Essentials of Orthopedics RM Shenoy
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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.
  1. A force of considerable magnitude is necessary to cause these injuries (Unless the bone is already weak or the structure of a joint is already disturbed due to disease).
  2. The resultant failure pattern (deformation) is directly proportional to the nature, magnitude and direction of the force.
  3. It is possible to classify these failure patterns with certain limitations.
  4. The treatment protocol is based on the nature of the failure pattern and follows a definite path which is consistent, with minor variations.
  5. Healing is indirectly proportional to the severity of the injury.
  6. Complications that develop with these injuries are related to the severity of the deforming force, the resultant failure pattern and the site and multiplicity of the injury.
  7. Though the terms ‘Fracture and Dislocation’ refer to the bone and joint pathology, one should always remember that in a skeletal injury, there is considerable damage to the soft tissue envelope that surrounds the bones and the 2joints. Namely the periosteum and the muscles. This soft tissue injury has an inverse relation to the normal healing process.
 
Fractures
 
Definition
Fracture is a break in continuity of a bone or loss of normal anatomical continuity of a bone.
 
Types of Fracture
  1. Depending on basic nature
    1. Closed or simple.
    2. Open or compound (Figs 1.1A to F).
  2. Depending on the displacements
    1. Displaced fracture
    2. Undisplaced fracture.
      • Incomplete fracture
      • Complete fracture.
  3. Depending on the nature of the fracture line (Figs 1.2 to 1.8)
    1. Transverse fracture.
    2. Oblique fracture.
      • Long oblique
      • Short oblique
    3. Spiral fracture.
      • Long spiral
      • Short spiral
    4. Comminuted fracture: In this type, there are more than two fragments at one fracture site.
    5. Segmental fracture: In a single bone, fracture occurs at two different levels.
    6. Intra-articular fracture: A fracture that involves (extends into) the articular surface of a joint.
    7. Avulsion fracture: This is a fracture occurring due to a pull by a muscle, tendon or a ligament at its insertion to the bone, e.g. mallet finger, fracture of the olecrenon process of the ulna.
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      Figure 1.1: Classification of open fractures—based on the classification by Gustilo and Anderson Criteria for classification: Extent of injury to skin, soft tissue, bone, vessels and the degree of contamination.
      Type I: Wound smaller than 1 cm in diameter, no skin crushing with no or little contamination. Fracture pattern is not complex
      Type II: A lacerated wound larger than 1 cm but without significant soft tissue crushing, no degloving, or contusion with moderate contamination.
      Fracture pattern may or may not be complex.
      Type III: An open injury with extensive soft tissue crushing and contamination, fracture pattern is single or complex. Injury is further subdivided into three types:
      1. Adequate soft tissue coverage of the fracture can be acquired at closure.
      2. Periosteal stripping is seen. Inadequate soft tissue coverage at closure. Hence, soft tissue reconstruction is necessary.
      3. Open fracture that is associated with vascular injury (or nerve injury or both) and that needs repair.
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      Figure 1.2: Radiograph showing fracture of radius and ulna. Note the transverse nature of the fracture line.
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      Figure 1.3: Radiograph showing a short oblique fracture at the neck of the 5th metacarpal bone of the left hand.
    8. Multiple fractures: Many bones are fractured in the same individual.
 
Deforming Forces
The deforming forces causing fractures can be classified as:
  1. Direct
  2. Indirect
Direct impact causes severe injuries, e.g. open fractures, comminuted fractures, etc.
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Figure 1.4: Radiograph showing a short spiral fracture of the tibia and the fibula, in the lower third.
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Figures 1.5A and B: Radiograph showing fracture of upper and lower humerus respectively and comminution at the fracture site with many fragments of bone which are displaced.
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Figure 1.6: Radiograph of an open segmental fracture of tibia and fabula with secondary infection and changes of chronic osteomyelitis. Bone resorption is seen at the fracture site. Both the fracture sites are showing features of nonunion.
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Figure 1.7: Radiograph showing fracture of the head of the femur. This is a very rare injury and generally associated with a dislocation of the hip. In this case, there was posterior dislocation which was reduced. The reduction achieved is obviously not congruous.
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Figure 1.8: Radiograph of an avulsion fracture of the base of distal phalanx. The resultant deformity is a ‘Mallet finger’. The patient is a goal keeper and the injury happened during a soccer match when he blocked a goal kick. Avulsion force is exerted by the lateral slips of the extensor expansion.
Indirect impact causes less severe injuries and is classified as follows:
  1. A bending force—produces a transverse fracture.
  2. A torsional force—produces a spiral fracture.
  3. A combination of both bending and torsional force—produces a comminuted fracture with a butterfly fragment/fragments.
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Figure 1.9: Radiograph showing greenstick fracture of both, the radius and the ulna. Note the gross deformity.
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Figure 1.10: Radiograph showing a compression fracture of L2 vertebra. Note the decrease in anterior height of the vertebral body.
 
Specific Types of Fractures
 
Greenstick Fracture (Fig. 1.9)
It is called so 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.
 
Compression Fracture (Fig. 1.10)
It is seen in the vertebral column wherein the height of the vertebral body decreases following fracture.
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Figure 1.11: Radiograph showing a Giant cell tumor arising from the upper end of tibia with multiple pathological fractures due to thinning of the cortex. Pathological fracture is a late feature of a Giant cell tumor
 
Pathological Fracture (Fig. 1.11)
It is a fracture occurring as a result of 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.
 
Stress Fracture (Fig. 1.12)
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.
 
Signs and Symptoms of a Fracture
  1. Pain and Swelling
  2. Deformity.
  3. Loss of continuity.
  4. Irregularity.
  5. Crepitus.
  6. Bony tenderness.
  7. Loss of function.
  8. Abnormal mobility.
(Abnormal mobility is a sign to be observed and not a sign to be elicited in a fresh fracture. It is very painful because the movement is taking place at the fracture site. It is the sure sign of a fracture and further examination to ascertain the fracture is unnecessary.)
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Figure 1.12: Radiograph showing ‘March fracture’ at the neck of 2nd metatarsal. Note the healing response by formation of abundant callus.
 
Healing of a Fracture
Healing takes place in stages and over a period of time (approximately 4 weeks minimum). Four distinct stages are recognized (Fig. 1.13).
 
1st Stage: Stage of Hematoma Formation
This is an important stage of fracture healing. During the process of fracture the blood vessels are torn and hence bleeding occurs almost immediately. Hematoma acts as a vehicle delivering required material for union and clearing the 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.
(Hence open fractures are to be converted into closed fractures as early as possible to promote healing. Many a times this is not possible and nonunion is accepted and treated accordingly at a later date.)
 
2nd Stage: Stage of Cellular Proliferation
Within 8 hours of the fracture there is inflammation resulting in 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.
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Figure 1.13: Stages of healing of fracture
 
3rd Stage: Stage of Primary Woven Bone Formation (Soft Callus)
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), 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 is supposed to occur during 2nd and 3rd week.
 
4th Stage: Stage of Lamellar Bone Formation (Hard Callus)
Mineralization occurs and this primary woven bone is transformed into lamellar bone. This is supposed to occur between 3 and 6 weeks
This is hard bone and is seen as a bridge or a cuff across the fracture site. It indicates early stage of fracture union.
 
Stage of Remodeling
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 and 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.
 
Factors Influencing Healing
  1. Factors not (at all) in control of the treating doctor
    • Nature of the trauma
      • High velocity trauma.
      • Low velocity trauma.
    • Nature of the fracture.
    • Vascularity of the bone.
    • Age of the patient.
  2. Factors in control (some control) of the treating doctor.
    • Proper reduction.
    • Adequate fixation.
    • Adequate immobilization.
    • Prevention of distraction.
    • Prevention of infection.
    • Maintaining adequate nutrition.
    • Adequate management of other comorbid conditions.
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Management of a Fracture
The treatment begins at the site of injury. The first step is to apply a splint to the injured part and look for other associated injuries. Namely, the vascular, the visceral and the neurological, by doing a thorough general and systemic examination. 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, the breathing and the blood pressure and treatment of shock and hemorrhage is essential. A skilled paramedical team should be available to transport a severely injured patient to the specialized center where definitive treatment is instituted. Delay is detrimental.
 
Basic Methods of Treating a Fracture
  1. Immobilization in a cast.
  2. Closed reduction and immobilization in a cast.
  3. Open reduction and internal fixation.
  4. Closed reduction and internal fixation (with the help of C-Arm imaging).
  5. External fixation.
  6. Tractions.
All the above methods are practised and can be employed to treat a fracture depending on the indication. All these methods help to enhance the biological process of healing by maintaining the anatomical alignment and providing the necessary stability at the fracture site. Every method has its own merits and demerits and to be chosen carefully. Aim of fracture treatment is to minimize the confinement to bed, achieve union at the earliest and make the patient to regain his activity as early as possible.
 
Complications
Following are the complications that can occur after a fracture.
  1. Specific and local complications
    1. Nonunion.
    2. Delayed union.
    3. Malunion.
    4. Sudecks atrophy.
    5. Associated nerve injuries.
    6. Associated vascular injuries (Fig.1.14).
    7. Associated visceral injuries.
    8. Infection leading to osteomyelitis and pyogenic arthritis.
      (as a consequence of open fracture or surgical sepsis.)
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      Figure 1.14: A femoral artery arteriogram showing injury to the femoral artery secondary to a badly displaced fracture of the lower third of the shaft of the femur (Vascular injury in a fracture is an emergency. Hemorrhage, shock and compartment syndrome is common. It has to be treated immediately to save the limb and the life of an individual)
  2. Systemic and general complications.
    1. Shock and hemorrhage.
    2. Fat embolism.
    3. Crush syndrome.
    4. Pulmonary embolism.
A. Specific Complications
 
Nonunion
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 is known as nonunion.
Clinically, it is diagnosed by painless abnormal mobility. Radiologically, it shows rounding of the ends of the bones, sclerosis of the margins and poor callus. The fracture site is not viable and the biological response at union has ceased.
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Figure 1.15: Radiograph showing lateral view of wrist and hand showing malunited Colles’ fracture with a classical ‘Dinner fork’ deformity.
 
Delayed Union
A fracture is said to have gone in for delayed union when there is undue delay at union.
This is so because the attempt at union for some reason does not proceed towards complete union or the attempt at union is not strong enough or adequate enough to progress towards complete union.
Clinically, it is diagnosed by painful abnormal mobility. Radiologically, it shows callus but callus formation is not adequate enough to bridge the fracture site and cause complete union. The fracture site is viable and there exists a biological response at the fracture site (but inadequate).
Abnormal mobility is a sign to be elicited in nonunions and delayed unions.
 
Malunion (Figs 1.15 and 1.16)
When a fracture unites in anatomical malalignment it is known as malunion. These malalignments are angulation, rotation and over-riding. Single or malalignment in one plane is rare. Usually, there is combination of two or all the three malalignments. Angulation causes angular deformity, rotation causes rotational malalignment and over-riding causes shortening.
Clinically, it is diagnosed by the presence of deformity with no abnormal mobility. Radiologically, it shows deformity and malalignment with adequate bridging callus.
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Figure 1.16: Radiograph showing malunion of a comminuted intertrochanteric fracture.
Note the neck shaft angle. It is reduced. Hence, there is Coxa vara deformity at the hip.
(Left alone most of the intertrochanteric fractures unite in coxa vara. This happens because of the cancellous nature of the bone that is present at the fracture site).
 
Classification of Delayed and Nonunions
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 or nonunion. They show both clinical and radiological features of the same.
Depending on Strontium 85 uptake at the ends of the fracture site the vascularity (viability) is assessed and classified as hypervascular (hypertrophic) and avascular (atrophic). (Based on Description by Weber BG and Cech, O Pseudarthrosis, Berne Switzerland 1976, Hans Huber Medical Publisher)
Hypervascular nonunions (true delayed unions) (Fig.1.17A)
  1. Elephant foot type: Presents with exuberant expansile callus and the picture resembles the foot of an elephant. It is the result of movement occurring at the fracture site before union has occurred, e.g. premature weight-bearing.
  2. Horse hoof type: Presents with little callus and picture resembles a horse hoof. Perhaps, this is the result of instability at the fracture site following inadequate reduction or fixation.
  3. Oligotrophic type: These are hypervascular but are not hypertrophic and do not show callus.
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Figure 1.17: (A) Hypervascular type (B) Avascular type
(Ref: Based on description by Weber BG and Cech O; Pseudarthrosis, Berne Switzerland 1976, Hans Huber Medical Publisher).
They are considered to be the result of major displacement/distraction persisting after treatment.
Avascular nonunions (true nonunions) (Fig.1.17B)
  1. Torsion wedge type: Seen when there is an intermediate fragment with poor blood supply. It unites on one side but does not unite on the other.
  2. Comminuted type: Is the result of many intermediate fragments with poor blood supply.
  3. Defect type: Seen when there is bone loss.
  4. Atrophic type: Seen when intermediate fragments are small and are missing. The defect is replaced by scar tissue.
(See the X-ray pictures in the Figs 1.18A to G in the next page).
 
Treatment of Delayed and Nonunions
Standard methods: Cancellous bone grafting is the procedure of choice to achieve union. Cancellous bone grafting is done only after confirming good apposition of the ends of bone without any soft tissue interposition. Freshening the edges of the fractured bone is a must. Cortical grafting is done in cases of defect non unions to bridge the defect, prior to the placement of cancellous graft.
(In delayed union with exuberant callus and when the cause is certain that it is the movement taking place at the fracture site which is preventing union, rigid fixation and immobilization alone may result in union).
To conclude the role of cortical graft is to bridge the defect. The role of cancellous graft is to induce osteogenesis. Hence, when the need is osteogenesis only, cancellous bone grafting is the procedure of choice. When the need is to bridge the defect as well as to induce osteogenesis both cortical and cancellous bone grafting (corticocancellous grafting) procedure is to be chosen.
The procedure needs immobility at the site for the incorporation of the graft and the union to take place. Thus internal fixation/external immobilization is necessary.
 
Sources of bone graft
  1. Allo/Homograft from the same species, e.g. bank bone, maternal fibula.
  2. Auto/Isograft from the same individual.
Source of cancellous graft: Iliac crest, excised ribs, excised head and neck of femur.
Source of cortical graft: Upper 2/3 of the fibula, anteromedial tibia.
 
Specialized Methods for the Treatment of Delayed Unions and Nonunions
  1. Distraction/compression osteogenesis based on the principle of Illizarov; It is proved by Illizarov that controlled progressive distraction and/or compression leads to tissue regeneration. This principle is of immense use when the skin condition does not permit open bone grafting procedures (Figs 1.19A and B).
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    Figures 1.18A to G: Radiographs showing the different types of pseudarthrosis based on the description by Weber BG and Cech O. Figure 1.18G shows a bone distraction (transportation) procedure in an attempt to salvage the limb, being carried out in a combined, both defective and atrophic nonunion, employing Illizarov methodology.
  2. Bone marrow grafting procedure; in this the bone marrow is aspirated and injected into the site of nonunion/delayed union. The sample may be injected de novo before clotting or may be injected in a concentrated form with anticoagulants after centrifuging and obtaining the concentrate under aseptic precautions (Figs 1.20A and B).
 
Treatment of Malunions
Malunions are treated by the help of a surgical procedure known as 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 with only external cast). Immobilization is continued till healing takes place.
Osteoclasis: This is a closed procedure wherein the malunited bone is broken manually, reduced and aligned and immobilized in appropriate cast. This procedure is indicated in early cases of malunion and in children when the bridging callus has just formed and the callus formed is soft. Osteoclasis should never be attempted after consolidation of callus.
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Figures 1.19A and B: (A) Nonunion of fracture shaft femur associated with shortening of the limb, (B) Procedure of compression/ distraction osteogenesis
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Figures 1.20A and B: Radiographs showing union in a 12 weeks old ununited type III open fracture tibia fibula after 2 injections of de novo bone marrow grafting at 6 weekly intervals
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Figures 1.21A and B: Radiograph showing a normally united Colles’ fracture with Sudeck's Osteodystrophy. Note the severe nature of demineralization and rarefaction in the cancellous areas of the bones of the forearm wrist and the hand.
 
Sudeck's Atrophy (Figs 1.21A and B)
Synonyms are Reflex Sympathetic Dystrophy, Complex Regional Pain Syndrome, Causalgia, Shoulder hand Syndrome.
It is a chronic condition characterized by pain and stiffness in the extremity as a result of dysfunction of central or peripheral nervous system.
Pathogenesis is thought to be due to
  1. Activation of pain pathways by the release of catecholamines, e.g. norepinephrine following injury.
  2. Exaggerated inflammation and immune response following injury.
Signs and symptoms
  1. Burning pain.
  2. Skin temperature changes (warm initially, cold later).
  3. Skin color and texture changes.
  4. Alteration in nail and hair growth.
  5. Swelling and stiffness of joints.
  6. Impairment of function of extremity.
Diagnosis
Diagnosis is made by clinical signs, X-ray (shows demineralization) and nuclear bone scan (shows increased uptake).
Treatment
Treatment aims at reducing sympathetic overactivity.
Drug therapy is given using following drugs as per need:
  • Opiates.
  • Anti-inflammatory analgesics.
  • Antidepressants.
  • Antiepileptics.
  • Calcitonin.
  • Corticosteroids.
Interventional therapy as follows
  • Physical and exercise therapy.
  • Psychotherapy to relieve anxiety and depression.
  • Sympathetic nerve block.
  • Spinal cord stimulation.
  • Intrathecal drug pump.
B. Systemic and General Complications
 
Shock and Hemorrhage
Hemorrhagic shock: This is the most common complication of a severe injury. Inadequate oxygenation of tissues leads to a chain of events resulting in hypotension, multi organ failure and death.
Measures to be adopted include
  1. Adequate oxygenation of tissues by maintaining the airway and administration of oxygen (important and to be employed in all types of shock).
  2. Immediate stoppage of bleeding.
  3. Treatment of lost volume by infusing Saline/Ringer lactate and Blood.
Diagnosis of hemorrhagic shock is made by cold and clammy feeling of the body, hypotension (initially diastolic and later both systolic as well as diastolic). Tachycardia, tachypnea and poor urine output. Loss of more than 40% of the blood volume will pose grave danger to life.
Neurogenic shock: This type of shock is commonly seen in spinal cord injury. The disturbance in sympathetic innervation 13causes 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: This type of shock is the result of 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.
It is characterized by increased warmth of the body, tachycardia, hypotension (little fall in systolic but marked fall in diastolic pressure) tachypnoea. Multiorgan failure is common. Septicemia with gram-negative organism may not increase the body warmth.
Aggressive antibiotic therapy along with all other supportive measures is essential for the recovery.
 
Fat Embolism
In a long bone fractures always, there is 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 the fat embolism syndrome. The syndrome is more common in a young patient with multiple fractures.
Diagnosis of the fat embolism is difficult. But the following features developing after a fracture should arouse the suspicion.
  1. Confusion and restlessness.
  2. Increased body temperature and tachycardia in a patient who is otherwise normal and not in a state of shock.
  3. Breathlessness.
  4. Petechiae over the chest, back, axilla, the conjunctival folds and the retina.
In severe cases of pulmonary embolism, there can be blood tinged frothy secretion which is coughed out by the patient or in case of cerebral embolism patient may become comatose. There is no definite treatment for fat embolism except supportive measures of giving high concentration of oxygen and maintaining capillary perfusion. Low molecular weight dextran may help in maintaining capillary perfusion. If the oxygen saturation falls severely, intubation and ventilation is the treatment of choice. If there is blood loss and hemoglobin is low, blood tansfusion is to be given. Good quality blood is essential for maintaining the oxygen saturation.
 
Crush Syndrome
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-time 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 are released into the bloodstream.
The flow of oxygenated blood through the damaged area causes formation reactive oxygen metabolites resulting in further damage to the tissues. The resultant hyperkalemia, hypocalcemia and metabolic acidosis may cause cardiac arrest. Renal failure may occur when myoglobinuria is severe and blocks the renal tubules.
Management: Large amount of fluid infusion to dissolve the metabolites and simultaneous forced diuresis with 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
Pulmonary embolism commonly occurs in those patients who are confined to bed for a prolonged period after the fracture and in those elderly high-risk patients who present with major fractures. Heparinization of blood with the help of low molecular weight heparin and prevention is the treatment of choice.
 
Recent Concept of Fracture Healing
Regenerative Medicine
Regenerative medicine is an evolving branch which tries to restore the normalcy from a diseased state, by going deep into the cellular and molecular response. Thus if fracture healing is analysed, it is found that the healing process begins with inflammation. As a result of this a series of events follow, bringing to the site of fracture an outflow of chemical mediators, cells and growth factors (TGF, etc). This in turn initiates a chain of reactions resulting in fracture healing (Flow chart 1.1).
Thus, after understanding the exact process of healing, these days, methods which are different from conventional ones have evolved.
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Flow chart 1.1: Schematic representation of a chain of events occurring at the cellular level which is responsible for the healing of the fracture.
Bone marrow grafting, Stem cell injection alone or insertion of a Scaffold mixed with Stem cells are some of the methods currently practiced. In the years to come this concept is going to revolutionize the treatment of fractures and nonunions.
 
Dislocations
 
Definition of Dislocation and Subluxation
When the two articular surfaces are totally out of contact it is known as dislocation.
(Total loss of contact between the two articular surfaces)
When the two articular surfaces are partly in contact and partly out of contact it is known as subluxation. Subluxation is also known as partial dislocation.
(Partial loss of contact between the two aritcular surfaces).
 
Types of Dislocation (Figs 1.22A to D)
  1. Traumatic.
  2. Pathological, e.g. pyogenic arthritis
  3. Paralytic, e.g. poliomyelitis
  4. Congenital, e.g. DDH
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. minor segment occupies in relation to the major segment gives the name for the dislocation as anterior, posterior, medial, lateral, central, etc.
When there is a fracture involving the articular surface of a joint along with dislocation or a fracture of the adjoining part of the bone along with dislocation the term fracture dislocation is used to describe the injury (Figs 1.23A and B).
 
Diagnosis
Clinical diagnosis is simple because of the classical attitude and the signs. Total loss of joint movement is characteristic and any attempted movement results in severe pain.
 
Treatment
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, e.g. joint capsule, muscles and tendons and rarely vessels and nerves.
Following successful reduction, immobilization for a minimum period of three weeks is essential. This is necessary for healing of the damaged soft tissues.
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Figures 1.22A to D: Radiographs showing different types of dislocations. (A) Traumatic Anterior dislocation of the Hip. (B) Pathological dislocation secondary to Tuberculosis of the Hip joint. (C) Paralytic dislocation secondary to Postpolio Residual Paralysis. Note a recent fracture in a thin femur. (D) Neglected Developmental Dysplasia of the Hip.
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Figures 1.23A and B: Radiograph, AP view of the hip joint showing (A) Fracture of the Acetabulum with posterior subluxation of the hip joint. (B) Comminuted Intertrochanteric fracture with posterior dislocation of the hip joint. Both are fracture dislocations.
Poor healing of damaged soft tissues increases the chance of recurrent dislocation and subluxation.
 
Complications of Dislocation
  1. Injury to the neighboring nerves and vessels, e.g. Sciatic nerve injury in posterior dislocation of the hip, Popliteal artery in posterior dislocation of the knee, etc.
  2. Recurrent dislocation.
  3. Habitual dislocation.
  4. Avascular necrosis.
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Revision Questions
Q. Define a fracture. How do you classify fractures? Add a note on fracture healing.
Q. Define and classify non unions. Discuss the management.
Q. Enumerate the complications of a fracture. Discuss their management.
Note: For questions on dislocations refer Chapter 4.
Further Reading
  1. Orr HW, Nicolas Andry. Founder of the orthopaedic specialty. Clin Orthop 1954; 4: 3–9.
Open Fracture Management
  1. Dedmond BT, Kortesis B, Punger K, Simpson J, et al. The use of negative-pressure wound therapy(NPWT) in the temporary treatment of soft-tissue injuries associated with high-energy open tibial shaft fractures. J Orthop Trauma 2007; 21: 11–7.
  1. Fischer MD, Gustilo RB, Varecka TF. The timing of flap coverage, bone-grafting, and intramedullary nailing in patients who have a fracture of the tibial shaft with extensive soft tissue injury. J Bone Joint Surg 1991; 73A: 1316–22.
  1. Gustilo RB, Anderson JT. Prevention of infection in the treatment of one thousand twenty-five open fractures of long bones: Retrospective and prospective analysis. J Bone Joint Surg 1976; 58A: 453–8.
  1. Gustilo RB, Mendoza RM, Williams DN. Problems in the management of type III (severe) open fractures; A new classification of type III open fractures. J Trauma 1984; 24: 742–6.
  1. Knapp TP, et al. Comparison of intravenous and oral antibiotic therapy in the treatment of fractures caused by low-velocity gunshots. A prospective, randomized study of infection rates. J Bone Joint Surg 1996; 78A: 1167–71.
  1. Zalavras CG, Marcus RE, Levin LS, Patzakis MJ. Management of open fractures and subsequent complications. J Bone Joint Surg Am 2007; 89 (4): 884–95.
Complex Regional Pain Syndrome (Sudeck's Atrophy)
  1. Oaklander AL, Fields HL. Is reflex sympathetic dystrophy/complex regional pain syndrome type I a small-fiber neuropathy? Ann Neurol 2009; 65 (6): 629–38.
  1. Schwartzman RJ, Erwin KL, Alexander GM. The natural history of complex regional pain syndrome. Clin J Pain 2009; 25 (4): 273–80.