Fractures complications of the bones are many and very important to be known which will be discussed as follow these complications can be classified into the following items early general and early local complications and late general and late local complications

Early general complications

Hypovolaemic shock

Disseminated intravascular coagulation DIC

Systemic inflammatory response syndrome SRIS

Fat embolism syndrome

Early local complications

Arterial injury

Nerve injury

Compartment syndrome


Soft tissue compromise

Late general complications

Deep venous thrombosis DVT see articles of DVT

Pulmonary embolism PE

Urinary tract infections UTI

Respiratory tract infection

Disuse atrophy

Osteoporosis disorders

Psychosocial/economic factors

Late local complications

Delayed union/non-union/mal-union

Infection and Joint stiffness

Secondary osteoarthritis

Avascular necrosis

Myositis ossificans

Complex regional pain syndrome a.k.a. reflex sympathetic dystrophy or Sudeck's atrophy

Early general complications of fractures

Fractures and hypovolaemic shock

Approximate blood loss in closed fracture
Pelvis 1-5 litres

Femur 1-2.5 litres

Tibia 0.5-1.5 Iitres

Humerus 0.5-1.5 litres

Fractures and disseminated intravascular coagulation DIC

DIC is associated with trauma and massive transfusions. It causes consumption of clotting factors and platelets, resulting in uncontrolled bleeding from injured sites. It is treated by replacement of platelets and clotting factors, with surgical control of bleeding if required.

Fractures and systemic inflammatory response syndrome SIRS

This is the systemic response to major trauma, mediated by changes in the autonomic nervous system and the immune system. Some patients are more susceptible to it as a result of their genetics and immune system.

Features must have two or more

Pyrexia> 38 degree C or < 36 degree C
Tachycardia > 90 b.p.m
Tachypnoea > 20 b.p.m. or PaC02 < 32 mmHg
• WCC > 12 000 cells/M-2 or 10% immature (bands) forms

Patients with signs of SIRS should not be subject to major surgery until their condition improves. The additional (surgical) trauma may exceed their physiological capacity to auto-regulate the local organ and systemic circulation death. This is the 'second hit' hypoth­esis of trauma, and applies in particular to the intramedullary nailing of long bones which provokes a large immunological response in patients.

Fractures and fat embolism syndrome

This complication of long-bone (especially femur) fracture presents with a petechial rash, confusion, and hypoxia.

Fat embolism syndrome occurs as a result of

• Release of lipid globules from damaged bone marrow fat cells

• Increased peripheral mobilisation of fatty acids

• Increased synthesis of triglycerides by liver

It results in thromboembolism of the microvasculature with lipid globules. As any part of the microvasculature can be affected the clinical manifestations are varied

• Pulmonary: ventilation/perfusion mismatch

• Cerebral: ischaemia, infarction, oedema

• Cardiac: arrhythmias and impaired mechanical performance

• Renal: ischaemic glomerular/tubular dysfunction

• Skin: capillary damage, petechial haemorrhage

Diagnosis is made by detection of fat globules in body fluids in association with pulmonary and failure/dysfunction. of at least one other organ system. Treatment is to main­tain adequate tissue oxygenation.'The incidence may be reduced by early stabilisation of long-bone fracture

Fractures and arterial and nerve injuries

Common sites of nerve and arterial injuries

Proximal humeral fractures and shoulder dislocations axillary nerve is at risk for injury
Humeral shaft middle and distal third radial nerve at risk for injury

Peadiatric supracondyler fractures radial nerve commonest median nerve ulnar nerve and brachial artery all at risk for injuries

Distal radial fractures median nerve acute carpal tunnel syndrome at risk for injury

Pelvic fractures lumbar sacral plexus iliac vessels or superior gluteal artery all are at risk for injuries

Acetabular fracture or hip dislocation sciatic nerve at risk for injury

Knee dislocation popliteal artery and common peroneal nerve are at risk for injury

Open tibial fractures any lower leg artery or nerve at risk for injury

Priorities in management of neurovascular limb injury

• Haemorrhage control
Arterial and venous shunt
• Wound debridement
• Skeletal stabilisation
Arterial or venous reconstruction
Soft tissue coverage
Fasciotomy if required allow reperfusion
Nerve repair may be deferred, but it is suggested that best results are obtained if it is under taken within 10 days of injury
for more details see the articles of peripheral nerve trauma
summary nerve injury can be

Neuropraxia: conduction block, axon and nerve sheath intact. Usually full recovery by 6 weeks

Axonotmesis: axon divided, nerve sheath intact May recover (at rate of 1 mm/day), but fibrosis may prevent full recovery exploration and neurolysis may be indicated

Neurotmesis: axon and nerve sheath divided little chance of recovery unless primary surgical repair or nerve grafting. Unlikely to achieve full recovery even with surgical treatment

Fractures and compartment syndrome

Compartment syndrome is inadequate tissue perfusion and oxygenation in a compartment secondary to raised pressure within that compartment. It is a surgical emergency with dire consequences if missed immediate diagnosis and prompt surgery are vital to save limb function.

Pathophysiology of compartment syndrome

Swelling within a compartment bounded by bone and fascia, either secondary to oedema, inflammation or haematoma, will impede venous outflow, increasing the compartment pressure further, and preventing inflow of oxygenated blood. This leads to muscle ischaemia, which will increase the oedema and inflammatory response, so exacerbating the problem. It must be treated by immediate surgical decompression. ischaemia will lead to tissue necrosis, resulting in long-term disability. Muscle necrosis and rhabdomyolysis may result in acute renal failure and death.

The commonest site is the anterior compartment of the lower limb. It can occur in any fibro-osseous compartment including hands, feet, thigh, buttock and forearm.

Causes of compartment syndrome

Can occur after any injury

Crush injuries

Prolonged compression of limb eg tight cast, prolonged surgery, collapsed patient after drug overdose

Occurs in both open and closed fractures

Reperfusion injury eg after delayed arterial repair, or prolonged tourniquet time

Clinical features of compartment syndrome

The cardinal sign is pain that is out of proportion to the injury sustained. On examination there is muscle tenderness and the compartment feels tense. There is typically pain on passive stretch. Weakness, parasthaesia and pulses should be looked for. A pale cool limb and loss of pulses are Very late signs and suggest that the window of opportunity for successful treatment has been missed. Initially, distal circulation and pulses are normal with warm. pink skin.

Management of compartment syndrome

If comportment syndrome is suspected clinically then plaster immobilisation and any bandaging must be removed immediately. Compartment presvores should be measured if there is doubt about the diagnosis, and, if elevated (> 30 mmlHg (or lower If diastolic. BP is low), urgent fasciotomy must be performed.

Fasciotomy for compartment syndrome in the calf requires decompression of four compartments through two incisions

• Lateral incision: peroneal and anterior compartment

• Medial incision: superficial and deep posterior compartments

The skin and fascial incisions could extend the full length of the compartment. The inci­sions are left open and closed when the swelling subsides

Regional anaesthetic techniques (such as nerve blocks, spinals or epidurals) may mask the symptoms of compartment syndrome, resulting in a missed diagnosis. Therefore these techniques should be avoided where there is a high risk of compartment syndrome (tibial shaft fractures). If these techniques must be used, or the patient's (conscious level is reduced, then compartmental pressure monitoring should be considered.

Fractures and infection

post-traumatic infection osteomyelitis, post-operative infection, necrotising fasciitis, tetanus and gas gangrene.

Fractures and soft tissue problems

Open fractures with soft tissue injury or loss require soft tissue cover. The infection rate is inversely related to the time to definitive cover (ie any delay increases the risk of infec­tion). Soft tissue cover may be achieved by primary closure, split-skin graft, local flaps, or free microvascular flaps. If there is an associated bony defect an acute shortening procedure may be appropriate. Best results are obtained by early involvement of the plastic surgical team.

Swelling complicates all injuries - severe swelling around the fracture site may result in fracture blisters. Moderate to severe swelling will result in an increased rate of wound problems and infection. Open reduction and internal fixation should be deferred until the soft tissues permit. Ankle and calcaneal fractures are particularly prone to swelling. All unstable ankle fracture may be temporarily held in a cast or with an external fixator until the soft tissues settle.

Fractures and avascular necrosis AVN

Joints with extensive, convex articular surfaces are at risk of Avascular necrosis AVN. The blood supply to subchondral bone enters the bone at a site distant from the articular surface. Fractures across this bone, carrying the blood supply, will result in AVN. Increased displacement and associated soft tissue stripping increase the risk of AVN. Early and anatomical reduc­tion and fixation may reduce the incidence of AVN.

Typical sites for AVN
Femoral head from intracapsular fracture of the proximal femur

• Proximal scaphoid from a fracture of the waist of the scaphoid

• Humeral heard from proximal humeral fracture (typically three- or four-part fracture where articular and tuberosity fragments are separate

• Body of talus from a neck of talus fracture

Clinical features of AVN


• Chondrolysis and flaps seen on MRI

• Articular collapse seen on plain films

Management of AVN

• Avoid weight bearing across the joint - may revascularise given time (revascularisation demonstrated by MRI or bone scan, or by evidence of bone resorption on plain tilms

. Revascularisation procedures such as vascularised fibula grafts in the femoral head or core decompression

Arthrodesis or arthroplasty

Fractures and myositis ossificans

Myositis ossificans may occur following a fracture or soft tissue injury may involves avul­sion of the periosteum and local haematoma. It is thought that periosteal cells proliferates within the haematoma and ossify it. therefore markedly reducing the range of movement. and often resulting in permanent limitation.

Typical sites for myositis ossificans

• Quadriceps

• Gluteals

• Biceps

• Intrinsic muscles of the hand

Treatment of myositis ossificans

• Differentiate from other calcifying lesions eg osteosarcoma

• Symptomatic treatment in the acute phase 3-6 months

• May be excised if still symptomatic when calcification is mature 12-18 months

• NSAIDs and radiotherapy have been used to reduce incidence but no definite benefit has been proven

Fractures and complex regional pain syndrome CRPS
It divided into two types CRPS type I and CRPS type II
CRPS type I Also known as

Reflex sympathetic dystrophy (RSO) Sudeck's atrophy


Shoulder-hand syndrome

CRPS type II: same features as CRPS type I, but with a demonstrable nerve lesion
Also known as: Causalgia

CRPS type I

Also known as

• Reflex sympathetic dystrophy (RSD

• Sudeck's atrophy

• Algodystrophy

• Shoulder-hand syndrome

This is a poorly understood condition. It may be an exaggeration of the normal sympa­thetic response to injury. CRPS type I occurs in the upper and lower limbs. It is seen in up to 30% of cases following distal radial fracture. It may occur after any minor or major injury (including injury to a nerve as a result of surgery or cast immobilisation.

Primary clinical features of CRPS type I

• Pain out of proportion to the injury

• Swelling

• Stiffness

• Colour change usually redness, but the limb may take on pale or blue colouration

Other signs

• Temperature change

• Sudomotor changes initially hyperhidrosis; later dry skin

• Trophic skin changes and osteoporosis

• Palmer fibromatosis

Three stages of CRPS type I

• Stage I: pain and tenderness, with warm, dry and swollen erythematous limb

• Stage II: cool, sweaty and swollen cyanotic limb

• Stage III: stiffness, atrophy and osteoporosis

Causes of CRPS type I

Many theories have been proposed

Injury alters afferent neurons

This results in altered sympathetic activity, through interaction either locally or in the cord lead to

Altered sympathetic activity (vasomotor and sudomotor) results in swelling, stiffness and colour change and this lead to

Reduced venous drainage perpetuates condition this may be due to vasomotor changes dependent limb or subclavian vein stenosis,

Treatment of CRPS type I

Usually this is a self-limiting condition in minor cases, but it may result in permanent decreased function if swelling and stiffness are allowed to persist. The cycle of pain­ swelling-stiffness-pain must be broken

• Intensive physiotherapy and splintage if required

• Optimised analgesia

• Sympathetic blockade or surgical sympathectomy

• Release of subclavian vein compression has been shown to be beneficial in some resistant cases of CRPS.The compression is due to abnormal anatomy, and is thus present from birth, but does not cause a problem until CRPS is established
CRPS type II

This is also known as causalgia. It has the same features as CRPS type I, with a demonstra­ble nerve lesion.

Surgical decompression and neurolysis may be of benefit in resistant cases that do not respond to non operative treatment


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