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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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