Chapter 1: General Principles of Orthopedics Compound fracture/ Open fracture: Introduction: A fracture with break in the overlying skin and soft tissues, leading to the fracture communicating with the external environment. Mechanism: This type of fracture occurs when enough force hits the bone to cause it break and stick out through the skin. Types: 1. Internally open: The sharp fracture end pierces the skin from within 2. Externally open: The object causing the fracture lacerates the skin and soft tissues over the bone and finally break the bone to cause a fracture. Symptoms and warning signs: * History of a major trauma * Symptoms are mainly due to broken bone and open wound: pain, swelling, bleeding, infection etc. © Warning signs to be kept in mind: i. Stretch pain: Indicates compartment syndrome ii, Pallor pulselessness: Indicates arterial injury ili, Foul odour: Indicates infection due to open wound Grading of compound fracture [Gustilo classification] Type | Open fracture with a skin wound <1 em in length and clean, Type Open fracture with a laceration >I em in length without extensive soft tissue damage, flaps, or avulsions. Type IIL Open segmental fracture with >10 cm wound with extensive soft tissue injury or a traumatic amputation (special categorie: in Type III include gunshot fractures and open fractures caused by farm injuries) Il, Adequate soft tissue coverage. Il Significant soft tissue loss with exposed bone that requires soft tissue transfer to achieve coverage. Mle Associated vascular injury that requires repair for limb preservation,Treatment: Principles and steps of treatment: 1. Primary survey and early resuscitation 2. Bleeding control (by direct pressure) 3. Temporary immobilization of the fracture 4. Decontamination (Wound irrigation with NS [at least 3 litres] + Antiseptic/ Antibiotic solution) Tetanus prophylaxis (Inj. Tetanus toxoid 0.5 ml IM) . Early administration of prophylactic antibiotic (Commonly used: 1* Generation cephalosporin [type 1 and 2] + Aminoglycoside [type 3]) 7, Thorough wound debridement (Wound exploration + detection and removal of foreign material + nonviable tissue + bacterial contamination) 8. Repair damaged structures (Consult CTVS surgeon in case of major vascular injury/ plastic surgeon in case of nerve/ tendon injury) 9. Reduce and stabilize the fracture (External splinting [slab/ cast/ traction]; Early internal fixation (pin/ nail/ plate and screw] + External fixators: Method of choice) 10.Wound coverage (Direct suture/ skin graft/ flap). oe Complications: * Infection © Damaged structures © Compartment syndrome * Bone defect: delayed union/ non-union. Non-union of [closed] fracture: Introduction: Non-union is a permanent failure of healing following a fracture. Definition: A fracture that in a minimum of 9 months post occurrence and is not healed and has not shown radiographic progression by 3 months.Classification: There are 2 main types: 1. Atrophic non-union: Osteogenesis seems to have ceased, The bone ends are tapered or rounded with no suggestion of new bone formation. 2. Hypertrophic non-union: Bone ends are enlarged, suggesting that osteogenesis is still active but not quite capable of bridging the gap. Etiological/ Risk factors: Patient Related Treatment Related) - Old Age - Bone Loss - Inadequate immo- - Poor Nutrition - Open Injuries -bolisation - Steroid Therapy = #Blood supply - Implant Failure - Radiation Therapy| | - Infection - Fragment malposi- - Smoking - Muscle Injury -tion - Alcoholism Common sites Femur * Scaphoid * Lower third of the tibia * Lower third of the ulna © Lateral condyle of the humerus. Clinical features: © Persistent pain © Pain on stressing the fracture * Mobility © Increasing deformity at the fracture site. Radiological features: * Absence of bridging trabeculae * Sclerotic fracture edges © Persistent fracture lines # Lack of evidence of progressive change toward union in serial X-Ray* Progressive deformity. Treatment options: 1. Open reduction + Internal fixation + Bone grafting: This is the commonest operation performed for non-union. The grafts are taken from iliac crest. 2. Excision of fragments: This can only be done where excision of the fragment does not cause any loss of functions. An excision may or may not need to be combined with replacement with an artificial prosthesis. Ex.: In non-union of fracture of the neck of femur in an elderly, the head of the femur can be replaced by a prosthesis (replacement arthroplasty). 3. No treatment: Some non-unions do not give rise to any symptoms, and hence require no treatment. Ex.: Some non-unions of the fracture scaphoid. 4, llizarov’s method: llizarov method is a system in which bone is fixed with thin wires and rings. Extremity lengthening and reconstruction techniques are used for filling bone defects and correcting and lengthening bones with deformity. Compartment syndrome: Introduction: Limbs contains muscles, blood vessels and nerves covered by tough fascia. All these together forms a “compartment”. Introduction: Compartment syndrome is a clinical condition characterized by an elevation of intra-compartmental pressure, resulting in a decreased blood supply of the muscles and nerves within it; causing ischemic damage which may progress into necrosis of both muscles and nerves. Risk factors: 1. Direct trauma leading to edema of muscles2. Soft tissue bleeding from fractures/ operations 3. Prolonged compression by tight plaster/ bandage 4. Direct pressure in a comatose patient lying on a hard surface. The common sites of fractures notorious for developing compartment syndrome are elbow, forearm bones, proximal 1/3" of tibia, multiple fractures of hand and foot. Pathophysiology: © The increased pressure within the compartment compromises the circulation leading to further muscle ischemia. * Avicious-cycle is thus initiated and continues until the total vascularity of the muscles and nerves within the compartment is jeopardized. This results in ischemic muscle necrosis and nerve damage. * The necrotic muscles undergo healing with fibrosis, leading to contractures. * Nerve damage may result in motor and sensory loss. 4 Injury ‘Swelling 4 Blood supply Muscle ischaemia NU? According to the progression, compartment syndrome may be of 2 types: Types: 1. Acute: Ex: Volkmann’s contracture It is a complication of supracondylar fracture of humerus where there is injury/ compression of the brachial artery, leading to ischemia of flexor digitorum profundus and flexor pollicis longus, resulting in a permanent flexion contracture of wrist joint and fingers.2. Chronic: Ex: Chronic exertional compartment syndrome In some of the long distance runners, there is swelling of the anterior calf muscle, causing a chronically elevated compartment pressure, leading to ischemia of deep peroneal nerve, resulting in pain along the anterolateral aspect of calf; precipitated by muscular exertion. Clinical features: |. Often a H/O a risk factor (fracture/ operation/ compression/ infection) is present ll Classical features of ischemia (5P): Pain Pallor Paresthesia Paralysis Pulselessness, All of these clinical features may not be present, but presence of any of them should raise suspicion of an impending compartment syndrome in the mind of the clinician in a background of risk factor(s). Ill Stretch test: * This is the earliest sign of impending compartment syndrome. * The ischemic muscles, when stretched, give rise to pain. * Its possible to stretch the affected muscles by passively moving the joints in a direction opposite to that of the damaged muscle's action. Ex: When the toes/ fingers are passively hyperextended, there is increased pain in the flexors of calf/ forearm. Diagnosis: Rene * Confirmation of the diagnosis can be made by measuring the intra- compartmental pressure. * Adifferential pressure (AP) — the difference between diastolic pressure and compartment pressure — of <30 mmkg is an indication for immediate compartment decompression.Management: Compartmental syndrome is a medical emergency: |, Remove any cast/ bandage/ dressing immediately ll. Elevate the limb to increase blood supply Ill The AP should be carefully monitored; if it falls below 30 mmHg, immediate open fasciotomy (opening compartments through incisions) is performed. The wounds should be left open and inspected 2 days later: v lf there is muscle necrosis, debridement can be carried out; Y If the tissues are healthy, the wounds can be sutured (without tension) or skin-grafted. Crush syndrome: Introduction This is seen when a limb is compressed for extended periods, e.g. following entrapment in a vehicle or rubble, but also after prolonged use of tourniquet. Consequences of Crush syndrome: Crushed limb -—>|—Underperfusion >] Necrosis of muscles ——se Release of toxic metabolites (Reactive ‘oxygen metabolites) when limb is freed —— >| Tissuedamage L_>| Swelling Compartment ‘Ageravating ischemia |-—> ayndtanne* Tissue necrosis also causes systemic problems such as renal failure from free myoglobin, which is precipitated in the renal glomeruli. Myonecrosis may also cause a metabolic acidosis with hyperkalaemia and hypocalcaemia. Clinical features: * The compromised limb is pulseless and becomes red, swollen and blistered; sensation and muscle power may be lost. * If not treated adequately within 2-3 days, acute tubular necrosis sets in, producing signs of deficient renal functions such as scanty urine, apathy, restlessness and delirium. Treatment: + The most important measure is prevention. * Ahigh urine flow is encouraged with alkalization of the urine with sodium bicarbonate, which prevents myoglobin precipitating in the renal tubules. If oliguria or renal failure occurs then renal haemofiltration will be needed. Ifa compartment syndrome develops, and is confirmed by pressure measurements, then a fasciotomy is indicated. Excision of dead muscle must be radical to avoid sepsis. Similarly, if there is an open wound then this should be managed aggressively. If there is no open wound and the compartment pressures are not high, then the risk of infection is probably lower if early surgery is avoided. Fat embolism: Introduction: A fat embolism is a type of embolism that is often caused by physical trauma such as fracture of long bones, soft tissue trauma and burns. Fat embolism occurs in about 90% of individuals with severe skeletal injuries. Common skeletal injuries causing fat embolism: * Fracture femur+ Fracture tibia * Multiple fractures. Fat embolism syndrome (FES). It is distinct from the presence of fat emboli. Symptoms usually occur 1-3 days after a traumatic injury and consists of the following symptoms: * Pulmonary: Shortness of breath, hypoxemia + Neurological: Agitation, delirium, coma * Dermatological: Petechial rash + Hematological: Anemia, thrombocytopenia. Pathogenesis: * The pathogenesis of fat emboli syndrome probably involves both mechanical obstruction and biochemical injury. * Fat microemboli and associated RBC and platelet aggregates can occlude the pulmonary and cerebral microvasculature. * Release of free fatty acids from the fat globules exacerbates the situation by causing local toxic injury to endothelium; and resultant platelet activation and granulocyte recruitment. Treatment: * Oxygen + Heparinisation + Low molecular weight dextran * Ventilator support and ICU management. Myositis ossificans: Definition: Myositis ossificans is defined as heterotopic ossification in the muscles after an injury. Age: The patient is usually a fit young man.Most common clinical conditions that may lead to myositis ossificans: 1. Dislocation of elbow. 2. Blow to brachialis/ deltoid/ quadriceps. 3. Unconscious/ paraplegic patients. Clinical and radiological features: * Soon after the injury, the patient complains of pain; there is local swelling and soft-tissue tenderness. X-ray is normal. * Over the next 2-3 weeks the pain gradually subsides, but joint movement is limited; X-ray may show fluffy calcification in the soft tissues. * By 8 weeks the bony mass is easily palpable and is clearly defined in the X- ray, Treatment: = The joint should be rested in the position of function until pain subsides; gentle active movements are then begun. * Months later, when the condition has stabilized, it may be helpful to excise the bony mass. = Indomethacin or radiotherapy should be given to help prevent a recurrence. Pathological fracture: Definition: It is defined as a fracture in a bone which has already become week by some underlying diseases. Most common cause: * The most common cause of pathological fracture is osteoporosis. * The most commonly involved bones are thoracic and lumber vertebral bodies, ‘* Other common fractures associated with osteoporosis are fracture neck of femur and Colles’ fracture.Causes of pathological fractures at different ages: Age Most common cause(s) At birth Osteogenesis imperfecta 0-5 years © Osteogenesis imperfecta Osteomyelitis Osteomyelitis Primary bone cyst Primary bone malignancy Cystic lesions of bone Malignancy Osteomalacia Giant cell tumor Osteoporosis Multiple myeloma Metastasis to the bones 5-20 years 20-50 years After 50 years Diagnostic clues: * A fracture without a significant trauma, Ahistory of mild discomfort in the region of fracture for some days before the fracture occurred. ‘* When patient is already diagnosed with a disease that may cause pathological fractures (Ex.: malignancy). Treatment: The treatment of a pathological fracture consists of: a. Detection of the underlying disease that is making bone weak. b. Assessment of the capacity of fractured bone to unite. ©. Achievement of maximum stable fixation. Detection of the underlying disease that is making bone weak To detect the underlying disease, the following tests should be done:. CBC, ESR. . Kidney and liver function tests. . Calcium, phosphorus and alkaline phosphatase (Osteoporosis, Osteomalacia, Bone tumors). . Plasma protein electrophoresis (Multiple myeloma). . Tumor markers: a. CA 19-9 (Colorectal cancer). CA 125 (Ovarian cancer). . CA 15-3 (Breast cancer). . B2-Microglobulin (Lymphoma). . Alpha-fetoprotein (Hepatocellular cancer). PSA (Prostatic cancer) Assessment of the capacity of fractured bone to unite m~epeans It is well known that depending upon the etiology of pathological fracture, there are differences in the capacity of the bone to reunite. Ex.: In diseases like Osteogenesis imperfecta and Osteoporosis, the fracture is amenable to reunite with conventional methods whereas, in diseases like Osteomyelitis and Malignancy, fractures may fail to reunite despite best efforts. Achievement of maximum stable fixation Non-operative treatment options: 1. Bisphosphonates. 2. Radiotherapy. Rw . Pain control. . DVT control. . Splints/ traction/ braces etc. Operative treatment options: i a Note: Internal fixation; Preferable intra-medullary fixation with/ without bone grafting/ cementing (in case of big cavities), Resection and replacement. Surgery should be followed by postoperative radiotherapy to prevent recurrences.Stress fracture: Introduction: Stress fracture, also known as hairline fracture; is a special type of fracture sustained due to chronic repetitive injury (stress) causing a break in bony trabeculae. Mechanism: It results from accumulated trauma from repeated submaximal loading. Types: 1. Fatique fracture: Occurs secondary to an abnormal amount of stress applied to a normal bone. Ex.: Runners, dancers, military recruits etc. 2. Insufficiency fracture: Occurs with normal stress placed on an abnormal bone. Ex.: Osteoporosis, osteomalacia, Paget's disease, drug induced (corticosteroids and methotrexate). Clinical features: * There may be a history of unaccustomed and repetitive activity or a strenuous physical exercise programme. * Acommon sequence of events is: pain after exercise —> pain during exercise —> pain without exercise, © The affected site may be swollen or red. It is sometimes warm and usually tender; the callus may be palpable. * Occasionally the patient presents only after the fracture has healed and may then complain of a lump (the callus). Investigation: * X-Ray: Early on, the fracture is difficult to detect. When taken a few weeks later, it may show a small transverse defect in the cortex and/or localized periosteal new-bone formation. * Best diagnostic test for unilateral stress fracture is MRI* Best diagnostic test for bilateral stress fracture is Bone scan: will show increased activity at the painful spot Note: The great danger is o mistaken diagnosis of osteosarcoma; scanning shows increased uptake in both conditions and even biopsy may be misleading. Treatment! ‘Most stress fractures need no treatment other than an elastic bandage and avoidance of the painful activity until the lesion heals. ‘+ An important exception is stress fracture of the femoral neck. This should be suspected in all elderly people who complain of pain in the hip for which no obvious cause can be found. If the diagnosis is confirmed by bone scan, the femoral neck should be internally fixed with screws as a prophylactic measure. Classification of nerve injuries: Seddon’ classification (1942): Term Description Example ‘Neurapraxia | A reversible physiological nerve conduction block with loss of | Saturday some types of sensation and muscle power followed by right palsy spontaneous recovery within a few days or weeks. ‘Axonotmesis | Axonal interruption with loss of conduction but the nerveisin | Closed continuity and the neural tubes are intact. fracture Distal to the lesion, axons disintegrate and are resorbed by and phagocytes. This phenomenon is called Wallerian degeneration. | dislocations Recovery takes months to occur. Neurotmesis | When the injury is more severe, whether the nerve is in ‘Open continuity or not, recovery will not occur. wound As in axonotmesis, there is rapid Wallerian degeneration, but here the endoneurial tubes are destroyed over a variable segment and scarring takes place, which interferes with regenerating axons regaining entry into the distal seament. Instead, regenerating fibers mingle with proliferating Schwann cells and fibroblasts in a jumbled knot or ‘neuroma’ at the site of injury, Even after surgical repair, many new axons fail to reach the distal segment.Chapter 2: Infection of bones and joints Pyogenic osteomyelitis, Etiopathogenesis: Introduction: Infection of bone by any pyogenic organism is called pyogenic osteomyelitis. It is of 2 types: acute and chronic. Acute pyogenic osteomyelitis Responsible organisms: Staphylococcus aureus (commonest), followed by streptococcus and pneumococcus. Route of entry to bone: 1. Primary/ hematogenous (commonest, often seen in children) 2. Secondary (following an open fracture/ bone operation, less common). Etiopathogenesis: 1. ‘Hairpin arrangement’ of the vessels in the metaphysis of long bone makes the blood flow sluggish in this area and makes this area being the commonest area to lodge the organisms (/ower femoral metaphysis is the commonest among them). 2. The host bone initiates an inflammatory reaction in response to the bacteria. This leads to bone destruction and production of an inflammatory exudate which may spread to the following directions: Epiphysis Motaphysis [Spread of pus from metaphysis: A) Along medullary cavity, B) Out of the cortex, C) To the joint, D) Abscess formation]1. Along the medullary cavity: The pus may spread along the medullary cavity, causing thrombosis of medullary arteries and veins; cutting blood supply to a portion of bone. 2. Qut of the cortex: The pus travels along Volkmann’s canals and comes to lie sub-periosteally. The periosteum is thus lifted off the underlying bone, resulting in damage to the periosteal blood supply to a part of the bone. ‘A segment of bone is thus rendered avascular and is called sequestrum. 3. Abscess and sinus formation: Eventually the periosteum is perforated, letting the pus out into the muscle or subcutaneous plane, where it can be felt as an abscess. The abscess, if unattended, bursts out of the skin, forming a discharging sinus. 4, To the joint: The capsular attachment at the epiphysis - metaphysis junction prevents the pus from entering the nearby joint. In joints with an intra-articular metaphysis, the pus can spread to the joint and cause acute pyogenic arthritis e.g., hip, shoulder etc. Diagnosis: Parts of diagnosis Description Age Childhood History A recent history of infection (Ex: sore throat, ear discharge etc.) Chief complaints ‘Acute onset of pain and swelling at the end of a bone systemic symptoms like fever, malaise etc. Examination Pulse rate is very high and temperature is raised Acute tenderness near one of the largest joints Joint movement is restricted (pseudoparalysis) Local signs of inflammation (redness, edema, swelling, warmth) are usually late features and signifies that pus has escaped from the interior of the bone. Investigation Blood: CRPS, ESR, WBC count (PMN leucocytes) X-Ray: Earliest classic sign is periosteal new bone formation at the metaphysis (by the 2"! weeks) Confirmatory: The most certain way to confirm the clinical diagnosis is to aspirate pus or fluid from the metaphysealsubperiosteal abscess/ extra-osseous soft tissues/ an adjacent joint, followed by gram stain. Treatment: Supportive _| Analgesics at repeated intervals and IV fluid to correct dehydration Splintage Simple skin traction/ plaster slab for comfort and prevent contracture Antibiotics Blood and aspiration material is sent immediately, but the administration of antibiotic should be prompt without waiting for result. The empirical antibiotic recommendations are: Age/ group Antibiotic of choice Upto 6 months IV (Floxacillin + 3 gen. cephalosporin* 6 months- 6 years -Do- Older children + IV (Floxacillin + Fusidic acid) previously fit adults Elderly + previously | IV (Floxacillin + 2/3" gen. cephalosporin) unfit adults Sickle cell disease _| IV (3gen. cephalosporin/ fluoroquinolone~) Drug addicts/ HIV -Do- MRSA IV (Vancomycin + 3“ gen. cephalosporin) Drainage If the clinical features do not improve within 36 hours of starting treatment/ if there are signs of deep pus (swelling, edema, fluctuation) / if pus is aspirated, the abscess should be drained by open operation under general anesthesia. Complications: 1. Chronic osteomyelitis PWN Causes: . Acute pyogenic arthritis . Pathological fracture . Growth plate disturbances causing deformity of the limb. Chronic osteomyelitis 1. Delayed and inadequate treatment 2. Reduced host resistance (malnutrition/ HIV etc.)Diagnosis: Parts of diagnosis Description Chief complaints A chronic discharging sinus The type discharge is sero-purulent Pain & fever become evident in times of acute exacerbations. Examination A chronic discharging sinus Thickened, irregular bone when compared to the normal side Mild tenderness on deep palpation Stiffness of the adjacent joint may be present. Investigation X-Ray: ¥ Thickening and irregularity of the cortices ¥ Patchy sclerosis giving the bone a honeycomb appearance ¥_ Sequestrum and involucrum may be visible, Treatment: Aims of surgery: 1. Removal of dead bone 2. Elimination of dead space 3. Removal of infected granulation tissue and sinus. Surgical options: Option Description Presentation Sequestrectomy | A window is made in the overlying involucrum and the sequestrum removed. One must wait for adequate involucrum formation before performing sequestrectomy.Saucerization The bone-cavity is converted into a ; 7 'saucer' by removing its wall. This allows ~ free drainage of the infected material. \ Curettage The wall of the cavity, lined by infected granulation tissue, is curetted until the underlying normal-looking bone is seen. Excision of the infected bone Itis done when the affected bone can be excised en-bloc without compromising the functions of the limb. Amputation It is preferred in a long standing discharging sinus when sinus undergoes malignant change. Sequestrum, Ring sequestrum: Introduction: It is a dead piece of bone which is formed in some infective conditions of bone. Common conditions associated with sequestrum: 1. Acute osteomyelitis 2. Chronic osteomyelitis 3. TB spine. Pathogenesis: 1. Incase of acute osteomyelitis. * The bacteria gets lodged into the bone (commonly metaphysis) usually through a hematogenous route © Inresponse, the bone initiates an inflammatory reaction against the invading bacteria, resulting in formation of inflammatory exudate (pus). * When the pus spread into medullary cavity, travels along the Volkmann’s canal and ultimately come to the subperiosteal space. © The periosteum is thus lifted off the underlying bone, resulting in damage/ cut off to the periosteal blood supply to a part of the bone. * Asegment of bone becomes avascular and dead.Sub-periosteal space Bacteria in medullary cavity Cutting off the blood supply and formation of sequestrum V/ Passage through ‘Volkmann's canal 2. Incase of chronic osteomyelitis: Delayed and inadequate treatment of acute osteomyelitis results in the pus giving the time to spread within medullary cavity and sub-periosteally; resulting in a diminished blood supply and formation of a dead piece of bone. 3. Incase of TB spine: * Inthe commoner paradiscal type of spinal TB, the bacteria lodge in the contiguous areas of two adjacent vertebrae. * The granulomatous inflammation results in erosion of the margins of these vertebrae. * The nutrition of the intervening disc, which comes from the endplates of the adjacent vertebrae is compromised. * This results in disc degeneration and sequestra formation and as the process continues, complete destruction of the vertebra. Elevation of periosteum.Relevant operative procedures: Sequestrectomy: This means the removal of sequestrum. If it lies within the medullary cavity, a window is made in the overlying involucrum (it is the dense sclerotic bone overlying a sequestrum) and the sequestrum removed. One must wait for adequate involucrum formation before performing sequestrectomy. Brodie’s abscess: Introduction: Itis a special type of subacute osteomyelitis in which the body's defence mechanisms have been able to contain the infection so as to create a chronic bone abscess. Common age of presentation: 11-20 years Common sites: Upper end of the tibia and lower-end of the femur. Clinical features: * The patient is usually a child or adolescent who has had chronic persistent deep boring pain near one of the larger joints for several weeks or even months. © The pain may become worse at night and in some instances, it becomes worse on walking and is relieved by rest. © He or she may have a limp and often there is slight swelling, muscle wasting and local tenderness. * The temperature is usually normal and there is little to suggest an infection. Laboratory investigations: The WBC count and blood cultures usually show no abnormality but the ESR is sometimes elevated. Radiological features: * The radiological appearance of Brodie’s abscess is diagnostic. © The typical radiographic lesion is a circumscribed, round or oval radiolucent ‘cavity’ 1-2 cm in diameter surrounded by a halo of sclerosis.© Most often it is seen in the tibial or femoral metaphysis. Management: © Surgical evacuation and curettage is performed under antibiotic cover. © If the cavity is large, it is packed with cancellous bone chips. TB hip: Introduction: Hip is the second most common site for bone TB (after TB spine) is the commonest cause of pain in the hip in children in countries where TB is stil prevalent. Initial focus of infection: 1. Acetabular roof (most common) 2. Head of femur. Stages along with clinical features: Stage Pathology Clinical feature Stage of Joint effusion Flexion, abduction and external rotation synovitis, (FABER) deformity Apparent lengthening of the affected limb. Stage of early Damage to the Flexion, adduction and internal rotation arthritis articular damage (FAdIR) deformity Apparent shortening of the affected limb. Stage of late | Gross destruction of Flexion, adduction and internal rotation arthritis articular cartilage, (FAdIR) deformity femoral head + True shortening of the affected limb acetabulum * Considerable restriction of hip movements. Stage of Pathological * Migrating (Wandering) acetabulum advanced dislocation or * Mortar and pestle appearance: Femoral arthritis subluxation of the hip head and neck grossly destroyed, collapsed and small in size,Radiological features: 1. Haziness of the bones around the hip: Earliest sign 2. Reduction of joint space: Due to arthritis of cartilage 3. Irregular outline of articular surface of bone: Because of destruction process 4. Acetabular changes: Wandering acetabulum/ Mortar & pestle appearance. Other diagnostic tools: . CBC: Lymphocyte count + . ESR: May be * . Aspiration of synovial fluid . Aspiration of cold abscess (if any) . Biopsy and histopathological examination from lesion . CXR: Should be routinely done to rule out pulmonary TB. Oupune Treatment: A. Conservative management: |. Care of the hip: The affected hip is put to rest by immobilisation using below-knee skin traction. Il General care: = High protein diet = Control of infection by prompt initiation of anti-tubercular chemotherapy. Start with HRZE for 3 months. Ill. Gradual mobilisation of the hip B. Operative intervention: |. FNAC/ Biopsy: When diagnosis is in doubt I. Cold abscess: Aspiration/ evacuation lll. To provide a painless, mobile but unstable joint: Excision arthroplasty (Girdlestone arthroplasty) IV. To provide a painless, stable but fixed joint: Arthrodesis (surgical fusion of the joint).Chapter 3: Upper limb Fractures occurring due to fall on outstretched hand (FOOSH): Depending on where the forces from FOOSH are applied, fractures and dislocations can occur at the wrist, forearm or elbow. Wrist fractures Mechanism: When falling on outstretched hand, palm strikes the ground with the wrist in hyperextension. (a i Examples of wrist fractures resulting from FOOSH: Diagram shows lateral view of bones of forearm and wrist: humerus (HUM), which includes capitulum (CAP); radius and radial head articulating with capitulum; ulna and olecranon wrapping around trochlea; and scaphoid (S) articulating with distal articular surface of radius Arrow indicates hyperextension of wrist that occurs during fall on outstretched hhand, Inset shows enlargement of area Indicated by outline and rotated to typical orientation of wrist radiographs. Lightning bolts represent common sites of fractures due to falls on outstretched palm: Fractures caused: A= Colles, 8 = Dorsal Barton, C= Scaphoia. Example General description Colles fracture Transverse fracture through the distal metaphysis of radius Dorsal Burton Fracture through the dorsal rim of distal articular surface of fracture radius Scaphoid fracture Usually non-displaced fracture of the scaphoidForearm and elbow fractures Mechanism: Not only does a FOOSH cause hyperextension of the wrist, but it also transmits an axial load along the length of the forearm, from wrist to elbow, which may result in specific patterns of fractures, Diagram shows frontal view of bones of forearm: humerus (HUM), whieh Includes capitulum (CAP) and trochlea (TRO); radius with head articulating with capitulum; ulna with olecranon wrapping around trochlea; and carpus as one unit, Falling on outstretched hand [downward arrow) results in transmission of axial forces up forearm (upward arrows), Examples of forearm and elbow fractures resulting from FOOSH: (See pictures on next page) Example General description Both Bone Forearm _| Transverse fractures of the shafts of both the radius and Fracture ulna, particularly seen in children Monteggia Fracture- | Ulnar shaft fracture with radial head dislocation Dislocation Galeazzi Fracture- | Radius fracture with dislocation of the distal ulna at the Dislocation distal radioulnar joint Radial head fractures __| Simple radial head fractures are common and usually are isolated injuries. Severely comminuted radial head fractures are uncommon; ex.: Essex-Lopresti fracture.@ Monteggia Fracture-Dislocation @ Galeazzi Fracture-Dislocation © Essex-Lopresti fracture: 1. Application of axial load to radius alone, impacting radial head into capitulum (CAP) and causing comminuted radial head fracture. II Asymmetric axial load between radius and ulna causes tearing along length of interosseous membrane (IOM) and disrupts distal radioulnar joint (DRUJ). Volkmann’s ischemic contracture (VIC): Definition: VIC is the result of vascular insult to deep tissues of limb producing ischemia, primarily of the muscles and secondarily of nerves, as a sequel of compartment syndrome (an elevation of interstitial pressure in a closed osseofascial compartment). Causes: . External compression (tight bandage/ plastering) . Crush injuries . Fractures . Post burn contracture . Repeated intra-arterial injections (in drug addicts) . Internal bleeding (hemophilia). OyRwNECommon sites: 1. Volar aspect of forearm 2. Hand and foot 3. Anterior and deep posterior compartments of leg Pathology: Raised intra- comer >) al fos] Saumael Ly] mownel pressure Muscles can't Replaced by Contracture regenerate [| fibrooustissue [>| (vic) Clinical features: (4Ps) © Pain: It increases with extension of fingers i.e. stretching of flexor muscles. So it is called “stretching pain”. Gentle passive extension of fingers causes severe pain. * Pallor: Earliest feature. © Paresthesia: Late feature. * Pulselessness: It is not a constant feature of VIC as radial pulse is often found in ischemic hand. Volkmann's sign: © When wrist is extended, MCP and IP joints become more flexed. © When wrist is flexed, MCP and IP joints can be extended. Management: Impending VIC (it is a medical emergency) * All bandage/ plasters/ splints are removed immediately. * Limb is elevated to the level of heart. * Elbow is straightened to 30° flexion. «Limb is frequently observed for signs of ischemia.«Ifo improvement occurs, fasciotomy operation must be done to decompress the osseofascial compartment. Established VIC Mild variety Splinting and physiotherapy. Moderate | Max page muscle slide operation + Neurolysis + Tendon transfer Severe Scar excision +- Muscle slide +- Proximal row carpectomy +- Wrist arthrodesis. | Colles fracture: Introduction: It is the most common fracture in people >40 years of age. Site: This is a transverse fracture of distal end of radius, at the cortico-cancellous junction (2 cm proximal to distal articular surface). Relevant anatomy: Normally, the radial styloid is about 1 cm distal to the ulnar styloid. In Colles fracture, both the styloids lie almost at the same level. Mechanism; Fall on an out-stretched hand/ post-menopausal osteoporosis. Typical deformities: © Dorsal displacement. } it © Dorsal tlt. > * Lateral displacement. © Lateral tilt. 2 a impaction of fragments. a i * Supination AP. Lateral \ Proximal shit Proximal shit Radial shift Dorsal shift Fadia tit Dorsal tit Clinical features: The patient presents with pain, swelling and d examination, tenderness and irregularity of the lower end of the radius Is found. There may be a classical ‘dinner-fork deformit leformity of the wrist. OnThe wrist is broadened and radially deviated with prominent ulnar head and there is dorsal and lateral tilt. Wrist movements are restricted. Radiological features: * Most of the displacements are evident on X-Ray, except Supination which can be appreciated only clinically. © A-P view: Normally the distal articular surface of radius is faced medially. When it faces laterally, a lateral tilt is present. * Lateral view: Normally the distal articular surface of radius is faced ventrally. When it faces neutral/ dorsal position, a dorsal tilt is present. This dorsal tilt is the most characteristic displacement of Colles fracture. Treatment: * For an undisplaced fracture, immobilisation in a below-elbow plaster cast for 6 weeks is sufficient. * For displaced fractures, the standard method of treatment is manipulative reduction followed by immobilisation in Colles' cast. Technique of closed manipulation: * The muscles of forearm must be relaxed, either by general or regional anesthesia, The surgeon grasps the injured hand as if he were ‘shaking hands’. © The first step is to disimpact the fragments which have often been driven together. This is achieved by firm longitudinal traction to the hand against the counter-traction by an assistant who grasps the arm above the flexed elbow. Some displacements are corrected by traction alone. * The surgeon now presses the distal fragment into palmar flexion and ulnar deviation using the thumb of his other hand.« As this is done, the patient's hand is drawn into pronation, palmar flexion and ulnar deviation. A plaster cast is applied extending from below the elbow to the metacarpal heads, maintaining the wrist in palmar flexion and ulnar deviation. This is Colles' cast. ‘coumrsmscton ‘actor Colles cast: (a) In palmar flexion (b) In ulnar deviation. eau ” Sere Monteggia fracture-dislocation: Introduction: Fracture of the upper-third of the ulna with dislocation of the head of radius. Mechanism of injury: Fall on outstretched hand. Types: Type Angulation of ulnar Angulation of radial fracture fragment dislocation Extension Anteriorly Anteriorly Flexion Posteriorly PosteriorlyClinical features: © The ulnar deformity is usually obvious but the dislocated head of radius is masked by swelling. « Auseful clue is pain and tenderness on the lateral side of the elbow. © Wrist and hand should be examined for signs of injury to radial nerve. Diagnosis: With isolated fractures of the ulna, it is essential to obtain a true antero-posterior [A-P] and true lateral view of the elbow. Always obtain a full length X-Ray of forearm and hand. Treatment: Confirmation of diagnosis Attempt at reduction under general anaesthesia Successful Failed Check X-rays weekly for! Open reduction and r internal fixation using a the initial 3-4 weeks aE Complications: 1. Nerve injury 2. Mal-union 3. Non-union.Dislocation of shoulder: Shoulder joint is the most commonly dislocated joint among the large joints. The causes behind this vulnerability are: a. Shallow glenoid socket. b. Extraordinary range of movement. c. Sheer vulnerability of this joint during stressful activities of upper limb Anterior dislocation Mechanism: Dislocation is usually caused by a fall on the hand. The head of the humerus is driven forward, tearing the capsule and producing avulsion of the glenoid labrum (the Bankart lesion). Clinical features: * Severe pain. Patient support the affected arm with the opposite arm. The arm must always be examined for nerve and vessel injury before reduction is attempted. X-Ray: © A-P view: It will show the overlapping shadows of the humeral head and glenoid fossa, with the head usually lying below and medial to the socket. ¢ Lateral view: It will show the humeral head out of line with the socket.— eet 7 pre Treatment: a. Stimson’s technique: The patient is left prone with the arm hanging over the side of the bed. After 15 or 20 minutes the shoulder may reduce. b. Hippocratic method: Gently increasing traction is applied to the arm with the shoulder in slight abduction, while an assistant applies firm counter- traction to the body. ©. Kocher’s method: TEA-I (Traction, external rotation, adduction and internal rotation applied serially), This technique has been abandoned due to high risk of injury to vessels and nerves and bone fracture. Post-operative care: * An x-ray is taken to confirm reduction and exclude a fracture. When the patient is fully awake, active abduction is gently tested to exclude an axillary nerve injury and rotator cuff tear. The median, radial, ulnar and musculocutaneous nerves are also tested. © The pulse is felt. Complications. Early complications Rotator cufftear |Nerve injury (axillary nerve: most common) | Vessel injury (axillary artery: most common) Fracture-dislocation of proximal humerus | _ Late complications Shoulder stiffness Unreduced dislocation (in the elderly) Recurrent dislocation (in case of tear of capsule of shoulder joint)Posterior dislocation It is rare (<2% of all shoulder dislocations). Mechanism: Indirect force producing marked internal rotation and adduction needs be very severe to cause a posterior dislocation. This happens most commonly during a fit or convulsion or with an electric shock. Clinical features: © The arm is held in internal rotation and is locked in that position. © The front of the shoulder looks flat with a prominent coracoid, but swelling may obscure this deformity. When seen from above, the posterior displacement is usually apparent. X-ray: © A-P view: As humeral head is medially rotated, it looks abnormal in shape (like an electric light bulb). The humeral head stands away from the glenoid fossa (the empty glenoid sign). «Lateral view: It is very important to take as it actually shows the posterior dislocation/ subluxation. Treatment: Reduction of dislocation by ADLRI (adduction, lateral rotation and immobilization done serially) Complications: * Unreduced dislocation. © Recurrent dislocation and subluxation. Recurrent dislocation of shoulder: Introduction: «fan anterior dislocation tears the shoulder capsule, repair occurs spontaneously following reduction and the dislocation may not recur.© Butif the glenoid labrum is detached (particularly in young patients) or the capsule is stripped off in front of the neck of glenoid, repair is less likely and recurrence is more common. Epidemiology: 1, Common in young patients (~20 years) 2. Common in males 3. Most recurrences occur within first 2 years of first episode 4. May be classified into 2 types: traumatic and atraumatic. Clinical features: * History: The history is diagnostic. The patient complains that the shoulder dislocates with relatively trivial everyday actions. Often he can reduce the dislocation himself. « Any doubt as to diagnosis is quickly resolved by a) the apprehension test. if the patient’s arm is passively placed behind the coronal plane ina Y position of abduction and lateral rotation, his ONG \ immediate resistance and apprehension are pathognomonic. Radiological features: 1. Hill sach’s lesion: Posterolateral humeral head compression fracture 2. Bankart’s lesion: Fracture-dislocation of anteroinferior aspect of glenoid. Treatment: Surgery is indicated for patients having >3 episodes, Commonly done operations are: 1. Bankart's operation: Glenoid labrum and capsule are re-attached to the front of the glenoid rim 2. Arthroscopic Bankart repair: Faster and easier rehabilitation but expensive procedure 3. Putti-Platt operation: Double-breasting of the subscapularis tendon to prevent recurrences, a» AeSupracondylar fracture of humerus: Introduction: This is one of the most serious fractures in childhood as it is often associated with complications. Mechanism: «Fallon outstretched hand «As the hand strikes the ground, the elbow is forced into hyperextension resulting in fracture of the humerus above the condyles The fracture line extends transversely through the distal metaphysis of humerus just above the condyles. Types: Depending upon the displacement of the distal fragment, supracondylar fracture may be of 2 types: A. Extension type (80%): The distal fragment is extended (tilted backwards) in relation to the proximal fragment. B. Flexion type (20%): The distal fragment is flexed (tilted forwards) in relation to the proximal fragment. Displacements and Radiological investigation Commonly, a supracondylar fracture is displaced. The distal fragment may be displaced in the following directions [ Displacements Evident in which view of X Ray? 1. Proximal shift 2. Lateral/ medial shift A-P view. Medial tilt . Proximal shift . Dorsal shift . Dorsal tilt Lateral view Diagnosis: Internal rotation is not visible in X Ray and only diagnosed clinically Chief complaint The child is brought to the hospital with a history of fall on outstretched hand followed by pain, swelling, deformity and inability to move the affected elbow. Examination Early presentation Late presentation Unusual posterior prominence of tip of olecranon (because of dorsal tilt) may be present Since the fracture is supra- condylar, the 3 bony point relationship is maintained, as in a normal elbow. Gross swelling makes the diagnosis difficult Signs of ischemia may be present (5P: Pain, pallor, paresthesia, paralysis, pulselessness) Radial and ulnar pulses may be absent Look for median nerve injury (pointing-index) Look for radial nerve injury (wrist-drop). Classification of supracondylar fracture: Classification Description Type 1 UndisplacedType 2 Angulated fracture with posterior cortex still in continuity Type 20 Distal fragment merely angulated Type 2b Distal fragment is angulated and malrotated Type 3 A completely displaced fracture Treatment of choice according to classification Classification _ Treatment of choice Type1 | Immobilization in plaster slabs for 3 weeks, with elbow in maximal flexion and forearm in pronation that does not jeopardize the radial pulse. Extent of plaster is from deltoid muscle insertion to proximal palmar crease just short of the knuckles, excluding the thumb. Type 2a __| Reduction under general anesthesia by the following step wise maneuver: 1. Traction and counter traction above the elbow 2. Reduction by pressure over olecranon, while maintaining traction 3. Gradual elbow flexion and forearm pronation, while checking radial pulse and capillary return. \ = ® N , % Type 2b & 3 | The fracture should be reduced under general anesthesia as soon as possible, by the method described above, and then held with percutaneous crossed smooth K-wires. Other options for severe fractures: 1. Open reduction 2. Continuous traction (Ex: Dunlop traction).Complication of supracondylar fracture of humerus: Nature Time Name immediate At the time of fracture © Vascular injury © Nerve injury Early Within first 2-3 days of fracture | Volkmann's ischemia Late Weeks to months after fracture | Malunion © Myositis ossificans © Volkmann's ischemic contracture (VIC) Immediate complications Vascular injury Commonly injured artery: Brachial artery Mechanism of injury: The brachial artery is usually injured by the sharp edge of the proximal fragment. « Complications: v Forearm edema and compartment syndrome ¥ Absent pulse ¥ Volkmann's ischemia (ischemic damage to flexors of forearm) ¥ Peripheral gangrene. Definite management options: v Extension of elbow and removal of all dressings Y Repair/ grafting of vessel + fasciotomy ¥ Operative exploration in extreme cases. Nerve injury Commonly injured nerves: ¥ Radial nerve ¥ Median nerve v Ulnar nerve, * Management: Y Loss of function is usually temporary and recovery is expected within 3-4 months. Y If there is no recovery then the nerve should be explored.Early complications Volkmann’s ischemia Introduction: This is an ischemic injury to the muscles and nerves of the flexor compartment of the forearm caused by occlusion of brachial artery by a complicated supracondylar fracture of humerus. Commonly affected muscles: The muscles supplied by the anterior interosseous artery are most susceptible to ischemic damage because this artery is an end-artery. Most commonly affected muscles are the flexor pollicis longus and flexor digitorum profundus (medial-half). Clinical features: Early diagnosis of Volkmann's ischemia is of extreme importance. v Severe pain in the forearm Y Stretch pain: Pain in the flexor aspect of forearm when fingers are extended passively ¥ Inability to move fingers fully Y Tenderness on pressing forearm muscles. Treatment: Volkmann’s ischemia is an emergency of highest order: v Remove any splints or bandages v Elevate the forearm Y Encourage to move the fingers ¥ If no improvement within 2 hours: Perform fasciotomy operation. Late complications Malunion This is the commonest complication of a supracondylar fracture. Cause: ¥ Failure to achieve good reduction ¥ Displacement of the fracture fragment within plaster. Type of deformity: Cubitus varus. Other name: ‘Gunshot deformity’.Treatment: Supracondylar corrective osteotomy (French osteotomy). Myositis ossificans introduction: Itis characterized by ectopic new bone formation around the elbow joint, resulting in stiffness. Cause: Massage following the injury. Treatment: v Early stages: = Elbow is put to rest by an above-elbow slab = Gentle elbow mobilization is started. v Late stages: Treatment options are: * Excision of the myositic bone * Excision arthroplasty of elbow. Volkmann’s ischemic contracture (VIC) Introduction: This is a sequel to Volkmann's ischemia. The ischemic muscles are gradually replaced by fibrous tissue, which contracts and draws the wrist and fingers into flexion, If the peripheral nerves are also affected, there will be sensory loss and motor paralysis in the forearm and hand. Clinical features: (4Ps) ¥ Pain: Pain in the flexor aspect of forearm when fingers are extended Passively. Itis called ‘stretching pain’, ¥ Pallor: Earliest feature. Y Paresthesia: Late feature.Pulselessness: It is not a constant feature of VIC. Volkmann’s sig) = When wrist is flexed, MCP and IP joints can be extended. = When wrist is extended, MCP and IP joints become more flexed. * Treatment: Severity of deformity Treatment options Mild Passive stretching of muscles using Volkmann’s splint Moderate Maxpage operation: Here the flexor muscles are released from their origin at medial epicondyle and ulna | Severe Bone operations such as shortening of the forearm bones, carpal bone excision etc. may be required Fracture clavicle: Introduction: In children the clavicle fractures easily, but it almost invariably unites rapidly without complications. In adults this can be a much more troublesome injury. Classification/ types: Clavicle fractures are usually classified into 3 types on the basis of their location:Fracture clavicle Group 1: Middle thied fracture Group 2: Lateral third fracture (21-28%) Group 3: Medial third fracture (69-82%) (23%) Group 2b Coracoclavicular ligament torn/ ‘detached Group 23: Coracociavicular ligament intact Group 2c: Intra- articular fracture [*Group 2b fractures are unstable and often cause asymptomatic non-union] Mechanism of injury: Cause: Fall on outstretched hand/ shoulder In the common middle third fracture: = The inner half is held upwards by the sternomastoid muscle and * The outer fragment is pulled downwards by the gravity and pull by pectoralis major muscle. In the less common lateral third fracture: = 2a: There is little displacement = 2b: There may be severe displacement.Clinical features: Diagnosis is simple in most cases. There is a history of trauma followed by pain, swelling, crepitus etc, at the site of fracture. One must look for any evidence of neuro-vascular deficit in the upper limb on the affected side. Imaging: © X Ray of shoulder: 1, Antero-posterior view 2. 30° cephalic tilt view * The fracture is usually in the middle third of the bone, and the outer fragment usually lies below the inner. © With medial third fractures it is also wise to obtain X-Rays of the sterno- clavicular joint. Treatment: | Type of fracture Recommendations Middle third | Non-operative management: application of a sling for 1-3 weeks (Group 1) __ | until the pain subsides, followed by mobilization within the limits of pain. Lateral third 2a | Non-operative management: application of a sling for 2-3 (Group 2) weeks until the pain subsides, followed by mobilization within the limits of pain (as group 1). 2b | Surgery to stabilize the fracture (reserved for cases of symptomatic non-union only): Use of a coracoclavicular screw * Plate and hook plate fixation * Suture and sling techniques. Medial third _ | Non-operative management unless the fracture displacement (Group 3) threatens the mediastinal structures. Complications of fracture clavicle: Early complication Late complication Injury to subclavian vessels/ brachial Shoulder stiffness plexus Symptomatic non-unionTennis elbow (lateral epicondalgia): Introduction: Pain and tenderness over the lateral epicondyle of the humerus is a common complaint among tennis players, but even more common in non-players who perform similar activities involving forceful repetitive wrist extension. Pathology: The extensor carpi radialis tendon (which automatically extends the wrist when gripping) is pathological in tennis elbow. Age of presentation: 30-40 years Typical history: Pain comes on gradually, often after a period of unaccustomed activity involving forceful gripping and wrist extension. It is usually localized to the lateral epicondyle, but in severe cases it may radiate widely. It is aggravated by movements such as pouring out tea, turning a stiff door handle, shaking hands or lifting with the forearm pronated, Examination: The elbow looks normal; flexion and extension are full and painless. Characteristically there is localized tenderness at/ just below the lateral epicondyle The pain can be reproduced actively by having the patient extend the wrist with the elbow straight/ passively by stretching the wrist extensors (by the examiner acutely flexing the patient’s wrist with the forearm pronated).Treatment: * 90% of ‘tennis elbows’ will resolve spontaneously within 6-12 months. ‘= The first step is to identify, and then restrict, those activities which cause pain. ‘Symptomatic treatment: The patient is initially treated with analgesics-anti-inflammatory drugs for a week or so. © If there is no response, a local injection of hydrocortisone at the point of maximum tenderness generally brings relief. Operative treatment: Tennis elbow surgery may involve: © Releasing the tendon © Removing inflamed tissue from the tendon * Repairing tendon tears. Dupuytren’s contracture: Introduction: This is a condition characterized by a flexion deformity of one or more fingers due toa thickening and shortening of the palmar aponeurosis. Epidemiology: Dupuytren’s contracture is common in Europeans, epileptics receiving phenytoin, diabetic and cirrhotic patients. Relevant anatomy: ¢ Normally, the palmar aponeurosis is a thin but tough membrane, lying immediately beneath the skin of the palm. * Proximally, it is in continuation with the palmaris longus tendon. « Distally, it divides into slips, one for each finger. The slip blends with the fibrous flexor sheaths covering the flexor tendon of the finger, and extends up to the middle phalanx.Pathoanatomical changes in Dupuytren’s contracture: © The essential problem in Dupuytren’s contracture is proliferation of myofibroblasts, the cause of which remains unknown. * After an initial proliferative phase, fibrous tissue within the palmar aponeurosis slowly contracts, drawing the fingers into flexion at the metacarpophalangeal (MCP) and proximal interphalangeal joints (PIP). © The ring finger is the one affected most commonly. The contracture is generally limited to the medial 3 fingers. 3 e PIP joint MP joint~ MA ‘The Dupuytren’s deformity may not allow the hand to be placed flat on a table top. History and chief complaint: © The patient (usually a middle-aged man) complains of a nodular thickening in the palm. © Gradually this extends distally to involve the ring or little finger. © Pain may occur early on but is seldom a marked feature © The palm is puckered, nodular and thick. © If the subcutaneous cords extend into the fingers they may produce flexion deformities at the MCP and PIP joints. About 60% of patients give a family history. Flexion Contracture of Left Ring Finger Grade2 Grade 3 \_Dupuytren's Contracture—! ‘— Dupuytren’s DiseaseDifferential diagnosis 1. Skin contracture: Previous skin laceration is obvious 2. Tendon contracture: Finger deformity changes with wrist position 3. PIP contracture: History of joint injury. Treatment options: 1. Non-surgical a. High energy radiation therapy (usually X Ray) b. Injection of enzyme (Collagenase clostridium histolyticum) 2. Surgical (from mild to severe cases) a. Needle fasciotomy b. Open fasciotomy c. Fasclectomy under general anesthesia Mallet finger: Introduction: After a sudden flexion injury (e.g. stubbing the tip of the finger), the terminal phalanx droops and cannot be straightened actively. Types of injuries: 2 broad types of injuries can occur in a mallet finger: 1. Avulsion of the most distal part of extensor tendon 2. Avulsion of a bone fragment (small/large) from base of terminal phalanx, Normal Increased tension Mallet ‘of cantral slip f Snaer Tendon ruptureTreatment: The TIP joint should be immobilized in slight hyperextension, using a special mallet-finger splint which fixes the distal joint but leaves the proximal joints free. Duration of splint: 1. For tendon avulsion: 8 weeks constant + 4 weeks only at night 2. For bone avulsion: 6 weeks (as bone heals early than tendon). Complications: 1. Non-union 2. Persistent droop 3. Swan neck deformity. Trigger finger/ Digital Tenovaginosis: Introduction: It is a condition characterized by entrapment of a flexor tendon at the entrance into fibrous digital sheath, preventing free gliding of that contained flexor tendon. Epidemiology: « Female > Male Common age group: 40-60 years Predisposing diseases: 1. Diabetes mellitus 2. Rheumatoid arthritis. Pathophysiology: The flexor tendon can become irritated as it slides through th sheath tunnel. As it becomes more al e tendon nd more irritated, the tendon maythicken and nodules may form, making its passage through the tunnel more difficult. * The tendon sheath may also thicken, causing the opening of the tunnel to become smaller. Symptoms: * Initially, the only symptom is pain at the base of the affected finger, especially on trying to passively extend the finger. cc © Any digit may be affected, but the thumb, — on tendon, ring and middle fingers most commonly; sometimes several fingers are affected. © The affected finger initially remains bent at the PIP joint but with further effort it suddenly straightens with a snap. * A tender nodule can be felt in front of the MCP joint and the click may be reproduced at this site by alternately flexing and extending the finger. Belt loop (pulley) Treatment: Injection of In early stage Lo} cortcosteroitinto tne Lp} Recurtentcses(especity in digital tendon sheath eS . . ‘A second injection is often needed >| Refractory cases L>| ee Tue Fracture olecranon: Introduction: This is usually seen in adults. It results from a direct injury as in a fall onto the point of the elbow.Clinical Presentation: Patients typically present with the upper extremity supported by the contralateral hand with the elbow in relative flexion. Clinical evaluation: « Look: Abrasions over olecranon or hand can be indicative of the mechanism of injury * Feel: Palpable defect at fracture site * Move: Inability to extend the elbow actively against gravity indicates discontinuity of triceps mechanism * Neurosensory evaluation: Associated ulnar nerve injury is possible, especially with comminuted fractures from high-energy injuries. Mayo classification of olecranon fracture with treatment options of choice: Type | Subtype Description Treatment of choice 1 1A _| Non-comminuted | Long arm cast or posterior splint (Nondisplaced) 1B Comminuted with early mobilization 2 (Displaced, 2A | Non-comminuted Tension band wiring/ stable): intramedullary fixation Most common 28 Comminuted Tension band wiring + Additional type interfragmentary plate & screw fixation/ Fragment excision & triceps advancement (in elderly) 3 (Displaced, 3A__|Non-comminuted | _ Rigid plate and screw fixation unstable) 38 Comminuted Rigid plate & screw fixation + External fixator + Bone graft Complications: 1. Hardware prominence requiring removal (most common) . Stiffness . Non-union }. Miscellaneous: BWN a. Ulnar neuropathy b. Post-traumatic arthritisc. Infection d. Heterotopic ossification. Carpal tunnel syndrome: Definition: It is a syndrome characterized by compression of median nerve as it passes beneath the flexor retinaculum. Age group involved: 40-50 years, common in females. Thenar Flexor muscles retinaculum Hypothenar Causes: MEDIAN TRAP = Myxoedema = Edema premenstrually = Diabetes = Idiopathic = Agromegaly * Neoplasm = Trauma = Rheumatoid arthritis = Amyloidosis = Pregnancy.