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SPONDYLOARTHROPATHIES

Definition: Group of inflammatory rheumatic


diseases with common characteristics that can
include inflammation of the spine, eye,
gastrointestinal tract, and skin. Other joints can be
involved, as can tendons and ligaments near the
spine or affected joint. Spondyloarthropathies
have been linked to the HLA-B27 gene. Patients
with a spondyloarthropathy are typically negative
for rheumatoid factor (seronegative).
SPONDYLOARTHROPATHIES
The following conditions are classified as
spondyloarthropathies:
1. Ankylosing spondylitis
2. Psoriatic arthritis
3. Reactive arthritis
4. Enteropathic arthritis
5. Undifferentiated spondyloarthropathy
6. Juvenile spondyloarthropathy
ANKYLOSING SPONDYLITIS
Greek word:
“ankylos” = bent ;“spondylos” = spinal vertebra
Also called Strumpell-Marie Arthritis
Description: Characterized by ossification of the
ligaments of the spine causing pain and stiffness in
the spine and by involvement also of the hips and
shoulders. Bones in the spine may fuse (ankylosis)
resulting in a rigid and inflexible spine.
10 times more common in men and usually begins
between the ages of 20 and 30 years.
Features of Ankylosing Spondylitis
1. Non-specific symptoms of malaise and fatigability
and weight loss
2. Pain and stiffness
3. Pain first appears in the hips, buttocks or
lumbosacral area which is followed by stiffening
which progresses very slowly from the lower back
and farther upward until finally the entire spine
becomes ankylosed
4. In the later stages, the ankylosis may take place
with the head, neck and thorax in severe flexion
5. May be associated with plantar fasciitis, tendinitis
of Achilles tendon, heel pain and inflammatory
eye disease
Ankylosing Spondylitis

Inflammatory back pain


Onset before age 40 years
Insidious onset
Improvement with exercise
No improvement with rest
Pain at night (with
improvement upon arising)
Ossification of the
longitudinal ligaments
and periphery of the
annulus fibrosus and
bony bridging of the
laminae and spinous
process
Diagnosis of Ankylosing Spondylitis
X-ray is the standard of diagnosing for Ankylosing
Spondylitis however they have poor sensitivity in
early stages of the disease.

Grade 1 – Blurring of joint margins


Grade 2 – Small erosions and narrowing appear in
the facet joints
Diagnosis of Ankylosing Spondylitis

MRI
Most sensitive imaging
Schober's Test
The patient is in a standing position the examiner
makes a mark approximately at the level of L5. The
examiner then places one finger ~5 cm below this
mark, and another, second, finger, ~10 cm above
this mark. The patient is asked to touch his/her
toes without flexing the knee joints. By doing so,
the distance between the two fingers of the
examiner increases.
Schober's Test
Chest Expansion
Measured at the level of 4th ICS
The difference between maximum inspiration and
expiration is measured.
An expansion of less than 2.5 cms is abnormal
Lateral Spinal Flexion
Heel and back against the wall
Measure distance from middle finger to floor
Bend sideways without bending knees and repeat
measurement
Greater than 10 cm is normal
Treatment for Ankylosing Spondylitis
1. NSAIDS – relieves inflammation, pain and
stiffness
2. Tumor Necrosis Factor Blockers (TNF) - TNF is a cell
protein that acts as an inflammatory agent in
rheumatoid arthritis. TNF blockers target this
protein to help reduce pain, stiffness, and tender
or swollen joints.
Adalimumab (Humira)
Etanercept (Enbrel)
Infliximab (Remicade)
Golimumab (Simponi)
Treatment for Ankylosing Spondylitis
3. Range-of-motion and stretching exercises can help
maintain flexibility in your joints and preserve
good posture. In addition, specific breathing
exercises can help to sustain and enhance your
lung capacity.
4. The two types of surgical treatment that are
sometimes needed by people with AS are:
A. Joint replacement surgery
B. Spinal corrective surgery
Reiter’s Syndrome
Definition: It is one of a family of arthritic
disorders affecting the spine. It commonly
involves the joints of the spine and the sacroiliac
joints.
Characteristic features of the disease include
inflammation of the joints, urinary tract and eyes.
More recently doctors have recognized a fourth
major feature: ulcerations of the skin and mouth.
It primarily affects young white men between the
ages of 20 and 40 although it can occur in older
people or children.
Causes of Reiter’s Syndrome
1. Direct cause of Reiter's syndrome is not known
2. 75 percent of people with Reiter's syndrome have
a gene called HLA-B27
3. Usually follows a bout of diarrhea caused by
eating foods contaminated with bacteria such as
salmonella, shigella campylobacter or yersinia.
Treatment for Reiter’s Syndrome
1. Exercises to increase the mobility of joints and
strengthen surrounding tissues
2. Nonsteroidal anti-inflammatory drugs usually are
sufficient to suppress the swelling heat and pain
of the joints. In some cases injections of the
hormone cortisone to control pain and
inflammation in specific joints.
3. In the few people for whom management does
not prevent severe joint damage surgical
reconstruction of the joints
4. Health care specialist – Ophthalmologist,
Urologist, Dermatologist...
ORTHOPEDIC INFECTIONS
1. Life-threatening soft tissue infections and its
treatment
2. Common bone infections and its principles of
treatment
3. Infections involving joints, its complications and
basic treatment guidelines
LIFE-THREATENING SOFT
TISSUE INFECTIONS
Skin and soft-tissue infections usually follow minor
traumatic events or surgical procedures are caused
by a wide spectrum of bacteria, less frequently, the
infections occur spontaneously.
Most of the infections are self-limited and easily
treated with local measures and/or antibiotics.
Others are life-threatening, requiring prompt
diagnosis and aggressive surgical debridement in
addition to the wise choice of antibiotic agents to
limit tissue loss and preserve life.
Common Skin and Soft-Tissue Infections
1. Impetigo - Common bacterial infection of the
skin. It is highly contagious and can occur at any
age, from infancy to adulthood, but it is most
commonly seen in preschool-aged children;
usually associated with a heavy mixed flora of
both staphylococci and streptococci.
These lesions are most common in warm, moist
areas of the body. Predisposing factors include
warm ambient temperatures, humidity, poor
hygiene, and crowded living conditions.
Impetigo

Treatment: Antibiotics and eradication of the


environmental factors thought to be influential in
the development of the process
Common Skin and Soft-Tissue Infections
2. Folliculitis - Pyoderma that arises within a hair
follicle. These lesions occur most frequently in the
moist areas of the body and in areas subject to
friction and perspiration. Host factors known to
predispose to folliculitis include obesity, blood
dyscrasias, defects in neutrophil function, and
immune deficiency states.
The causative organism in most
immunocompetent patients is S. aureus;
however, when immunosuppression impairs host
defenses, gram-negative organisms (Klebsiella,
Enterobacter, and Proteus species) can be
involved.
Folliculitis
Common Skin and Soft-Tissue Infections
3. Cellulitis - Acute infection of the skin and
underlying soft tissues. Its presentation is that of
a rapidly expanding, tender, erythematous, firm
area of skin. Offending organisms are most
commonly group A β-hemolytic Streptococcus
species and S. aureus.
Common Skin and Soft-Tissue Infections
4. Abscess - Enclosed collection of liquefied tissue,
known as pus.
Treatment: Antimicrobial
Incision and drainage
Common Skin and Soft-Tissue Infections
5. Carbuncle - Abscess larger than a boil, usually with
one or more openings draining pus onto the skin.
It is usually caused by bacterial infection, most
commonly Staphylococcus aureus, or
Streptococcus
Saucerization
Life-Threatening Soft-Tissue Infections
1. Group A β-hemolytic streptococcal gangrene -
Extremely rapid–progressing skin and soft-tissue
infection. The causative organisms secrete
hemolysins, streptolysins O and S (which are
cardiotoxic), and leukocidins.
Streptococcal
gangrenous infection
(so-called flesh-eater)
of the arm, involving
skin and subcutaneous
tissues, that followed
a minor penetrating
traumatic event.
Group A β-hemolytic streptococcal gangrene

Elbow of the patient displaying obvious necrosis of


superficial tissues. The potential for extensive tissue
loss and mortality exists, especially if treatment is
delayed. Therefore, prompt, aggressive tissue
debridement and antibiotic therapy are necessary for
a favorable outcome
Life-Threatening Soft-Tissue Infections
2. Clotridial myonecrosis “gas gangrene” -
Destructive infectious process of muscle
associated with infections of the skin and soft
tissues. It is often associated with local crepitance
and systemic signs of toxemia, which are caused
by the anaerobic, gas-forming bacilli of the
Clostridium genus.
Most often occurs after abdominal operations on
the gastrointestinal tract; however, penetrating
trauma, such as gunshot wounds and frostbite,
can expose muscle, fascia, and subcutaneous
tissues to these organisms.
Life-Threatening Soft-Tissue Infections
Clostridia are gram-positive, spore-forming,
obligate anaerobes that are widely found in soil
contaminated with animal excreta. They may also
be isolated from the human gastrointestinal tract
and from the skin in the perineal area. Clostridium
perfringens is the most common isolate (present in
80% of cases). This organism produces
collagenases and proteases that cause widespread
tissue destruction, as well as α-toxin, which has a
role in the high mortality rate associated with
clostridial myonecrosis. The α-toxin causes
extensive capillary destruction and hemolysis,
leading to necrosis of the muscle and overlying
fascia, skin, and subcutaneous tissues.
Clostridial Myonecrosis

The muscle is pale, edematous, and unresponsive to


stimulation. As the disease process continues, the
muscle becomes frankly gangrenous, black, and
extremely friable. Gas in the wound is a relatively late
finding, and by the time crepitance is appreciated, the
patient may be near death.
Treatment of Clostridial Myonecrosis
1. Surgical debridement
2. Parenteral antibiotic
3. Hyperbaric oxygen - 100% oxygen has been
reported to reduce associated tissue loss and
mortality;
Clostridial Myonecrosis
Life-Threatening Soft-Tissue Infections
3. Necrotizing Fasciitis - Aggressive soft-tissue
infection involving the fascia, with characteristic
extensive undermining and tracking along
anatomic planes.
This usually occurs in patients with significant
comorbidity, such as diabetes mellitus or
peripheral vascular disease, but it is also seen in
obese or malnourished patients and in IV drug
abusers.
Classically associated with group A β-hemolytic
streptococci and staphylococci, the disease is now
known to be caused by a variety of organisms,
including coliforms, as well as anaerobic
Peptostreptococcus and Bacteroides species.
Necrotizing Fasciitis

Diabetic patient who developed necrotizing


fasciitis after drainage of perirectal abscess. Initial
debridement has been done, in addition to a
diverting colostomy.
Necrotizing Fasciitis

Daily inspection and additional debridements


were done as indicated.
Idiopathic or Spontaneous necrotizing fasciitis - often
arises without any obvious portal of entry

Extensive tissue loss in a patient who developed


spontaneous group A streptococcal idiopathic
necrotizing fasciitis.
Life-Threatening Soft-Tissue Infections
4. Fournier's gangrene - Characterized by necrosis of
the skin and soft-tissues of the scrotum and/or
perineum that is associated with a fulminant,
painful, and severely toxic infection.
Definitive diagnosis is made by identification of a
necrotic black area on the scrotum that is
associated with local and systemic signs of
infection.
Fournier's gangrene

Fournier's gangrene, with pathognomonic "black


spot" on the involved scrotum.
Fournier's gangrene

Tissue loss in the patient resulted in the need to


debride all of the genital organs. A Foley catheter,
which had been placed into the bladder, is seen at
bottom.
Life-Threatening Soft-Tissue Infections
5. Ecthyma gangrenosum - Characteristic skin lesion
may develop, with erythematous macular
eruptions that quickly become bullous with
central ulceration and necrosis . This lesion may
resemble a decubitus ulcer with the characteristic
black eschar
STOP
1-8-2016
COMMON BONE AND JOINT INFECTIONS
Causes of Bone/Joint Infections
A. Hematogenous spread - Bacteremia
B. External inoculation – Open fracture, penetrating
wound and or following surgery
C. Direct extension from an adjacent soft tissue
infection
Hematogenous Osteomyelitis
Distant Infection/Surgery

Organisms gain access to the blood (bacteremia)

Metaphyseal side of the epiphyseal plate

Osteomyelitis
Hematogenous Osteomyelitis
Nutrient artery is an artery that supplies the
marrow of a long bone. The branches of nutrient
artery terminate in the metaphysis. Circulation is
sluggish in this area and pathogenic organism may
gain seed in this area.

- Cells in this area have


no phagocytic activity
Clinical Picture of Osteomyelitis
1. Malaise
2. General weakness
3. Fever
4. Pain on affected area
5. Protective muscle spasm on the affected part
6. Blood culture is frequently positive
7. Leukocytosis
8. Elevated ESR
9. Localize tenderness, swelling, redness over
affected area
10. X-ray findings do not appear until a week or two
later
Treatment of Osteomyelitis
1. Antimicrobial – GS and culture and sensitivity;
Staphylococcus in 80% of cases
2. Drainage or debridement
3. Rest of affected
limb
4. Blood transfusion
5. Fluids and electrolytes
6. Amputation
Complications of Osteomyelitis
1. Chronic osteomyelitis - Severe, persistent, and
sometimes incapacitating infection of bone and
bone marrow (+/-) sinus
Complications of Osteomyelitis
2. Muscle atrophy
3. Joint contractures
4. Septicemia
5. Bone asymmetry and angular deformity
6. Squamous cell carcinoma
Chronic Granulomatous
Disease of Childhood
Also called Bridges–Good syndrome, Chronic
granulomatous disorder, and Quie syndrome.
Hereditary diseases in which certain cells of the immune
system have difficulty forming the reactive oxygen
compounds (superoxide radical) used to kill certain
ingested pathogens. This leads to the formation of
granulomata in many organs.
The recurrent infections they acquire are: Pneumonia,
abscesses of the skin, tissues, and organs, suppurative
arthritis, osteomyelitis, bacteremia/fungemia, superficial
skin infections such as cellulitis or impetigo.
Osteomyelitis usually involves small bones of the hands
and feet.
Brodie’s Abscess
It is a localized form of chronic hematogenous
osteomyelitis which manifest as an abscess of
bone surrounded by dense fibrous tissue and
sclerotic bone.
The most common site is at the lower end of the
tibia in children or young adults and more
commonly seen in boys.
This disease has an insidious onset, mild local
symptoms (typically nocturnal), few or no
constitutional symptoms, and lacks a systemic
reaction, and supportive laboratory data (normal
values) are inconsistent.
Brodie’s Abscess
Diagnosis usually difficult to diagnose because the
characteristic signs and symptoms of the acute
(osteomyelitis) form of the disease are absent.

Treatment:
A. Antimicrobial
B. Drainage and Debridement
C. Rest of affected extremity
Brodie’s Abscess
EXOGENOUS OSTEOMYELITIS
Definition: Infection of the bone through direct
contamination from an open wound which may be
secondary to the following:
A. Open fracture
B. Punctured wound
C. GSW
D. Surgery
Infection of the bone will depend on the number
and virulence of bacteria entering the wound,
extent of tissue devitalization, type of organism
and host resistance.
HEMATOGENOUS EXOGENOUS
OSTEOMYELITIS OSTEOMYELITIS
Extensive dissection and Localized or infection is
massive involucrum confined to one part of the
formation bone
Often insidious 36-48 hours following open
fracture, punctured wound,
GSW or surgery
Treatment of Osteomyelitis
1. Antimicrobial – GS and culture and sensitivity;
Staphylococcus in 80% of cases
2. Drainage or debridement
3. Rest of affected
limb
4. Amputation if develops
into squamous CA
OSTEITIS PUBIS
Noninfectious inflammation of the pubis
symphysis occuring most often after prostatic
operations (male), pelvic surgery (female) or after
pregnancy.
The incidence and etiology of osteitis pubis as an
inflammatory process versus an infectious process
continues to fuel debate among physicians when
confronted by a patient who presents complaining
of abdominal pain or pelvic pain and overlapping
symptoms.
Clinical Picture of Osteitis Pubis
Sudden onset of pain over the symphysis pubis 2 –
8 weeks after prostatic and pelvic surgery. The pain
becomes more severe, especially with activity and
is worse on coughing, defecation and urination
Treatment for Osteitis Pubis
1. Rest and immobilization
2. Ice 48 – 72 hours
3. Heat after 72 hours
4. Gentle stretch exercises
5. Antimicrobials if (+) infection
6. If (+) pus aspiration or I & D
Intervertebral Disc
Inflammation(Discitis)
Inflammation of the intervertebral disc which is
common in children below 6 years of age. The
upper back (thoracic) and low back (lumbar) disks
are most commonly affected.
Discitis can be caused by a bacterial or viral
infection, or it can be caused by other
inflammation, such as from autoimmune diseases
Signs and Symptoms of Discitis
Back pain
Difficulty getting up and standing
Increased curvature of the back
Irritability
Low-grade fever
Recent flu-like symptoms
Refusal to sit up, stand, or walk (younger
child)
Stiffness in back
Test for Discitis
Bone scan
CBC
ESR
MRI of the spine – Narrowing of the disc space
X-ray of the spine
Discitis
Discitis destroys two
adjacent endplates (yellow
and white arrows) and the
intervening disk space.
Treatment for Discitis
1. Rest with immobilization of body cast – In the
absence of systemic manifestations
2. Antimicrobial if with systemic manifestations
together with rest and immobilization
3. Consider biopsy of the intervertebral dics if no
improvement
SEPTIC ARTHRITIS/PYOGENIC
INFECTION OF JOINT
Definition: Bacterial infection of the joint which
causes intense inflammatory reaction with
migration of the polymorph nuclear leukocytes
and subsequent release of proteolytic enzymes.
This could lead to destruction of the articular
cartilage and later the joint. Hip and knee are the
most frequent sites of infection.
Newer Definition: A positive synovial fluid culture or
a synovial fluid WBC count of greater than 50,000
with 75% polymorphic neutrophils and a negative
lyme titer
Causative Organisms in Septic
Arthritis
1. Staphylococcus aureus - 50%
2. Streptococcus – 20%
3. Pneumococcus – 10%
4. Gonococcus
5. E. coli
6. H. influenza
Routes of Entry of Organisms
1. Primary focus is in RS, GIT
2. Pyogenic osteomyelitis
3. Punctured wounds
4. Pneumonia, typhoid
5. Primary focus within the joint, absent in few
Predisposing Factors in Septic
Arthritis
1. Trauma
2. Diabetes
3. Steroid therapy
4. Malignancy
Sites of Involvement of the
Joints
ADULT
1. Knee – 53%
2. Hip – 20%
3. Elbow – 17%
4. Shoulder – 10%

CHILDREN
1. Knee – 39%
2. Hip – 32%
Clinical Features of Septic
Arthritis
A. 90% of cases of septic arthritis are monoarticular
and 10% are polyarticular
B. Fever is only seen in 50% of the cases
C. Limp is a common complaint
D. Severity of clinical manifestations depends upon
the severity of disease
E. 1/3 suffer from loss of joint function
Septic Arthritis
Diagnostic tools in Septic Arthritis
1. Blood culture is positive in only 60% of cases
2. Joint aspirate and synovial fluid analysis – This is the
most accurate diagnostic tool for septic arthritis. The
synovial fluid is tested for cells, sugars and proteins.
Gram staining is positive in 60% of the cases for
gram positive.
3. WBC are raised to 50,000 to 1,000,000 (80%)
4. ESR increase more than 20 mm/hr – 50%
5. Hb percentage decreases
6. CRP – if CRP is < 10 mg/dl, the probability that the
patient does not have septic arthritis is 87%.
Treatment for Septic Arthritis
1. Arthrotomy or joint drainage – Joint is aspirated
first if pus is present, open arthrotomy is
indicated. Pus is cultured and gram staining is
done. Antibiotics is given
2. Immobilization of the joint by using plaster of
Paris splints in functional position reduces pain
3. Radical treatment - If cartilage is destroyed, aim
for ankylosis in functional position by plaster
cast.
Arthrotomy Arthrocentesis
Pyogenic Arthritis of the Hip in Infants
It generally arises as a sequela to acute infectious
diseases such as scarlet fever, pneumonia, typhoid
fever, diphtheria. The blood stream as a rule,
conveys the pathogenic organism to the
predisposed joint.
Complications of Pyogenic Arthritis of Hip
1. Complete destruction of the joint
2. Spontaneous or pathologic dislocations
3. Ankylosis
Treatment of Pyogenic Arthritis of the Hip
1. Antimicrobial - Haemophilus influenzae type b
was the most common causative agent identified
and 82% of such cases occurred in children
between 6 and 24 months of age
2. Surgical drainage
3. Immobilization using spica cast
Gonococcal Arthritis
This is a complication of inadequately treated
acute gonorrheal urethritis. Since gonorrhea is less
commonly recognized (asymptomatic) and
therefore less treated in women than in men,
gonococcal arthritis is more common in women.
Gonococcal Arthritis
The age of predilection is 20 – 30 years of age.
Joint involvement usually appears 2 – 3 weeks
after the onset of urethral or vaginal discharge.

Polyarticular or monoarticular with the knee joint


as the most commonly affected joint followed by
the ankle.
Gonococcal Arthritis

Note the rash

Chronic gonococcal arthritis may involve both hands,


as well as other joints. Many physicians, particularly
those in upscale urban practices, forget that this is
still the most common cause of infectious arthritis.
Diagnosis of Gonoccocal Arthritis
1. Identification of urethral or vaginal discharge
2. Arthrocentesis – Gonoccocci in the aspirate in the
early stages
Treatment of Gonococcal Arthritis
1. Antimicrobial
2. Arthrotomy or arthrocentesis
3. Rest of affected part
Salmonella Osteomyelitis and Arthritis
Infection of the bone and joint secondary to
Salmonellosis. The incidence of this is significant
among people with sickle cell anemia.
Several bones may be involved with local pain and
tenderness.
Diagnosis is made based on the culture of
organism.

Treatment is the same with other forms of


arthritis.
SICKLE CELL ANEMIA
Definition: Inherited disorder of hemoglobin
synthesis in which adult hemoblogin is partly or
completely replaced by abnormal sickle
hemoglobin (HgbS); Prevalent in African-
American

Precipitating Factors:
1. Fever
2. Emotional or physical stress
3. Increased blood viscosity

Clinical manifestations:
1. Dyspnea, chest pain and cyanosis
2. Cardiac murmurs, dysrhythmias and
cardiomegaly
3. Uremia
Pathogenesis of Infection
Capillary occlusion secondary to intravascular
sickling may devitalize and infarct the gut,
permitting Salmonella invasion. Reduced function
of the liver and spleen, together with interference
with reticuloendothelial system function due to
erythrophagocytosis, suppresses clearing of these
organisms from the blood stream.
Brucella Osteomyelitis & Arthritis
Brucellosis is a zoonosis, or an infectious disease in animals
that can be transmitted to humans, which is caused by the
bacterial genus Brucella. This usually infects cattle, swine,
goats, sheep and dogs. When exposed to infected animals or
animal products, humans may contract brucellosis.
There are three ways of transmitting Brucellosis to humans:
A. By ingesting infected meat or animal products;
B. Through inhalation of the organism; or,
C. By having the bacteria enter the body through an open
wound.
The most common cause of Brucellosis in humans is by
consuming unpasteurized milk or cheese from an infected
animal. Human to human transmission, though uncommon,
may be through sexual contact or breastfeeding.
Diagnosis of Brucellosis
A. Blood tests and blood/tissue cultures
B. Testing for antibodies against the bacteria
C. A biopsy of body tissue - from the bone marrow
or the liver
D. Additional blood tests may demonstrate
anemia, low platelets, a low white blood cell
count, and elevated liver function tests.
Treatment of Brucellosis
1. Antimicrobial is the mainstay of treatment - The
antimicrobials most commonly used include
doxycycline (Vibramycin), streptomycin, rifampin
(Rifadin), gentamicin (Garamycin), and
trimethoprim-sulfamethoxazole (Bactrim, Septra).
Skeletal Tuberculosis
Skeletal tuberculosis is always secondary, the
primary foci being either in the lungs, lymph nodes
or gastrointestinal tract.
The incidence of bone and joint tuberculosis is 2-
3%. Fifty percent of these cases are found in the
vertebral column. The other major areas affected
in order or predilection are hip, knee, foot, hand,
shoulder and others...
Skeletal tuberculosis occurs mostly in the first
three decades of life but no age is immune.
Etiology of Skeletal Tuberculosis
TB bacillus:
A. Mycobacterium tuberculosis
B. Mycobacterirum bovine

Route:
A. Blood e.g. Batson’s plexus in TB of the spine
B. Lymphatic channel
C. Direct

Precipitating factors:
A. Anemia, debility help precipitate the infection
B. Local factors like trauma
What happens after infection with
the tubercle bacilli?
Pathophysiology of TB
Pathophysiology of Osteoarticular TB
Primary Focus

May be active /quiescent(Lungs, tonsils, medistinum,mesentery etc)

Bacillemia

Through the arteries and veins
(Batson’s plexus in the spine)

Reach the skeletal system

Tubercle develops
Clinical Features of Skeletal TB
Insidious Onset

Monoarticular Constitutional Symptoms


Diagnostic Procedures
1. Mantoux test
2. X-ray – An outstanding characteristic of TB of the
bone is destruction with little tendency toward
the formation of new bone; almost complete lack
of regeneration in the early cases
3. Biopsy of regional lymph nodes
4. Arthrocentesis – ZN stains of acid-fast bacilli in
the aspirate
Principles of Treatment of TB of the Bones
1. Nutritious diet and rest
2. Immobilization – If disease is osseous aim at
ankylosis in functional position by
immobilization. If the disease is synovial, aim at
mobility by traction
3. Surgery – Partial capsulectomy, synovectomy,
osteotomy, curettage depending on the stage of
tuberculosis
4. Treatment of tubercular abscess – Drainage and
or aspiration versus conservative management
5. Chemotherapy
Chemotherapy for Skeletal TB
A. First line of drugs
R – Rifampicin
I – INH
P – Pyrazinamide
E – Ethambutol
S – Streptomycin
B. Second line of drugs – Resistant strains
C - Capriomycin
A - Amikacin
K - Kanamycin
E - Ethionamide
C - Cycloserine
A – Amino salicylic acid
T - Thiacetazone
Pott’s Disease
Tuberculous spine. This is the most common form
of skeletal tuberculosis.

REGIONAL DISTRIBUTION
Cervical 12%
Cervicodorsal 5%
Dorsal 42%
Dorsolumbar 12%
Lumbar 26%
Lumbosacral 3%
Reasons for the Site of Predilection
1. There is large amounts of spongy tissue within
the vertebral body
2. Degree of weight bearing, which is comparatively
more
3. More vertebral mobility is seen here
Sites of Involvement within the Vertebra
E
F A
D
C B

A Metaphyseal (98%)D True arthritis


B Anterior E Appendiceal
C Central F Posterior Spinal Elements
Sequences of Pathological Events
Tuberculous endarteritis which develops following
an infection, results in marrow devitalization.
Lamellae are destroyed and the vertebral body is
easily compressed.
TYPES OF VERTEBRAL REACTION
Exudative Reaction Caseative Reaction
Common Rare
Severe hypergic reaction causes severe Mechanism of formation and spread of
osteoporosis destruction is similar to exudative type
but is slower
Rapid spread
Abscess formation if formed frequently
Constitutional symptoms are pronounced
Clinical Features of Pott’s Disease
1. Back pain localized over the site of involvement
of specific nerve root
A. Cervical roots – Pain radiates to arm
B. Dorsal roots – Girdle pain
C. Lumbar roots – Groin pain
D. Sacral roots – Complains of sciatica
2. Back stiffness
3. Paraplegia
4. Wasting of back muscles
5. Cold abscess
6. Kyphotic deformity – 95% of cases
Typical Attitudes in Skeletal TB
Upper Cervical Wryneck
Lower Cervical Military position
Lower Thoracic Alderman’s gait
Upper Lumbar Prominent abdomen
Lower Lumbar Increased lordosis
TB Cold Abscess
Cold abscess is called
“cold” because it is not
associated with features
like redness, heat as in
pyogenic abscess
Kyphotic Deformity of TB
Diagnostic Procedure
1. X-rays – Disk space narrowing, anterior wedge
compression and paravertebral shadow (abscess)
2. CT scan – Assess the degree of neural compromise
3. MRI – Helps detect cord compression
4. US – Detect the size of cold abscess
5. Culture – Before starting treatment
Objectives of Surgery in TB of Spine
A. To excise the infected tissue
B. Decompress the intraspinal neural elements
C. Reduce the spinal instability
D. Provide stability by spine fusion techniques
Indications for Surgery for TB of Spine
1. Neurological symptoms
2. Kyphosis with several vertebral involvement,
severe kyphosis, progressive kyphosis etc
3. Resistance to chemotherapy
4. Cord compression
5. Progressive impairment of pulmonary function
6. Spinal instabiliy
Complications of Pott’s Disease
1. Paraplegia
2. Cold abscess
3. Sinuses
4. Secondary infection
5. Death
Syphilis of Bones and Joints
Skeletal syphilis can happen in two forms namely
congenital and acquired.

CONGENITAL SYPHILIS ACQUIRED SYPHILIS


Osteochondritis Periostitis
Pseudoparalysis Osteomyelitis
Periostitis Gummatous Arthritis
Clutton’s joints Charcot’s joint
Parrot’s Syphilitic Osteochondritis
Within the first 8 months of life, osteochondritis of
the long bones and ribs, may cause
pseudoparalysis of the limbs. This is an epiphysitis
which occurs during the first few months of life. It
affects the upper limbs more frequently than the
lower, and is often associated with an effusion into
the adjacent joint.
Separation of the epiphysis may occur and give rise
to unwillingness to move the joint-syphilitic
pseudoparalysis.
Clutton’s Joints
It occurs between 5 and 20 years of age in both
sexes. This condition results in symmetrical joint
swelling seen in patients with congenital syphilis.
It is also known as symmetrical hydrarthrosis
of childhood. Knees are most commonly affected
by synovitis and joint effusions followed by the
ankles, elbows, wrists and fingers. It is usually
painless and usually no disability associated with
the joint swelling.
Clutton’s Joints
Diagnostic Test for Skeletal Syphilis
1. Joint fluid aspiration and synovial fluid analysis
2. Wassermann’s test - Wassermann reaction (WR)
is an antibody test for syphilis
Fungal Infections of Bones and Joints
Rare
Mimics TB by granuloma formation

Route of Spread:
1. Systemic – hematogenous
2. Direct extension
Fungal Infections of Bones and Joints
1. Blastomycosis - Caused by the fungus Blastomyces dermatitidis.
The fungus lives in moist soil and in association with decomposing
organic matter such as wood and leaves.
2. Coccidiomycosis - Fungus found in the soil of dry, low rainfall
areas. Also known as Valley Fever, is a common cause of
pneumonia in endemic areas.
3. Cryptococcossis - Two species – Cryptococcus neoformans and
gattii – cause nearly all cryptococcal infections in humans and
animals. C. neoformans can be found in soil throughout the world.
People at risk can become infected after inhaling microscopic,
airborne fungal spores.
4. Sporotrichosis – Caused by Sporothrix schenckii. The fungus lives in
soil, plants, and decaying vegetation. Cutaneous infection is the
most common form of infection and usually occurs after handling
contaminated plant material, when the fungus enters the skin
through a small cut or scrape.

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