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Orthopaedic Surgery - Osteochondritis Dissecans of the Knee
Basics
Osteochondritis dissecans (OCD) of the knee is a disorder of the subchondral bone and overlying articular cartilage in which a localized segment of subchondral bone becomes abnormal and may eventually separate from the surrounding bone.
The process can lead to:
Cartilage injury
Fragment instability
Loose-body formation
Secondary osteoarthritis
The knee is the most commonly affected joint, although OCD can also occur in the:
Elbow, particularly in throwing athletes and gymnasts
and
Ankle, where lesions may be associated with recurrent instability or trauma.
Age at Presentation
OCD occurs most commonly during the:
Second decade of life
but can also occur in younger children and adults.
Lesions that develop before skeletal maturity are referred to as:
Juvenile OCD
whereas lesions in skeletally mature patients are generally considered:
Adult OCD.
Healing potential is better when the growth plates remain open.
Older adolescents and adults are less likely to heal with nonoperative treatment alone.
Common Locations
The classic location is the:
Posterolateral aspect of the medial femoral condyle, accounting for approximately 65% of lesions.
Other reported sites include:
Inferocentral lateral femoral condyle – approximately 30%
Patella – approximately 2%
Lateral femoral trochlea – approximately 2%
Central trochlea – less than 1%
Lateral tibial plateau – less than 1%
Epidemiology
OCD is uncommon.
Historical incidence has been estimated at approximately:
10 cases per 100,000 population.
It is more common in:
Males
than females.
Bilateral Disease
Approximately:
8–30% of patients
may have bilateral lesions.
For this reason, the contralateral knee should be considered during clinical and radiographic evaluation.
Risk Factors
Potential risk factors include:
High levels of sports participation
Repetitive mechanical stress
Abnormal mechanical axis
Discoid meniscus
Generalized ligamentous laxity
Obesity
Abnormal intraosseous blood supply
Genetics
Familial clustering has been reported.
However, most cases do not follow a clearly established Mendelian inheritance pattern.
Etiology
The exact cause is probably multifactorial.
Proposed contributing mechanisms include:
Repetitive microtrauma
Subchondral ischemia
Abnormal biomechanics
Altered vascular supply
Genetic susceptibility
Repeated loading may impair the integrity of the subchondral bone, eventually compromising the overlying cartilage.
Diagnosis
Diagnosis is based on:
History
Physical examination
Radiographs
and often
MRI.
Signs and Symptoms
Early lesions commonly present with:
Insidious, activity-related knee pain.
The pain may be vague and poorly localized.
Late Symptoms
As the lesion becomes unstable, patients may develop:
Swelling
Catching
Locking
Mechanical clicking
These symptoms may indicate:
Fragment instability or loose-body formation.
History
Important questions include:
Duration of symptoms
Activity-related pain
Participation in repetitive or high-impact sports
Episodes of swelling
Locking or catching
Previous knee injury
Previous treatment
Physical Examination
A complete knee examination should be performed.
Range of Motion
Assess:
Flexion
Extension
and any:
Painful or mechanical restriction.
Tenderness
Localized tenderness may be present over the involved femoral condyle.
Effusion
Joint effusion should be graded as:
Mild
Moderate
or
Large.
Effusions are more common when the lesion is unstable or when there is significant cartilage irritation.
Meniscal Examination
The McMurray test can be used to assess for associated meniscal pathology.
Ligament Examination
The Lachman test should be performed to assess for ACL injury when appropriate.
Gait
An:
Antalgic gait
may be present.
Muscle Atrophy
Chronic symptoms may lead to:
Quadriceps or thigh atrophy.
Contralateral Knee
Because bilateral lesions are not uncommon, the opposite knee should be examined.
Imaging of the contralateral side may be considered when clinically appropriate.
Imaging
Plain Radiographs
Initial radiographs commonly include:
AP
Lateral
Tunnel
Merchant or patellofemoral views
Tunnel View
The tunnel view is commonly obtained with the knee flexed approximately:
45°
and improves visualization of the posterior femoral condyles, where classic OCD lesions frequently occur.
Merchant View
The Merchant or patellofemoral view helps assess uncommon OCD lesions involving the:
Trochlea
or
Patella.
Bilateral Imaging
Bilateral radiographs can be obtained when there is concern for:
Contralateral involvement.
Physeal Status
The growth plates should be evaluated carefully.
Open physes are generally associated with:
Better healing potential and a more favorable prognosis.
Early Radiographic Findings
Early lesions may appear as:
A localized area of radiolucency or subchondral irregularity.
Late Radiographic Findings
Chronic or more advanced lesions may demonstrate:
Subchondral cysts
Sclerotic margins
Fragmentation
Separation of the osteochondral fragment
A prominent sclerotic rim may indicate reduced healing potential.
Radiographic Healing
Healing is suggested by:
Resolution of radiolucency
Progressive incorporation of the lesion
Disappearance of cystic or fragmentary changes
MRI
MRI is particularly useful for:
Characterizing the lesion
Assessing stability
Measuring lesion size
Evaluating cartilage
Detecting loose bodies
Identifying associated knee pathology
MRI Findings
Important features include:
Bone marrow edema
Lesion dimensions
Subchondral cysts
Fluid beneath the fragment
Articular cartilage defects
Loose bodies
MRI Classification
A commonly used MRI staging system includes:
Stage I
There is:
Small or poorly defined signal alteration without clear lesion margins.
Stage II
The OCD fragment has:
Well-defined margins
but there is:
No fluid between the fragment and underlying bone.
Stage III
Fluid is:
Partially visible between the fragment and underlying bone.
This raises concern for partial instability.
Stage IV
Fluid:
Completely surrounds the fragment.
This strongly suggests instability.
Stage V
The fragment is:
Displaced.
MRI Signs of Instability
Features associated with an unstable lesion include:
A high-signal line greater than approximately 5 mm between the lesion and underlying bone
A homogeneous high-signal area greater than approximately 5 mm beneath the lesion
A focal articular-surface defect greater than approximately 5 mm
A high-signal line extending through the subchondral plate into the lesion
Fluid Behind the Fragment
A high-signal fluid line behind the fragment is particularly concerning for:
Loss of attachment and instability.
It is also commonly seen in lesions that fail nonoperative treatment.
MRI Accuracy
MRI is highly sensitive for detecting instability.
However, specificity is lower in skeletally immature children because:
Normal developmental vascularity and ossification patterns may mimic instability.
Thus, MRI findings should be interpreted together with:
Age, symptoms, radiographs, and clinical course.
Pediatric Considerations
In children younger than approximately 7 years, irregularities of the distal femoral ossification center may resemble OCD.
These normal developmental variants should not be mistaken for pathological lesions.
Pathological Findings
Pathology may show:
An osteochondral fragment composed of articular cartilage with attached abnormal or necrotic subchondral bone.
If separation progresses, the fragment may become unstable and eventually detach.
Differential Diagnosis
Stress Fracture
Stress injury may cause activity-related pain but often has a different imaging pattern.
Some stress fractures present more acutely.
ACL Injury
ACL injury is suggested by:
Instability
and
A positive Lachman test.
Normal Ossification Variant
Young children may have physiologic irregularity of the distal femoral epiphysis that resembles OCD on radiographs.
Meniscal Injury
Meniscal tears may produce:
Locking
Catching
Joint-line pain
and a:
Positive McMurray test.
Osteonecrosis
Spontaneous or secondary osteonecrosis of the knee may enter the differential diagnosis, particularly in adults.
Potential risk factors include:
Corticosteroid exposure
Alcohol use
Other causes of impaired bone blood supply
Treatment
General Principles
Treatment depends on:
Age
Physeal status
Lesion size
Location
Stability
Symptoms
Radiographic stage
Favorable Lesions
The lesions most likely to heal without surgery are:
Small
Stable
Covered by intact cartilage
and present in:
Skeletally immature patients with open physes.
Unstable Lesions
An unstable or detached lesion generally requires:
Operative treatment, regardless of skeletal maturity.
Nonoperative Treatment
Conservative management is preferred initially for many stable lesions that present before physeal closure.
Very small lesions may sometimes be treated with:
Observation and activity modification alone.
Three-Phase Nonoperative Protocol
A structured three-phase treatment approach can be used.
Phase 1: Initial Protection
During approximately the first 6 weeks, treatment may include:
Knee immobilizer or cast
Unloader brace
Crutch-assisted or protected weight bearing
The patient should become:
Pain-free before progressing.
Radiographs are generally repeated at the end of this phase.
Phase 2: Rehabilitation
From approximately 6–12 weeks:
Weight bearing is progressively increased as tolerated
Immobilization is discontinued
Physical therapy begins
The focus is on:
Knee range of motion
Quadriceps strengthening
The patient should remain pain-free before further activity progression.
Repeat radiographs may be obtained.
Phase 3: Return to Activity
Beginning around:
3 months
activity is gradually advanced under supervision.
Impact Restrictions
High-impact and shear-loading activities should remain restricted until the patient has:
No pain
No swelling
Improving imaging findings
and has remained symptom-free for a sustained period.
Repeat MRI
MRI may be repeated when:
Healing is uncertain
Symptoms persist
Instability is suspected
Return to sport is being considered
Failed Nonoperative Treatment
If the lesion progresses, symptoms recur, or imaging demonstrates instability, immobilization may be resumed or surgery may be considered.
Surgery
Surgery is recommended for:
Detached lesions
Unstable lesions
Displaced fragments
Relative Surgical Indications
Surgery may also be considered for:
Symptomatic patients approaching physeal closure who fail conservative treatment
Stable lesions that show no healing after approximately 6–9 months
Arthroscopic Drilling
Drilling is most appropriate for:
Stable lesions with intact articular cartilage.
Mechanism of Drilling
Small channels are created through or around the lesion to stimulate:
Revascularization and bone healing.
Techniques include:
Transarticular drilling
and
Retrograde drilling through the epiphysis.
Drilling Outcomes
Historical series report healing in approximately:
85% of patients with open physes
and
75% of patients with closed physes.
Factors Associated With Failure
Less favorable results have been associated with:
Atypical lesion location
Multiple lesions
Underlying medical disorders
Skeletal maturity
Fragment Reduction and Fixation
Unstable but salvageable fragments may be:
Reduced anatomically and fixed.
Bone Grafting
If there is subchondral bone loss, the crater may be filled with:
Autologous bone graft
before or during fragment fixation.
Fixation Options
Possible implants include:
Headless compression screws
Conventional screws
Osteochondral plugs
MRI-compatible implants are preferred when future MRI surveillance is anticipated.
Chronic Loose Fragments
Longstanding detached fragments may have:
Poor vascularity
Altered shape
Poor healing potential
and may not be suitable for fixation.
Unsalvageable Lesions
If the fragment cannot be preserved, treatment is based on the size of the residual defect.
Marrow Stimulation
For smaller defects, options include:
Drilling
Abrasion arthroplasty
Microfracture
These techniques stimulate marrow-derived cells and produce:
Fibrocartilage repair tissue.
Osteochondral Plug Transplantation
Autologous or allograft osteochondral transplantation may be used for:
Moderate-sized defects, particularly those unsuitable for simple marrow stimulation.
Historically, lesions under approximately:
2 cm in diameter
have often been considered for osteochondral plug techniques.
Autologous Osteochondral Transfer
Healthy osteochondral plugs are harvested from a low-load portion of the patient’s knee and transplanted into the defect.
This restores:
Subchondral bone and hyaline cartilage.
Osteochondral Allograft
Larger defects may be reconstructed using:
Fresh osteochondral allograft tissue.
This avoids donor-site morbidity but introduces considerations related to:
Graft availability and incorporation.
Autologous Chondrocyte Implantation
Autologous chondrocyte implantation may be considered for:
Large cartilage defects
particularly in:
Skeletally mature patients.
Cartilage cells are harvested, cultured, and later implanted into the defect.
Follow-Up
Stable lesions treated nonoperatively require close surveillance to determine whether they are:
Healing
Remaining unchanged
or
Becoming unstable.
Imaging Follow-Up
Serial radiographs or MRI may be obtained approximately every:
3–6 months
depending on symptoms, lesion characteristics, and treatment.
Prognosis
Small, stable, nondisplaced lesions in patients with:
Open growth plates
have the best prognosis and often heal.
Poor Prognostic Factors
Less favorable outcomes are associated with:
Skeletal maturity
Large lesions
Unstable lesions
Displaced fragments
Sclerotic margins
Failure of prolonged conservative treatment
Long-Term Outcome
Large or unstable lesions that fail to heal may result in:
Persistent symptoms and early degenerative osteoarthritis.
Complications
Potential complications include:
Persistent OCD despite treatment
Nonunion of a repaired fragment
Progression from stable to unstable lesion
Loose-body formation
Loss or displacement of fixation hardware
Failure or displacement of osteochondral plugs
Overgrowth or hypertrophy of cartilage repair tissue
Secondary osteoarthritis
Patient Monitoring
Patients should be monitored for:
Pain
Effusion
Mechanical symptoms
Range of motion
Quadriceps strength
Radiographic healing
Development of instability
Return to impact sports should occur only after clinical and imaging evidence suggests satisfactory healing.
Key Principle
Osteochondritis dissecans of the knee is a subchondral bone disorder that may secondarily compromise the overlying articular cartilage.
The most important treatment determinants are:
Skeletal maturity and lesion stability.
Small, stable lesions in patients with open physes often heal with protected activity and rehabilitation, whereas:
Unstable, detached, displaced, or persistently symptomatic lesions usually require surgical treatment.
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Orthopaedic Surgery - Metacarpal Fracture
Basics
A metacarpal fracture is a break involving one of the five metacarpal bones of the hand, which form the skeletal base of each digital ray.
These fractures are classified according to the anatomic location of the break:
Head
Neck
Shaft
Base
A fracture through the neck of the fifth metacarpal is commonly called a boxer’s fracture because it often results from striking an object with a clenched fist.
Boxer’s Fracture
A boxer’s fracture is usually a fracture through the neck of the fifth metacarpal.
The classic mechanism is:
Axial loading through the fifth metacarpophalangeal joint during a punch.
The fracture typically develops an apex-dorsal angulation.
Thumb Metacarpal Fractures
Fractures involving the base of the thumb metacarpal are commonly divided according to:
Whether the fracture is intra-articular or extra-articular and the degree of comminution.
Several characteristic patterns have eponymous names.
Bennett Fracture
A Bennett fracture is an intra-articular fracture-dislocation of the base of the first metacarpal.
A volar-ulnar fragment remains attached to the carpometacarpal joint, whereas the remainder of the metacarpal base is displaced by deforming muscular forces.
Because of this displacement, Bennett fractures are inherently unstable.
Rolando Fracture
A Rolando fracture is a comminuted intra-articular fracture of the first metacarpal base.
The classic pattern is Y- or T-shaped and involves the thumb carpometacarpal joint.
Rolando fractures generally have a worse prognosis than simple Bennett fractures because of the degree of articular comminution.
Epidemiology
Metacarpal fractures are among the most common injuries of the hand.
They account for approximately 20% of upper-extremity fractures in older epidemiologic studies.
An estimated 264,000 cases per year have historically been reported in the United States.
Age and Sex
These injuries occur most frequently in:
Male patients between approximately 15 and 55 years of age.
Risk Factors
Common risk factors include:
Fighting
Contact sports
Falls
Bicycle injuries
Occupational hand trauma
Etiology
Metacarpal fractures may result from:
Direct trauma
Crush injury
Axial loading through the metacarpal head
Axial loading is a particularly common mechanism.
Sports Injuries
Sport-related trauma can produce:
Neck, shaft, or base fractures, depending on the direction and magnitude of force.
Falls and Bicycle Injuries
A fall onto the hand or direct impact during a bicycle accident can produce metacarpal fractures, sometimes with associated soft-tissue injury.
Diagnosis
Signs and Symptoms
The diagnosis is usually established by combining:
History, physical examination, and plain radiographs.
Patients commonly complain of:
Pain, swelling, bruising, and deformity, most prominently over the dorsum of the hand.
Physical Examination
Inspection
Look for:
Swelling
Ecchymosis
Loss of normal knuckle contour
Angular deformity
Open wounds
Metacarpal Shortening
Shortening may cause an apparently absent or flattened knuckle when the patient makes a fist.
The involved metacarpal head may appear recessed compared with adjacent digits.
Rotational Alignment
Rotation is one of the most important components of the examination.
Assess the finger cascade both:
At rest and during active fist formation.
Normally, the fingers converge toward the scaphoid region without crossing.
Malrotation
Any overlap or scissoring of the fingers suggests rotational deformity.
Unlike some degree of angulation, clinically evident malrotation is not acceptable because it substantially affects hand function.
Neurovascular Examination
Document:
Capillary refill
Digital perfusion
Light-touch sensation
Two-point discrimination
Motor function should also be assessed when possible.
Skin Examination
Any break in the skin must be examined carefully.
The clinician should determine whether the injury represents an open fracture.
Fight Bite Injury
An apparently small laceration over the MCP joint after punching another person may represent a human bite injury involving the joint or metacarpal head.
These injuries are potentially serious because a tooth may penetrate the:
Skin, extensor mechanism, joint capsule, and articular surface.
They require urgent recognition and treatment.
Laboratory Tests
Routine laboratory tests are not required for uncomplicated closed metacarpal fractures.
Laboratory investigations may be appropriate if infection or another systemic issue is suspected.
Imaging
Plain radiographs are the standard initial study.
Obtain:
AP
Lateral
Oblique views
True Lateral View
A true lateral radiograph is particularly important for assessing:
Fracture angulation.
Focused Views
Dedicated views centered on the involved metacarpal may provide better definition of:
Fracture pattern, displacement, comminution, and articular involvement.
Pathological Findings
Acute fracture produces:
Disruption of the cortex and periosteum with hematoma formation.
Healing subsequently progresses through:
Callus formation, consolidation, and remodeling.
Differential Diagnosis
Important alternatives or associated injuries include:
MCP joint dislocation
Extensor tendon injury
Flexor tendon injury
Soft-tissue contusion
Ligament injury
Treatment
General Principles
Most metacarpal fractures can be treated nonoperatively if:
Alignment is acceptable, rotation is normal, the fracture is stable, and there is no important articular displacement.
Treatment commonly consists of:
Reduction when required, splinting or casting, followed by early range-of-motion exercises.
Immobilization
Many uncomplicated fractures are immobilized for approximately 3 weeks, although the exact duration depends on stability, location, and symptoms.
Prolonged immobilization should be avoided because it increases the risk of stiffness.
Intrinsic-Plus Position
When the fingers are included in the splint, the hand is traditionally immobilized in the intrinsic-plus or safe position.
This generally places the:
MCP joints in flexion and the interphalangeal joints relatively extended.
This position helps maintain collateral ligament length and reduces the risk of stiffness.
However, several studies have found little difference in final outcomes among different splinting techniques for many stable fractures.
Initial Symptomatic Care
Initial management should also include:
Ice
Elevation
Analgesia
These measures reduce swelling and discomfort.
Reduction
Closed reduction is performed when angulation, shortening, or displacement exceeds acceptable limits.
The patient should be advised that surgery may become necessary if satisfactory reduction:
Cannot be obtained or cannot be maintained.
Acceptable Angulation: Metacarpal Neck Fractures
Acceptable apex-dorsal angulation increases from the radial to ulnar side because the ring and small-finger CMC joints permit greater compensatory motion.
Reasonable historical guidelines are:
Index metacarpal: approximately 10°
Long metacarpal: approximately 10°
Ring metacarpal: approximately 20–30°
Small-finger metacarpal: approximately 40–70°
Clinical function, fracture stability, shortening, and rotation must also be considered.
Acceptable Angulation: Metacarpal Shaft Fractures
Shaft fractures generally tolerate less deformity than neck fractures.
Approximate historical limits are:
Index metacarpal: essentially no significant angulation
Long metacarpal: essentially no significant angulation
Ring metacarpal: approximately 20°
Small-finger metacarpal: approximately 30°
Rotation
Unlike angular deformity:
No clinically significant rotational deformity should be accepted.
Even a small amount of metacarpal rotation may produce major overlap of the fingertip during flexion.
Intra-Articular Fractures
Fractures involving a joint surface require particularly careful assessment.
Significant:
Articular step-off, displacement, or instability
may require operative reduction.
The goal is to restore joint congruity and reduce the risk of post-traumatic arthritis.
Open Fractures
Open metacarpal fractures require prompt treatment.
Management may include:
Antibiotics
Tetanus prophylaxis when appropriate
Irrigation
Surgical débridement
Fracture stabilization
Fight-Bite Injuries
Human-bite injuries over the MCP joint are treated aggressively because of the high risk of infection.
Treatment commonly includes:
Early antibiotics, surgical irrigation and débridement, and evaluation of the joint, tendon, and bone.
Fracture Healing
Most uncomplicated metacarpal fractures achieve substantial union within approximately 6–8 weeks.
Clinical healing and functional recovery may occur at different rates.
Physical Therapy
Early motion is important.
Finger Range of Motion
Gentle active and passive exercises should begin as soon as fracture stability permits.
For many fractures, finger motion should begin within approximately 3 weeks of injury, and often earlier if fixation is stable.
Wrist Motion
Wrist range of motion should also be restored progressively when immobilization no longer requires restriction.
Goals of Rehabilitation
Therapy aims to restore:
Finger flexion and extension
Wrist motion
Grip strength
Tendon excursion
Fine motor function
Surgery
Operative treatment includes:
Closed reduction with percutaneous fixation
and
Open reduction with internal fixation.
Surgical Goals
The goals are:
Stable reduction
Preservation of length and rotation
Minimal soft-tissue disruption
Early mobilization
Indications for Surgery
Operative treatment is considered for:
Unstable fractures
Multiple metacarpal fractures
Significantly displaced intra-articular fractures
Open fractures
Unacceptable angulation
Metacarpal shortening with functional consequences
Any persistent malrotation
Failure of closed reduction
Loss of reduction during follow-up
Surgical Fixation Options
Fixation methods include:
Percutaneous Kirschner wires
Plate-and-screw fixation
Lag screws
Intramedullary fixation
External fixation
The choice depends on fracture pattern, location, soft-tissue condition, and surgeon preference.
Percutaneous Pinning
K-wire fixation provides relatively minimally invasive stabilization and is commonly used for:
Neck, shaft, and base fractures.
Pins may be placed transversely, intramedullary, or across adjacent metacarpals depending on the injury.
Plate and Screw Fixation
Plate fixation provides rigid stability and is particularly useful when:
Length or rotational stability cannot otherwise be maintained
or
The fracture is comminuted or associated with bone loss.
Because plates require greater soft-tissue exposure, they may have a higher risk of tendon irritation, adhesions, and stiffness than less invasive methods.
Intramedullary Fixation
Intramedullary devices can provide stable fixation of selected:
Metacarpal neck or shaft fractures
while limiting soft-tissue dissection.
External Fixation
External fixation is rarely required but may be useful when there is:
Severe comminution, major bone loss, extensive soft-tissue injury, or an open high-energy fracture.
Thumb Metacarpal Base Fractures
Bennett Fracture
Bennett fractures are often treated surgically because they are inherently unstable.
Nonoperative treatment may be appropriate only when:
Displacement is minimal and joint congruity can be maintained reliably.
Fixation
Percutaneous pinning is a common technique.
Other options include:
Screw fixation or open reduction, depending on fragment size and displacement.
Rolando Fracture
Comminuted intra-articular fractures of the thumb base are more difficult to reconstruct.
Treatment may involve:
K-wires, screws, plates, or external fixation, depending on the number and size of fragments.
Follow-Up
Radiographic Monitoring
Radiographs are commonly obtained approximately 1 week after reduction to confirm maintained alignment.
Repeat imaging may be performed another 2–3 weeks later or according to fracture stability.
Early Motion
Finger motion should begin early, generally within approximately 3 weeks, and often earlier when fixation permits.
The goal is to prevent:
MCP and interphalangeal stiffness and tendon adhesions.
Prognosis
The overall prognosis is good to excellent for most appropriately treated metacarpal fractures.
Stable fractures treated nonoperatively generally heal well with useful hand function.
Percutaneous Fixation Outcomes
K-wire and intramedullary fixation can provide excellent results for:
Metacarpal neck fractures.
K-wire fixation can also produce good outcomes in:
Shaft and base fractures.
Plate Fixation Outcomes
Plate fixation provides strong stability but may have a higher complication burden than nonoperative care or less invasive fixation.
Nevertheless, it can be essential for:
Unstable, comminuted, or bone-loss fractures.
Thumb Base Fracture Prognosis
Bennett fractures generally have good results when:
Articular alignment and CMC stability are restored.
Comminuted Rolando-type fractures have a less favorable prognosis because articular reconstruction is more difficult.
Complications
Soft-Tissue Injury
The original trauma may damage:
Skin, tendons, nerves, and soft tissues.
Repeated aggressive reduction attempts can worsen this injury.
Tendon Dysfunction
Flexor or extensor tendons may develop:
Adhesions, reduced excursion, or mechanical irritation.
Metacarpal shortening can also alter tendon mechanics.
Malunion
Malunion may produce:
Angular deformity, shortening, or rotation.
Rotational malunion is particularly poorly tolerated because it causes digital overlap during grip.
MCP Stiffness
Immobilizing the MCP joint in excessive extension may allow the collateral ligaments to shorten.
This can produce persistent stiffness.
Early motion and appropriate positioning help reduce this risk.
Surgical Complications
Potential complications include:
Infection
Delayed wound healing
Sensory nerve injury
Tendon irritation or adhesions
Hardware prominence
Loss of fixation
Joint stiffness
Patient Monitoring
Follow-up should assess:
Pain, swelling, rotational alignment, fracture stability, neurovascular status, and finger motion.
Radiographs are used to confirm maintenance of reduction and progression of healing.
Key Principle
Successful treatment of metacarpal fractures depends less on eliminating every degree of angulation than on preserving:
Rotation, length, joint congruity, stability, and early finger motion.
In particular, malrotation should not be accepted, because even modest rotational deformity can substantially impair hand function.
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I. Definition & Epidemiology:
- Definition: Parkinson's disease is a neurodegenerative disorder. Clinically, it's characterized by parkinsonism (a group of motor symptoms); histologically (microscopically), it's defined by neuronal loss in the brain and the presence of Lewy bodies (abnormal protein aggregates) concentrated in the substantia nigra. Crucially, parkinsonism itself is not diagnostic of Parkinson's Disease.
- Epidemiology: Primarily affects the elderly. Prevalence is approximately 1% in individuals over 60 years old.
- Mostly Unknown: The cause of most Parkinson's cases remains unclear.
- Genetic Factors (Rare Cases): Rarely, inherited mutations in the PARK1 gene (chromosome 4), which codes for α-synuclein (a protein component of Lewy bodies), are implicated.
- Dopamine Deficiency: Neurons in the substantia nigra project to the putamen and globus pallidus (basal ganglia structures crucial for movement). These neurons release dopamine, a neurotransmitter essential for controlling movement. In Parkinson's, dopamine release is significantly reduced.
- Movement Disorder: The lack of dopamine leads to the characteristic movement disorders.
- Parkinsonism: The classic triad of symptoms includes:
- Tremor: Involuntary shaking.
- Rigidity: Stiffness and resistance to movement.
- Bradykinesia: Slowness of movement.
- Important Note: Parkinsonism can result from various causes (drugs, toxins, infections, trauma) and isn't solely indicative of Parkinson's disease.
- Macroscopy (Gross Examination): Shows pallor (loss of color) in the substantia nigra and locus ceruleus (brain regions).
- Histopathology (Microscopic Examination): Reveals:
- Loss of pigmented neurons in the substantia nigra.
- Presence of Lewy bodies within remaining neurons.
- Treatment: Dopamine-replacement therapies can alleviate parkinsonism symptoms. However, these treatments do not slow or stop the disease's progression.
- Variable Progression: The rate of disease progression varies significantly between individuals.
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I. Definition & Epidemiology:
- Definition: Bleeding into the subarachnoid space (the space between the arachnoid mater and pia mater surrounding the brain).
- Incidence: Approximately 8 cases per 100,000 people annually.
- Age of Onset: Most common in adults aged 35-65.
- Primary Cause: Rupture of a berry aneurysm (a small, saccular aneurysm, usually at arterial bifurcations).
- Aneurysm Formation: Hypothesized to result from a congenital defect in the tunica media (middle layer) of cerebral vessels, exacerbated by later-life atherosclerosis and hypertension. Crucially, most berry aneurysms do not rupture.
- Location of Aneurysms: Most commonly found at the base of the brain, specifically:
- Anterior communicating artery (40%)
- Middle cerebral artery (34%)
- Internal carotid artery (20%)
- Posterior cerebral artery (4%)
- Rupture Mechanism: Rupture leads to extensive subarachnoid hemorrhage, potentially extending into the brain parenchyma (brain tissue itself).
- Cardinal Symptom: Sudden, severe headache, often described as a "thunderclap" headache or feeling like being hit on the back of the head.
- Precipitating Factors: Exertion or straining can trigger rupture.
- Severity: Can range from unconsciousness to immediate death in severe cases.
- Macroscopy: Blood is found in the subarachnoid space, frequently accumulating around the circle of Willis at the brain's base. The ruptured berry aneurysm may be visible after clot removal.
- Histopathology: The aneurysm wall lacks a muscular media layer; it consists of a thick fibrous intima (inner layer) and an outer adventitia (outer layer).
- Tripartite Outcome: Prognosis is generally categorized into thirds:
- ⅓ Immediate Death: Due to tonsillar herniation (brain stem compression) from massive intracranial pressure increase.
- ⅓ Unconscious with High Risk: High risk of mortality or permanent neurological deficits.
- ⅓ Good Outcome: Provided there is no re-bleeding.
- Congenital Weakness: The underlying congenital defect in the arterial wall is crucial to understanding aneurysm formation.
- Atherosclerosis & Hypertension: These conditions exacerbate the congenital weakness, increasing rupture risk.
- Location Matters: The specific location of aneurysms dictates potential neurological consequences based on affected arteries.
- Rapid Onset: The sudden, severe headache is a hallmark symptom reflecting the acute nature of the hemorrhage.
- Variable Outcome: The significant variability in outcomes highlights the severity and unpredictable nature of SAH.
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I. Definition & Epidemiology:
- Definition: Alzheimer's disease (AD) is a neurodegenerative disorder clinically characterized by dementia and histopathologically by neuronal loss in the cerebral cortex, accompanied by amyloid plaques and neurofibrillary tangles. Crucially, it's the most common cause of dementia.
- Epidemiology:
- Incidence dramatically increases with age (5% >65 years old, 20% >80 years old).
- Represents a significant socioeconomic burden on healthcare systems.
- Aetiology (Cause): The cause is unknown in most cases. A small percentage are familial, linked to genetic mutations in the amyloid precursor protein (APP) gene on chromosome 21.
- Pathogenesis (Mechanism):
- AD is considered a "proteinopathy," focusing on the abnormal accumulation of amyloid-beta (Aβ) and tau proteins.
- Aβ peptides are derived from APP through secretase enzymes.
- The exact mechanism by which Aβ and tau accumulation leads to neuronal loss remains unclear—this is a key area of ongoing research.
- Early Stages: Begins with memory loss, especially recent memory and new learning difficulties. Progressive decline in daily activities (finances, shopping).
- Middle Stages: Loss of motor skills impacts dressing, cooking, and cleaning.
- Late Stages: Agitation, restlessness, wandering, and disinhibition emerge, causing distress for family and caregivers. Eventually, speech loss, immobility, and incontinence occur.
- Macroscopy (Gross Anatomy):
- Reduced brain weight (often <1000g).< />pan>
- Cortical atrophy, particularly in the temporal lobe and hippocampus.
- Histopathology (Microscopic Anatomy):
- Key Features: Abundant neuritic plaques and neurofibrillary tangles in the cerebral cortex, alongside neuronal and synaptic loss.
- Neuritic Plaques: Spherical collections of distorted neuronal processes around a central amyloid core, primarily composed of Aβ protein.
- Neurofibrillary Tangles: Intracellular accumulations of paired helical filaments within neurons; mainly composed of tau protein.
- Death typically occurs approximately 10 years post-diagnosis, often due to complications like pneumonia.
- Amyloid-beta (Aβ) plaques: Extracellular deposits, key hallmark of AD.
- Neurofibrillary tangles: Intracellular accumulations of tau protein, another hallmark of AD.
- APP (Amyloid Precursor Protein): A protein implicated in familial forms of AD.
- Tau protein: A microtubule-associated protein whose abnormal accumulation contributes to neurofibrillary tangles.
- Proteinopathy: A disease caused by misfolded or aggregated proteins.
- The relationship between Aβ and tau accumulation and neuronal death needs further study.
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This guide summarizes key information on Multiple Sclerosis to aid understanding and effective study.
I. Definition & Epidemiology:
- Definition: MS is a relapsing-remitting, demyelinating disease of the Central Nervous System (CNS). Neurological disturbances affect different CNS areas at different times. Think intermittent attacks in different locations.
- Epidemiology:
- Peak onset: 20-30 years old.
- Slightly more common in females.
- Significant geographical variation: higher incidence at higher latitudes (farther from the equator), near absence near the equator. This hints at environmental factors.
- Aetiology (Cause): Unknown. Leading hypothesis: immune-mediated demyelination triggered by a childhood infection in genetically susceptible individuals. Think infection + genetics = trigger.
- Pathogenesis (Mechanism):
- Demyelination episodes cause acute neurological deficits (symptoms) developing over days and lasting weeks.
- Early stages: Complete recovery is typical.
- Progression: Slower recovery, residual deficits, axonal death, and permanent disability due to extensive axonal loss. Think initial recovery, then progressive damage.
- Optic Nerve: Blurred vision, loss of color vision.
- Cerebellum: Vertigo, incoordination.
- Brainstem: Eye movement disorders.
- Spinal Cord: Patchy numbness/tingling, progressing to paraplegia (paralysis of lower limbs), incontinence, and sexual dysfunction.
- Macroscopy (Gross Examination): Well-circumscribed grey plaques in CNS white matter. Common locations: optic nerves, periventricular white matter, brainstem, cervical spinal cord. Think visible lesions in specific areas.
- Histopathology (Microscopic Examination):
- Active plaques: Inflammatory infiltrate, myelin sheath destruction.
- Established plaques: Complete myelin loss, reduced oligodendrocytes (myelin-producing cells), relatively normal or slightly reduced axon numbers (initially).
- Most patients experience progressive disease.
- Significant complications due to disability: pneumonia, urinary tract infections, pressure sores. Think disability leads to secondary complications.
- Relapsing-remitting: Periods of attacks followed by periods of remission (partial or complete recovery).
- Demyelination: Damage to the myelin sheath surrounding nerve fibers, impairing signal transmission.
- Geographical variation: Strong evidence for environmental influence.
- Progressive axonal loss: The ultimate cause of permanent disability.
- Location-specific symptoms: The location of the demyelination dictates the presenting symptoms.
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I. Encephalitis
A. Definition: Infection of the brain parenchyma (functional tissue of the brain).
B. Etiology: Primarily viral, most commonly Herpes Simplex Virus (HSV).
C. Pathogenesis: HSV encephalitis typically results from reactivation of latent HSV in the trigeminal ganglion, leading to infection of the temporal lobe.
D. Presentation: * Confusion * Behavioral changes * Altered consciousness * Seizures (severe cases) * Key diagnostic clue: Simultaneous perioral (around the mouth) involvement.
E. Diagnosis: * Imaging: Brain imaging (e.g., MRI) may show temporal lobe abnormalities. * Laboratory: Polymerase chain reaction (PCR) on cerebrospinal fluid (CSF) to identify HSV DNA. * Histology: Necrotizing inflammation with characteristic herpetic intranuclear inclusions in neurons and glial cells (post-mortem).
F. Treatment: Urgent antiviral treatment is essential.
II. Cerebral Abscess
A. Definition: Localized brain infection with tissue destruction.
B. Etiology: Primarily bacterial, often mixed infections.
C. Pathogenesis: * Direct spread: From paranasal sinuses, middle ear, or teeth. * Hematogenous spread: From septic emboli (e.g., infective endocarditis).
D. Presentation: Symptoms of an infected intracranial mass: * Headache * Nausea * Vomiting * Fever * Seizures * Focal neurological signs (depending on abscess location).
E. Diagnosis: Primarily through CT scan.
F. Treatment: Surgical drainage and prolonged antibiotic therapy.
G. Prognosis: High mortality (20%) and significant morbidity (50% of survivors have persistent neurological deficits or epilepsy).
III. Progressive Multifocal Leukoencephalopathy (PML)
A. Definition: Demyelinating disease of the central nervous system white matter.
B. Etiology: JC virus (polyomavirus).
C. Risk Factors: Virtually exclusive to immunocompromised individuals (e.g., HIV/AIDS, transplant recipients).
D. Pathogenesis: JC virus infection leads to multiple foci of demyelination in the white matter, which can coalesce.
E. Histology: Viral inclusions in the nuclei of astrocytes, macrophages, and oligodendrocytes within demyelinated areas.
F. Diagnosis: * Clinical presentation: Neurological symptoms. * Imaging: Characteristic MRI findings. * Laboratory: Detection of JC virus DNA in CSF.
G. Prognosis: High mortality (up to 50% within 3 months).
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I. Definition & Epidemiology
- Definition: Cerebral infarction is ischemic (lack of blood flow) necrosis (tissue death) of a brain region. This is crucial to understand
- the fundamental nature of the condition.
- Epidemiology: It's the most common type of stroke (~80%), predominantly affecting the elderly. Remember this high prevalence and its association with age.
- Thromboembolism: The majority of cases result from blood clots (thromboemboli) originating in the internal carotid artery or the left side of the heart. These clots travel to and block a cerebral artery. Understand the source of the emboli is key here.
- In situ thrombosis: A smaller percentage arises from clots forming directly within a cerebral artery, often due to atherosclerosis (hardening of the arteries). Distinguish between emboli and in situ thrombosis.
- Artery Occlusion: Sustained blockage of a cerebral artery leads to ischemia and subsequent necrosis in the brain area supplied by that artery. The longer the occlusion, the greater the damage.
- Rapid Onset: Cerebral infarction presents with a sudden onset of neurological symptoms specific to the affected artery's distribution. This is a hallmark of stroke.
- Middle Cerebral Artery Involvement: Most infarctions affect the middle cerebral artery, resulting in contralateral (opposite side) hemiplegia (paralysis) or hemiparesis (weakness), homonymous hemianopia (loss of half of the visual field in both eyes), and dysphasia (language impairment). Memorize these common symptoms and their locations.
- Transient Ischemic Attacks (TIAs): TIAs are brief episodes of focal neurological symptoms (less than 24 hours) that serve as significant warning signs for future infarction. Recognize TIAs as crucial predictors.
- 24 hours: The infarcted area softens, and the grey-white matter boundary becomes indistinct. Cerebral edema (brain swelling) and midline shift may occur.
- 48 hours - 10 days: The infarct becomes gelatinous, and the distinction between infarct and normal tissue clarifies.
- 10 days - 3 weeks: Liquefaction (conversion to liquid) and cystic changes (cavity formation) develop.
- Hemorrhagic Infarct: Reperfusion (restoration of blood flow) can sometimes lead to bleeding into the infarcted area.
VI. Histopathology (Microscopic Changes)
- First 48 hours: Ischemic neuronal changes (shrunken, eosinophilic neurons) and neutrophil (white blood cell) infiltration are observed.
- Later Stages: Mononuclear cells (other white blood cells) remove myelin debris, and astrocytes (glial cells) proliferate as the infarct heals.
- Mortality: High initial mortality (20% at 1 month), followed by a 10% annual mortality rate.
- Complications: Pneumonia, depression, contractures (muscle shortening), constipation, bedsores, and significant emotional impact on the family are common. Remember the range of potential complications.
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I. Definition:
- Infection of the subarachnoid space (the area between the brain and the protective membranes).
- Viral Meningitis: Approximately 11 cases per 100,000 people per year.
- Bacterial Meningitis: Approximately 3 cases per 100,000 people per year. Note the significantly lower incidence compared to viral meningitis.
- Viral Meningitis: Most commonly caused by echoviruses and coxsackieviruses. No organism is cultured from CSF.
- Bacterial Meningitis:
- Most common causes: Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus).
- Neonates (newborns): Escherichia coli and Group B streptococci are significant causes.
- CSF culture and/or blood cultures will yield the causative organism.
- Bacterial Meningitis: Bacteria typically enter the bloodstream from the nasal cavity (often following a viral upper respiratory infection). Their capsules provide resistance to phagocytosis (immune cell engulfment) and complement (part of the immune system). Bacteria exploit weaknesses in the blood-brain barrier (e.g., the choroid plexus) to access the subarachnoid space. Rapid bacterial multiplication in the cerebrospinal fluid (CSF) triggers an acute inflammatory response within the meninges.
- Viral Meningitis: The pathogenic mechanisms are less detailed in the provided text, but it implies a similar entry point via the bloodstream but without the bacterial capsule-related resistance to immune response.
- Common Symptoms (both viral and bacterial): Headache, fever, neck stiffness (meningismus), photophobia (light sensitivity).
- Severity: Bacterial meningitis typically presents with more severe symptoms than viral meningitis.
- Lumbar Puncture (Spinal Tap): CSF analysis is crucial.
- Viral Meningitis: CSF will show a predominance of lymphocytes (a type of white blood cell).
- Bacterial Meningitis: CSF will show a predominance of neutrophils (another type of white blood cell).
- Gram Staining (Bacterial Meningitis): Helps identify the bacteria present in the CSF, aiding in rapid diagnosis and treatment.
- Culture (Bacterial Meningitis): CSF and/or blood cultures are used to grow and identify the specific bacteria.
- Viral Meningitis: Generally mild, with complete recovery expected.
- Bacterial Meningitis: Much more serious; potentially life-threatening if not treated promptly with appropriate antibiotics. Severe cases can lead to permanent neurological complications including hearing loss, learning disabilities, paralysis, and epilepsy.
