1 - general complications of fractures - d3

8/2/2019 1 - General Complications of Fractures - D3

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General complications offractures

presented by:

Anas AL-Karasneh

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General complications

** Deep vein thrombosis and pulmonaryembolism.

**Tetanus.**Gas gangrene.** Fat embolism syndrome.

** hypovolemic Shock.crush syndrom .**

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Deep vein thrombosis and pulmonary embolism.

** DVT is very common complication after fracture andmajor orthopedic operation .

** Site : leg, thigh and pelvic vein.

**Risk factors: Knee and hip replacement

ElderlyImmobilityMalignancy and CV diseaseTrauma ( fracture of spine , pelvis , femur and

tibia)hypercoagulable status

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Symptoms and signs

1. Pain and tenderness in calf or thighusually unilateral

2. swelling3.hotness4. positive homan s sign.

5. pulmonary embolism as primarypresentation ( dyspnea, hemoptysis ,tachypnea and fever).

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Diagnosis:Duplex ultrasonography , V-Q scan,

spiral CT and angiography.

Prevention:

1.Elastic stockings. 2.Elevation the foot.

3.Early mobilization. 4.Low molecular weigh heparin 40mg\day .

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Tetanus.C.tetani** Is wound infection caused by

** Tetanus toxin passes to anterior horn cellswhere it fixed and cant be neutralized so

produces hyper excitability and reflex musclespasm.

Symptoms:**Tonic and clonic contractions of esp. jaw, face,

around the wound itself ,neck ,trunk, finallyspasm of the diaphragm and intercostal

muscles leads to asphyxia and death.

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:Prophylaxis:DTP for general population(pediatrics)

>10 years booster dose of toxoid afterall trivial skin wound Not immunized and wounded ? wound

toilet and antibiotic ( consider antitoxin ifcontaminated wound and give the toxoidimmunization )


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Treatment:1. IV antitoxin.2. IV antibiotics (penicillin).3. Muscle relaxant.

4. Tracheal intubation.5. Control respiration.


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Gas gangreneCause:It caused by clostridium (perfringens) andthis organism survive and multiply only intissue with low oxygen tension.Characterized by rapid and extensivenecrosis of muscle accompanied by gasformation and systemic toxicity .

Its associated with traumatic wounds thatare deep, necrotic and without

communication to the surface.www.icareunit.com


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Clinical features:1. sudden onset of pain localized to theinfected area.2. swelling , edema3.no pyrexia (cool)4.profuse serous discharge with sweetish

and mousy odor .5. Gas production

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Treatment:1. early diagnosis .2. surgical intervention and debridementare the mainstay of treatment.3. IV antibiotics4.fluid replacement.

5. hyperbaric Oxygen

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Fat embolismUsually occurs in young adult after closedfractures of long bone .Characterized by occlusion of the smallblood vessels by fat globules.Risk factors

Closed fractures-

Multiple fractures-- Pulmonary contusion

- Long bone/pelvis/rib fractureswww.icareunit.com


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Closed/openFracture

Fat in bonemarrow

escape

Formation offat globules in

vessels

Fat embolusStick in

pulmonarybed

Triggerclottingcascade


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Clinical feature:

- Sudden onset dyspnoea- Hypoxia

- tachypnea and tachycardia

- Confusion, coma, convulsions--Transient red-brown petechial rash affecting

upper body, especially axilla

*no defenitive test, but hypoxia


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Treatment :

- Supportive treatment- O2 administrated.-Blood, fluid replacement - Iv steroid + heparin ( mayreduce pulmonary edema and IV

clotting )-Surgical stabilization of fracture

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shock**A generalized state of decreased tissueperfusion.**If prolonged it may lead to irreversibledamage of the life supporting organs.causes:

Cardiogenic :direct injury to heart, thepump is not working properly ( massiveMI).

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II. Neurogenic : injury to brain stem(vasomotor center) spinal cord loss ofsympathetic tone increase venouscapacitance low venous return lowcardiac output ( but bradycardia )

III.Hypovolaemic : reduction of blood volumethe most important one to be dealt with firstly


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Low cardiacoutput Low B.P

Decreasedtissue

perfusion

Hypoxia andacidosisProgressivecell damageORGANFAILURE


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Clinical featuresThirst, rapid shallow breathing, the lipsand skin are pale and the extremitiesfeel cold,if the compansation fails..impaired renal function test anddecreased urinary output.

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treatment1.IV morphine and oxygen: to arrestbleeding and replace blood loss.

2.Early reduction and splinting offracture.3.Restoration of blood volume by rapidinfusion of crystalloid solution.4.Keep monitoring of vital signs.

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If no quick respond, blood transfusionis mandatory ( we can use O bloodgroup Rh (-) until cross matching isavailable

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CRUSH syndrome

Serious medical condition characterized by majorshock & renal failure following a crushing injury toskeletal muscles or tourniquet left too long

Its a re -perfusion injury seen after the releaseof crushing pressure, there will be release ofmuscular breakdown products(myoglobin,k+,p) whichhave nephrotoxic effect on the kidney


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When compressionreleased

Myohaematinrelease from cells

To kidneyBlock tubules

Alternative mechanism : renal artery spasm tubular necrosis


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Clinically:Shock

Pulsless limb redness swellingLoss of muscle sensation and powerDecrease renal secretionUremia, acidosis


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CRUSH syndrome :treatment

Avoid the disaster by amputationabove the site of compression andbefore compression release

If compression is already released cool the limb and treat for shock andrenal failure (dialysis)


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1 - general complications of fractures - d3

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