1. General complications of fractures presented by: Anas AL-Karasneh
Medical ppt

2. General complications
** Deep vein thrombosis and pulmonary embolism.
**Tetanus.
**Gas gangrene.
** Fat embolism syndrome.
** hypovolemic Shock.
crush syndrom.**

3. 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

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

5. 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 .

6. Tetanus ** Is wound infection caused by C.tetani .
** Tetanus toxin passes to anterior horn cells
where it fixed and can’t 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.

7. :Prophylaxis :…DTP for general population (pediatrics) …>10 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 )

8. Treatment: 1. IV antitoxin. 2. IV antibiotics (penicillin). 3
Treatment: 1. IV antitoxin. 2. IV antibiotics (penicillin). 3. Muscle relaxant. 4. Tracheal intubation. 5. Control respiration.

9. 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.

10. 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

11. Treatment: 1. early diagnosis .
2. surgical intervention and debridement are the mainstay of treatment.
3. IV antibiotics
4.fluid replacement.
5. hyperbaric Oxygen

12. 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

13. Fat in bone marrow escape Trigger clotting cascade
Closed/open Fracture
Fat in bone marrow escape
Formation of fat globules in vessels
Fat embolus
Stick in pulmonary bed
Trigger clotting cascade

14. 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 <60mmHg after major trauma is suspicious

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

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

17. 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

18. Decreased tissue perfusion Progressive cell damage
Low cardiac output
Low B.P
Decreased tissue perfusion
Hypoxia and acidosis
Progressive cell damage
ORGAN FAILURE

19. 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.

20. 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.

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

22. CRUSH syndrome
Serious medical condition characterized by major shock & renal failure following a crushing injury to skeletal muscles or tourniquet left too long…
It’s 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…

23. When compression released Myohaematin release from cells
To kidney
Block tubules
Alternative mechanism : renal artery spasm  tubular necrosis

24. Clinically: Shock Pulsless limb  redness  swelling
Loss of muscle sensation and power
Decrease renal secretion
Uremia, acidosis

25. CRUSH syndrome: prognosis
If renal secretion return within 1 week the patient survive
But most of them die within 14 days

26. 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)

27. Medical ppt