complications of fracture

Complications of Fractures
Dr. Ali Ahmed Mohamed (Ali Ades)

MBBS, MS (Orthopedics & Traumatology)
Introduction
These are 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
Classifications
1. Immediate complications
A. Systemic
• hypovolemic shock
B. Local injury
• major vessels
• muscles and tendons
• joints
• viscera
2. Early complications
A. Systemic
• Hypovolemic shock
• ARDS
• Fat embolism syndrome
• DVT and Pulmonary embolism
• Aseptic traumatic fever
• Septicemia (in open fractures)
• Crush syndrome
B. Local
• Infection
• Compartment syndrome
3. Late complications
Imperfect union of the fracture
• Delayed union
• Non-union
• Malunion
• Cross union
Others
• Avascular necrosis
• Shortening
• Joint stiffness
• Sudeck’s dystrophy (Reflex Sympathetic Dystrophy)
• Osteomyelitis
• Ischaemic contracture
• Myositis ossificans
• Osteoarthritis
Hypovolemic shock
Commonest cause of death following fractures of major bones such as
the pelvis and femur.
Cause:
 External hemorrhage or internal hemorrhage.
 External hemorrhage: compound fracture injuring vessels of the
limb.
 Internal hemorrhage: massive bleeding in the body cavities such as
chest, abdomen or pelvis.
 Internal hemorrhage is more difficult to diagnose.
 #pelvis (1500–2000 ml), and #femur (1000–1500 ml).
Prevention
Excessive blood loss from fractured bone may be prevented:

 Avoiding shifting of the patient
 for pelvic fracture- temporary stabilization with external fixator
emergency angiography and embolization of the bleeding from
deeper vessels.
Management
• Start even before the cause is stablished
• put in at least two large bore I.V. cannulas (No. 16 or No. 14).
• 2000 ml of crystalloids (preferably Ringer lactate), should be infused
rapidly, followed by colloids (Haemaccel) and blood if needed.
• Localize the site of lesion – if in the body cavities, then perform
needle aspiration from the chest, or diagnostic peritoneal lavage.
Sometimes a simple X ray is enough
• Chest bleeding- chest tube
• Abdominal bleeding- laporatomy
Adult respiratory distress syndrome
• ARDS can be a sequelae of trauma with subsequent shock.
• Causes: not define, but it is supposed to be due to release of
inflammatory mediators which cause disruption of microvasculature of
the pulmonary system.
• The onset is usually 24 hours after the injury.
Features
a) Tachypnea
b) Laboured breathing
c) Xray- diffuse pulmonary infiltrates.
d) Arterial PO2 falls to less than 50.
Management
• 100% oxygen and assisted ventilation.
• It takes from 4-7 days for the chest to clear, and the patient returns to
normal.
• If not detected early, death occurs by multiorgan failure or cardio-
respiratory failure.
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 vessels by any material

which is brought to the site from elsewhere by bloodstream.
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.
Clinical features
a) Common
Patechial rash of anterior neck,
anterior axillary fold or conjunctiva.
b) Cerebral type
• Drowsiness
• Restlessness
• Disorientation
• Coma
c) pulmonary type
• Tachypnoea
• Tachycardia
• Respiratory failure
(If untreated, and sometimes despite treatment, the patient develops

respiratory failure and dies).
Diagnosis
• Retinal artery emboli
• Urine and sputum: fat globules
• CXR: patchy pulmonary
infiltration (Snow storm
appearance)
• Clinical features
Management
• Respiratory support
• Heparinisation (treat with heparin)
• i.v. low mol wt dextran (Lomodex-20)
• Corticosteroid
• 5% Dextrose solution and 5% alcohol infusion to emulsify fat.
Deep vein thrombosis (DVT)
It is a common complication
originating from altered Trauma
hemodynamics in lower limb
and spinal injuries. Immobilization
DVT proximal to the knee is a Venous stasis

common cause of life
threatening complication of Thrombosis
pulmonary embolism.
• flow rate of
the blood
(stasis)
• damage to the
blood vessel
wall
• hypercoagulabi
lity
Pathology
Virchow's
triad
Clinical features
• Elderly and obese patients are at
risk.
• Leg swelling
• Local redness, warmth
• Calf tenderness
• Pain exaggerated by in passive
dorsiflexion (Homan sign)
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-
thrombotic syndrome, which can manifest
itself as edema, pain or discomfort and skin
problems.
Diagnosis
a. D-dimers
b. Doppler ultrasound
c. Venography
d. Clinical features
Treatment
Prophylaxis Management
• Active/ passive calf pump and • Complete rest with elevation
toe movement • Thrombolysis
• Elevation • Anticoagulant therapy
• Deep breathing exercise • graduated compression stockings
• Elastic stockings or intermittent pneumatic
• Early internal fixation to provide compression devices.
early mobility. • Respiratory support in case of
pulmonary embolism
pneumatic compression devices stoking
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 &
hyperkalemia
Clinical features
(appear within 2-3 days of injury) Signs of deficient renal function:
a) Oliguria
b) Restlessness
c) Delirium
d) Cardiac arrhythmia & failure
e) Hypothermia
f) Shock
Treatment
Prophylaxis Treatment
Application of tourniquet and Treated as acute renal failure.
gradual release to slowly allow the
myoglobin to reach the kidneys
Compartment syndrome
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
Etiology
1) Trauma with bleeding/swelling

2) Bleeding disorders
3) Burns
4) Tight wraps (Casting)
5) Traction
6) Surgical positioning
7) Pneumatic anti-shock garment
8) Reperfusion swelling
Pathophysiology:
Increased compartment pressure

leads to increased venous
pressure which decreases A-V
gradient resulting in muscle and
nerve ischemia.
Eaton and green cycle for compartment syndrome

Compartments
Most common
• Forearm
• Leg
Other compartments
• Hand
• Finger
• Gluteal
• Thigh
• Foot
Diagnosis
• History
• Clinical exam: the 6 P’s
• Compartment pressures > 40 H2O
• Laboratory tests
- CPK
- Urine myoglobin
Clinical features
The six ‘Ps’:

1. Pressure: palpation of compartment and its tension or firmness
2. Pain: Exaggerated with passive stretch of the involved muscles in
compartment. Earliest symptom but inconsistent
3. Paresthesia: Peripheral nerve tissue is more sensitive than muscle to
ischemia. Will progress to anesthesia if pressure not relieved
4. Paralysis: late finding
5. Pallor
6. Pulselessness
Treatment
1) Elevation of Lower leg to level of the heart
2) Remove cast
3) Split all dressings down to skin
4) Fasciotomy or Fibulectomy if continued clinical findings and/or
elevated compartment pressure
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.
Causes
1. Related to patient
• Old age
• Associated systemic illness: ex. Malignancy
2. 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
3. Causes related to treatment:
• Inadequate reduction: # shaft of long bones
• Inadequate immobilization:# shaft of long bones
• Distraction (excessive) during treatment::# shaft of femur.
Types of non-union
• Atrophic: no or minimal
callus formation
• Hypertrophic: callus is
present but it does not
bridge the fracture site.
Types pf non union a) atrophic b) hypertrophic

Common sites
I. Neck of femur
II. Scaphoid
III. Lower third of tibia
IV. Lower third of ulna
V. Lateral condyle of humerus
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.
Treatment: Delayed union
• Most commonly prolonged conservative management

• Surgical intervention: bone grafting with or without internal fixation.
Treatment: non union
Depends upon site and resulting disability. Following are the options.
• Bone grafting: commonest.
• 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.
• Illizarov method
• No treatment: when there is no disability, eg. # scaphoid.
Mal union
When a fracture does not unite in

proper position it is said to have
malunited.
Causes:
• Improper reduction
• Unchecked muscle pull(e.g., fracture
of the clavicle)
• Excessive comminution (e.g., Colles’
fracture)
Common sites
Fractures at the ends of a
bone always unite, but
they often mal-unite e.g.,
supracondylar fracture
of the humerus, Colles’
fracture etc.
Consequences
• Deformity
• Shortening of limb
• Limitation of movements
Treatment
• Osteoclasis: refracture, done in children to correct mild to moderate
angular deformities under general anestethia.
• Redoing the fracture surgically: most common. ORIF is generally
done along with bone grafting.
• Corrective osteotomy: performed at a site away from the fracture.
e.g., Supra-condyle fracture of humerus.
(No treatment may be necessary if remodeling occurs).
A 7 year old boy sustained with both bone fracture of left forearm
Two weeks after cast
Six weeks after cast
Mahadsanid!

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complications of fracture

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Complications of Fractures

Dr. Ali Ahmed Mohamed (Ali Ades)

Early diagnosis and aggressive treatment is necessary to minimize

Excessive blood loss from fractured bone may be prevented:

Embolism is the process of occlusion of blood vessels by any material

(If untreated, and sometimes despite treatment, the patient develops

DVT proximal to the knee is a Venous stasis

It is renal failure following

An increased pressure within enclosed osteofascial space that reduces

1) Trauma with bleeding/swelling

Increased compartment pressure

Eaton and green cycle for compartment syndrome

The six ‘Ps’:

Types pf non union a) atrophic b) hypertrophic

• Most commonly prolonged conservative management

When a fracture does not unite in

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