General complications of fractures presented by: Anas AL-Karasneh

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General complications of fractures
presented by
Anas AL-Karasneh
Medical ppt
http//hastaneciyiz.blogspot.com
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General complications

• Deep vein thrombosis and pulmonary embolism.
• 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
  and major orthopedic operation.
• Site leg, thigh and pelvic vein.
• Risk factors
• ? Knee and hip replacement
• ? Elderly
• ? Immobility
• ? Malignancy and CV disease
• ? Trauma ( fracture of spine , pelvis ,
  femur and tibia)
• ? hypercoagulable status

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Symptoms and signs

• 1. Pain and tenderness in calf or thigh usually
  unilateral
• 2. swelling
• 3.hotness
• 4. positive homans sign.
• 5. pulmonary embolism as primary presentation (
  dyspnea, hemoptysis , tachypnea and fever).

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DiagnosisDuplex ultrasonography , V-Q scan,
spiral CT and angiography. Prevention1.Elasti
c stockings.2.Elevation the foot.3.Early
mobilization.4.Low molecular weigh heparin
40mg\day .
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Tetanus

• Is wound infection caused by C.tetani .
• Tetanus toxin passes to anterior horn cells
• where it fixed and cant be neutralized so
• produces hyper excitability and reflex muscle
  spasm.
• Symptoms
• Tonic and clonic contractions of esp. jaw,
  face, around the wound itself ,neck ,trunk,
  finally spasm of the diaphragm and intercostal
  muscles leads to asphyxia and death.

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ProphylaxisDTP for general population
(pediatrics)gt10 years ? booster dose of
toxoid after all trivial skin wound Not
immunized and wounded ? ? wound toilet and
antibiotic ( consider antitoxin if contaminated
wound and give the toxoid immunization )
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Treatment1. IV antitoxin.2. IV antibiotics
(penicillin). 3. Muscle relaxant.4. Tracheal
intubation.5. Control respiration.
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Gas gangrene

• Cause
• It caused by clostridium (perfringens) and this
  organism survive and multiply only in tissue with
  low oxygen tension. Characterized by rapid and
  extensive necrosis of muscle accompanied by gas
  formation and systemic toxicity .
• Its associated with traumatic wounds that are
  deep, necrotic and without communication to the
  surface.

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Clinical features

• 1. sudden onset of pain localized to the infected
  area.
• 2. swelling , edema
• 3.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 debridement are the
  mainstay of treatment.
• 3. IV antibiotics
• 4.fluid replacement.
• 5. hyperbaric Oxygen

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Fat embolism

• Usually occurs in young adult after closed
  fractures of long bone .
• Characterized by occlusion of the small blood
  vessels by fat globules.
• Risk factors
• Closed fractures-
• Multiple fractures -
• - Pulmonary contusion
• - Long bone/pelvis/rib fractures

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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 lt60mmHg after
  major trauma is suspicious

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Treatment - Supportive treatment - O2
administrated.-Blood, fluid replacement - Iv
steroid heparin ( may reduce pulmonary edema
and IV clotting )-Surgical stabilization of
fracture
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shock

• A generalized state of decreased tissue
  perfusion.
• If prolonged it may lead to irreversible damage
  of the life supporting organs.
• causes
• Cardiogenicdirect injury to heart, the pump is
  not working properly ( massive MI).

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• II. Neurogenic injury to brain stem (vasomotor
  center) spinal cord ?loss of sympathetic tone ?
  increase venous capacitance ? low venous return ?
  low cardiac output ( but bradycardia )
• III.Hypovolaemic reduction of blood volume the
  most important one to be dealt with firstly

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Clinical features

• Thirst, rapid shallow breathing, the lips and
  skin are pale and the extremities feel cold,if
  the compansation fails.. impaired renal function
  test and decreased urinary output.

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treatment

• 1.IV morphine and oxygen to arrest bleeding and
  replace blood loss.
• 2.Early reduction and splinting of fracture.
• 3.Restoration of blood volume by rapid infusion
  of crystalloid solution.
• 4.Keep monitoring of vital signs.

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• If no quick respond, blood transfusion is
  mandatory ( we can use O blood group Rh (-) until
  cross matching is available

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CRUSH syndrome

• Serious medical condition characterized by major
  shock renal failure following a crushing injury
  to skeletal muscles or tourniquet left too long
• Its a re-perfusion injury seen after the release
  of crushing pressure, there will be release of
  muscular breakdown products(myoglobin,k,p) which
  have nephrotoxic effect on the kidney

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Alternative mechanism renal artery spasm ?
tubular necrosis
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• Clinically
• Shock
• Pulsless limb ? redness ? swelling
• Loss of muscle sensation and power
• Decrease renal secretion
• Uremia, acidosis

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CRUSH syndrome prognosis

• If renal secretion return within 1 week the
  patient survive
• But most of them die within 14 days

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CRUSH syndrome treatment

• Avoid the disaster by amputation above the site
  of compression and before compression release
• If compression is already released ? cool the
  limb and treat for shock and renal failure
  (dialysis)

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Medical ppt
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