COMPLICATIONS OF FRACTURE AND THERE MANAGEMENTS

Presentation by
DR.ARUN MEENA

RESIDENT(2011-2014) DEARTMENT OF ORTHOPAEDICS SAWAI MAN SINGH MEDICAL COLLEGE AND ATTACHED HOSPITALS, JAIPUR

COMPLICATION OF FRACTURE

General

Local

Early

Late

General Complications

General Complication
Shock Metabolic Response Respiratory Dysfunction Crush Syndrome Venous Thrombosis and Pulmonary embolism Tetanus Fat Embolism

Shock:

Hypovolemic shock Neurogenic shock:1.Spinal cord injury 2.Regional anesthesia 3.Drugs 4.Neurological disorders

Septic shock Vasoconstriction,

hypotension,oliguria, mental status. altered
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ARDS
First described in 1967. Diffuse alveolar damage, Hypoxemia Mortality- 40%-60%

Criteria:- Respiratory failure Bilateral infiltrate on CXR PCWP <18

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MANAGEMENT OF ARDS

Mechanical ventilation corrects hypoxemia/respiratory acidosis Fluid management correction of anemia and hypovolemia

Pharmacological intervention Dopamine to augment C.O. Diuretics Antibiotics Corticosteroids - no demonstrated benefit early disease, helpful 1 week later Mortality continues to be 50 to 60%

Crush syndrome
Occur in Muscle crushed Tourniquet - TOO long What happened??? 1st theory Compression released acid myohaematin enter the circulation kidney blocks the tubules SHOCK 2nd theory Renal artery SPASManoxic tubule cells necrosis SHOCK

What we can see?

SHOCK!!
Limb
Pulse less Red Swollen

Renal
Secretion diminished Low output uraemia Acidosis

Neurologically
Drowsy not treated

DEATH

Mangled Extremity Severity Score (MESS Score)

Limb Ischemia for > 6 hr Limb Ischemia Yes- Limb Ischemia Points x2 Reduced Pulse but Normal Perfusion +1 Pulseless, Paresthesias, Slow Capillary Refill +2 Cool, Paralysis, Numb/Insensate +3 0 30-50 years old +1 50 years old +2

Patient Age Range

Shock

SBP > 90 Consistently 0 Hypotension Transiently +1 Persistent Hypotension +2

Low Energy (stab, gunshot, simple fracture) +1 Medium Energy (dislocation, open/multiple fractures) +2 High Energy (high speed MVA or rifle shot) +3 Very High Energy (high speed trauma with 10

Injury Mechanism

How to treat it?

IV FLUIDS BICARBONATES MANNITOL

Limb crushed severely(>6hrs) MESS of 7

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Venous thrombosis & Pulmonary Embolism

Commonest Complication

Most frequently Proximal of thigh pelvis Calf Pulmonary Embolism Incidence 5% & Fatal 0.5%

Cause:-

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High risk group:Old people Cardiovascular Disease Bedridden patient Patients undergoing hip arthroplasty

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Signs:Pain the calf or thigh Soft tissue tenderness Sudden slight incr. temp. Sudden incr. P/R

Homan's Sign positive-pain at back of knee

or calf while knee is flexed and dorsiflexion at ankle is done .

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How to diagnose DVT?

Ascending venography Radioactive iodine labelled fibrinogen(clot) Doppler technique (measure blood flow) CT or MRI scans. Imaging can provide visual images of your veins.

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Treatment: Bed rest. Elastic stockings Heparin bolus of 5000 units followed by i.v. infusion@ 1400 u/h OR Low dose sub cut. heparin (17,500 unit). Warfarin (oral anticoagulant) Surgical Thrombectomy. Placement of Inferior Vena Cava Filters. Replacement of Venous Valves.
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Pulmonary embolism

Difficult to diagnose only minority have symptoms (chest pain, dyspnoe, heamoptysis)

So high risk patients should be examine for pulmonary consolidation

X-ray Lung scintigraphy Pulmonary angiography
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High risk group:Old people Cardiovascular Disease Bedridden patient Patients undergoing hip arthroplasty

How to prevent it?

Prophylactic treatment: Foot elevation Graduated compression stockings Exercise Anticoagulant treatment
Subcut. low dose heparin 5000 units pre ops & 3/7day post ops (but C/I in older patient bleeding) Change to low molecular weight heparin (less likely to cause bleeding)

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Treatment:Cardio respiratory resuscitation Vasopressor for shock Oxygen Large dose heparin Streptokinase (dissolve clot) Antibiotics (prevent lung infection)

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TETANUS

What is Tetanus?
Tetanus organism live only in dead tissue Exotoxin blood & lymph to CNS anterior horn cell Will develop
Tonic clonic contraction
Jaw and face (trismus and risus sardonicus) Neck and trunk Diaphragm and Intercostal muscle spasmASPHYXIA

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Prophylaxis:Active immunization (tetanus toxoid) Booster doses (immunized patients) Non Immunized patients

Wound toilet & antibiotics If wound contaminated antitoxin

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Treatment for Tetanus:IV antitoxin Heavy Sedation Muscle Relaxant drug Tracheal Intubation Controlled respiration

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FAT EMBOLISM

Only minority patients with circulating fat globules from bone marrow will develop POST TRAUMATIC
RESPIRATORY DYSFUNCTION.

Trauma fat from bone marrow influence of CRP reached to heart lung fatty acids disruption of alveolar capillary membrane haemorrhaegic pulmonary edema. Usually in MULTIPLE CLOSED FRACTURE But other condition also reported (burns, renal infarction, cardiopulmonary operation)

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How can we detect it?

Usually young adults with LL fracture Early warning signs (72/24HR of injury)

Rise in temperature and pulse rate

More pronounced case

Breathlessness Mild mental confusion Petechia (chest & conjuntival fold)

Most severe case

Marked respiratory distress coma ARDS
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Gurds and wilson Criteria

Major Features (at least 1) Minor Features (at least 4) Lab Features (at least 1) Fat macroglobulinemia Anaemia Thrombocytopenia High ESR

Respiratory Insufficiency Pyrexia Cerebral involvement Petechia Rash Tachycardia Retinal changes Jaundice Renal changes

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How to treat it?

Monitoring of blood PsO2

Signs of hypoxia (<8kPa @ 60mmHg)

Oxygen If severe
Intensive care with sedation and assisted ventilation Swan ganz Catheterization (monitor cardiac Fx) Fluid balance. Supportive
Heparin-thromboembolism Steroids-pulmonary edema Aprotinin-prevent aggregation of chylomicrons
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EARLY LOCAL COMPLICATION OF FRACTURE

Arise during the first few weeks

following injury.

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Early Complication
Local Visceral Injury Vascular Injury Nerve Injury Compartment Syndrome Haemarthrosis Infection Gas gangrene

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Local visceral Injury

Pelvic fracture
rupture.

Bladder and urethral Penetration to the

Rib fracture
lungs

Pneumothorax

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Vascular injury

Clinical features

Pt with ischemia may have 5 Ps: - paraesthesia / numbness - pain - pallor - pulselessness - paralysis Investigate: Angiogram

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Treatment

Emergency treatment All bandages/splints removed The fracture X-Ray again Circulation reassessed for next half hour If no improvement, do vessels exploration Suture torn vessels, vein grafting, if thrombosed do endarterectomy Aim: to restore blood flow

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Nerve Injury
TYPE Neurapraxia:-It is physiological disruption of conduction
in the nerve fiber; no structural changes occurs.

Axonotmesis:-the axons are damaged but the internal

architecture of the nerve is preserved.

Neurotmesis:-the structure of a nerve is damaged by

actual cutting or scarring of a segment.

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Nerve Axillary Radial Median Ulnar

Trauma Dislocation of shoulder # of humerus Supracondylar # of humerus # medial epicondyl humerus Post dislocation of hip Knee dislocation # neck of fibula

Effect Deltoid paralysis Wrist drop Pointing index Claw hand

Sciatic
Common peroneal

Foot drop
Foot drop

Radial nerve is most frequently damaged nerves.

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In closed injuries nerve is seldom severed and spontaneous recovery should be awaited In open fractures complete lesion (neurotmesis) : the nerve is explored during wound debridement and repaired.

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Compartment Syndrome

Definition
Compartment syndrome involves the compression of nerves and blood vessels within an enclosed space, leading to impaired blood flow and nerve damage.

Causes:
-any injury/infection leading to edema of muscle -fracture hematoma within the compartment -ischemia to the compartment leading to muscle edema -Due to tight bandages or casts
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Vicious cycle of Volkmanns ischemia

TRAUMA

ISCHEMIA

EDEMA

DEC. BLOOD FLOW

INCREASED COMPARTMENT PRESSURE

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Hallmark Symptoms:
- severe pain that does not respond to elevation or pain medication. - In more advanced cases, there may be decreased sensation, weakness, and paleness of the skin. -Stretch test positive(earliest sign)

Injuries with a high risk of developing Compartments synd: # of the elbow # of the forearm bone # of the proximal third of the tibia (M.C.)

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A vicious cycle cont. until the total vascularity of the muscles and nerves is jeopardized.

This result in ischemic muscle necrosis and nerve damage. (within 12 hours)
The necrotic muscle undergo healing with fibrosis, leading to Volkmanns contracture. Nerve damage may result in motor and sensory loss. In extreme case gangrene

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Treatment
First removed all the bandages & dressing. Fasciotomy is performed. The wound should be left open and inspected 2 days later. If there is muscle necrosis debridement If muscle is healthy suture/ skin grafted / simply heal by 2 intention.

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Haemarthrosis
Fractures involve joints, leads to collection of blood within the joints. Feature :-The joint is swollen and tense and patient will resists any movement. Tx : the blood should be aspirated before dealing with the fracture

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Infection

Causes:

Open fracture (common) Use of operative method in the Tx of # Wound becomes inflamed and starts draining seropurulent fluid. Infection may be superficial, moderate (osteomyelitis), severe (gas gangrene). Post-traumatic wound infection is most common cause of chronic osteomyelitis union will be slow and chance of refracturing.

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Treatment:
Antibiotic Excising all devitalized tissue

If Sign of acute infection and pus formation : tissue around the fracture should be opened & drained.

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Gas gangrene

anaerobic orgs : Clostridium sp. infections. Toxins produced will destroy the cell wall and leads to tissue necrosis C/f:--- intense pain - swelling around the wound - brownish discharge - gas formation - pyrexia - characteristic smelling - PR - toxaemic coma death Inability to recognize may lead to unnecessary amputation for the non-lethal cellulitis.
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swelling around the wound, brownish discharge

gas formation

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How to prevent it?

Deep penetrating wound should be

EXPLORED ALL dead tissue completely EXCISED Doubt about tissue viability left it OPEN No antitoxin

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Treatment for gas gangrene

The key = EARLY DIAGNOSIS General measures (fluid, IV antibiotics) Hyperbaric oxygen (limiting spread) Decompression of wound Removal of all dead tissue Amputation (advanced case)

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LATE COMPLICATIONS

Delayed union Non-union Malunion Joint stiffness Myositis ossificans Avascular necrosis Shortening Sudecks dystrophy Osteomyelitis Volkmanns Ischaemic contracture Osteoarthritis
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DELAYED UNION

A fracture that has not healed after a reasonable time period (the time in which it was expected to heal) has passed.

Causes
Inadequate blood supply Severe soft tissue damage Periosteal stripping Excessive traction Insufficient splintage Infection
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PERKINS TIME TABLE

Upper Limb Callus visible Union Consolidation 2-3 wks 4-6 wks 6-8 wks Lower Limb 2-3 wks 8-12 wks 12-16 wks

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Clinical features Fracture tenderness

(Esp. when subjected to stress)

X-Ray Visible fracture line

Very little callus formation or periosteal reaction.

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Conservative:(1) eliminate any possible cause of delayed union. (2) Promote healing by providing the most appropriate biological environment. (3) immobilization. (4) Union stimulus by encouraging muscular exercise and weight bearing cast or brace

Operative :Delayed union more than 6 months without signs of callus formation Internal fixation or bone grafting are indicated

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NON-UNION

Condition when the fracture will never unite w/o intervention Healing has stopped. Fracture gap is filled by fibrous tissue (pseudoarthrosis) Causes: Improper Tt. of delayed union. Too large gap. Interposition of periosteum, muscle or cartilage between the fragments. Chronic sub acute infection.
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Types:SEPTIC NON-UNION ASEPTIC NON-UNION

Atrophic(TRUE NON-UNION)

Oligotrophic

Hypertrophic(HYPER VASCULAR)

TORISON WEDGE

COMMINUTED

DEFECT TYPE ELEPHANT FOOT

HORSE HOOF

OLIGOTROHIC

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Hypertrophic non-union

Atrophic non-union.
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Elephant foot type :-expansile callus present, it is result of movement occurring at fracture site before union has occurred. Horse hoof type:-little callus due to instability at fracture site following inadequate reduction and fixation. Torision wedge type:-when intermediate fragment with poor blood supply unite at one end but do not unite at other end.

Communited type:-due to many intermediate fragments with poor blood supply.

Defect type:- occurs in bone lose.

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Clinical features:-

Painless movement at the fracture site

X-Ray:-

Fracture is clearly visible Fracture ends are rounded, smooth and sclerotic

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Treatment
Conservative: 1.Occasionally symptom less, needing no treatment 2.Functional bracing may be sufficient to induce union 3.Electrical stimulation promotes osteogenesis Operative Hypertrophic non-union (Esp. long bone) Rigid fixation (internal / external) sometimes need bone grafting Atrophic non-union Fixation & bone grafting

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MALUNION

Fragments join in an unsatisfactory position (unacceptable angulation, rotation or

shortening)
Causes: Failure to reduce a fracture adequately Failure to hold reduction while healing proceeds Gradual collapse of osteoporotic bone Clinical feature: 1.Deformity & shortening of the limb 2.Limitation of movements
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 Treatment

Angulation in a long bone (> 15 degrees) Osteotomy & internal fixation Shortening less than 2 cm: compensated by shoe raise Shortening more than 2 cm: limb length equalization procedures

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Cross union

Sometimes radio-ulnar and tibiofibular fractures may undergo cross union.

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AVASCULAR NECROSIS

Circumscribed bone necrosis Causes:Interruption of the arterial blood flow Slowing of the venous outflow leading to inadequate perfusion

Common sites:Femoral head Femoral condyles Humeral head Capitulum of humerus Scaphoid (proximal part) Talus (body) Lunate
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Clinical features:Joint pain, stiffness, swelling Restricted movement

Diagnosis:-

X-ray shows increase in bone density

(consequence of new bone ingrowth in the necrotic segment and disuse osteoprosis in the surrounding parts )

Bone scan:- changes can be seen before X-ray changes,

Visible as cold area on the bone.

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Avascular necrosis of the head of the femur (Bone scan)

Treatment
Avoid weight bearing on the necrotic bone Revascularisation (using vascularised bone grafts) Excision of the avascular segment Replacement by prostheses

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Conditions associated with AVN

Perthes disease Certain fractures Epiphyseal infection Sickle cell disease Caisson disease Gauchers disease Alcohol abuse High-dosage corticosteroid

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ALGODYSTROPHY
(COMPLEX REGIONAL PAIN SYNDROME)

Previously known as Sudecks atrophy. Post-traumatic Reflex sympathetic dystrophy. Usually seen in the foot / hand(after relatively trivial injury)

Clinical features
Continuous burning pain. Early stage:- Local swelling, redness, warmth Later:Atrophy of the skin, muscles Movement are grossly restricted

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X-Ray
Patchy rarefaction of the bones ( patchy

osteoporosis )

Treatment
Physiotherapy (elevation & active exercises) Drugs - Anti-inflammatory drugs - Sympathetic block or sympatholytic drugs (Guanethidine)

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OSTEOARTHRITIS

A fracture involving a joint may damage the articular cartilage and give rise to post traumatic osteoarthritis within a period of months. TYPES:Post-traumatic OA: Joint fracture wt severely damaged articular cartilage Within period of months

2O OA: Cartilage heals Irregular joint surface may caused localized stress2O OA Years after joint injury

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Clinical features
Pain Stiffness Swelling Deformity Restricted movement

Treatment
Pain relief : Analgesics/Anti-inflammatory agent Joint mobility : Physiotherapy Load reduction : wt reduction Realignment Osteotomy (young pt.) Arthroplasty (pt > 60yr)

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JOINT STIFFNESS
Common site : knee, elbow, shoulder,
small joints of the hand.

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Causes:-

Oedema & fibrosis of the capsule, ligaments, muscle around the joint Adhesion of the soft tissue to each other or to the underlying bone (intra & peri- articular adhesions) Synovial adhesions due to haemarthrosis

Treatment 1.Prevention:I. Exercise II. If joint has to be splinted Make sure in correct position 2.Joint stiffness occurred:I. Prolonged physiotherapy II. Intra- articular adhesions Gentle manipulation under anesthesia followed by continuous passive motion III. Adherent or contracted tissues Released by operation
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MYOSITIS OSSIFICANS
Heterotopic ossification in the muscles after an injury. It may also happens because of the ossification of the hematoma around a joint after a compound fracture.

Usually occurs in
Dislocation of the elbow A blow to the brachialis / deltoid / quadriceps

Clinical features
Pain, soft tissue tenderness Local swelling Joint stiffness Limitation of movements Extreme cases: - Bone bridges the joint - Complete loss of movement (extra-articular ankylosis)
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X-Ray

Normal Fluffy calcification in the soft tissue

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Treatment
Early stage : Joint should be rested Then : Gentle active movements When the condition has stabilized:- Excision of the bony mass Anti-inflammatory drugs may joint stiffness

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Volkmanns ischemic contracture

Sequel to Untreated or inadequately treated compartment syndrome in which necrotic muscles and nerve tissues has been replaced by fibrous tissues. If the peripheral nerves are also affected, sensory or motor paralysis may happen

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Clinical features:- Severe pain that does not respond to elevation or pain medication. - In more advanced cases, there may be decreased sensation, weakness, and paleness of the skin. - 5 Ps 1.pain 2.pallor 3.paraesthesia 4.paralysis 5.pulselessness
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TREATMENT:I. II. Physiotherapy Tendon lengthening III. Muscle sliding IV. Tendon transfer V. Amputation VI. JESS distracter

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Osteomyelitis

Osteomyelitis is the progressive infection of bone and bone marrow by micro-organisms, resulting in inflammatory destruction of bone, bone necrosis and new bone formation. Infection with a bacterium called Staph. aureus is the most common cause. Fungus is a rare cause.

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Chronic osteomyelitis exists in the presence of any of the following conditions:1.Infection lasting 6 weeks or more (with radiologic evidence)

2.Sequestrum formation or sclerosis

3.Relapse or persistence after initial treatment of acute osteomyelitis 4.Osteomyelitis associated with foreign bodies 5.Osteomyelitis associated with peripheral vascular disease 6.Osteomyelitis from organisms that produce chronic, indolent disease e.g Mycobacterium tuberculosis.

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Classification:Waldvogel classification 1.Haematogenous osteomyelitis 2.Osteomyelitis secondary to contigous focus of infection 3.No generalized vascular disease 4.Generalised vascular disease 5.Chronic osteomyelitis (Necrotic bone)

Cierny-Mader classification Anatomic types Type I: --Endosteal or medullary osteomyelitis Type II: --Superficial osteomyelitis limited to the surface Type III:--Localized, well marked lesion involving the entire cortical thickness with sequestration and cavity formation Type IV: --Diffuse Osteomyelitis

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Radiological investigations
X-RAYS:1.A sequestrum surrounded by an involucrum gives a typical bone-in-bone picture . area merely appears densely sclerotic with surrounding regional 2.Infected Osteoporosis. Computerized Tomography (CT):- is more useful in chronic osteomyelitis. Magnetic Resonance Imaging (MRI) is very sensitive even in the early phase of bone infections. Scintigraphy:Ultrasonography:Can localize subperiosteal fluid.

Treatment of Osteomyelitis :1.Antibiotics 2.Surgical debridement

bone-in-bone

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Shortening

It is a common complications of fractures and results from:Mal union of the long bones Crushing: Actual bone loss Growth defects: growth plate or Epiphyseal injuries

Treatment: 1.Shortening of upper limbs goes unnoticed 2.For lower limb treatment depends upon the amount of shortening: Shortening less than 2 cm: compensated by shoe raise Shortening more than 2 cm: limb length equalization Procedures

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