Introduction to Fractures and Dislocations1

Fractures and dislocations are among the most common injuries seen in day-to-day practice. It is important to remember the following basic facts to understand these injuries.

Fracture can be defined as a break in continuity of a bone or the loss of normal anatomical continuity of a bone.

Note: Multiple fractures is the terminology used when many bones are fractured in an individual. This should not be confused with segmental or comminuted fracture (see above).

The deforming forces causing fractures can be classified based on impact as:

The fracture got its name because the bone breaks like a greenstick branch of a tree. Only a part (one side) of the bone breaks and rest of the bone bends. It is an incomplete break occurring in the bone and seen in children whose bones are more elastic, soft and pliable. There is no abnormal mobility.

It is seen in the vertebral column where in the height of the vertebral body decreases following fracture.

It is a fracture occurring in a bone with pre-existing pathology. The pathology softens the bone considerably and this soft bone yields to a very trivial trauma and fractures, e.g. malignancy, osteomyelitis, etc.

It is a type of pathological fracture due to unaccustomed stress getting concentrated on one part of the bone, e.g. March fracture seen in soldiers after a long route march.

Healing takes place in stages and over a period of time which is said to be a minimum of 4 weeks approximately. Four distinct stages are recognized (Fig. 1.13).

This is an important stage of fracture healing. As the bone fractures, the blood vessels are torn and hence bleeding occurs almost immediately. Hematoma acts as a vehicle delivering the required material for union and clearing unwanted material by a process of chemotaxis of cells. If this stage of hematoma is deficient as seen in cases of open fractures, healing is interfered with and fracture fails to unite.

Within 8 hours of fracture there is inflammation subsequently leading to subperiosteal and endosteal cellular proliferation. These cells surround the broken ends of the bone. At the same time, the clotted hematoma progressively gets absorbed and new capillaries start infiltrating these cellular masses.

The proliferating cells which are mainly osteogenic and chondrogenic start to get incorporated into the fibrogenic matrix under the influence of bone morphogenic proteins (BMP), the transforming growth factor beta (TGF-β) and fibroblast growth factor (FGF), thus forming primary woven bone. This bone is soft as it is not fully mineralized. This occurs during the 2nd and 3rd week.

Mineralization occurs and the primary woven bone is transformed into lamellar bone. This occurs between 3 and 6 weeks.

This stage is better not considered as one of the stages of fracture healing because remodeling takes place only after the fracture unites (heals) and takes months and years. Here, the body attempts to give the normal shape and strength to the fractured bone or in other words to restore its preinjured status. Remodeling is rapid in children and in growing bones, slow in adult bones and almost nil in osteoporotic bones.

Note: Healing of a fracture in a cancellous bone does not follow these stages. Cancellous bone heals by direct formation of osteoblastic new bone.

The treatment begins at the site of injury. The first step is to apply a splint to the injured part. After this a thorough general and systemic examination is performed to look for other injuries such as vascular visceral and neurological. Visceral injuries when present may be life-threatening, e.g. liver laceration, splenic rupture, hemopneumothorax, etc. Early repair of these structures is of paramount importance. In polytrauma, maintaining the airway, breathing and blood pressure (by treating of shock and hemorrhage) is essential. A skilled paramedical team should be available to transport a severely injured patient to a specialized center where definitive treatment is instituted. Delay can be detrimental.7

Management of open fracture is an emergency and has to be carried out precisely. Apart from imparting primary care for the open wound, it is important to maintain vital parameters and attend other associated injuries (when present).

As soon as the patient is stable and fit for surgical intervention definitive treatment is instituted. Aim of treatment is to convert a contaminated wound into a clean wound and an open fracture into a closed fracture as early as possible.

Following are the complications that can occur after a fracture.

When a fracture fails to show progressive signs of union at review, both clinically and radiologically, for a consecutive period of three months after the specified time expected for union, it can be defined as nonunion.8

A fracture is said to have gone in for delayed union when there is undue delay at union.

Note: Abnormal mobility is a sign to be elicited in nonunions and delayed unions. It can be elicited only in a case where implant has not been used or when implant used, has failed (loosening or breaking).

When a fracture unites in anatomical malalignment, it is known as malunion. Possible malalignments are angulation, rotation and over-riding. Single or uniplanar malalignment, is rare. Usually, there is combination of two or all the three malalignments.

Malalignment causes deformity. Angulation causes angular deformity, rotation causes rotational deformity and over-riding causes shortening.

Basically, fractures which do not unite and need a secondary procedure for achieving union are considered as the ones that have gone in for delayed union or nonunion. They show both clinical and radiological features of the same.

Bone grafting

Source of cancellous graft: Iliac crest, excised ribs, excised head and neck of femur.

Source of cortical graft: Upper 2/3rd of the fibula, anteromedial tibia.11

Corrective osteotomy: In this procedure, the site of malunion is osteotomized surgically and the deformity is corrected accordingly. The alignment thus obtained, is maintained by internal fixation devices and appropriate external immobilization (very rarely by external cast alone). Immobilization is continued till healing takes place.

Osteoclasis: This is a closed procedure wherein the malunited bone is broken manually, reduced, aligned and immobilized in an appropriate cast. This procedure is indicated in early cases of malunion in children whe re the soft bridging callus has just formed. Osteocla sis should never be attempted after consolidation of callus.

Synonyms are Sudeck's osteodystrophy, r eflex s ympathetic d ystrophy, c omplex r egional p ain s yndrome, c ausalgia, s houlder hand s yndrome.

Pathogenesis is thought to be due to:

Diagnosis is made by clinical signs, X-ray (shows demineralization) and nuclear bone scan (shows increased uptake).

Treatment aims at reducing sympathetic overactivity.

Interventional therapy as follows:

Hemorrhagic shock: This is the most common complication of a severe injury. Inadequate oxygenation of tissues leads to a chain of events resulting in multiorgan failure and death.

Measures to be adopted include:

Neurogenic shock: This type of shock is commonly seen in spinal cord injury. The disturbance in sympathetic innervation causes decrease in the heart rate, dilatation of peripheral vessels and as a result fall in blood pressure. Monitoring the central venous pressure and infusion of plasma expanders help in the management of this difficult problem.

Cardiogenic shock: In a trauma setting, this type of shock commonly results from chest injuries, e.g. tension pneumothorax impeding venous return, myocardial contusion, etc. should be managed promptly depending on the underlying cause.

Septic shock: This type of shock is seen as a result of septicemia and usually occurs several days after the open injury as a result of septicemia.

In long bone fractures, there is always dissemination of fat globules from the marrow into the bloodstream. This can also happen from a spongy bone. At times, these fat globules block the capillaries of the pulmonary and the cerebral vessels causing fat embolism syndrome. The syndrome is more common in a young patient with multiple fractures.

First described by a British physician Eric Bywaters in the year 1914. It is a traumatic rhabdomyolysis occurring because of crushing. Also known as reperfusion injury, it occurs in those whose limbs are compressed for a long-time, e.g. limb trapped in a vehicular collision or buried in a land slide, etc. Such a limb is deprived of blood flow for quite a long period and the tissues release toxic metabolites because of cell death. When the compression is released and reperfusion occurs, myoglobin from the dead muscle and the toxic metabolites enter the bloodstream.

Management: Large amount of fluid infusion to dissolve the metabolites and simultaneous forced diuresis with the help of diuretics is the treatment of choice till myoglobinuria becomes negligible. Crushed tissues should be radically debrided and a tight compartment when present should be adequately decompressed. Dialysis may be necessary when renal failure is observed.

Pulmonary embolism commonly occurs in those patients who are confined to bed for a prolonged period after fracture. Elderly high-risk patients who present with major fractures are more prone to develop pulmonary embolism. Prevention by heparinization of blood with the help of low molecular weight heparin is the best measure employed in such patients.

Regenerative medicine is an evolving branch which tries to restore the normalcy from a diseased state, by analyzing the cellular and molecular responses. Thus, if fracture healing is analyzed, it is found that the healing process begins with inflammation. A series of events following inflammation, deliver to the site of fracture several chemical mediators, cells and growth factors (TGF), etc. This in turn initiates a chain of reactions which results in fracture healing (Flow chart 1.2).

When the two articular surfaces are totally out of contact, it is known as dislocation.

Note: In a dislocation, the part which loses contact with the rest of the body is considered as minor segment. The position which this part, i.e. the minor segment occupies in relation to the major segment classifies the dislocation as anterior, posterior, medial, lateral and central.

For a traumatic dislocation to occur, the force should be of a considerable magnitude.

Clinical diagnosis is simple because of the classical attitude and signs. Total loss of joint movement is characteristic and any attempted movement results in severe pain.

Any dislocated joint has to be reduced under anesthesia as early as possible. Delay poses difficulty in reduction. This is because of re-organization of muscles and soft tissue structures around the joint. Irreducibility under anesthesia with adequate muscle relaxation, indicates entanglement of the dislocated part in the surrounding tissues such as joint capsule, muscles and tendons and rarely vessels and nerves.

Pathological dislocation is a type of dislocation where the dislocation is the result of a pre-existing pathology. In this, it is important to ascertain whether the primary pathology that was responsible for dislocation, is still active. If it is active and persistent, e.g. persistent infection in a pathological dislocation due to infective arthritis, control of infection is achieved first before the dislocation is treated. The secondary changes that have occurred as a result of primary insult are treated by means of reconstructive procedures. These reconstructive procedures vary with respect to joint and age. They are categorized as joint replacement procedures, osteotomies and arthrodesis.

In this, the dislocation occurs due to muscle imbalance secondary to muscle paralysis. Whenever possible, the paralyzed muscles are substituted with normal muscles by carrying out procedures such as muscle and tendon transfers. When not possible, e.g. in cases of long standing paralytic dislocation, procedures like osteotomy and arthrodesis are considered.