Reza Omid MD

Orthopaedic Basic Science

1)

Science of Bones

Bone Histology

Lamellar Bone: normal bone, stress oriented

o
Less osteocytes and turnover than woven bone
o
2 subtypes of lamellar bone:
Cortical: aka compact bone

makes up 80% of skeleton

mainly diaphyseal

composed of tightly packed osteons or haversian

systems connected by haversian (or volkman) canals

slow turnover

high Youngs module (E)

Cancellous: aka spongy bone or trabecular bone

mainly metaphyseal/epiphyseal, vertebral body,

calcaneus

less dense and more remodeling according to lines of

stress

high turnover

more elastic and smaller Youngs module (E)

*Cement lines are found in cortical bone indicating where bone resorption
has stopped and new bone formation has begun. Cement lines define the
outer border of an osteon

Woven Bone: immature/pathologic bone, NOT stress oriented

o
More osteocytes and turnover than lamellar bone
o
Weaker and more flexible than lamellar bone
o
Immature bone found in embryonic skeleton & fracture callus
o
Pathologic bone found in osteogenic sarcoma and fibrous dysplasia

Cell Types Found in Bone

1. Osteoblasts: form bone
a. Derived from undifferentiated mesenchymal cells (osteoprogenitor
cells) found in periosteum, endosteum and haversian canals
b. Produce bone so produce:
i. alkaline phosphatase
ii. type 1 collagen
iii. osteocalcin
c. more Golgi, ER and mitochondria than other cells
d. 2 subtypes:
i. more differentiated, activated cells that line bone surfaces

Reza Omid MD

less active resting cells which maintain the ionic mileu of

bone. Disruption of the lining cell layer activated these cells
e. Respond to several factors:
i. PTH (releases RANKL to stimulate osteoclastic activity)
ii. Vitamin D (stimulates matrix and alkaline phosphatase
synthesis and production of bone-specific proteins such as
osteocalcin which then upregulates osteoblasts)
iii. Glucocorticoids (decreases bone production)
iv. Prostaglandins (increase cAMP to cause increased
resorption)
v. Estrogen (anabolic and anticatabolic to increase bone
production)
vi. PDGF
vii. Cbf-1:RUNX2 is the main activator of osteoblasts.
Cbf-1:RUNX2 is also critical during the process of
chondrocyte hypertrophy and terminal differentiation and
mice without Cbf-1:RUNX2 have an absence of
hypertrophic chondrocytes in some growth plates
1. Mutations of Cbf-1:RUNX2 result in cleidocranial
dysplasia (abnormal/absent clavicles with face)
f. Certain antiseptic agents are toxic to cultured osteoblasts including:
i. Hydrogen peroxide
ii. Betadine
iii. Bacitracin is less toxic
2. Osteoclasts: resorb bone
a. Multinucleated irregularly shaped giant cells from hematopoetic
tissues (monocyte progenitors form giant cells by fusion)
b. Possess ruffled brush borders (which are plasma membrane
enfoldings that increase surface area and are important for bone
resorption) and surrounding clear zone
c. RANK ligand (from osteoblasts) binds to osteoclasts on RANK to
increase bone resorption. This mechanism is inhibited by
osteoprotegerin binding to RANK-L and preventing interaction
with osteoclasts and induces apoptosis.
d. Synthesize TRAP (tartrate-resistant acid phosphate)
+
e. Bind to bone via integrin (vitronectin) and produce H ions (via
carbonic anhydrase) to decrease the pH and increase solubility of
hydroxyapatite crystals [Ca 10 (PO 4 ) 6 (OH) 2 ] and organic
matrix is removed by digestion.
f. Have calcitonin receptors but NOT PTH receptors
g. Responsible for bone resorption in metastasis and multiple
myeloma and total joint osteolysis.
ii.

Reza Omid MD
h. IL-1 is a potent stimulator of osteoclastic bone resportion and has

been found in the membranes surrounding loose total joint

implants.
i. IL-10 suppresses osteoclast formation
j. Bisphosphonates inhibit osteoclast resportion by preventing ruffed
borders from forming and inducing apoptosis
3. Osteocytes: maintain bone
a. 90% of cells found in mature bone
b. are former osteoblasts trapped in newly formed matrix (which they
help preserve)
c. high nucleus to cytoplasm ration with long interconnecting
cytoplasmic processes
d. important for control of extracellular calcium and phosphate
concentration
e. directly stimulated by calcitonin
f. inhibited by PTH
4. Osteoprogenitor cells: become osteoblasts

Line Haversian canals, endosteum and periosteum

Await stimulus to differentiate into osteoblasts

5. Lining cells: narrow flattened cells that form an envelope around bone
Wnt- catenin Pathway
-Wnt (mammalian homologue of wingless in drosophila) is very similar to BMP
(essential for osteogenesis) but uses a different signaling pathway
-Wnt binds to receptors frizzled and LDLR5 and LDLR6 and activates
catenin which go to the nucleus to regulate gene expression
-Sclerostin and Dickkopf (DKK-1) are antagonists of Wnt
-BMP uses smad to cause gene expression
Bone Matrix
-Composed of organic (40%) and inorganic component (60%)
-Organic component is composed of:
1. primarily type I collagen
2. proteoglycans (provides compressive strength)
3. non-collagenous matrix proteins (osteocalcin, osteonectin, osteopontin)
4. growth factors and cytokines
-Inorganic component is composed of:
1. calcium hydroxyapatite (provides main compressive strength)
2. osteocalcium phosphate (brushite)
-Collagen is layed down in an arrangement that forms hole zones (which are
gaps between two consecutive fibrils and pores which are gaps between two
side to side fibrils. Mineral deposition (calcification) occurs within the
hole zones and pores. Cross linking decreases collagen solubility and
increases its tensile strength.

Reza Omid MD

-Osteocalcin is the most abundant non-collagenous matrix protein. It is

inhibited by PTH and stimulated by vitamin D. Osteocalcin levels can be
measured in the serum or urine as a marker of bone turnover. Increased levels
of osteocalcin can be seen in Pagets disesase, Renal osteodystrophy, Hyper-PTH
-Osteonectin (aka SPARC) is secreted by platelets and osteoblasts and
regulates calcium and organizing the mineral in bone matrix
-Osteopontin is a cell binding protein (similar role to integrins)

Bone Physiology

-Wolffs Law: bone remodels in response to mechanical stress. Increased

stress causes increased bone gain and less stress results in loss of bone (disuse
osteopenia). Bone loss seen with paraplegia/quadriplegia occurs throughout the
skeleton (except the skull) for about 16 months and then levels off at 2/3 of the
original bone mass.
-Bone remodels in response to electrical changes. Compressive side is
electronegative and stimulates osteoblasts. Tension side is electropositive and
stimulates osteoclasts.
-Hueter-Volkmann Law: bone remodeling occurs in small packets of cells
known as basic multicellular units (BMU), modulated by systemic hormones and
local cytokines. Mechanical factors can influence longitudinal growth, bone
remodeling and fracture repair. Compressive forces inhibit growth and tensile
forces stimulate growth. This law is seen in the progression of scoliosis and
Blounts disease.
Bone Remodeling
-Cortical bone remodeling occurs by osteoclastic tunneling (cutting cones),
followed by layering of osteoblasts and successive deposition of layers of
lamellae (after the cement line has been laid down) until the tunnel size has
narrowed to the diameter of the osteonal central canal. The head of the cutting
cone is made up of osteoclasts, which bore holes through hard cortical bone.
Behind osteoclasts are capillaries, followed by osteoblasts that lay down osteoid
to fill the resorption cavity.
-Cancellous bone remodeling occurs by osteoclastic resorption, followed by
osteoblasts laying down new bone.
Bone Blood Supply
-Bone receives 5-10% of cardiac output.
-Long bones receive blood from 3 sources:
1. Nutrient artery: gives rise to the medullary blood supply and
supplies the inner 2/3. This supply is disrupted by fracture and
reaming
a. High pressure system
2. Metaphyseal-Epiphyseal system: arises from periarticular
vascular plexus (ex: genicular arteries)

Reza Omid MD

3. Periosteal system: supplies the outer 1/3

a. Low pressure system
-Blood flow is normally centrifugal (inside to outside) in adults due to high
pressure of the nutrient artery and low pressure of the periosteal system. In a
completely displaced fracture with disruption of the endosteal (nutrient) system,
the periosteum predominates and flow becomes centripetal (outside to inside).
Blood flow in immature bones is centripetal due to the very well developed
periosteum.
-Venous flow in mature bones is centripetal (outside to inside) from sinusoids to
emissary veins
-Hypoxia, hypercapnia, and sympathectomy increases blood flow to the bone
-Regional acceleratory phenomenon is the response of blood flow to a
fracture and is initially decreased due to vascular disruption at the fracture site
and within hours to days, blood flow increases and peaks at 2 weeks and returns
to normal between 3-5 months.
Enchondral Ossification
-Bone replaces a cartilage model (but cartilage is NOT converted to bone)
1. Undifferentiated cells secrete a cartilaginous matrix and differentiates into
chondrocytes
2. Matrix mineralizes and is invades by vascular buds that bring
osteoprogenitor cells into the matrix
3. Osteoclasts resorb calcified cartilage and the osteoblasts form bone
-Examples of enchondral ossification:

Embronic long bones

Longitudinal growth (physis)

Fracture callus (relative stability)

Bone formed via use of BDM

-Achondroplasia is a disease of abnormal enchondral ossification
Intramembranous Ossification
-Bone formation without a cartilage model
1. Undifferentiated mesenchymal cells aggregate into layers (or membranes)
2. These cells differentiate into osteoblasts and deposite organic matrix that
mineralizes to form bone
-Examples of intramembranous ossification:

Embryonic flat bone formation (pelvis, clavicle, vault of skull)

Bone formation during distraction osteogenesis

Blastema bone (occurs in young children with amputations)

Bone formed with absolute stability

-Cleidocranial dystosis is a disease of abnormal intramembranous ossification
Appositional Ossification
-Osteoblasts align themselves on existing bone surface and lay down new bone

Reza Omid MD

-Examples of appositional ossification:

Periosteal bone enlargement (width)

Bone formation phase of bone remodeling

-Diseases of abnormal appositional ossification:

Melorheostosis

Pagets disease

Caffeys disease (infantile hyperostosis)

Physeal Zones
1. Epiphysis
2. Reserve zone: cells store lipids, glycogen and PG aggregates for later
growth and matrix production
-Decreased oxygen tension
o
Affected by lysosomal storage diseases (Gaucher),
Pseudoachondroplasia, Kneist syndrome, Gaucher disease,
Diastrophic dysplasia (Reserve Place Kicker has Good
Distance)
3. Proliferation zone: longitudinal growth occurs with stacking of chodrocytes
(top cell is the dividing mother cell)
-Increased oxygen tension
-Increased PG in surrounding matrix inhibiting calcification
-Cellular proliferation and matrix production occurs in this zone
o
Affected by Gigantism and Achondroplasia (GPA)
4. Hypertrophic zone: chondrocytes increase 5 times in size and accumulate
calcium in their mitochondria and then die to release calcium.
-Decreased oxygen tension
-rate of chondrocyted maturation is regulated by systemic hormones and
local growth factors. PTHrP inhibits chondrocyte maturation. Indian
hedgehog is produced by growth plate chondrovytes and regulates
expression of PTHrP
-Composed of 3 sub-zones:
Maturation zone
Degenerative zone
Zone of provisional calcification
-This zone widens in Rickets
-Encondromas originate here
o
Affected by Rickets, SCFE, Mucopolysaccaridoses, Osteomalacia,
Rickets, Encondroma, SCFE, Physeal fractures (MORE Sex
Please)
5. Metaphysis:
Primary spongiosa
Secondary spongiosa
o
Affected by SCFE with endocrinopathy

Reza Omid MD
6.

Diaphysis

Bone Injury
-Fracture healing is a continuum proceeding from inflammation through repair
(soft callus followed by hard callus) and ending in remodeling
-Most important factor in bone healing is blood supply
-Head injury can increase the osteogenic response to fracture (HO)
-Nicotine increases time to fracture healing and increases the risk of non-union
(tibia) and decreases strength of the facture callus. Also it increases the risk of
pseudoarthrosis after a lumbar fusion by up to 500%
-NSAIDs also adversely affect fracture repair and lumbar spine fusions
-Inflammation phase starts with bleeding from the fracture site and
surrounding soft tissue creating a hematoma which provides a source of
hematopoietic cells capable of secreting growth factors. Fibroblasts,
mesenchymal cells and osteoprogenitor cells are present at the fracture site.
Granulation tissue forms at the fracture ends
-Repair phase is when the primary (soft) callus forms at about 2 weeks and at
this stage shortening does not occur but angular deformity can still occur.
During callus formation, type 2 collagen is expressed early followed by type 1
collagen.
-Remodeling phase begins during the middle of the repair phase and
continues long after the fracture has clinically healed (up to 7 years). Fracture
healing is complete when there is repopulation of the marrow space.
-Cortisone decreases callus proliferation
-Thyroid and PTH increase bone remodeling
-Growth hormone increases callus volume
-Low-intensity pulsed ultrasound accelerates fracture healing and increases
the mechanical strength of callus, including torque and stiffness. The proposed
mechanism is that cells responsible for fracture healing respond favorably to the
mechanical energy transmitted by the ultrasound signal.

Allograft

-Fresh allograft is most immunogenic and most osteoinductive

-Fresh-Frozen is less immunogenic but still preserves BMP
-Freeze-Dried allograft is least immunogenic but looses structural integrity
and depletes BMP. Purely osteoconductive (crutons)

Distraction Osteogenesis
-Use of distraction to stimulate formation of bone. Under optimal stable
conditions, bone forms via intramembranous ossification (unstable conditions
form enchondral ossification or even pseudoarthrosis).
-Histologic phases:
1. Latency phase: 5-7 days

Reza Omid MD

2. Distraction phase: 1mm/day (divided into 0.25mm per 6 hours) or 1 inch

per month.
3. Consolidation phase: twice as long as the distraction phase
-Uses for distaction osteogenesis:
o Limb lengthening
o Hypertrophic non-union
o Deformity correction via differential lengthening (Taylor spatial
frame for Blounts disease)
o Segmental bone loss via bone transport
-Conditions that promote optimal bone formation during distraction
osteogenesis:
o Low energy corticotomy/osteotomy (corticotomy is better because leaves
medullary canal intact)
o Minimal soft tissue stripping at corticotomy site
o Stable ex-fix construct
o Latency period of 5-7 days (no lengthening done during this time)
o Distraction done at 0.25mm/6 hours
o Neutral fixation interval (no distraction done during consolidation phase)
o Normal physiologic use of the extremity including weight bearing

Bone Metabolism
-Bone serves as a reservoir for >99% of the bodys calcium. Plasma calcium
(<1%) is about equally free and bound (to albumin). Calcium is absorbed in the
duodenum by active transport (requires ATP, calcium binding proteins and
Vitamin D 3 ) and passive diffusion in the jejunum. The kidney reabsorbes 98% of
the calcium (60% in the proximal tubule). The primary homeostatic regulator of
serum calcium are PTH and vitamin D 3 . Most people have a positive calcium
balance during the first 3 decades and a negative balance during their 4th decade
and after that. 400 mg of calcium is released from bone daily.
-Dietary requirement of elementary calcium is:
o Children <10: 600 mg/d
o Age 10-25: 1300 mg/d
o Age 25-65: 750 mg/d
o Pregnancy: 1500 mg/d
o Lactating: 2000 mg/d
o Fractures: 1500 mg/d
o Post-menopausal: 1500 mg/d
o Elderly >65: 1200 mg/d
-8oz of milk has 250mg of elementary calcium
-Phosphate is 85% in the bone and is mostly unbound in the serum. Resorbed
by the proximal tubules. Dietary intake of phosphate is usually adequate (1001500 mg/d)
-Parathyroid hormone is a peptide secreted from the chief cells of the
parathyroid glands. PTH directly activates osteoblasts and modulates renal

Reza Omid MD

phosphate filtration. Decreased calcium levels in the extracellular fluid stimulates

2 cells to release PTH. PTH acts on the intestines, kidney and bone and causes
bone resportion to increase serum calcium levels.
-Vitamin D is a naturally occurring steroid activated by UV sunlight and from
dietary intake. Vitamin D helps actively absorb calcium from the duodenum and
also at the kidney. Phenytoin (as well as most other anticonvulsant meds)
causes impaired metabolism of vitamin D. Primary function of vitamin D is to
increase the calcium and phosphate absorption by the intestines. Daily intake of
vitamin D should be 800 mg/d.
-Vitamin D metabolism is shown below:

-Calcitonin is a peptide produced by clear cells of the thyroid gland. Increased

serum calcium levels cause secretion of calcitonin (controlled by 2 receptors).
Calcitonin decreases osteoclast number and activity and leads to a decrease in
serum calcium.
-Markers of bone resorption:
1. Urinary hydroxyproline
2. Pyridoline cross-links
-Serum alkaline phosphatase is a marker of bone formation

Reza Omid MD

Osteomalacia

Description
o Failure of mineralization of bone due to multiple etiologies (see
table below).
o Rickets is osteomalacia in children
o Lack of vitamin D is the underlying factor
Poor nutritional intake
Lack of sunlight
Renal or Liver disease
History & Physical
o Most common symptom is pain, sometimes localized, more often
bilateral and symmetrical; often initially vague but gradually
becomes severe.
o May be proximal muscle weakness
Etiology

-Seen commonly in chronic alcoholics

Pathophysiology
o The total amount of bone is normal (unlike osteoporosis) but there
is a lack of mineralization
o Serum calcium is low normal, phosphate is very low and alkaline
phosphatase is very high
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Reza Omid MD

o Serum vitamin 25-OH-D is markedly depressed, while 1,25(OH)

levels may be initially normal, although they too eventually fall.
o PTH levels tend to rise considerably, resulting in relative
preservation of the serum calcium (at the expense of the bones)
Imaging
o Radiographs reveal generalized osteopenia
Classically multiple bilateral and symmetrical cortical lucent
areas in the ribs, scapula, pelvis and femoral neck. These
lucent areas represent stress fractures and typically lie
perpendicular to the long axis of the bone (sometimes
referred to as Loosers zones or Milkmans lines)
The axial skeleton is more often affected clinically than the
peripheral skeleton
Pathology
o Microscopic examination (transiliac bone biopsy) is required for
diagnosis and must reveal at least 10% of total bone volume
constituted by non-mineralized matrix (osteoid) and widened
osteoid seams are seen.
Treatment
o Large doses of vitamin D

Primary Hyperparathyroidism
-Overproduction of PTH from an hypertrophy/adenoma/carcinoma which leads to
increased serum calcium and decreased serum phosphate.
-Leads to osteopenia, osteitis fibrosa cystica (fibrous replacement of marrow),
brown tumors (giant cells, RBC and hemosiderin) and chondrocalcinosis
-Radiographic findings include deformed osteopenic bones, fractures, areas of
radiolucency (at tufts of phalanges, distal clavicle, vertebral end plates), soft
tissue calcifications

Albright Hereditary Osteodystrophy

-Form of pseudohypoparathryroidism (lack of effect of PTH at target cells,

PTH levels normal to high) associated with:
st th th
1. Short 1 /4 /5 metacarpals and metatarsals
2. Brachydactyly
3. Exostosis
4. Obesity
5. Diminished intelligence
-Pseudo- pseudohypoparathryroidism is a normocalcemic disorder which is
phenotypically similar to pseudohypoparathryroidism however there is a normal
response to PTH.

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Reza Omid MD

Renal Osteodystrophy (Secondary

Hyperparathyroidism)
-Abnormal bone metabolism in patients with chronic renal disease.
-Glomerular damage causes phosphate retention and hyperphosphatemia,
inhibits vitamin D production and decreased GI absorption of calcium and also
increased phosphate which leads to ectopic calcification (basal ganglia)
-Tubular damage causes loss of -hydroxylase activity so decreased vitamin D
production which decreases GI absorption of calcium leading to hypocalcemia
and secondary hyperparathyroidism. Phosphate retention also occurs which
causes a rise in PTH as well. The elevated PTH then causes osteitis fibrosa,
ectopic calcifications and osteomalacia (osteopenia & fragility fractures).
-Traditionally, patients on dialysis were also having worsening of their
osteomalacia due to the high aluminum levels in the dialysis fluid. The aluminum
competed with other ions to prevent proper formation of the hydroxyapatitie
crystals. Now days the dialysis fluid is not made with aluminum so this is not so
much of a problem.
-Treatment of renal osteodystrophy is to give phosphate binders as well as high
levels of vitamin D

Rickets
-In children the equivalent to osteomalacia in adults
-Failure of mineralization leading to changes in the physis in the zone of
provisional calcification (increased width and disorientation of the physis)
-Cortical thinning and bowing
-Several subtypes of Rickets:
1. Nutritional Rickets
a. Vitamin D deficiency: rare except for in Asians, premature
babies and patients with sprue (malabsorption). Low calcium and
phosphate, increased PTH, low vitamin D levels.
i. Rachitic rosary
ii. Bowing of the knees
iii. Codfish vertebrae
iv. Coxa vara
v. Milkmans fracture (Loosers lines)
vi. Growth retardation
vii. Muscle hypotonia
-Treatment is 5000 IUD Vitamin D
b. Calcium deficiency
c. Phosphate deficiency
2. Hereditary Vitamin D-dependent Rickets
-Similar to vitamin D deficiency rickets but worse
-Patients may have total baldness
a. Type I: defect in renal 25-OH Vitamin D 1-hydroxylase enzyme

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Reza Omid MD

3.

b. Type II: defect in intracellular receptor for 1,25 (OH) 2 vitamin D

Familial Hypophosphatemic Rickets
-aka phosphate diabetes
-X-linked dominant
-Due to impaired renal tubular reabsorption of phosphate
-Vitamin D resistant rickets (impaired vitamin D response)
-Normal GFR
-Treatment is phosphate replacement and high dose vitamin D

Osteoporosis
-Quantitative (not qualitative) defect of bone
-2.5 SD below the peak bone mass of a 25 year old
-Vertebral body fracture is the most common
-Lab values are normal, need DEXA scan
-Z-scores give results for age controlled
-T-scores gives results for young normal adults
-Must rule out hyperthyroidism, hype-PTH, Cushings and malignancy
-Risk Factors: sedentary, thin Caucasian women of norther European descent,
smokers, heavy drinkers, dilantin use, poor diet, breast feeders, family history,
premature menopause.
-History of 2 osteoporotic vertebral fractures is the strongest predictor of
subsequent vertebral fractures in post-menopausal women.
-3 major types of osteoporosis:
1. Senile (age-related): affects trabecular bone and cortical bone
a. Related to poor calcium absorption
b. Hip fractures and Pelvis fractures
2. Post-menopausal (high turnover): affects trabecular bone primarily
a. Vertebral body and distal radius fractures
b. Distal radius fractures
3. Glucocorticoid induced (low turnover):
-Treatment for Osteoporosis:
1. Diet and adequate calcium and vitamin D
2. Weight bearing exercise
3. Estrogen therapy evaluation (works best when started within 6 years of
menopause)
4. Bisphosphonates (Fosamax): bind farnesyl disphosphate synthase and
cause apoptosis in osteoclasts.. Can also be used for OI, Padgets,
Osteopetrosis and metastasis
5. Calcitonin
6. Tamoxifen
7. SERMs

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Reza Omid MD
8.

Anabolic: PTH (Forteo) is PTH given intermittently to stimulate

osteoblasts but can only give for 2 years, may cause osteosarcoma

Idiopathic Transient Osteoporosis of the Hip

-Uncommon disorder of exclusion
-Most commonly seen in 3rd trimester of pregnancy but also occurs in men
(middle age)
-Present with groin pain, limited ROM and localized osteopenia (without history
of trauma)
-MRI is highly sensitive but not specific and must rule out infection,
osteonecrosis and neoplasm.
-Self-limited disease and resolves within 6-8 months with restricted WB and pain
control.

Osteochondroses
-Osteochondrosis is a disease causing degenerative changes in the ossification
centers of the epiphysis of bones, particularly during periods of rapid growth in
children. The process can continue to AVN. AKA traction apophysitis. May or
may not be associated with trauma, inflammation of joint capsule, or vascular
insult/secondary thrombosis.
-Examples of osteochondroses:
1. Van Necks Disease: ischiopubic synchrondosis
2. Legg-Calve-Perthese Disease: femoral head
3. Osgood-Schlatter Disease: tibial tuberosity
4. Sinding-Larsen-Johansson Syndrome: inferior patella
5. Blouts Disease: proximal tibial epiphysis
6. Severs Disease: calcaneus
7. Kohlers Disease: navicular
nd
8. Friedbergs Infraction: 2
metatarsal head
9. Scheuermanns Disease: discovertebral junction
10. Panners Disease: capitellum
11. Thiemanns Disease: phalanges of the hand
12. Kienbocks Disease: lunate
th
13. Iselins Disease: 5 metatarsal base
14. Preisers Disease: scaphoid

2)

Science of Joints

Articular Cartilage

-Articular cartilage is a resilient load bearing tissue that forms the articulating
surface of joints. It provides a surfaces with low friction and absorbs mechanical
shock and spreads the load onto subchondral bone.
-Contains no nerves, blood vessels or lymphatics

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Reza Omid MD

-Collagen of articular cartilage provides tensile strength

-Proteoglycans of articular cartilage provides compressive strength
-Thickest cartilage is under the patella
-4 Zones of Articular Cartilage:
1. Superficial zone: resists shear force, 10-20%
a. Lamina splendens (unique superficial layer that consists of fibrils
and little or no PG and no cells
b. Ellipsoidal chondrocyte layer
-High water content
-Low PG content
-Acts as a barrier against movement of molecules between the synovium
and the articular cartilage
-Damage to this zone may contribute to development of OA. Also damage
to this zone could release molecules into the synovial fluid and stimulate a
immune response.
2. Middle (Intermediate) zone: resists compressive forces, 40-60%
-Rounded chondrocytes spread out
-Most metabolically active
-Randomly arranged collagen fibers
3. Deep zone: resists compressive forces, 30%
-Chondrocytes in columns
-Low water content
-High PG content
-Largest collagen fibers, fibers arranged vertical (perpendicular to surface)
*Tidemark separates the deep zone from the calcified zone. It resists
shear forces.
The number of tidemarks increases with age as the tissue is remodeled.
4. Calcified zone:
-seperates the articular cartilage from the subchondral bone
-anchors the cartilage to the bone (equivalent of Sharpys fibers with
ligaments)
-Articular Cartilage Composition:
1. Water: 65-80% of total weight
a. Resists compression
2. Type II collagen: 10-20% of total weight (50% of dry weight)
a. Provides tensile properties and acts as a framework to immobilize
ECM & PG
3. Proteoglycan Aggragate: 5-10% of total weight
a. GAGs contain carboxyl & sulfate groups (keratin and chondroitin
sulfate). GAGs are negatively charged and bind water (act like a
sponge) and the negative charges repel each other maximizing
volume.

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Reza Omid MD

Chondrocytes: 2% of total weight

a. Produce all the ECM macromolecules and degradative enzymes.
b. Chondrocytes are responsible for formation of all ECM
macromolecules and maintenance of articular cartilage. They are
derived from mesenchymal cells and are metabolically active
(anaerobic). There numbers decrease with age. Chondrocytes
respond to environmental stimuli. Exposure of IL-1 may lead to
degredation of ECM.
-Articular cartilage nutrition is via diffusion and requires joint mobilization to
allow for movement of the synovial fluid over the articular surface.
4.

Collagen
-At least 15 types of collagen, all triple helix structures composed of 3 -chain
polypeptides with large quantities of glycine and praline. Also contain
hydroxyproline, hydroxylysine and glycosylated hydroxylysine.
-Hydroxylation of collagen requires vitamin C
1. Type 1 Collagen: most common type of collagen
a. Found in bone, tendon, ligament, meniscus, annulus fibrosus of
discs, skin, pubic symphysis, articular discs (AC/SC joints)
b. Any site where fibrocartilage is found (microfracture)
2. Type 2 Collagen:
a. Found in articular (hyaline) cartilage, nucleus pulposus of discs.
b. Early fracture callus
3. Type 3 Collagen: Found in skin and blood vessels
4. Type 4 Collagen: Found in basement membranes
5. Type 6 Collagen:
a. Minor component of normal articular cartilage
b. Increases significantly in early OA
6. Type 9 Collagen: Adhesive cartilages which link together with Type 11
collagen and other type 2
7. Type 10 Collagen:
a. Found only near calcified cartilage (calcified zone of articular
cartilage and hypertrophic zone of growth plate)
b. Produced by hypertrophic chondrocytes during enchondral
ossification seen in:
i. Fracture callus
ii. Growth plate
iii. HO formation
iv. Calcifying cartilaginous tumors
c. Genetic defect of type 10 collagen seen in Schmidss metaphyseal
chondroplasia
8. Type 11 Collagen: More adhesive than type 9
9. Type 12 Collagen: Found in tendons

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Reza Omid MD

-Proteoglycans (PG) are complex macromolecules that consist of a protein

core with covalently bound GAG chains aka proteoglycan aggregate. Half life of
PG are 3 months. PG produce cartilages porous structure and trap and hold
water (regulate and retain water in the matrix)
-95% of proteoglycans are chondroitin and keratin sulfate. The sulfate
molecules are the negative charge that attracts positive cations (Na+& K+) and
increase osmotic pressure to inflate the elastic meshwork with water for
compression properties. Proteoglycan aggregate are made up of a hyaluronic
acid with several aggregan molecules bond to it. Each aggrecan molecule has
several regions: chondroitin rich region and keratin rich region. Aggregate size
decreases with age.
-Glycosaminoglycans are long chain disaccharide units that make up PG once
bound to hyaluronic acid. Types of GAG:
1. Chondroitin Sulfate (most prevalent, found in articular cartilage,
concentrated at ends of aggrecan molecules)
a. 4-isomer decreases with age
b. 4-isomer increases with OA
c. 6-isomer remains constant with age
d. total chondroitin decreases with age
2. Keratin Sulfate (articular cartilage, concentrated in middle of aggrecan
molecules)
a. Increases with age
b. Decreases with OA
3.
4.

Dermatan Sulfate
Hyaluronate (HA)

a. HA is unique because it is not sulfated like the other GAG and not
covalently bound to a protein core so not part of a PG
-Glucosamine and Chondroitin Sulfate supplements are over the counter
chondroprotective agents. Glucosamine stimulates chodrocytes and synoviocyte
activites. Chondroitin sulfate inhibits degredative enzymes and prevent sfibrin
thrombus formation in periarticular tissue. These supplements improve pain,
joint line tenderness, ROM and walking speed but no studies show that they
affect mechanical properties or biomechanical consistency of articular cartilage.
-Cartilage Oligometric Protein (COMP) is a protein concentrated primarily in
the chondrocyte territorial matrix. COMP appears to be present mainly in
articular cartilage and binds to chondrocytes and serves as a serum marker for
cartilage turnover and of progression of cartilage degeneration in patients OA/RA
or any inflammatory arthritis. COMP can also be used for monitoring efficiency
of treatment.
-Creep is a time-dependent deformation of a viscoelastic tissue (articular
cartilage) due to a constant load). Rate of creep is governed by the rate at
which fluid may be forced out from the tissue, which in turn, is governed by the
permeability and stiffness of the matrix. The tissue will creep until an
equilibrium value is reached.

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Reza Omid MD

-Mechanosignal transduction occurs via integrins in chodrocytes as pressure

or deformation is transmitted to the cell to increase mRNA expression.

Synovium
-Composed of 2 distinct layers:
1. Intimal lining: in direct contact with IA cavity and responsible for
production of hyaluronic acid
a. Loosely organized and avascular layer 1-2 cells layers thick
2. Sublining: lies beneath the intimal lining and is acellular and contains
scattered blood vessels, fat cells and fibroblasts.
-Cell types present in the synovium:
1. Type A cells: macrophage like (phagocytosis)
2. Type B cells: fibroblast like (produce synovial fluid)
-Synovial fluid consists of HA, lubricin, proteinase, collagenase and PG. It is an
ultrafiltrate of plasma and contains no RBC, clotting factors or hemoglobin

Meniscus
-Deepens the articular surface of synovial joints and found in the:
1. AC joint
2. SC joint
3. Glenohumeral joint
4. Hip joint
5. Knee joint
-The meniscus broadens the contact area and distributes the load. More elastic
and less permeable than cartilage.
-Composed of type 1 collagen (fibrocartilage)
-Medial meniscus of the knee is semicircular (C-shaped)
-Lateral meniscus of the knee is circular
-2 meniscofemoral ligaments run from the posterior horn of the lateral
meniscus to the medial femoral condyle. Anterior to the PCL is the ligament of
Humphrey and posterior to the PCL is the ligament of Wrisberg.
-2 cell types found within meniscus:
1. Fusiform cells in the superficial zone
2. Fibrochondrocytes (ovoid/polygonal cells) found in the remainder of the
tissue. These cells are responsible for meniscal healing in the peripheral
zone. Meniscal tears with a rim width <4mm have the best healing
characteristics
-Meniscus collagen fiber orientation is principally circumferential. A few radial
fibers act as ties to provide rigidity and help resist longitudinal splitting. 3
framework layers are found in the menisci:
1. Superficial layer: fine fibrils in meshlike matrix
2. Surface layer: irregularly aligned bundles
3. Middle layer: circumferential large coarse fibrils which are main force
resisting fibers
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Reza Omid MD

-Meniscus motion (excursion is AP displacement) occurs with knee range of

motion of 0-120:
o
Medial meniscus excursion is 5.1 0.96
o
Lateral meniscus excursion is 11.2 3.27
-Limited peripheral blood supply to the meniscus originates from the lateral and
medial genicular arteries (both inferior and superior). It penetrates 10-30% of
the medial meniscus and 10-25% of the lateral meniscus. The medial inner 2/3
of the meniscus derives nutrition from the synovial fluid via mechanical pumping.
-Anterior and posterior horns of the menisci are most richly innervated
(particularly the posterior horn). During extremes of flexion/extension, the horns
of the menisci become taut and this increases tension then activates the
mechanoreceptors. 3 types of mechanoreceptors found:
1. Ruffini endings
2. Golgi tendon organs
3. Pacinian corpuscles
-Following ACL transaction, the meniscus undergoes alterations in ECM, including
increased water content and decreased GAG concentration. With age, meniscus
undergo discoloration and increased deposition of calcium pyrophosphate
dehydrate crystals, but water content does not change with age (unlike articular
cartilage). However there is an increased chondroitin 6 to chondroitin 4 ratio
with age (similar to articular cartilage).

Synovial Fluid
-Synovial fluid id an acellular plasma ultrafiltrate that lubricates the joint. Its
high viscosity gives it important mechanical properties and is related to large
amounts of polymerized hyaluronic acid.
-Should be sent for gram stain, culture, WBC with differential, and crystal
analysis
-Dye should be injected only after fluid is obtained from the joint because the
bactericidal effect of iodinated contrast material can cause a false negative
culture result.
-Non-inflammatory synovial fluid contains 200 WBC, 25% PMN, glucose and
protein values equal to serum values and volume <3.5 cc.
-Inflammatory synovial fluid contains 2,000-75,000 WBC, 50% PMN, glucose
levels moderately decreased and volume >3.5 cc. Inflammation decreases
viscosity of synovial fluid so it decreases the string sign length.
-Infectious synovial fluid contains >50,000-80,000 WBC, 75% PMN, glucose
levels significantly decreased and protein levels increased. Inflammation
decreases viscosity of synovial fluid so it decreases the string sign length.

Non-Inflammatory Arthritis
1.

Osteoarthritis:
a. Most common form of arthritis (most common in knee)
b. Increased water content (age causes decreased water content)
19

Reza Omid MD

c.
d.
e.
f.
g.
h.

2.

Increased chondroitin 4 sulfate

Decreased keratin sulfate
Increased cathepsins B&D
Increased metalloproteinases (collagenase, gelatinase)
IL-1 increases synthesis of these enzymes
Post-menopausal arthritis of the medial clavicle seen on the
dominant extremity
i. OA may be primary (intrinsic defect) or secondary (trauma,
infection, congenital)
j. Pathologic changes of OA include:
i. subchondral cysts (arise secondary to microfracture and may
contain an amorphous gelatinous material)
ii. osteophytes (as a compensation to abnormal joint forces)
iii. joint space narrowing
iv. eburnation of joint surface
v. chondral cloning (>1 chondrocyte per lacunae)
vi. replication and breakdown of tidemark
vii. sclerotic bone formation
k. Radiographic changes of OA include:
i. Osteophytes
ii. Joint space narrowing
iii. Subchondral sclerosis
iv. Subchondral cyst
v. Hand (DIP/PIP/CMC)
vi. Knee (asymmetric involvement
vii. Hip (superolateral involvement)
Neuropathic Arthritis (Charcot Joint Disease):
a. Extreme form of OA caused by disrupted sensory innervation
(neuropathy)
b. Present with swelling, warmth, erythema, minimal pain, variable
WBC & ESR (very similar to osteomyelitis and both are common in
DM)
c. Charcot joint is usually a contraindication for a total joint
arthroplasty
d. Causes of Charcot joint:
i. Diabetes Mellitus
ii. Syphilis
iii. B-12 deficiency
iv. Leprosy (2nd most common cause for UE involvement)
v. Syringomyelia (most common cause for UE involvement)
vi. Myelomenigocele/Spinal cord injury
e. Radiographic evaluation of Charcot joint:
i. Severe destruction of both sides of the joint

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Reza Omid MD

3.

4.

ii. Scattered chunks of bone embedded in fibrous tissue,

fragmentation of bone, heterotopic ossification
iii. Very difficult to distinguish between osteomyelitis and
Charcot on x-ray, MRI and labs
iv. Technitium bone scan may look similar (hot) for both
osteomyelitis and Charcot.
v. Indium leukocyte scan may be hot or positive for
osteomyelitis and cold or negative for Charcot
f. Eichenholtz Classification:
i. Development phase: fragmentation of bone
ii. Coalescense phase: absorption of small bone fragments and
fusion of joints
iii. Remodeling phase: healing and new bone formation
g. Treatment of Charcot Arthropathy:
i. Initial treatment is to off load the foot with a total contact
cast, usually for 3-6 months
ii. Involvement side skin temperature similar to the uninvolved
side is the best indicator for D/C of the cast. Acute phase
(fragmentation and collapse) of Charcot is characterized by
an increase of 3-4F between involved (hot) and uninvolved
side.
iii. If total contact casting fails, reconstructive fusion and finally
amputation may be needed.
Acute Rheumatic Fever:
a. Arthritis and arthralgias following untreated group A -hemolytic
strep infection (pharyngitis not cellulitis)
b. Acute onset of red, tender, extremely painful joint effusions
c. Carditis, erythema marginatum (painless macules), subcutaneous
nodules (extensor surface of UE) and chorea
d. Arthritis is migratory and involves multiple large joints
e. Diagnosis by Jones criteria (2 major or 1 major and 2 minor)
f. Antistreptolysin O titers elevated in 80% of patients
g. Treatment is PCN and ASA
Ochronosis:
a. Degenerative arthritis secondary to alkaptonuria
b. Error of homogentisic acid oxidase enzyme system (tyrosine and
phenylalanine catabolism)
c. Excess homogentisic acid deposited in joints and then polymerize
(turn black)
d. Black urine
e. Onchronotic spondylitis (calcification and narrowing of the
intervertebral discs) in 4th decade of life.

Inflammatory Arthritis
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Reza Omid MD
1.

Rheumatoid arthritis:
a. Required diagnostic criteria: morning stiffness, swelling, nodules,
positive lab values and radiographic findings.
b. Cell mediated (T-cell) response against soft tissue, then cartilage
and bone
c. Mononuclear cells are primary cellular mediator of tissue
destruction in RA
d. Associated with HLA-DR4 and HLA-DW4
e. Elevated ESR, CRP and RF (IgM or IgG against the Fc portion of
IgG), decreased complement levels
f. Subcutaneous nodules (are strongly associated with + RF) are seen
in 20% of patients with RA
g. Hands with ulnar deviation of MCP, Hallus valgus, claw toes
h. Common in knee, elbow, shoulder, ankle and c-spine.
i. Systemic manifestations include: rheumatoid vasculitis, pericarditis,
pulmonary disease (pleuritis, nodules, fibrosis), c-spine
destabilization
j. Radiographic finding of RA:
1. periacetabular erosions
2. symmetric joint involvement
3. osteopenia
4. protrusion acetabuli
k. Feltys syndrome: RA + splenomegaly + leucopenia
l. Stills disease: acute onset arthritis + fever + rash +
splenomegaly
m. Rheumatoid factor is positive for:
1. RA
2. Sjorgrens syndrome
3. Sarcoidosis
4. SLE
n. Rheumatoid factor is negative for:
1. Ankylosing spondylitis
2. Gout
3. Psoriatic arthritis
4. Reiters syndrome
o. Antinuclear antibodies are found in:
1. SLE
2. Sjogrens syndrome
3. Scleroderma
p. Synovectomy decreases pain and swelling associated with the
synovitis but does not prevent radiographic progression or the
future need for total knee arthroplasty nor does it improve joint
ROM. After synovectomy, the synovium initially regenerates
normally but degenerates to rheumatoid synovial tissue over time.

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Reza Omid MD
2.

3.

4.

5.

Sjogrens Syndrome:
a. Autoimmune exocrinopathy
b. Similar presentation as RA
c. Decreased salivation
d. Decreased lacrimal gland secretion (keratoconjunctivitis) sicca
complex
e. Lymphoid proliferation
Systemic lupus erythematosus (SLE):
a. African american women
b. Fever butterfly malar rash, pancytopenia, nephritis, pericarditis and
polyarthritis.
c. Joint involvement is most common feature (75%), acute red tender
swelling of PIPs, MCPs, carpus, knee and other joints.
d. Not as destructive as RA
e. Mortality related to renal disease
f. Positive ANA
g. Polymyalgia Rheumatica: aching and stiffness of shoulder and
pelvic girdle, malaise, HA and anorexia. Markedly elevated ESR,
anemia and increased alkaline phosphatase. May be associated
with temporal arteritis (which requires biopsy for definitive
diagnosis). Treat symptomatically or with steroids if refractory.
Temporal arteritis needs urgent steroids to prevent blindness.
Relapsing polychondritis:
a. Episodic inflammation
b. Diffuse self-limited arthritis
c. Progressive cartilage destruction systemic vasculitis
d. Primarily involves the ears (thickening)
e. Also seen are inflammatory eye disorders, tracheal involvement,
hearing disorders and sometimes cardiac involvement.
f. Autoimmune disease involving type 2 collagen
g. Supportive treatment, consider dapsone
Juvenile rheumatoid arthritis:
a. 3 major types of JRA:
1. systemic (20%)
2. pauciarticular (30%): 4 joints involved
3. polyarticular (50%): 5 joints involved
b. early onset is before teens, late onset is as teen or later
c. Seronegative polyarticular JRA seen in girls
d. Seropositive polyarticular JRA seen in girls and frequently
develops into adult RA
e. Early onset pauciarticular JRA seen in girls and associated with
iridiocyclitis in 50%
f. Late onset pauciarticular JRA seen in boys

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Reza Omid MD

6.

g. Treatment of JRA is high dose ASA with frequent ophthalmologic

examinations. Only occasionally is gold or remittive drugs used.
Spondyloarthropathies
-HLA-B27 is positive for all these conditions
-aka enthesopathies (occur at ligament insertion onto bone)
-RF negative
a. Ankylosing Spondylitis:
1. bilateral sacroiliitis acute uveitis
2. HLA-B27 is diagnostic
rd th
3. insidious onset of back pain and hip pain during 3 -4
decade
4. progressive spinal kyphosis (chin to chest deformity)
5. squaring of vertebrae
6. vertical syndesmophytes
7. obliteration of SI joints
8. whiskering of enthesis
9. difficult c-spine fractures associated with epidural
hemorrhage
10. associated with protrusion acetabuli
11. often associated with heart disease and pulmonary fibrosis
12. extraarticular manifestations include: amyloidosis,
arachnoiditis, aortitis, iritis, colitis, sarcoidosis
13. DISH is very similar to AS except the radiographic findings
are non-marginal syndesmophytes (AS has marginal
syndesmophytes) and appears as melting wax. It is
predominantly on the right side in the thoracic spine.
b. Reiters Syndrome:
1. classic triad: conjunctivitis, urethritis, oligoarticular arthritis
(cant see, cant pee, cant climb a tree)
2. painless oral ulcers, penile ulcers and pustular lesions on
extremities, palms, soles (aka keratoderma
blennorrlagium)
3. plantar heel pain is common (fluffy periosteal calcifications
near calcaneal spur.
4. metatarsal head erosion and calcaneal periostitis is
common with reoccurrence
5. HLA-B27 positive
6. sacroilitis is 60%
7. Treatment is NSAIDs, PT, sulfa drugs
c. Psoriatic Arthropathy:
1. 5-10% of patients with psoriasis
2. HLA-B27 seen in 50%
3. oligoarticular involvement which affects small joints of the
hands and feet.

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Reza Omid MD

nail pitting, fragmentation and discoloration

sausage digits
6. pencil in a cup deformity with DIP involvement
d. Enteropathic Arthritis:
1. 10-20% of patients with crohns disease and ulcerative
colitis
2. 5% or more experience axial disease
3. common in large weight bearing joints
4. presents as acute monoarticular synovitis that precedes
bowel symptoms
5. HLA-B27 in 50%
Crystal deposition disease
a. Gout:
1. disorder of nucleic acid metabolism causing hyperuricemia
which leads to monosodium urate crystal deposition in
joints.
2. crystals activate inflammatory mediators, activate platelets,
IL-1 and complement.
3. inflammatory mediators inhibited by colchicines
4. phagocytosis is inhibited by indomethacin and
phenylbutazone
5. great toe involvement (podagra)
6. tophi deposition (ear, eyelid, olecranon, Achilles)
7. renal disease/stones in 2%
nd
8. kidneys are 2
most commonly affected organ
9. x-ray: punched out periarticular erosions with sclerotic
overhanging borders
10. needle shaped crystals
11. negative bifringent crystals (yellow): means the long axis
of the crystal is parallel to the compensator and the crystal
is yellow (if the gout crystal was perpendicular it would
appear blue)
b. Pseudogout:
1. aka calcium pyrophosphate deposition disease (CPPD)
2. a disorder of pyrophosphate metabolism
3. acute attacks (like gout) but especially prevalent in the
knee
4. short blunt rhomboid-shaped crystals
5. weakly positively bifringent (blue): means the long axis of
crystal is parallel to compensator and crystal is blue (if the
CPPD crystal was perpendicular it would appear yellow)
6. chondrocalcinosis is common
-Chondrocalcinosis: calcification of the cartilage and meniscus.
Seen commonly in:
4.
5.

7.

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Reza Omid MD

pseudogout (CPPD)
ochronosis
3. hyperparathyroidism
4. hypothyroidism
5. hemachromatosis
6. old trauma
c. Calcium Hydroxyapatite Crystal Deposition
1. destructive arthropathy due to IA deposition of calcium
hydroxyapatite crystals which releases enzymes
(collagenase and neutral proteases)
2. commonly seen in knee and shoulder
3. in the shoulder results in cuff tear arthropathy (aka
Milwaukee shoulder)
1.
2.

Infectious Arthritis
1.

2.

3.

Pyogenic:
a. From hematogenous spread or extension of osteomyelitis
b. At risk patients include:
i. IVDA
ii. Sexually active (GC is most common: intracellular
diplococcus)
iii. DM
iv. RA
v. Trauma (open facture or CFI)
vi. Surgery
c. Destruction of cartilage occurs via 2 mechanisma:
i. Direct (proteolytic enzyme degredation)
ii. Indirect (increased pressure and lack of nutrition)
d. Treatment is I&D with 2-3 weeks IV antibiotics
Tuberculous:
a. Chronic granulomatous infection (mycobacterium tuberculosus)
b. Via hematogenous spread
c. Most common in spine and LE
d. 80% monoarticular
e. positive PPD and acid fast bacilli on synovial gram stain
f. granulomas with langerhan giant cells on histology
g. radiographic changes seen:
i. subchondral osteoporosis
ii. cystic changes
iii. notch-like bony destruction at joint edges
iv. osteolytic changes on both sides of the joint
h. treatment is I&D with R.I.P.E. antibiotics
Lyme disease:

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Reza Omid MD

4.

a. acute self-limited joint effusions, especially in the shoulder and

knee
b. recur frequently
c. borrelia burgdorferi (spirochete)
d. transmitted by Ioxodes tick bite
e. stages of disease:
i. Rash (erythema chronicum migrans) and arthralgia
ii. Myocarditis, Bells palsy, meningitis and heart block
iii. Arthritis and chronic CNS changes
f. immune complexes and cryoglobulins accumulate in the synovial
fluid
g. diagnosis is via ELISA because gram stain is negative
h. treatment in doxycycline in stage 1 and ceftriaxone in stage 2 or 3.
Fungal:
a. more common in neonates, AIDs patients and IVDA
b. candida albicans
c. KOH prep of synovial fluid
d. treat with 5-flucytosine
e. blastomycosis, coccidiomycosis and histo often require
amphotericin and sometimes given IA to limit systemic effects

Hemorrhagic Arthritis
1.

Hemophilic Arthropathy:
a. X-linked recessive
b. Factor 8 deficiency (hemophilia A) or factor 9 (hemophilia B)
c. Repeat hemarthrosis due to minor trauma, leading to synovitis,
cartilage destruction and joint deformity
d. Disease severity:
i. mild is 5-25% levels
ii. moderate is 1-5% levels
iii. severe is 0-1% levels
e. Knee is most commonly involved followed by elbow > ankle>
shoulder>spine
f. Radiographic findings:
i. Squared off patella = Jordans sign (also seen in JRA)
ii. Widening of intercondylar notch
iii. Enlarged femoral condyles that appear to fall off the tibia
g. Iliacus hematoma can cause femoral nerve palsy
h. Management is to replace the factor levels, splint, compression,
steroids, synovectomy and arthroplasty
i. Synovectomy reduces the incidence of recurrent hemarthrosis (less
pain and swelling)

27

Reza Omid MD

2.

3.

j. Synoviorthesis (destruction of synovium with IA injection of

radioactive P32 chromic phosphate) for treatment of chronic
hemophilic synovitis that is resistant to conventional treatment
k. Factor levels should be maintained @100% during the first post-op
week and 50-75% during the 2nd week. Presnec of inhibitor that
represents an IgG to the clotting factor proteins (causes the patient
to have no response to factor replacement therapy) is a relative
contraindication to any elective procedure. This inhibitor is seen in
5-25% of patients.
l. New monoclonal factor 8 is prone to induce inhibitors
Sickle Cell Disease:
a. Leads to local infarction due to capillary stasis
b. Bone infarcts and ischemic necrosis may occur in multiple bones in
sickle cell disease
c. Thalassemia does not produce infarcts or necrosis
d. Dactilitis with metacarpal/metatarsal periosteal new bone formation
may also be seen.
e. Osteomyelitis is uncommon (staph aureus is most common but
salmonella is most characteristic). Salmonella spread can come
from gallbladder infection
f. AVN of the femoral head is common requiring THA
g. Results of TJA are poor with sickle cell due to ongoing negative
bone remodeling
PVNS

Growth and Development of the

Skeleton
3)

Limb Development

-The appendicular skeleton forms between the 4th and 8th weeks of gestation.
The limb bud begins as an out-pouching from the lateral body wall and initially
consists of both ectodermal and mesodermal layers.
-This initial outgrowth appears to be under the control of the FGF family

because FGF-1, FGF-2 and FGF-4 all are able to induce the formation of
ectopic limb buds.

-The progressive enlargement of the limb bud results from biomechanical

signaling between the layer of ectodermal cells at the distal layer, apical
ectodermal ridge (AER), and the rapidly proliferating mesodermal cells,
progress zone, adjacent tot his ectodermal layer.
-The apical ectodermal ridge (AER) is to promote the outgrowth of the
limb bud in the proximal distal direction by maintaining the mesodermal
cells in an undifferentiated state.

28

Reza Omid MD

-The role of the progress zone is to secrete a factor that maintains the
AER. If the AER is experimentally removed, the cells immediately subjacent to

the AER undergo massivce cell death, and the limb formation is truncated at a
variable proximal-distal level, depending on the timing of the AER removal. The
severe transverse phocomelic birth defects caused by thalidomide exposure
during the 1st trimester of pregnancy have been postulated to involve damage to
the progress zone.
-Surgical replacement of the AER or implantation of a bead loaded with FGF-4
prevents this cell death and restores the normal proximal-distal axis of limb
formation. The proximal-distal axis of limb formation is therefore under control
of the FGF family.
-As the limb bud enlarges, its constituent cells acquire a positional identity with
respect to each of the three axes (proximal-distal, anterior-posterior, dorsalventral) that ultimately specifies cell fate and sculpts the mesenchymal
condensations that form the precursors of the skeletal elements of the limb.
This positional identity is acquired as cells pass through the progress zone
beneath the AER.
-Cells located in the zone of polarizing activity (ZPA) in the posterior

aspect of the limb bud direct both the number and type of digits
formed. This organizing activity of the ZPA has been traced to the product of
the Sonic hedgehog (Shh) gene. Shh controls the formation of digits by
activating the expression of homeobox (HOX) genes.
-Limb formation along the dorsal-ventral axis of the limb bud is under
the control of a member of the Wnt gene family, Wnt-7a. This regulatory

molecule is expressed in a restricted area on the dorsal aspect of the limb bud
and specifies dorsal-ventral patterning. Misexpression of Wnt-7a on the ventral
aspect of the limb bud in mice results in digits that flex in the dorsal direction
and extend in the ventral direction.
-During the 6th week of development, mesenchymal condensations within the
limb bud, which serve as models for skeletal development, undergo
chondrogenesis as the cells begin the synthesize a cartilage extracellular matrix.
This transformation into cartilage tissue is regulated by the activity of
members of the SOX gene family, specifically SOX5, SOX6 and SOX9.
-Mutations of SOX9 have been linked to camptomelic dysplasia ().
-Three dimentional regulatory axis of limb bud pattern formation:
1. Proximal-Distal: FGF
2. Dorsal-Ventral: Wnt-7a
3. Anterior-Posterior: Shh

4)

Science of Muscluar Tissue

-Myotendon junction is the weakest link in the muscle. It is often the site of
tears, especially with eccentric contractions (muscle lengthens while contracting)

29

Reza Omid MD

-Sarcomere is composed of thick (myosin) and thin (actin) filaments intricately

arranged to allow the fibers to slide past each other. The sarcomere is arranged
into bands and lines:
o H-band: contains myosin only
o I-band: contains actin only
o A-band: contains actin and myosin
o M-line: interconnecting site of myosin
o Z-line: anchors the thin (actin) filaments
-Neuromuscular junction: stimulus for a muscle contraction comes from the
brain and travels down the spine to the muscle. The motor endplate (specialized
synapse formed between the nerve and muscle) releases ACh from presynaptic
vesicles. The Ach then binds to a postsynaptic receptors to cause depolarization
of the SR which then releases calcium into the muscle cytoplasm. Calcium binds
to troponin (on thin filaments) causing them to change the position of
topomyosin (also on the thin filaments) and expose the actin filaments. Actinmyosin cross bridging forms and with ATP breakdown of ATP the thick and thin
filaments slide past one another causing contraction of the muscle.
-Botunlinum A toxin blocks ACh release presynaptically
-Non-depolarizing drugs (curare, pancuronium and vecuronium)
competitively bind to ACh recepts to block impulse transmission (long term
paralytic)
-Depolarizing drugs (succinylcholine) binds to ACh receptors to cause
temporary depolarization of muscle membrane (short term paralytic)
-Anticholinesterases (neostigmine, edrophonium) act at the autonomic
ganglia, prevents breakdown of ACh to enhance its effects. These meds are
reversal agents for non-depolarizing drugs. These meds have muscarinic effects
(bronchospasm, bradycardia, bronchorrhea)
3 Types of Muscle Contraction:
1. Isotonic Contraction:
-muscle tension is constant throughout the ROM.
-measure of dynamic strength
-free weight exercise is an example
-has several phases:
i. Concentric contraction: the muscle shortens during
contraction
ii. Eccentric contraction: the muscle lengthens during
contraction
2. Isometric Contraction:
-muscle tension is generated but length remains unchanged.
-a measure of static (not dynamic) strength
-increases strength at a specific joint angle at which the training is
being affected

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Reza Omid MD

-benefits seem to occur during the early stages of training or

rehab
-optimal effects occur at maximal contraction and long enough
duration to recruit as many fibers as possible and best when done
several times per day
-example is wall sits
3. Isokinetic Contraction:
-muscle tension is generated as the muscle maximally contracts at
a constant velocity over a full ROM
-best for maximizing strength and are a measure of dynamic
strength
-effective at slow speeds (60/sec)
-cybex machines (exerts a force that equals that exerted by the
person)
i. Concentric contraction phase
ii. Eccentric contraction phase
-Eccentric contraction is a phase of muscle contraction, not a type of
muscle contraction. The muscle lengthens during the contraction (internal
force is less than the external force). Eccentric contractions have the
greatest potential for high muscle tension and muscle injury.
Example is a negative. It is questionable if it is more effective than
other forms of training, some say no.
-Concentric contraction is a phase of muscle contraction, not a type of
muscle contraction. The muscle shortens during the contraction (internal
force exceeds the external force).
-Plyometrics are a special type of exercise. It is implosion training in
which the muscles are loaded suddenly and forcefully stretched before
they can contract. It is very effective at power generation. Like eccentric
loading, it has been shown to increase muscle soreness and have an
increased risk of injury. Examples are catching and throwing a medicine
ball, jumping down from a box and jumping back up. The stretch stores
elastic energy which increases the force of the concentric contraction.
-Closed-chain exercises include loading an extremity with the most
distal segment stabilized or not moving (on the ground). This allows
muscular co-contraction around a joint, which minimizes joint shear
(places less stress on the ACL). Stationary bike is an open chain exercise
and is harmful to an ACL reconstruction.
-Type 1 Muscle Fibers:
o Slow twitch
o Oxidative (red) fibers (slow red ox)
o Aerobic therefore more mitochondria and high capillary density
o Good for endurance sports
o First muscles lost without rehabilitation
o Low anaerobic capacity

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Reza Omid MD

-Type IIA Muscle Fibers:

o Fast twitch
o Glycolytic (white) and oxidative fibers (FOG fast oxidative
glycolytic)
o Not as prevalent in humans (seen in humbingbirds)
o Good for strength
-Type IIB Muscle Fibers:
o Fast twitch
o Glycolytic (white) only (unlike IIA)
o Anaerobic
o Quick contractions with larger and stronger motor units
o Good for sprinters and strength atheletes
o Strength training causes hypertrophy of these fibers
ATP-CP System
-aka Phosphogen system
-meets the metabolic requirement for intense muscle activity that lasts up to 20
sec, such as sprinting a 100-200 meter dash.
-converts stored carbohydrates from within the muscle fiber itself to energy
-does not use oxygen
-does not produce lactate
-energy is derived from the high energy phosphate bonds of ATP
-creatine supplements can increase the amount of work that is produced in 1st
few max-effort anaerobic trials but does not increase peak force production
Lactic Anaerobic System
-meets the metabolic requirement for intense muscle activity that lasts 20-120
sec, such as a 400 meter dash.
-involves hydrolysis of on glucose molecule to ultimately produce lactic acid plus
energy converting 2 molecules of ADP to 2 molecules of ATP
Aerobic System
-when oxygen is available, the aerobic system replenishes ATP through oxidative
phosphorylation and the Krebs cycle. It uses glucose or fatty acids to produce
ATP. Meets the metabolic requirements for episodes of longer duration and
lower-intensity muscle activities.
-Aerobic exercise in a healthy adult is recommended for 3-5 days per week for
20-60 min per session. Training should be at 60-90% of max heart rate. Max
heart rate is approximately 220 bpm age. Aerobic conditioning has proved
effective in lowering the incidence of back injury in workers and in helping
elderly remain ambulatory. A significant decline in aerobic fitness occurs after
just 2 weeks of no training (detraining)
Basic Science of Sports Medicine

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Reza Omid MD

-Unhealthy weigth loss due to fluid and food restriction (seen in wrestlers,
fighters and jockeys) is associated with:
1. reduced cardiac output
2. increased heart rate
3. smaller stroke volume
4. lower oxygen consumption
5. decreased renal blood flow
6. electrolyte loss (hypokalemia)
-Fluid replacement regimen for a competitive athlete is to replace enough
water to maintain pre-practive weight and maintain a normal diet. Fluid
carbohydrate and electrolyte replacement is most effective when the osmolarity
of the replacement fluid is <10% (glucose polymers minimize osmolarity). Fluid
absorption by the gut is enhanced by solutions of low osmolarity
-Female athlete triad:
1. Amenorrhea: from decreased percentage of body fat and changes in the
hypothalamic-pituitary axis.
2. Osteoporosis: decreased estrogen levels cause bone loss and amenorrhea
3. Anorexia: loss of appetite and desire to lose weight
-Initial management is increasing weight, decreasing exercise and possibly
administration of cyclic estrogens or progesterones.
-Muscle strain is the most common sports injury seen. Most muscle strains
occur at the myotendinous junction in muscles that cross 2 joints (such as the
hamstring or gastrocnemius) and have increased type 2 fibers. Muscle strains
occur most commonly at the myotendinous junction often during a rapid (high
velocity) eccentric contraction (eccentric contraction develops the highest forces
observed in skeletal muscle). Muscle tears heal with dense scarring. Surgical
repair of clean lacerations in the midbelly of skeletal muscle usually results in
minimal regeneration of muscle fibers distally, scar formation at the laceration
and recovery of approximately half of the muscle strength.
-Muscle activation via stretching allows twice the energy absorption prior to
failure. Bouncing types of stretches are deleterious.
-Muscle soreness that apprears 24-48 hours after strenuous exercise is termed
delayed muscle soreness. It is an overuse injury commonly experienced. It
is more common with eccentric contractions. It is associated with changes in the
I-band. Torn tissue, muscle spasm and connective tissue damage may cause
muscle soreness.
-Muscle strength gains during the 1st 10 days of rehabilitation are due to
improved neural firing patterns. Later strength gains are due to increases in
ROM, muscle fiber size, muscle repair and tendon repair. Trunk extensors are
stronger than trunk flexors.
-Immobilization of injured muscle changes the number of sarcomeres at the
musculotendinous junction and accelerates granulation tissue reponse in the
injured muscle. Immobilization in lengthened positions decreases contractures
and maintain strength. Atrophy can result from disuse and altered nervous

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Reza Omid MD

system recruitment. Electrical stimulation (US therapy) can help offset these
effects.

4)

Science of Nervous Tissue

CNS Injuries
-Patients may continue to improve up to 6 months after a stroke and up to 18
months after traumatic brain injury. Most common mechanism of spinal cord
injury in adults is MVA. If <3hrs from injury: 30mg/kg for 1st hour then
5.4mg/kg/hr for the next 23 hours. If injry is between 3-8 hours: 30mg/kg for
1st hour then 5.4mg/kg/hr for the next 47 hours. This regimen is associated with
improved root function and the level of injury, although improvement of spinal
cord function may or may not be seen. Regimen is not indicated for GSW,
brachial plexus injuries and nerve root deficits.
-Concussion is a jarring injury to the brain that results in disturbance to some
degree of cerebral function. 3 grades of severity:
1. Grade 1 (mild): no loss of conciousness, no retrograde amnesia
o
Return to play as soon as asymptomatic
2. Grade 2 (moderate): + loss of conciousness <5min, + retrograde
amnesia (there is always some permanent loss of memory regarding the
injury itself), confusion and disorientation resolved rapidly
o
Return to play afte asymptomatic for 1 week
o
Repeat episode requires long term suspension
3. Grade 3 (severe): prolonged unconsciousness, permanent retrograde
amnesia, confusion persists
o
Long term suspension is required
-Meissners corpuscle:
o
Mechanoreceptor with A fiber type
o
Rapidly adapting
o
Moving 2 point discrimination
o
Well equipped for analysis of motion
-Merkels receptor:
o
Mechanoreceptor with A fiber type
o
Slowly adapting
o
Static 2 point discrimination
o
Responds to a small area of skin pressure
-Pacinian corpuscle:
o
Mechanoreceptor with A fiber type
o
Rapidly adapting
o
Flutter
-Ruffinis corpuscle:
o
Mechanoreceptor with A fiber type
o
Slowly adapting

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Reza Omid MD
o

Vibration

Peripheral Nerve Morphology

-Axon coated with a fibrous tissue called endoneurium, group into nerve bundles
called fascicles, which are covered with a connective tissue called perineurium.
Peripheral nerves are composed of one (mono), a few (oligo) or several (poly)
fascicles and surrounding areolar connective tissue (epineurium) enclosed within
an epineurial sheath. Perineurium which surrounds the bundles of fascicles
within a peripheral nerve is the primary structure responsible for tensile strength.
Epineurium is thicker but has less tensile strength and may function more to
resist compressive forces.
-Blood supply to nerves is from an extrinsic blood supply from vessels that run in
loose connective tissue surrounding the nerve trunk. Intrinsic blood supply is
from vascular plexus in the epineurium, perineurium and endoneurium (with
interconnections between these three plexus)
-Peripheral nerve injury leads to death of the distal axons and Wallerian
degeneration (of myelin) which extends distal to the somatosensory receptor.
Proximal axonal budding occurs (after 1 month delay) and leads to regeneration
at rate of about 1mm/day (possibly 3-5mm/day in children). Pain is the first
modality to return
-Nerve regeneration is influenced by:
1. Contact guidance: attraction to basal lamina of the Schwann cell
2. Neurotrophism: factors enhancing growth
3. Neurotropism: preferential attraction towards nerves rather than other
tissues
-Upper Motor Neuron Signs (brain or spinal cord):
o
Decreased strength
o
Increased tone
o
Hyperreflexia
o
Babinski
o
Hoffman
o
Clonus
-Lower Motor Neuron Signs (nerve injuries):
o
Decreased strength
o
Loss of tone
o
Loss of reflexes
o
Fasciculations
o
Atrophy of muscles
-Types of Nerve Injuries:
o
Neuropraxia: reversible coduction block characterized by local
ischemia and selective demyelination of axon sheath
Most common
Best prognosis

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Reza Omid MD

Axonotmesis: more severe injury with disruption of the axon and

myelin sheath but leaving the epineurium intact
o
Neurotmesis: complete nerve division with disruption of the
endoneurium
Worst prognosis
-Football stingers or burners are neuropraxia from a brachial plexus
stretch injury. Nerve stretching can affect function as 8% elongation can
diminish a nerves microcirculation and 15% elongation disrupts axons. A +
histamine response implies that there is an intact reflex arc indicating that the
lesion is proximal to the ganglion (pre-ganglionic)
-It is crucial to properly align nevre ends during surgical repair in order to
maximize potential for functional recovery. Types of nerve repair include:
1. Direct muscular neurontization: insert nerve stump into the muscle
belly
2. Epineural repair: primary repair of outer connective tissue
a. Used for smaller nerves (digital nerves)
b. Remember kissing but no sex
3. Grouped fascicular repair: reapproximation of individual fascicles under
a microscope.
a. No significant improvement in results over epineural repair has
been documented
b. Used for larger nerves.
o

5)

Science of Connective Tissue

-Tendons insert into bone via four transitional tissues (for force dissipation):
1. Tendon
2. Fibrocartilage
3. Mineralized fibrocartilage (Sharpys fibers)
4. Bone
-Consists of fibroblasts arranged in parallel rows in fascicles of type 1 collagen
(85%) with surrounding loose areolar tissue called the peritenon. Tendons
attach muscle to bone (via Sharpeys fibers). Immobilization leads to increased
tendon strength at the expense of ROM but decreases tendon strength at the
tendon-bone interface. Tendon repairs are weakest at 7-10 days and regain
maximum strength at 6 months. Two types of tendons are found in the body:
1. Paratenon-covered tendons
2. Sheathed tendons
-Paratenon tendons are vascularized tendons. They have many vessels
supplying a rich capillary system. They heal better than sheathed tendons.
Examples include the patellar tendon and Achilles tendon
-Sheathed tendons have a mesotenon (vincula) which carries a vessel that
supplies only one tendon segment. Avascular areas receive nutrition via

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Reza Omid MD

diffusion from vascularized segments. Examples include flexor tendons of the

hand.
-Ligaments stabilize joints (connect bone to bone) and are composed of type 1
collagen (70%). Fibers are more variable than tendons and have higher elastin
content. They have uniform microvascularity (unlike tendons) and receives its
supply at the insertion site. They also possess mechanoreceptors and free nerve
endings. They insert onto bone via direct or indirect insertion. Early healing is
via type 3 collagen which is converted to type 1 collagen. Mobilization increases
strength of the ligaments.
-Ligament sprains include 3 grades:
1. Grade 1 Sprain: ligament is stretched but remains intact and results in
no instability
2. Grade 2 Sprain: partial tears that lead to mild instability
3. Grade 3 Sprain: complete tears that result in significant joint instability
-Rupture of sequential series of collagen fiber bundles distributed throughout the
body of the ligament (as opposed to localized to one specific area) is most
common mechanism of ligament failure. Ligaments doe not plastically deform.
Midsubstance tears are common in adults. Avulsion injuries (with small piece of
bone) are more common in children. Ligament avulsion typically occurs between
the unmineralized and mineralized fibrocartilage layers. Local injections of
corticosteroids at a site of injured ligament is detrimental to the healing process.
-Fibrillin is a component of elastic fiber system. Fibrillin metabolism defect has
been demonstrated in some patients with adolescent idiopathic scoliosis as well
as Marfans.
-Magic angle of MRI occurs when a tendon or ligament is oriented near 55 to
the magnetic field, T1 images may appear to have increased signal and create
false appearance of pathology. Most commonly seen in the shoulder, knee and
ankle
-Intervertebral discs of the spine contains various neuropepties including
substance P, calcitonin gene-related peptide, vasoactive intestinal peptide (VIP)
and c-flanking peptide of neuropeptide (CPON). They are composed of 2
components:
1. Central Nucleus Pulposus: hydrated gel with compressibility
i. High GAG and low collagen
ii. Type 2 collagen
2. Annulus Fibrosis: increased tensile strength
i. High collagen and low GAG
ii. Type 1 collagen
iii. Superficial layer contains nerve fibers

6)

Science of Perioperative Problems

Blood Gas Evaluation

1) pO 2 = 7(FiO 2 )-pCO 2

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Reza Omid MD

pO 2 is the anticipated or normal pO 2 in a normal person given

FiO 2 . pCO 2 is from the ABG value obtained
2) Once pO 2 (anticipated) is calculated, you subtract this from the pO 2
given from the ABG to determine the Aa-gradient
o
Aa-gradiant = Anticipated pO 2 Observed pO 2
3) Calculate the percentage physiologic shunt from the Aa-gradient as:
o
Percentage physiologic shunt = Aa-gradient/20
o

Thromboembolism Risk Factors

o
History of thromboembolism
o
Obesity
o
Malignancy
o
Age
o
CHF
o
Birth control pills
o
Varicose veins
o
Smoking
o
General anesthesia
o
Increased blood viscosity (factor V leiden)
o
Immobilization
o
Paralysis
o
Pregnancy
Virchows Triad
1) Venous stasis
2) Hypercoagulability
3) Intimal injury
Deep Vein Thrombosis
-Pain, swelling and + Homans sign
-Venography is the gold standard (97% accurate)
-I125 labeled fibrinogen (op-site has false positive)
-Duplex US (B-mode) is 90% accurate
-Doppler is good for bedside study
-DVT is uncommon after elective spine surgery so only mechanical prophylaxis is
recommended.
-Treatment is indicated for all thigh DVTs but below the popliteal fossa is
controversial
-Pre-op identification of DVT in a patient with lower extremity or pelvic trauma is
an indication for placement of a vena cava filter
-Coumadin inhibits hepatic enzymes (vitamin-k dependent epoxide and
reductase) to decrease carboxylation of the vitamin k-dependednt proteins:
1) Factor 2 (prothrombin)
2) Factor 7

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Reza Omid MD

Factor 9
Factor 10
-Effects of coumadin can be reversed with vitamin K or more rapidly with fresh
frozen plasma. Rifampin and phenobarbital are antagonistic to coumadin.
Erythromycin is contraindicated with coumadin use. COumadin is most effective
for DVT prophylaxis/treatment but takes 3-5 days for full effect and the initial
few days there is a hypercoagulable state so recommended to bridge with
lovenox. Treatment for DVT is for 3 months with INR at 2-3. Coumadin is
monitored with PT/INR
-Heparin is antithrombin III inhibitor and can be monitored via PTT
-Lovenox inhibits clotting factors by forming complexes with antithrombin III
and factors IIa and Xa but you cannot monitor and must use with caution in
patients with renal disease. Bleeding/oozing is a concern with lovenox.
-Indomethacin is a very potent NSAID and acts at lipooxygenase side of
arachadonic acid metabolism (as opposed to COX), which results in inhibition of
leukotriene inflammatory mediators.
3)
4)

Pulmonary Embolism
-Acute onset of pleuritic chest pain, tachypnea, tachycardia.
-Work up includes:
1) EKG (RBBB, RAD, ST depression or T-wave inversion in lead III)
2) CXR (hyperlucency)
3) ABG (respiratory alkylosis due to low CO 2 , but normal ABG does not
exclude this diagnosis)
4) V/Q scan
5) Pulmonary angiogram (gold standard)
6) CTPA (CT pulmonary angiogram) but not as good as pulmonary
angiogram
-Treatment is with heparin or therapeutic lovenox (1mg/kg/BID) for 7-10 days
followed by 3 months of coumadin
-Thrombolytic agents indicated if patient is unstable
-IVC filters in select cases
Coagulation
-A cascade of enzymatic reactions ending with fibrin clot formation via 2
interconnected pathways:
1) Intrinsic pathway: monitored by PTT
a. Activated when factor 12 contacts collagen of damaged vessels
2) Extrinsic pathway: monitored by PT
a. Activated by thromboplastin released into circulation after cellular
injury (surgery or trauma)
-Bleeding time measures platelet function

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Reza Omid MD

-Fibrinolytic system is responsible for dissolving clots. Plasminogen is

converted to plasmin (with help of tissue activators, factor 12a and thrombin)
and plasmin dissolves fibrin clots.
Adult Respiratory Distress Syndrome
-Acute respiratory failure secondary to pulmonary edema after trauma, shock or
infection.
-Causes of ARDS include:
1) Pulmonary infection
2) Sepsis
3) Fat embolism (from multiple long bone fractures)
4) Microembolism
5) Aspiration
6) Fluid overload
7) Atelectasis
8) O 2 toxicity
9) Pulmonary contusion
10) Head injury
-Complement activation leads to further progression
-Tachypnea, dyspnea, hypoxemia and decreased lung compliance
-Clinical diagnosis of ARDS after long bone fractures is best made with ABGs
-50% mortality associated with ARDS
-Treatment is ventilation with PEEP or high frequency percussive ventilation
-Steroids are not useful
-Stabilization of long bones decreases risk but must contemplate damage control
versus early definitive stabilization.
Fat Embolism Syndrome
-Usually occurs at 24-72 hours after trauma (before the time frame for PE)
-Clinical findings include:
o
Hypoxemia (PO 2 <60mmHg)
o
o

CNS depression
Petechial rash (axilla, conjunctivae, palate)

Tachypnea
o
Tachycardia
-May be caused by bone marrow fat (mechanical theory), chylomicron changes
as a result of stress (metabolic theory) or both
-Can result in ARDS
-Early skeletal stabilization decreases incidence of clinically significant fat
embolism
-Over-reaming the femoral canal can decrease the incidence of fat embolism
during TKA
o

Nutrition

40

Reza Omid MD

-Malnutrition is present in 50% of surgical ward patients.

-Work up includes:
o
Anergy panel
o
Albumin (2-3 weeks life) >3-3.5g/dl
o
Pre-albumin (2 days life) >20mg/dl
o
Transferrin (1 week life) ~0.16-0.36g/dl
o
Fibronectin (1 day life)
-Arm muscle circumference measurement is the best indicator of mutritional
status
-Wound dehiscence, infection, pneumonia and sepsis can result from poor
nutrition.
-Lack of enteral feeding can lead to atrophy of the intestinal mucosae, leading in
turn to bacterial translocation
-Enteral protein supplements have proven effective in patients at risk of
developing multiple organ system failure. Provide patients with:
1) Boost with meals TID
2) MVI Qday
3) Vitamin C 500mg Qday or BID
4) Zinc Sulfate 220mg Qday
5) Iron Sulfate 325mg BID or TID
-Wound healing measurements:
1) TcPO 2 > 30mmHg
2) ABI > 0.45
3) Toe pressure > 40mmHg
4) Albumin > 3.0g/dl
3
5) Total lymphocyte count >1500 cells/mm
6) Total protein >6.2 g/dl
7) Hemoglobin >10g/dl
-Frostbite: treat with general rewarming of entire body plus rapid rewarming of
hands and feet in a warm bath (104F or 40C for 15-30min). Also splint, give
tetanus, antibiotics and provide analgesics. Severe swelling may occur upon
rewarming so monitor for compartment syndrome
-Kneeling frame for spine surgery causes:
o
Decreased intraabdominal pressure
o
Decreased pressure on the IVC
o
Decreased pressure on vertebral venous system
o
Decreased blood loss
Malignant Hyperthermia
-Autosomal dominant hypermetabolic disorder of skeletal muscle, has impaired
sarcoplasmic reticulum and calcium homeostasis
-Masseter muscle spasm, increased temperature, rigidity and acidosis

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Reza Omid MD

-Most accurate method of diagnosis is muscle biopsy

-Occurs with halothane and succinylcholine
-Patients at risk are:
1) Duchennes muscular dystrophy
2) Arthrogryposis
3) Osteogenesis imperfecta
-Treat with dandrolene, correct electrolytes and increase uring output as well as
cooling measures.
Surgical Tourniquet
-Can injure nerves and muscles (EMG abnormalities may occur in 70% of
patients using the tourniquet.
-Careful application, wide cuffs, lower pressures (200mmHg for the UE and
250mmHg in the LE or 100-150mmHg above systolic pressure for LE)
-Double cuffs are useful to prevent pain at the tourniquet site. 1st inflate the
proximal cuff and infuse with lidocaine, then inflate the distal cuff (now
anesthetized) and deflate the proximal cuff.
-Equilibrium can be re-estabilished within 5 min after 90 minutes of use but
requires 15 minutes after use for 3 hours. Do not exceed 2 hours of use at a
time.
-Esmark bandage and elevation (for 5 min) can be used to prevent a venous
tourniquet. Only 2 layers of webril are required when using a tourniquet, as
more will decrease the pressure.

Science of Biomaterial &

Biomechanics
7)

Biomaterials
-Loads: forces that act on a body (compression, tension, shear and torsion)
-Deformations: temporary (elastic) or permanent (plastic) change in the shape
of a body. Changes in load produce changes in deformation
-Stress = force/area (N/m2) in pascals
-Normal stresses (compressive or tensile) are perpendicular to the surface on
which they act.
-Shear stresses are parallel to the surface on which they act
-Strain=change in length/original length
-Strain is a relative measure of the deformation
-Hookes Law: stress is proportional to the strain up to a limit (proportional
limit)
-Youngs Modulus (E): measure of the stiffness of a material or its ability to
resist deformation.
-E=stress/strain (slope of the curve)
-The larger the E the more stress shielding seen
-Comparison of different materials/tissues (from highest E to lowest):
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Reza Omid MD

1) Ceramic (Al 2 O 3 )
2) Co-Cr-Mo (Alloy)
3) Stainless steel (iron, chromium and nickel)
4) Titanium
5) Cortical bone
6) PMMA
7) Polyethylene
8) Cancellous bone
9) Tendon/Ligament
10) Cartilage
-Yield point (proportional limit) on a stress strain curve is the transition
point from the elastic to the plastic range.
-Ultimate strength: maximum strength obtained by the material
-Breaking point: point where the material fractures
-Plastic deformation: change in length after removing the load (before the
breaking point) in the plastic range.
-Strain energy: the capacity of a material (such as bone) to absorb energy. On
a stress strain curve it is illustrated as the area under the curve. Total strain
energy is recoverable energy (resilience) + dissipated strain energy. A
measure of the toughness (ability to absorb energy before failure) of a material
-Materials/Structures:
1. Brittle materials: exhibit a linear stress strain curve up to the point of
failure (PMMA). Undergo only fully recoverable (elastic) deformation
before failure and have little or no capacity to undergo permanent
(plastic) deformation before failure
2. Ductile materials: undergo a large amount of plastic deformation prior to
failure (metal). Ductility is a measure of post-yield deformation.
3. Viscoelastic materials: exhibit stress-strain behavior that is time-rate
dependent (bone and ligament); the materials deformation depends on
the load and the rate at which the load is applied. The modulus of a
viscoelastic material increases as the strain rate increases. Viscoelastic
behavior is a function of the internal friction of a material.
4. Isotropic materials: possess the same mechanical properties in all
directions (golf ball)
5. Anisotropic materials: have mechanical properties that vary with the
direction of the applied load (bone)
6. Homogeneous materials: have a uniform structure or composition
throughout
-Fatigue failure: occurs with repetitive loading cycles at stress below the
ultimate tensile strength. Fatigue failure depends on the magnitude of the stress
and the number of cycles. If the stress is less than a predetermined amount of
stress, called the endurance limit (the max stress under which the material will
not fail regardless of how many loading cycles are applied), the material may be
loaded an infinite number of times without breaking.

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Reza Omid MD

-Creep (aka Cold Flow): progressive deformation of metals (or other materials
such as PE) in response to a constant force applied over an extended period. If
sudden stress, followed by constant loading, causes a material to continue to
deform, it demonstrates creep. Creep can produce a permanent deformity and
may affect mechanical function (such as in a TJA)
-Corrosion: chemical dissolving of metals as may occur in the high-saline
environment of the body.
316L stainless steel is the most likely metal to undergo pitting and
crevice corrosion
The risk of galvanic corrosion is highest between 316L stainless steel
and cobalt-chromium (Co-Cr) alloy.
Modular components of THA have direct contact between either similar
or dissimilar metals (at the modular junction) and thereby have
corrosion products (metal oxides, metal chlorides, etc).
-Galvanic corrosion can be decreased by using similar metals (plates and
screws with similar metals), with proper design of implants and with
passivation (a thin layer that effectively separates the metal from the solution
(stainless steel coated by chromium oxide)

8)

Orthopaedic Infectious Disease

-Microorganisms gain access to muscluloskeletal system via 3 mechanisms:

1) Hematogenous
2) Spread from a contiguous source (adjacent osetomyelitis)
3) Direct inoculation (trauma/surgery)
-Virulence is the ability of an organism to overcome the host defenses and
cause infection.
-Defense mechanisms of Staphlococcus aureus include:
1) Excretion of protein A: inactivates host IgG
2) Production of capsular polysaccarides: inhibits opsonization and
phagocytosis
3) Formation of a biofilm
-Host factors that facilitate infection:
1) Reduced vascularity (arterial disease, venous stasis, irradiation,
scarring, smoking)
2) Neuropathy
3) Presence of implants
4) Trauma (predisposes by compromising the soft tissue, by creating a
dead space with hematoma)
5) Renal or liver disease
6) Malignancy
7) Rheumatologic disease
8) Alcoholism
9) Immunocompromised state (HIV/AIDS)

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Reza Omid MD
10)

IVDA

Inflammatory Markers
-Become elevated with infections, fractures and chronic inflammatory diseases
1) ESR (erythrocyte sedimentation rate):

Unreliable in neonates, patients with sickle cell disese and patients

taking steroids.

Unreliable in patients with short period of symptoms (<48hrs)

Elevated with Ewings sarcoma (CRP does not)

Peak elevation at 3-5 days

Returns to normal at 3 weeks after treatment started

Drawbacks include:
i. Indirect measure of acute phase reaction
ii. Results influenced by age/gender, pregnancy, temperature,
drugs (steroids/ASA, and smoking
2) CRP (C-reactive protein):

Synthesized in the liver in response to infection or inflammation

Much more sensitive and specific for infections than ESR

Not elevated with Ewings sarcoma

Increases within 6 hours of infection

Peak elevation at 2 days

Returns to normal at 1 week

Direct measure of acute phase reaction (ESR is indirect measure)

-Plain radiographs are useful to show soft-tissue swelling, joint space narrowing
or widening and bone destruction (lytic lesions). Bone destruction is not
apparent on x-ray until an infection has been present for 10-21 days. Also ~3050% of bone matrix must be lost before it becomes apparent on x-rays. Wheat
et al found that <5% of x-rays were initially abnormal in bone/joint infections
and <30% were abnormal at 1 week but 90% were abnormal at 3-4 weeks.
Bone Scans
1) Technetium-99 m Phosphate Scan: used to detect osteomyelitis
within 48 hours. Reflects increased blood flow and metabolic activity
(osteoblastic) in areas of infection, neoplasia or trauma. Can get
whole body view or pin-hole view (more details).
a. 3 phases of the study:
i. Flow phase (immediate): demonstrates blood flow
ii. Blood pool/Equilibrium phase (30 min): shows relative
vascular flow and distribution of isotope into ECM space
iii. Delayed phase (4 hours): shows areas of osteoblastic
activity (hot spots)
b. If blood flow to an area is decreased by subperiosteal pus or
necrosis (sequestrum) a cold scan may result.

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Reza Omid MD

Cellulitis will show up during 1st two phases but not 3rd phase as
opposed to osteomyelitis
d. Bone marrow scan (technetium-99 m sulfur colloid) can be
combined with bone scanning (technetium-99 m methylene
diphosphate), within 24 hours, to differentiate between bone
infarction and osteomyelitis in children.
i. Bone infarction: decrease on bone marrow scan and
increase on bone scan
ii. Osteomyelitis: normal on bone marrow scan and increase
uptake on bone scan
Gallium-67 Citrate Scan: used to localize areas of inflammation or
neoplasia probably because of exudation of labeled serum proteins.
a. Specifically is poor when used alone so its commonly used in
conjunction with technetium-99 m phosphate scans as a double
tracer technique.
b. Requires delayed imaging 24-48 hours
c. Less dependent on vascular flow than technetium-99 m phosphate
and may identify foci that would have otherwise been missed.
d. Difficult to distinguish between cellulitis and osteomyelitis
Indium 111-Labeled Leukocyte Scan: suggested for use to
differentiate osteomyelitis from neoplasia or reactive bone formation.
a. Positive at earlier stages of osteomyelitis than technetium-99 m
phosphate (more accurate for osteomyelitis)
b. Blood is taken from the patient and PMN separated and labeled
with indium 111 and placed back in the patient and scanned at 24
hours.
c. Hot spots occur in areas where PMN accumulate so helpful for
acute osteomyelitis but may not be good for chronic osteomyelitis
(lymphocytes predominate)
c.

2)

3)

MRI
-T1 images have short TR and TE, bright fat
-T2 images have long TR and TE, bright water
-STIR (short au inversion recovery) are fat suppression and are almost 100%
negative predictive value for osteomyelitis.
-In osteomyelitis, marrow fat is replaced with edema and cellular infiltrates that
are lower signal on T1 than fat and higher signal that fat on T2 and STIR
therefore:
Classic findings of osteomyelitis on MRI are a decrease in

normally high marrow signal on T1 and normal or increased

signal on T2 images

-Gadolinium contrast helps distinguish an abscess (bright signal involved abscess

with no enhancements of the fluid within the abscess) from cellulitis.

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Reza Omid MD

Culture Studies
-Cultures should be obtained before antibiotics started.
-Cultures of superficial wounds or sinus tracts should be used with caution
because not reliable for deep infection and are usually polymicrobial (unless
staph. aureus groups)
-Preferred specimen is aspiration fluid (joint or pus)
-Deep wound biopsy or cultured specimen after cleaning the wound is acceptable
-Specimens should be sent from:
1. sinus tract tissue
2. sinus tract pus
3. soft tissue
4. bone from curettage
5. bed of involved bone
6. tissue surrounding implant for aerobic, anaerobic, fungal and TB
-Sinus tract should be sent for histologic evaluation to rule out malignancy
Glycocalyx
-An exopolysaccaride coating that envelops bacteria
-A biofilm is an aggregation of microbe colonies embedded within a glycocalyx
matrix that usually develop on implants or devitalized bone surfaces.
-Glycocalyx shields bacteria from antibodies and antibiotics
Bacterial Types
1. Gram + Bacteria:
a. No outer membrane (unlike gram -)
b. Have thick cell wall on outside of cell which is where a lot of
antibiotics work on (gram have no cell wall)
c. Resistant to antibodies and complement mediated killing
2. Gram Bacteria:
a. Have an outer membrane which contains endotoxins (lipid A) which
cause sepsis.
b. Have very thin cell wall between the OM and IM
c. Susceptible to antibodies and complement mediated killing
d. Antibodies must penetrate porins in the outer membrane so not
susceptible to some antibiotics
3. Encapsulated Organisms:
a. Streptococcus pneumoniae
b. Neisseria meningitites
c. Haemophilus influenzae
d. Patients who have splenectomy or hypogammaglobulinemia are at
increased risk for these encapsulated organisms
Transient Synovitis of the Hip
-May mimic septic arthritis of the hip

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Reza Omid MD

-An immune-mediated mechanism after viral infection.

-Less signs of systemic illness
-Kocher criteria include:
1. History of fever
2. Non-weight bearing of that side
3. ESR >40
4. WBC > 12,000
- Probability of septic arthritis with positive predictors:
o 1 out of 4: 5%
o 2 out of 4: 62%
o 3 out of 4: 97%
o 4 out of 4: 99.8%
Osteomyelitis
-Infection of bone and bone marrow
-Bone inflammation secondary to microbial pathogens
-May be caused by: hematogenous, direct inoculation or spread from adjacent
tissue
-May be acute, subacute or chronic
-Tibia is the most common location of adult osteomyelitis
-Most common pathogen is staph. aureus
-Diagnosis is based on clinical findings (pain, erythema, sinus drainage and
systemic symptoms), lab values (ESR, CRP, CBC, Blood cultures), imaging (MRI,
x-ray, bone scan), gram stain and cultures.
-Cultures needed from deep tissue and from multiple sites (sinus tract cultures
are no good)
-Sequestra is dead bone with surrounding granulation tissue
-Involucrum is periosteal new bone formation.
1. Pathology of osteomyelitis: the peculiarity of an abscess in bone is
that it is contained within a firm structure with little chance of tissue
expansion. As the infection progresses, purulent material works its
way through the haversian system and Volkmann canals and lifts the
periosteum off the surface of bone. The combination of pus in the
medullary cavity and in the subperiosteal space causes necrosis of
cortical bone. This necrotic bone (sequestrum) can continue to harbor
bacteria despite antibiotics. Antibiotics and inflammatory cells cannot
be adequately delivered to this area of avascularity, resulting in failure
of medical treatment for osteomyelitis.
2. Acute Hematogenous Osteomyelitis: staph aureus is most
common, group A strep, strep pneumonia, group B strep (neonates).
Most common in metaphyseal region of bones (seen where fastest
bone growth (distal femur).
3. Joints at Risk for Septic Arthritis in Children: joints where
metaphysic lies within the capsule.

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Reza Omid MD

a. Proximal femur (hip)

b. Proximal humerus (shoulder)
c. Distal fibula/istal lateral tibia (ankle)
d. Radial head/neck (elbow)
4. Osteomyelitis in newborn up to 4 months old: most common
organisms include s. aureus, gram bacilli and group B strep. 70%
have + blood cultures.
5. Osteomyelitis in children 4 years up to 21 years old: most
common organisms include s. aureus, group A strep and coliforms
(uncommon). Because of immunizations, H.influenzae has become
obsolete
6. Chronic Osteomyelitis: may result from inappropriately treated
acute osteomyelitis, trauma, soft tissue spread. Especially seen in
Cierny type C patients, immunosuppressed, DM and IVDA. Sinus tract
may develop squamous cell CA (marjolin ulcer). Operative sampling of
deep specimens from multiple foci is most accurate means of identify
organisms. Most common organisms are s. aureus, enterobacter, p.
aeruginosa.
7. Cierneys Anatomic Class:
a. Medullary: requires 6 weeks IV Abx
b. Superficial: requires 2 weeks IV Abx
c. Localized: requires 6 weeks IV Abx
d. Diffuse: requires 6 weeks IV Abx
8. Cierneys Physiologic Class:
a. Type A Host: normal immune response, non-smoker, minimal
risk of surgery
b. Type B Host: local or mild systemic deficiency, smoker and
moderate risk of surgery
c. Type C Host: major nutritional or systemic disorder, smoker
and severe risk, too risky for surgery and must consider non-op
treatment
9. Subacute Osteomyelitis: usually discovered radiographically in a
patient with a painful limp and no systemic signs or symptoms. May
arise secondary to partially treated acute osteomyelitis or occasionally
develop in a fracture hematoma. WBC and blood culture often normal.
ESR, bone culture and radiographs are helpful. Brodies abscess seen
radiographically. Most often in the femur or tibia.
10. Brodies Abscess: a localized radiolucency usually seen in the
metaphysic of long bones. Seen with subacute osteomyelitis.
Differential diagnosis includes Ewings sarcoma. Treatment in surgical
curettage. On x-ray seen as a lytic lesion with rim of sclerotic bone
and localized abscess caused by low virulence organism.
11. Sinography: can be performed if a sinus tract is present with a
radioopaque dye for pre-op planning. Methelylene blue can be

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Reza Omid MD

injected 24 hours before surgery or in the OR to make all the area

needing to be resected visualized
12. Surgical Treatment of Osteomyelitis:
a. Radical debridement of all non-viable tissue and skeletal
stabilization. Debridement until bleeding is noted (paprika
sign). Culture from multiple sources
i. Removal of sequestrum (infected dead bone) and
resection of scarred infected bone and soft tissue is vital.
ii. A cortical window is outlined with a drill and an
osteotome is used to create a window around the
sequestrum
b. Deadspace from debridement is filled with antibiotic beads in
bead pouch format or papineau graft or myoplasty
c. Culture specific IV Abx for 6 weeks
d. Soft tissue coverage, possible flaps usually done 3-7 days after
initial debridement.
e. Address bone defect once soft tissue has healed (usually 6-8
weeks after flap placed) by elevating the flap or using
posterolateral (harmon) approach to the tibia. Bone defects up
to 6 cm can be done with autograft/allograft but defects >6cm
requires vascularized bone graft or distraction osteogenesis.
13. Papineau Grafting: open bone grafting technique for chronic
osteomyelitis. Based on several principles:
a. Granulation tissue markedly resists infection
b. Autogenous cancellous bone grafts are rapidly revascularized
and are resistant to infection
c. Infected area is completely excised
d. Adequate drainage is provided
e. Adequate immobilization is provided
f. Antibiotics are used for prolonged periods
g. Steps of the technique include:
i. Debridement of all infected tissue and stabilized with
hardware. Treat with wound care for 4-5 days
ii. Autogenous cancellous bone grafting to fill cavity and
apply dressing soaked with antibiotics for 1-2 weeks
iii. Wound coverage (sometimes epithelializes
spontaneously)
14. Pelvic Osteomyelitis: usually an intraabdominal source is the cause
so must rule out colonic fistula or abdominal/pelvic abscess with triple
contrast CT (IV/PO/PR). Must account for anaerobic coverage.
15. Epiphyseal Osteomyelitis: caused almost exclusively by s. aureus.
Must rule out other lesions (chondroblastoma). Requires surgical
drainage only if pus is present, otherwise 48 hours of IV Abx followed
by 6 weeks of oral Abx.

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Reza Omid MD

16. Chronic Sclerosing Osteomyelitis of Garre: unusual infection that

primarily involves diaphyseal bones of adolescents. Typified by intense
proliferation of the periosteum leading to bony deposition. May be
caused by anaerobic organisms. Insidious onset, dense progressive
sclerosis on radiographs and localized pain and tenderness are
common. Must rule out malignancy.
17. Chronic Multifocal Osteomyelitis: multiple metaphyseal lytic
lesions with minimal symptoms and low grade fevers. Especially
medial clavicle, distal femur and distal tibia. 70% of patients have
pustulous palmoplantaris. ESR is elevated and cultures are invariably
negative. Usually resolves spontaneously without antibiotics.
Erysipelas
-Superficial infection (more superficial than cellulitis) of the epidermis
-Prograssively enlarging, well demarcated, red raised, painful plaque.
-Can be quite severe in diabetics
-Caused by group A strep, s. aureus, clostridia and enterobacter
Cellulitis
-Infection of the subcutaneous tissue
-Generally deeper and less distinct margins than erysipelas
-Most commonly due to group A strep, less commonly s.aureus
Necrotizing Fascitis
-Infection of the muscle fascia
-Associated with DM, vascular disease, IVDA, HIV
-Most commonly due group A strep but may be polymicrobial
-Clinically you see non-pitting edema with dishwater fluid, possibly some bullae
and the patient may become unstable and die within hours
-Treat with extensive debridement and antibiotic regimen should include
Vancomycin + Clindamycin + Zosyn
Gas Gangrene
-Infection of the muscle
-Commonly seen in grossly contaminated traumatic wounds, particularly those
that are closed primarily (reason why we leave all open fractures open at the
traumatic site)
-Similar picture clinically to necrotizing fascitis
-Gas seen on x-rays (facilitates rapid spread of the infection)
-Caused by clostridium perfingens or clostridium specticum (gram +) which
produce exotoxins that cause necrosis of fat and muscle and thrombosis of local
vessels.
-Treat with surgical debridement and Clindamycin and Penicillin G

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Toxic Shock Syndrome-Staphlococcal

-A form of toxemia, not septicemia, seen secondary to colonization of surgical or
traumatic wounds (even after minor trauma)
-Fever, hypotension, erythematous macular rash with a serous exudates
-IV Abx and surgical I&D with fluid resuscitation
Marine Injuries
-Careful history of fishing or marine exposure
-Vibrio vulnificus is most likely the organism in infected wounds that were
exposed to brackish water or shellfish
-Treatment with Ceftazidime or Doxycycline
-Mycobacterium marinarum is an indolent infection which should be treated with
doxycycline or clarithromycin
-Cultures must be take at 30C or 86F and may take weeks to grow out
Clenched Fist Injuries
-Injury to the MCP or PIP joints of the hand from a human bite.
-Ekinella corrodens is the most offensive bug
-Surgical debridement is essential and must note tendon, joint capsule, articular
surface
-Treatment with IV Ertapenem
-If extensor tendon is lacerated, do not repair the tendon acutely, wash and
splint and consider delayed repair of tendon
Nail Punctures to Foot
-Must cover for Pseudomonas aeruginosa if the patient was wearing tennis shoes
(only if it goes through the sole of the shoe, not just anywhere through the
shoe)
-Foot is divided into 3 zones (according to Patzakis et al):
1. Zone 1: from MT heads to tips of the toes
2. Zone 2: from MT heads to calcaneus
3. Zone 3: overlies calcaneus
-Patzakis showed that puncture to zone 1 was highest risk for osteomyelitis,
pyarthrosis or both so all zone 1 need admit for I&D with IV Abx. Zone 3 was
next most likely to cause serious infection but zone 2 and 3 only require
admission if there was a history of bone involvement.
-Osteomyelitis develops in 1-2% of children who sustain a puncture wound
through the sole of the tennis shoe
Human Bite
-Organisms involved are strep viridians (100%), ekinella corrodens, bacteroides,
s. epidermidis, peptostreptococcus, s. aureus, corynebacterum
-Treat with Augmentin for prophylaxis and ertapenem if infected

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Reza Omid MD

Dog Bite
-Organisms involved are capnocytophaga, pasteurella multocida, bacteroides,
fusobacterium, s. aureus
-Treat with Augmentin and consider antirabies treatment
Cat Bite
-Organisms involved are pateurella multocida, s.aureus
-Cat bite penetrates bone deeper than dog bites (sharper teeth) so must
consider surgical debridement
-Treat with Augmentin
Rat Bite
-Strep. Moniliformis
-Treat with Augmentin and antirabies is not indicated
Pig Bite
-Polymicrobial (aerobic/anaerobic)
-Treat with Augmentin
Septic Arthritis
-Commonly follows hematogenous spread or extension of metaphyseal
osteomyelitis in kids. Most cases involve infant hips (proximal femur) but may
include the elbow (radial head), ankle (distal fibula and lateral tibia) and shoulder
(proximal humerus) in children because all these are within their respective joint
capsule.
-Most common site at which septic arthritis follos acute osteomyelitis is proximal
femur/hip
-Most commonly due to gonococcus and second most common is s.aureus
-Rheumatoid arthritis and IVDA are predisposing factors
-Open vs arthroscopic drainage is required with 3-4 weeks of IV Abx
-SI joint septic arthritis is diagnosed with FABER test, ESR, CT and is treated with
IV Abx (surgical debridement is not indicated for SI joint septic arthritis)
-Surgical decompression by arthrotomy or arthroscopic irrigation relieves
pressure and evacuates enzymes and bacteria
-Repeat aspirations may be satisfactory in some knee infections but not be used
in hip or small joints.
-Synovial biopsy and culture is recommended for all joints undergoing
arthrotomy
-Synovectomy is warranted if very infected
-Antibiotics is usually 4 weeks for non-gonococcal and 1 week for gonococcal
arthritis
1. Newborn up to 3 months:
a. S.aureus, Group B strep, Enterobacter and N. Gonnorrhea
b. Adjacent bony involvement seen in 70%

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Reza Omid MD

2.

3.

4.

5.
6.

7.

c. Blood cultures commonly positive

Age 3 months to 14 years:
a. S.aureus, Strep Pyognes, Strep Pneumoniae, H.influenzae, Gram
bacilli
Acute Monoarticular Septic Arthritis in Sexually Active Adults:
a. N. gonorrhea (most common) treat with ceftriaxone for 1 week
nd
b. S. aureus (2
most common)
Acute Monoarticular Septic Arthritis in Non-Sexually Active
Adults:
a. Most commonly S. aureus
Chronic Monoarticular Septic Arthritis:
a. Brucella, Norcardia, Mycobacteria, Fungi
Polyarticular Septic Arthritis:
a. Gonococci, Borrelia burgdorferi (lyme dz), cute rheumatic fever,
viruses
Infected Total Joint:
a. Diagnosed with WBC > 2,500 and PMN >50%
b. Can be acute (2-4 weeks), chronic or hematogenous (same as
acute but same treatment as acute).
c. Acute can be washed with poly exchange and head exchange (all
modular components) with IV Abx for 6 weeks. Chronic requires
full 2 staged I&D with Abx for 6 weeks and sometimes life.
d. Most common organism is stap epidermis

Tetanus
-Potentially neuroparalytic disease caused by an exotoxin of clostridium tetani
-Give 0.5ml of toxin booster if indicated
-Give Ig in an area different than the booster
Rabies
-An acute infection of CNS that may be followed by paralysis and death
-Neurotropic virus present in saliva of rabid dog, cat, bat, skunk, raccoons and
foxes.
-Not seen with squirrels, rabbit, rodents, chipmunk.
-If animal available observe it for 10 days
Cat Scratch Fever
-Caused by Bartonella henslea
-Transmitted by cats
-Painful erythematous lymphadenitis
-Do not I&D, treat with IV Abx (Azithromycin)
Meningococcemia
-Can develop in patients with multiple infants, such as those with electrical burns

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Reza Omid MD

Marjolins Ulcer
-Squamous cell CA
-Develops in patients in chronic drainage from sinus tracts seen in untreated
chronic osteomyelitis
Sporothrix
-Occurs in plant handles (roses)
-Treat with potassium iodide solution
IVDA Infections
Serratia marcescens
Pseudomonas aeruginosa
Meat Handleers Infection: Brucella (gram -), tetracycline
Skin Preparation Pre-Op
-Skin and hair can be sterilized with alcohol, iodine, hexachlorophene or
chlorhexidine but it is almost impossible to sterilize the hair follicles and
sebaceous glands where bacteria normally reside and reproduce.
-Skin preps have a limited effect on sebaceous glands and hair follicles because
they do not penetrate an oily environment
-Disinfectants that penetrate the oily environment are absorbed by the body and
have toxic side effects (hexachlorophene is neurotoxic).
-Hair removal at op-site is not recommended unless done in the OR. Shaving the
op-site the night before surgery can cause local trauma that produces a
favorable environment for bacterial reproduction.
Antibiotic Beads
-PMMA is mixed with antibiotic powder (vancomycin + tobramycin) and rolled
into several small beads and must have a closure of the skin with ioban to form a
pouch.
-Antibiotics elute from the PMMA beads with an exponential decline over a 2
week period and cease to be present locally in significant levels by 6-8 weeks.
-PMMA may cause foreign body reaction so beads must always be removed.
-Mix 2 grams of Abx per 40g of powdered PMMA to not affect compressive
strength as higher doses of Abx (4-5 g) significantly reduces compressive
strength.
-Cannot use fluoroquinolones, tetracycline and polymyxin B (they burn up in the
polymerization process)
-Should change pouch at 72 hours and repeat I&D
Prophylactic Antibiotics
-Used to prevent SSI (surgical site infections)

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Reza Omid MD

-Given 30-60 min pre-op (recommendation is within 60 min and Dr. Holtom
recommends that Abx be in 30 min prior to cuff inflation and cut time.
-Continue antibiotics for 24 hours only, not longer even if drains or foley are still
in place.
-Give 1g Ancef (2g if patient weights >80kg) or 900mg Clinda or 1g Vancomycin
-Repeat intraop Q4 hours or if blood loss is >1000ml.
-Contaminated bone from an open fracture may be sterilized (100% effective) by
immersion in chlorhexidine gluconate scrub and an antibiotic solution.
Antibiotics
1. Aminoglycosides:
a. gram and polymicrobial coverage
b. binds 30S ribosomal units
c. gentamycin and tobracycin good for pseudomonas
d. SE: auditory toxicity, nephrotoxicity, neuromuscular blockage
2. Aztreonam:
a. gram coverage (similar to aminoglycosides)
b. no anaerobic coverage or gram + coverage
c. good for pseudomonas and serratia
d. good for zosyn allergy
3. Ceftriaxone:
a. Used to treat N.gonorrhea septic arthritis but if patient are post-op
they must be treated with cefotoxime because ceftriaxone cannot
be given with calcium supplements in the IV fluids (LR) because
FDA black label warning due to renal lithiasis in neonates
4. Erythromycin:
a. broad spectrum but still gram + coverage
b. good alternative for PCN allergy
c. contraindicated in patients on anticoagulants (coumadin)
d. increased level of digoxin
e. ototoxic
f.
inhibits 50S ribosome
g. same family as axithromycin and clarithromycin
5. Clindamycin:
a. gram + coverage and anaerobic coverage
b. covers proprionobacterium (shoulder surgery)
c. pseudomembranous colitis
d. achieves intraosseous concentration similar to serum concentration
e. covers some MRSA
6. Tetracycline:
a. broad spectrum coverage especially gram +
b. good for PCN allergy
c. binds 30S subunit
d. stains teeth up to age 8

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Reza Omid MD
7.

8.

Quinolones:
a. broad spectrum activity (especially gram -)
b. good for pseudomonas coverage
c. inhibits DNA gyrase
d. SE: tendon ruptures
e. antacids (Mg or Al) reduce absorption of cipro
f.
theophylline increases serum concentration of cipro
Antibiotics for DM foot infections:
a. Flagyl + Levaquin for 10-14 days

Orthopaedic Rehabilitation

I. Gait

-Step is the distance between initial swing and initial contact of the same limb.
-Stride is initial contact to initial contact of the same limb
-Walking requires that one foot be in contact with the ground at all times (singlelimb support) and running involves a period when neither limb is in contact with
the ground.
-Stance phase of walking occupies 60% of the cycle
-Swing phase of walking occupies 40% of the cyle
-During the initial swing, the hip and knee flex and the ankle starts dorsiflexion.
-The center of gravity of the body mass (70% is made up of the head,

neck, trunk and arms) is just anterior to T10, which is 33cm above the
hip joints.

-During gait the non-weight bearing side of the pelvis drops 5 (which means the
hip abductors are eccentrically contracting
-Most muscle activity during gait is eccentric (gluteus medieus, hip
adductors, hip abductors, quadriceps, hamstrings, tibialis anterior and
gastroc/soleus). Gluteus maximus and iliopsoas are concentric.
-ACL decicient knee has a quadriceps avoidance gait (which is a lower
than normal net quadriceps moment during midstance)
-Gluteus medius weakness causes abductor lurch (trendeleburg gait) and

can be treated with hip abductor strengthening or a cane in the contralateral

hand or a suitcase in the ipsilateral hand.
-Joint reaction force (R): force generated within a joint in response to forces

acting on the joint (both intrinsic and extrinsic). Muscle contractions about the
joint are the major contributory factor to the joint reaction force. Values of R
correlate with the predisposition to degenerative changes. Joint contact pressure
(stress) can be minimized by decreasing R and increasing contact area.
-The hips R (joint reaction force) can reach three to six times body weight (W)
and is primarily due to contraction of muscles crossing the hip.

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Reza Omid MD

-An increase in the ratio of A/B decreases the joint reaction force (R) and can be
accomplished with:
1. medialization of the acetabulum
2. long-neck prosthesis
3. lateralization of the greater trochanter
-The hips R (joint reaction force) and abductor moment (M) are both reduced by
shifting the body weight over the hip (Trendelenburg gait).
-A cane in the contralateral hand produces an additional moment and can
reduce the joint reaction force up to 60% because it decreases the abductor
moment (M) needed to stabilize the hip. Also carrying a load (suitcase) in the
ipsilateral hand also decreases the joint reaction force at the hip.
-Crutches improve stability by providing two additional loading points.
-Forces across the knee may be 4-7 times body weight and 70% of the load
across the knee occurs through the medial compartment.

II. Amputations
-Amputations typically occur as the result of tumors, trauma or other medical
conditions such as DM or infection.
-Absolute indication for amputation after trauma is an ischemic limb
with a vascular injury that cannot be repaired.
-Biologic amputation level is the most distal functional amputation level with
a high probability of supporting wound healing. This is why any patient without
a palpable pulse requires vascular studies to determine the level of amputation
which will heal.
-Patients who have amputations for trauma are much worst off with knee
disarticulations than BKA. Also atypical soft-tissue flaps have to be used.
-The most important risk factors for amputation in diabetic patients are the
presence of peripheral neuropathy and development of deformity and infection.
Gangrene In The Upper Extremity In Diabetic Patients

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Reza Omid MD

-UE gangrene (fingers) that is not due to Raynauds or Bergers disease is an

end-stage disease, especially in patients with DM (JBJSAm 1989:257-264):
a. Most patients (77.3%) die within 2 years after the appearance of
gangrene, 27% will die within 4 months!
b. Preop assessment of the viability of the limb is crucial in these
patients as a limited amputation is unlikely to heal in these patients
and they require a higher level than expected (transradial level is
preferred level for finger/hand gangrene to achieve wound healing
during the final months of the patients life).
Amputation Levels
1. Wrist Disarticulation
-Advantages over below elbow amputation is preservation of more FA
rotation because of preservation of the DRUJ and improved prosthetic
suspension because of the flare of the DR.
-hard to make a prosthesis for so not very useful
2. Below-Elbow Amputation
-Forearm rotation and strength are directly related to the length of the
transradial residual limb.
-The optimal length is the junction of the middle and distal 1/3 of the FA,
where the soft-tissue envelope can be repaired by myodesis (repair to
bone) and the components of a myoelectric prosthesis can be hidden
within the prosthetic shank.
-Best for patients with complete brachial plexus injury and a nonfunctioning hand and FA
3. Elbow Disarticulation
-May be used for patients with complete brachial plexus injury and a nonfunctioning hand and FA but transradial is better
4. Above-Elbow Amputation
5. Tikhoff-Linberg Amputation
-consists of en bloc removal of the scapula, distal clavicle, and proximal
humerus and preservation of the arm.
-First true limb-sparing procedure of the upper extremity
6. Shoulder Disarticulation
7. Toe Amputations
-Little morbidity associated with toe amps.
-Traumatic amputees lose some late-stance-phase stability with toe amps.
-GT amps should be distal to the FHL insertion if possible
-Isolated 2nd toe amps should be performed just distal to the proximal
phalanx metaphyseal flare, leaving it to act as a buttress and prevent late
hallux valgus.
8. Transmetatarsal Amputations
-Crush injuries, frostbite and lawnmower injuries are the most common
excluding DM foot infections

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Reza Omid MD

9.

10.

11.

12.

13.

-Single outer (1st and 5th) ray resections function well in standard shoes.
-Resection of more than one ray leaves a narrow forfoot that is difficult to
fit in shoes and often results in a late equines deformity.
-Central ray resections are complicated by prolonged wound healing and
rarely outperform midfoot amputations.
-Quality of soft-tissue coverage is more important in the ultimate
outcome than bone length.
-There is little functional difference between TMA and Lisfranc amps
-Long plantar flaps are preferable to the fish-mouth flaps
Lisfranc Amputation
-Percutaneous TAL should be performed to prevent equinus or
equinovarus contractures.
-Late varus can be corrected with transfer of the TA to the neck of the
talus.
Chopart Amputation
-Midfoot amputation done across the talonavicular joint and
calcaneocuboid joint
-Advantage is limited ambulation without a prosthesis
-Disadvantage is equines deformity which leads to ulceration (but this can
be prevented by attaching the tibialis anterior to the calcaneus at the time
of amputation and doing a percutaneous TAL.
-Indicated for elderly patients and pediatric patients with congential
deformities
-Avoid in DM or vascular insufficiency
Boyd Amputation
-Amputation through the calcaneus horizontally
-Percutaneous TAL should be performed to prevent equinus or
equinovarus contractures.
-Late varus can be corrected with transfer of the TA to the neck of the
talus
Pirogoff Amputation
-Amputation through the calcaneus vertically
-Percutaneous TAL should be performed to prevent equinus or
equinovarus contractures.
-Late varus can be corrected with transfer of the TA to the neck of the
talus
Syme Amputation
-Ankle disarticulation and removal of malleolar bone
-Better functionally than a BKA because allows direct load transfer and is
rarely complicated by late residual limb ulcers or tissue breakdown
(patient is able to get up in the middle of night and ambulate without a
prosthesis if she forgets it.
-Provides a stable gait pattern that rarely requires prosthetic gait training
after surgery.

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14.

15.

16.

17.
18.
19.

-Most patients need a prosthesis for routine walking though.

-A patent posterior tibial pulse and heel viability are essential to
do a Syme amputation
Below-Knee Amputation
-Transtibial amputation is a very common and functional amputation.
-Mangled extremities are most commonly treated with a BKA
-BKA can be performed as long as the extensor mechanism is intact but
the recommended length for a BKA is 12-15 cm of tibial length. The fibula
should be slightly shorter and consideration should be given to fusion
between the tibia and fibula (especially in young active patients)
Knee Disarticulation
-Patella tendon is sutured to the cruciate ligaments in the notch, leaving
the patella o the anterior femur
-This level is usually used for the non-ambulator who can support wound
healing at the transtibial or distal level.
-Muscle balanced amputation and provides an excellent weight-bearing
plateform for sitting and provides a lever arm for transfer.
-When performed in a potential walker, it provides a direct load transfer
(end-bearing) residual limb.
Above-Knee Amputation
-Optimal length is 12 cm above the knee joint to accommodate the
prosthetic knee. Minimal length of bone for prosthesis is 10 cm of femur.
-Adductor myodesis is important for maintaining femoral adduction during
the stance phase to allow for optimal prosthetic function.
-Medially based flap is essential
-Major deforming force is into abduction and flexion
-Adductor myodesis at normal muscle tension eliminates the problem of
adductor roll in the groin. Sectioning of adductor magnus results in a loss
of 70% of adductor pull.
-Prone position post-op is very important to prevent flexion contractions of
the hip.
Hip Disarticulation
Internal Hemipelvectomy
-Removal of the hemipelvis internally so the leg is salvaged
External Hemipelvectomy
-Removal of the hemipelvis with removal of the entire lower extremity

Energy Expenditure for Amputations

-The metabolic cost of walking is increased with proximal-level amputations,
being inversely proportional to the length of the residual limb and the number of
functional joints preserved.
-Oxygen consumption is increased with more proximal level amputations, thus
the AKA with peripheral vascular disease uses close to maximum energy
expenditure during normal self-selected velocity walking.

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-Energy expenditure above baseline for:

long BKA is 10%
average BKA is 25%
short BKA is 40%
bilateral BKA is 41%
AKA is 65%
-Cardiac output is increased by 35% in BKA
-Cardiac output is increased by 50% in AKA
Load Transfer
-Load transfer (weight bearing) occurs by either direct or indirect means.
-Direct load transfer (end-weight bearing) is accomplished with knee
disarticulation or ankle disarticulation (Symes). Intimacy of the prosthetic socket
is necessary only for suspension.
-Indirect load transfer is when amputation is performed through a long bone
(BKA or AKA) and the end of the stump does not take all the weight and the load
transferred indirectly by the total contact method. This process requires an
intimate prosthetic socket fit and 7-10 of flexion of the knee for BKA and 5-10
of adduction and flexion of the femur for AKA.
Wound healing measurements:
1) TcPO 2 > 30mmHg
2) ABI > 0.45
3) Toe pressure > 40mmHg
4) Albumin > 3.0-3.5g/dl
3
5) Total lymphocyte count >1500 cells/mm
6) Total protein >6.2 g/dl
7) Hemoglobin >10g/dl
-Amputation wounds generally heal by collateral flow, so arteriography is rarely
useful for predicting wound healing.
-In patients with DM or peripheral vascular disease, Doppler waveform tracings
may be falsely elevated due to the noncompressibility and noncompliance of
calcified peripheral arteries. The toe pressures ischemic index of >0.5 is
more accurate in these patients.
-TcPO 2 is the gold standard measure of vascular inflow. It records the
oxygen-delivering capacity of the vascular system to the level of the
comtemplated surgery. Values >40mmHg correlate with acceptable wound
healing rates without false-positive values seen in noncompliant peripheral
vascular diseased vessels. Pressures <20mmHg are predictive for poor healing
potential.
Pediatric Amputations
-Disarticulations should be performed when possible to maintain maximal
residual limb length and to prevent terminal bony overgrowth.

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-Amputation is rarely indicated in congential upper limb deficiency; even

rudimentary appendages can be functionally useful.
-In the lower limb, amputation of an unstable segment may allow direct load
transfer and enhanced walking:
Fibular hemimelia: ankle disarticulation (Symes)
Tibial hemimelia: knee disarticulation
o Only long bone deficiency with a known inheritance pattern

(autosomal dominant)

-Overgrowth is the most common complication of amputations in children and

overgrowth is most common in the humerus>fibula>tibia>femur.
Overgrowth is most common in diaphyseal amputations
-Surgical revision is best treatment option with adequate resection and bone or
autogenous osteochondral stump capping procedure.
Technical Considerations
-Periosteal stripping should be sufficient to allow for bone transaction; this
minimizes regenerative bone overgrowth.
-Wounds should not be sutured under tension.
-Muscles are best secured directly to bone at resting tension (myodesis) rather
than to antagonist muscle (myoplasty).
-All transected nerves form neuromas so the nerve end should come to lie deep
in a soft-tissue envelope away from potential pressure areas. Crushing the nerve
may contribute to post-op phantom or limb pain.
-Rigid dressings post-op help reduce swelling, decrease pain, and protect the
stump from trauma. Rigid dressings also prevent contractures and compressive
bandages help reduce swelling. No weight-bearing should be done till all
sutures/staples are removed and wound is healed.
Complications
-Phantom limb sensation is the feeling that all or part of the amputated limb
is present, and occurs in almost all adults who have undergone amputation. It
usually decreases with time.
-Phantom pain is a burning, painful sensation in the amputated part. It is
diminished by prosthetic use, physical therapy, compression and TENS. A
common cause of residual pain is complex regional pain syndrome (RSD) or
causalgia. Amputation should NOT be performed for this condition!
-Post-op edema occurs after amputation and may impede wound healing. Rigid
post-op dressings and compression sleeves may reduce this problem. Swelling
occurring after stump maturation is usually caused by poor socket fit, medial
problems or trauma. Persistence of chronic swelling may lead to verrucous
hyperplasia, which is wart-like overgrowth of skin with pigmentation and
serous discharge. This is treated with total contact casting.
-Hip or knee contractures are common.

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III. Prosthetics
-For patients to learn to walk with a prosthesis and care for their stump and
prosthesis, they must possess certain cognitive capacities: memory, attention,
concentration and organization. Patients with cognitive deficits or psych
disorders have a low likelihood of becoming successful prosthesis users.
Upper Limb Prosthetics
-Prosthetic fitting should be done as soon as possible, even before complete
wound healing has occurred. Outcomes of prothetic limb use vary from

70-85% when prosthetic fitting occurs within 30 days of amputation

(for transradial amputations) in contrast with <30% when started late.
-Myoelectric prostheses provide good cosmesis and are used for sedentary work
and are most successful in the midlength transradial amputee.
-Body-powered prostheses are used for heavy labor and are activated

by shoulder flexion and abduction. Elbow flexion and extension are

controlled by shoulder extension and depression.

-Optimal mechanical efficiency of figure-eight harnesses requires the harness

ring to be at the spinous process of C7 and slightly to the non-amputated side.
-When the residual forearm is so short as to preclude an adequate lever arm for
driving the prothesis through space, supracondylar suspension (Munster socket)
and step-up hinges can be used to augment function.
-The best function with the least weight at the lowest cost is provided by hybrid
prosthetic systems combining myoelectric, traditional body-powered, and bodydriven switch components.
Lower Limb Prosthetics
-Prosthetic feet are available in several designs:
1) Single-axis foot is based on ankle hinge that provides dorsiflexion
and plantar flexion
a. Disadvantages include poor durability and cosmese
2) SACH foot (solid ankle, cushioned heel) has been the standard for
decades and was appropriate for general use in low-demand patients.
Its use has been discontinued.
a. It may lead to overload problems on the non-amputated foot.
3) Articulated dynamic response foot allows inversion/eversion and
rotation of the foot and are useful for activities on uneven surfaces.
a. They may absorb loads and decrease shear forces to the residual
limb.
-Most dynamic response feet have a flexible keel and are the new standard for
general use. Correct dynamic prosthetic foot selection requires information
about the patients height, weight, activity level, access for maintenance,
cosmesis, and funding.
-Dynamic response feet may be grouped into articulating and non-articulating
feet, which have short or long keels.

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-The keel deforms under load, becoming a spring and allowing dorsiflexion,
thereby decreasing the loading on the sound side and providing a spring-like
response for push-off. Shortened keels are not as responsive and are

indicated for the moderate activity ambulatory, whereas long keels are
for very high-demand activities.

-Prosthetic shanks are the structural link between prosthetic components and
exist as endoskeletal and exoskeletal. Rotator units exist for patients who play
golf.
-Polycentric (Four-Bar Linkage) knee has a moving center of rotation that
provides for different stability characteristics during the gait cycle and may allow
increased flexion for sitting. It is recommended for patients with knee
disarticulations, AKA and bilateral amputees.
-Fluid-control (hydraulic and pneumatic) knee allows adjustment of
cadence response by changing resistance to knee flexion via a piston
mechanism. The knee is best used in active patients who prefer greater utility
and variability at the expense of more weight.
-Constant friction knee has a hinge that dampens knee swing. It is a general
utility knee and may be used on uneven terrain. It is the most common knee
used in children. It allows for only single-speed walking and relies solely on
alignment for stance-phase stability and therefore not recommended for older,
weaker patients.
-Variable friction (cadence control) knee allows resistance to knee flexion
to increase as the knee extends to allow for walking at different speeds but is
not durable and is not available in endoskeletal systems.
-Manual locking knee consists of a constant friction knee hinge with a positive
lock in extension that can be unlocked to allow function similar to that of a
constant friction knee. The knee is often left locked in extension for more
stability. Used primarily in weak, unstable patients and those just learing to use
prosthetics and for blind amputees.

Suspension Systems
-In general, suction and socket contour are the primary suspension modalities
used. Use of straps and belts are usually for supplementation. The suction
socket provides an airtight seal via a pressure differential between the socket
and atmosphere. Total contact support of the residual limb surface prevents
edema formation.
-Transtibial suspension is best with gel liner suspension systems with a
locking pin. The liners provide suspension through suction and friction and act
as the socket interface.
-Supracondylar suspension is recommended when the residual limb is
less than 5cm long.

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Common Prosthetic Problems

-Pistoning during swing phase of gait is usually caused by an ineffective
suspension system.
-Pistoning in the stance phase is due to poor socket fit or volume

changes in the stump

-Pressure-related pain or redness should be corrected with relief of the

prosthesis in the affected area.
-Too soft a foot results excessive knee extension
-Too hard a foot results in excessive knee flexion and lateral rotation of
the toes.
-Valgus strain (proximal-lateral and distal-medial) pain at the stump
and broad based gait is due to foot being too outset.
-Varus strain (proximal-medial and distal-lateral) pain at the stump
and circumduction gait is due to foot being too inset.
-A premature loss of anterior support (knee buckling) can occur if:
the foot is too far posterior
the foot is too dorsiflexed
the interface is too flexed
overly-firm heel
-Knee hyperextension (increased knee extension and patellar pain) at
heel-off can occur if:
the foot is too far anterior
the foot is too plantarflexed
the interface is not flexed enough
overly-soft heel
-Lateral trunk bending gait occurs with:

short prosthesis
weak abductors

poor fit
-In general, amputees climb stairs by leading with their normal limb and
descend by leading with their prosthetic limb (the good goes up and the
bad comes down)

IV. Orthoses
-With few exceptions, orthoses are not indicated for correction of fixed
deformities or for spastic deformities that cannot be easily controlled manually.
-Extra-depth shoes with a high toe box to dissipate local pressures over bony
prominences are recommended for diabetic patients.
-A rocker sole can lessen the bending forces on an arthritic or stiff midfoot
during the midstance as the foot changes from accepting the weight-bearing
load to pushing off. It is useful in treating metatarsalgia, hallux rigidus, and
other forefoot problems. For the rocker sole to be effective, it must be rigid.
-Medial heel outflare is used to treat severe flat foot of most causes. A foot
orthosis is also necessary. Most foot orthoses are used to align and support the

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foot, prevent, correct or accommodate foot deformities and also improve foot
function.
-Three main types of foot orthoses are used: rigid, semirigid and soft. Rigid foot
orthoses limit joint motion and stabilize flexible deformities. Soft orthoses have
best shock-absorbing ability and are used to accommodate fixed deformities of
the feet, especially neuropathic, dysvascular and ulcerative disorders.

V. Stroke
-Maximum spontaneous motor recovery is 6 months for stroke
- Maximum spontaneous motor recovery is 12-18 months for traumatic brain
injury.
-Surgical intervention in adult-acquired spasticity is delayed until the patient
achieves maximum spontaneous motor recovery.
-Balance is the best predictor of a patients ability to ambulate after acquired
brain injury.

VI. Spinal Cord Injury

-The functional level in a patient with spinal cord injury is determined by the
most distal intact functional dermatome (sensory level) and the most distal
motor level where most of the muscles at the level function at least at a fair
motor grade.
-Above C4 functional level: respiratory dependent
-C4 functional level: no use of arms, wheelchair chin/puff
-C5 functional level: elbow flexors intact but no function below the elbow,
electric wheelchair
-C7 functional level: no grasp, wheelchair but independent and can groom and
dress themselves and cut meat. BB function can be controlled with rectal
stimulation and intermittent cath
-L1 functional level: minimal ambulation with KAFO
-L2 functional level: household ambulatory with KAFO
-L3 functional level: community ambulator with AFO (quads work)
-Majority of pathologic fractures (secondary to disuse osteopenia in paralytics)
occur about the knee (supracondylar femur fractures) and is also known as the
paralytic fracture
-Autonomic dysreflexia is a catastrophic hypertensive event can occur with
injuries above T5. It is usually caused by an obstructed urinary catheter or fecal
impaction.

VII. Postpolio Syndrome

-Polio affects the anterior horn cells of the spinal cord.
-Postpolio syndrome is not a reactivation of the polio virus. It is an aging
phenomenon whereby more nerve cells become inactive. These patients use a
high proportion of their capacity for normal activities of daily living. With aging
and the drop-off of muscle units, they no longer have the reserves to perform

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their daily activities. Treatment is limited exercise combined with periods of rest,
so muscles are maintained but not overtaxed.

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