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Periwound skin DFu

Consider normal, erythematic (document/draw extent), streaking, stasis changes, trophic changes


acronym for wound descrption

Acronym 3D MOBB (depth, diameter, drainage, measure, odor, base, border


ABIs for DFU

-Values >0.9 associated with good healing potential
-Values 0.5-0.9 associated with PVD and delayed healing
-Values <0.5 associated with ischemia and problematic healing
-Be wary of elevated values secondary to vessel calcification


TcPO2 for DFU

-TcPO2: -Values >30mmHg associated with good healing potential [Mars M. Transcutaneous oxygen tension as a predictor of success
after an amputation. JBJS-Am. 1988; 70(9): 1429-30.]
-Values <20mmHg associated with microcirculatory problems and delayed/problematic healing.


absolute pressures and absolute relative skin temp

-Absolute Pressures: -Should have 40mmHg at ankle and 20mmHg at the digits for healing potential.
-Absolute/Relative skin temperature: compare B/L (normal around 94° F)


vascular things to look for for DFU

CFT, pedal hair
absolute pressures
Absolute/relative skin temperatures


neurological things for DFU

-Sensory testing:
-Posterior column: Vibratory, Proprioception
-Anterior column: Light touch (5.07 SWMF)
-Lateral column: Pain and temperature
-Motor testing:
-Expect intrinsic weakness with advanced neuropathy
-Manual Muscle Testing
-Spinal Reflexes (Achilles, Patellar, Babinski)
-Increase in skin temperature
-Lack of sweating leading to xerosis
-Any other relevant neurologic tests (you should have an awareness of Dellon’s work and the PSSD).


MSK for DFu

-Document any/all foot deformities, especially osseous prominences.
-Expect intrinsic muscle weakness leading to digital deformities.
-Overall foot type



[Wagner FW: The dysvascular foot: a system of diagnosis and treatment. Foot Ankle 2: 64–122, 1981]
0: Pre-ulcerative area without open lesion
1: Superficial ulcer (partial/full thickness)
2: Ulcer deep to tendon, capsule, bone
3: Stage 2 with abscess, osteomyelitis or joint sepsis
4: Localized gangrene
5: Global foot gangrene
Modified with the following risk factors:
A: Neuropathic
B: Ischemic
C: Neuroischemic
-So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: Wagner 4B


-University of Texas: [Lavery LA, Armstrong DG, Harkless LB: Classification of diabetic foot wounds. J Foot Ankle Surg 35:528–531, 1996

0: no open lesion
1: superficial
2: Tendon capsule
3: Bone Joint

A: no ischmia/infection
B: infection
c: ischemia
D: both


PEDIS system

-Recommended by the Infectious Disease Society of America.
-PEDIS is an acronym standing for perfusion (measure of vascular supply), extent/size, depth/tissue loss, infection,
and sensation.
-Each of the 5 categories is graded from 0 (minimal) to 2 (severe).
-Based ona 10-point scale with 10 being most serious ulcer with greatest difficulty in treatment


-Liverpool Classification System: Dfu


-Modified with:
-Complicated (cellulitis, abscess, OM, etc.)



Glucose (HA1c)
Wound culture and sens:
-gram stain
Blood Cultures
Bone Biopsy
If surg candidate get:



-Total Leukocyte Count (~4-10 x 10^3 leukocytes/ul)
-Leukocyte is a generalized term for any WBC including neutrophils/granulocytes, monocytes,
lymphocytes, eosinophils and basophils. So an increased leukocyte count can indicate a rise in any or all of
these. This is the reason why a differential is so important.


PMN/granulocytes in DFU

-Neutrophils/Granulocytes (Usually ~54%; increased >85%)
-Part of the humoral system.
-Phagocytic cells in the inflammatory process.
-Normally take 8-14 days to mature. Functionally last 1-2 days. Half-life 6 hours.
-Would be increased in an inflammatory state.
-PMNs: Mature neutrophils that you would expect to see in an infection.
-Band cells: Immature neutrophils. Presence indicates active, ongoing infection.
-A left shift is an increased neutrophil percentage in the presence of band cells


Monocytes in DFU

-Monocytes (Usually ~6%)
-Phagocytic, bacteriocidal macrophages in the humoral system.
-Accumulate after neutrophils in acute infection.
-Presence indicates post-inflammatory state or chronic infection


Lymphocytes in DFU

-Part of the cellular system.
-Produce immunoglobulins and express cellular immunity (T and B cells).
-Not normally increased in bone/soft tissue infections.
-Possibly increased in a foreign body reaction.


Eosinophils in DFU

-Part of the cellular system.
-Generally involved in allergic and immune responses.
-Develop in the same line as lymphocytes.
-Increased with acronym NAACP
-(Neoplasm, Allergy, Addison’s, Collagen vascular disorder, Parasites


basophils in DFU

-Part of cellular immunity.
-Involved with acute allergic responses and histamine release


Glucose and Ha1c


-HbA1C: Measure of glycosylated hemoglobin and long-term glucose control:
-1% equals approximately 20 glucose points (7% equals ~140ug/ul)
-Note that the stress of infection will probably cause a hyperglycemic state


ESR for DFu

Normal: 60mm/hr

-Analyzed using the Westergren method, which measures the distance erythrocytes fall in one hour in a vertical
column of anti-coagulated blood under the influence of gravity (even though gravity is just a theory).
-Sensitive, but not specific for infection as it is increased in any inflammatory state with increased fibrinogen.
-Also elevated in: Pregnancy, DM, ESRD, CAD, CVD, Malignancy, Age, etc.
-[Karr JC. The diagnosis of osteomyelitis in diabetes using ESR. JAPMA 2002 May; 95(5): 314.]
-[Lipsky BA. Bone of contention: diagnosing diabetic foot osteomyelitis. Clin Infect Dis. 2008 Aug; 47(4): 528-30.]



-Normal: 0-0.6mg/dl
-Measures a liver protein only present in acute inflammation (not normally found at all).
-Sensitive, but not specific for infection.
-Also elevated in: RA, Malignancy, MI, SLE, Pregnancy, etc.
-More expensive and technically difficult to perform compared to the ESR.
-[Jeandrot A. Serum procalcitonin and CRP concentrations to distinguish mildly infected from non-infected diabetic foot ulcers: a pilot study.
Diabetologia. 2008 Feb; 51(2): 347-52.]


wound culture swabs can be easily contaminated.

What is ideal situation to swab

The ideal situation is a deep wound specimen of tissue (not just a swab)
following incision and drainage with pulse lavage before beginning antibiotic therapy


blood cultures and biopsy consideration for dfu

-Blood Cultures
-Should be drawn from 2 sites; 20 minutes apart.
-Indicates bacteremia/septicemia
-Bone Biopsy
-Gold standard for diagnosis of osteomyelitis (discussed further later)


aerobic gram pos cocci

Staph Aureus
Staph Epi
Strept pyogenes (A)
Strept agalactia (B)
Strept Bovis (D)
Strept viridans


Anaerobic gram pos cocci



aerobic gram pos rods

Bacillus anthracis
Corynebacterium diphtheriae
Listeria Monocytogene


Anaerobic Gram Positive Rods

Clostridium perfringens
Clostridium difficile
Clostridium tetani


aerobic gram neg rods

e coli
Y. pestis
e. corrodens
paturella multicide

morganella morganii(?)


anaerogic gram neg rods

bacteroides fragilis


aerobic gram neg cocci




Treponium pallidum
Borrelia burgdorferi


Imaging for DFU

bone scan
wbc scan
PET scan


xrays for dfu

-Soft Tissue: Infection characterized by radiolucent area. One should be able to see a soft tissue deficit if an ulcer is present. It is very important
to rule out emphysema (gas in the tissues) with a plain film. Can also appreciate soft tissue edema.
-Osseous Tissue:
-Early Osteomyelitis (OM) signs: No reliable ones. Rarefaction and periostitis are possible.
-Subacute OM signs: Brodie’s abscess (lytic lesion surrounded by sclerotic rim).
-Chronic OM: Lysis, Malformation, Involucrum, Cloaca, Sequestra.
-Plain film radiographs are 67% specific, 60% sensitive for OM [Termaat, JBJS 2005]


mri for dfu

T1: Diffuse and infiltrative decreased signal intensity as inflammation replaces fat.
T2 and STIR: Increased signal intensity.

T1/T2/STIR: Homogeneous increased signal intensity.
-Note that pus/necrotic tissue has a decreased intensity compared to inflammatory fluid.

T1: Decreased signal intensity, cortical lysis and intramedullary changes.
-Increased signal intensity in known OM indicates healing as fat infiltrates.
T2: Increased signal intensity, cortical lysis, and intramedullary changes.
-Rim sign: thin layer of active infection surrounding normal bone.
-60% Specificity, 85% sensitivity per Termaat.


bone scans for dfu

-A radio-isotope is injected into the patient and imaged at specific intervals.

-Immediate Angiogram (1-3sec): Essentially an arteriogram.
-Blood Pool (3-5min): Demonstrates blood pooling in capillaries and veins.
-Delayed (2-4 hours): Increasingly specific to activity patterns and pathology.
-4th Phase (varying times): Increasingly specific to activity patterns and pathology


technitium 99 bone scan for dfu

-Binds to calcium hydroxyapatite and measures osteoblast/osteoclast activity.
-Half-life: 6 hours
-Excreted through kidneys which will show homogenous control signal.
-Mucomyst 600mg PO q12 day before and of surgery as renal ppx.
-Cellulitis: Focal uptake in blood pool; Negative in delayed phase.
-OM: Diffuse uptake in blood pool; Hot increased uptake in delayed phases.
-45% Specificity; 86% sensitivity per Termaat


types of wbc scans for dfu

gallium 67 citrate
indium 111 oxime
technetium 99m HMPAO
technetium 99m sulfur colloid marrow scan
Combination Sequential Technitium-Gallium scans


explain combo sequential technetium gallium scans

-Scan at 4 hours, then at 48-72 hours. Based on half-lives.
-Increased specificity for infection if gallium has higher uptake then technetium.
-Can use any other combination


explain technetium 99 m sulfur colloid marrow scan for dfu

-Specific for bone marrow and neutrophil production
-Has shown promise in differentiating OM from Charco


technetium 99m HMPAO for dfu

-WBCs isolated from blood samples, tagged and re-injected. Scan at 3 hours.
-Tagged molecule is HMPAO (hexamethylpropyleneamine oxime) ->you will get asked this!)
-Technically easier with less radiation than indium


indium 111 oxime for dfu

-WBCs isolated from blood sample, labeled and re-injected.
-Scan at 24 hours. Half life: 67 hours.
-Predominantly uptaken by neutrophils, so it demonstrates acute infections better than chronic infections


gallium 67 citrate

-Uptake by siderophore complex (direct bacteria) and lactoferrin (protein-released by bacteria)
-Scan taken 48-72 hours after injection or done in triphasic manner.
-Has longer half-life
-42% Specificity; 80% Sensitivity per Termaat


ct scans for dfu

Radiograph altered by computer to highlight specific “windows”. You can isolate soft tissue or different aspects of bone, for example.
-Soft tissue infection: Exact locations and anatomy of abnormal soft tissue density.
-OM: Increased density in the marrow.
-CT scans can be combined with contrast


explain PET scan

-A tracer is injected/inhaled into the patient which releases radioactive positrons. The positrons collide with electrons and produce gamma rays.
->90% Sensitivity and Specificity per Termaat (best in study

High sens,spec


3 pathogenesis of dfu

trauma leading to ulcer
impaired wound healing


pathogenesis of dfu

explain neuropathy

-30-50% of diabetics have some form of sensory, motor and/or autonomic neuropathy.
-Sorbitol accumulation in Schwann cells leads to hyperosmolarity of the nerve cells in turn leading to swelling and cellular lysis. This leads to decreased nerve signal conduction. Microvascular damage to the nerve (described later) also impairs healing of the damaged nerve.

-Sensory Neuropathy
-Loss of light touch/protective sensation (anterior spinothalamic tract)
-Loss of vibratory/proprioception mechanisms (posterior tract)
-Loss of pain/temperature sensation (lateral tracts)
-The patient has no warning of current, developing or impending trauma.

-Motor Neuropathy
-“Intrinsic Minus” foot-type with wasting of the intrinsic muscles and extensor substitution.
-Undetected excess plantar pressures develop.

-Autonomic Neuropathy
-Damage occurs in the sympathetic ganglion
-AV shunting occurs with global LE edema not relieved by diuretics or elevation.
-Increased skin temperature predisposes to ulceration (Armstrong)
-Decreased sweating leads to xerosis and fissuring (portal for infection)


pathogenesis dfu

explain traum leading to ucleration

-Abnormal anatomy: extrinsic and intrinsic abnormalities secondary to motor neuropathy and tendon glycosylation.
-Decreased joint mobility: secondary to non-enzymatic glycosylation and excess collagen cross-linking of tendons,
ligaments, joint capsules (especially at the STJ and the MTPJ).
-Equinus: Increased cross-linking of collagen in the Achilles tendon (leads to increased forefoot pressures).
-Skin stiffness: secondary to glycosylation of keratin.
-Intrinsic skin weakness: trophic changes associated with PVD.
-All lead to increased plantar pressures, which is the driving force behind ulceration.


explain impaired wound healing for dfu pathogenesis

-Can be thought of as increased inflammation, decreased vasculature and decreased catabolism.
-Increased Inflammation
-The inflammatory phase of the healing process actually lasts longer than necessary.
-Inflammation initially not as effective due to decreased leukocyte adhesion and morphologic changes to
the macrophages.
-Prolongation occurs due to decreased chemotaxis of growth factors and cytokines.
-MMPs increase their activity and continue to produce an “inflammatory soup.”
-All contribute to a wound “stuck” in the inflammatory phase.
-Decreased Vasculature
-Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation.
-Microangiopathy: Thickened basement membrane decreases diffusion at capillary level.
-Mechanism behind neuropathy, nephropathy and retinopathy
-Think of it in terms of a decreased TcPO2
-Endothelial dysfunction:
-Decreased nitric oxide (NO) and prostaglandin to promote vasodilation
-Decreased smooth muscle cell relaxation to promote vasodilation
-AV shunting secondary to autonomic neuropathy
-Decreased vasodilation and membrane permeability in response to trauma/damage/inflammation:
-Usually regulated by substance P and vasomodulators from damaged cells and nociceptors.
-Overall leads to a “sluggish” vasculature with decreased inflow, diffusion, outflow and angiogenesis.
-Decreased Catabolism
-Decreased collagen synthesis, both in peptide production and post-translational modification
-Morphologic changes to keratinocytes
-Decreased angiogenesis


surgical layers of dissestion used for dfu depth measurement

Superficial Fascia
-First Dissection Interval containing superficial neurovascular structures
Deep Fascia
-Second Dissection Interval containing muscular and deep neurovascular structures
-Third Dissection Interval


OM definitions per Resnick:

Brodies Abscess
Sclerosing OM of Garre

-Periostitis: Inflammation of the periosteum
-Osteitis: Inflammation of the cortex
-Osteomyelitis: Inflammation of the medullary canal
-Sequestrum: piece of dead bone floating in pus/inflammation
-Involucrum: sheath of bone surrounding pus/inflammation
-Cloaca: tract through an involucrum
-Brodie’s Abscess (1832): Chronic abscess in bone surrounded by sclerosis
-Sclerosing OM of Garre: low grade inflammatory condition


waldvogel and lew article on definitions

acute OM
chronic OM
Contiguos/Direct extension
Hematogenous spread
vascular impairment

-Acute Osteomyelitis: Systemic clinical signs of infection
-Chronic Osteomyelitis: Subacute clinical signs of infection
-Contiguous/Direct Extension: spread of infection to bone from exogenous source or adjacent tissue.
This can be described as an “outside-in” spread invading the cortex and proceeding to the medullary canal.
-Hematogenous Spread: Infective agent reaches medullary canal of bone from the vascular supply. This
can be described as an “inside-out” infection invading the medullary canal first and spreading to the cortex.
-Vascular Impairment: Decreases the effectiveness of the inflammatory response and Abx delivery.


Other people who differnetiate acute vs chronic OM

Weiland: Describes chronic OM as lasting > 6months.
-Schauwecker: Describes chronic OM as lasting > 6 weeks and one failed episode of tx.


AJM classification for OM

-Acute Osteomyelitis
-Contiguous/Direct Extension
-Hematogenous Spread

-Chronic Osteomyelitis
-Contiguous/Direct Extension
-Hematogenous Spread


-Cierny-Mader-Penninck Classification [A clinical staging system for adult osteomyelitis. CORR. 2003; (414): 7-24.

-Anatomic Stage
Stage 1: Medullary: infection of only the medullary canal
Stage 2: Superficial: infection of only the superficial cortex
Stage 3: Localized: infection of only the cortex
Stage 4: Diffuse: infection of both the cortex and medullary canal

-Physiologic Stage
A: Normal Host
Bs: Compromised Host with systemic risk factors (eg DM)
Bl: Compromised Host with local risk factors (eg smoking)
C: Treatment worse than the disease

-So a smoking DM patient with infection of only the superficial portion of the cortex is: 2Bs
-Obviously much more work needs to be done on the topic of osteomyelitis classification.


OM diagnosis

-Subjective Findings (See Diabetic Infection Work-up)
-Objective Findings (Diabetic Infection Work-up)
-Probing to bone 89% positive predictive value (Grayson JAMA 1995).
-Gold Standard: Bone biopsy. This is ideally performed when the patient has been free of antibiotics for 2 weeks.
-Imaging Studies:
-Review plain films, MRI, Bone Scans, WBC scans, CT, PET in Diabetic Infection Imaging Sheet.
-These all add evidence, but are rarely exclusively diagnostic.
-Blood Cultures: Hematogenous OM diagnosed with positive BCx and positive bone scan.


general OM treatment

-There is much controversy regarding long-term Abx (PO vs. IV vs. PMMA) vs. Surgical Debridement.
-The Cierny-Mader Classification makes some general recommendations:
-CM Stage 1: 2 weeks IV + 2-4 weeks PO Abx
-CM Stage 2: Surgical Debridement + 2 weeks IV
-CM Stage 3&4: Surgical Debridement + 4-6 weeks IV Abx


OM abx administration options

-Long-term Abx (4-8 weeks) is a conservative option because many people believe you can never cure OM and that
it can reactivate at any time for years to come.


OM abx PO

-Doxycycline and Ciprofloxacin are reputed to have the best bone penetration.
-Keep in mind that most ID docs would never substitute coverage for bone penetration.
-Your Abx choices should be culture driven.


OM abx IV

-Culture driven
-Access options: IV, PICC, Infusion pump, etc.


OM PMMA beads

-PMMA: polymethylmethacrylate
-PMMA is a combination of monomer (liquid) and polymer (powder).
-Comes in 20, 40 and 60g packets.
-7% elusion in the first 24 hours with activity noted for 14 days.
-Demonstrates exponential release.
-Cierny proposes a 1:5 ratio of Abx:PMMA. Another common standard is 4-8g:40-60g.
-Increased Abx means increased elution, but decreased bead hardening.
-Smaller beads means increased overall surface area and increased elution.
-The Abx must be heat-labile
-Gentamycin, Tobramycin, Vancomycin, Ticarcillin, Cefazolin, Moxalactam, Cefotaxime


IDSA General Treatment Recommendations
Soft Tissue

[Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections.
IDSA Guidelines. CID 2004; 39: 885-910.]

Soft Tissue Only

Topical or oral 1-2 weeks up to 4 weeks

Oral 2-4 weeks

Initial parenteral, then switch to oral 2-4 weeks


IDSA General Treatment Recommendations
'bone or joint

[Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections.
IDSA Guidelines. CID 2004; 39: 885-910.]

No residual infection Parenteral or oral 2-5 days

Residual infected soft tissue
Parenteral or oral 2-4 weeks

Residual infected (but viable) bone
initial parenteral, then switch to oral 4-6 weeks

Residual dead bone post-operatively
Initial parenteral, then switch to oral >3 months


charcot defintion

Neuropathic osteoarthropathy first described by Musgrave in 1703 and named for JM Charcot in 1868


NV/french/theory of charcot pathogenesis

-Trophic centers in the anterior horn of the spinal cord maintain nutrition to joints.
-Trauma to these trophic centers leads to increased blood flow and osteoclastic activity.
-Evidence for the Neurovascular Theory:
-Autonomic neuropathy in DM leads to increased AV shunting, edema and skin temperature.
-Boulton: Increased PO2 in venous system of Charcot pts (63mmHg vs. 46mmHg)
-Shows increased perfusion in neuropathic diabetics
-Edmonds: Increased blood velocity in neuropathic diabetics
-Young: Decreased bone density in patients with decreased nerve conduction velocities
-Cundy: Decreased bone density in Charcot patients
-Gough: Increased osteoclastic activity in Charcot patients


Neurotraumatic/German/Theory of Virchow and Volkmann

-Repeated trauma from biomechanical stresses during ambulation on an insensate foot.
-Evidence for the Neurotraumatic Theory:
-Eloesser and Johnson: Trauma is the necessary predisposing factor, and not underlying bone weakness, to
create Charcot changes in a neuropathic limb.
-Common sense
-Two opposing, fighting theories (with two opining blowhards on either side getting red-faced)? Probably a little bit of both.


etiology of charcot

-First described: Tabes Dorsalis (Charcot 1868)
-Most common: DM
-3 most common: DM, Syringomyelia (longitudinal cavities lined by dense tissue), and Tabes Dorsalis
-C: Myelomeningocele, Spina Bifida, CMT, MS, CP, Syringomyelia, Congenital insensitivity
M: DM, Alcoholic neuropathy, Uremia, Pernicous Anemia
I: Tabes Dorsalis, Polio, Leprosy, TB
N: Tumors in brain, spinal cord, peripheral nerve
T: Trauma to brain, spinal cord, peripheral nerve
D: Indomethacin, Intra-articular corticosteroids, phenylbutazone


ddx of charcot

Inflammatory arthritis
septic arthritis


charcot clinical findings

-Presents similar to infection
-Red, hot, swollen, deformed foot +/- pain
-Readily available pulses (often described as bounding)


radiograhpic findings in charcot

-With osteopenia, pencil&cup deformities, resorption of bone ends
-Without osteophytes, sclerosis, fragmentation, soft tissue debris

-With joint space narrowing, fractures, fragmentation, ST debris, periosteal rxn, subluxation
-Without osteoporosis
-Be aware of both types


classifications for charcot

-Eichenholtz Classification
-Brodsky Classification
-Schon Classification


treatment for charcot

-Strict and immediate NWB and immobilization for 12-16 weeks.
-Edema control (Jones cast, ACE inhibitors, Diuretics, Posterior splint, Elevation, Ex Fix, etc.)
-Education and family support
-FXR every 4-6 weeks with relatively few cast changes

-Transition to WB (CAM walker, CROW, Bracing, MAFO, Shoes, etc.)

-Surgical correction of underlying deformity
-Consider TAL, Arthrodesis, Wedging osteotomies, Amputation

-Bone stimulators
-Bisphosphonates: -Pamidronate (Aredia): 60-90mg over 24h. 3 doses in 2 weeks.
-Alendronate (Fosamax): 5mg PO q24h


eichenoholtz 1966 classification of charcot

-Based on plain film radiographic findings
-Originally described Stages 1Æ3, but Stage 0 added later (Yu given credit, but really Schon).
-[Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. JAPMA. 2002; 92(4): 210-20.]

-Stage 0:
High risk pre-Charcot
-Radiograph: Unremarkable. Maybe increased ST density, bone flecks or change in foot architecture.
-Clinical: Sudden onset of non-pitting edema, erythema, calor, +/- pain, bounding pulses, intrinsic atrophy.
-Normal skin temp: 94°F; can increase by 12°
-Uptake in all three phases of Tc-99 bone scan

-Stage 1: Acute/Developmental
-Radiograph: Capsular distention, fragmentation, debris, subluxation
-Clinical: Red, hot, swollen foot with joint laxity

-Stage 2: Coalescence
-Radiograph: Sclerosis, resorption of debris, fusion
-Clinical: Subjectively decreased red, hot, swollen

-Stage 3: Reconstruction
-Radiograph: Decreased sclerosis (with increased vascularity) and remodeling
-Clinical: Decreased joint mobility with increased stabilization


Brodsky Classification (1992)
[Brodsky JW. The diabetic foot. In: Coughlin and Mann’s 1992 edition.

of charcot

-Type 1: Lisfranc joint (27-60% incidence)
-Type 2: Chopart’s joint and STJ (30-35% incidence)
-Type 3A: Ankle joint (9% incidence)
-Type 3B: Posterior calcaneus
-Type 4: Multiple combinations of above
-Type 5: The forefoot


-Schon Classification
[Charcot neuroarthropathy of the foot and ankle. CORR. 1998; 349: 116-131.

I: Lisfranc Pattern
-AÆC with increasing deformity to medial rockerbottom and ulceration.
II: Naviculocunieform Pattern
-AÆC with increasing deformity to lateral rockerbottom and ulceration.
III: Perinavicular Pattern
-AÆC with lateral rockerbottom, Talar AVN and ulceration.
IV: Transverse Tarsal Pattern
-AÆC with increasing deformity to central rockerbottom and ulceration.


Differentiate charcot of OM General

-Please keep in mind that these are not mutually exclusive and both can be present!
-These are just general guidelines and many people will vehemently argue about them.
-The gold standard is a bone biopsy which would show infection in OM and not in Charcot.


OM vs charcot subjective and objective

-OM: Constitutional signs and symptoms of infection, infectious risk factors, history of infection.
-Charcot: Uncontrolled DM, history of Charcot, history of recent trauma.

-OM: Necrosis, purulent drainage, elevated white count, cultures, positive bone biopsy.
-Charcot: Increased joint laxity, non-pitting edema, bounding pulses, rockerbottom deformity, negative bone biopsy.


OM vs charcot imaging

-Not enough evidence yet, but some believe that OM is positive on bone scans and WBC scans for greater than 24 hours
whereas Charcot neuroarthropathy is only positive during the first 24 hours.
-The Tc99 Sulfur Colloid scan would also theoretically be positive for infection, but not for Charcot.


keys to describing plain films

-Increased or Decreased
-Radiolucency or Radiodensity
-Everything that you see on a radiograph can be described using these terms. So while you may not be able
to “see” a fracture, you can describe an area of radiolucency within bone consistent with a fracture. And
while you may not be able to “see” an infection, you can describe an area of radiolucency within the soft
tissue consistent with emphysema.


reading MRI

bone scans


-Increased or Decreased
-Signal intensity
-Bone scans:
-Increased or Decreased
-Signal uptake
-Hyperechoic or Hypoechoic


bugs- cellulitis with an open wound

-Staph Aureus (SA) (if no streaking present)
-Strept (with streaking and palpable border)
-Usually monomicrobial


Infected ulcer in abx naive pateint

Staph Au


chronically infected ulcer in abx naive pt

Staph Au
usually polymicrobial


macerated infected ulcer



Chronic, non-healing ulcer with prolonged Abx therapy:

-Staph epi
-Enterococci -VRE
-Diptheroids (Corynebacterium)
-Extended GNR
-Usually polymicrobia


Fetid Foot with necrosis and gangrene

-Resistant Gram positive cocci
-Mixed GNR


OM with hemodialysis



OM with IVDA



OM with decubitus

gram negatives


OM with hemoglobulinopathy



Human mouth pathogens

cardiobacterium hominis
eikenella corrodens
kingella kingae


water exposure

aeromonas hyprophilia


Puncture through a shoe



any dirt or soil



Cat bite

pasteurella multocida


dog bit

strep virdans
capnocytophaga canimorsus


immunocompromised pt

gram negatives


septic burisitis

Staph aureus


gas gangrene



post op infection following implant

staph epi


fruity odor/green hue



foul smelling discharge



creamy yellow discharge



White discharge

Staph epi


generalized gram pos coverage

-2ndGeneration PCN -2ndGeneration Quinolones
-4thGeneration PCN -Macrolides
-1stGeneration Cephs -Bactrim
-2ndGeneration Cephs
-Carbapenems -Clindamycin


generalizd MRSA coverage

-Vancomycin -Synercid


gram neg coverage

3/4 PCN
2/3/4 quinolones


Generalized Pseudomonas Coverage

-Cephalosporins x 3 (Fortaz, Cefobid, Maxipime)
-PCN x 2 (Zosyn, Timentin)
-ACRONYM: FAT CIAZ (Fortaz, Aztreonam, Timentin, Cefobid, Imipenin, Aminoglycosides, Zosyn)



1/2/3/4 Ceph


IDSA source citation

-from Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910.


IDSA uninfected wound

-Definition: No purulence, inflammatory manifestations, or systemic manifestations
-Empiric Therapy: None


IDSA Mildly infected wound

-2+ Manifestations of Infection (purulence, induration or erythema/pain/warmth)
-<2cm of erythema
-Limited to skin and subcutaneous tissue
-No systemic complaints

-Empiric Therapy Recommendations:
-2-PCN -Bactrim
-Clinda -Augmentin
-Keflex -Levo


IDSA Moderately Infected Wound

-As above, in a systemically/metabolically stable patient PLUS
->2cm cellulitis OR streaking OR involvement of deep tissue

-Empiric Therapy Recommendations:

-Bactrim -Invanz
-Augmentin -Ceftin + Flagyl
-Levo -Timentin
-2-Ceph -Zosyn
-3-Ceph -Levo + Clinda
-Daptomycin + Aztreonam -Cipro + Clinda
-Zyvox + Aztreonam


IDSA Severely Infected Wound

-Definition: -Infection as above in a patient with systemic toxicity and metabolic instability

-Empiric Therapy Recommendations:

-Vanco + Fortaz
-Vanco + Fortaz + Flagyl
-Cipro + Clinda
-Levo + Clinda


empiric therapy if MRSA is likely

-Vanco + Fortaz
-Zyvox + Aztreonam
-Vanco + Fortaz + Flagyl
-Daptomycin + Aztreonam


empiric therapy to cover all bases

Vanco + Aztreonam + Flagyl


DOC Staph aureus








DOC Staph Epi






DOC Enterococci






Strep pyogenes Group A Strep DOC

Strep agalactiae (B)

Strep bovis (D)

Strep Viridans



Peptostreptococcous DOC



bacillus antracis doc



conynebacerium diptheriae doc



liseria monocytogenes



clostridium perfringens doc



c diff doc



clostridium tetani doc



pseudomonas doc



e coli doc

3 cep


enterobacter doc



proteus doc



vibrio doc



y. pestis doc



shigella doc



salmonella doc



klebsiella doc



serratia doc



e. corrodens doc



p. multocida doc



bacteroides fagilis doc



neisseria doc



spirochetes doc

t. pallidum
borrelia burgdorferi



staph aureus
po/iv dosing

Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid
Zithromycin -500mg PO day 1, 250mg PO days 2-5

Ancef -1g IV q8
Vancomycin -1g IV q12
Clindamycin -600mg IV q8



po and iv dosing

Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid

Ancef -1g IV q8
Vancomycin -1g IV q12
Clindamycin -600mg IV q8



po and iv dosing

Vancomycin -1g IV q12

Bactrim -1 tablet PO bid
Rifampin 300mg
-100mg PO bid


enterococcus dosing chart

Amoxicillin -250-500mg tid
Augmentin -875mg bid or 500mg tid (or bid)
Zyvox -600mg PO bid

Vancomycin -1g IV q12
Zyvox -600mg IVq12


VRA/VRE dosing iv and po

Zyvox -600mg PO bid

Zyvox -600mg IV q12
Synercid -7.5mg/kg/hr over 1 hour q12


pseudomonas dosing iva nd po

Ciprofloxacin -250-750mg PO bid

Ciprofloxacin -400mg IV q12
Fortaz -2g IV q12
Aztreonam -1g IV q8


e coli, proteus dosing iv and po

-PO: Keflex -500mg PO tid or 750mg PO bid
Cipro -250-750mg PO bid
Levaquin -500mg PO qday
Tequin -400mg PO qday

-IV: Ancef -1g IV q8
Cipro -400mg IV q12
Levaquin -500mg IV qday
Tequin -400mg IV qday


dosing of penicilliins

1st Generation:
-Pen V: 500mg q6 PO
-Pen G: 250,000 units/kg/day IV

2nd Generation: -Dicloxacillin: 250mg q6 PO
-Oxacillin: 1-2g q4 IV
-Nafcillin: 1-2g q4 IV

3rd Generation: -Amoxicillin: 500mg q8 PO
-Ampicillin: 1g q4-6 IV

4th Generation: -Augmentin: 875mg q12 PO
-Unasyn: 3g q6 IV
-Zosyn: 4.5g q6 IV
-Timentin: 3.1g q6 IV


cephalosporins dosing

1stGeneration: -Keflex: 500mg q8 PO or 750mg PO bid
-Duricef : 2g q24 PO
-Ancef: 1g q8 IV

2ndGeneration: -Ceftin: 500mg q12 PO
-Zinacef: 1.5g q8 IV
-Mefoxin: 1g q6 IV

3rd Generation: -Omnicef: 300mg q12 PO
-Vantin: 400mg q12 PO
-Rocephin: 1g q24 IV
-Fortaz: 1g q8 IV
-Cefobid: 2g q12 IV

4th Generation: -Maxipime: 2g q12 IV


quinolones dosing

2ndGeneration: -Ciprofloxacin: 750mg q12 PO/400mg q12 IV

3rdGeneration: -Levofloxacin: 500mg q24 PO/IV

4thGeneration: -Tequin: 400 q12 PO/IV
-Avelox: 400 q24 PO


Macrolines dosing

-Biaxin: 500mg q12 PO
-Ketek: 800mg q24 PO
-Zithromax: 500 q12 IV/ 500mg PO Day 1; 250 mg PO Day2-5
-Erythromycin 500mg q6 PO


carbapenems dosing

-Invanz: 1g q24 IV
-Primaxin: 500mg q8 IV
-Merrem 1g q8 IV


Aminoglycosyides dosing

-Amikacin: 1500mg/day
-Tobramycin: 3-5mg/kg/day
-Gentamycin: 3-5mg/kg/day


tetracyhclines dosing

-Minocycline: 100mg q12 PO/IV
-Doxycycline: 100mg q24 PO
-Tetracycline: 500mg q6 PO


bactrim dosing

160/800mg q24 PO


vanco dosing

1g q12 iv


clindamycin dosing

600mg q8 IV
300 mg q6 PO


Zyvox dosing

600 mg q12 PO/IV


Synercid dosing

7.5mg/kg q8 IV


Flagyl dosing

500mg q8 PO


Trauma Work-up

ABCDEs of primary survey
Tetanus Status
NPO Status


ABCDES of Primary survey

-Airway: Three common forms of airway obstruction are cervical spine injury, swollen tongue and facial fracture.
-Breathing: Note how this is different than an established airway. Someone can have an airway, but still not be
-Circulation: Assess vascular status in all four extremities. Two large-bore (18-gauge) IV’s should be started
immediately if fluid replacement is considered necessary.
-Deficits (Neurological): There are two ways to assess this.
---Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive
---Glasgow Coma Scale
----Based upon three criteria: eye opening, verbal response, motor response.
-Based on scale of 0-15 with a higher score indicating a better prognosis.
-13+ associated with a good prognosis; 7- associated with a poor prognosis.
-Exposure: Complete exposure of the patient to evaluate further, unknown damage


trauma secondary survery

HPI, PMH, etc and physical exam


Racquet-shpaed gram positive bacillis

Releases exotoxin causing a pre-sympathetic blockade

Clostridium Tetani


Triad of tetanus symptoms

trismus - Lockjaw
Risus Sardonicus - spasms causing smiling
Aphagia - can't swallow


Charateristic of a tetanus prone wound

greater than 6 hours old,
clinical signs of infection,
deep, devitalized
traumatic mechanism of injury, etc


Tatanus algorithm

-Unknown tetanus status:
-Clean wound: Give the toxoid; Hold the TIG
-Tetanus-prone wound: Give the toxoid; Give the TIG

-Incomplete tetanus status:
-Clean wound: Give the toxoid; Hold the TIG
(No booster within 5 years) -Tetanus-prone wound: Give the toxoid; Give the TIG

-Complete tetanus status:
-Clean wound: Hold the toxoid; Hold the TIG
(Booster within 5 years) -Tetanus-prone wound: Hold the toxoid; Hold the TIG


dosages of tetanus treatments

toxoid 0.5ml
TIG (tetanus immunoglobulin) 250 to 300 units


NPO status considerations

-All trauma patients are potential surgical candidates, so get this information for the weenie anesthesiologists

-Traditional guidelines recommend:
-Nothing by mouth after midnight the night before elective surgery
-Nothing by mouth within 6-8 hours of any type of surgery
-These strict guidelines are in the process of changing however, particularly with regard to allowing the ingestion
of small amounts of clear liquids up to the time of surgery


What are considered podiatric surgical emergencies

-Infection with emphysema (gas gangrene)
-Open fracture/dislocation
-Compartment syndrome
-Necrotizing Fasciitis
-General Neurovascular compromises


Mangled Extremity Severity Score MESS

-Based on 4 criteria: Skeletal/Soft Tissue Injury, Limb Ischemia, Age, and Shock
-Based on a scale from 1-11 with a higher score leading to an increased incidence of amputation.
-A score of 7+ has an increased likelihood of amputation.


Open fractures generally

-Note that 30% of lower extremity open fractures are associated with polytrauma.
-Mainstays of treatment: Aggressive incision and drainage with copious lavage.
-It is generally recommended to never primarily close an open fracture until devitalized soft tissue has demarcated,
but this certainly isn’t always the case in practice. In fact, the Ortho Trauma service at Inova routinely primarily
closes open fractures following I&D with ORIF.


guistillo anderson classification of open fractures

I. Clean Wound 5cm in diameter with extensive soft tissue damage
-Abx choice: Ancef (or high dose PCN), Clindamycin and Aminoglycoside
-IIIA: Adequate soft tissue coverage
-IIIB: Extensive soft tissue damage with periosteal stripping and massive contamination
-IIIC: Arterial damage requiring primary repair


fracture blisters general

-Location: Subepidermal
-Note that the fluid is sterile. Fracture blisters are histologically similar to 2nd degree burns.
-Most common LE etiology? Secondary to high-energy trauma such as ankle fx, calcaneus fx or Lisfranc injury.
-2 Common Types of Fracture Blisters
-Clear fluid: Most common (75%). Very tense in appearance.
-Hemorrhagic: Most severe. Roof is flaccid. Takes longer to re-epithelialize.
-Treatment is controversial, but the conservative approach is to never incise through a fracture blister and to delay
surgery until re-epithelialization


signs and symptoms of shock

delayed capillary refill,
decreased pulse pressure,
change in
mental status,
decreased systolic pressure,
decreased urinary output
decreased H&H


Types o f shock

-Hypovolemic: most common; defined as the acute loss of circulating blood. Treatment is aggressive fluid
-Cardiogenic: induced by myocardial dysfunction.
-Neurogenic: secondary to decreased sympathetic tone from head and spinal cord injuries.
-Septic: shock secondary to infection


goal of treating shock

Restore organ perfusion


When should a foreign body be removed?

-Clinical signs of infection, known contaminated object, pain, object close to NV elements, intra-articular


-Recommended imaging studies for a foreign body?

-Plain film radiography (no oblique views!), fluoroscopy, CT, MRI, US


-How will wooden objects appear on US

-Hyperechoic with a hypoechoic dark shadow


-How large must a glass foreign body be to be visible on plain film radiography? Does leaden matter

A piece of glass, regardless of whether it is leaden, must be >5mm to be visibl


-Classification for foreign bodies?

-Resnick Classification
-Patzakis Classification


-Resnick Classification

-I. Superficial/cutaneous: usually visible without signs of infection.
-II. Subcutaneous or articular without signs of infection.
-IIIA. Subcutaneous or articular with signs of infection.
-IIIB. Bone penetration without signs of infection.
-IV. Bone penetration with known osteomyelitis.


-Patzakis Classification

Wound site as a predictore of complications following deep nail puctures of foot.

-Zone 1: Toe to met head (50% incidence of osteomyelitis in this limited study.)
-Zone 2: Midfoot (17% incidence of osteomyelitis in this limited study.)
-Zone 3: Calcaneus (33% incidence of osteomyelitis in this limited study.


puncture wound most common bug

Staph Aureus

Beta Hemolyitc strept


puncture thru shoe



puncture on farm



Human bite

Eikenella corrodens


cat bites

pasteurella multocida


dog bites



mainstay of foreign body punture/wound treatment

Tetanus status
aggressive I& D


Gunshot wounds genreral

-High velocity GSWs are characterized by speeds >2500 ft/s. This is significant because high velocity GSWs have a tendency
to yaw and tumble leading to increased cavitation.


describe cavitation


Large wound is created under a situation of negative pressure. This negative pressure “sucks” outside
contaminants into the wound


Compartment syndrome

-Results when interstitial pressure exceeds capillary hydrostatic pressure, so the microcirculation shuts down


symptoms of compartment syndrome

-P’s of Compartment Syndrome (These are very generalized)
-Pain out of proportion and not controlled by analgesics -Paralysis
-Pain with passive dorsiflexion of the toes -Pulselessness
-Paresthesia -Pressure


normal compartment pressures

0 to 5 mmHg


treatment of compartment syndrome

-Decompression via fasciotomy, debridement of necrotic tissue, copious lavage and delayed closure
-Incision approaches: Consider dorsal vs. medial approaches


how is compartment syndrome dx made

wick or slit catheter to measure pressures


complications of compartment syndrome

-Complications: permanent loss of function with structural deformity (Volkmann contractures), myoneural necrosis, sensory
loss, chronic pain



-Intermetatarsal Compartments X 4: Contains the interossei muscles
-Medial Compartment: Abductor Hallucis
-Lateral Compartment: Abductor digiti minimi
-Superficial Central Compartment: FDB
-Deep Central Compartment: Adductor Hallucis
-Calcaneal Compartment: Quadratus Plantae and late
Dorsal: EHB and EDB


comparmtent syndrome suspected but why still have DP andPT pulses

lie above fascial compartments so they are the last to go.


Digital fx, subjective

-History of trauma. “Bedpost” fracture describes stubbing your toe while walking at night. Also common are injuries from
dropping objects on the foot


Objective for digital fractures

-Edema, erythema, ecchymosis, open lesions, subungual hematoma, and onycholysis should all be expected.
-Any rotational/angulation deformities should be identified on plain film radiograph.


digital fx classification

-Rosenthal Classification [Rosenthal EA. Treatment of fingertip and nail bed injuries. Orthop Clin North Am. 1983; 14: 675-697.]
-Zone I: Injury occurs with damaged tissue completely distal to the distal aspect of the phalanx.
-Zone II: Injury occurs with damaged tissue completely distal to the lunula.
-Zone III: Injury occurs with damaged tissue completely distal to the most distal joint (IPJ in hallux; DIPJ in


digital fractures treatment by zone

-Zone I Injuries
-If injury involves no exposed bone and a total tissue loss less than 1cm squared, then:
-Allow to heal in by secondary intention.
-If injury involves a total tissue loss greater than 1cm squared, then:
-A STSG or FTSG should be used depending on weight-bearing position.

-Zone II Injuries
-Flaps and Skin Grafts generally employed:
-Atasoy flap: plantar V to Y advancement

-Kutler flap: biaxial V to Y advancement

-Zone III Injuries
-Usually requires distal amputation (Distal Symes amputation)


Most common forefoot fracture



digital fracture without nail involvement or displacement tx



if subungal hematoma is present than there is a what chance of what

25% incidienc of underlying phalanx fracture


if subungal hematoma is greater than 25% then

remove nail


for proper nail function and adherence there should be no onyholysis within what of what

5mm of lunula


Transverse groove often associated with trauma

beau's line


sesamoid trauma subjective

-History of trauma is very important in this case. You want to differentiate between acute and chronic conditions involving
the sesamoids. Be careful to elicit any neurologic complaints that could be present


Objective for sesamoid trauma

-Expect edema, erythema, ecchymosis and open lesions. Take the time for proper palpation.
-Joplin’s neuroma is irritation of the medial plantar proper digital nerve.
-Associated with rigidly plantarflexed first metatarsals, anterior cavus, etc.
-One of the most difficult things to differentiate is an acute sesamoid fracture from a bipartite sesamoid. There are
several generic plain film radiographic characteristics found in acute fractures:
-Jagged, irregular and uneven spacing
-Large space between fragments
-Abnormal anatomy
-Bone callus formation
-Comparison to a contra-lateral view


1st MTPJ dislocation classification




-Type I
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Intact
-Fracture?: No sesamoid fracture
-Treatment: Requires open reduction

-Type IIA
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: No sesamoid fracture
-Treatment: Closed reduction/Conservative Care

-Type IIB
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: Fracture of at least one sesamoid
-Treatment: Closed reduction/Conservative Care

-Type II Variant
-Mechanism: Dorsal dislocation of the hallux
-Intersesamoid ligament: Ruptured
-Fracture?: Separation of a bipartite sesamoid
-Treatment: Closed reduction/Conservative Care


Treatment of sesamoid injuries

-Immobilization (NWB SLC, PWB SLC, Surgical Shoe, CAM Walker, etc.)
-Dancer’s Pad

-Excision of the fractured fragment or entire sesamoid


agenesis of fibular sesamoid

Ilfeld's disease


incidience of bipartite sesamoid

35.5% (kewenter)
10.7% (Inge) with 75% being unilateral


met fractures subj and obj

-Will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct blunt trauma, shearing, ankle sprains, etc.
-Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are necessary to accurately describe
displacement/angular/rotational abnormalities


met head/impaction fractures

-MOI: Direct or indirect trauma

-Radiographic findings:
-Examine for evidence of displacement/angulation/rotation
-Expect a shortening mechanism
-Examine for intra-articular nature of fracture

-Closed reduction generally unsuccessful
-ORIF with fixation of K-wire, screws or absorbable pins
- Immobilization for 4-6 weeks and NWB
-Early PROM suggested
-Subsequent arthrosis is a common complication


met neck fractures
radiograph findings

Shearing forces or direct trauma

-Radiographic findings:
-Expect elements of shortening, plantarflexion and lateral displacement of the distal segment.

-Treatment: -Conservative
--Closed reduction generally unsuccessful
--ORIF effective in restoring and maintaining alignment with K-wires, IM pinning and plates.
--NWB in SLC for 4-6 weeks


vassal principle for met neck fx

Adjacent fractures generally improve alignment after reduction of the initial fracture because soft tissue structures are
returned to their normal position through traction.


Midhsaft met fractures

Result of direct, blunt or torsional injuries

-Radiographic findings:
-Expect oblique fracture line, but transverse, spiral and comminuted are all possible.
-Expect elements of shortening, plantarflexion and lateral displacement of the distal segment.

-Based on displacement and fracture type:
-Non-displaced fractures: NWB SLC 4-6 weeks
-Fractures with >2-3mm of displacement and >10 degrees of angulation: ORIF

-Transverse displaced fractures
-Consider buttress plate, compression plate, IM percutaneous pinning, crossed K-wires
-Long oblique or spiral fractures
-Consider screws, plates, IM pinning, cerclage wiring
-Consider screws, plates, cerclage wiring, K-wires and external fixation


Metatarsal Base fractures

Direct trauma (MVA, fall from height, etc.) Usually associated with Lisfranc’s trauma.

-Radiographic findings: -Generally remain in good alignment/angulation because of surrounding stable structures.

-Treatment: -Conservative
-NWB SLC 4-6 weeks with good alignment
-ORIF with displacement/alignment/angulation


-First Metatarsal Fractures

Direct trauma (MVA, fall from height, crush, etc.) and indirect trauma (torsional, twisting, avulsions, etc.)

-Radiographic findings:
-Examine for distal intra-articular fractures
-Examine for avulsion-type fractures
-SLC 4-6 weeks with non-displaced fractures
-Be wary of closed reduction because extrinsic muscles may displace after apposition.
-Various ORIF techniques detailed above
-Percutaneous pinning and cannulated screws are option in first metatarsal
-ORIF should be utilized if intra-articular fracture involves >20% of articular surface


5th met base fractures subj and obj

-All will point to some form of traumatic injury. Common injuries leading to metatarsal fracture include direct trauma, blunt
trauma, shearing, ankle sprains, etc.
-Most important in your work-up will be how you read the plain film radiographs. Remember that at least two views are
necessary to accurately describe displacement/angular/rotational abnormalities.


diagnostic classification of 5th met base



Stewart type I

Extra-articular fx at metaphyseal-diaphyseal junction (True Jones Fracture)
-MOI: Internal rotation of the forefoot while the base of 5
met remains fixed
-Radiographic findings: -Usually oblique or transverse fx at metaphyseal-diaphyseal junction
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement >5mm
-Misc: -Fracture first described by Sir Robert Jones in 1902 from injuring himself while ballroom
-Very unstable fracture with high incidence of non-union/delayed union secondary to variable
blood supply. Remember that the diaphysis and metaphysis are generally supplied by two
different arterial sources.


stewart II

Intra-articular avulsion fracture
-MOI: Shearing force caused by internal twisting with contracture of peroneus brevis tendon
-Radiographic findings: -1 or 2 fracture lines
-Intra-articular in nature
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement >5mm


stewart III

-MOI: Reflex contracture of peroneus brevis with ankle in plantarflexed position
-Radiographic findings: -Extra-articular; Involvement of styloid process
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF (pins, screws, tension-band wiring) for displacement >5mm
-Consider excision of fragment and reattachment of peroneus brevis tendon


steward IV

Intra-articular, Comminuted fracture
-MOI: Crush injuries with base of 5
met stuck between cuboid and the external agent
-Radiographic findings: -Multiple fragments; joint involvement
-Treatment: -NWB SLC 4-6 weeks for non-displaced fractures
-ORIF with displacement
-Consider bone grafting and fragment excision with severe comminution
-Misc: -High rate of non-union/delayed union


stewart V

Extra-articular avulsion fractures of the epiphysis
-MOI and treatment similar to Type II and III fractures
-Note that this can only occur in children (similar to a Salter-Harris Type I fracture)


classifcation of jones fractures describing potential for non-union



explain Torg

-Radiographic classification of Jones fractures describing potential for non-union development.
-Type I: Acute injuries
-Radiographic findings: Narrow fracture line without intra-medullary sclerosis
-Type II: Delayed Union
-Radiographic findings: Widened fracture intersurface with evidence of IM sclerosis
-Type III: Non-Union
-Radiographic findings: Complete sclerotic obliteration of the IM canal


Stress fracture other names

March fx, Hairline fx, Fatigue fx, Insufficiency fx, Deutschlander’s dz, Bone exhaustion, etc


subjective for stress fracture

-CC: Patient presents complaining of a diffuse foot and ankle pain. Classic patient is a military recruit or athlete.
-HPI: -Nature: Pain described as “sharp with WB” or “sore/aching.” May have element of “shooting” pain.
-Location: Described as diffuse, but can be localized with palpation. Common areas include dorsal metatarsal or
distal tib/fib.
-Course: Subacute onset. Usually related to an increase in patient’s physical activity.
-Aggravating factors: Activity
-Alleviating factors: PRICE
-PMH: -Look for things that would weaken bone (eg. Osteoporosis)
-SH: -Look for recent increases in physical activity or a generally active patient
-PSH/Meds/All/FH/ROS: Usually non-contributory


Objective of stress fx

Physical Exam
-Derm: -Generalized or localized edema
-Ecchymosis is rare
-Vasc/Neuro: Usually non-contributory
-Ortho: -Painful on localized palpation (positive pinpoint tenderness!!)
-Possible pain with tuning fork


stress fracture imagin

-Plain Film Radiograph: -Localized loss of bone density and bone callus formation are hallmark signs
-Note that there must be a 30-50% loss of bone mineralization before radiographic presentation
of decreased bone density. This generally takes 10-21 days in a stress fracture.
-Bone Scan: -Increased uptake in all phases regardless of time of presentation


80 to 90% of stress factures occur where



most common bones for stress fractures in LE

metatarsals (2nd most common) and distal tib/fib


2 mechanisms of stress fractures

-Chronic strain upon a normal bone
-A chronic, normally benign strain upon a weakened bone


stress fx treatment

-Immobilization and NWB for 4-6 weeks (SLC, Unna boot, surgical shoe, etc.)
-Be certain of anatomic position with no angulation/rotation/displacement (very uncommon)


lisfracn histor

-Dr. Jacques Lisfranc was a French gynecologist who was called into the service of Napoleon’s army where he served as a trauma surgeon in the 1820’s and
30’s. He also served under Dr. Dupuytren during this time.
-Del Sel first described Lisfranc dislocations following equine injuries (JBJS 1955).


Anatomy of Lisfranc

-Tarsometatarsal joint: 9 bones, ~13 joints, 7 weak dorsal ligaments, 5 strong plantar ligaments, the Lisfranc ligament (+2 other interosseous ligaments)
-Myerson described three functional columns of the Lisfranc joint. Ouzounian and Shereff described the sagittal plane motion of each of these columns.
-Medial Column: 1st
met and medial cuneiform: 4mm of motion in the sagittal plane.
-Central Column: 2
mets and central/lateral cuneiforms. 1mm of motion in sagittal plane.
-Lateral Column: 4
mets and cuboid. 10mm of motion in the sagittal plane.


Mechanism of injury of lisfranc

-Accounts for 0.2% of all traumatic injuries. Most common in MVA and sports injuries.
-Occurs either by direct crushing (i.e. dropping something on the foot) or indirectly (usually a plantarflexed and abducted foot).


clinical diagnosis of lisfranc

-Midfoot pain and tenderness. Possibly exacerbated with pronation, abduction or plantarflexion.
-Plantar ecchymosis
-Be wary of compartment syndrome! Always check neurovascular status


Plain films of lisfranc

-Plain Film Radiography
-Pathognomonic “fleck sign” representing an avulsion fx in the 1st
IM space.
-Look for deviations from normal in the AP, MO and Lat views. Normal is:
-AP: Medial border of the 2
met continuous with the medial border of the central cuneiform. Lateral border of the
medial cuneiform continuous with the medial border of the central cuneiform.
-MO: Medial border of the 4th
met continuous with the medial border of the cuboid. Lateral border of the 3rdmet
continuous with the lateral border of the lateral cuneiform.
-Lat: No sagittal displacement. Look for lateral column shortening with a “nutcracker fracture” of the cuboid.
-“Lisfranc variant” is fracture damage extending proximally into the cuboid-navicular region.
-Consider stress radiographs with the foot in plantarflexion or abduction


lisfranc imaging for full diagnostic and peri-operative planning

CT scan


Classification for Lisfranc


originally called Quenu and Kuss the modified by Hardcastle


Myerson classification of lisfranc

-Type A: Total incongruity in any plane (QK: Homolateral)
-Type B: Partial incongruity (QK: Isolateral)
-B1: 1stmet goes medial
-B2: Lesser mets go lateral
-Type C: Divergent (QK: Divergent)
-C1: Partial (only 1st
and 2nd
mets involved)
-C2: Total (all mets involved)


ORIF literature indication

-Literature strongly favors ORIF with any displacement (>2mm between the 1st
and 2nd mets). Exact anatomic reduction is the key to prognosis.


-Non-operative treatment for lisfranc

-If plain film and stress radiographs show no displacement, then NWB SLC for 6 weeks with films q2 weeks looking specifically for


-Operative treatmentfor lisfranc

-Goal: Reduction and stabilization of the medial and central columns. You must reduce the lateral column, but it is usually left unfixed because
of the pronating mobile adapter mechanism. The medial and central columns do not have as much sagittal plane motion, but you still don’t want
excess compression with associated chondrolysis to develop.
-1st met to medial cuneiform, 2nd met to central cuneiform, and 3rd met to lateral cuneiform with crossed 0.062” K-wires (removed at 8 weeks), cannulated cancellous screws (removed at ~12 weeks) or 3.5mm corticals. Consider putting a notch 1.5cm distal to the joint
for screw to prevent stress risers. Drill the hole for the screw in the superior aspect of the notch and not the base to prevent splitting
the base.
-Consider 4th met to cuboid and 5th
met to cuboid with a single 0.062” K-wire
-Lisfranc Screw: Medial cuneiform to 2nd
met base, screw in a lag fashion
-Length of the lateral column must be restored following a “nutcracker fracture.” Consider using an H-plate or external fixation.
-Usually longitudinally over the dorsal-medial 1
, proximal 2nd
interspace (for access to 2,3) and proximal 4th


Post OP for Lisfranc

-NWB SLC for 8 weeks transitioned to PWB SLC for 4 weeks transitioned to rehab. High impact activity can usually be resumed at 6 month


Lisfranc compications

ARTHROSIS! essentially everyone develops post-traumatic arthritis to some extent


Navicular trauma subjective

-History of trauma ranges from contusions to ankle sprains to forced abduction/plantarflexion of the forefoot


Navicular trauma Objective

-Manual muscle testing (MMT) of the posterior tibialis tendon is important in these cases.
-Multiple view plain film radiographs are extremely important because of the possible obliquity of some fractures. CT scans
and MR images may also be necessary for complete visualization and analysis of stress fractures.


Relevant anatomy for navicular

-The navicular is surrounded by a number of joints of varying stability. The TNJ proximally is very mobile, while the distal
NCJ and lateral NCJ are very stable. The navicular is also very stable medially because of the insertion of the PT tendon.
-Vascular anatomy to the navicular can be extremely important as described by Sarrafian:
-It has been demonstrated that the central 1/3 of the navicular is relatively avascular.
-The dorsalis pedis artery adequately supplies the dorsal and medial aspects.
-The medial plantar artery adequately supplies the plantar and lateral aspects.
-The central 1/3 has variable, radially-projecting branches from anastomosis of these arteries


Navicula trauma diagnositic classification

I - Nav Tuberosity fx
II - Dorsal Lip avulsion fx
III - Navicular body fx
--IIIA - Coronal Plane fx with no angulation
--IIIB - Dorso-lateral to Plantar Medial fx with adduction of the forefoot
---IIIC -Comminuton with abduction of the forefoot
IV - Stress fracture of navicular


Watson Jones Type I

and treatment

-Type I: Navicular Tuberosity Fractures
-Occur secondary to eversion and posterior tibialis contracture
-Watch for associated “nutcracker fracture” of cuboid and anterior calcaneal process fractures
-Must be differentiated from accessory navicular

-Displacement 5mm consider:
-Excision of fragment with reattachment of tendon
-ORIF with a cancellous screw


Watson Jone Type II

-Type II: Dorsal Lip Avulsion Fractures
-Occur secondary to plantarflexion/frontal plane mechanisms.
-Must differentiate from os supranaviculare and os supratalare accessory ossicles.
-Generally intra-articular
-Generally treated with conservative immobilization


Type III Watson Jones

Navicular Body Fractures. Described by Sangeorzan.
-[Sangeorzan BJ, et al. Displaced intra-articular fractures of the tarsal navicular. JBJS-Am. 1989; 71(10): 1504-10.]
-IIIA: Coronal Plane Fracture with no angulation
-~100% successful reduction usually achieved
-IIIB: Dorso-lateral to Plantar-medial fracture with adduction of the forefoot
-67% successful reduction usually achieved
-IIIC: Comminution with abduction of the forefoot
-50% successful reduction usually achieved


Principles of ORIF for Type III tx (Watson Jones

-Must achieve 60% reapproximation of proximal joint space
-Incision placed dorsal-medial, between the TA and TP
-Complications involve post-traumatic arthritis and/or AVN


Fixation options for Type III Watson Jones fx

-Fixation Options using 3.5mm Cortical Screws:
-Two screws directed lateral to medial
-Two crossed screws directed proximal to distal
-One screw directed proximal-medial to distal-lateral into the middle cuneiform
-Consider FDL transfer in the presence of a weakened PT tendon


Watson Jones Type IV fx

-Generally occurs secondary to running
-Torg describes typical stress fracture occurring in central 1/3 of body in the sagittal plane.
-DDx: Tibialis anterior tendonitis
-Usually plain films, CT and bone scans are necessary to diagnose


Talar fx general

-Talar fractures are generally associated with high energy trauma, and a standard evaluation with primary and secondary surveys
should precede any specific talar evaluation. The following describes unique subjective findings, objective findings, diagnostic
classifications and treatment considerations.


talar fx subjective

-History of trauma with a high incidence of MVC. The classic description of a talar neck fracture comes from a forced dorsiflexion
of the foot on the ankle (“aviator’s astragulus”). Talar fractures account for approximately 1% of all foot and ankle fractures.


Objective fortalar fractures

-Important to verify neurovascular status, and rule out dislocations and compartment syndromes


Imagng for Talar fx

-Canale View: Plain film radiograph taken with the foot in a plantarflexed position. The foot is also pronated
15 degrees with the tube head orientated 75 degrees cephalad. This view allows for evaluation of angular
deformities of the talar neck.
-CT scan is essential for complete evaluation and surgical planning.


Big concern for talar fratures



Relevant Anatomy for talar fractures

-Dorsalis Pedis: Supply the superior aspect of the head and neck (artery of the superior neck)
-Anastomoses with the peroneal and perforating peroneal arteries
-Artery to the sinus tarsi: supplies the lateral aspect of the talar body
-Forms an anastomotic sling with the artery of the tarsal canal

-Posterior Tibial Artery:
-Deltoid branch: medial aspect of the talar body
-Artery of the canalis tarsi: majority of the talar body
-Forms an anastomotic sling with the artery of the tarsal sinus
-Also sends branches to the posterior process

-Peroneal/Perforating Peroneal Artery: supplies posterior and lateral aspects of the talar body
-Anastomoses with the dorsalis pedis artery branches


4 classifications for talar fx

Berndt Hardy
Modified Hawkins


Hawkins classification

Hawkins Classification: Talar neck fractures
Type I: Non-displaced (~13% incidence of AVN)
Type II: Displaced fracture with STJ dislocation (~50% incidence)
Type III: Displaced fracture with STJ and ankle dislocation (~95%)
Type IV: Displaced fracture with STJ/ankle/TN dislocation (>95%)
-(Type IV added by Canale and Kelly)


Berndt Harty

Berndt and Harty: Talar dome fractures
Type 1: Chondral Depression
Type 2: Partial chondral fracture, seen on MRI
Type 3: Nondisplaced complete osteochondral fracture
Type 4: Displaced complete osteochondral fracture



Sneppen: Talar body fractures
Type 1: Osteochondral fracture
Type 2: Sagittal, Coronal, Transverse body fracture
Type 3: Posterior tubercle fracture
Type 4: Lateral process fracture
Type 5: Crush fracture


Modified Hawkins

Modified Hawkins: Lateral process fractures
Type I: Simple bipartite fracture
Type II: Comminuted fracture
Type III: Chip fracture of anteroinferior lateral process


acute fx of posterolateral talar process

Shepheds fracture


Acute fx of posteromedial talar process

Cedells fracture


Snowboarders fx

lateral process fracture


Talar fx treatment

-NWB in SLC 6-8 weeks versus ORIF depending on nature of fracture and degree of displacement.
-Titanium hardware may be used so that MRI evaluation may be used in post-operative period to evaluate for AVN!


Hawkins sign

-Hawkins sign: radiolucency of the talar body noted at 6-8 weeks after fracture. This sign is indicative of intact vascularity.
However, the absence of this sign does not indicate that osteonecrosis and talar collapse are eminent.


calc fx demographis

-Demographics: Men>Women; Age range generally 30-60; account for ~2% of all fractures; 2-10% are bilateral; 10% associated
with vertebral fracture (most commonly L1); 1% associated with pelvic fracture and urethral trauma


calc fx common mech of injury

Direct axial load, vertical shear force, MVC, gastroc contraction, stress fracture, ballistics,
iatrogenic surgical fracture


with calc fx ask what

back pain
compartment syndrome


calc fx on physical exm

-Pain with palpation to heel
-Mondor’s Sign: characteristic ecchymosis extending into plantar medial foot
-Short, wide heel
-Hoffa’s sign: less taut Achilles tendon on involved side
-Inability to bear weight -Must rule out compartment syndrome
-Imaging: -Plain film Imaging: -Bohler’s Angle: normally 25-40 degrees (decre


Imaging for calc fx

-Bohler’s Angle: normally 25-40 degrees (decreased with fracture)
-Critical Angle of Gissane: normally 125-140 degrees (increased with fracture)
-Both demonstrate loss of calcaneal height

-Broden’s View: Oblique views to view the middle and posterior facets
-Isherwood Views: 3 oblique views to highlight all facets
-Calcaneal Axial View: demonstrates lateral widening and varus orientation

-CT Scan: -Gold standard for evaluation and surgical planning
-The coronal view forms the basis of the Sanders Classification


Sanders classificatio

-Type I: Non-displaced articular fx
-Type II: Two-part posterior facet fx
-Type III: Three-part posterior facet fx
-Type IV: Four-part/comminuted fx

-A, B and C further describe the fx (lateralÆmedial)
-A/B: divide posterior facet into equal 1/3’s
-C: divides posterior facet from sus tali


Rowe classification for calc fractures

-Type I: -Type IA: Plantar tuberosity fractures (medial more common than lateral)
-Type IB: Sus tali fracture (remember FHL: pt will have pain with hallux PROM)
-Type IC: Anterior process fractures (remember your anatomy: bifurcate ligament)
-further divided into three parts by Degan Classification
-Type II: -Type IIA: Extra-articular “beak” fracture of posterior-superior calcaneal body
-Type IIB: Intra-articular “tongue-type” Achilles avulsion fracture
-Type III: Extra-articular calcaneal body fracture
-Type IV: Intra-articular joint depression fracture
-Type V: Intra-articular comminuted fracture


Essex lopresti

-Differentiated between extra-articular (~25%) and intra-articular (~75%) fractures and further sub-divided intra-articular fractures
into tongue-type and joint depression fractures (both with the same primary force, but different secondary exit points).


zwipp classification for calc fx

-Assigns 2-12 points based on:
-Number of fragments
-Number of involved joints
-Open fracture or high soft tissue injury
-Highly comminuted nature, or associated talar, cuboid, navicular fracture


Goals of calc fx treatment

Restore calc height
decrease widening
take it out of varus
Articular reduction


incision for calc treatme

lateral extensile surgical approach


comlications for calc fx

wound healing
lateral ankle impingement


ankle fx treatment

-The standard trauma work-up again applies with primary and secondary surveys. The following describes unique subjective
findings, objective findings, diagnostic classifications and treatment considerations.
-Residents and attendings love to ask questions about ankle fractures for whatever reason, so this is certainly a subject where
you should know the classification systems cold, and do a lot of the additional readings. We’ll keep it brief here


ankle ligaments to consider

-Lateral: ATFL, CFL, PTFL
-Medial: Superficial Deltoid: superficial talotibial, naviculotibial, tibiocalcaneal
Deep Deltoid: anterior talotibial and deep posterior ligaments


Syndesmotic ligaments

AITFL, PITFL (and inferior transverse tibiofibular ligament), Interosseous ligament


Ottawa ankle rules

-Developed by ED docs to minimize unnecessary radiographs following ankle sprains. X-ray only required if:
-Bone tenderness along distal 6cm of posterior edge of fibula or tibia
-Bone tenderness at tip of fibula or tibia
-Bone tenderness at the base of the 5
-Bone tenderness on the navicular
-Inability to bear weight/walk 4 steps in the ED


Mueller classification for ankle f

for medial malleolor fx

A - avulsion
B- transvers at level of mortise
C - Oblique
D - Vertical


Danis weber/AO

A1 - isolated
A2 - with medial mall
A3 - with post-medial mall

B - Transysdesmotic
B1 - Isolated
B2 - With medial mall fx or deltoid
B3 - with media lesion and poserolateral tibial fx

C - Suprasyndesmotic
C1 - simple diaphyseal fibular fx
C2 -Complex diaphyseal fibular fx
C3 - Proximal fib fx


-Tillaux-Chaput fx

AITFL avulsion from the anterolateral tibia


Wagstaff fx

AITFL avulsion from the anteromedial fibula


Volkmann fx

PITFL avulsion for postlat tibia


bosowrth fx

PITFL avulsion from the posterior-medial fibula


Maisonneuve fx

Weber C-type proximal fibular fracture that occurs within 10cm of the fibular neck


-Pott’s fx

Generic term for a bimalleolar ankle fracture


-Destot fx

Generic term of a trimalleolar ankle fracture


Dupuytren fx:

At least a bimalleolar fracture when the talus gets lodged up between the tibia and fibula


-Posterior Malleolar Fractures:

Different than an avulsion fracture of the PITFL; this is a true fx involving a portion of the
tibial plafond cartilage. CT is usually done to estimate a percentage of the involved joint space. The rule of thumb (although
certainly not proven) is that fractures involving >25-30% of the joint space require ORIF.


principles of fixation of ankle ORIF

Restore fib length
Restore ankle mortise
Fix syndesmosis


Restore fib length considerations

-Most people agree that the fibular fracture is the dominant fracture. In other words, if you adequately reduce
the fibula, then the other fractures and dislocations more or less fall into line because of the soft tissues (poor
man’s definition of the Vassal Principle). It doesn’t mean that the other fractures don’t require fixation, but
it means there’s no real sense in fixating the other fractures unless you have the dominate fracture fixated (or
at least reduced).
-The other concept is that a fixed fibula is essentially acting as a buttress, keeping the talus within the ankle
-The fibula is generally shortened in ankle fractures, so you want to get the full length back with your
reduction (generally visibly seen by reduction of the posterior spike on a lateral view)


restore ankle mortise principles

-This goes back to the fibula keeping the talus in the ankle mortise. The classic article you need to know is
Ramsey and Hamilton that showed a 42% decrease in the tibiotalar contact area when the talus was displaced
1mm laterally. From this, people inferred that if the talus isn’t perfectly reduced back into the mortise, then
gross instability occurs.
-This is assessed by:
-Medial clear space (from the talar shoulder): Should be ~4mm or less after reduction
-Tib-Fib Overlap: Approximately >10mm on AP view at 1cm superior to the joint line
-Talar Tilt: <5 degrees compared to other side


fix syndesmosis principles

-Another area of controversy where there is no clear answer is when and how to fixate the syndesmosis with
internal fixation. One point is clear: the purpose of placing internal fixation across the syndesmosis is to
stabilize the fibula against the tibia to prevent lateral migration of the talus and instability. If the fibula is
stable against the tibia with all of your other fixation, then you don’t really need any additional fixation.
How can you tell? Radiographic findings and the Cotton hook test for instability intra-operatively.
-Other questions where people have opinions, but no clear answers are: What type of screws? How many
screws? How many cortices? How far above the ankle? Temporary vs. permanent fixation? Weightbearing? etc.


Lateral mall fixation

-Fracture is primarily reduced and fixated with a single 2.7 or 3.5mm cortical screw with interfrag compression.
-Then a generic 1/3 tubular plate or a specialized contoured plate is used for buttress stabilization.
-Attempt for 6 cortices proximal to fracture with 3.5 bicortical screws
-Get as many distal screws as you can. 3.5 bicortical if above the ankle joint. 4.0 unicortical if not.
-Proximal fibular fractures still amendable to 1/3 tubular plating, but may need to double-stack the plates.
-Should appreciate the concept of lateral vs. posterior anti-glide plating


Medial mall fx

-Several options including 4.0 cancellous, K-wires, plating, cerclage, etc


General tendon trauma mechanism of trauma

-Tendon is actually the strongest part of the muscle-tendon-insertion system. It is much more likely for the complex
to fail at the myotendinous junction or at the tendinous insertion, but acute tendon injuries do occur. They are usually the
result of direct trauma, or overload on an intrinsically weakened tendon.
-Tension overload on a passive muscle
-Eccentric overload on an actively contracting muscle
-Blunt Trauma


Factors which can intrinsically weaken tendons

-Increased age:
-increased cross-linking of collagen fibrils decreases tendon elasticity
-decreased reaction time and muscular contraction speed
-decreased vascularity

-Sex: -M>F

-Systemic inflammatory process: -RA, SLE, Gout, etc.

-Underlying endocrine dysfunction: -Xanthoma (hyperbetalipoproteinemia), DM, Hyperparathyroidism
secondary to renal failure, hyperthyroidism, infection, intratendinous calcifications, etc.

-Medications: -Fluoroquinolones, Corticosteroids


Tendon healing

-As with most tissue, there is a generalized inflammation, reparative and remodeling phase.
-Week 1: Severed ends fill in with granulation tissue
-Weeks 2-3: Increased paratenon vascularity; collagen fibril alignment
-Week 4: Return to full activity without immobilization


Plain films in acute tendon injry

-May see avulsions, soft tissue swelling, accessory bones/calcifications


Tenograph for tendon injury

-Radiopaque dye injected into tendon sheath and viewed on plain film radiograph
-Technically difficult with many false positives and negatives


Ultrasound for tendon injry

-Tendon normally appears hyperechoic to muscle on US.
-Look for discontinuity of fibers, possible alternating hyperechoic/hypoechoic bands, and an area
of intensely hyperechoic hematoma.
-It is very important that the US head is held perpendicular to the long axis of the tendon.


CT for tendon injury

-Tendon normally appears as a homogenous, well-circumscribed oval surrounded by fat on CT. It
normally has a higher attenuation than muscle.
-Will be able to appreciate discontinuity on CT with injury.


MRI for tendon injry

-T1: Tendons normally have a uniform low-intensity (very black). Will be uniform with variable
high-intensity signal with injury.
-T2: Tendons are normally relatively low-intensity. Will light up with high-intensity signal with


Magic angle phenomenon

Any MRI signal shot at 55 degrees to the course of
the tendon will show a false-positive damage signal. Very common in the peroneals


Principle of tendon repair

-It is possible, but rare to get acute tendon injury to any of the long tendons of the leg. An Achilles tendon work-up
will be featured in another AJM sheet, but realize there are some basic principles that apply to any tendon.
-One is generally able to primarily repair the tendon. Non-absorbable suture is preferred.
-Special attention should be paid to vascular supply. Remember that the majority of a tendon’s vascularity comes
from the mesotenon, and therefore should be preserved as much as possible.
-If primary repair is not possible, consider using lengthening tendon slides, tendon grafts, tendon transfers and
biomaterials such as Graft-Jacket (allograft dermal tissue matrix) or Pegasus (equine pericardium) to restore the
integrity of the tendon.
-The goal of treatment should be to allow early PROM without gapping of the tendon


acilles truamaCC and HPI

CC: Typical complaint is pain, weakness and swelling in the back of the leg following an acute injury. The typical patient is
the “weekend warrior” type. This is a 30-50 y/o male participating in a strenuous athletic activity after a generally inactive
HPI: Nature: Pain, weakness and swelling. Pain is surprisingly non-intense allowing the patient to ambulate. The patient
may relate an audible “pop” or “snap”. They may also relate feeling like they were “kicked or shot” in the back of the leg.
Location: Distal posterior leg. The left leg is more affected. Some people theorize that this has to do with the
majority of people having right-handedness and a greater strength and proprioception of the RLE.
Duration, Onset, Course: Acute onset with gradually progressive increase in swelling and edema.
Mechanism of Action: -Three classic MOA are described:
-Unexpected dorsiflexion with triceps contraction
-Pushing off during WB with the leg extended (tennis lunge)
-Violent dorsiflexion on a plantarflexed ankle
-Also consider lacerations and blunt trauma
Previous History: obviously more likely to re-rupture


Achilles tendon trauma pMH

-Inflammatory conditions: RA, SLE, Gout
-Endocrine dysfunction: DM, Renal failure with hyperparathyroidism, hyperthyroidism, Xanthoma
-Infection: Syphilis


Achilles tendon trauma and Social history

Meds: -Corticosteroid injection
-Fluoroquinolone use
SH: -Smoking
-Sedentary lifestyle with weekend activity


Basic Objective exam for Achilles trauma

Derm: -Posterior, Medial and Lateral Ecchymosis
-Open lesion associated with laceration
Vasc: -Posterior, Medial and Lateral edema
Neuro: -Sural Neuritis
Ortho: -Palpable gap (“hatchet strike defect”)
-Positive Thompson test
-Negative Jack’s test
-Pain in the area
-Increased PROM ankle dorsiflexion
-Decreased AROM ankle plantarflexion
-Retraction of proximal gastroc belly
-Apropulsive gait


other specific tests for Achilles traua

-Mattles test: Foot should be in plantarflexed position with patient prone and knee at 90°

-Simmonds’ test: Foot should be in plantarflexed position with patient prone
-Various needle tests (O’Brian, Cetti)

-Toygar’s skin angle: Normally 110-125 degrees. Increases to 130-150 degrees with rupture


Imagin for Achilles trauma

-Plain film:
-r/o Rowe Type IIB avulsion fracture
-Radiodense gap
-Obliteration of Kager’s triangle
-Soft tissue edema

-Alternating hyperechoic and hypoechoic bands
-Hyperechoic hematoma

-TI: -Ill-defined low-intensity with mixed high-intensity signal
-T2: -High-intensity signal from hematoma


Achilles tendon anatomy review

-Muscles of the Triceps Surae (origins, insertions, NV supply, action)
-Plantaris (origins, insertions, NV supply, action)
-Segmental Blood Supply of Tendon
-“Twisting” of tendon


Specific information regarding the Watershed area of achilles

-Lagergren and Lindholm
-Used microangiographic technique on human cadavers
-Found decreased vascularity 2-6cm proximal to insertion
-Theorized this was secondary to atrophy from inactivity

-Conflicting information from laser Doppler flowmetry studies
-Found uniform vascularity throughout tendon
-Found decreased vascularity with age and in men
-Found decreased vascularity with physical loading/stress of tendon, specifically at insertion

-Found increased stress/strain at the watershed area regardless of vascularity


Achilles ruptures clssifican



kuwada classifiction

-Type I: Partial tear involving 6cm deficit


chronic achiles pathology classification



puddu classifitio

-Peritendonitis: Inflammation of the surrounding tissues, not the tendon itself. This pain will remain stationary as the tendon is taken through a
range of motion.
-Tendonosis: Intra-tendinous degeneration. This pain will move proximally and distally as the tendon is taken through a range of motion.
-Peritendonitis with tendonosis: combination of the two pathologies.


3 options for Achilles tendontrauma

do nothing
cast immobilize
surgical repair


cast immobilization for achilles

-AK cast versus SLC
-Some are proponents of AK casting
-Knee should be in a 20 degree flexed position

-General recommendations:
-Gravity equinus cast x 4 weeks
-Reduction of 5 degrees every 2 weeks to a neutral ankle position (~4-6 weeks)
-Heel lift and PT until normal ankle PROM
-Return to full activity at approximately 6 months


Achilles surcal approach

-Midline to medial incision to avoid superficial neurovascular structures
-Pt in a prone or supine frog-legged position
-Use full-thickness flaps with emphasis on atraumatic technique


achillesprimary open repair

-Keith needles with non-absorbable suture (or fiberwire) with absorbable sutures to reinforce
-There are three common stitches used:
-Bunnell: Figure of 8 or weave stitch
-Krakow: Interlocking stitch
-Kessler: Box stitch


Achilles augmented open primary repair

-Lynn: Plantaris is fanned out to reinforce
-Silverskoild: 1 strip of gastroc aponeurosis brought down and twisted 180 degrees
-Lindholm: Utilizes multiple strips of gastroc aponeurosis
-Bug and Boyd: Strips of fascia lata are used to reinforce
-VÆ Y lengthening of the proximal segment with primary repair
-Reinforcement with FHL
-Graft Jacket, Pegasus, etc.


percutaneous primary repair

Ma and Griffith described a bunnel type approach
may be associated with high re-rupture rates


post op Achilles tx

SLC in gravity equinus over 6 to 10 weeks.


Admission orders

Ambulataroy Staus
Ancillary consults


Admission Orders

Pt is admitted to the general medical floor on the Podiatric Surgery Service under Dr. Attending.
Most patients on the podiatric surgery service are admitted to the general medical floor or a surgical floor. Any pts
admitted to a critical care unit or telemetry unit will probably be on a medicine service with a podiatric surgical consult.


Admission orders

Infection of bone of right 2
Always use terminology that everyone in the hospital can understand, but also be as specific as possible.


Admission orders Condtion


Most are stable or fair


Admision orders

Vitals recorded q8 hours per nursing.

Recored how often
Consider NV checks


Admission orders AmbulaaryStatus

-CBR (Complete bed rest)
-As tolerated
-OOB to chair
Always designate which leg the order is for. Be specific with PWB status (“toe-touch” or “heel-touch”). If order is for
CBR, consider DVT ppx and a bed pan order. If the order is OOB, specify # of times and length per day.
Also consider Physical Therapy and/or Occupational Therapy orders here.


Admision orders
Nursing instructions

-Accuchecks (how often and when?) -Ice and elevation
-Bedside Commode -Dispense Post-op shoe/Crutches
-Wound Care -Dressing Instructions
-Drain management -Off-loading instructions


Admision orders

-Regular diet
-ADA 1800-2200 calorie
-Mechanically soft
-Renal diet
-Cardiac diet
-Decreased Na
-Decreased K


Admisson orders

-Measurement and recording of Ins and Outs (especially dialysis pts)
-IV Fluids


admission orders

-CBC with diff
-Chem-7/Met Panel
-Type and Screen
-Wound cultures
-Blood cultures

Always detail when the labs should be done. For example, initial CBC and Chem-7 should be taken “upon arrival to the floor.” Additionally, 2 sets of blood cultures should be taken from 2 different sites.


Admission orders

-Write out all at-home medications in full
-Pain medication
-DVT ppx
-Sliding Scale Insulin (SSI)
-Throat lozenges
Be as specific as possible. SSI needs to be written out in full. Many medications require hold parameters. For example,
fever medications should not be given unless the temperature reaches 101.5° F. Anti-HTN agents should be held if the blood
pressure or heart rate drops too low


Admission Orders
Ancillary Consults

-General Medicine
-Infectious Disease
-Vascular Surgery
-Social Work
-Home Care
-Case Manager


Electrolytes normal values

Na: 135 to 145
K: 3.5 to 5
Cl: 95 to 105
Co2: 24 to 32
BUN: 5 to 20
Cr: 0.5 to 1/5
Glucose < 110 mg/dL



Hyponatremia Manifestation and treatment

-Manifestations: Primarily neurologic, lethargy, headache, confusion, obtundation
-Treatment: -Restrict water intake and promote water loss -Correct underlying disorder
-Replace Na+ deficit


Hypernatremia manifestations and trement

-Manifestations: Change in mental status, weakness, neuromuscular irritability, focal neurologic deficits, coma,
-Treatment: -Replace water loss and promote sodium excretion
-Water deficit = ([Na+]-140)/140 x Total Body Water in liters
-Rapid correction of either of these disorders is dangerous due to rapid shifts of water in and out of brain cells. It should
therefore be corrected slowly over 48-72 hours. Aim correction at 0.5 mEq/L/hr with no more than a 12 mEq/L correction over
the first 24 hours.


Main reason a surgery can be cancelled electrolyte wise



Hypokalemia manifestaions and treatment

-Manifestations: Fatigue, myalgia, muscular weakness, cramps, arrhythmia’s, hypoventilation, paralysis, tetany
-Treatment: -Minimize outgoing losses -Treat underlying cause
-Correct K+ deficit via oral or IV means (K+ riders added to fluid, oral KCL, etc.)


Hyperkalemia manifestations and treatent

-Manifestations: Cardiac toxicity (peaked T waves, prolonged PR, torsades de pointes), muscle weakness, paralysis,
-Treatment: -Increase cellular uptake of K+
-Insulin (10-20 units) with 50 g IV glucose
-IV NaHCO3 (3 ampules in 1L of 5% dextrose)
-Albuterol (5-10mg nebulized over 30-60 minutes)
-Increase K+ excretion
-Loop diuretic, Thiazide diuretic
-Kayexalate (cation exchange resin) (25-50mg mixed with 100ml 20% sorbitol to prevent constipation)
-Calcium Gluconate (10ml of 10% solution over 2-3 minutes emergently to reduce membrane excitability


chloride and carbon dioxide

-Not going to talk much about this, but you should have a basic understanding of Acid-Base Regulation.
-Equation for determining Anion Gap:
Anion gap (all units mmol/L) = (Na + K) - (Cl + [HCO3-])
-Normal gap (~8-20mmol/L)
-Negative/lowered gap (20mmol/L): Acidotic state
-MUDPILES algorithm: methanol/metformin, uremia, diabetic ketoacidosis, propylene glycol,
infection, lactate, ethanol, salicylate/starvation


BUN and Creatinine cosiderations

-Measures of kidney function and hydration status
-BUN (Blood Urea Nitrogen): Protein metabolism waste product eliminated by the kidneys. This can be increased if your
kidneys aren’t eliminating it properly, or in a dehydrated state where it’s a relatively high concentration.
-Creatinine: A more direct measure of kidney function from elimination of this skeletal muscle waste product.
-Creatinine clearance and estimated glomerular filtration rate (GFR) with the Cockcroft-Gault Equation:
[(140-Age in years) x Weight in kg] / [72 x Serum creatinine] x 0.85 if female
-GFR < 60 ml/min indicates chronic kidney disease; < 15 indicates kidney failure
-Antibiotics and other drugs should be dosed appropriately in these situations
-Renal protective agents are utilized prior to procedures that are known to affect the kidneys in patients with kidney
disease. A common example of this is an angiogram with dye to evaluate the vascular status of a patient with diabetic
foot disease.
-Pre-procedural hydration -Mucomyst (N-acetylcysteine) (also used for acetaminophen OD)
-Sodium Bicarb Protocols


Blood Glucose level higher than150 to 175 significantly limits what

function of the immune system for a period of days, particularly cytokine activation and


sulfonylureas mechanism and specifi meds

Bind to β-cell receptors stimulating insulin release
-Glyburide (Micronase) -Glipizide (Glucotrol) -Glimepiride (Amaryl


Biguaides mechanisms and specific med

Decrease production of glucose in the liver
-Metformin (Glucophage)


Thiazolidinediones mechanimsand specific d

Increase peripheral cellular response to insulin
-Rosiglitazone (Avandia) -Pioglitazone (Actos)


-α-glucosidase inhibitors mechanism and specific meds

Reduce intestinal carbohydrate absorption
-Acarbose (Precose) -Miglitol (Glyset


Rapid acting

Lispro (Humalog)
Aspart (Novolog)
10-15 minutes
10-15 minutes
1-2 hours
1-2 hours
3-5 hours
3-5 hours


Short acting insulin
onset, peak, duration

2-4 hours
4-8 hours


Intermediate Acting
onset, peak, duration


1-3 hours
2-4 hours

4-10 hours
4-12 hours

10-18 hours
12-20 hours


Long acting insulins

Glargine (Lantus)
Detemir (Levemir)

2-3 hours
1 hour


24+ hours
24 hours


Combinations insulins



In-patient recommendatons for insulin and diabetes

-There is increasing data that sliding scales are completely inefficient at in-patient glucose management.
Sliding scales are passive, reactionary scales that compensate after a hyperglycemic incident occurs. Inzucchi
recommends the following, instead of a sliding scale:
-Basal Rate: Lantus or other long acting
-Start 0.2-0.3 Units/kg/day; then increase 10-20% q1-2 days prn
-Prandial Coverage: Novolog or other rapid acting
-Start 0.05-0.1 Units/kg/day; then adjust 1-2 Units/dose q1-2 days prn


Diabetic NPO recommendaions for Type 2

-1/2 the normal dose of long acting if they get any
-BG checks q6 hours with short acting agent available for coverage
-D5W or D5-1/2NS at 50-75cc/hr while NPO


Diabetic NPO recommendations for Type 1

- Strongly consider an insulin drip
-1/2 – 2/3 normal dose of long acting agent
- BG checks q6 hours with short acting agent available for coverage
- D5W or D5-1/2NS at 75-100cc/hr while NPO


Why use fluid balance

It can be
used to maintain fluid balance in a patient who is NPO, correct electrolyte disturbances, and/or provide glucose to name just a
few examples. This sheet will cover the basics of short-term maintenance therapy and show differences in electrolyte
concentrations between the most common fluids.


Maintenance therapy r NPO patient

-An NPO patient is still losing water that needs to be replaced to ensure homeostasis. Sources of water loss include:
-Urine output: At least 500ml/day
-Insensible water losses (Skin and Respiration): At least 500ml/day
-This can increase by 150ml/day for each degree of body temperature of 37°C.
-Gastrointestinal losses: Extremely variable
-Direct blood volume loss from the surgery itself
-Electrolytes are also lost to varying degrees. In the short term, it is usually only necessary to replace Na+, K+ and
glucose. The other electrolytes usually do not need replacement until around 1 week of parenteral therapy.


Mintenance therapy for NPO patient with pediatric considerations

-Pediatric patients should be aggressively rehydrated after a surgical procedure for two reasons:
-They will lose a higher percentage of their total fluid volume during a procedure.
-They have a tendency to “third space” and shift fluid balances in the perioperative period.
-To determine the total intravascular volume of a pediatric patient:
-The first 10kg of body weight account for about 80ml/kg.
-So a 7kg kid would be (7x80) = 560ml
-The next kg’s account for about 70ml/kg
-So a 25kg kid would be (10x80 + 15x70) = 1850


Maintenae Theapy for NPO patien general recommendatns

-At the very least you should replace fluid to account for water loss. This is at least 1L/day, but you can
certainly increase this and lose the excess through the urine.
-It is also recommended to provide some electrolyte supplementation:
-Na+: 50-150 mEq/day
-K+: 20-60 mEq/day
-Glucose: 100-150g/day to minimize protein catabolism and ketoacidosis


Review in prism common parenteral solution



Common administrations of commonparenteral solutions

-Normal adult: NS or 1/2 NS or LR at 75-120ml/hr +/- 20mEq KCl
-Diabetic patients: D5-1/2NS at 50-100ml/hr +/- 20mEq KCl while NPO
There usually isn’t a need to deliver extra glucose (D5) to diabetic patients while they are PO


Key to fluid manageme

-The key to fluid management is an understanding and knowledge of exactly why you are giving fluids in the first place, what
you hope to accomplish, what substances you are giving in the fluid and how much you are giving.
-Obvious care needs to be taken with diabetic patients, those with renal pathology, and those with CHF.


Genera Info Post op fever

-When dealing with a fever work-up, always note what the baseline temperature of the patient is and the method of
-Fever in most institutions is defined as greater than 101.5° F.
-Temperatures between 98.6-101.5° are low-grade fevers


Intra-op cuases of fever

-Inflammatory process of the surgical procedure itself
-Transfusion Reaction
-Malignant Hyperthermia
-Pre-existing Sepsis


Post op fever Timeline general guide

-0-6 hours post-op: Pain, anesthesia rxn, rebound from cold OR, endocrine causes (thyroid crisis, adrenal
-24-48 hours post-op: atelectasis, aspiration pneumonia, dehydration, constipation
-72+ hours: infection (3-7 days), DVT, UTI, drug allergy, thrombophlebitis


Temperature General Guid

-107: Anesthetic Hyperthermia
-106: --105: Blood transfusion reaction
-104: Closed abscess
-103: Atelectasis; pneumonia; drug reaction; liver disease
-102: Wound infection
-101: Draining abscess
-100: Benign post-op fever; post-anesthesia overshoot


what 2 agents can cause a fever within a few hours of surgery

Group a strep
Clostridium perfingens


Post of fever and dialysis pts

-Dialysis patients typically run approximately 1 degree F cooler than the normal population, so a fever for HD
patients wound be defined as 100.5° F. This is hypothesized to be due to a resetting of the hypothalamic set point


purpose of fever work up is the workup and to what

find the source


DVT signs and symptoms

-Homan’s Sign: Pain in calf with dorsiflexion of the ankle
-Pratt’s Sign: Pain with compression of the calf
-Palpation of clot


Virchows triad

-Hypercoagulable state
-Vessel Wall Injury


acronym fr DVT risk factors

-There is also the acronym I AM CLOTTED: Immobilization,
Longevity (age),
DVT/PE history.


Diagnosis for DVT

-Compression Ultrasound: can actually visualize the clot
-D-Dimer > 500μg/ml: Not sufficient as a stand alone test
-Consider full coagulation work-up for hypercoagulable states
-Contrast venography
-Impedance plethysmography


goals of dvt treatment

1. Prevent pulmonary embolism
2. Prevent clot extension
3. Prevent recurrence


dvt immediate anti-coagulation

-IV Unfractionated Heparin
-Law of 8018
-Initial Dose 80mg/kg IV bolus and then 18mg/kg/hour
-PTT should be checked q6 until it stabilizes at 1.5-2.5X normal (46-70s)
-Goal is to get PTT in this range

-LMWH may also be used
-Enoxaparin (Lovenox): 1mg/kg subcutaneous q12

-Heparin Dosing Guide
-Initial Dose: Law of 8018 with PTT checks q6
-If PTT 90s: Hold infusion for 1 hour, then decrease infusion rate by 3 units/kg/hr


dv continued anti-coagulation

-Warfarin (Coumadin)
-Load at 10mg or 7.5mg PO qdaily for 2 days
-Decrease/adjust dose to a target INR=2.5
-DO NOT stop heparin infusion until INR reaches 2.5
-INR should be maintained at 2.5 for 3-12 months
-Consider placement of IVC filter (inferior vena cava)


PE s/s triad

-PE occurs when a clot from a peripheral location embolizes to the pulmonary vasculature
- <25% of deep vein thromboses distal to the iliac veins go on to develop PE.
-The more proximal the clot, the more likely it is to develop into a PE.
-“Classic Triad” of signs and symptoms of a PE: Dyspnea/SOB, Chest Pain, Hemoptysis
-Please note that less than 14% of patients experience the classic triad


PE diagnosis

-Gold standard: Pulmonary Angiography, Spiral CT
-V/Q study


Treatment of PE

-Thrombolytic Therapy:
-Urokinase: 4400units/kg IV over 10 min, then 4400units/kg/hr for 12 hours
-Streptokinase: 1.5 million units IV over 60 minutes

-Pulmonary Embolectomy
-Various filter


aO histor

-Plates and screws for fx fixation first described by Alain Lambotte in 1907.
-Robert Danis (Belgium surgeon) published “The Theory and Practice of Osteosynthesis” in 1949.
-Described use of compression plate called a coapteur.
-Maurice Müller, a pupil of Danis, founded AO with other Swiss surgeons in 1958.


AO Principles

1. Accurate and precise anatomic reduction of fracture fragments (especially in joints).
2. Atraumatic surgical technique with emphasis on preservation of blood supply.
3. Rigid/Stable fixation
4. Early mobilization


Why have lag tenchinque

generates compression which leads to lack ofmotion and therefore primary bone heali


Motion and lag techniqu

Motion disrupts angiogenesis, decreases oxygen tension levels and inhibits osteogenesis. So, it is the lack of motion and
NOT the compression that is osteogenic


general principles of laq technique

-Orientation of the screw 90° to the fracture line obtains optimal compression.
->20° displacement from perpendicular is significant
-Weakest in translation from axial loading
-Orientation of the screw 90° to the long axis optimally prevents displacement with axial loading.
-Weak in compression
-Ideal screw placement for a long, oblique fracture:
-One central anchor screw 90° to the long axis
-One proximal and one distal compression screw 90° to the fracture line


AO prinples of insertion

-AO Recommendations: Overdrill, Underdrill, Countersink, Measure, Tap, Screw
-Some underdrill before overdrill
-Some don’t overdrill until after tapping
-Two finger tightness = 440-770lbs.

-To prevent thermal necrosis:
-Sharp tip
-Fast advancement (2-3mm/sec)
-Slow drill speed (300-400rpm)
-Firm force (20-25lbs)

-Screw Pull-out
-Directly proportional to screw diameter, screw length and bone strength (cortical nature).
-Indirectly related to pilot hole diameter.
-To increase screw pull-out, maximize bone-screw contact.


Fatigue falure
stress shielding

-Stress: pressure on a material
-Strain: measurable deformation following a given stress
-Fatigue Failure: failure from repetitive cyclic loading
-Creep: temperature dependant permanent deformation of a metal
-Stress Shielding: Internal fixation absorbs physiologic stress from bone and results in bone resorption per Wolff’s


stress strain curve definitions

-Elastic Range: -Non-permanent strain/deformation with a given stress
-Proportional stress and strain (Hook’s Law)
-Slope of the line is the stiffness (Young’s Modulus of Elasticity)
-Yield Point: -Past the yield point, a given stress causes a non-proportional increase in strain.
-Plastic Range: -Permanent deformation past the yield point
-Ultimate Failure Point


screw definitions
thread diameter
core diameter
rake angle
thread angle

-Head: more efficient hexagonal vs. cruciate
-Land: underside of the head which contacts the near cortex. Want as much land-bone contact as possible to reduce
stress at any one location. This is the same principle as washers and countersinking.
-Shank: unthreaded portion of the screw
-Run-out: junction between the shank and the threads. Represents the weakest portion of the screw.
-Thread diameter: diameter of threads + core (major diameter)
-Core diameter: diameter without the threads (minor diameter)
-Pitch: distance between threads
-Tip: can be round, trocar or fluted
-Axis: central line of the screw
-Rake Angle: thread to axis angle
-Thread Angle: angle between the thread


Memorize Table 1 on page 76 mcglam



Cortical and cancellous screws

-Cortical: tighter pitch designed for hard cortical bone (1.25mm)
-Cancellous: higher pitch designed for metaphyseal and epiphyseal bone (1.75mm


self tapping screws

-Fluted tip that clears debris as it is advanced
-Require larger pilot holes, have decreased thread-bone contact and have the ability to cut its own path
different from the underdrill


cannulated screws

-Classically 3.0, 4.0, and 7.3mm, but really have just about any size available now
-Advantages: self-drilling, self-tapping, good for hard to visualize fractures, avoids skiving of cortical bone on
insertion and has definite co-axial nature with K-wire.
-Disadvantages: hollow core, decreased thread-core ratio, decreased pull-out strength


Herbert screws

-Proximal and distal threads separated by a smooth shaft. Headless.
-Leading threads have increased pitch, so it draws the trailing threads.
-Does generate interfragmental compression, but not a lot.


Interferencs screws

-FT, headless screw
-Prevents axial displacement. Does not generate compression.


Malleolar screws

-Essentially a self-cutting, PT cortical screw.


quarter tubular plate

or use with screws from the mini fragment set


1/3 tubular plate

: For use with screws from the small fragment set


Dynamic compression plate

Wider/Deeper holes that allow for eccentric drilling and axial compression


Limitd conact pressue

Essentially grooves on the underside of the plate that limit periosteal contact


gener plate funcions

-Interfragmentary Compression
-Tension Band


AO basic stabilization rule

Ideally you want 3 or 4 cortical threads in each main fragment distally, and 5 or 6 proximall


Absorbale suture types

-pig gollagen, chromc



Describe Vicryl

-Braided. May be coated (polyglactin 370 or calcium stearate)
-65% tensile strength at 14 days
-Hydrolyzed (to CO2 and H20) in 80-120 days
-Vicryl Rapid: Hydrolyzed in 42 days; loses strength in 7-10 days
-Vicryl Plus: Coated with broad spectrum antibiotic Triclosan (also found in toothpaste


describe Dexon

hydrolyzed 100 to 20 days


PDS describe

70% tensile strength at 14 days
hydrolyzed in 90 dyas


describe Maxon

hydrolyzed in 180 dyas
Longest lasting absorbable


describe Monocril

-20-30% tensile strength at 14 days
-Hydrolyzed in 90-120 day


Nonabsorble types and specifics


-Stainless steel


Weakest suture



describe silk

-Made from silk worm
-Actually very slowly absorbed (hydrolyzed in 1 year)
-Very low tensile strength


describe Nylon

-Both monofilament and braided available
-Highest “knot slippage” rate: monofilaments are at a higher risk of knot slippage


describe polypropylene suture

Prolene, surgilene
-Can be used in contaminated/infected wounds (Nonabsorbable, synthetic, monofilaments best
in this situation). This is the least reactive suture.


Polyester tures

-Strong suture. May be used for tendon repair.
-Braided. May be coated with silicone.


describe stainless steel suture

-Monofilament or braided (braided is called Flexon)
-Strongest suture with longest absorption rate
-Used for bone fixation and tendon repair, but may corrode bone at stress points


Other suture notes

-Sutures are also classified according to size. They can range from 0-0 (very thick) to 9-0 (extremely thin).
-Surgeon’s choice is extremely variable and you usually just work with what you are used to, but here are some safe bets:
-Capsule closure: 2-0 or 3-0 Vicryl
-Subcutaneous tissue closure: 3-0 or 4-0 Vicryl
-Skin: 4-0 Nylon or Prolene
-Skin sutures are removed at 10-14 days because at this point the tensile strength of the wound equals the tensile strength of the


surgical instruments are composed of what

stainless steel


stainless steel is composed of what

-Carbon: gives instrument “hardness”
-Chromium: chromium oxide layer prevents corrosion of instrument
-Tungsten Carbide: extreme “hardness” for grasping surfaces (teeth of needle drivers)


2 different seies of stainless steel and depends on what

-There are two different series of stainless steel depending on how it is manufactured:
-300 series Austenitic: Implants and internal fixation. Resists corrosion with resilience.
-400 series Martenitic: Cutting instruments. Hardness maintains sharp edges and jaw alignments.


surgical blades

-Most common: 10, 15, 11, 62 on a minihandle
-Purpose: Sharp (blade) and blunt (handle) dissection
-Cutting edge width: 0.015”



-Most common: Tissue: Metzenbaum, Mayo, Iris, Crown&Collar (Sistrunk)
Non Tissue: Suture, Utility, Bandage

Purpose dissection



-Most common: Mosquito (Halsted), Kelly, Crile
-Purpose: Grasping and holding



-Most common: 1-2 (Rat tooth), Adson-Brown, Atraumatic (Potts-Smith)
-Purpose: Grasping and Holding



-Most Common: Hand Held: Skin Hooks, Senn, Ragnell, Malleable, Army-Navy, Volkmann Rake,
Self-retaining: Weitlaner, Holzheimer, Heiss
-Purpose: Retraction and exposure


6. Elevators

-Most Common: Freer, Sayre, Key, Crego, McGlamry, Langenbeck
-Purpose: Dissection



-Most Common: Joseph, Maltz, Bell, Parkes
-Purpose: Cutting


Other instruments to know

-Bone-Cutting Forceps
-Bone Handling Clamps
-Reduction Forceps (Lewin, Lane, Lowman, Verbrugge)
-Needle Holders (Mayo-Heger, Sarot, Ryder, Halsey, Webster)
-Suction-Tip (Frazier)


hardest material in human body

teeth enamel


power instruments developed by



power sources 3 types



describe pneumatic

-Advantages: Delivers high power and torque, does not overheat, cheap
-Disadvantages: Does not operate at slow speeds, bulky, burdensome, cords prone to contamination
-General: -Most commonly driven by compressed nitrogen
-Tank pressure > 500 psi
-Dynamic instrument pressure: 90-110 psi


describe electric instrumentation

-Advantages: Light, quiet, small, good for office use
-Disadvantages: Prone to overheating, expensive
-General: -Utilizes an alternating current drive


describe battery instrumentation

-Advantages: No cords
-Disadvantages: Loses power quickly, bulky handling
-General: -Utilizes direct current


brands of power instrumentaton



define torque

Measurement of power and force. Units: Newtons/cm^2
-Cortical bone requires more torque to cut through than cancellous bone


speed pod procedures require

20,000 rpm


how to decrease thermal necrosis

decrease torque
and increase seed


define collet

distal end of a saw where the saw blade attaes


define stroke

one area excursion for a saw blade


define oscillation

One back and forth motion of a saw blade. (Two strokes equal one oscillation).


types of power saws

-Sagittal Saw: Cuts in the same plane as the instrument
-Better for longer and deeper cuts
-4° arc of excursion
-Blade may be positioned anywhere within a 160-180° arc.
-Oscillating Saw: Cuts in plane perpendicular to instrument
-7° arc of excursion
-Blade may be positioned anywhere within a 360° circle


types of saw blades

-Vary by cutting depth, width, thickness, shape and number of teeth
-Shapes: straight (most commonly used), inward flair, outward flair
-The angulation of the teeth and NOT the thickness of the blade determine the thickness of a cut.
-Blades may contain holes which collect debris, thereby decreasing heat and friction


types and sizes of wire drivers

-K-Wires (Kirshner wire)
-Sizes: 0.028”, 0.035”, 0.045”, 0.062”
-Threaded vs. Non-threaded. Note that the direction of the driver only matters with threaded wires.
-K-Wires provide splintage (stability, but no compression)
-Steinman Pins
-Sizes: 5/64”-3/16”


-Rotary Cutting types

-Power Drill Bit Sizes: 1.1, 1.5, 2.0mm
-Shapes: Round, Barrel, Straight, Straight-tapered
-Definitions: -shank vs. shaft vs. head
-flute vs. blade
-edge angle vs. clearance angle vs. rake angle


surgeons hands provide 3 functions

-The surgeon’s hands provide 3 functions when operating power instrumentation:
-Control of power of the instrument
-Control of direction of the instrument
-Stability between the instrument and the surgical site


in mcglamry or elsewhere review concepts of

axis guide
reciprocal pinning



other power instrumentation pearls

-With a saw or K-wire, always divot perpendicular to the cortex, and then redirect.
-The spin of a burr should be parallel to the grain of the cortex or parallel the ridge of bone to be removed


-Properties of the ideal implant material:

clinically inert, no inflammatory or foreign body response, noncarcinogenic,
nonallergenic, structurally stable, capable of sterilization, capable of fabrication in desired forms, serve as a scaffold for new
bone growth and gradual biodegradation


Host response to implant

cellular response (acute)
tissue remodeling response
infectin potential


describe cellular response to implant

-Immediately after implantation, implants are covered with a coat of proteins that denature and elicit an
inflammatory response. Denatured fibrinogen accumulates neutrophils and macrophages.

-Detritic Synovitis: Foreign body reaction to shards of silicone materials in the lymphatic system.

-Environmental Stress Cracking: Surface defects on polyetherurethane implants secondary to chronic
inflammation. Chronic inflammation results from fragmentation and leads to intracortical lysis and cyst


normal for implants to hat during tissue remodeling phase

fibrous capsule formation


implants infection potenl

-Susceptible to S. Aureus and S. Epidermidis infections
-Malignancy and Type III hypersensitivity reactions extremely rare



-PLLA (Polylactic-L-Acid: L is enantiomer)
-Degrades to lactic acid via hydrolysis
-Retains strength 36 weeks and degrades in 2-3 years
-Available in FT 2.0, 2.7, 3.5 and 4.5mm screws

-PGA (Polyglycolic Acid)
-Degrades to glycolic acid and glycine
-Elliptical. Provides compression secondary to shape.
-Brittle and rigid
-Highest likelihood of FB rxn or complication (<4%)

-PDS (Poly-para-dioxanone)
-Tapered form swaged on metallic wire. Provides compression secondary to shape.
-Flexible and malleabl


advantages and disadvants of biomaterial

-Increased degradation times are good because it decreases the load the body has to clear.
-These screws don’t “bite” like metal screws, but swell 2-4% in the first 48 hours.
-Advantages: decreased stress shielding, no second operation for removal.
-Disadvantages: more expensive than metallic screws, but are cheaper in the long run if you remove >31% of
metallic screws in your practice.


3 types of metallic implants

-Surgical Stainless Steel
-316LVM (low carbon vacuum remelting)
-Iron, 17-25% chrome, 10-14% nickel, 2-4% molybdenium, 1% carbon
-Nickel most commonly causes reaction: allergic eczematous dermatitis.

-Very inert, integrates into surrounding bone, resists corrosion, decreased capsule formation
-Addition of 6% aluminum and 4% vanadium increases the strength similar to steel
-Nitrogen implantation forms a stable oxide layer
-Black metallic wear debris is often seen. No toxicity or malignancy associated with this.

-Cobalt Chrome and Alloys
-30% cobalt, 7% chromium, <0.034% moly/carbon
-Used in joint replacement prostheses


define corrosion

-Corrosion: breakdown of metallic alloys because of electrochemical interactions within the environment


history of ex fix

-377BC: Hippocrates with wood from a cornel tree
-1904: Codvilla (Italy) used unilateral fixator for limb lengthening
-1951-1991: Ilizarov (Siberia, Russia). Father of modern ex-fix and developer of external ring fixator for WWII vets from old bus parts.


-Tension-Stress Effect (Ilizarov)

-Distraction performed at proper rate and in the proper area leads to tissue growth similar to hormone-mediated growth at adolescent
growth plates.
-Too fast: Stretching and traction injuries
-Too slow: Bone callus consolidation preventing future distraction
-An important principle is that all tissues (bone, skin, muscle, NV structures, etc.) become mitogenically active and grow. They proliferate as
opposed to “stretching”. Much of this has to do with the distraction serving as a mechanical stimulus for growth factor release (such as
osteoblastic growth factor) and dramatic increases in vascularity


tension stress effect influences

-Stability: increased stability leads to increased osteoblastic activity
-Rate: Ideal is 1mm/day in 4 increments
-Bone Cut: Best to keep medullary canal and as much periosteum intact as possible. Best technique is a percutaneous subperiosteal
corticotomy with a Gigli saw or osteotome/mallet.
-Location of Bone Cut: Metaphysis found to be superior to other area


-Behrens Principles of External Fixation

-Avoid and respect neurovascular structures
-Allow access to injured area for future fixation
-Meet mechanical demands of the patient and the injury


-Tajana’s Stages of Callus Development

-Colloidal (0-2 weeks): formation of microreticular network
-Fibrillar (2 weeks-1 month): collagen organization
-Lamellar (1 month-years): formation of compact lamellar tissue and calcification


-Advantages of Ex-Fix

-Decreased soft tissue dissection
-Immobilization of multiple regions
-Allows for post-operative adjustment
-Skin grafting and wound debridement available
-Early ROM and WB


-Complications of Ex-Fix

-Complications of Ex-Fix
-Pin tract infection vs. irritation
-Cage rage
-NV injury


anatom of ex-fix

-Knowledge of cross-sectional anatomy is essential for the application of external fixation. There are numerous manuals and tests available
demonstrating proper pin and wire placement in a given location.
-The key is to have solid bone with avoidance of neurovascular structures.
-As a general rule, the medial and anterior aspects of the tibia are safe locations.


types of exfi

hybrid fixators
taylor spatial frames


describe unilateral fixators

-EBI Dynafix and Orthofix
-Can be straight (uniplanar) or articulated (multiplanar)
-Allow for compression/distraction in a single plane only
-Attached to bone via half-pins
-Rigidity and stiffness determined by half-pins/bone interface. Want pins spread over a large area.
-Weak in the sagittal plane


describe circular fixato

-Generate compression/distraction in multiple planes
-Tensioned wires generate stability; half-pins generate rigidity.
-Best if these are located 90° to each other for optimal stability
-Can be formulated to allow for immediate WB


hybrid fixators

-Orthofix, Dynafix, Smith&Nephew, Rancho
-Combination of unilateral and circular fixato


describe taylor spatial frames

-Allows for reduction of triplanar complex deformitie


indications for ex fix

-Limb Lengthening/Distraction
-Percutaneous metaphyseal subperiosteal corticotomy with Gigli saw or osteotome/mallet
-Apply fixation before corticotomy
-Distraction begins 7-14 days after corticotomy at 1mm/day

-Angular Deformities
-CORA principle (center of rotational angulation)
-Double Taylor spatial frame
-Dynamization: release of tension from wires and loosening of half-pins to allow bone a period of introductory WB

-Ligamentotaxis: pulling of fracture fragments into alignment with distraction



Bone properties 2 component system consit of what

-Bone is a two component system consisting of minerals (increases the yield and ultimate strength of bone) and collagen (mostly
Type II).


For bone, define

-Porosity. Increased porosity leads to increased compressive strength of bone. Cortical bone has <15% porosity and
cancellous bone has ~70% porosity.
-Strength. Strength is defined as the amount of force a material can handle before failure. Bone can handle a 2%
increase in length before failure. Bone is has the greatest strength in compression, followed by tension and is weakest
in shear. Strength is affected by collagen fiber orientation, trabecular orientation, age, presence of defects and
-Stiffness. Cortical bone has 5-10 times the stiffness of cancellous bone


Vaular supply to bone

-Blood supply to bone comes from two sources. A nutrient artery feeds the endosteal and medullary vessels and supplies the
inner 2/3-3/4 of bone. The periosteal vessels supply the outer 1/3 of bone from muscle and tendon attachments.
-The amount of vascular disruption following a fracture depends on the force/displacement of the fracture and which vascular
systems are disrupted.


Phases of bone healing

inflammation (10%)
Reparative/Regeneration (40%
Remodeling (70%)


describe inflammation phase of bone healing

-Hematoma fills the area with fibrin, RBCs, neutrophils, platelets, macrophages, fibroblasts (from PMNs).
-Mesenchymal cells from the cambium layer differentiate into osteoblasts and chondrocytes.
-Chemotaxis by growth factors (transforming growth factor beta, platelet derived, and macrophage derived)


describe reparative phase of bone healing

-Soft callus forms and is replaced by bone.
-Cartilage, fibrocartilage, collagen and hydroxyapatite deposition
-Cartilage replaced by bone like endochondral ossification


describe remodeling phase of bone healing

-Callus completely replaced by bone
-Vascular network is normalized
-Remodels according to Wolff’s Law
-Piezoelectric Effect: appearance of electrical potentials within bone in response to the application of an external force
-Compression side: electronegative leading to bone production
-Tension side: electropositive leading to bone resorption


types of bone heali

-Direct Osseous Repair (Primary Intention, Direct Healing)
-No callus formation; no motion
-Cutting cone: Osteoclasts in the front, osteoblasts in the back. Travels across the fx line (Schenk and Willinegger).
-Gap Healing: Bone deposition at 90° to the orientation of bone fragments
-Indirect Osseous Repair
-Callus formation


3 phases of wound healing

1. Substrate/Lag/Inflammatory Stage (Days 1-4)
-Inflammation characterized by edema/erythema/calor/dolor
-PMNs start out dominating, but are eventually taken over by macrophages
2. Proliferative/Repair Phase (Days 3-21)
-Collagen proliferation and macrophages
-Myofibroblasts also begin working
3. Remodeling/Maturation Phase (Day 21+)


HAV radiograph read

“In the area of the patient’s presenting complaint I see a (mild, moderate, or severe) hallux abductovalgus deformity at
the level of the metatarsal-phalangeal joint as defined by a (mildly, moderately, or severely) increased intermetatarsal angle,
(mildly, moderately, or severely) increased hallux abductus angle, and approximate tibial sesamoid position of (1-7). The PASA
and DASA of this joint appear (within normal limits or deviated). There (does or does not) appear to be a hallux interphalangeus
deformity as defined by the (increased or normal) hallux interphalangeus angle. The overall length of the first metatarsal appears
(normal, shortened, or long) compared to the remainder of the lesser metatarsal parabola on the AP view. On the lateral view the
first metatarsal appears (dorsiflexed, plantarflexed, or normal) compared to the second metatarsal using Seiberg’s index. There
(is or is not) an underlying metatarsus adductus as defined by the metatarsus adductus and Engle’s angles. Generally, the
rearfoot appears (rectus, pronated, or supinated) as defined by…”


Fltfoot xray read

“Consistent with the patient’s presenting complaint we see a (mild, moderate, or severe) pes planovalgus deformity. In
the sagittal plane I see a (decreased or increased) calcaneal inclination angle, talar declination angle, talar-calcaneal angle, first
metatarsal inclination angle, Meary’s angle, and medial column fault on the lateral view. I would also evaluate the patient for
equinus using the Silfverskiold test to determine a sagittal plane deformity. In the transverse plane I see a (decreased or
increased) talar-calcaneal angle, cuboid abduction angle, talar head coverage, talar-first metatarsal angle, metatarsus adductus
angle on the AP view. In the frontal plane we can see the Cyma Line is (anteriorly displaced, posteriorly displaced or normal) on
the lateral view, and that the subtalar joint alignment, ankle joint alignment and calcaneal position are (normal or abnormal) on
the long leg calcaneal axial views.”


flatfoot script for procedure recommendation

Now that you have defined the deformity on your own terms, you can now suggest how to fix it using the same tools.
“I would consider performing a (Gastroc recession, TAL, Cotton osteotomy, medial column arthrodesis, etc.) to correct for the
sagittal plane deformity, a (Evans osteotomy, CC joint distraction arthrodesis, etc.) to correct for the transverse plane deformity,
and a (medial calcaneal slide, STJ implant, etc.) to correct for the frontal plane deformity.


Subjective for digital deformities

-CC: Pt can complain of generalized “corns, calluses and hammertoes.”
-HPI: -Nature: “Sharp, aching and/or sore” type pain. May have a “tired feeling” in the feet.
-Location: Usually dorsal PIPJ/DIPJ of the toes or submetatarsal
-Course: Progressive onset and course.
-Aggravating factors: WB, shoe gear (especially tight shoes)
-Alleviating factors: NWB, wide shoebox, sandals
-PMH/PSH/Meds/Allergies/SH/FH/ROS: Usually non-contributory


derm things to ook for in digital deformities

-Derm: -Hyperkeratotic lesions can be seen submetatarsal, dorsal PIPJ or DIPJ of the lesser digits, distal tuft of the lesser digits, or
interdigitally. All can have erythema, calor and associated bursitis.
-5th digit is usually dorsolateral at the PIPJ, DIPJ or lateral nail fold (Lister’s corn). Hyperkeratotic lesion of the adjuvant 4th
interspace may also be present (heloma molle).


MS things to ook for in digital deformities

-Positive Coughlin test: Vertical shift of >50% of the proximal phalanx base on the met head. Also called the “draw sign” or
Lachman’s test.

-Kelikian push-up test: Differentiate between a soft-tissue and osseous deformity

-Specific to the 5th digit:
-Toe usually has a unique triplanar deformity (dorsiflexion, adduction and varus).
-Bunionette, splay foot and equinus may be present
-The 5th digit is in the most susceptible position in terms of a muscular imbalance deformity because the FDL has such
an oblique pull on the 5th
digit as opposed to the relatively axial pull of the other digits.


hammertoe radiograph sign

gun barrel sign


Mallet toe
claw toe
curly toe
digitus aductus
digitus abdctus
heloma molle

-Hammertoe: Extension at MPJ level; flexion at PIPJ level, neutral/extended DIPJ
-Mallet toe: Neutral at MPJ and PIPJ level; flexion at DIPJ level
-Claw toe: Extension at MPJ level; flexion at PIPJ and DIPJ level
-Curly toe: Claw/hammertoe deformity with an additional frontal plane component
-Digitus Adductus: Digital deformity with adduction in the transverse plane
-Digitus Abductus: Digital deformity with abduction in the transverse plane
-Heloma Molle: Generally occurs in the 4th
interspace with a curly toe deformity of the 5th
digit. Using this example, the head of the
proximal phalanx of the 5th
digit abuts the base of the proximal phalanx of the 4th
digit causing a hyperkeratotic lesion in the proximal 4th


Prism thoughts on pathomechanics

During weight-bearing, the toes cannot function in propulsive gait to aid in load
transfer if the most distal segment is not stabilized. The distal phalanx is stabilized by the long flexor tendons holding it solidly against the
weight-bearing surface. With the distal phalanx stabilized, the short flexor tendon can hold the middle phalanx against the weight-bearing
surface. With the middle phalanx stabilized, the lumbrical muscles hold the proximal phalanx against the ground. The lumbrical muscles
must work against the extensor tendon complex, but this complex is usually not actively firing to extend the MPJ during propulsion. The
interosseous muscles also stabilize the proximal phalanx in the transverse plane. When the proximal phalanx has been effectively
stabilized against the weight-bearing surface, the head of the metatarsal can effectively move through its range of motion and transfer load
across the metatarsal parabola. Any disruption in the stabilization process will lead to abnormal biomechanics and deformity


describe for stabilization

-Most common origin of hammertoe deformity
-Occurs when the PT muscle is unable to effectively resupinate the midtarsal and subtalar joints at
the beginning of propulsion. To compensate, the FHL and FDL fire earlier, longer and with
greater force to resupinate the foot. This puts too much force on the distal and middle phalanges
causing the toe to “buckle” in a dorsiflexed position at the MPJ. This retrograde buckling puts the
PIPJ in a vulnerable dorsal position and also pushes the metatarsal head plantarly.


flexor stabilization

-Occurs when the triceps surae muscle group is unable to effectively plantarflex the foot during
propulsion for whatever reason. To compensate, the muscles of the deep posterior compartment
(PT, FHL, and FDL) again fire earlier, longer and with greater force leading to the same type of


extensor substition

-Can occur in two ways
-One way is when the TA is unable to dorsiflex the foot through the swing phase. In this case the
EDL and EHL fire earlier, longer and with greater force than normal and are actually actively
extending the MPJ. This easily overpowers the lumbricals and leads to retrograde buckling.
-The other way is in a situation with anterior cavus where the EDL is actually at a mechanical
advantage over the lumbricals. Passive stretch of the EDL, rather than active contraction,
overpowers the lumbricals and leads to deformity


conservative tx of digital deformities

-Do nothing: Digital deformities are not a life-threatening condition and can be ignored if the patient is willing to put up
with it.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions
-Splints/Supports: -Metatarsal sling pads
-Silicone devices
-Toe crests
-Orthotics: -Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity


Surgery options for HToes

-Head arthroplasty: Post procedure (1882)
-Extensor hood and PIPJ capsule release
-Extensor tendon lengthening
-Capsulotomy (MPJ)
-Arthrodesis (PIPJ)
-Tendon transfer (flexor longus tendon transfer to function in MPJ plantarflexion


extensor tendon lengthening for haertoes

-Done proximal to MPJ level with a Z-lengthening


capsulotomy for hammertoes

-Of the PIPJ and MPJ
-Remember the “J” maneuver for release of the collateral ligaments
-Extensor hood release is also usually performed
-Some use the McGlamry elevator in this step to free plantar attachments


PIPJ arthroplasty for HT

-Post procedure 1882
-Resection of the head of the proximal phalanx at the surgical neck


-PIPJ Arthrodesis for HT

-Fusion of the PIPJ using a variety of techniques: table-top, V, peg-in-hole, etc.
-Fusion maintained with K-wire crossing the MPJ extending into the distal 1/3 of the metatarsal


-Flexor Tendon Transfer for HT

-Transfer of the FDL tendon dorsally to act as a more effective plantarflexor of the proximal
-Girdlestone-Taylor technique: Tendon is bisected, crossed and sutured on the dorsal aspect.
-Kuwada/Dockery technique: Tendon is re-routed through a distal drill hole
-Schuberth technique: Tendon is transferred through a proximal drill hole


-Syndactyly for HT

-Soft tissue fusion of one digit to a normal adjacent digit to help “bring it down”
-Interposing skin is removed and the digits are sutured togethe


know NV for each toe for HT surgery



5th digit skin incision

-It is possible to alter your skin incision to incorporate a derotational element to your skin closure. While the osseous work can be accomplished using a longitudinal or lazy “s” incision (proximal medial to distal lateral), those are really best for uniplanar deformities. 5th
digit HT is usually a triplanar deformity.

-Two semi-elliptical incisions directed proximal lateral to distal medial.
-The more oblique the incision is, the greater transverse plane correction.
-The more longitudinal the incision is, the greater the frontal plane correction.


Lesser Met deformity work up SUBj

-CC: Pt presents complaining of “pain in the ball of my foot.”
-HPI: -Nature: Generalized pain (aching, sharp, sore, etc.)
-Location: Submetatarsal. Can usually be localized to an exact metatarsal.
-Course: Gradual and progressive onset. “Has bothered me for years.”
-Aggravating factors: WB for long periods, shoe gear, etc.
-PMH/PSH/Meds/All/SH/FH/ROS: Usually non-contributory


Lesser et OJB and Imaging

Derm: -Diffuse or focal hyperkeratotic lesions submetatarsal
Vasc/Neuro: Usually non-contributory
-Many of the same signs/symptoms as HT digital deformity. HT often present.
-Anterior displacement of the fat pad
-Hypermobility of the first ray
-Anterior Cavus foot type
-Hypermobility of the fifth ray

Objective: Imaging
-Plain film radiograph:
-Look for irregularities of the metatarsal parabola
-Look for excessively plantarflexed or dorsiflexed position on lateral/sesamoid axial views


Possible etiologies of lesser met problems

-Retrograde force from hammertoes. Please see AJM Sheet: Digital Deformities.
-An excessively long and/or plantarflexed metatarsal leads to increased load bearing under that particular metatarsal.
-An excessively short and/or dorsiflexed metatarsal can lead to increased load bearing on the adjacent metatarsals.
-Hypermobility of the first ray leads to increased load bearing under at least the second metatarsal.
-Hypermobility of the fifth ray leads to increased load bearing under at least the fourth metatarsal.
-Anterior cavus and equinus deformities lead to increased pressures across the forefoot.
-Before a surgical option is considered, it is extremely important to understand where the increased load is coming from. The goal of
treatment should be to restore a normal parabola and weight-bearing function to the foot. Failure to correct the underlying deformity will
dramatically increase the rate of recurrence and transfer lesions.


Conservative tx for lesser mets

-Do nothing: Lesser metatarsal deformities are not a life-threatening condition.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions

-Splints/Supports: -Metatarsal sling pads
-Toe crests
-Silicone devices

-Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity


Surigicl tx for lesser met

distal met proc
Met shaft proc
met base proc


described the distal met proc for lesser met

-Duvries: plantar condylectomy on both sides of the MPJ
-Jacoby: “V” shaped cut in the metatarsal neck to allow for dorsiflexion of the head
-Chevron: “V” shaped cut similar to a Jacoby, but with removal of a wedge of bone to obtain metatarsal shortening as well.
-Dorsiflexory wedge osteotomy: similar to a Watermann of the first metatarsal
-Weil: Distal dorsal to proximal plantar oblique cut to allow for distal metatarsal dorsiflexion and shortening. Can be
made in several planes to obtain desired dorsiflexory/shortening effects.
-Osteoclasis: Through and through cut through the metatarsal neck allowing the distal head to find its own plane.


Met shaft proc for lesser met probs

-Cylindrical shortening
-Giannestras step-down procedure: Z-shaped cut which can allow for shortening and distal dorsiflexion.


Met base proc for lesser met probs

-Dorsiflexory wedge: (1mm of proximal dorsal shortening equivalent to ~10 degrees of dorsiflexion)
-Buckholtz: Oblique dorsiflexory wedge which allows for insertion of a 2.7mm cortical screw


complations for leser met surgery

floating toe
transfer lesions


study that shows osteoclastic procedures allowing the distal segment to find their own plane without internal fixation have
the least occurrence of recurrence and transfer lesions, but they also have a higher rate of malunion, delayed union and non-union.

-[Derner and Meyr. Complications and Salvage of Elective Central Metatarsal Osteotomies. Clinics Pod Med Surg. Jan 2009


tailorbunon imaging

-4-5 Intermetatarsal Angle > 9 degrees (Normal is 6.47 degrees per Fallat and Buckholtz)
-Lateral Deviation Angle > 8 degrees (Normal is 2.64 degrees per Fallat and Buckholtz)
-[Fallat LM, Buckholtz J. J Am Podiatry Assoc. 1980 Dec; 70(12): 597-603.]
-Splay Foot Deformity
-Plantarflexed 5th
metatarsal position
-Structural changes to 5th
metatarsal head


etiology of tailor'sbunion

-Numerous authors have chimed in on the etiology of the 5
Metatarsal Deformity:
-Davies: incomplete development of deep transverse metatarsal ligament
-Gray: malinsertion of adductor hallucis muscle
-Lelievre: forefoot splay
-Yancey: congenital bowing of metatarsal shaft
-Root: abnormal STJ pronation
-CMINT, etc, etc, etc


Treatment conservattais bunion

-Do nothing: 5th metatarsal deformities are not a life-threatening condition.
-Palliative care: Periodic sharp debridement of hyperkeratotic lesions
-Splints/Supports: -Shoe gear modification with large toe box
-Derotational tapings
-Orthotics: -Cut-outs of high pressure areas
-Metatarsal pads to elevate the metatarsal heads
-Correction of the underlying deformity


surgical tx for taiors buion

-Exostectomy: Removal of prominent lateral eminence from 5thmet head
-Arthroplasty: Removal of part/whole of 5thmet head
-Distal Metatarsal Osteotomies:
-Reverse Hohmann
-Reverse Wilson
-Reverse Austin
-Crawford: “L” shaped osteotomy allows for insertion of cortical screws
-LODO (Long Oblique Distal Osteotomy): similar to Crawford but simply oblique
-Read [London BP, Stern SF, et al. Long oblique distal osteotomy of the fifth metatarsal for correction of tailor's bunion: a
retrospective review. J Foot Ankle Surg. 2003 Jan-Feb;42(1):36-42.] Especially if externing at Inova!
-Medially-based wedge
-Proximal Osteotomies:
-Transverse cuts
-Oblique cuts
-Medially based wedges