Presentation on theme: "Fracture healing. Bone heals by the formation of normal bone bone has a fine fibroid structure nonunion when a bone heals by a fibroblastic response instead."— Presentation transcript:
Bone heals by the formation of normal bone bone has a fine fibroid structure nonunion when a bone heals by a fibroblastic response instead of by bone formation
for cortical and cancellous bone from the diaphysis, epiphysis, or metaphysis all have same microscopic structure Bone will, therefore, heal by the same mechanism wherever it breaks.
Fracture healing can be divided into primary and secondary healing In primary healing, the cortex attempts to reestablish itself without the formation of callus (osteonal or haversian healing) This occurs when the fracture is anatomically reduced, the blood supply is preserved, and the fracture is rigidly stabilized by internal fixation
Secondary fracture healing results in the formation of callus and involves the participation of the periosteum and external soft tissues This fracture healing response is enhanced by motion and is inhibited by rigid fixation
Fracture healing can be conveniently divided, based on the biologic events taking place, into the following four stages 1. Hematoma formation (inflammation) and angiogenesis. 2. Cartilage formation with subsequent calcification 3. Cartilage removal and bone formation 4. Bone remodeling
Hematoma Formation and Angiogenesis Initially, there is an inflammatory phase characterized by an accumulation of mesenchymal cells around the fracture site. The formed hematoma is a source of growth factors. Transforming growth factor beta (TGF-) and platelet derived-growth factor (PDGF) are released from platelets at the fracture site TGF- induces mesenchymal cells and osteoblasts to produce type II collagen and proteoglycans. PDGF recruits inflammatory cells at the fracture site.
Bone morphogenetic proteins (BMPs) are osteoinductive mediators inducing metaplasia of mesenchymal cells into osteoblasts. IL-1 (interleukin-1) and IL-6 recruit inflammatory cells to the fracture site.
mesenchymal cells ensheathe the fracture and differentiate into chondrocytes or osteoblasts. Low-oxygen tension, low pH, and movement favor the differentiation into chondrocytes; high-oxygen tension, high pH, and stability predispose to osteoblasts.
This initial callus acts as an internal splint against bending and rotational deformation and, less effectively, against shearing and axial deformation. Clinically, the fracture becomes "sticky," and although some motion is detectable, the fracture is stable.
Cartilage Formation with Subsequent Calcification Radiologic evidence of mineral formation signals the onset of this phase. Cartilage in callus is replaced by woven bone
Mineralization causes the chondrocytes themselves to degenerate and die Capillary buds then invade the mineralized cartilage, bringing osteoblasts, which resorb part of the calcified cartilage and deposit coarse fibroid bone on its residuum. The proliferating cambium layer of the periosteum also lays down new bone on the exposed surface of the bone, if conditions are favorable.
The phase of mineralized callus leads to a state in which the fracture site is enveloped in a polymorphous mass of mineralized tissues consisting of calcified cartilage, woven bone made from cartilage, and woven bone formed directly
3; Cartilage Removal and Bone Formation The woven-bone mineralized callus has to be replaced by lamellar bone arranged in osteonal systems to allow the bone to resume its normal function. Before this stage of remodeling can start, it is necessary to consolidate the fracture site.
The concept of consolidation is poorly defined but includes filling the gaps left by the previous phase between the ends of the bone; it is also called gap-healing bone.
This bone has three major characteristics: 1. It forms only under conditions of mechanical stability; 2. It has the ability to replace fibrous or muscle tissue; and 3. It forms within the confines of the bone defect Gap-healing bone is essentially coarse fibroid bone and, therefore, is not normal lamellar bone.
Remodeling This final phase involves the replacement of woven bone by lamellar bone in various shapes and arrangements and is necessary to restore the bone to optimal function. This process involves the simultaneous meticulously coordinated removal of bone from one site and deposition in another.
Two lines of cells, osteoclasts and osteoblasts, are responsible for this process. Osteoclasts are derived from monocytes and are large multinucleated cells that remove bone. They are located on the resorption surfaces of the bone. Osteoblasts are mononuclear and are responsible for the accretion of bone.
Complications General 1-Shock: Some fractures may be associated with signiﬁcant bleeding causing severe hypotension. Pelvic fractures, femoral fractures, fractures with vascular injury.
Asses for symtoms and signs of shock, pulse, BP, temperature of limbs etc. Mild, moderate and severe shock Stop external source of bleeding, immobilize fractures Internal bleed, Inititial replacement with colloids like Ringers lact Blood transfusions Irreversible shock
2-Fat embolism: Fat droplets from the fracture site act as emboli and may cause vascular occlusion in the lungs, brain and other parts of the body. Respiratory failure, cerebral dysfunction and petechiae are important clinical ﬁndings.
3-Deep vein thrombosis and pulmonary embolism: Immobility causes venous stasis and clot formation in the deep veins of the leg. If a clot becomes dislodged and embolizes into the pulmonary vasculature, it can lead to respiratory failure.
4-Septicaemia: Open fractures are associated with a signiﬁcantly high risk of local infection, which can spread through the blood stream and involve multiple organs.
Complications Local 1-Infection: This may occur as a result of the initial injury or surgery. The infection of the bone is called ‘osteomyelitis’. Chronic infection is difﬁcult to treat and may lead to long-term functional disability.
2-Nerve damage: Nerves may get stretched, contused or transected as a result of the fracture. A radial nerve palsy occurring after a fracture of the shaft of humerus is a common example.
3-Vascular injury: Ischaemia may occur due to vascular compression, intimal tear, stretching, kinking and transection. Pale, cold, pulselessness, paresthesia Surgical emergancy to restore circulation, repair or graft Ischemia time 6-8 hrs
4-Compartment syndrome: Signiﬁcant vascular comprise can give rise to a ‘compartment syndrome’. This condition is characterized by a signiﬁcant rise of pressure in the osteofascial compartment of the limb or body part. Pain on passive stretching of the muscles is the most common feature of this condition. Failure of urgent treatment (fasciotomy) may result in irreversible ischaemic damage to muscles, which subsequently undergo ﬁbrosis.
Volkmann’s ischaemic contractures after a supracondylar fracture of the humerus) may follow as a result of ﬁbrosis in muscles and joints.
5-Associated soft tissue injuries (e.g. ruptured ligaments or tendons): Delayed rupture of the Extensor Pollicis Longus tendon may occur after a Colles’ fracture.
6-Delayed union: In a delayed union a fracture takes longer to unite than expected. Possible causes of delayed fracture healing are severe soft tissue damage, inadequate blood supply, infection, insufﬁcient immobilization or excessive traction.
7-Malunion: Union of a fracture in a non-anatomical position is usually due to poor immobilization and loss of reduction can produce functional limitations.
8-Non-union A fracture may fail to unite as a result of infection, ischaemia, excessive fracture mobility, soft tissue interposition and many other factors. Painless abnormal mobility at the fracture site ( pseudo-joint ) is a common feature. Such fractures frequently require operative treatment with bone graft.
9-Avascular necrosis: A fracture may induce ischaemia and disintegration of the bone architechture. Joint function is signiﬁcantly affected and post traumatic osteoarthritis may occur. A common example is ‘avascular necrosis’ of the femoral head following an intracapsular fracture of the neck of femur.
10-Myositis ossiﬁcans: Benign heterotopic ossiﬁcation in the soft tissues may occur in association with some fractures near elbow. If severe may bridge across joint and markly restrict joint movements.
11-Joint stiffness: Joint stiffness is one of the most common complications of fracture treatment. Immobility, soft tissue injuries, surgery and intra-articular injury are important contributing factors.
12-Chronic regional pain syndrome (CRPS or Sudek’s dystrophy): This is a painful condition that usually affects the hands or feet. It is believed to be a sympathetic vasomotor phenomenon induced by an injury. Characteristic features are regional pain, swelling, temperature change, cyanosis or pallor and motor dysfunction. Treatment consists of analgesia, physiotherapy, sympathetic blockade and psychological support.
13-Post-traumatic arthritis: Articular damage and unequal weight shifting (malunion) resulting from injury may cause persistent joint symptoms such as pain, stiffness and instability.