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Complication of traumatology theme lecture
This document discusses fracture complications from Dr. Utkarsh Shahi of King Faisal University. It begins by outlining immediate, early, and late complications of fractures both locally and systemically. Immediate complications include hemorrhage, vascular injury, and nerve injury. Early complications include infection, compartment syndrome, fat embolism syndrome, and delayed union. Late complications consist of non-union, malunion, avascular necrosis, and arthritis. The document then provides details on diagnosing and treating specific complications like hemorrhage, nerve injury, and compartment syndrome. It emphasizes the importance of early diagnosis and management to prevent long-term issues.
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Complication of traumatology theme lecture
- 1. COMPLICATIONS IN TRAUMATOLOGY DR.UTKARSH SHAHI ASSISTANT PROFESSOR IN ORTHOPEDICS DEPARTMENT OF SURGERY KING FAISAL UNIVERSITY AL AHSA, KSA
- 2. LEARNING QUESTIONS • Whatare the immediate complications of a fracture? Describe the diagnosis & treatment. • What are the early complications of a fracture? Describe the diagnosis & treatment. • What are the late complications of a fracture? Describe the diagnosis & treatment. • What are the advantages, disadvantages and complications of a fracture treatment using traction, plaster cast, external fixator, plate & screw osteosynthesis, cerclage & intramedullary pin fixation?
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- 4. IMMEDIATE COMPLICATIONS EARLYCOMPLICATIONS LATE COMPLICATIONS Systemic Hypovolemic shock (Haemorrhage) Systemic Hypovolemic shock ARDS (Adult respiratory distress syndrome) Fat embolism syndrome Deep vein thrombosis Pulmonary Embolism Crush syndrome DIC: Disseminated Intravascular Coagulation Aseptic traumatic fever Septicaemia (in open fracture ) Imperfect union of the fracture (Deformity) Delayed union Non union Mal union Cross union Aseptic Necrosis Shortening Others Joint stiffness Myositis ossificans Traumatic Chondromalacia Osteomyelitis Ischaemic contracture Osteoarthritis CRPS : Chronic Regional Pain Syndrome Local Injury to major vessels Injury to muscles and tendons Injury to joints Injury to viscera Local Compartment syndrome Infection
- 5. FRCATURE SHARP BONE ENDS CAUSING DAMAGETO BLOOD VESSELS HYPOVOLAEMIC SHOCK HAEMORRHAGE BLEEDING FROM BONES HYPOVOLAEMIC SHOCK HAEMORRHAGE
- 6. HEMORRHAGE: DIAGNOSIS Complete Blood Count Coagulation studies Urineand stool for blood Radiographic studies
- 7. HEMORRHAGE: INTERVENTIONS Direct pressure Surgicalintervention as indicated Use of autologous or synthetic clotting material Vitamin K or clotting replacement factors Volume replacement and blood transfusion as necessary Iron supplementation
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- 9. BLOOD VESSELS :VASCULAR INJURY Relatively uncommon event when associated with fractures. When it occurs, it is always an emergent situation. Injury to the artery is classically associated with several specific fractures involving such sites as : • Clavicle • Supracondylar region of the elbow (especially in children) • Femoral shaft • Around the knee
- 10. NERVE INJURY Typically, anerve is compressed, contused, or stretched. Classic examples include: • Radial nerve injury secondary to fractures of the distal humerus • Sciatic nerve injury following posterior fracture dislocations of hip
- 11. Neuropraxia. • Death ofthe axon does not occur. • The condition is generally caused by pressure or contusion and usually improves by itself in a few weeks. • The nerve is anatomically intact and physiologically nonfunctional. Axonotmesis. • Is an anatomic disruption of the axon in its sheath. • Improvement follows regeneration, the axon growing at a slow rate of 1 mm a day along the existing axonal sheath. Neurotmesis. • Is an anatomic disruption of the nerve itself. • Surgical repair is required if recovery is to be anticipated.
- 13. MUSCLE AND TENDONINJURY With any fracture or dislocation there is always some associated muscle damage. The extent of this damage and the results will vary depending on the site in consideration. Myositis ossificans is a specific complication of muscle damage in which heterotopic bone forms within the damaged muscle. The quadriceps and brachialis are specifically predisposed to develop this complication.
- 14. ADULT RESPIRATORY DISTRESSSYNDROME Also known as Shock lung or wet lung. Can follow slight fluid overload and is made worse if: • There is any damage to the lungs • Aspiration into the lung or over-transfusion. Oedema and electrolyte retention secondary to the trauma also contribute to it. Treatment is by oxygen and ventilation. Do not over-transfuse with crystalloids!
- 15. FAT EMBOLI SYNDROME(FES) Mechanical blockage of blood vessels by circulating fat particles Occurs following • Long bone fracture • Pelvic fracture • Total hip arthroplasty
- 16. FES: CLINICAL MANIFESTATIONS Signsand symptoms can appear 12- 72 hours post injury • Change in mental status • Increased respiratory distress • Petechial of skin & mucosa (appear above nipple line and blanch)
- 17. FES: DIAGNOSTICS No specificlabs Fat globules may be detected in blood, urine or sputum PO2 drops to < 50 mm HG Chest X Ray with diffuse “snowstorm” effect VQ scan to r/o PE
- 18. FES: INTERVENTIONS Early recognitionto prevent morbidity and mortality Minimize movement of long bone fractures Respiratory support • Intubation • Ventilator management • ICU monitoring
- 19. DEEP VEIN THROMBOSIS(DVT) AND PULMONARY EMBOLISM (PE) Formation of fibrin leads to development of a thrombus (fibrin clot) Clinical symptoms appear when thrombus is large enough to impede blood flow in a large vessel When venous thrombosis or part of a thrombus dislodges from its primary site, it becomes an embolus Embolus can enter pulmonary circulation and perfusion distal to the embolus can be partially or completely occluded
- 20. DVT: CLINICAL MANIFESTATIONS Unilateralswelling of thigh/lower leg Discomfort in leg Erythema Warmth Tenderness Palpable, tender venous cord in popliteal space
- 21. DVT: DIAGNOSTICS Contrast venography Dopplerultrasonography Magnetic Resonance Imaging (MRI) Radionuclide venography
- 22. PE: DIAGNOSTICS Arterial bloodgas (ABG) Chest x-ray (CXR) Electrocardiogram (EKG) Ventilation-perfusion scan (VQ scan) Pulmonary angiography CT scan
- 23. DVT & PE:PREVENTION External pneumatic compression Graduated compression stockings Early ambulation and range of motion Elevation of lower extremities
- 24. DVT & PE:PREVENTION Prophylactic inferior vena cava filter Anticoagulation • Heparin • LMWH (low molecular weight heparin) • Warfarin (Coumadin)
- 25. DVT & PE:PREVENTION Full dose anticoagulation with heparin/warfarin Oxygen therapy for PE Thrombolytic therapy • Urokinase • streptokinase Surgical embolectomy Inferior vena cava filter
- 26. CRUSH SYNDROME Also knownas traumatic rhabdomyolysis or Bywaters' syndrome It is characterized by major shock and renal failure after a crushing injury to skeletal muscle. It is compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body. Cases occur commonly in catastrophes such as earthquakes, to victims that have been trapped under fallen masonry. Treatment is complex & it should be started at the earliest to avoid irreversible damage
- 27. DISSEMINATED INTRAVASCULAR COAGULATION Alsoknown as Diffuse intravascular coagulation (DIC) Can follow any injury and is due to a disturbance of the clotting mechanism. Treatment is done with: • Fresh frozen plasma • Platelets • Heparin.
- 28. COMPARTMENT SYNDROME “A conditionin which the circulation and function of tissues within a closed space compromised by an increased pressure within that space” The muscles and nerves of the extremity are enclosed in fascial spaces or compartments and are therefore susceptible to this condition
- 29. COMPARTMENT SYNDROME RISK FACTORS External CompressionForce • Tight cast • Tight dressing • Prolonged compression • Crush injuries Internal Factors • Bleeding • Swelling/edema • Exertional Miscellaneous Factors • Acute trauma • Fracture • Infection • Skin traction • Tibial nailing • Exercise • Insensate extremity
- 30. COMPARTMENT SYNDROME: 5PS Pain on passive stretch Pallor Pulselessness Paresthesia Paralysis
- 31. PERIPHERAL VASCULAR ASSESSMENT Color •Pale • White • Pink • Dusky • Cyanotic • Mottled Edema • Pitting Temperature • Cold • Warm • Hot Capillary refill • normal < 3 seconds Peripheral pulses • Distal to injury • Bilateral • If non- palpable: doppler
- 32. PERIPHERAL NEUROLOGICALASSESSMENT Sensation Motor function Bothelements evaluate: • Upper extremity: Radial, Median & Ulnar Nerves • Lower extremity:Tibial, Peroneal, Femoral & Sciatic nerves
- 33. COMPARTMENT SYNDROME: DIAGNOSTICS Muscledamage indicated by: • Myoglobin in urine • Elevated CPK, LDH and SGOT Intracompartmental pressure monitor • Pressures of 30-45 mm HG a concern
- 34. INTRACOMPARTMENTAL PRESSURES (ICP) Paincan be unreliable especially in the trauma patient. It can range from being mild to severe, and in the unconscious patient important clinical symptoms and signs can be difficult to elicit. Techniques have been developed to measure ICPs. The normal tissue pressure within closed compartments is 0–10mmHg. This pressure markedly increases in compartment syndrome
- 35. COMPARTMENT SYNDROME PREVENTION Early recognitionis key to preventing or minimizing negative outcome Astute nursing intervention to identify pathologic pain in the presence of good pain control (epidural, PCA) The key to successful treatment of acute compartment syndrome is early diagnosis and decompression of the affected compartments
- 36. COMPARTMENT SYNDROME: INTERVENTIONS Relieve pressuresource • Remove constrictive dressing • Bivalve cast Initiate pain management Elevate extremity at heart level Ongoing neurovascular assessments Fasciotomy if indicated
- 38. WOUND/SSI CLINICAL MANIFESTATIONS Increased pain Feveror chills Foul smell from wound Edema Increased temperature around incision or wound Erythema around wound or incision Purulent exudate, poor wound healing Elevated WBC, ESR, C-reactive protein
- 39. WOUND/SSI: INTERVENTIONS Wound care Systemicantibiotics Adequate perfusion Adequate oxygenation Optimal nutritional intake
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- 41. NON-UNION • Delayed union non-union. • No progression of healing over serial radiographs • On x-ray : • Hypertrophic …due to excessive mobility • Atrophic…due to poor blood supply • Needs intervention.
- 43. NON-UNION TREATMENT • Conservative; •No symptoms no treatment or removable splint. • Symptomatic • Hypertrophic (functional Bracing) • EMG Stimulation • Pulsed US • Operative • Hypertrophic fixation • Atrophic excision , bone graft and fixation
- 44. MALUNION • Union inan unsatisfactory position: • Angulation • Rotation • Shortening • Causes: • Failure to reduce fracture adequately • Failure to hold reduction while healing • Gradual collapse of comminuted or osteoporotic bone
- 45. MALUNION • Clinical Features: •Deformity • Usually visible in X - ray • May be not apparent in some cases • On x-ray: • Check the position in the 1st 3 weeks
- 46. MALUNION TREATMENT • Canbe started before the fracture is fully united. • Adults reduce to the anatomical position • More than 10 to15 degrees may need; • Re-manipulation • Osteotomy • Internal fixation
- 47. MALUNION TREATMENT • Children •Angular deformity resolve without treatment • Rotational deformity needs intervention • In lower limb shortening ( 2cm or more ) : lengthening
- 48. AVASCULAR NECROSIS • Bonedeath due to interruption of blood supply • Certain regions more than others include: • Head of femur • Proximal part of scaphoid • Lunate • Body of talus • It is an early complication because of ischemia but radiological findings are seen later
- 50. COMPLEX REGIONAL PAINSYNDROME
- 51. COMPLEX REGIONAL PAINSYNDROME
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- 56. SUMMARY Introduction to postureand factors affecting it. Ideal versus Normal Posture. Fundamentals of postural defects. Growth Variation in lower limbs. Congenital Telipes Equinovarus. Developmental disorders of spine. Syndromes affecting posture: • Osteogenesis Imperfecta • Down’s Syndrome • Marfan’s Syndrome
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