chance of refracturing.

76. Treatment:
 Antibiotic
 Excising all devitalised tissue
 If Sx of acute infx and pus formation : tissue
around the fracture should be opened &
drained

77.  Produced by anaerobic orgs : Clostridium sp infections.
 These orgs can survive in ↓ O2 tension
 Toxins produced will destroy the cell wall and leads to
tissue necrosis
 C/feature: within 24hr. Pt complains:
- intense pain
- swelling around the wound
- brownish discharge
- gas formation
- pyrexia
- characteristic smelling
- PR ↑
- toxaemic  coma  death
 Inability to recognize may lead to unnecessary amputation
for the non-lethal cellulitis.

78. 
swelling around the wound,swelling around the wound,
brownish dischargebrownish discharge
gas formationgas formation

79. Prevention:
 deep penetrating wound in muscular tissue are
dangerous;should be explored, all dead tissue
should be completely excised, and if there doubt
about the tissue viability should left open the
wound
Treatment:
 Early Dx is life saving
 General measures:
 Fluid replacement & IV Antibiotic (immediate)
 Hyperbaric O2(limiting the spread of gangrene)
 Mainstay : prompt decompression & remove
dead tissue

80. • Delayed union
• Non-union
• Malunion
• Joint stiffness
• Myoisitis ossificans
• Avascular necrosis
• Algodystrophy
• Osteoarthritis
• Joint instability
• Muscle contracture
(Volkmann’s contracture)
• Tendon lesions
• Nerve compression
• Growth disturbance
• Bed sores

81.  Fracture takes more than the usual time to unite.
 CausesCauses
 Inadequate blood supply
 Severe soft tissue damage
 Periosteal stripping
 Excessive traction
 Insufficient splintage
 Infection

82. Upper LimbUpper Limb Lower LimbLower Limb
Callus visibleCallus visible 2-3 wks2-3 wks 2-3 wks2-3 wks
UnionUnion 4-6 wks4-6 wks 8-12 wks8-12 wks
ConsolidationConsolidation 6-8 wks6-8 wks 12-16 wks12-16 wks

83.  Clinical featuresClinical features
 Fracture tenderness
(Esp when subjected to stress)
 X-RayX-Ray
 Visible fracture line
 Very little callus formation or
periosteal reaction

84. Severe soft tissueSevere soft tissue
damagedamage
InfectionInfection ExcessiveExcessive
tractiontraction
Intact fibulaIntact fibula

85.  TreatmentTreatment
 ConservativeConservative
- To eliminate any possible cause
- Immobilization
- Exercise
 OperativeOperative
- Indication :
Union is delayed > 6 mths
No signs of callus formation
- Internal fixation & bone grafting

86.  Condition when the fracture will never unite w/o
intervention
 Healing has stopped.
Fracture gap is filled by fibrous tissue
(pseudoarthrosis)
 CausesCauses
 Improper Tx of delayed union
 Too large a gap
 Interposition of periosteum, muscle or cartilage between
the fragments

87.  Clinical featuresClinical features
 Painless movement at the fracture site
 X-RayX-Ray
 Fracture is clearly visible
 Fracture ends are rounded, smooth and sclerotic
 Atrophic non-unionAtrophic non-union : - Bone looks inactive
(Bone ends are often tapered / rounded)
- Relatively avascular
Hypertrophic non-unionHypertrophic non-union : - Excessive bone formation
` - on the side of the gap
- Unable to bridge the gap

88. Hypertrophic non-unionHypertrophic non-union Atrophic non-unionAtrophic non-union

89.  TreatmentTreatment
 Ununited scaphoid fracture → asymptomatic
 Hypertrophic non-union (Esp long bone)
→ Rigid fixation (internal / external)
sometimes need bone grafting
 Atrophic non-union
→ Fixation & bone grafting

90.  Condition when the fragments join in an
unsatisfactory position (unaccepted angulation,
rotation or shortening)
 CausesCauses
 Failure to reduce a fracture adequately
 Failure to hold reduction while healing proceeds
 Gradual collapse of comminuted or osteoporotic bone.

91.  Clinical featuresClinical features
 Deformity & shortening of the limb
 Limitation of movements
 TreatmentTreatment
 Angulation in a long bone (> 15 degrees)
→ Osteotomy & internal fixation
 Marked rotational deformity
→ Osteotomy & internal fixation
 Shortening (> 3cm) in 1 of the lower limbs
→ A raised boot OR
Bone operation

93.  Common complication of fracture Tx following
immobilization
 Common siteCommon site : knee, elbow, shoulder,
small joints of the hand
 CausesCauses
 Oedema & fibrosis of the capsule, ligaments, muscle
around the joint
 Adhesion of the soft tissue to each other or to the
underlying bone (intra & peri-articular adhesions)
 Synovial adhesions d/t haemarthrosis

94.  TreatmentTreatment
 Prevention :Prevention :
- Exercise
- If joint has to be splinted → Make sure in correct position
 Joint stiffness has occurred:Joint stiffness has occurred:
- Prolonged physiotherapy
- Intra-articular adhesions
→ Gentle manipulation under anaesthesia
followed by continuous passive motion
- Adherent or contracted tissues
→ Released by operation

95.  Heterotopic ossification in the muscles after an
injury
 Usually occurs in
 Dislocation of the elbow
 A blow to the brachialis / deltoid / quadriceps
 CausesCauses
 (thought to be due to) muscle damage
 w/o a local injury (unconscious / paraplegic patient)

96.  Clinical featuresClinical features
 Pain, soft tissue tenderness
 Local swelling
 Joint stiffness
 Limitation of movements
 Extreme cases: - Bone bridges the joint
- Complete loss of movement
(extra-articular ankylosis)
 X-RayX-Ray
 Normal
 Fluffy calcification in the soft tissue

97.  TreatmentTreatment
 Early stage : Joint should be rested
 Then : Gentle active movements
 When the condition has stabilized :
Excision of the bony mass
 Anti-inflammatory drugs may ↓ joint stiffness

98.  Circumscribed bone
necrosis
 CausesCauses
 Interruption of the arterial
blood flow
 Slowing of the venous
outflow leading to
inadequate perfusion
 Common siteCommon site ::
 Femoral headFemoral head
 Femoral condyls
 Humeral head
 Capitulum of humerus
 ScaphoidScaphoid (proximal part)
 TalusTalus (body)
 Lunate

99.  Conditions a/w AVNConditions a/w AVN
 Perthes’ disease
 Certain fractures
 Epiphyseal infection
 Sickle cell disease
 Caisson disease
 Gaucher’s disease
 Alcohol abuse
 High-dosage corticosteroid

100.  Clinical featuresClinical features
 Joint pain, stiffness, swelling
 Restricted movement
 X-RayX-Ray
 ↑ bone density
 Subarticular fracturing
 Bone deformity

102.  TreatmentTreatment
 Avoid weight bearing on the necrotic bone
 Revascularisation (using vascularised bone grafts)
 Excision of the avascular segment
 Replacement by prostheses

103.  Previosly known as Sudeck’s atrophy
 Post-traumatic reflex sympathetic dystrophy
 Usually seen in the foot / hand
(after relatively trivial injury)
 Clinical featuresClinical features
 Continuous, burning pain
 Early stage : Local swelling, redness, warmth
 Later : Atrophy of the skin, muscles
 Movement are grossly restricted

104.  X-RayX-Ray
 Patchy rarefaction of the bones (patchy osteoporosis)
OsteoporosisOsteoporosis AlgodystrophyAlgodystrophy

105.  TreatmentTreatment
 Physiotherapy (elevation & active exercises)
 Drugs
- Anti-inflammatory drugs
- Sympathetic block or sympatholytic drugs
(Guanethidine)

106.  Post-traumatic OAPost-traumatic OA
 Joint fracture wt severely damaged articular cartilage
 Within period of months
 22OO
OAOA
 Cartilage heals
 Irregular joint surface may caused localized stress → 2O
OA
 Years after joint injury

107.  Clinical featuresClinical features
 Pain
 Stiffness
 Swelling
 Deformity
 Restricted movement
 TreatmentTreatment
 Pain relief : Analgesics
Anti-inflam agent
 Joint mobility : Physiotherapy
 Load reduction : wt reduction
 Realignment osteotomy (young
pt)
 Arthroplasty (pt > 60yr)