COMPLICATIONSOF

FRACTURES

CLASSIFICATION

•Complications of fractures tend to beclassified according to whether theyare local or systemic and when theyoccur –

IMMEDIATE EARLY LATE

IMMEDIATE HYPOVOLAEMIC SHOCK

Commonest cause of death following fractures

Cause- external/internal haemorrhage Treatment Iv crystalloids-ringer lactate,followed by

colloids and blood

EARLY COMPLICATIONS

•Early complications occur at the timeof the fracture (immediate) or soonafter.

•They are again classified into- local Systemic •Early local complications tend to affect mainly the soft tissues

LOCAL EARLY COMPLICATIONS

•Vascular injury causing haemorrhage, internal or external •Visceral injury causing damage to structures such as brain, lung or bladder •Damage to surrounding tissue, nerves

or skin •Haemarthrosis •Compartment syndrome {volkmanns

ischemia}

•Wound Infection, more common for open

fractures •Tetanus

•Gas gangrene

•Injury to joints

VASCULAR INJURY

Blood vessels lie close proximity to bones ,hence liable to injured

Popliteal is commonly injured one Consequences- exercise ischemia-

ischemic contracture-gangrene Signs-5ps-pain,absent

pulse,pallor,parasthesia,paralysis

VISCERAL INJURIES Commonly seen

in pelvic and rib fractures

NERVE AND SKIN TISSUE DAMAGES

Radial nerve is commonly injured Consequences- lead to

neurapraxia,axonotmesis or neurotmesis Axillary n-dislocatn of shoulder-deltoid

paralysis Radial n-#shaft of humerus-wrist drop Median n-supracondylar# of humerus-

pointing index Ulnar n-#medial epicondyle humerus-

claw hand Sciatic n- posterior dislocation of hip-

foot drop

HAEMARTHROSIS

Bleeding in the joint because of fracture

COMPARTMENT SYNDROME

•Fractures of the limbs can cause severeischaemia, even without damage to a major bloodvessel

•. Bleeding or oedema in an osteofascialcompartment increases pressure within thecompartment, reducing capillary flow and causingmuscle ischaemia

•A vicious circle develops of further oedema and pressure build-up, leading swiftly to muscle and nerve necrosis.

Limp amputation may be required if untreated

•Compartment syndromes can also result from ;

Crush injuries caused by falling debris orfrom a patient’s unconscious compressionof their own limb

Swelling of a limb inside an over tight cast

•Compartment syndrome can occur in anycompartment, e.g. the hand, forearm,upper arm, abdomen, buttock, thigh, andleg.

•40% occur following fracture of the shaftof the tibia (with an incidence of 1-10%)and about 14% following fracture of aforearm bone.

•Risk is highest in those under 35 years

•COMPARTMENTAL SYNDROME MAY LEADTO THE VOLKMANN'S ISCHAEMIA

Presentation:- Signs of ischaemia (5 P's:

Pain,Paraesthesia, Pallor, Paralysis,Pulselessness)

Signs of raised intracompartmental pressure: 1.Swollen arm or leg 2.Tender muscle - calf or forearm pain on passive extension of digits

3.Pain out of proportion to injury4.Redness, mottling and blisters

Watch for signs of renal failure{low-output uraemia with acidosis)

MANAGEMENT

Remove/relieve external pressures (fasciotomy) Prompt decompression of threatened compartments by open fasciotomy Debride any muscle necrosis Treat hypovolaemic shock and oliguria urgently Renal dialysis may be necessary

•Complications Acute renal failure secondary to rhabdomyolysis DIC Volkmann's contracture (where infarcted

muscle is replaced by inelastic fibroustissue)

GAS GANGRENE

•Clostidium welchii ( perfringens )

•Clinical presentation Subcutaneous

crepitations Myonecrosis

•Treatment Debridement pencillin

TETANUS

Causative agent

Clostidium tetani

TRISMUS DYSPHAGIA RISUS

SARDONICUS OPIS THOTONUS

Treatment

Bed rest and sedation

Immunoglobulin Respiratory

support pencillin

SYSTEMIC EARLYCOMPLICATIONS

•Fat embolism•Shock•ARDS•Thromboembolism (pulmonary or venous)

•Exacerbation of underlying diseases such as diabetes or CAD Pneumonia Aspectic traumatic fever Septicemia Crush syndrome

FAT EMBOLISM •This is a relatively uncommon disorder that occurs

in the first few days following trauma with amortality rate of 10-20%

•Fat drops are thought to be released mechanicallyfrom bone marrow following fracture, coalesce andform emboli in the pulmonary capillary beds andbrain, with a secondary inflammatory cascade andplatelet aggregation

•An alternative theory suggests that free fatty acidsare released as chylomicrons following hormonalchanges due to trauma or sepsis

•Risk factors Closed fractures

Multiple fracturesPulmonary contusionLong bone/pelvis/rib fractures

•PRESENTATION

•Sudden onset dyspnoea•Hypoxia•Fever•Confusion, coma, convulsions•Transient red-brown petechial rash

affecting upper body,especially axilla Diagnosis Retinal artery emboli-striate hges &

exudates Sputum & urine-fat globules X-ray chest –snow storm appearance

TREATMENT :-

Respiratory support Heparinisation Intravenous low molecular weight dextran(lomodex 20) and corticosteroids Iv 5% dextrose solution with 5% alcohol

–helps in emulsification of fat globules

DEEP VEIN THROMBOSIS

Common complication associated with lower limb injuries and with spinal injuries •D.V.T. proximal to the knee

is a common cause of lifethreatening complication of pulmonary embolism

Causes Immobilization following trauma Fracture of legSymptomsLeg swellingCalf tenderness

CONSEQUENCES:-

pulmonary embolism Tachypnoea Dyspnoea 4-5 days after trauma

•Treatment:- Elevation of the limb Anti coagulating therapy Respiratory support and heparin therapy{ respiratory embolism} Early internal fixation of fractures Active mobilization of the extremity

ASEPTIC TRAUMATIC FEVER

•Aseptic traumatic fever: This issupposed to be due to absorption offibrin ferment taking place.

•It may, however, be due to someirritation, as of a badly fitting splint,and disappears on removal of it

SEPTICAEMIA

•Because of trauma a large amount of bacteria can enter in the blood stream and may cause septicemia

Symptoms Rash Fever and vomiting Cold extremitis Rapid breathing Stomach pain and joint pain drowsy

MANAGEMENT

Initial Resuscitation - ABC 1.Secure airway 2. Support breathing 3.Restore circulation Fluid therapy Inotropic Support Antimicrobial therapy Respiratory Support

CRUSH SYNDROME

•Crushing injury to skeletal muscles because of the fracture Cause- crushing of muscles- myohb enters

to circulation-ppt in renal tubules-a/c renal failure

•Complications shock Renal failure •Management To avert disaster, a limb crushed severely and for several hours should be amputated

LATE COMPLICATIONS

•Late complications are those which occurafter a substantial time has passed andare as a result of defective healingprocess or because of the treatment itself.

•They are again classified in to 2 groups Imperfect union of the fracture others

OTHER LATE COMPLICATIONS

•Avascular necrosis•Shortening•Joint stiffness•Sudeck’s dystrophy•Osteomyelitis•Volkmann’s Ischaemic contracture•Myositis ossificans•Osteoarthritis

IMPERFECT UNION OF THEFRACTURE

•They are again classified into four sub groups: Delayed union Non union Mal-union Cross-union

DELAYED UNION

•When a fracture takes more than theusual time to unite, it is said to havegone in delayed union

•Causes: Inadequate blood supply infection Incorrect splintage 1.Insufficient splintage 2.excessive traction

•Signs: The fractured site is usually tender The bone may appear to move in one piece,

if however, it is subjected to stress , pain isimmediately felt and the bone may angulate;

The fracture is not consolidated X-ray: the fractured site is still clearly

visible, but the bone ends are not sclerosed

•TREATMENT

Conservative: 1.Plaster should be sufficiently

extensive and must fit accurately

2.Replace traction by plaster splintage3.Use of functional bracing

Operative: Bone grafting with or without IF

NON-UNION

•When the process of fracture healingcomes to a stand before itscompletion, the fracture is said tohave gone in non –union.

•It is not before six months that a fracture can be so labelled.  Nonunion is one endpoint of delayed

union

CAUSES :

The injury 1.Soft tissue loss 2. Bone loss 3.Intact fellow bone 4.Soft tissue inter position The bone 1.Poor blood supply 2. Poor haematoma

3. Infection4. Pathological lesion

PRESENTATION

Pain at fracture site Nonuse of extremity Tenderness and swelling Joint stiffness (prolonged >3 months) Movement around the fracture site (pseudarthrosis) Investigations Absence of callus (remodelled bone) or lack of

progressive change in the callus suggests delayed union.

Closed medullary cavities suggest nonunion. Radiologically, bone can look inactive, suggesting

the area is avascular (known as atrophic nonunion) or there can be excessive bone formation on either side of the gap (known as hypertrophic nonunion).

TREATMENT

Conservative: 1.Occasionally symptom less, needing no treatment 2.Functional bracing may be sufficient to induce union 3.Electrical stimulation promotes osteogenesis Operative 1.Very rigid internal fixation with hypertrophic non-union 2.Fixation with bone graft is needed in case of

atrophic non union

MAL-UNION

 occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction.

Causes

primary 1.The fracture was never reduced and has united in a deformed position. 2.Shortening is, of course, one type of deformity.

Secondary 1.The fracture was reduced but the reduction was not

held 2.Redisplacementmay occur during the first week, and a check x-ray at 1 week is adviseable

. •Signs: The deformity is usually obvious There may be painful limitation of joint movements At elbow, valgus deformity may present with delayed ulnar nerve palsy

TREATMENT

Conservative 1.If shortening is the main feature a raised shoe is usually sufficient 2.In child usually no treatment is required

because it is expected to correct byremodelling

Operative 1. Osteotomy 2.Excision of protruding bone 3. Osteoclasis 4.Redoing the fracture surgical

AVASCULAR NECROSIS

•Blood supply of some bones is suchthat the vascularity of a part of it isseriously jeopardized followingfracture, resulting in necrosis of thepart.

CONSEQUENCES:-

Avascular necrosis causesdeformation of the bone. This leads, afew years later, to secondaryosteoarthritis and causes painfullimitation of joint movement.

Diagnosis:-

X-ray changes:-- 1.Sclerosis of the necrotic area 2.Deformity of the bone 3. Osteoarthritis Bone scan:- changes can be seen before X-ray changes: 1.Visible as cold area on the bone

•Treatment:- Avascular necrosis canbe prevented by early, energeticreduction of susceptible fracturesand dislocations. Treatment options:

1.Delay weight bearing till revascularization

to prevent collapse 2. Revascularization 3.Excision of the avascular segment 4.Total joint replacement

SHORTENING

•It is a common complications of fractures and results from:- 1.Mal union of the long bones

2.Crushing: Actual bone loss3.Growth defects: growth plate or epiphyseal injuries

TREATMENT:-

Shortening of upper limbs goes unnoticed For lower limb treatment depends upon

the amount of shortening: 1.Shortening less than 2 cm: compensated

by shoe raise 2.Shortening more than 2 cm: limb length equalization procedures

JOINT STIFFNESS

•It is a common complications of fracture treatment. •Shoulder, elbow and knee joints are

particularly prone to stiffnessfollowing immobilization

CAUSES

Intra-articular or Para-articular adhesions secondary to immobilizations Contracture ofthe musclesaround a joint because of prolonged immobilizations Tethering of muscles at fracture site Myositis ossificans •Consequences:- Hampers the normal physical activity Results in late osteoarthritis

TREATMENT:-

Heat therapy and exercise Manipulation of the joint under

anesthesia Surgical interventions 1.To excise an extra articular bone block

2.To lengthen contracted muscles3.Joint replacement, if there is pain due tosecondary arthritis

ALGODYSTROPHY/ SUDECK'S DYSTROPHY

•Also known as Reflex Sympathetic Dystrophy. •Involves a disturbance in the sympathetic nervous system. •Consequences:- pain Hyperaesthesia Tenderness Swelling

Skin become red, shiny and warm in early

stages Progressive atrophy of the skin, muscles

and nails in later stages Joint deformity and stiffness ensues X-ray shows characteristic spotty

rarefraction

TREATMENT:-

Occupational therapy and physiotherapy constitutes the principle modality of treatment. Use of β-blocker. In resistant cases, sympathetic blocks

have been shown to aid in recovery

OSTEOMYELITIS

•Osteomyelitis is an infection of a bone. •Many different types of bacteria can cause osteomyelitis. •However, infection with a bacterium

called Staph. aureus is the mostcommon cause. Infection with afungus is a rare cause

TREATMENT:-

•After operative treatment of fracturebacteria may spread to the bone andmay cause osteomyelitis.

antibiotics Surgery: 1.in case of abscess formation 2.The infection presses on other important structures 3.The infection has become 'chronic' (persistent) and some bone has been destroyed. 4. Hyperbaric oxygen

VOLKMANN’S ISCHAEMICCONTRACTURE

•This a sequel to Volkmann's ischaemia. •The ischaemic muscles are replaced by fibrous tissue •If the peripheral nerves are also

affected, sensory or motor paralysismay happen

Clinical features:- Marked atrophy Flexion deformity Nails shows atrophic changes Skin becomes dry and scaly

TREATMENT:-

Mild deformity can be corrected by passivestretching using a turn-buckle splint(Volkmann's splint)

For moderate deformities, a soft tissue slidingoperation, where the flexor muscles arereleased from their origin, is performed

For a severe deformity, bone shortening operations may be required

MYOSITIS OSSIFICANS

•Myositis ossificans is wherecalcifications and bony massesdevelop within muscle and can occuras a complication of fractures.

•It may also happens because of the ossification of the hematoma around a joint after a compound fractures

CLINICAL FEATURES:-

Pain Tenderness , Focal swelling, and Joint/muscle contractions •Treatment:- Massage following injury is strictly

prohibited. In early stages rest is advised NSAIDS may help to reduce pain

In late stages Occupational and Physiotherapy is prescribed to regain movements Ultra sound In some cases surgical excision of

myositic mass is done

OSTEOARTHRITIS

•Osteoarthritis is liable to followmalunion and traumatic injuries to thejoints.

•Joint surfaces become incongruent •Direction of stress transmission is abnormal •Increase wear and tear at the joint

TREATMENT:-

Osteoarthritis cannot be cured, but it can be treated The goal of every treatment for arthritis is to:- 1.reduce pain and stiffness,

2.allow for greater movement, and3.slow the progression of the disease

Anti-Inflammatory Medications

Cortisone Injections Occupational and physiotherapy Weight Loss Activity Modification Diet: obesity is a risk factor for

developing osteoarthritis

IATROGENIC COMPLICATIONS

Casts

Pressure ulcers Thermal burns during plaster hardening Thrombophlebitis

TRACTION

Traction prevents patients mobilising, causing additional muscle wasting and weakness. Other complications include:

Pressure ulcers Pneumonia/urinary tract infections Permanent footdrop contractures Peroneal nerve palsy Pin tract infection Thromboembolism

EXTERNAL FIXATION

Problems include: Pin tract infection Pin loosening or breakage Interference with movement of the joint Neurovascular damage due to pin

placement Misalignment due to poor placement of

the fixator

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