This document discusses various complications that can arise from fractures. It classifies complications as immediate, early, or late. Immediate complications include hypovolaemic shock, injuries to major vessels or internal organs. Early complications include hypovolaemic shock, ARDS, fat embolism, DVT, and infections. Late complications are related to imperfect union like delayed union, non-union, or malunion. Other late complications include avascular necrosis, joint stiffness, osteomyelitis, and osteoarthritis. The document provides details on pathogenesis, clinical features, diagnosis, and management of various common complications like hypovolaemic shock, fat embolism, DVT, crush syndrome, compartment syndrome, and

1. Subhanjan Das

2. Introduction
These are the associated pathologies other than the loss
of bone continuity which either co exist or originate
due to the fracture.
early diagnosis and aggressive treatment is necessary
to minimize disabilities.

3. Classification
I.IMMEDIATE
A.Systemic
hypovolaemic Shock
B.Local
injury to
1. major vessels
2. Muscles and tendons
3. Joints
4. viscera

4. II.EARLY
A.Systemic
1. Hypovolaemic shock
2. ARDS
3. Fat embolism
4. DVT & pulmonary embolism
5. Aseptic traumatic fever
6. Septicaemia
7. Crush syndrome
B. Local
1. Infection
2. Compartment syndrome

5. III. LATE COMPLICATIONS
A. Related to imperfect union
1. Delayed union
2. Non union
3. Mal union
4. Cross union
B.Others
1. Avascular necrosis
2. Shortening
3. Joint stiffness
4. Sudeck’s dystrophy
5. Osteomyelitis
6. Ischemic contracture
7. Myositis ossificans
8. OA

6. Hypovolaemic shock
 Commonest cause of death in fractures of major bones
Like pelvis or femur

7. cause
 External or internal haemorrhage.
 External: compound fractures injuring major vessels of
the LIMB
 Internal: injury to body cavities- chest or pelvis
 Internal is more difficult to diagnose.
 # pelvis (1.5-2 litres) # femur (1-1.5 litres) produces
major haemorrhage.

8. Prevention
 Early stopping of bleeding
 Avoiding shifting of the patients
 For # pelvis- temporary stabilization with external
fixator
 Emergency angiography and embolisation of bleeding
vessels for deeper vessels.

9. 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
 Cut down if peripheral vasoconstriction is present
 Localise the site of lesion- if in body cavities, perform
chest aspiration or diagnostic peritonial lewage.
Sometimes a simple x ray is enough.
 Chest bleeding-ICDT
 Abdominal bleeding- laperotomy

10. ARDS
 Respiratory distress following a trauma
 Cause- not definite. Hypothesized to be by release of
Inflammatory cells and proteinaceous fluid that
accumulate in the alveolar spaces leading to a decrease
in diffusing capacity and hypoxemia. The
microvasculature in dysrupted.
 Onset- 24 hours after injury

11.  Features:
 Tachypnea
 Laboured breathing
 X- ray- diffused
pulmonary infiltrates
 Arterial Po2 below 50

12. management
 100% O2 and assisted ventilation
 It takes upto 7 days to get the chest clear
 If not detected early death occurs by multiorgan
failure or cardiorespiratory failure.

13. Fat Embolism
It is a life threatening complication of fracture where fat
globules occlude the small blood vessels.
Embolism is the process of occlusion of blood vessel by
any material which is brought to the site from
elsewhere by bloodstream.

14. Pathogenesis
Injury to large bones (e.g. femur) release fat globule
from bone marrow to blood stream. Alternatively fat
can also be released from the adipose tissue.
The fat globules obstruct capillary vasculature of the
lungs.
Also, fat is converted to free fatty acid, which induces
toxic vasculitis followed by thrombosis which obstruct
the microvasculature.

15. Clinical features
COMMON
Patechial rash of anterior
neck, anterior axillary
fold or conjunctiva
CEREBRAL TYPE
Drowsiness
Restlessness
Disorientation
Coma
PULMONARY TYPE
Tachypnoea
Tachycardia
Respiratory failure

16. Diagnosis
Retinal artery emboli
Urine: fat globules
CXR: pulmonary infiltration/
Snow storm appearance
Clinical features

17. management
 Respitarory support
 Heparinisation
 i.v. low mol wt dextran
 Corticosteroid
 Dextrose and alcohol infusion to emulsify fat.

18. Deep Vein Thrombosis
It is a common complication
originating from altered
hemodynamics in lower
limb and spinal injuries.
Pathology:

19. pathology
Virchow's triad
1. decreased flow rate of
the blood
2. damage to the blood
vessel wall
3. hypercoagulability
trauma
immobilisation
Venous stasis
thrombosis

20. Clinical features
Elderly and obese patients are at risk.
Leg swelling
Local redness, warmth
Calf tenderness
Pain in passive dorsiflexion (Homan sign)
Venography shows DVT

21.  Sequale
1. The venous thrombosis can get dislodged and
produce embolism elsewhere. If it is pulmonary
embolism the condition is life threatening.
Embolism usually occurs within 4-5 days after injury.
2. A late complication of DVT is the post-phlebitic
syndrome, which can manifest itself as edema, pain
or discomfort and skin problems.

22. Other causes
compression of the veins
physical trauma
cancer
infections
inflammatory diseases
stroke
heart failure
nephrotic syndrome
Risk factor:
Surgery
hospitalization
immobilization
orthopedic casts
economy class syndrome
smoking
Obesity
age
certain drugs (such as estrogen
or erythropoietin)
thrombophilia
pregnancy
postnatal period.

23. diagnosis
D-dimers
doppler ultrasound
venography
Clinical features

24. treatment
Prophylaxis
 Active/ passive calf pump
and toe movement
 Elevation
 Deep breathing exercise
 Elastic TED stockings
 Early internal fixation to
provide early mobility.
Management
Complete rest with elevation
thrombolysis
Anticoagulant therapy
graduated compression
stockings (
thromboembolic deterrent
stockings) or
intermittent pneumatic
compression devices.
Respiratory support in case
of pulmonary embolism

25. Crush syndrome
It is renal failure following
extensive crushing injury
of muscles.
Pathogenesis:
Crushing of muscles causes
entry of myoglobin into
circulation. Myoglobin
precipitates in renal
tubules causing acute
tubular necrosis,
metabolic acidosis &
hperkalemia
Clinical features
(appear within 2-3 days of injury)
Signs of deficient renal function:
Oliguria (Scanty urine)
Apathy
Restlessness
Delirium
Cardiac arrhythmia & failure
Hypothermia
Shock

26. Treatment
Prophylaxis
Application of tourniquet
and gradual release to
slowly allow the
myoglobin to reach the
kidneys
Treatment
Treated as acute renal
failure.

27. An increased pressure within enclosed
osteofascial space that reduces capillary per-
fusion below level necessary for tissue
viability; the underlying mechanism is:
- increased volume within space
- decreased space for contents
- combination of both
Compartment syndrome

28. Etiology
 Trauma with
bleeding/swelling
 Bleeding disorders
 Burns
 Tight wraps
 Traction
 Surgical positioning
 Pneumatic antishock
garment
 Reprefusion swelling
 Casting & Wraps

29. Pathophysiology:
Increased compartment pressure
leads to increased venous pressure
which decreases A-V gradient resulting
in muscle and nerve ischemia.

30. Compartments
 Most common
 Forearm
 Leg
 Other compartments
 Hand
 Finger
 Gluteal
 Thigh
 Foot

31. Diagnosis
 History
 Clinical exam: the Ps
 Compartment pressures
 Laboratory tests
 CPK
 Urine myoglobin

32. Clinical features
 The six ‘Ps’:
 Pressure: palpation of compartment and its tension or
firmness
 Pain: Exaggerated with passive stretch of the involved
muscles in compartment
 Earliest symptom but inconsistent
 Paresthesia:Peripheral nerve tissue is more sensitive than
muscle to ischemia
 Will progress to anesthesia if pressure not relieved
 Paralysis: late finding
 Pallor
 Pulselessness

33. Treatment
 Lower leg to level of the heart
 Remove cast
 Split all dressings down to skin
 Fasciotomy if continued clinical findings and/or
elevated compartment pressure

34. Forearm

35. Leg Anatomy

36. Leg Single Incision Technique

37. Leg Two Incision Technique

38. Hand Compartments

39. Foot Compartments

40. Delayed/ Non union
When a fracture takes more than the usual time to unite
it is said to have gone in delayed union.
When the process of healing stops before completion
the fracture is said to have gone for non union. To
diagnose non union the fracture has to be minimum
six months old.

41. causes
I. Related to patient
 Old age
 Associated systemic illness: ex. Malignancy
II. Related to fracture
 Distraction at fracture site
Muscle pulling the fragments: ex. # patella
Gravity: ex. # shaft of humerus
 Soft tissue interposition: ex. # shaft of humerus
 Bone loss during fracture: ex. # tibia open type
 Infection from open fracture: ex. # tibia
 Damage to blood supply of # fragment: ex. # scaphoid
 Pathological fracture: ex. # osteomyelitic tibia

42. III causes related to treatment:
 Inadequate reduction: # shaft of long bones
 Inadequate immobilisation:# shaft of long bones
 Distraction (excessive) during treatment::# shaft of
femur.

43. types
1. Atrophic: no or minimal callus formation
2. Hypertrophic: callus is present but it does not bridge
the fracture site.

44. Common sites
Neck of femur
Scaphoid
Lower third of tibia
Lower third of ulna
Lateral condyle of humerus

45. Clinical features
 Pain
 Deformity
 Abnormal mobility
 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.

46. Treatment: Delayed union
1. Most commonly prolonged conservative
management
2. Surgical intervention: bone grafting with or without
internal fixation.

47. Treatment: non union
Depends upon site and resulting disability. Following are
the options.
1. Bone grafting: commonest.
2. Excision of fragments: when it can be done with
minimal loss of function. A prosthesis may be used
to replace the lost part, eg. In # neck of femur the
head can be replaced with an austin moore
prosthesis.
3. Illizarov menthod
4. No treatment: when there is no disability, eg. #
scaphoid.

48. Mal union
 When a fracture does not unite in proper position it is
said to have malunited.
Causes:
1. Improper reduction
2. Unchecked muscle pull
3. Excessive communication

49. Consequences
Deformity
Shortening of limb
Limitation of movements

50. treatment
1. osteoclasis: refracture, done in children to correct
mild to moderate angular deformities under GA.
2. Redoing the fracture surgically: most common. ORIF
is generally done along with bone grafting.
3. Corrective osteotomy: performed at a site away from
the fracture. Eg. Supracondyle # of humerus.
4. Excision of protruding bone.

51.  No treatment may be necessary if remodelling occurs.