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Short Notes of Orthopaedics
Edited by:
Prithwiraj Maiti, MBBS
House physician
Department of Internal Medicine, R.G.Kar Medical College
Author: ͞ An Ultimate Guide to Community Medicine͟
Author: ͞ A Practical Handďook of Pathology Specimens and Slides͟
[Both published by Jaypee Brothers Medical Publishers, India]
Table of contents Chapters Contents Page no. General principles of orthopaedics
Compound fracture [14, supple], Non-union of fracture [13, supple], Non-union of closed fracture [09, supple], Compartment syndrome [12, supple], Crush syndrome [06], Fat embolism [09], Myositis ossificans [09], Pathological facture [09] [15], Stress fracture [08, supple], Classification of nerve injuries [06]
Infections of bones and joints
Pyogenic Osteomyelitis [12], Aetiopathogenesis of acute osteomyelitis [09], Sequestrum [08] [11, supple] [12, supple], Ring sequestrum [16], Brodie’s Aďscess [11] [14, supple], TB hip joint [10, supple]
Upper limb Fractures occurring due to fall on outstretched hand [14], VolkmaŶŶ’s ischaeŵic CoŶtracture [06] [08] [13] [10, supple] [15], Colles fracture [13] [08, supple], Monteggia fracture-dislocation [13, supple], Shoulder dislocation [06] [11], Recurrent dislocation of shoulder [13, supple], Supra condylar fracture of Humerus [12] [16], Complication of supracondylar fracture of humerus [08] [09, supple],
Fracture clavicle [12], Tennis Elbow [12],], DupuytreŶ’s contracture [12] [10, supple], Mallet finger [12], Trigger finger [11], Fracture olecranon [12, supple], Carpal tunnel syndrome [11] [09] [13, supple] [14, supple] [16], Frozen shoulder [08] [11, supple] [14, supple], De QuervaŶ’s disease [08] [11, supple] Lower limb Fracture of patella [14] [08, supple], Mechanism of patellar fracture [11], Ruptured Tendoachilles [12], Avascular necrosis of femoral head [10, supple], Fracture neck femur- types and complication [09]
Spine and vertebra Slipped disc [12, supple], Spondylolisthesis [10], TB spine [10], Clinical feature of TB spine [08, supple], Gibbus [08, supple], Spina bifida [14][09]
Paediatric age group Greenstick fracture [14], CTEV/ Clubfoot [08] [13, supple] [11, supple] [10, supple]
Bone cysts and tumours
Osteochondroma/ Exostosis [14] [15] [10], EwiŶg’s tuŵour [13] [11] [10] [14, supple], Radiological features of osteosarcoma [12, supple], Management of osteosarcoma [09, supple], Giant cell tumor [10, supple] [16], Bone cyst [08, supple]
Miscellaneous Bone graft [13], External fixation [13, supple], Indications of limb amputation [12, supple] [09, supple], Ideal amputation stump [15] [06], CodŵaŶ’s triaŶgle [11, supple], Bone scan [10], Paget’s disease of ďoŶe [09, supple], Tension band wiring [09, supple], SP Nail [11, supple]
References: Essential Orthopaedics by J.Maheshwari (5ed), Apley’s System of Orthopaedics and Fractures (9ed), Handbook of Orthopedic Examination by K. Banerjee (5ed), Radiopaedia.org and others. Disclaimers: This document is created for helping the undergraduate MBBS students for examination purpose. The pictures used in this document are property of the authors/ publishers and used here solely for educational, non- commercial use.
Treatment:
Principles and steps of treatment:
- Primary survey and early resuscitation
- Bleeding control (by direct pressure)
- Temporary immobilization of the fracture
- 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: 1st Generation cephalosporin [type 1 and 2] ± Aminoglycoside [type 3])
- Thorough wound debridement (Wound exploration + detection and removal of foreign material + nonviable tissue + bacterial contamination)
- Repair damaged structures (Consult CTVS surgeon in case of major vascular injury/ plastic surgeon in case of nerve/ tendon injury)
- 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).
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:
- Atrophic non-union : Osteogenesis seems to have ceased. The bone ends are tapered or rounded with no suggestion of new bone formation.
- Hypertrophic non-union : Bone ends are enlarged, suggesting that osteogenesis is still active but not quite capable of bridging the gap.
Etiological/ Risk factors:
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
- Soft tissue bleeding from fractures/ operations
- Prolonged compression by tight plaster/ bandage
- 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 1/3rd^ of tibia, multiple fractures of hand and foot.
Pathophysiology:
The increased pressure within the compartment compromises the circulation leading to further muscle ischemia. A vicious-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.
Types:
According to the progression, compartment syndrome may be of 2 types:
1. Acute: Edž: VolkŵaŶŶ’s coŶtracture 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:
I. Often a H/O a risk factor (fracture/ operation/ compression/ infection) is present II. 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). III. Stretch test : This is the earliest sign of impending compartment syndrome. The ischemic muscles, when stretched, give rise to pain. It is 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:
Confirmation of the diagnosis can be made by measuring the intra- compartmental pressure. A differeŶtial pressure (ΔP) – the difference between diastolic pressure and compartment pressure – of <30 mmHg is an indication for immediate compartment decompression.
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. A high 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. If a 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 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.
Causes of pathological fractures at different ages:
Age Most common cause(s) At birth Osteogenesis imperfecta 0-5 years (^) Osteogenesis imperfecta Osteomyelitis 5-20 years Osteomyelitis Primary bone cyst Primary bone malignancy 20-50 years Cystic lesions of bone Malignancy Osteomalacia Giant cell tumor After 50 years Osteoporosis Multiple myeloma Metastasis to the bones
Diagnostic clues:
A fracture without a significant trauma. A history 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. c. 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:
1. 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). b. CA 125 (Ovarian cancer). c. CA 15-3 (Breast cancer). d. β2-Microglobulin (Lymphoma). e. Alpha-fetoprotein (Hepatocellular cancer). f. PSA (Prostatic cancer). Assessment of the capacity of fractured bone to unite
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:
- Bisphosphonates.
- Radiotherapy.
- Pain control.
- DVT control.
- Splints/ traction/ braces etc.
Operative treatment options:
- Internal fixation : Preferable intra-medullary fixation with/ without bone grafting/ cementing (in case of big cavities),
- Resection and replacement. Note : Surgery should be followed by postoperative radiotherapy to prevent recurrences.
Best diagnostic test for bilateral stress fracture is bone scan : will show increased activity at the painful spot. Note: The great danger is a 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: SeddoŶ’s classificatioŶ (1942): Term Description Example Neurapraxia A reversible physiological nerve conduction block with loss of some types of sensation and muscle power followed by spontaneous recovery within a few days or weeks.
Saturday night palsy
Axonotmesis Axonal interruption with loss of conduction but the nerve is in continuity and the neural tubes are intact. Distal to the lesion, axons disintegrate and are resorbed by phagocytes. This phenomenon is called Wallerian degeneration. Recovery takes months to occur.
Closed fracture and dislocations
Neurotmesis When the injury is more severe, whether the nerve is in continuity or not, recovery will not occur. 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 segment. Instead, regenerating fibers mingle with proliferating Schwann cells aŶd fiďroďlasts iŶ a juŵďled kŶot or ͚ neuroma ’ at the site of injury.
Open wound
Even after surgical repair, many new axons fail to reach the distal segment.
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. Out of the cortex: The pus travels along VolkŵaŶŶ’s caŶals aŶd coŵes to lie suď-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: C‘P↑, ES‘↑, WBC couŶt↑ (PMN leucocytes) X-Ray: Earliest classic sign is periosteal new bone formation at the metaphysis (by the 2nd^ 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 + 3rd^ gen. cephalosporin* 6 months- 6 years -Do- Older children + previously fit adults
IV (Floxacillin + Fusidic acid)
Elderly + previously unfit adults
IV (Floxacillin + 2nd/3rd^ gen. cephalosporin)
Sickle cell disease IV (3rd^ gen. cephalosporin/ fluoroquinolone~) Drug addicts/ HIV -Do- MRSA IV (Vancomycin + 3rd^ 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:
- Chronic osteomyelitis
- Acute pyogenic arthritis
- Pathological fracture
- Growth plate disturbances causing deformity of the limb.
Chronic osteomyelitis
Causes:
- Delayed and inadequate treatment
- Reduced host resistance (malnutrition/ HIV etc.)
