nattapong pholpradubpet complication of fracture

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NATTAPONG PHOLPRADUBPET COMPLICATION OF FRACTURE

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Page 1: NATTAPONG PHOLPRADUBPET COMPLICATION OF FRACTURE

N AT TA P O N G P H O L P RA D U B P E T

COMPLICATION OF FRACTURE

Page 2: NATTAPONG PHOLPRADUBPET COMPLICATION OF FRACTURE

OUTLINE

• Vascular injury• Compartment Syndrome• Thromboembolism• Fat Embolism Syndrome• Complex Regional Pain Syndrome (CRPS)

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VASCULAR INJURY

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ETIOLOGY

• Vast majority of arterial injuries associated with fractures are secondary to Gunshot wounds

• Type• Intimal flaps• Disruptions or subintimal hematoma• Wall defect• Complete transection• A-V fistula

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ARTERIAL INJURY

• Associate with fractures in areas where the vessels are close to osseous structure or held in a fixed position• fracture dislocation around the knee

The presentation may be delayed (intimal flap or thrombosis), so the absence of classic signs of acute ischemia & the presence of palpable pulses in no way rule out the possibility

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VENOUS INJURY

• Commonly associate with arterial injury • Often multiple, lacerations, producing hematoma• Venous repair esp. in the groin or popliteal area • may be helpful after arterial repair to prevent hematoma

formation, distal edema, & progressive tissue destruction

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DIAGNOSIS

• Awareness• Signs & Symptoms:

• Absence of distal pulse, pallor, differential gradient in temp, rapidly progressing edema or hematoma formation• Paralysis, paresthesia

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INVESTIGATION

• Investigation• Doppler U/S• Duplex U/S (real time B-mode U/S & pulsed Doppler flow

detection)• Arteriogram • Venogram

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TREATMENT

• Initial• Early resuscitation• Immobilization the traumatized limb• Do not elevate the affected limb• Direct pressure• Avoid tourniquet (temporary use only if necessary)

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• Pre-op preparation• Optimal period for restorative surgery is 6 - 8 hr• Correct acidosis & volume depletion• Splint or traction is applied

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BONE VS VESSEL: WHAT SHOULD BE REPAIRED FIRST?

• Depends on• ischemic time (6 hr golden period)• amount of contamination• extent of wound• mechanism of injury• associated injury

• Team approach• Adjust individually

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• Surgery• Constructive dialogue with vascular surgeon• Drape to permit access to sapheneous or cephalic vein• Temporary shunt ???• Fasciotomy

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• Fixation• Closed fracture: internal fixation• Open fracture: external fixation • place pin away from the open wound & position the bar away

from the operative field for vascular repair

• Delayed definitive fixation

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COMPARTMENT SYNDROME

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DEFINITION

• An increased pressure within an enclosed osteofascial space that reduces the capillary blood perfusion below a level necessary for tissue viability

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COMMON CAUSE

• Fracture• Soft tissue injury• Arterial injury• Limb compression• Burns

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SIGN & SYMPTOM

• Symptoms• Pain out of proportion !!!• Pain is unrelenting• No relief following splinting or removal of casts &

bandages• Paresthesia

• Signs• Pain on palpation of compartment• Tense / swollen compartment• Passive muscle stretch severe pain • Sensory deficit of nerve in the compartment• Muscle weakness

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•Warnings• Pulses are present early and their absence occurs late in

the development• Normal capillary refill also present early in development• Paresthesia and paralysis are too late• Pain out of proportion & pain on passive stretching are 2

most important findings

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COMPARTMENT PRESSURE MEASUREMENT (WHITESIDE)

• Sterile saline is used• 18- gauge needle is inserted

into the muscle at the level of fracture

• Read when saline meniscus is “flat”

• Do not depress the plunger too strongly (avoid saline leakage)

• 2 readings should be made• Repeat readings should be

made at 1 hr interval

Same level with tip of needle

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• What is the magic number?• 30 mmHg (corresponds with normal capillary pressure)

• 45 mmHg (capillary pressure rises in compartment syndrome)

• 20 mmHg below DBP

• 30 mmHg below DBP

Mubarak, SJ & Hargens, AR

Matsen, FA

Whiteside, TE

McQueen, MM & Court-Brown, CM

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MANAGEMENT

• Release constrictive dressings, bivalve cast & webril • Fasciotomy

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• Fracture stabilization• External fixator is the implant of choice

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THROMBOEMBOLISM

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• Risk depends on• Age• Extent & duration surgery• Type of anesthesia • Spinal & epidural lower than GA

• Degree & duration of immobilization• Severity of underlying systemic disease

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CLINICAL SYMPTOM

• Leg pain• Swelling• Warmth• Dilated vein• Erythema• Pitting edema

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PHYSICAL EXAMINATION

• Measure leg circumference• Tenderness along deep venous system• Homans’ sign• Pain in the calf or popliteal region on forceful & abrupt

dorsiflexion of ankle with knee in a “FLEXED” position

PHE has low sensitivity & specificity

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INVESTIGATION

• Duplex ultrasound• Venogram

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MANAGEMENT

• Prophylaxis• LMWH 30 mg subcutaneously twice daily no monitor is

required• Warfarin 5 - 10 mg/day INR 2 -2.5

• Treatment• Heparin intravenously

5,000 units followed by cont infusion of 30,000 - 35,000 units / 24 hr APTT

• Warfarin 5 - 10 mg/day starts 24 hr later INR 2 - 3

• Stop heparin when therapeutic range of INR is achieved for at least 2 days

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FAT EMBOLISM SYNDROME

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DEFINITION

• Presence of fat globules in lung parenchyma & peripheral circulation after fracture of long bone & pelvis, other major trauma, or non-traumatic conditions• “Fat embolism syndrome” term to describe a

serious manifestation of the phenomenon of fat emboli

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PREVALENCE

• Fat emboli: • 90% after major trauma

• Fat embolism syndrome • 0.25-1.25%• Higher prevalence in multiple bone fractures

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• Mostly have a latent period of 12 - 72 hr after trauma• Movement of unstable fracture ends & reaming of

medullary cavity promote entrance of marrow contents to the circulation

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CLINICAL FINDINGS

• Classic triad • Pulmonary• Cerebral• Cutaneous manifestations

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• Pulmonary• Tachypnea, pleuritic chest pain, dyspnea, cyanosis,

tachycardia, pyrexia• PHE: rales, rhonchi, pleural rub• Hypoxemia

• Cerebral• Headache, irritability, delirium, stupor, convulsion, coma• Focal neurological deficit (rare)

• Cutaneous• Manifest on 2nd or 3rd day in 50% of pts• Petechial rash in nondependent portions of body:

chest, ant axillary fold, conjunctiva• Retinal findings

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INVESTIGATION

• Blood gas: hypoxemia• Blood test: thrombocytopenia, anemia, hypocalcemia• EKG:

• Right axis deviation (prominent S in lead I, Q in III, ST segment changes)

• CXR: • Varies• Severe cases:• diffuse, bilateral infiltration (interstitial or

alveolar)• opacify both lungs diffusely (capillary

permeability-type edema)

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TREATMENT

• Supportive pulmonary care• Pulse oximetry: < 90% blood gas

(maintain PaO2 > 90)• Persistent or worsening hypoxemia (PaO2 <

60) & resp. distress despite O2

ET tube + ICU• Early fracture stabilization • Appropriate fluid resuscitation to avoid shock

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COMPLEX REGIONAL PAIN SYNDROME (CRPS)

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CLINICAL FEATURES

• biphasic condition • early swelling and vasomotor instability • late contracture and joint stiffness

• hand and foot are most frequently involved• usually begins up to a month after the

precipitating trauma

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BONE CHANGES

• increased uptake on bone scanning in early CRPS • Later, the bone scan returns to normal • there are radiographic features of rapid bone loss• visible demineralization with patchy, subchondral or

subperiosteal osteoporosis• metaphyseal banding• profound bone loss

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INCIDENCE

• early features of CRPS show that they occur after 30% to 40% of every fracture and surgical trauma • severe, chronic CRPS associated with severe

contracture is uncommon with a reported prevalence of less than 2% in retrospective series

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CLINICAL DIAGNOSIS IN AN ORTHOPAEDIC SETTING

• 1 Pain• 2a Vasomotor instability• 2b Abnormal sweating• 3 Edema and swelling• 4 Loss of joint mobility and atrophy• 5 Bone changes

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INVESTIGATIONS

• CRPS is a clinical diagnosis and there is no single diagnostic test• Magnetic resonance imaging (MRI)• early bone and soft tissue edema with late atrophy and

fibrosis

• Computed tomography (CT) • bony compressing lesion

• Electromyographic and nerve conduction studies • normal in CRPS 1 but may demonstrate a nerve lesion in

CRPS 2

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MANAGEMENT

• Reassurance• excellent analgesia• intensive, careful physical therapy avoiding

exacerbation of pain

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Six-Pack Exercises

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• Analgesia• Nonsteroidal anti-inflammatory drugs may give better

pain relief than opiates• centrally acting analgesic such as amitriptyline is often

useful even at this early stage

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• Secondline treatment• centrally acting analgesic > amitriptyline, gabapentin, or

carbamazepine• regional anesthesia• Calcitonin• membrane-stabilizing drugs > mexilitene• sympathetic blockade and manipulation• desensitization of peripheral nerve receptors > capsaicin

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• Immobilization and splintage should generally be avoided • if used, joints must be placed in a safe position and

splintage is a temporary adjunct to mobilization

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• Pain desensitization• reminded that simple stroking cannot by definition be

painful • instructed to stroke the affected part repetitively while

looking at it and repeatedly saying “this does not hurt, it is merely a gentle touch.”

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• Surgery• rarely indicated• treat fixed contractures • delayed until the active phase of CRPS has completely

passed at least 1 year since

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THANK YOU