1st Ray Procedures

Hallux Abductus Angle PASA DASA

(HAA) Normal: 0-8 Normal: 0-8
Normal: 0-16 *line perpendicular to *line perpendicular to
* >16 in all HAV deformities articular cartilage of articular cartilage of base
head of 1st met & long of 1st prox phalanx &
bisection of 1st met longitudinal bisection of 1st
*best measured prox phalanx
intraoperatively (effective
PASA)

Parameter Positional Structural Combined

HAA > 16o > 16o > 16o

PASA &/or DASA Normal Abnormal Abnormal

PASA + DASA: HAA < 0 <

Joint Position Deviated / Subluxed Congruous Deviated / Subluxed

(lines representing articular (lines representing articular
surfaces intersect outside joint) surfaces intersect inside joint)

IM Angle HIP Angle Metatarsus Adductus Angle

Normal: Normal: 8-10 Normal: 0-14
1-2: 0-8
2-4: 16 + 4
4-5: 8 + 2
 Distal HAV Surgeries
-True IM up to 16 degrees (8-16): True IM = Apparent IM + abnormal met adductus (ma-15)
-No DJD (apparent= what you measure) (if met adductus <15, apparent IM is the true IM)

Youngswick Mitchell Reverdin

*Increased IM *Long first metatarsal *Abnormal PASA
*Elevated first metatarsal *Normal PASA 1) Distal cut: Parallel to articular surface
*Hallux Limitus 2) Proximal cut: perpendicular to long axis
-Thickness of bone removed usually
1-2mm PLUS width of blade
*Absence of DJD of metatarsal

-If IM is increased can be modified and -Maintain lateral cortical hinge

applied. My opinion must be 12 or less. -Inherent problems-sesamoid pain
Larger lateral ledge corrects for IM

Roux
*Similar to Mitchell with the addition
of an ABNORMAL PASA
*Modification of Mitchell where distal
cut made parallel to articular surface for
PASA correction.

Reverdin Green (Distal L) Reverdin Laird Hohman

*Abnormal PASA (most common for this) *Abnormal PASA and IM *Abnormal PASA and IM
*Protects the sesamoids i.e. PASA >8, IM>8<16. *Must be an increase in met length.
*Lateral Hinge still maintained *Protects the sesamoids *The cut allows for rotation in the
*No Lateral cortical hinge, frontal plane.
1) Plantar cut
2) Distal cut: parallel to articular surface allowing translation of capital
3) Prox cut: perpendicular to met long axis fragment laterally to reduce IM.
Pearl: plantar cut, leave blade in, get new
blade for dorsal cuts.

The Todd Modification takes this

osteotomy and PF it as well.
Wilson AUSTIN
*Long first met + Increased IM *60 degree cuts
*Very stable in all planes but transverse
*Normal PASA
*Increased IM up to 16 unless met width is
large
*K-wire fixation-Dorsal Proximal Medial to
Plantar Lateral Distal is most stable
(DPM PLD)
*Can use screw fixation-same orientation as
above OR Dorsal Distal to Plantar Proximal

DF: Plantar Medial to Dorsal Lateral

PF: Dorsal Medial to Plantar Lateral
Shorten: Distal Medial to Proximal Lateral
Lengthen: Proximal Medial to Distal Lateral

Kalish Modification SCARF

*same indications as Austin, but *Long cut through diaphyseal bone
need more screws due to poor *Allows for `swivelinga of met.
cortices -Divide Cortex at 50/50 or 66/33
*Angle between arms is reduced to -Make Distal and Prox cut at 60-70
as low as 40 degrees degree angle
-Avoid `troughinga
-Easy dorsal to plantar screw fixation
Diaphyseal vs Metaphyseal bone
-decreased vascularity
-more cortical vs. cancellous
-good for AO fixation because of hard bone
-need for rigid fixation
*For an increased IM angle
*Watch out for Troughing in frontal plane (prevent with bone graft)

Ludloff Osteotomy MAU Osteotomy

*IM angle 13-20 degrees *Minimizes potential of elevates
*Abnormal HAA -Dorsal Distal to Plantar Proximal, parallel to WB Surface
*Can lengthen, PF, rotate laterally (for abnormal -Can translate laterally, rotate, DF, lengthen
PASA) -Need Rigid fixation
-Combine w/R. Green to correct for PASA
-Weight bearing causes elevation of capital fragment
and met head Post op elevates, lesser metatarsalgia
-Dorsal Proximal to Plantar Distal
-Need good bone stock for ridged AO screw fixation (Requires
rigid fixation)
*If the 1st metatarsal is as long, or longer than the 2nd than a base procedure may be performed, (Remember a
Base procedure will shorten the 1st Metatarsal) Therefore: Contraindicated in patient with short 1st metatarsals
*18 gauge needle is used to locate the metatarsal cuneiform joint (leave it in so you donjt hit joint)
*Anatomical Structures
k Medial Dorsal Cutaneous Nerve: Crosses the base of 1st Metatarsal
k Deep Plantar Artery: Runs between 1st and 2nd Metatarsals
k Deep Plantar Vein: Crosses Base of 1st Metatarsal

Closing Base Wedge Oblique Closing Base Opening Base Wedge

Make cuts 1-1.5 cm from joint Wedge *For Short 1st Met (maintains 1st
1) Distal: perpendicular to shaft axis, (Juvara Procedure) met length)
2) Proximal: parallel to desired *Angled at 40 degrees to the long *Must use bone graft
articular surface of met head -Use Autogenous Bone - Resected
axis of the 1st metatarsal shaft
medial eminence, or Cortico-
*Allows better screw fixation cancellous graft from calcaneus
*Good for Juvenile HAV because it
avoids open physeal plates
*Patient compliance is extremely
important (long recovery)

In Sagittal Plane:
*The osteotomy is made perpendicular to
the weight bearing surface (NOT to met
shaft. Will result in Met Primus Elevatus)

Crescentic Base Osteotomy Logrescino Lapidus Procedure

(Weinstock) * Increased PASA & Increased IM *1st Metatarsal l Cuneiform fusion
*Primarily in the transverse plane: *1st Metatarsal l Cuneiform fusion *Eliminates hypermobility of 1st
(allows easy correction of transverse plane deformity) *Eliminates hypermobility of 1st ray l can get some lengthening
*Need to use Crescentic Blade ray (Multi-planar correction) *Must be NWB for 6-8 weeks
*Elevatus is most common problem
postop.
-Cut 1.5cm distal to the metatarsal-
cuneiform joint
-Concave portion faces distally
-Convex portion faces proximally
-Segment is rotated until desired
correction is obtained

Sequential Release of Plantar Lateral Contracture

-Skin incision is between EHL and proper digital branch of medial dorsal cutaneous nerve
 -Cut through DTIL tendon to expose plantar structures
-Sequence of Release:
1) Adductor halluces tendon freed from its attachment to MTPJ and sesamoid apparatus
2) Fibular sesamoid ligament released by stab incision
3) Tenotomy of lateral head of FHB on the proximal and distal margins of the fibular sesamoid
4) Excision of fibular sesamoid
-Between each step, check status of release by viewing placement of medial rim of the base of the
proximal phalanx in the tibial sesamoidal sagittal groove.

3 Intervals of dissection
1) Skin = 1st incision, cut full thickness through skin, and separate the skin from the sub q
2) Sub q = cut through the sub q to the bone and try to keep it all one layer
3) Periosteum = dissect the periosteum off the bone
4) Then you have to suture all 3 layers individually.

Good example of Austin: [Link]

Complications
Over Correction Hallux Varus
Causes of Hallux Varus:
-Excessive resection of medial eminence (staking of 1st met head)
-Osteotomy that creates negative IM angle
-Overzealous medial capsuloraphy (suture of capsule: triangle piece of
capsule w/base plantar)
-Fibular sesamoidectomy
-Aggressive lateral capsulotomy
-Bandaging
Anesthesia

Physical Status Exam

American Society of Anesthesiologists
Class 1: Normal and Healthy (no known disease)
Class 2: Mild Systemic Disease (presence of essential HTN or mild type II diabetes)
Class 3: Severe Systemic Disease that is not incapacitating (severe DM, type 1 w/vascular comprimises)
Class 4: Incapacitating Systemic Disease thatIs a threat to life (advanced cardiac, renal, hepatic problems, etc.)
Class 5: Moribund Patient whoIs not expected to live w/o surgery
Emergency Operation: any of the above classes in emergency operation (letter E is placed next to classification)

Risky Patient Types

Advanced or Uncontrolled Cardiovascular Disease
P Hypertension (>140/, or >/90): Stabilize BP prior to anesthesia (have PCP take BP before anesthesia)
P Coronary Artery Disease
W Nitroglycerin pre-op
W How old is YOld MIZ (no surgery if MI <3months, <6 for elective)
W Monitor ST segment in II (right coronary artery) and V5 (left coronary artery)
W Avoid conditions known to lead to ischemia (no strenuous activity before surgery, like shoveling snow)
Asthma
W Treat with bronchodilators before to avoid any issues
W Steroids to reduce inflammation
W Cromolyn sodium to stabilize mast cells (surgery may introduce cell mediators into blood and lead to an attack)
W Beta-2 agonists for acute bronchospasm
COPD
W Continue inhalation treatment, steroids, etc.
W Stop smoking for 24 hours improve oxygen carrying
W Stop smoking for 6-8 weeks will mucus production, ciliary function, & decrease alveolar macrophages
Diabetes Mellitus
W Check blood glucose pre-operatively (too high is ok, too low is bad, so avoid hypoglycemia)
W Patient should not take morning insulin dose. Will check it and treat accordingly on patient arrival
W Resume Insulin as soon as the patient can tolerate oral intake of fluids/food
W Anticipate higher Insulin requirements
End Stage Renal Disease
W Potassium (is a reason to stop surgery because K affects rate and rhythm of the heart)
W Dialysis schedule (schedule dialysis right after to get rid of injected stuff during surgery)
Allergic reactions
P Anaphylaxis:
W Immune mediated hypersensitivity w/in 10 min of exposure to antigen (Involve production of IgE AbIs)
P Anaphylactoid reaction:
W Not an immune mediated hypersensitivity and do not involve production of IgE antibodies
W Massive release of histamine from basophils and mast cells occurs.
P Cannot distinguish between Anaphylaxis and Anaphylactoid reactions on the basis of clinical observations
P Plasma tryptase levels may be elevated for few days (anaphylaxis.)
P Muscle relaxants account for about 60% of drug induced allergies during anesthesia
P Treatment:
W Oxygenation
W Fluids to replace intravascular volume (If someone is red and vasodilated, give fluids)
W Epinephrine by injection or as a continuous infusion
W Antihistamines (diphenhydramine), inhaled beta agonist agents (Epinephrine), phosphodiesterase
inhibitors (aminophylline) steroids
 Conscious Sedation
IV sedatives and analgesics are used to increase patientIs comfort
P Obtain informed consent
P A separate physician/nurse administers the sedative or other appropriate medications
P This physician/nurse monitors the patient
P Common Analgesics (pain elimination): P Common Sedatives (will fall asleep, but still feel pain):
W Morphine W Midazolan [Versed]
W Meperidine [Demerol] W Diazepam [Valium]
W Fentanyl W Lorazepam
*donIt give Demerol to pt with renal failure, it will accumulate and cause seizures
• Common Reversal Agents:
W Naloxone: narcotics antagonist
W Flumazenil: sedative antagonist

Airway Evaluation
Mallampati Classification
P Ability to view posterior pharynx.
P Examine open mouth to visualize the Faucial pillars, soft palate, and uvula
Class1: All can be visualized
Class 2: Uvula is masked by the base of the tongue (see pillars and soft palate)
Class 3: Only soft palate can be visualized

General Anesthesia
Reversible unconsciousness with loss of sensation of pain over whole body
Order of CNS descending depression:
1) cortical and psychic centers
2) basal ganglia and cerebellum
3) medullary centers
4) spinal cord

P Advantages:
W Patient preference to be YasleepZ
P Disadvantages:
W More complex, therefore higher cardiac and respiratory risks
W Slower recovery

Steps
1) Start IV
2) Administer pre anesthesia medications
W Sedatives/Anxiolytics (midazolam)
Pentobarbital and Secobarbital: Used before surgery for anxiety and tension (cerebral cortex
depression). Have no analgesic component
Chloral Hydrate: Good alternative to barbiturates in kids and elderly
Diazepam (valium): prevent/treat convulsions, anxiety
Hydroxazine: Excellent pre-medication for patients with bronchial asthma history
W Anticholinergics (atropine, glycopyrrolate) to make patient dry so pt doesnIt choke on spit
W Medications to reduce stomach acid production and facilitate emptying (pepcid, metachlopromide (reglan)
 3) In the OR: connect patient to monitors
4) Administer a narcotic (usually Fentanyl)
Fentanyl: produces short depression of ventilation. Reversed by antagonist
Morphine: constricts bronchi (due to histamine release)
Meperedine (Demerol): has analgesic, sedative, and spasmolytic properties. Contraindicated in patients
with atrial flutter (can cause tachycardia)
5) Induction of anesthesia (best through IV)
IV:
Thiopental (sodium pentothal)
Ethomidate
Propofol
Inhaled:
Volatile Liquids (Can cause malignant HTN)
MoA: binding to ion (potassium, sodium) channels in cholinergic neurons.
Advantages: Rapid Induction, Pleasant smell, Bronchodilator, nonemetic
Disadvantages: Liver damage (hepatotoxicity), myocardial depression
Enflurane
Disadvantages: smooth muscle relaxant, increase HTN w/increase depth of
anesthesia
Isoflurane
Advantages: excellent muscle relaxation, maintains stable cardiac rhythm
Disadvantages: shivering postop
Gaseous Agents
Nitrous Oxide
-least potent of the anesthetic gases, and most frequently used inhaled anesthetic
-Oxygen 100% must be given at end of surgery to prevent diffusion hypoxia
Advantages: doesnIt sensitize the myocardium to epinephrine,
Disadvantages: No muscle relaxation, possible marrow depression and fatal
agranulocytosis from prolonged exposure
6) When the patient loses consciousness determine if you can ventilate the patient using mask
W Yes, continue as planned
W No, allow the patient to breath spontaneously until awake, and then use an alternate plan
7) Administer a muscle relaxant
* Succinylcholine (can cause malignant HTN)
* Atracurium
* Vecuronium, rocuronium
8) Intubation
9) Connect the patient to a ventilator and administer a mixture of oxygen and the anesthetic gases.
10) When the procedure ends, turn the gasses off and administer 100% oxygen.
11) When the patient wakes up, remove the endotracheal tube

Anesthetic Phases
Stage 1: Analgesia
Plane 1- Preanalgesia (normal memory and sensation)
Plane 2- partial analgesia and amnesia
Plane 3- total analgesia and amnesia
Stage 2: Delirium (extends from loss of consciousness until beginning of surgical anesthesia.)
-Excitement and voluntary activity marked (irregular breathing, pupils dilated)
Stage 3: Surgical anesthesia
Plane 1 (sleep)- Rhythmical breathing, eyeball centrally fixed, faint lid reflex
Plane 2 (sensory loss)- Pupils slightly dilated, pulse and BP normal
Plane 3 (muscle tone loss)- Intercostal paralysis begins, increase pulse rate and decrease BP
Plane 4 (intercostal paralysis)- Cessation of respiratory effort (requires artificial ventilation)
Stage 4: Medullary Paralysis
Plane 1- Reversible respiratory failure
Plane 2- Irreversible cardiovascular collapse
 Local Anesthetics
-MoA: Na+ channel blocker, preventing depolarization -Pain and Temp is lost first. Touch and Motor later
Esters:
-Hydrolized by pseudocholinesterase in the plasma
-High potential for allergenicity due to PABA chemistry
Procaine (Novocaine): most toxic, used to compare other locals
Chlorprocaine: least toxic, rapid plasma hydrolysis
Tetracaine: longest duration
Amides:
-Hydrolized in the liver
-Injection into an acidic area (infection) converts the anesthetic chemically and does not allow for penetration into
cell membrane and lessens effectiveness
Lidocaine (xylocaine): shortest duration and fastest action
Mepivicaine: donIt use in renal ds patient
Bupivicaine (Marcaine): long duration, donIt use in children under age of 12
Etidocaine (Duranest): 4x more potent than lidocaine, but only twice as toxic

Vasoconstrictors (epinephrine)
Reduces vascularity (from vasoconstriction) and absorption rate
Cautious in patients with hyperparathyroidism, arteriosclerosis, HTN, peripheral vascular disease
Avoid in patients receiving Halothane (bc it sensitizes myocardium in presence of catecholamineIs)
Hyaluronidase (Wydase):
More rapid spread of solutions into tissues to facilitate regional block anesthesia. Increased incidence of toxic
reactions caused by local anesthetic drugs when hyaluronidase is used

Regional Nerve Blocks

Ankle Block:
Saphenous- only nerve in ankle from femoral nerve. Medial to great saphenous vein
PT- branch of sciatic nerve. Lies in 3rd compartment of lacinate ligament
Sural- Branch of tibial and common peroneal
Sup. Peroneal-
Deep Peroneal- between EHL and Anterior Tibial

Maximum Allowable single dose in adults

Plain w/Epinephrine
Novocaine(1-2%) 750mg 1000mg *Is no advantage in using a
Pontocaine (.1-.25%) 75mg 100mg higher % solution (no stronger or
Lidocaine (1-2%) 300mg 500mg longer anesthesia), so with a
Carbocaine (1-2%) 500mg lower % solution you can inject
Marcaine (.25-.75%) 175mg 225mg more volume
Complications of Local
Systemic Reactions
-Cardiovascular: Myocardial depression, HTN, pallor, clammy sweaty skin, arrhythmias, cardiac arrest
[use vasopressors (Ephedrine, methoxamine, phenylephrine), IV fluid, CPR]
-Medullary Center: depressed respiration (O2, artificial ventilation, airway control), apnea
-CNS: N/V, talkative, euphoria, restlessness. Followed by twitching, convulsions [Valium (ultra-short
acting barbiturate) and artificial ventilation] lung and heart failure
Vasovagal Reflex (Syncope): dilation of vessels in leg, slow heart rate temporary loss of consciousness
Anaphylactic reaction
Allergic reaction: If pt has paraben sensitivity, prep w/o araben and w/o epinephrine (masks positive skin test)
* Cross reactivity does not exist between amide and ester local anesthetics
Local reactions: skin slough, swelling, abscess, ulceration
 IV Anesthesia
Ultra –Short acting Barbiturates: in sufficient amounts provides all anesthetic stages for short procedures. Frequently
used for Induction.
-Neuroleptanalgesia: somnolence w/o total unconsciousness, indifferent to environment, no voluntary
movement, analgesia, satisfactory amnesia. For high-risk patients (old, liver damage)
Neuroleptic drug (tranquilizer: droperidol)
Narcotic (opioid) analgesic (fentanyl)
-Neuroleptanesthesia: (for pts w/low cardiac reserve)
Injectable anesthetic (Nitrous Oxide)
Low does neuroleptic (droperidol)
Short acting analgesic (fentanyl)
Muscle relaxants
-Dissociative anesthesia
Ketamine Produces state where pt is mentally dissociated from enviornment
-Total Intravenous Anesthesia (TIVA): These drugs are eliminated within minutes and irreversible. Are used to
reduce the risks associated with accumulation and avoids unwanted effects of inhalational agents and the need for
complex apparatus.
Injectable anesthetics (propofol and etmidate)
Analgesics (alfentanil and remifentanil)
Muscle relaxant (mivacurium)

Lumbar Epidural and Cuadal Anesthesia

Sensory Only!
P Advantages:
W An epidural catheter can be placed for repeated injections
W Longer lasting Sympathetic block
W Longer lasting Post operative analgesia (by Epidural administration of Morphine)
P Disadvantages:
W Hypotension
W Bleeding/hematoma inside the spine
W Post Dural Puncture headache
Injection of local anesthetic into epidural space in 2nd lumbar or below for foot
Indications: pt with lung problems, R.A. affecting cervical spine, and myasthenia gravis (canIt take muscle relaxants)
Contraindications: septicemia, preoperative headache, chronic backache
Advantages over spinal (inject in cerebral spinal fluid in subarachnoid space): segmental anesthesia, no post-op headache
Advantages of spinal over epidural: less drug needed, less time needed, predictable, easier to perform
Anatomy: dura attaches to foramen magnum, preventing drugs to pass from peridural space into cranial activity. Dura
sac ends at lower border of S2. Epidural space is between dura and ligamentum flavum and contains spinal nerve root
 Spinal Anesthesia
P Meds: Procaine (45min), cloprocaine, tetracaine (6-8hrs), lidocaine (1.5hrs)
P Advantages:
W Simple, easy, fast, reliable
W Sympathetic block in addition to the motor and sensory block.
W Post operative analgesia (if preservative free Morphine is added to the spinal anesthetics)
P Disadvantages:
W Hypotension
W Bleeding/hematoma inside the spine
W Post Dural Puncture headache

General Complications of Anesthesia

Hypoxemia:
Control of Ventilation: (PaCO2 is most important regulator of ventilation)
-Respiratory reaction to hypoxia is on peripheral chemoreceptors, most importantly carotid bodies
Causes:
-Hypoventilation (drugs, encephalitis, guillain barre, m. dystrophy), Absolute shunt [perfusion (process of
delivery of blood to a capillary bed) w/o ventilation], Shunt (dead space): blood flow or ventilation does not meet the
Relative shunt (ventilation perfusion inequity), other in the lung as it should for gas exchange to take place
Diffusion block (lung cant diffuse oxygen to blood)
Biochem changes: oxidative phosphorylation in mitochondria stops anaerobic metabolism H+ & lactate
-Increased heart rate -Pulmonary vasoconstriction (compensation: hyperventilation)
-Acute renal failure - hepatic portal circulation (compensation: hemoglobin)

Hyponatremia (Serum sodium <136 mEq/L):

Symptoms: depend on rate, and amount of decrease.
-occurs when Na+ falls below 125
-confusion, anorexia, lethargy, N/V, coma, seizures
Treatment: correct underlying disorder
-hypovolemic-hypotonic: isotonic saline
-hypervolemic-hypotonic: restriction of water and diuretics

Hypokalemia (Serum potassium <3.5 mEq/L)

Symptoms: disorders of muscle physiology
-Depressed myocardial contractility arrhythmias (Respiratory arrest if <2mEq/L)
- GFR, aldosterone, insulin release

Hyperkalemia
Symptoms: muscle weakness, paresthesias (peripheral nerves), cardiac conduction (dangerous if >7mEw/L)

Hypothermia
Effects - Is O2 consumption and Is CO2 production by 7-9%/°C in all tissues
-Blood WGas transport: hemoglobinIs affinity for O2 Is 6%/°C decrease
-Respiration
-Cardiovascular: HR and CO as temp falls. Prolonged QT on EKG, dysrhythmias at 28°C
- GFR by 60%
Malignant Hyperthermia
-Etiology: genetic (do genetic testing)
-Hypermetabolic Crisis (everything thatIs working is working at the max resulting in temp overload)
*Occurs when a susceptible individual is exposed to a triggering anesthetic agent.
-Common triggering anesthetic agents:
W All volatile inhalation anesthetic gases [not Nitrous Oxide: not a volatile inhalation gas]
W Depolarizing muscle relaxant [succinylcholine]
-Safe to use:
W Nitrous Oxide
W All non-depolarizing muscle relaxants
W Narcotics
W Local and Regional anesthesia
-Clinical and laboratory signs:
W Muscle rigidity (muscle not working myoglobin not working dark cola urine)
W Dark (like cola) urine [myoglobinuria] (if you see this, itIs MH until proven otherwise)
W Acidosis, hyperkalemia, myoglobin in blood and urine, increased CPK (normal 25-30)
W Skin mottling
W DIC (Disseminated Intravascular Coagulation)
-Diagnosis:
W Muscle biopsy and Caffeine and Halothane contracture test
W In the USA: genetic [RYR1] screening for MH suseptibily
-Treatment:
W Aggressive cooling (ice everywhere)
W IV Dantrolene (will lower body temp)
W Treat all manifestations: acidosis, hyperkalemia, myoglobinuria

Pediatric Patient
Clarks rule: Adult Dose X (Weight ÷ 150) = Childs dose [eg. 300mg x (70lb ÷ 150) = 235mg]
Fried’s rule: (Age in month X adult dose) ÷ 150 = Child dose [eg. (96 x 300) ÷ 150 = 192mg]
Cowlings rule: (Age at next birthday in years X adult dose) ÷ 24 = Child dose [eg. (8 x 300) ÷ 24 = 100mg]

Anesthesia: create warm environment bc kids have poor autothermoregulation mechanisms (inability to shiver)
-If not, child may become cold and cyanotic, especially after 2hrs of surgery. Hypothermia depressed
respiration and hypoxia predisposition to arrhythmias and v-fibrillation. This is most common cause
of cardiac arrest and shock in young.

Inhalation Agents: Halothane and Nitrous Oxide w/neuromuscular blockade. (add Fentanyl for short procedures)
-Fentanyl reduces inhalation requirements, coughing while providing post-op analgesia and shorter
discharge time. Give 1 microgram/kg IV 20 minutes prior to end of surgery

Succinylcholine: muscle relaxant used to quickly establish airway (nicotinic antagonist).

Biomechanics
TALIPES CALCANEUS
! A fixed structural position in which the foot is positioned above a transverse plane which runs through the heel.
! In other words the person walks on their heels

TALIPES EQUINAS
! A fixed structural position in which the foot is positioned below a transverse plane which runs through the heel.
! Translation - person walks on their toes

SWING PHASE MOTIONS (Open Kinetic Chain)

! During swing phase the foot pronates then supinates
! Pronation- functionally shortens the limb to help the foot clear the ground just after toe off
! Supination- stabilizes the osseous structure of the foot preparing it for heel strike

STANCE PHASE (Closed Kinetic Chain) (60% of gait cycle)

1. Contact Period (27% of stance phase)
*Occurs between heel strike & toe off of the opposite foot (Forefoot loading)
-At heel strike the foot is supinated (remember at the end of swing phase the foot is supinating)
Closed kinetic Chain Pronation
-STJ pronates (calcaneus everts; talus PF’s, adducts); absorb shock & adapt to terrain (mobile adapter)
*As forefoot loads, OMTJ pronates (DF & abduction from EDL contraction) & LMTJ supinates (inverts)
-This is why 5th met head strikes first
*Ankle joint PFXs (is DFXed prior to contact)
*The leg internally rotates

2. Midstance period (40% of stance phase)

*Occurs between toe off of opposite foot & heel lift
Closed kinetic chain Supination
-STJ begins to Supinate (Calcaneus Inverts; talus DF’s, abducts)
Midtarsal Joint Movement
-OMTJ is pronated (DFXed & abducted) due to vertical ground reactive forces
-When calcaneus inverts, LMTJ pronates (everts) until the forefoot locks
-Once OMTJ & LMTJ are max pronated, the forefoot locks on the rearfoot, (midtarsal joint is locked!)
-Because OMTJ is pronated and LMTJ is pronating, the foot changes from mobile adapter to rigid lever
Rigid Lever: STJ Supination MTJ pronation (piling of the tarsal bones) rigidity
*Ankle begins to DF, keeping our heel in contact with the ground
3. Propulsive period (33% of stance phase)
*Occurs between heel lift and toe off
Closed kinetic chain Supination
-STJ continues supinating maintaining foot as a rigid lever for propulsion
-Immediately before toe off the STJ pronates slightly
Midtarsal Joint Movement
-Forefoot is locked on the rearfoot.
-Peroneal muscles lift the lateral side of the forefoot to transfer weight medially for propulsion
*Because of lateral to medial loading of the forefoot, the OMTJ supinates (PF and adduction),
keeping digits on the ground
-LMTJ remains pronated
*The first ray PFXs and Everts to maintain contact between the first metatarsal head and the ground
*Leg externally rotates
IF PRONATING DURING PROPULSION:
-Foot & leg muscles must work harder, resulting in fatigue of foot and leg musculature
-Also results in hypermobility of bones due to foot being a mobile adapter
-Can shearing forces between bones of forefoot and skin calluses

JOINT’S PLANES OF MOTION

1st MPJ planes of Motion
1. Transverse (add. & abd.)
2. Sagittal (DF &PF):
a. Minimum ROM needed for propulsion: 65°-75°

1st Ray planes of Motion

1. As 1st ray Dorsiflexes, it Inverts
2. As 1st ray Plantarflexes, it Everts
*1st ray must DF to remove stress from sesamoids during forefoot loading &
to compensate for eversion of the calcaneus during contact period pronation
-hallux rigidus (PFed 1st ray) will prevent full eversion (pronation) of STJ
-Compensation results in supination of the STJ in contact period
st
*1 ray must PF during propulsion for lat. side of foot to lift off ground as forefoot loads from lat. to med.

Midtarsal Joint
*Consist of 2 joints which function about 2 common axis of motion (both have supination/pronation axis)
2 Joints
1. The talo-navicular joint
2. The calcaneo-cuboid joint
2 Axis of motion
1. LMJA: eversion and inversion
2. OMJA:
-No abduction or adduction w/o PF or DF and vice a versa
*This allows the forefoot to lock on the rearfoot during loading when both heel
and forefoot are in contact with the ground (In other words your forefoot doesn't
bend back onto your tibia during forefoot loading)
*MTJ locks on rearfoot when both the LMTJ & OMTJ axis are max pronated
 STJ
Transverse plane: 42° abduction & adduction
Frontal plane: 48° Inversion & Eversion
Sagittal plane: 16° PF & DF
*Neutral: position of STJ when there is twice as much inversion of calcaneus as eversion of calcaneus
*Need total ROM of 8 to 12° of Inversion/Eversion at the STJ for normal locomotion.

Ankle joint
*Minimum ROM of the ankle joint for normal locomotion is 10° of DF and 20° of PF

SELETAL STABILITY
Hypermobility
! Any motion in a direction outside the normal plane of motion causes instability (called hypermobility)
! Hypermobility causes momentary subluxation of a joint
Subluxation
-State of partial dislocation: joint margins compress on one side and
separate on the opposite side
-Causes trauma to the joint and results in functional adaptation or
degenerative joint disease
Pronated foot: angulation of forces, stability (muscles work harder to maintain
stability muscle imbalance)
Supinated foot: angulation of forces, stability

COMPENSATORY FUNCTION
Abnormal Compensation
! Accomplished by pronation or supination of the subtalar or midtarsal joint
! STJ joint is the primary joint in the lower extremity for compensation
! Compensation for STJ pronation (rearfoot eversion) is forefoot inversion (supination of the LMTJ)
-Result: 1st ray dorsiflexes, MTJ unlocks, foot bears weight primarily on 2nd metatarsal head
! Forefoot cannot compensate for rearfoot supination [as STJ supinates (invert), forefoot also inverts]
-MTJ axis are loaded and maximally pronated thus locked (no more forefoot motion can occur)
Forefoot Varus
-Structural inversion of the forefoot on the rearfoot when the MTJ is locked (maximally pronated)
-Compensation seen for forefoot varus is STJ pronation through midstance and propulsion

MEDIAL COLUMN
! Primary role in shock absorption and terrain adaptation (mobile adapter)
! Remember first ray dorsiflexes to compensate for STJ pronation and to alleviate stress on the sesamoids

LATERAL COLUMN
! Primary role in balance
! Remember when forefoot everts so does the calcaneus to adapt to terrain

PLANTAR FASCIA
WINDLASS MECHANISM
! When we DF the digits, especially the hallux, (as in propulsive phase) we see an in the height of the
medial arch as the medial slip of the central band tightens plantarflexing the first metatarsal
! Also will see inversion of the calcaneus, again due to tightening of the plantar fascia
! This makes plantar fascia a passive supinator
PRONATED FOOT
Are two categories
1. Foot functions around an abnormally pronated position
2. Foot moves in a direction of pronation when it normally should be supinated
Abnormal Pronation
Occurs because:
1. Compensation for an osseous or soft tissue abnormality of the foot or lower extremity
2. Response to forces which load the medial side of the foot prematurely
3. Muscle imbalance due to neuromuscular disorder
4. Result of tonic muscle spasm

COMPENSATORY PRONATION
FOREFOOT VARUS (forefoot inverted in relation to the rearfoot)
-Compensation is eversion of the rearfoot to bring medial aspect of the foot to the ground
-Results in STJ joint pronation throughout the stance phase of gait
-This prevents normal supination of the foot during propulsion
NON - RIGID FOREFOOT VALGUS
-Forefoot everted on rearfoot. However, forefoot not rigidly fixed in valgus position
-When weight is placed on medial column, it DFXs, causing inversion of the forefoot on the rearfoot
-Behaves like a forefoot varus
TIBIAL VARUM (tibia is angulated in varus on the frontal plane)
-Causes heel and forefoot to be inverted in relation to the ground
-STJ pronates to bring the medial aspect of the foot to the ground
REARFOOT VARUS (Neutral position of STJ results in inverted calcaneus)
-As with tibial varum, results in forefoot being inverted to the ground
-STJ pronates to get the medial side of the foot to the ground.
INTERNALLY ROTATED LIMB
-The entire lower extremity is internally rotated when the hip is in neutral transverse plane position.
-Results in leg, ankle, and foot being internally rotated as the individual walks.
-Compensation is abduction of the foot on the leg, accomplished by STJ pronation (foot appears straight)
ANKLE DORSIFLEXION
-Congenitally or developmentally short gastrocnemius muscle.
-Results in inability to DF ankle joint the 10 degrees w/STJ joint in neutral required for normal gait.
-Made up at the STJ through pronation - foot a loose bag of bones.
LIMB LENGTH
One limb is longer than the opposite. STJ Pronation will shorten the longer limb by flattening the foot.

MUSCLES IN GAIT
BLIX CURVE
-When muscle is at its normal physiologic length or resting length, the muscle is then capable of
developing its maximum tension.
-Normal physiologic length is roughly 50% of the length of the muscle.
ELASTIC RESPONSE
-Muscle as well as ligaments has proprioceptors present to sense the position of the muscle or joint on
which the ligament is working to stabilize.
-These proprioceptors generally are activated in response to stretch placed on the structure they are in.
-When the structure is deformed they activate to return it to its normal shape.
EXAMPLE: Spring Ligmanet: When stretched during pronation or decrease of the medial arch height,
will elicit the elastic response and muscles that supinate the foot will counteract the pronation.
 Foot pronators
prime mover
peroneus longus eversion + plantarflexion
peroneus brevis pure eversion
During gait cycle, pronation of the foot occurs at foot flat and midstance
Foot supinators
prime movers
triceps surae inversion + plantarflexion
medial head of the gastrocnemius
lateral head of the gastrocnemius
soleus
tibialis anterior inversion + dorsiflexion
tibilais posterior pure inversion
During gait cycle, supination of the foot occurs at initial strike and propulsion.

GAIT ANALYSIS
1. HEAD
a. Tilt could mean extraocular muscle problems, scoliosis, spinal DJD, neurological problem
2. SHOULDERS
a. Scoliosis, limb length difference (shoulder will tilt toward shorter side), kyphosis
(slumped forward)
3. ARM SWING
a. One arm wider than other may mean neurological disorder (circumducting)
4. PELVIC & TRUNK ROTATION
a. Increase in one side could mean limb length discrepancy
5. KNEE
a. Knock knees = Genu Valgum w/coxa vara
b. Bow Legged = Genu Varum w/coxa valgum (normal at birth 15-20°)
c. Genu Recturvatum = knees hyperextended >10° in sagittal plane
6. ANGLE & BASE of GAIT
a. Normal angle of gait = 8-15° foot abduction
b. Normal base of gait = 1-1.5r between medial malleoli
7. FOOT
a. STJ viewed through calcaneal position in all phases
i. Start of contact: slight inversion
ii. Contact period: begin seeing eversion
iii. Midstance: inverting on through propulsive period. Reach neutral at end of midstance
b. Look for Abductory twist at toe-off (abnormal)
i. Seen in equinus or foreffot valgus
c. MTJ
i. Midtrsal Joint break occurs at the end of midstance
d. MPJ
i. Propulsive: Flexing of MPJ during propulsion
ii. Apropulsive: No flexing of MPJ during propulsion

RCSP: will be eversion-neutral

NCSP: will be inverted-neutral
BONY ANGLES
FEMUR

TIBIA
Talar tosions:
-normal 25-30°
II Exam Content Outline
205 questions
I. Medicine – 25%
A. Infectious diseases
1. Bacterial
2. Viral
3. Fungal
4. Parasitic
B. Neurology
1. Peripheral neuropathies
2. Central nervous system disorders
C. Cardiovascular medicine
1. Peripheral artery disease
2. Congestive heart failure
3. Murmurs
4. Myocardial infraction
5. Coronary artery disease
6. Lymphedema
D. Rheumatology
1. Myopathies
2. Arthritides (infectious, rheumatoid, osteoarthritis, collagen diseases, seronegative diseases,
and gout)
E. Endocrinology
1. Diabetes mellitus
2. Cushing disease
3. Addison disease
4. Hypothyroid and hyperthyroid disease
5. Osteoporosis
F. Hematology (leukemia and anemias)
G. Immunology (allergic and sensitivity reactions and immunosuppressive states)
H. Pulmonology (asthma, COPD, and emphysema)
I. Behavioral medicine (depression, chemical dependency, abuse, anger disorders, and noncompliant
patients)
J. Emergency medicine (medical/surgical)
K. Dermatology
1. Infections
3. Dermatoses
4. Local and systemic manifestations
5. Tumors
II. Medical Imaging – 20%
A. Radiation protection and safety
1. Radiation physics, biological effects of radiation, operator and patient protection
2. Radiographic technique and development
B. Positioning
 C. Normal radiographic anatomy, anatomical variations, developmental landmarks, and biomechanical
interpretation
D. Radiographic pathology
1. Congenital conditions
2. Infectious disease
3. Arthritic disease
4. Trauma
5. Metabolic disease
6. Neoplastic disease
7. Avascular necrosis
8. Biomechanical interpretation
E. Special imaging modalities (CT scan, MRI, MRA, contrast studies, ultrasonography, and nuclear
imaging)
III. Orthopedics, Biomechanics, and Sports Medicine – 20%
A. Function and structure
1. Osseous system
2. Muscular system
3. Neurologic system
B. Trauma
1. Sprains, strains, and soft tissue injuries
2. Fractures and dislocations
3. Overuse syndrome
4. Compartment syndrome
C. Physical medicine and rehabilitation
D. Pediatric orthopedics (congenital and developmental)
E. Biomechanics and pathomechanics
F. Kinesiology, kinematics, kinetics, and gait analysis
G. Functional devices (footgear, orthoses, bracing/immobilization, and prosthetics)
IV. Anesthesia and Surgery – 28%
A. General anesthesia (types of anesthetics [including pharmacological and clinical properties,
indications, contraindications, and complications] and preoperative assessment)
B. Regional and local anesthesia
1. Spinal anesthesia (including pharmacological and clinical properties – indications,
contraindications, and complications)
2. Regional and local anesthesia (including pharmacological and clinical properties – indications,
contraindications, and complications)
3. Techniques of regional and local anesthesia
C. Intravenous sedation (including pharmacological and clinical properties – indications,
contraindications, complications, and techniques)
D. Surgical principles
1. Wound healing
2. Wound management
3. Perioperative emergencies
4. Surgical hemostasis
5. Surgical anatomy
 6. Biomaterials
7. Fixation
E. Podiatric surgery (indications and procedures)
1. Foot
2. Ankle
3. Lower leg
F. Perioperative management
1. Complications
2. Trauma
3. Infections
4. Systematic disease
G. Hospital and operating room protocol
1. Wound dressing, bandaging, and casting
2. Sterile technique
3. Preparation of the patient
4. Surgical instruments and materials
5. Positioning
H. Pain management
V. Community Health, Jurisprudence, and Research – 7%
A. Medical literature analysis (research design, basic biostatistics, epidemiology, and principles of
evidence-based medicine)
B. Diversity (cultural, age, gender, economic, religious)
C. Disease prevention and control
1. Acute and chronic diseases
2. Universal precautions
3. OSHA regulations
D. Health care management
1. Delivery systems
2. Standards and quality assurance
3. HIPAA
4. Prevention of medical errors
5. Quality improvement
E. Jurisprudence and ethics
1. Doctor-patient relationship
2. Medical-legal issues (assault, negligence, and malpractice)
3. Licensure and scope of practice
4. Controlled substances
5. Statutes of limitations
6. Informed consent
7. Medical records
8. Mandatory reporting
Dermatology
Lichen Planus
Not contagious
Description
Four P’s:
*papule (elevation in skin)
*purple
*polygonal
*pruritic (severe itching)
Papules, flat-topped, 1 to 10 mm, sharply defined, shiny
Violet, with white lines
Distribution:
Predilection for flexural aspects of arms and legs (Wickham’s striae)
In the mouth milky-white reticulated papules; may become erosive and even ulcerate
Pruritus; in the mouth, pain
Therapy:
Topical and systemic glucocorticoids, cyclosporine
Triamicinolone 0.1% cream Disp: 20gm tube Sig: apply to affected area qid

Tinea Pedis
Dermatophytic infection of the feet
Dry scaling soles that are KOH positive for segmented branching hyphae, (-) on woods lamp
Clinical findings
*Erythema, scaling, maceration, and/or bulla formation
*In most cases of epidermal dermatophytosis, the infection occurs initially on the
feet ( T. rubrum ), and, in time, spreads
Synonyms: Athlete’s foot. Jungle rot
Treatment:
Topical Antifungal
Apply to all affected sites twice daily. Treat for 2–4 weeks
Apply bid to involved area optimally for 4 weeks including at least 1 week after lesions have cleared
Apply at least 3 cm beyond advancing margin of lesion
Miconazole 2% solution Disp: 29-57ml sig: apply twice a day

Contact Dermatitis
The spectrum of changes ranges from erythema to vesiculation and caustic burn with
necrosis. Acute ICD represents sharply demarcated erythema and superficial edema,
corresponding to the application site of the toxic substance. Lesions do not spread beyond
the site of contact. In more severe reactions vesicles and blisters arise within the
erythematous lesions, followed by erosions and/or even frank necrosis. No papules.
Configuration often bizarre or linear (“outside job” or dripping effect)
Treatment:
Topical class I glucocorticoid preparations. In severe cases, systemic glucocorticoids may be indicated
Prednisone: 2-week course, 60 mg initially, tapering by steps of 10 mg.
Psoriasis
Elbows and scalp also affected
Description:
Salmon-pink papules and plaques sharply marginated with silvery white
scale. Scales are lamellar loose and easily removed by scratching. Removal of
scale produces minute blood droplets. Lesions are round, oval, polycyclic,
anular, linear, and arranged in arciform, serpingious patterns or scattered
Treatment:
Rx: Topicort 0.25% cream Disp: 60gm tube sig: apply to affected area bid
-Pathogenesis not completely understood, but there are triggers
-Smoking increases the risk of getting psoriasis and also has an impact on the severity. Possible enviromental trigger

Erythrasma
In woods lamp exam: organism is fluorescing a coral red
Clinical findings
*well-demarcated red or tan patches, ± scale
Organism
*most likely is Corynebacterium minutissimum
Treatment
*topical Erythromycin 2% gel Disp one, 30 gram tube Sig. apply a thin layer
to the affected area bid
Prevention
Wear socks with shoes, Clean & dry feet/toes thoroughly, avoid walking barefoot, use antibacterial soaps

Pitted Keratolysis
Smelly feet and heels for several months
Cause: Micrococcus sedentarius, Dermatophilus congolensis,
Corynebacterium
Treatment:
1) Educate patient about limiting the use of occlusive footwear,
changing socks frequently to prevent moisture around the feet, and overall good foot health
2) Rx. Erythromycin topical 2% gel Disp. one, 60g tube Sig. Apply a thin layer to the affected area bid.
3) F/U with the patient. If the condition is not improving, we can try oral erythromycin or even Bactroban.

Palmar Plantar Keratoderma

Fissured hyperkeratosis of heels and hands
Fungal culture is negative and non-segmented hyphae present
Elbows knees and scalp are clear
Treatment:
Start with scalpel debridement to reduce the keratotic masses, and
dispense topical keratolytic agents: 10-20% salicylic acid ointment, corn plasters (20-
40% salicylic acid). 40-60% propylene glycol under overnight occlusion
These conditions are life-long, so continue topical agents used to soften the thickened skin and make them less
noticeable. Also recommend avoidance of walking or prolonged standing if possible
Chronic neurodermatitis
Left foot for 18 months
He rubs his foot with a pumice stone to relieve the itching.
Treatment:
desoximetasone topical (Topicort Emollient Cream 0.25%) Sig: apply bid
Disp: one, 60 gram tube
Toss the pumice stone

Dyshidrotic Eczematous Dermatitis DED

Repeated KOH and fungal cultures have been negative
Description:
*Diffuse hyperkeratotic plaque with fissuring, scaling, and some excoriations. The
lesions appears to be primarily located at the weight bearing portions of the foot
Treatment
*Wet Dressing for vesicular stage: Burow wet dressings. Fissures: topical
application of flexible collodion. Intralesional injection with triamcinolone 3mg/mL
*Ultravate 0.50% Cream Disp: 1 50g tube Sig: apply to all affected areas as directed
by physician twice daily for no more than 2 weeks

Scabies
Management:
*Apply a mite-killing agent like Permethrin (Elimite) to the affected areas and
leave this on over night and then rinse off in the morning. This process is then
repeated in 7 days. This is a good agent of choice being that it is approved for
people 2 months of age and older. Also, an anti-histamine, like Benadryl, can
be taking to help relieve the itching symptoms
Treatment
Elimite 5% Cream Disp: 1 Tube (60 grams) Sig: Apply once at night, sleep with
cream applied, rinse off in the morning. Repeat once more in 7 days

DSLO
Description:
*Thickening and yellowing of distal lateral aspect of right hallux w/subungal hyperkeratosis
& debris. There is a separation of nail plate from nail bed along the distal lateral border
Treatment:
*Debride all onycholytic nail plate saving most proximal portion & swabbing subungal
debris for testing. Perform KOH wet mount prep, fungal culture & a fungal specific PAS stain
Lab
*If the PAS nail clip biopsy is positive we suspect a fungal agent most likely it is Trichophyton species not Tinea
since the fungal culture is negative. Treatment would consist of:
a. debride and remove all of the hyperkeratotic nail bed
b. a RX for a topical antifungal agent like
Disp: Penlac 8% 3.3ml nail lacquer Sig: Apply to affected area once daily and wait 8 hours before bathing
TDO
*You should order a KOH wet mount prep and a PAS special stain along with a fungal culture
*Debride all hyperkeratoic tissue and use a dremel to reduce thickness of the nail plate
Write a prescription for;
Disp: Terbinafine Tablets # 84 Sig: take one tablet daily for 12 weeks

Verrucae
Description:
*Sharply marginated papules and plaques with hyperkeratotic surface on plantar
aspect of right foot sub hallux IPJ, 1st, 2nd,3rd & 4th met heads, and on medial aspect
of 1st MPJ with brown-black central dots; Disrupted skin lines (dermatoglyphics)also
noted; lesions are white with yellowed fibrotic border
Treatment:
*Debridement until pinpoint bleeding;
*Imiquimod 5% cream, Disp 1 box (24packets); Sig: apply 3x/wk to affected area
before bedtime, wash off w/ soap and water after 6-10 hrs

Atopic Eczema
Description:
*Poorly defined erythematous patches, papules and plaques with some scale
and signs of lichenification (thickening and hardening of the skin)
Treatment:
*Cutivate, 0.05% cream; Disp: 60g tube; Sig: apply BID to area for 2 weeks

Candida Intertrigo
Description:
*Confluent, eroded pustules on erythematous base
Treatment:
*Keep area dry; avoid occlusive dressings/wrappings;
*Clotrimazole 1% cream; disp 30g tube; apply BID (am & pm) for 4wks

Venous Stasis Dermatitis

Getting computer access – TWO weeks prior to your start day
- Call 313-966-3053, ensure that your name is on the list of visiting podiatry students
- Fill out the paperwork, 3 pages total, attached at the end of this packet, one has to be faxed over. Follow instructions on
papers, fax number is at the bottom of the page.

Getting your ID badge

- Most likely done on day one of getting here, ask your assigned resident on first day to print out the student ID badge
form with your name on it. $10 at SGH/DRH.

Online Gmail account

- A few days before you begin, you should ask for the password for the online DMC podiatry Gmail account. Here you
will find our day to day schedule, calendar, and other information. Username is dmcpodiatry@[Link]. The password
changes from time to time and so contact us a couple of days prior.

Completing pre-operative paperwork including: consent, H&P, and discharge paperwork, drawing local anesthetics and
placing tourniquet, and pulling gloves and equipment
Coming prepared for cases
Assisting during cases

Each floor has a clean utility room, stuffing your pockets full of supplies and cutting time down on rounds will make you
look prepared! Load up on first day for: kerlix, 4x4s, packing, tape, scissors, cultures, adaptic, betadine, cotton tip
applications, etc. Bring your nail nippers. There are floor consults sometimes for nail care- you are a podiatry student,
nails are part of the foot. Always carry a stethoscope, scissors, pen, paper, etc.

On consults, you should do a full H&P, and also have an assessment and plan in mind to discuss with the resident. Each
floor has a clean utility, so stack up on bandage supplies etc. For in-patients, do a standard SOAP progress note.

Pre-Operative Evaluation: Get to the case at least 30-60 minutes early. Check with the resident, but generally, you can
do the following: H&P, evaluate limb for biomechanical evaluation if appropriate, and mark surgical site. Sign every form
you right on with date and time. Make sure resident co-signs. Make sure resident signs consent and that it is completed
properly.
OR Prep: Common courtesy- introduce yourself to the circulator and scrub tech. Write your name on the white board, as
well as the resident who is scrubbing. Pull gloves for yourself and resident. Ask scrub tech if you can do so. They may
want you to, or they may just want the sizes. Draw the local. Usually 20 cc total in 10 ml syringes of 1% xylocaine plain
and 0.5% marcaine plain. DOUBLE CHECK with THE RESIDENT/ATTENDING to make sure before drawing. Check
the expiration date. Get the tourniquet ready. Webril goes on first. Ask resident what they want it set to.
Post-Operative Note: Help bandage and/or apply cast. Write post-op note (SAPPAHEMIC). Stay with patient until they
are transported to recovery.
Diabetes Mellitus
Normal Glucose Process:

Pathogenesis of Diabetes
In Summary (Wukich 2008)
*Hyperglycemia Protein Glycolysization formation of Sorbitol & Polyols Neurovascular compromise
-Because of this, pts will demonstrate some degree of immune dysfunction, peripheral neuropathy,
nephropathy, retinopathy, retinopathy, and arthropathy

In More Depth (Wukich 2008)

*Hyperglycemia Direct neuronal injury and microvascular damage
-Cellular homeostasis relies on the tight regulation of reactive oxygen species (Nitric Oxide, Hydrogen
Peroxide and such) because they play a crucial role in the normal functioning of the cell and they
are also very sensitive to glycemic control
-If glycemic control is not managed it causes an imbalance and overproduction of harmful levels of
reactive oxygen species. These excessive reactive oxygen species cause damage to cellular
proteins and membrane lipids Thickening of the Basement Membrane
-This allows toxic peroxidation products to accumulate & bind to normal cellular nuclear material leading
to apoptosis, DNA damage, & axonal transport as well as in neurotrophic factors that are
responsible for health & maintenance of normal nerve function Nerve dysfunction
-Vascular Level The vasa nervorum, which supply blood to the nerve for healthy mainentance and
function, loose their ability to function because of the superoxide species accumulation
vasoconstricitioin and nerve ischemia Further Nerve Dysfunction

Impaired wound healing (Key Points)

*Think of increased inflammation (Or being stuck in a prolonged inflammatory phase)
*MMPVs causing an inflammatory soup
-Decreased vascularity
*Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation
*Microangiopathy: Thickened basement membrane Diffusion at capillary level
Again this is the mechanism behind neuropathy, nephropathy and retinopathy
-Overall this leads to a sluggish vasculature and decreased inflow, diffusion, outflow and angiogenesis
*Frykberg (2006) Y You most certainly should read this article to tie everything together
 Type I (Insulin dependent) Type II (Non-Insulin dependent)
Symptoms Abrupt Onset Thirst
Polyuria Pruritus (itch)
Polydipsia (thirst) Fatigue
Polyphagia (hunger) Obesity present in most
Rapid weight loss
Ketosis (¥) Yes
HLA gene association Yes
Islet Cell Antibody Yes
Insulin Secretion Severe deficiency Moderate to hyperinsulinism
Insulin Treatment Always
Insulin Resistance Defect Occasional: poor control excess antibody Usual: receptor
¥: Ketones are formed when glycogen stores in the liver have run out. The ketones are used for energy. Ketones are the fuel created by
the breakdown of fat stores. Ketosis is potentially a serious condition if ketone levels go too high (ketoacidosis).

Diagnosis
Hyperglycemia: fasting plasma glucose level >140mg/dl on more than one occasion
Oral Glucose Tolerance Test: 75g glucose dose dissolved in 300ml water after overnight fast; plasma glucose
>200mg/dl at both 2hrs after glucose water is administered and at least one other time between 0 and 2hrs
Hemoglobin A1c: (glycosylated hemoglobin) normal concentration is 3-6%
Reflection of the mean level of circulating glucose for the previous 2-3 months (RBC life Y 120 days)

Treatment
Diet: cornerstone of treatment. Provide balance if protein, fat and carbs to normalize weight
Oral Hypoglycemics: Sulfonylureas are recommended for patients with symptomatic Type 2 who canVt be controlled by
diet alone and in whom insulin addition is impractical
Insulin: Used for Type 1 who is hypoinsulinemic and prone to ketosis. Also for Type 2 who are not compliant with diet

Complications
Acute Complications
Ketoacidosis:
-When fat is used for fuel instead of glucose due to decreased insulin, byproducts of fat breakdown
(ketones) build up in the body
Triggering factors Characteristics Symptoms Treatment
-infection -pH <7.2 -nausea -fluids
-omission of insulin -hyperventilation -vomiting -bicarb (pH <7.1)
- BUN/Cr ketones in -abdominal pain -K replacement
blood and urine -altered mental status -insulin
-acetone halitosis -phosphate (insulin Vs cellular uptake of
(fruity breath) phosphate and plasma levels)
Hyperosmolar Nonketotic Hyperglycemia
-High blood sugars cause severe dehydration, in osmolarity (relative concentration of solute) and a high
risk of complications, coma, seizures and death
-Glucose >600mg/dl
-Type II
-Tx: fluid, insulin, electrolytes (K and phosphate)
Infection
Increased risk due to triopathy
1. Neuropathy: Compromises antibiosis
2. Vascular Insufficiency
3. Immunopathy: Granulocyte depletion and defective phagocyte ingestion
 Hypoglycemia (glucose <50mg/dl)
-Type I: imbalance between insulin and glucose
-Diagnosis: WhippleRs Triad
1. Risk of hypoglycemia
2. BS <40mg/dl
3. Immediate recurrence following administration of glucose
-Tx: related to cause
-Somogyi Phenomenon: hypoglycemia results in rebound hyperglycemia- may be due to excess
secretion of counter-regulatory hormones (glucagon and epinephrine)

Chronic Complications
Atherosclerosis
Macroangiopathy: plaque
Microangiopathy: increase basement membrane thickening
Ant Tib, Post Tib, and peroneal arteries Causes of Neuropathy: "DANG THERAPIST"
D diabetic
Retinopathy
A alcoholic
Nephropathy N nutritional (Vitamins B6, B12)
Neuropathy (see below under 9Diabetic Foot Ulcer=) G Guillain-Barre syndrome
Treatment: T toxic (lead, arsenic, vinblastine, others)
-Tricyclic Antidepressants = Amitriptyline, Nortriptyline He hereditary
R recurrent
* Binds 5-HT and noradrenaline re-uptake
A amyloid (protein fragments from marrow)
-Anticonvulsants (GABA antag) = Gabapentin, Carbamazapine P porphyria (motor involvement, intermittent)
* Unknown MoA I infections (AIDS, mononucleosis, leprosy)
-Topical = Capsaicin S systemic (CVD, uremia, dysproteinemia)
-Analgesics/Sedatives T tumor (paraneoplastic)

Diabetic Charcot Foot

Pathogenesis Theories
Neurovascular (French)
-Trophic centers in the anterior horn of the spinal cord maintain nutrition to joints Trauma to center
leads to blood flow and osteoclastic activity
-Evidence: Autonomic neuropathy in DM leads to in AV shunting, edema, and skin temp
Neurotraumatic (German)
-Repeated trauma from biomechanical stresses during ambulation on an insensate (w/o sensation) foot
-Evidence: Trauma is the necessary predisposing factor (not underlying bone weakness) to create Charcot
changes in a neuropathic limb

Etiology (anything that causes neuropathy)

Most common causes in order:
1. DM
2. Syringomyelia (longitudinal cavities in spinal cord lined by dense tissue)
3. Tabes Dorsalis (complication of untreated syphilis)

Clinical Findings (presents similar to infection)

Red, Hot, Swollen, Deformed foot +/- pain
Neuropathic
Readily available pulses (bounding)
Radiographic Findings
-Unilateral or bilateral asymmetric
-Typical sites are LisfrancVs or naviculo-cuneiform joint, MTJ, MPJs, IPJs, or ankle joint
-Destruction, density, debris, disorganization, dislocation
-ST welling + MTJ fragmentation + calcified vessels + multiple met fractures +/- infection
-nStep deformityo LisfrancVs dislocation or nCube-footo deformity
-Absent bone and joint spaces
Atrophic (diabetic osteolysis)
Extensive resorption of bone ends
Osteoperosis present, destruction of bone may lead to fractures/dislocations
No osteophytes, sclerosis, fragmentation, or ST debris
Can be mistaken for cellulitis/OM
Hypertrophic
-Osteoarthritis w/a vengeance (like getting a bowling ball dropped on your foot joint disorganization)
-Inflammatory S.T. swelling
-Severe subluxation &/or dislocation
-Marked new bone formation
*Joint space narrowing
*Generalized and marketed bony sclerosis
*Hypertrophic (big) nosteophyteso
-Profound fragmentation
Eichenholtz Classifications
-Based on plain film radiographs (see uptake in all 3 phases on Tc-99 bone scan)
0. High risk pre-Charcot
Radiograph: unremarkable. Maybe increased ST density, bone flecks
Clinical: Sudden onset of non-pitting edema, erythema, calor, +/- pain, bounding pulses
1. Acute/Developmental (destructive phase)
Radiograph: capsular distention, subluxation, osteochondral fragmentation
Clinical: Red, Hot, swollen foot w/joint laxity
2. Coalescence
Radiograph: sclerosis, resorption of debris, fusion of larger fragments to adjacent bone
Clinical: Subjectively decreased red, hot, swollen
3. Reconstruction
Radiograph: Decreased sclerosis, revascularization (why there is bone lysis; increased osteoclasts to the
bone from more blood vessels being there), remodeling of bone and fragments
Clinical: Decreased joint mobility with increased stabilization
Brodsky Classification
Type 1: Lisfranc joint (most common) (¥)
Type 2: Choparts joint and STJ (2nd MC) ( )
Type 3A: Ankle joint
Type 3B: Posterior Calcaneus
Type 4: multiple combos of above
Type 5: Forefoot

Treatment
Acute: Do not perform surgery during acute phase!!
-Immediate NWB and immobilization for 12-16 weeks
-Control edema (Jones cast, ACE inhibitors, Diuretics, Post. Splint, Elevation, Ex Fixation)
-FXR every 4-6 weeks w/few cast changes
Transition: transition to WB (CAM walker, CROW, Bracing, MAFO, Shoes)
Permanent: surgical correction of underlying deformity. Consider TAL, Arthrodesis, wedge osteotomies
Adjunctive: Bisphosphonates (Pamidronate, Alendronate) impair osteoclastic activity

OM vs Charcot (These are general guidelines)

Subjective
OM: constitutional signs and symptoms of infection, infectious risk factors, history of infection
Charcot: uncontrolled DM, history of charcot or recent trauma
Objective
OM: necrosis, pustular drainage, WBC, + bone biopsy
Charcot: Increased joint laxity, non-pitting edema, bounding pulses, rockerbottom feet, - bone biopsy
Imaging
OM is + on bone scans and WBC scans for >24 hrs.
Charcot is only + during first 24 hrs.
 Diabetic Foot Ulcers
*Abnormal pressure distribution secondary to neuropathy
-accentuated by faulty biomechanics/bone distortion and/or poorly fitted shoes
*Secondary to cuts or punctures from foreign bodies
*Prevention is cornerstone to treatment
The pathogenesis of the diabetic foot ulcer can be described via three mechanisms
*Primary cell in PNS,
1) Neuropathy
forms myelin sheaths
-30-50% of diabetics has some form of sensory, motor and/or autonomic neuropathy.
-Sorbitol accumulates in *Schwann cells hyperosmolarity of nerve cells swelling & cellular lysis nerve
signal conduction
Sensory Neuropathy Sensation Tract
*Loss of light touch/protective sensation Touch/protective (5.07 SWMF) Ant. spinothalamic
*Loss of vibratory/proprioception mechanisms Pain/Temperature Lateral spinothalamic
Vibratory/Proprioception Dorsal Column
*Loss of pain/temperature sensation
*The patient has no warning of current, developing or impending trauma
Motor Neuropathy
*Intrinsic Minus foot: intrinsic muscles in foot begin to atrophy leads to 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
*Decreased sweating leads to xerosis and fissuring (portal for infection)
2) Trauma leading to Ulceration
Abnormal anatomy: Extrinsic and intrinsic abnormalities secondary to motor neuropathy and glycosylation
Decreased joint mobility: Secondary to non-enzymatic glycosylation and excess collagen cross-linking of
tendons, ligaments, joint capsules (especially at STJ and MTPJ)
Equinus: Increased cross-linking of collagen in the Achilles tendon
Skin stiffness and weakness: Secondary to glycosylation of keratin
-All lead to increased plantar pressures, which is the driving force behind ulceration
3) Impaired Wound Healing
-Can be thought of as increased inflammation, decreased vasculature and decreased catabolism
Increased Inflammation Time
*Inflammation efficacy Vs due to in leukocyte adhesion & morphologic changes to macrophages
*Prolongation occurs due to decreased chemotaxis of growth factors and cytokines
*MMPs activity & continue to produce an ninflammatory soupo (wound nstucko in inflammatory phase)
Decreased Vasculature
Macroangiopathy: LDL oxidation cause Atherosclerotic obstructive disease of large vessels
Microangiopathy: Thickened basement membrane decreases diffusion at capillary level ( TcPO2)
-Mechanism behind neuropathy, nephropathy and retinopathy
Endothelial dysfunction:
- in NO and prostaglandin in smooth muscle relaxation vasodilation
*Overall leads to a nsluggisho vasculature with inflow, diffusion, outflow and angiogenesis
Decreased Catabolism
* collagen synthesis
*Morphologic changes to keratinocytes (predominant cell type and outermost cells in the epidermis)
Surgical Layers of Dissection Used for Diabetic Ulcer Depth Measurement
1. Skin
2. Superficial Fascia: First Dissection Interval containing superficial neurovascular structures
3. Deep Fascia: Second Dissection Interval containing muscular and deep neurovascular structures
4. Periosteum: Third Dissection Interval
5. Bone

Intercompartmental Communications
Medial Compartment Lateral Compartment Central Compartment
To Central Compartment via: To Central Compartment via: To Medial Compartment via:
-Adductor Hallucis tendon -Long flexor tendon to 5th digit -Adductor Hallucis tendon
-Flexor Hallucis Longus tendon -Short flexor tendon to 5th digit -FHL Tendon
-Peroneus Longus tendon -Lumbrical muscle to 5th digit -PL Tendon
-Neurovascular structures -Plant. interosseous muscle to 5th digit -NV structures penetrating medial IM septum
penetrating the medial IM septum -Peroneus Longus tendon
-Neurovascular structures penetrating To Lateral Compartment via:
To Distal Deep Leg via: lateral IM septum -Long flexor tendon to 5th digit
-Flexor Hallucis Longus tendon -Short flexor tendon to 5th digit
-Lumbrical muscle/tendon to 5th digit
-Plantar interosseous muscle to 5th digit
-PL tendon
-NV structures penetrating lateral IM septum

To Distal Deep Leg via:

-FHL tendon
-FDL tendon

To Dorsum of Foot via:

-Interosseous muscles

Wagner Classification
Wound Classifications 0 Pre-Ulcerative area w/o open lesion
University of Texas Classification 1 Superficial Ulcer (partial/full thickness)
0 No open lesion A No Infection/Ischemia 2 Ulcer deep to tendon, capsule, bone
1 Superficial Wound B Infection present 3 Stage 2 w/abscess, OM, & joint sepsis
2 Deep wound to Tendon/Capsule C Ischemia present 4 Local Gangrene
3 Deep wound to Bone/Joint D Infection & Ischemia 5 Global foot Gangrene

PEDIS Classification (Lipsky, 2004)

*Recommended by Infectious Disease Society of America
*PEDIS (perfusion, extent/size, depth/tissue loss, infection, sensation)
Grade Severity Description
1 Uninfected Lacking purulence (pus) or any manifestations of inflammation
2 Mild * 2 manifestations of inflammation
* Cellulitis/erythema 2cm around the ulcer
* Infection is limited to skin or superficial tissue with no systemic illness
3 Moderate * Infection (as above) in a patient who is systemically well and stable with addition of 1 of the following
characteristics:
Cellulitis extending 2 cm
Lymphangatic streaking spread beneath fascia
Deep tissue abscess
Gangrene
Involvement of tendon or bone
4 Severe * Infection in a patient with systemic toxicity or metabolic instability such as; Fever, chills, tachycardia,
hypotension, confusion, vomiting, leukocytosis
 Work Up of a Diabetic Patient
SUBJECTIVE
CC: Infection should always be in the differential diagnosis with any situation
HPI: (Important to inquire about the following from the patient)
NLDOCAT (nature, location, duration, onset, condition, alleviating or aggravating factors, treatment)
Signs of Infection
Systemic: N/V/D (quantity and quality), fever, chills, SOB, night sweats
Local: pain, erythema, temp, drainage (quantity and quality), odor
Ulcer Specific: Duration, size/depth/color changes, dressing changes, wound care
products, any history of hospitalization for infection, etc.
-It is extremely important to get an antibiotic history from the patient to determine risk factors.
Risk factors for infection due to current or past antibiotic use include:
Antibiotic use in last 6 months
Any fluoroquinolone use
Hospitalization in last 6 months
-Cardinal signs of inflammation:
Rubor (redness)
Calor (heat)
Dolor (pain)
Tumor (swelling)
Functio laesa (loss of function)
Tetanus Status: These seem to be academic questions that are easily missed
NPO status: If it is a severe infection you will be thinking O.R. ASAP
*Most important point here is to make sure you know the order of these things.
PMH:
*Complete DM history including length of ds, previous complications, glucose monitoring schedule,
HbA1c levels, and medications
*Complications of DM w/interventions/treatment: cardiac, vascular, HTN, retinopathy
*Ask about renal and liver disease (antibiotic therapy)
PSH: Previous amputations, foot/ankle surgeries and DM related surgeries
*Although the insulin sliding scale has been taught to us many times (Inzucchi et al) states that sliding
scales arevery inefficient and really for the most part shouldnVt be used, he recommends the following;
Basal rate: (a low rate of continuous insulin supply needed for controlling cellular glucose)
*Lantus or other long acting insulin
*Start 0.2 Y 0.3 Units/kg/day; then 10-20% q1-2 days prn
Prandial Coverage: (mealtime)
*Novolog or other rapid acting insulin
*Start 0.1 Units/kg/day; then adjust 1-2 Units/dose q1-2 days prn

Meds: Drugs, doses, and patient compliance to schedule

All: True allergies and reactions to drugs, food, products, etc
SH: Very important and not to be overlooked
Work: line of work, quantity of WB and ambulation
Diet and exercise
Home support (includes patient compliance & family understanding/education/compliance)
Smoking, alcohol, drug use
FH: Anything applicable.
ROS: Anything applicable.
OBJECTIVE
Vitals
Temp: Hyperthermia is a non-descript sign of infection. Monitor current and max temps regularly
*Armstrong (JFAS 1996 July): 82% of patients admitted for OM were afebrile on admission
Blood Pressure: Hypotension is a sign of sepsis and non-descript measure of infection
Heart Rate: Tachycardia is a sign of sepsis and non-descript measure of infection
Respiratory Rate: Increased respiratory rate is a sign of sepsis and non-descript measure of infection
Pain Level: Important to document (has been deemed the n5th vital signo by JCAHO)
Glucose Levels: Immune system is significantly impaired and essentially not working at 150-175 ml/dL
Vital Signs of Septic Patient
Temperature Usually
Blood Pressure
Heart Rate
Respiratory Rate

Physical Exam
Derm: Use classification system to describe wound characteristics (look above)
*Regardless of classification, you absolutely must document certain wound characteristics:
Base: Exact length, width and depth, consistency (ranging from red/granular to yellow/fibrotic to
black/necrotic. Estimate percentages for mixed bases)

Depth: Probe to bone? [Grayson JAMA 1995. 89% positive predictive value for OM]
Wound Edges: hyperkeratotic, macerated, necrotic, clean, epithelial, Undermining? Tunneling?
Drainage: Serous, sanguineous, purulent (describe color), combination, etc.
Serous: Looks clear or straw colored. Serous drainage supports healing process and
contains protein, electrolytes, white cells and some microorganisms. Platelets and
fibrin appear in the fluid in the first 48 to 72 hours.
Sero-sanguineous: Looks pink due to a small number of blood cells mixing with
serous drainage. Appears normally in the healing of wounds.
Sanguineous: Red drainage from trauma to a blood vessel that may occur with
cleaning of a wound or excessive movement of the individual. The consistency
appears thin and watery. Infrequent finding in a wound.
-Describe any odor (This may be most important variable in infection assessment!)
Periwound skin: Consider normal, erythematic, streaking, stasis changes, trophic changes

Vascular:
*Describe extent (anatomic level) and nature (pitting vs. non-pitting) of any edema
Pulses: DP, PP, PT, Pop, and Fem every time (Always doppler if nonpalpable at each level)
CFT, Pedal Hair
ABI: < .5 Severe arterial disease. Arterial ulcers (no compression bandaging used) and rest pain.
Associated w/ ischemia & problematic healing
.5 - .8 Moderate arterial disease. Mixed ulcers (use reduced compression bandaging) and Intermittent Claudication.
Delayed Healing
1 Normal (compression stocking for venous ulcer if ulcer is present)
Good Healing Potential
>1 Abnormal Vessel hardening from PVD (eg. Calcified Vessels) (venous ulcer full compression sticking)
Good Healing Potential
 TcPO2: (Transcutaneous oxygen tension) determined by blood flow & arterial oxygen tension. A
measurement of tissue perfusion in PVD
>30mmHg good healing potential
<20mmHg microcirculatory problems & delayed healing
Absolute Pressures: Should have 40mmHg at ankle and 20mmHg at digits for healing potential

Neurologic:
Sensory testing:
Sensation Tract
Touch/protective (5.07 SWMF) Ant. spinothalamic
Pain/Temperature Lateral spinothalamic
Vibratory/Proprioception Posterior Column
Motor testing:
-Expect intrinsic weakness w/ neuropathy leading to digital deformities (orthopedic)
-Spinal Reflexes (Achilles, Patellar, Babinski)
Autonomic:
- in skin temperature. Compare B/L (normal around 94° F)
-Lack of sweating leading to xerosis
Orthopedic:
-Document any/all foot deformities, especially osseous prominences
-Overall foot type
-Equinus

Basic Labs:
Complete Blood Count (CBC) with Differential:
Total Leukocyte Count
Neutrophils/Granulocytes (Usually ~54%; increased >85%)
Part of the humoral system
Increased in an inflammatory state
Band cells: Immature neutrophils. Presence indicates active, ongoing infection
A left shift is an increased neutrophil percentage in the presence of band cells
Monocytes (Usually ~6%)
Accumulate after neutrophils in acute infection
Post-inflammatory state or chronic infection hg
Lymphocytes (Usually ~37%)
Produce immunoglobulins and express cellular immunity (T and B cells)
Eosinophils (Usually ~2%)
Allergic and immune responses
Increased with acronym NAACP
(Neoplasm, Allergy, Addison s, Collagen vascular disorder, Parasites)
Basophils (Usually ~0.5%)
Acute allergic responses and histamine release
Leukocytosis: WBC. A leukocyte count indicates an increased level of inflammation, not
necessarily infection. There are many other causes of leukocytosis besides infection:
Drugs: Lithium, Corticosteroids
[Armstrong: Leukocytosis is a poor indicator of acute OM of the foot in DM. JFAS 1996]
Leukopenia: WBC.
Drugs: Methotrexate, Phenybutase, Dilantin, Salicylates
 Chem-7/Metabolic Panel
*Little information about specific infection, but insight into general health of patient:
-Acidosis: Non-descript finding in infection
- BUN: Dehydrated state
Minerals (Ca, Mg, P): good to know for renal function
Glucose, HbA1c:
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.

Advanced Labs:
Erythrocyte Sedimentation Rate (ESR)
Normal: <20mm/hr
Moderate elevation: 20-60mm/hr
Severe elevation: >60mm/hr
*Sensitive, but not specific for infection. Vs in any inflammatory state w/ increased fibrinogen
*Also elevated in: Pregnancy, DM, Malignancy
C-Reactive Protein (CRP)
*Measures a liver protein only present in acute inflammation (not normally found at all)
*Sensitive, but not specific for infection
*Also elevated in: Pregnancy, SLE, Malignancy
Nutrition Analysis
Albumin:
-Is a Transport protein in liver with important functions in catabolism
- Vs with inflammation and malnutrition
Wound Culture and Sensitivity
Swab cultures are easily contaminated by normal cutaneous flora, so should be taken as deeply as
possible without surface contamination. The ideal situation is a deep wound specimen (not just a
swab) following incision and drainage with pulse lavage before beginning antibiotic therapy.
Blood Cultures
*Should be drawn from 2 sites; 20 minutes apart
*Indicates bacteremia/septicemia

Conservative Treatment (Pillars of Wound Care)

-HBO therapy works by increasing the pressure in the blood which forces the oxygen into the plasma instead
which obviates the need of the RBC to carry the blood
-In conjunction with the pillars of wound care one must keep PinzurVs studies in mind *9* Pinzur (1986)
*Are 3 essential elements of healing an amputation in a diabetic & this can be applied for wound healing
-A minimum value of the following are essential for wound healing in diabetics:
*ABI of > 0.50
*Total Lymphocyte Count of 1500
*Serum Albumin > 3.5 g/dL
-Results of his studies are below:
*3 factors present = 92% rate of healing
*2 factors present = 37.5% rate of healing
*1 factor present = 40% rate of healing

The Five Pillars of Wound Care: Look in Peripheral Vascular Disease section
Pharmacology
 Endoscopic Plantar Fasciotomy (EPF)
Background
• Up to the early 90-s, it was thought to be that bone spurs were cause of plantar fasciitis. (1)
• Most procedures involved something in addition to a fasciotomy, like resecting the inferior calcaneal exostosis,
decompressing the first branch of the lateral plantar nerve or denerving the medial calcaneal nerve.
• This led to cadaver work which resulted in the practice of the EPF procedure.

Physical Exam
• Press on plantar aspect of the heel, elicit pain
• Inject heel with corticosteroid. If pain improves, can rule out plantar fasciosis as opposed to fasciitis

X ray Evaluation
• May or may not see a bone spur
• Used to rule out other possible pathologies

Conservative Management
• Stretching
• Boot
• Orthotics
• Steroid Injection

Indication of Procedure
• Failure of previous conservative treatment to work for at least 6 months (2)

Contraindications (3)
• Anticoagulated patients
• Patients with a bleeding disorder
• Patients with osteoporosis.

Pertinent Anatomy to Procedure

• Plantar fascia bands
• Medial calcaneal tubercle (base incision on this)

Incision Site
• Anterior and inferior to medial calcaneal tubercle based on NWB lateral x ray and/or palpation
• 5mm vertical stab incision (some do horizontal incision, but with vertical incisions, you are more likely to
encounter the fascia at variable locations)
• Blunt dissection to plantar fascia
Positioning of patient in OR
• Supine

Basic Description of Procedure performed

• Using small blunt dissecting scissors, separate the subcutaneous fat creating a portal.

• Introduce the fascial elevator into the incision. Advance the elevator across the inferior aspect of the fascia,
tenting the lateral aspect and creating a channel for introduction of the obturator/cannula.

• Introduce the obturator/cannula assembly in a similar manner. Once the tip of the obturator is palpated on the
lateral aspect, make a small vertical incision over the tip so the obturator can pass through the soft tissue.
Remove obturator.
 • Introduce a 4.0mm, 30° beveled scope in the medial portal and the hook blade in the lateral portal. Advance
hook blade medially across the fascia engaging the medial band edge. The double banded cannula marking
represents approximately where the medial fascia release begins and the single marking represents the location
the fascia release should be stopped. Withdraw the hook blade laterally, transecting the medial 1/3 of the
plantar fascia. Release any remaining fascia fibers.

Post Operative Care

• Patients may remove the dressing the next morning after surgery and shower regularly, but are prohibited from
immersing the foot, until one week after sutures are removed. Sutures are removed 10 14 days after surgery.
• Patients should not be on their foot in regular shoes more than 5 minutes per hour during the _rst 4 6 weeks, or
once the fascia has healed. If they require more time on their feet, it is recommend they wear a cast boot.

Potential Complication
• Side effects include erythema, bruising, numbness, tingling, and a tear in the fascia.

Advantages/Disadvantages
• This procedure allows direct visualization of the plantar fascia in an area that is at low risk for nerve entrapment.
• Surgical complications

1) Bergmann, JN. History and mechanical control of heel spur pain. Clin Pod Med Surg. 7:243 259, 1990.
2) Barrett SL, MEHPS: Multiple etiology heel pain syndrome. Oklahoma Podiatric Medical Assoc. Fall 2001 Scientific seminar. Monkey Island,
OK. Oct. 4, 2001.
3) Blake,[Link] et al; T1 61 vs Rohadur in Heel Spur Syndrome, JAPII A 87: 439
Hallux Limitus & Rigidus
Limitus: decreased ROM
Rigidus: Absent ROM, end result of hallux limitus
Normal 1st MPJ ROM:
-65° Dorsiflexion
-20-25° Plantarflexion
-90° total ROM

Etiology
-DF 1st met secondary to abnormal pronation and hypermobile 1st ray
-DF 1st met secondary to muscle imbalance effecting 1st ray
-DF 1st met secondary to sagittal plane structural misalignment of 1st met
-Long 1st met
-Prolonged 1st MTPJ immobilization
-Arthritic conditions of 1st MTPJ from trauma or metabolism
-Iatrogenic secondary to previous surgery

X-Ray Evaluation:
AP view:
-Asymmetrical joint space narrowing
-Spurring around sides
-Met head squaring
Lateral view:
-Dorsal flag sign
-Met primus elevates (prox phalanx articulates with the plantar aspect of 1st met head)
-Sclerosis
Seiburg Index
The distance between the cortices of the first and second metatarsals,
first at the distal neck of the bones and then 1.5 cm from the first
metarsal base

Structural vs Functional HL
-Moving joint when standing is functional HL
Functional: hallux DF decreases only when the forefoot is loaded. Responds well to orthotics with foot in neutral
and allowing the hallux to dorsiflex
Structural: Hallux DF decreases whether forefoot is loaded or unloaded. Orthotics does not help

Signs:
Pain on dorsum of 1st MPJ
Plantar callus of IPJ due to hyperextension of the IPJ

Treatment Goals:
-remove spurs
-create slack for flexor apparatus
-plantarflexion of elevated 1st met
Classification of Hallux Rigidus: Staging of Joint Pathology Based on Degree of Arthrosis

Stage I: Stage of Functional Limitus

• Hallux equinus/flexus
W Plantar subluxation proximal phalanx
W Metatarsus primus elevatus
W Joint dorsiflexion may be normal with non-weight bearing, but
ground reactive forces elevate the first metatarsal and yield limitation
W No degenerative joint changes noted radiographically
W Hyperextension of the hallucal interphalangeal joint
W Pronatory architecture

Stage II: Stage of Joint Adaptation

• Flattening of the first metatarsal head
W Osteochondral defect/lesion
W Cartilage fibrillation and erosion
W Pain on end ROM
W Passive ROM may be limited
W Small dorsal exostosis (new bone formation)
W Subchondral eburnation (Degeneration of bone into a hard, ivorylike
mass)
W Periarticular lipping of the proximal phalanx, the first metatarsal
head, and the individual sesamoids

Stage III: Stage of Established Arthrosis

• Severe flattening of the first metatarsal head
W Osteophytosis, particularly dorsally
W Asymmetric narrowing of the joint space
W Degeneration of articular cartilage
W Erosions, excoriations
W Crepitus
W Subchondral cysts
W Pain on full ROM
W Associated inflammatory joint flares
Stage IV: Stage of Ankylosis
• Obliteration of joint space
W Osteophytosis with loose bodies within the joint capsule
W <10° ROM
W Deformity and/or malalignment
W Total ankylosis may occur
W Inflammatory joint flares possible
W Local pain is most likely secondary to skin irritation or bursitis
caused by the underlying osteophytosis

Joint Preserving
Cheilectomy = Bonney-Kessel Waterman
*For Peripheral Osteophyytosis *For Hallux Equinus *For Hallux Equinus
*Modification: valenti (v-cheilectomy) *Dorsiflexory osteotomy of base of *Dorsiflexory osteotomy of 1st met head
*Dorsal Bumpectomy proximal phalanx *osteotomy .5cm prox to articular
Advantage: Advantage: cartilage, converting PF ROM to DF ROM
-allows for ROM sometimes -hallux is in dorsal position in Disadvantage:
-immediate post-op ambulation propulsive phase of gait -no etiology correction
Disadvantage: Disadvantages: *Modification (Green Waterman): DF
-potential capsulodesis -doesn_t increase ROM wedge osteotomy of 1st met head leaving
-no etiology correction -no etiology correction plantar articular cartilage intact

Lambernudi -Mitchell, Youngswick, &

*PF wedge osteotomy of base of 1st met. Sagital Z
*Corrects Met Elevatus -shortens and PF_s 1st met
Advantage: -Increases 1st ray ROM
-correction of structurally DF_ed 1st met
-Increase overall 1st MPJ ROM
 Joint Destructive
Keller Arthroplasty Implant Arthroplasty McKeever Arthrodesis
*Resection of 1/3 of base of proximal *Total or Hemi-Implant *Fusion of 1st met prox phalanx
phalanx *Can include proximal plantarflexory Advantage:
Advantage: osteotomy -eliminate joint pain
-eliminate joint pain, increase ROM -significant internal 1st ray stability
Disadvantage: Disadvantage:
-creates instability in 1st ray -elimination of all 1st MTPJ motion
-no etiology correction -restricts type of shoe you can wear

Lapidus Arthrodesis
*Fusion of 1st met med-cuneiform joint
*For pain or hypermobility at met-
cuneiform joint
Advantage:
-eliminate joint pain
-significant internal 1st ray stability
Disadvantage:
-elimination of all 1st MTPJ motion
-restricts type of shoe you can wear
Internal Fixation
4 Principles of IF:
1) Anatomical Reduction
2) Rigid Internal Fixation
3) Atraumatic Technique on soft tissue and bone
4) Early active pain free range of Motion during first 10 post op days

Bone Histology
Osteoblasts: produce bone matrix, & are trapped when bone calcifies. (Osteocytes: trapped osteoblasts)
Osteoclasts: bone resorption

Bone Healing
Three phases
1. Inflammatory phase (3-7days)
2. Reparative phase (4-6 weeks)
3. Remodeling phase (up to 2 years)
Primary Bone Healing: Contact healing (NO callus)
Two requirements:
1. Intact vascular supply to bone
2. RIGID fixation to the fragments
This process (PBH) is limited to gaps of 2-4 mm.
PBH does not lead to faster healing but rather to healing without excessive bone formation.
Secondary Bone Healing: Gap healing and callus formation, AKA- indirect osseous repair
Immobilization is the key to all bone healing
Revascularization occurs from 3 areas.
1) capillaries from periosteal tissue
2) capillaries from endosteal tissues
3) blood supplied by neighboring tissues
-This process increases O2 to the area allowing osteoprogenitor cells to lay down osteoid
(calcium hydroxyapatite) and callus is now seen on radiograph
Summary:
Movement = secondary bone healing = callus
Rigid fixation = primary bone healing = no callus
Screw
Cortical screws: smaller pitch, threaded their entire length greater # of threads come
in contact with thicker cortical bone. Sizes: 1.5, 2.0, 2.7, 3.5, 4.5

Cancellous screws: larger pitch, allows for more contact with less dense bone

Herbert Screw: Has threads on both ends, no head. Wider at one end to push bone
towards fracture site- other end is less wide to pull bone towards fracture site.

Absorbable Screw: Natural or Synthetic. They are based on alpha-hydroxy acids such as L-lactic acid,
glycolic acid, and para-diaxonone. Lasts 6-8 weeks.

Parts:
Land: Increases surface contact between screw and bone. Reduces chance of stress risers
Thread Diameter: This value is used to describe the screw size (eg: 3.0mm, 4.0mm)
Runout: junction where the shaft meets the threads- weakest point of the screw
Tip:
-Rounded: requires tapping
-Pointed and fluted: self-tapping
Lag Technique: (for a cortical bone screw: this example is for 2.7mm screw)
1) Under drill thread hole (2.0mm drill bit) near and far cortex
2) Counter sink
3) Over drill glide hole (2.7 mm drill bit) near cortex only (not needed in cancellous screw)
4) Measure
5) Tap (2.7mm) 3 reasons to countersink
6) Flush 1. uniform compressoin
7) Insert 2.7mm screw (2 finger tightness) 2. dec. stress risers (microfractures)
Lag by Design 3. clearance (so pt. doesnt feel it)
Same as above but use a screw with shank and donbt need to over-drill
*If you see a radiograph with black around the screw, the screw has been moving around. Want to see
white all the way around the screw

Kirschner Wires (K-wires)

Can be permanent or temporary. Threaded wires provide more stable purchase but are harder to remove
Sizes: .028, .035, .045, .062 inches

Steinman Pins
Larger than K-wires. Measured in 64ths: Sizes-8/64 or 1/8, 7/64, 6/64, etc.

K-wires and Steinman pins: DO NOT PROVIDE INTERFRAGMENTARY COMPRESSION, THEY CAN
MAINTAIN COMPRESSION, BUT AGAIN- THEY DO NOT PROVIDE COMPRESSION.
Monofilament Wire
Malleable steel
Provides interfragmentary compression
Measured in gauges
Cerclage fashion: circling around bone
Interfrag fashion: Always pull on proximal fragment. Most stable
Box-Wire fashion:

Tension Band Wiring

-Combines K-wires with monofilament wire
-K-wires placed parallel across fracture or osteotomy site and a figure 8 with the
monofilament wire is used around the pins.
-26 and 28 are common in Podiatry

Plates
Allow early passive ROM
6-8 cortices of purchase are needed above and below the fracture
Specific Plate Designs- semi tubular 1/3 tubular, 1/4tubular, T-and L-plates
Categorized on basis of function: Neutralization, Compression, Buttress and Bridge plates

Neutralization Plate
-Used with interfrag screw and shields the screw from torsional
or bending forces
-Guard against torsion and bend

Compression Plate
-Amount of compression depends on overall design, technique of application, and site of
application of these plates.
-Site of application: PLACE ON THE SIDE OF TENSION, THUS CREATING
COMPRESSION ACROSS FRACTURE SITE.
Technique of application;
-Offset drilling (load screw technique) technique can
provide compression (leave gap between middle 2 screws
and gap will close as you tighten)
-Holes closest to the fracture site are used first
-Only the first two screws are load screws.
-If more screws are used you may need to pre-bend the plate

The holes in the plate have sloped edges on the side of the hole distal from
the fracture. A screw can be inserted in the hole at the end close to the
fracture. This will lock the plate to the bone without moving the bone with
respect to the plate. This screw is inserted first. The screws on the left side of
the plate are inserted at the far end of the hole with the shank of the screw
touching the far end of the hole as shown in the top figure. As the screw is
inserted, the head will be forced to the right by the slope in the hole, moving
the bone and its attached screw toward the fracture compressing it as shown
in the bottom plate.
 Dynamic Compression Plate
-Incorporates the load screw technique in its design. The holes are cut oblong
-Problem with DCP is it impedes periosteal blood flow. This led to the
Limited Contact DCP, it is contoured and grooved on its underside to
decrease contact with the bone

Buttress Plate (anti-glide plate)

It is anchored to the main stable fragment but not necessarily to
the fragment itbs supporting. It supports load bearing bone.
Sometimes called an anti-glide plate

Bridge Plate
Used to span a comminuted unstable fracture

Plate Application Problems

Can impair vascular supply to bone, this decreases bone healing.
Compression forces can lead to Plate Associated Osteoporosis.
Plate irritation
Immune response (nickel)
Bone refracture after screw removal

Staples
Donbt use if cortical bone is greater than 2-3mm; may cause cortical fxbs or not seat in bone properly.

Soft Tissue Anchors

-Used for attachment or re-attachment of ligaments or tendons into bone
-Implantable devices with attached suture incorporated. Normally absorbable -2.0 suture. Takes about 4-
6 weeks for tenodesis to take place
-Complications
Ruptures
Improper placement
Failure to suture
Pullout of the anchor from bone
Infection
Lesser Met Pathologies
Joint Anatomy:
DTML attaches capsule to plantar plate (flexor plate) which absorbs shock and stabilizes

Musculature Function of Toes:

Extensors: dorsiflex MPJ, passive flexion at PIPJ/DIPJ
Flexors: actively plantarflex MPJ, PIPJ, DIPJ
Interossei: prevent buckling
Lumbricales: hold digits rectus (plantarflex MPJ, dorsiflex PIPJ/DIPJ)

Contracted Digit Etiology

Flexor Stabilization (most common)
Weak Intrinsic Interossei Quadratus Plantae advantage Pronated foot type (flexors fire longer
and harder in early gait, overpower Interossei) adducto varus deformity on 4th and 5th
Tx: derotational arthroplasty
Flexor Substitution (least common)
Triceps Surae weakness (flexors & TP gain mechanical advantage over extensors) Supinated foot
type in late stance phase of gait
Tx: suture FDL to Achilles tendon to strengthen muscle (must perform arthrodesis)
Extensor Substitution
Weak Tibialis Anterior (extensor gains mechanical advantage over lumbricals) Becomes rigid
(reduce early with weight bearing) Pes cavus/ equinas/ TA weakness swing phase abnormality
-deformity is demonstrated by having patient DF ankle in non-weight bearing situation
Tx: Arthrodesis if rigid, Hibbs tenosuspension if flexible (transferring EDL to metatarsal head or base)

See RGun BarrelT sign on radiograph

 Hammertoes
Shoes can cause deformity (especially on long second toe)
May see heloma on PIPJ and DIPJ
Hammertoe Sequential Reduction
1) Z-Plasty
2) Arthroplasty
3) Extensor Hood Release
4) MPJ Capsulotomy
5) Volar Plate Release
6) Tendon Transfer (Girdlestone, Kuwanda and Dockery, Hibbs)
*Kelikian Push-Up Test: do between each step. If DF occurs with GRF on met
head, proceed to next step

Soft Tissue Hammertoe surgical procedures

Tenotomy: stab incision medial or lateral to tendon deformity and proximal to
MPJ using No. 15 scalpel blade or No. 57 beaver blade.
-PF digit w/blade in place to sever tendon
Girdlestone
Capsulotomy
Tendon Transfer
Girdlestone: Transfer FDL and FDB to dorsal head of proximal phalanx to restore intrinsic function
Hibbs: Transfer EDL to base of proximal phalanx or met head
Kuwada & Dockery: Modified Girdlestone (drill hole in prox phalanx base & bring tendons through)
Lengthening: Z-Plasty at level of MPJ
Percutaneous stab incision and splint
*Complications: muscle spasm caused by overcorrection,
tenosynovitis, scarring, adhesion, nerve entrapment,
bowstringing
Osseous Hammertoe surgical procedures
Arthroplasty
Post: resection of base of proximal phalanx
Gotch & Kreuz: resect base of prox phalanx and syndactylize digits
Arthrodesis (high amount of shortening)
Lambrinudi: fusion of PIPJcs and DIPJcs
Young-Thompson: Peg-in-Hole Fusion (peg from prox phalanx)
Taylor: PIPJ fusion using K-wire

Claw Toe
Usually associated with cavus foot
Early Stage: may be flexible and straighten out with the push-up test
Late Stage: IP joints will flex when metatarsals are loaded

Mallet Toe
Associated with a long digit
Surgical correction: resection of head of middle phalanx
May need to release plantar contracture via tenotomy and capsultomy
 Floating Toe
-One or more toes fail to purchase weight bearing surface in stance phase from failed flexor mechanism
-Important is the loss of the internal cubic content from within MTP joint (this occurs with plantar
condylectomies, met head resection, and proximal phalangeal base resection)
-Correction is aimed at cause of floating toe. Eg:
*brachymetatarsia (short toe) lengthen the met
*base of prox phalanx resection syndactaly (see below)
-Syndactylization:
*Fusing together of 2 or more digits
*salvage procedure secondary to prior surgery (eg: prox base phalanx resection floating toe)
*3rd and 4th toe syndactilization is contraindicated since these digits lie between the lateral and
medial columns (thus 2nd toe is syndactylized to 3rd and 4th to 5th)
-V-Y Flap Advancement
*salvage procedure for iatrogenic floating toe

Nail Procedures

Rosenthal Classification, Nail Injuries

Zone 1: Distal to phalanx
Tx: w/o bony exposure, let granulate if <1cm, graft if >1cm
Zone 2: Distal to Lunula
Zone 3: Proximal to Lunula

Martixectomies
Basic
1) Ingrown nail border freed with spatula
2) English anvil splitter used to split offending edge
3) Matrix, nail bed, and posterior nail fold is curetted (imp step if using phenol to clear all debris)
4) Apply phenol on cotton swab for 30s 3xcs (follow with alcohol swab)
Winograd
-.25T of the edge of the nail along with matrix and nail bed is removed and
curetted. Strip of nail fold is removed

Frost
-Modification of Winograd
-Use transverse incision for better visibilty of underlying matrix

Terminal Syme
-Most radical procedure for dystrophic nails
-Remove entire nail, wall, and matrix
-Close defect with plantar skin flap after resecting distal half of distal phalanx
-Disadvantages: shortens toe, potential slough, bulbous at terminal stub

Zadik
-Removes nail matrix and nail without shortening distal phalanx
-Eponychium is excised and skin flap is advanced and sutured
-Donct do in vascular compromised or DM patients
-The flap is advanced and sutured to the nail bed without tension. As with certain other total nail
ablation procedures, nail bed resection is directed proximally and the nail bed distal to the lunula
is undisturbed
PERI-OPERATIVE MANAGEMENT
Malignant Hyperthermia (Peri-operative Fever)
Susceptible Patients Triggering Agents Signs/Symptoms Treatment
*elevated CPK pre-op *anesthetics (inhaled agents such *arrhythmia = 1st sign *Stop Anesthesia
(creatine phosphokinase) as halothane, enflurane) *masseter muscle spasm *change anesthetic tubing
(occurs in 70% of *neuromuscular blockers *rapid rise in temp *hyperventilate w/100% O2
susceptible patients) (succinylcholine) *acidosis (metabolic and *correct acidosis (Sodium
*family history (dominant *stress respiratory) bicarbonate)
inheritance) of anesthesia *dark, mottled skin *cool patient (pack w/ice)
problems *Dantrolene Na (Dantrium)
*EKG abnormalities
Dantrolene: skeletal muscle relaxant that prevents release of calcium
-intraoperative crisis: 1 mg/kg IV push & continue until symptoms subside or 10 mg/kg max is reached
-postoperative crisis: 4-8 mg/kg po (by mouth) in four divided doses over 1-3 days
-preoperative prophylaxis: same as postop but with last dose 3-4 hours before surgery

M. Hyperthermia: Induced by anesthetics or catecholamineUs produced by stress. Normally sarcoplasmic reticulum releases Ca++
into sarcoplasm for muscle contraction. To relax muscle, sarcoplasmic reticulum must reabsorb the Ca++ from sarcoplasm. In M.
Hyperthermia, the Ca++ canUt be reabsorbed by sarcoplasmic reticulum. This increases Ca++ concentration inside the cell, activating
metabolic reactions and leading to malignant hyperthermia. Dantrolene prevents Ca++ release from sarcoplasmic reticulum.

Diabetic Patient
*Give early morning surgical preference
-If surgery is delayed: start D5W IV (5% dextrose in water; 1 liter = 50gm carbUs. Pt needs 100gm/day) to avoid
hypoglycemia
-Hypoglycemia: causes organic brain damage and death (Better Sweet than Sour)
*Check pre-op potassium levels as insulin reduces serum potassium
*HbA1C (glycosylated hemoglobin): 3-6% (high # is Not reason to postpone surgery)
*Pt with severe autonomic neuropathy (can result in tachycardia and orthostatic hypotension): has increased incidence
of gastroparesis (delayed gastric emptying) and aspiration, increasing chance of sudden death

University of Washington Medical Consult Handbook

-Want plasma glucose between 150-250mg/dL
-On the day of surgery, the patient should begin fasting at midnight.
-One may administer D5W or D5 1/2NS unless the blood glucose level is >200 mg/dL. In these cases, the surgeon
can usually administer normal saline instead if there are no contraindications
-Remind patients to check fingerstick glucose levels before every meal and at bedtime
-Perioperative Steps for Type II diabetic w/controlled diet and oral hypoglycemics
*Do not take oral medication the morning of surgery
-Perioperative Steps for patient’s w/type 1 or 2 diabetes requiring multiple daily insulin injections
*Withhold all scheduled fast- or very fast-acting insulin.
*Cut intermediate or long-acting insulin in half.

*Avoid post-op hyperglycemia. BS >250 inhibits phagocytosis, leading to an in postop infections (esp. gram -)
Post-op BS levels managed as follows:
-150-199: 2 units -300-349: 8 units
-200-249: 4 units -350-399: 10 units
-250-299: 6 units ->400: 12 units
 Hypertensive Patient
*Mild to moderate HTN is not a significant risk if diastolic is <110mmHg
-If BP >160/90, postpone surgery until itUs under control
*Do NOT discontinue HTN meds, except Guanethidine (take at 6am for morning surgery)
*Get K+ levels on pts on diuretics. If K+ <3.5, replace before surgery
*If pt is Hypertensive post-op, treat causing factor, and if necessary, give one of the following:
-Procardia
-IV diuretic *Do NOT give Epinephrine to these patients (vessopressor)
-Nitroprusside or Nitroglycerine
Congestive Heart Failure Pt
-Swan-Ganz monitoring: essential if undergoing emergency surgery

Steroid Therapy Patient

Steroid Uses:
-Asthma, COPD
*For asthmatic: consider spinal or local anesthesia and continue asthma meds until 90min before surgery
-Autoimmune ds (RA)
-Malignancy
Three areas Steroids effects in Peri-operative setting:
1. Hypothalamus/Pituitary adrenal axis suppression (occurs if pt took >7.5mg/day for a week before surgery)*
2. Poor wound healing
3. Predisposition to infection
*if pt has taken >7.5mg/day, steroids must be supplied perioperatively to avoid Hypotension & Cardiovascular Collapse
-Minor procedures: Hydrocortisone IV @ 100mg evening before surgery, 100mg prior to procedure, and 100mg
Q8h for 24 hours
-Major procedures: same as above, except Q8h continues until stress of post-op period has passed

Patient on Anticoagulants
Indications for Anti-coagulants
1. Perioperative prophylaxis for DVT prevention
-Stop anticoagulants 3-6 days before surgery and reinstate post-op 24 hours after procedure
2. Ischemic heart ds
3. Atrial Fib Coagulation Factors
4. Mitral Stenosis and Prosthetic Heart valves Extrinsic path: 3, 7
Heparin Type Intrinsic path: 8, 9, 11, 12
Requiring vit K: 2, 7, 9, 10
-Inhibits intrinsic pathway
-Short term Therapy for prophylaxis against DVTUs
*5,000u subq 2hr before surgery & 5,000u subq Q 12h until pt is ambulatory
-Dosage regulated according to PTT levels (when used as treatment)
-Reversed by Protamine
Coumadin Type
-Inhibits extrinsic pathway
-Long term Therapy
-Dosage regulated according to PT levels
-Reversed by Vitamin K, or fresh frozen plasma
 Patient w/Clotting Abnormalities
Drugs that alter platelet function
-Aspirin (Bleeding Time is especially useful since Aspirin stops platelet aggregation)
*must stop Aspirin 1 week prior to surgery
-NSAIDS
-Steroids
-Antihistamines
-High doses of Penicillin
-Heparin
Bleeding Diseases
VonWillebrands: abnormal Factor VIII, prolonged PTT and bleeding time
Tx: Fresh Frozen Plasma
Hemophilia: prolonged PTT, but normal bleeding time
-Hemophilia A: factor 8 deficiency
-Hemophilia B (Christmas ds): factor 9 deficiency
-pt must achieve a level of 70-100% prior to surgery
Tx: Fresh Frozen Plasma, Cryoprecipitate
Vitamin K Deficiency: effects intrinsic and extrinsic pathUs. PTT and PT prolonged
Tx: 10mg of vitamin K subq. Normalizes pt in 8hrs

Rheumatoid Patient
Do cervical spine X-ray pre-op
-predisposed to atlas/axis dislocation
Patient on steroidUs: follow above protocol
Patient on Non-steroidal: discontinue perioperative bc it alters bleeding time
Patient on Immunosuppressive: consider preoperative antibiotics

Sickle Cell Patient (hemoglobin S disease)

Sickle Cell
-mutation in -chain results in amino acid change from glutamic acid to valine
-Diagnosis:
*Hemoglobin electrophoresis shows presence of hemoglobin S
-Signs and Symptoms:
*long bone pain
*avascular necrosis of femoral head
*chronic punched out lesions around the ankles
-Aplastic Crisis: during acute infections (especially viral), RBC marrow production slows
-Painful Crisis: Severe abdominal pain w/vomiting accompanied by back and joint pain
Respiratory depression
-Avoid with narcotics and sedatives
Hypoxia
-These patients are prone to hypoxia due to decreased oxygen carrying capacity
-Avoid hypoxia w/ Local Anesthetic
-Avoid tourniquet use
 Gouty Arthritis Patient
Important bc trauma of a surgical procedure can precipitate an acute attack of gouty arthritis
High risk patient: (one or more of the following)
Colchicine inhibits microtubule polymerization by binding to tubulin
1. Attack in past year Allopurinol is a xanthine oxidase inhibitor
2. Marked relief after a test course of colchicine -does not alleviate acute attacks of gout
3. Documented need for anti-hyperuricemic medication
Tx: Give 0.5mg Colchicine 3x/day for 2-3 days prior to operation and 4-5 days postoperatively
-Give Allopurinol if pt is excreting >600mg of uric acid in 24 hours
Moderate risk patient: (one or more of the following)
1. Prior episodes of an acute monarthritis clinically resembling gout.
2. A diagnosis of gout made by history, clinical observation, and the presence of hyperuricemia during the acute
episode, but not documented by a joint aspiration.
3. Prior symptomatic relief during a bout of monarthritis from use of a nonsteroidal anti-inflammatory
medication such as indomethacin.
Tx: Give Colchicine prophylactically as in high risk patient
Low risk patient: (one or more of the following)
1. Asymptomatic primary hyperuricemia.
2. Asymptomatic hyperuricemia secondary to some other medical condition or drug reaction.
Tx: none needed

Cardiac Patient
Recent MI: due to high mortality rates, surgery should be postponed at least 6 months
Old MI: if evidence of old MI is found on ECG w/o chest pain, obtain previous ECG to compare
Peripheral Vascular Diseases

VESSEL LAYERS

VIRCHOW’S TRIAD
 NON-INVASSIVE VASCULAR STUDIES
Serial Pressures (Wound Healing Pressures in Diabetics)
>55mmHg: Healing
45-55mmHg: Range of Uncertainty
<45mmHg: No wound healing
-At least 30mmHg required for healing of a wound on digits

Ankle/Brachial Index (Ischemic Index)

Ankle Systolic Pressure:
1) Put BP cuff above ankle & inflate until PT pulse canLt be felt with Doppler
2) Deflate cuff. Point at which arterial sound returns is systolic pressure
3) Repeat on DP and Peroneal arteries
4) Highest of three is used as ankle systolic pressure

Index Values: Divide ankle systolic by arm systolic

< .5 Severe arterial disease. Arterial ulcers (no compression bandaging used) and rest pain

.5 - .8 Moderate arterial disease. Mixed ulcers (use reduced compression bandaging) and
Intermittent Claudication
1 Normal (compression stocking for venous ulcer if ulcer is present)

>1 Abnormal Vessel hardening from PVD (eg. Calcified Vessels) (venous ulcer full
compression sticking)

Doppler Ultrasound
-Hold the probe at +/- 45°.
Triphasic: (Sharp, high pitch sound) systolic, diastolic and the elastic vessel wall recoil.
Biphasic: the recoil sound is lost.
Monophasic: (long XswishingY sound) Peripheral Vascular Disease (PVD). Can also be small vessels since the
blood flow is too smooth for backflow at this level

Buerger’s Elevation-Dependency Test

1) Elevate legs above heart for at least 30 seconds
2) Evaluate color on soles of the feet and grade 1-4 [1= no pallor in leg (normal); +4 = marked pallor]
3) Check for rubor of dependency. Sit the patient upright and observe the feet
*Feet quickly turn pink normal.
*Feet fill more slowly and they turn red like a cooked lobster Ischemia.
4) Evaluate together
*If thereLs pallor, but no erythema, occlusive disease is severe.
Exercise Test
1) Take pedal BP w/foot at heart level
2) Elevate leg to 30° and against slight resistance, dorsiflex and plantarflex for 1 minute
3) Return leg to heart level and record pedal BPLs again every 30 seconds for 2 minutes
4) Interpret results
-If ankle pressure drops >20% & doesnLt return to normal in 2 minutes, thereLs arterial occlusion. This is
because blood going into foot is diverted to exercising calf muscles where thereLs less resistance to flow

5 Minute Reactive Hyperemic Test

-Used to differentiate vasospastic from organic disease
1) Patient placed prone and foot is raised 30°
2) Foot is dorsiflexed and plantarflexed to empty venous blood
3) Inflate ankle cuff 100mmHg above ankle systolic pressure
4) Place foot at heart level and deflate after 5 minutes
5) Time interval between cuff let down and color returning to foot
Vasospastic Ds: Return of color is uniform, but delayed (5-8s) (especially to toes). Max erythema (redness)
takes about 2 minutes
*blood flow is limited by increased tone of smooth muscles surrounding the blood vessels
Organic Occlusive Ds: Return of color is Not uniform and requires >15s to reach toes. Max erythema takes >2
minutes and is lighter than normal
*material is clogging the lumen of the vessels

Perthes Test
Clinical test for assessing the patency of the deep femoral vein prior to varicose vein surgery
1) Elevate limb w/elastic bandage from toes to the upper 1/3 of the thigh to obliterate the superficial veins only.
2) With the bandage applied the patient is asked to walk for 5 minutes.
3) Results :
a. If deep system is competent, the blood will go through and back to the heart.
b. If the deep system is incompetent, the patient will feel pain in the leg.
Modified Perthes test
Apply tourniquet at sapheno-femoral junction to occlude the superficial pathway, and then ask
patient to move in situ. If the deep veins are occluded, the dilated veins increase in prominence
and pain occurs. This is a better test as it does not depend on patient's pain threshold.

Trendelenburg’s Maneuver
Determines the competency of the valves in the superficial and deep veins of the legs in patients with varicose veins
1) Patient in the supine position the leg is flexed at the hip and raised above heart level until the veins empty
2) Tourniquet is put around the upper thigh to compress superficial veins but not deep veins (30-60mmHg)
3) The leg is then lowered by asking the patient to stand.
4) Results:
a. Normal: Superficial saphenous vein fills from below in 3 to 5s as blood from capillaries reach the veins
b. If superficial veins fill more rapidly with the tourniquet in place there is valve incompetence below the
level of the tourniquet in the "deep" or "communicating" veins
c. After 20 seconds, if there is no rapid filling, the tourniquet is released. If there is sudden filling at this
point it indicates that the communicating veins are competent but the superficial veins are incompetent.
 STAGES OF ARTERIAL OCCLUSION
Intermittent Claudication
-Due to arteries inability to meet metabolic demands of exercising muscle
-B/L pain (usually in the calf) after walking
-Pain is relieved with rest and reoccurs with resuming of activity (Intermittent)
-Tx: Exercise or Angioplasty (mechanically widening narrowed or obstructed arteries)
Rest Pain
-As occlusion worsens, blood supply becomes insufficient for resting muscle
-Pain with rest (worst at night) (Night pain relieved by walking indicates venous problem)
-Tx: Dangle legs off bed to drain more blood into legs
Gangrene
-Death of tissue due to loss of vascular supply
Dry:
*Gradually onset as a result of occlusion of blood supply (usually arterial)
*Not usually associated with bacterial infection (bacteria fail to survive)
*A form of coagulative necrosis
*The affected part is dry, shrunken and dark reddish-black
*Dark coloration: liberation of hemoglobin from hemolyzed red blood
cells, acted upon by hydrogen sulfide produced by the bacteria,
formation of black iron sulfide that remains in the tissues
Wet:
*Result of sudden stoppage of blood (burns, freezing, embolism) w/subsequent bacterial infection
*Tissue is infected by saprogenic microorganisms (eg. Clostridium perfringens or Bacillus fusiformis)
which cause tissue to swell and emit a fetid smell
*Develops rapidly due to blockage of venous (mainly) and/or arterial blood flow
*Wet gangrene is coagulative necrosis progressing to liquefactive necrosis
Gas:
*Is a deadly form of gangrene caused by exotoxin (usually C. perfringens) found in soil
*Infection spreads rapidly as gases produced by bacteria expand and infiltrate healthy tissue
*Because of its ability to spread quickly, it should be treated as a medical emergency
*Can cause necrosis, gas production, and sepsis. Progression to toxemia and shock is often very rapid
 ARTERIAL INSUFFICEINCY
Arteriosclerosis is any hardening (and loss of elasticity) of medium or large arteries;
Arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries);
Atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque

ARTERIOSCLEROSIS
Arteriosclerosis Obliterans
Proliferation of the intima of the small vessels has caused complete obliteration of the lumen of the artery.
Signs/Symptoms Diagnosis Treatment
-Initial Symptom: Intermittent Claudication (Pain B/L -ABI: Daily walking to build up collateral
in calf after pt walks. Relieved by rest) Claudication (.7) circulation
-Cold, Numb foot Rest pain (.25) *walk until claudication pain occurs,
-Skin is dry and scaly Gangrene (.1) at which time they rest for 3 minutes
-Elevation increases pain -Treadmill test then walk again
-Hanging foot off bed (dependent position) relieves pain -Doppler Ultrasound *do 8 times/day

Arteriolosclerosis
Seen in HTN and DM patients
Hyaline: hyaline deposition in the intima and media
Hyperplastic: concentric proliferation of smooth muscle cells
and thickened, duplicated basement membrane.

Monckeberg arteriosclerosis
-Calcium deposits in Tunica Media of medium sized vessels
-Sclerotic but NOT occlusive decrease distensibility (does NOT decrease blood flow, but decreases pulses)
Signs/Symptoms Diagnosis Treatment

-Not associated w/symptoms unless -Incidental finding in -Exercise and diet

complicated by atherosclerosis, an X ray radiograph -In severe cases,
calciphylaxis, or by other disease -Arterial calcification: stents may be
-Presence is associated with poorer *ABI >1.3 to >1.5 required as well as
prognosis of disease surgical re-routing

Thromboangiitis Obliterans (Buerger’s Dz)

-Thrombosis (clotting) and inflammatory changes in small and medium vessels (ALs and VLs) of hand and feet
-Hypersensitivity to tobacco
-Begins distal and progresses proximal, causing gangrene
Signs/Symptoms Diagnosis Treatment

-Arterial ischemia & -Relies in exclusion of other diseases: -Same as

superficial phlebitis (vein -Diagnostic criteria: atherosclerosis
inflammation) *Males 20-40 yrs -Stop smoking
-RaynaudLs *Episodic w/quiescent periods of wks,
-Intermittent Claudication months, yrs
in arch of foot *More drastic and less progressive
 ACUTE ARTERIAL OCCLUSSION
Arterial Embolism
40% of embolic obstructions are in femoral A. and 20% in popliteal A.
Signs/Symptoms Diagnosis Treatment
5 PLs: -Angiography -Keep extremity below horizontal plane
*Pain -Fogarty Catheter -Immediate embolectomy is Tx of choice (best if
*Pallor within 4-6 hrs after embolic episode)
*Paresthesia (abnormal sensation) *Delayed embolectomy (12hrs after episode) when
*Paralysis there is ischemia or necrosis leads to high risk of
*Pulseless Extremity (distal to obstruction) actute respiratory distress syndrome or acute renal
Sudden onset of pain, numbness, coldness failure

Acute Arterial Thrombosis

-Arteriosclerotic artery narrow, irregular lumen sudden complete occlusion collateral flow, shunting the
blood (if not enough collateralization occurs, limb may be threatened)
Signs/Symptoms Treatment
Differentiate from embolism: NO SURGERY
*Thrombosis: *removing from an already sclerotic artery is difficult
-History of occlusive arterial ds (absent pulses, *extremity will most likely survive due to collateral
intermittent claudication, dystrophic skin) circulation
*Emboli: *segment of occlusion could be long
-History of heart dz (MI) and symptoms may or may Thrombolysis using streptokinase/urokinase or tissue
not be present plasminogen activator (tPA)

RAYNAUD’S
-Arteries to your fingers and toes go into vasospasm narrows vessels and temporarily limits blood supply
-Skin usually turns white first. Then, affected areas often turn blue, cold, numb, and your sense of touch is dulled.
-Primary Raynaud's: This is Raynaud's without an underlying disease or associated medical problem that could provoke
vasospasm. Also called Raynaud's disease, it's the most common form of the disorder.
-Secondary Raynaud's:
Scleroderma.
Lupus.
Rheumatoid arthritis.
Sjogren's syndrome.
Diseases of the arteries.
Treatment:
Calcium channel blockers: Nifedipine, Amlodipine. Also help heal skin ulcers on your fingers or toes.
Alpha blockers: Prazosin, Doxazosin
Vasodilators. Nitroglycerin cream to help heal skin ulcers
 VENOUS DISEASES
Varicose Veins
-From increased venous pressure due to prolonged standing, heavy lifting, obesity, or pregnancy
-Long saphenous & its tributaries are most common
-Thrombophlebitis (swelling of vein caused by blood clot) may
develop, especially in post-op patients, pregnancies, or women
taking oral contraceptives
-Sunburst Varices: dilations in sub-q venous plexuses that have
spider-like arrangement and purple color
Signs/Symptoms Treatment
-Larger than spider veins -Graduated Compression
-May be cramps at night Stockings (class II or III)
-Sx Excision
-Cramps at night = elevate

Thrombophlebitis of Superficial Veins

-Inflammation of Vein associated w/thrombus formation
-Presents as palpable linear indurated cord (Long Saphenous most involved)
-May be history of IV, or trauma
-See occult DVT in 20% of cases
-Thrombophlebitis Migrans: When it occurs repeatedly in different locations
Signs/Symptoms Diagnosis Treatment
-No significant swelling in extremity -based on the -Local Heat
-No calf tenderness (unless Deep thrombophlebitis) appearance of -Bed rest w/elevation
-Self Limiting and lasts 1-2 weeks, but firm cord may last much longer the affected area -Thrombolytics
-The linear rather than circular nature of the lesion and the course along the
vein differentiates it from cellulitis (skin infxn)
Venous Insufficiency
-From Deep Venous Thrombophlebitis (postphlebitic syndrome ) with valve destruction in deep veins and
superficial to deep vein flow in perforating veins reverses
-Calf muscle action becomes ineffective blood flows to superficial veins valves in superficial system
become incompetent antegrade venous flow increased pressure edema, fibrosis, pigmentation
(hemosiderin deposits) dermatitis (itching), cellulitis, ulceration seen later
*Hemosiderin Deposits: venous HTN distends (swells) local capillaries allowing RBCLs to leak into
tissue. Hemoglobin from these cells is metabolized and results in brawny skin appearance
Signs/Symptoms Treatment
-1st sign: progressive edema of leg -Bed rest w/legs elevated
-2nd sign: changes in skin and subQ -Support Hose
-Pitting Edema: sign of chronic venous -Use wet to dry dressing for ulcers w/normal saline change BID. Remove
obstruction or acute inflammation
necrotic tissue and debris when dry dressing is removed
-Diuretics for edema

Deep Venous Thrombosis (DVT)

-Partial or complete occlusion of a vein by thrombus w/secondary inflammatory reaction in wall of vein
-80% are in deep veins of the calf
-Results in venous valve destruction incompetent veins postphlebitic syndrome (venous insufficiency)
Signs/Symptoms Diagnosis Treatment
-Symptoms arise over period of Venography: -Elevate leg 15-20°, trunk kept horizontal
hours to 1-2 days Gold Standard -Bedrest until local tenderness and swelling subside
-Self-limiting (lasts 1-2 weeks) -Heparin: bolus of 5,000-10,000 unit IV followed by 500 units/kg
continuous IV infusion every 24hr
- (+) Homan’s sign: Dorsiflexion
-Start pt on long term Coumadin (anti-coagulant): 10mg/day until
of foot causes deep pain in calf PT increases.
 ULCERS
Arterial (Ischemic) Ulcers
-When pressure is put on skin, the skin is damaged & is unable to be repaired from lack of blood perfusing the tissue.
Causes Symptoms Location Description
Arterial Insufficiency (see below): -Severe Pain, relieved by -Lateral surface of the -Solitary, Irregular Border
-Temporary arterial occlusion (TAO) dependency ankle -Deep, Punched out
-Arteriosclerosis Obliterans -Trophic Changes: changes -Heel -Pale dry base
(fibrosis of tunica intima) resulting from interruption -Ends of toes or -Often extends to tendons.
(calcification of tunica media) of nerve supply between toes -Little drainage
-Absent pulses

-Tx: primary goal of the treatment of arterial ulcers is to increase circulation to the area. Wound should be as dry as possible to
decrease the risk of infection

Venous Ulcer
-Improper functioning venous valves Venous HTN: pressure in veins increase (Body needs pressure gradient between
arteries & veins in order for heart to pump blood forward through arteries & into veins. In venous HTN, blood isnLt
pumped as effectively in or out of the area and it pools) movement of inflammatory mediators into the sub Q tissues of
the lower extremity & subsequent breakdown of the tissue including skin. Occur in 70% to 90% of chronic wound cases.
Causes Symptoms Location Description
Venous Stasis -Slight pain, relieved Medial distal leg Base: Necrotic but granulating (connective tissue replaces fibrin
by elevation in healing wounds) vascular base: Red in color (may be yellow
-Hemosiderin Deposits fibrous tissue cover). Discharge present if ulcer is infected.
-Palpable Pulses Fluid drainage can be significant.
Borders: Usually shallow, irregular shape.
-Tx:
*Bisgaard regimen: 4E's s
Education
Elevation
Elastic compression
Evaluation
*Pentoxifylline (Trental)
-Xanthine derivative
-Improves blood flow through peripheral
blood vessels, helping with blood
circulation in the arms and legs
Neurotrophic Ulcer (Malum perforans pedis)
Occurs primarily in people with diabetes, although they can affect anyone who has an impaired sensation of the feet
Causes Symptoms Location Description
- or absent -Painless (Indolent) -At pressure points on Begins as subQ tissue breakdown
sensation -Necrosis (tissue bottom of the feet Base: Variable, depending on the patient's
(+) death) -Plantar heel circulation. May be pink/red or brown/ black.
-Repeated -Under boney Borders: Punched out, while the surrounding skin is
microtrauma prominence often calloused
-Tx: Avoid pressure &
weight-bearing on the
affected leg. Regular
debridement. Orthotics

Hypertensive Ischemic Ulcer (Martorelli's ulcer)

-Association with diastolic arterial hypertension
-Results from narrowing of small blood vessels located in the skin
-Predominantly in middle-aged women with poorly controlled HTN in the form of skin ulcers
Causes Symptoms Location Description
Systemic High BP Extreme Pain Lateral lower leg Multiple small homogeneous, symmetrical lesions.
*usually Diastolic *Posterior or Anterior May join together
*often over Achilles

Calciphylaxis
-Almost exclusively in patients w/Stage 5 chronic kidney disease [End Stage Renal Disease (GFR <15 mL/min)] with
secondary hyperparathyroidism.
-Calcification of tunica media and occlusion in the absence of vasculitis (inflammation of vessels)
Causes Symptoms Location Description
Skin cells die because of lack -Small vessel mural Trunk & Extremities -Violaceous (dark bluish
of blood supply (dry calcification purple) mottling in star-
gangrene). -Extravascular calcification shape.

-Tx: Most important initial step is to normalize the

calcium and phosphate product levels ( the levels).
Dialysis with a lower diasylate calcium concentration
is important initial management in the calciphylaxis
associated with renal failure
 “The Five Pillars of Wound Care”
“KEEP IT SIMPLE STUDENT”
*Our job is to identify the conditions that lead to the development of the wound and then institute a plan to
manage and reverse those conditions to allow the body to effectively heal itself
*At each visit, address each principle of wound healing that the pillars address and adjust your plan accordingly

1) OPTIMIZE PERFUSION
*Pulses, ABIs, Segmental Pressures & PVRs
*See guide for ideal PVR/ABI

2) TREAT INFECTION
*Empirical Antibiotic Therapy & Culture/Sensitivity
*Watch for autoinoculation of wound with patient self-care

3) CONTROL EDEMA
*Elevation s Feet at or above the level of the heart
*Compression s multiple pressures available; both in compression wraps and fitted garments

4) OFFLOAD PRESSURE
*Surgical shoes with plastazole insert with cutout s minimize pressure, friction & shear
*Minimize Ambulation if required

5) MOISTURE BALANCE
*Wound Debridement
*Dressings s Wound should be Xlike a damp wrung-out towelY
*Frequency of Change s Determined by need for debridement and drainage - Keep moisture off the wound

IMPORTANT SIDE NOTES

*Compression Garments s You donLt put them Xon & offY, the technical works are Xdon & doffY the garments
*Santyl to be applied Xto nickel thicknessY. Remember donLt apply Santyl w/dressings w/heavy metal cations
*Aquacel Ag is great due to its Xvertical wickingY properties. It pulls drainage out & away from wound surface
*Not all ulcers deserve to be debrided
*When differentiating types of edema, understand XStemmerLs SignY and its relation to lymphedema
Stemmer’s Sign: Thick fold of skin at base of 2nd toe that can be gently pinched & lifted
-Positive test result: skin can’t be lifted. Is an indication of the presence of lymphedema
-Absence of Stemmer sign: doesnLt rule out possibility of lymphedema.
*Differentiate Venous Stasis (edema stops at ankle) from Lymphedema (entire leg and foot)

INTRODUCTION TO WOUND CARE PRODUCTS

MOIST-TO-MOIST DRESSING
*Provides nonselective mechanical debridement. May be painful on dressing removal
*Do not over-saturate the dressing. (May macerate good tissue)
*Should be changed q8 -12 hours depending upon the wound
*Most common: Normal Saline Solution
*Alternate solutions: 3% Boric acid (astringent) or dilute Dakin's solution (antiseptic XBleachY)

HYDROGELS/HYDROCOLLOIDS
*Promotes moist wound environment, but also absorbs some exudate
*Facilitates autolytic debridement
*Intended for use on relatively clean, granular wounds
*Good alternative when patient cannot tolerate more aggressive debridement or other topical products
*Duoderm CGF patch has no off-loading properties
*Examples: Duoderm, Safe-Gel, Duoderm CGFpatch (careful on heels, may macerate!)
DEBRIDING AGENTS
*''Medicinal''' equivalent to mechanical debridement properties of moist-to-moist dressing
*Combine with appropriate sharp debridement and daily wound irrigation to increase effectiveness
*Do not use detergents, hexachlorophene, anti-septics to cleanse the wound or products with heavy metal ions when using
enzymatic compounds as these agents inactivate the enzyme
*Ointment vehicle of delivery may inhibit effectiveness in highly exudative wounds
*Examples: Collagenase Santyl, Accuzyme, Panafil

ALGINATES
*Primary function = absorption/packing
*No debridement properties. Safe under compression
*Wound fluid is absorbed by the alginate, which then forms a hydrophilic gel
*Maintains moist wound/dressing interface
*Examples: Aquacel, Nu-Derm, Sorbsan

COLLAGEN WOUND DRESSINGS

*Provides scaffold for granulation and epithelialization. (use in mild to moderate exudate)
*Primary dressing with sequential applications required
*May be combined with other topical agents, including growth factor
*Composite dressing binds MMP's
*Examples: Fibracol, Promogran, Nu-Gel, Oasis

ANTIMICROBIAL DRESSINGS
*Decrease/control wound bio burden. Not a substitute for systemic antibiotic therapy
*Various vehicles of delivery: gels, pads, impregnated gauzes, island dressings
*Various precautions according to individual products
*Examples: Aquacel Ag. Actisorb. Iodojlex. Silvasorb
FOAM DRESSINGS
*Provides absorption. Prevents peri-wound maceration
*Use as a secondary dressing only. Not intended for use as primary dressing
*Variable composition depends on the manufacturer
*Available: thick/thin, non-adhesive/adhesive wound contact surface, and with/without adhesive borders
*Examples: Allevyn, [Link], Tielle

ADVANCED WOUND CARE PRODUCTS

*Regranex = Topical wound gel that contains becaplermin, a recombinant human platelet-derived growth factor
*Apligraf = Living, bilayered skin substitute composed of human keratinocytes (neonatal foreskin) and fibroblasts in a
bovine Type I collagen lattice. One time application every 3 weeks
*Dermagraft = Similar to Apligraf, but dermal component only. Multiple applications recommended. (May apply weekly)

COMPRESSION DRESSINGS
*Compression Stockings (e.g. Jobst Ulcer Care, Vairox, Sigvaris)
*Dynaflex
*Profore
*Lymphapress
*Unna-Flex/Gelocast
*Tubigrip

MISCELLANEOUS
*Pramasone (Hydrocortisone acetate and pramoxine HCL) lotion 1%
*Good choice for stasis dermatitis as it contains moisturizing component in addition to corticosteroid
*Carmol 40 cream s aggressive keratolytic agent
*Xenaderm Ointment s Promotes local vasodilatation
Postoperative Care and Complication
Post-op Fever
*Fever is most common post-op problem. Time of occurrence is important for etiology
*Do NOT treat fever w/antipyretics until the cause is determined (exceptions: pt discomfort, delirium, convulsions)
Risk Factors
1. Surgery over 2 hours
2. Transfusion
3. Pre-existing infection
4. In place prosthesis or shunt
5 W’s
Wind: 12-24 hrs post-op
-Atelectasis: Lung collapsing as a result of a blocked airway or of pressure from outside the lung
- Anesthesia changes dynamics of airflow within the lungs, the absorption of gases and pressures,
all of which combine to cause some degree of collapse of the tiny air sacs (alveoli) in your lungs
-Post op Hyperthermia and pneumonia
Walk: 24 hrs post-op
-Thrombophlebitis
-Pulmonary Embolism
Water: 48 hrs post-op
-UTI
Wound: 72 hrs post-op
-Wound infection
Wonder Drug: anytime post-op
-Drug Fever
Other causes: anytime post-op
-IV catheter phlebitis/infection
-Catheter infection
-Constipation
-Benign post-op fever
Post-op Fever Work Up
-History Questions: SOB, chest pain, dysuria, pain at IV site
-See if patient is on new meds (heparin, antibiotics, etc)
-Inspect catheter sites
-Obtain blood cultures if fever is believed to be septic

DVT
Predisposing Factors
-Pneumatic Tourniquet use -Immobilization -Oral Contraceptives
-Obesity -Bed rest
Symptoms
-Fever after 24hrs -Calf tenderness *Painful swollen leg and a positive duplex scan
Diagnostic Test are criteria to initiate treatment for a DVT.
-Duplex scan However, a swollen, painful leg plus a
Treatment questionable requires a venogram
-Heparin IV
-Coumadin: used to prevent pulmonary emboli
 Compartment Syndrome
Definition: interstitial pressure > capillary hydrostatic pressure in perfusion ultimate ischemic changes to the
tissues on the compartment contractures and poorly functioning limbs

Ps 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
-Poikilothermia (canWt maintain temp, usually cooler than other leg) -Pressure

Diagnosis
-Wicks Catheter
Action Compartment Pressure
Rest ~ 5mmHg
During muscle contraction > 150mmHg
Muscle relaxation compartment pressure rapidly and returns to baseline in 5-10 minutes
*In compartment syndrome, there is no drop in pressure
-worry at 20-30 mmHg, consider surgical intervention at 30-40mmHg

Criteria for Diagnosis

1. A space thatWs limited by fascia, skin, or bone
2. compartment pressure caused by in compartment size or in size of compartment contents

Acute Compartment Syndrome

-Occurs when resting P in compartment exceeds available perfusion P
-Usually results from trauma with hemorrhage or gross muscular edema
-Necrosis is inevitable if it goes untreated

Chronic Compartment Syndrome

-Occurs when resting P is higher than normal resting P but not so high as to cause hypofusion
-Following exercise, the time for P to return to baseline is longer than normal
-Results in prolongation of the ischemic time resulting in symptoms following exercise

Compartments of the Foot

*Also important to know for spread of infection
Plantar:
_Deep fascia divides plantar surface of foot into a medial,
lateral, central, & interosseous compartment
_Medial: Abductor hallucis, tendon of FHL, and FHB
_Lateral: Abd digiti minimi, and flex digiti minimi
_Central: FDB, tendons of FDL, quadratus plantae, lumbricals, and adductor hallucis
_Interosseous: Dorsal and plantar interossei
Dorsal:
_Deep fascia encloses the tendons and forms a dorsal subfascial space that is continuous into the digits.
*Clinical note: The tendons of the lumbricales in the central compartment, and the tendons of the interossei in the
interosseous compartment are continuous onto the dorsum of the digits via the sides of the digits. Interdigital
infections can spread along these connections.

Treatment
*Release of compartment syndrome through dorsal incisions: 2 dorsal longitudinal incisions, one over 2nd met
and other over 4th (deepened down to met shaft) where hemostat is passed into each interosseous space and
interosseous muscle in stripped from metatarsal. Wound is secondarily closed in 5 days

Complications
*Loss of function w/structural deformity (Volkmann contractures), myoneural necrosis, sensory loss, chronic pain
-Volkmann contractures: permanent flexion of digits from acute ischemia/necrosis of the muscle fibers
of the flexor group due to arterial obstruction
 White Toe
*Arterial in nature onset of ischemia is rapid and severe (no time for collateral circulation to develop)
Signs and Symptoms
Excruciating pain
Pale coloration w/blue mottling
Paresthesia
Pulselessness
Treatment
Avoid nicotine/caffeine
D/C ice/elevation
Place foot in dependent position (standing or sitting, hang over bed)
Loosen bandage
Rotate toe on k-wire
Local nerve block proximal to area to provide distal vasodilation

Blue Toe
Stasis from poor arterial inflow or sluggish venous outflow
Etiology
Post op complication
Tight dressing/cast
bTourniquet effectc of large volume of local anesthetic
Poor tissue handling technique
Impingement of tissue between bone or fixation device
Transient vasospasm of digital vessels
Collagen vascular disease (R.A., SLE, scleroderma)
RaynaudWs disease or phenomena
Acrocyanosis (persistent blue or cyanotic discoloration of the extremities)
Treatment
D/C ice and elevation
Secondary to Venous Insufficiency (toe is warm and may blanch with pressure, unless severe)
Avoid dependency
Do NOT increase vascular perfusion
Secondary to Arterial Insufficiency (toe and cold does not blanch with pressure)
Thermostat controlled heat lamp over foot (not to exceed 90°)
Vasodilators (Nifedipine, Nitroglycerin)
PRE - OP MANAGEMENT
Laboratory Tests
Complete Blood Count (CBC)
WBC & WBC Differential
Normal Leukocytosis: >11,000 Leukopenia: <4,400
4,800-10,800/mm3 -Acute bacterial infx (viral usually has normal WBC count) -Severe infxn, septicemia
-Intoxication (gout, heavy metals, vaccines) -Hepatitis
-Hemolysis or Hemorrhage -Drugs (sulfa, analgesics)
-Stress -Myeloproliferative disorders
-Dehydration (most common)

Granulocytes
NeutrophilOs *First line of defense (neutrophil leukocytosis is a shift left, indicating acute bacterial infection)
(45-65%) -Neutropenia ( ): depressed marrow (neutropenia may be earliest clue to marrow failure); severe
bacterial, viral, or fungal infxn; maturation defect (vitamin defect)
-Neutrophilia ( ): Toxins; emotional or physical stress (strained defecation/valsalva maneuver)
EosinophilOs *Contain histamine, transports alkaline phosphatase
(1-3%) -Increase: intestinal parasite; GI disturbance; allergy
BasophilOs (0-1%) *Contains heparin, transports alk. phosphatase and histamine

Non-Granulocytes
Lymphocytes *Ab production (cell mediated immunity), graft rejection
(20-40%) -Increase: virus infxn (most common)
-Decrease: hodgkinYs, drugs
Monocytes *turn into macrophages which ingest/destroy bacteria
(4-8%) -Increase: Recovery from acute infxn, subactute bacterial endocarditis

Platelet Count
Normal *Suspect platelet disorder if patient exhibits petechiae (purple spots) in skin or mucosa
150,000-400,000 -Thrombocytopenia ( ): chemotherapy is #1 cause
*increase risk of hemorrhage. Give platelets if count <60,000
-Thrombocytosis ( ): spleenectomy

RBCOs Hemoglobin
Normal Normal
Male: 4,700,000-6,100,000mm3 Male: 12-17
Female: 4,200,000-5,400,000mm3 Female: 11-16

Reticulocyte Count
Normal -Increase: Iron deficiency (good RBC production, but peripheral cell destruction)
.5-1.5% of total RBC -Decrease: Aplastic anemia (marrow is pathology site: Best indicator to assess marrow activity)

Hematocrit (HCT)
Normal *Portion of total blood volume occupied by red cells vs plasma
Male: 43-53% *HCT is usually 3x Hb
Female: 35-47%

Mean Corpuscular Volume (MCV)

MVC = HCT/RBC *size of the red cell
-Increase: Pernicious anemia; Liver diseas; hypothyroidism; leukemia
-Decrease: Iron deficiency; Thalassemia (abnormal form of hemoglobin); lead poisoning
 AnemiaOs
Macrocytic: either megaloblastic (B12 or Folic Acid deficiency) or chronic liver disease
Normocytic: sudden blood loss, hemolytic anemia, impaired production, anemia of chronic disease (DM or RA)
Microcytic:
Hypochromic- iron deficiency, thalassemia, sideroblastosis
Normochromic- bone marrow suppression, hemolysis, chronic infxn, inflammatory disease
Pernicious: gut doesnYt make IF no B12 absorption DNA disturbance. Diagnose via Schilling Test

Hemostasis (Clotting)
Blood Clotting Stages
1) Vessel constricts and Platelets adhere to wounded vessel walls
2) Production of Plasma (extrinsic) or tissue thromboplastin (intrinsic) to form prothrombin activator
3) Conversion of fibrinogen to fibrin by proteolytic action of thrombin
Vitamin K
*Needed for factors II, VII, IX, X, Protein C, Protein S
*Coumadin: prevents conversion of Vitamin K to active form. Have patient stop Coumadin 2-3 days
before surgery. Coumadin is reversed by vit. K1 or fresh plasma administration

Prothrombin Time (PT)

Normal *measures Extrinsic blood coagulation [factor II (prothrombin), factor V, or factor X]
11-13s *Affected by Coumadin type anti-coagulants

Partial Thromboplastin Time (PTT)

Normal *measures Intrinsic blood coagulation
24-26s *should be within 5s of control

Bleeding Time
*measures effectiveness of platelet plug formation
*Given to patients with suspected platelet disorder (Pt took ASA or has Von WillebrandYs ds)

Serum Electrolytes
Sodium
Normal -Hypernatremia: kidney disease, too little water intake, water loss due to diarrhea and/or vomiting
135-145 mEq/L -Hyponatremia: liver and kidney disease, CHF, burn victims

Potassium
Normal *Very important for pre-op evaluation
3.5-5.1 mEq/L *Important in diabetic as Insulin decreases serum potassium levels
-Hyperkalemia: mineralcoricoids, acidosis, ketoacidosis
*produces cardiac pathology and arrhythmias (cardiac standstill when >7.5 mEq/L)
-Hypokalemia: alkalosis, diarrhea, insulin
*produces muscle cramps and arrhythmias (symptoms donYt start until <2.5 mEq/L)

Calcium
Normal -Increased: ds of bone demineralization (multiple myeloma, hyperparathyroidism, vit D intake)
4.5-5.5 mg/dl -Decreased: Renal failure, hypoparathyroidism

Chloride
Liver Studies
Alanine amino transferase (ALT) Aspartate amino transferase (AST)
Normal *measures hepatocellular activity Normal
7 - 56 IU/L 5 - 40 IU/L

Alkaline Phosphatase
Normal *Common bile duct obstruction is most common cause of increased levels
35-137 U/dl *Bed rest is second most common

Bilirubin
Normal *Is pigment of bile from RBC breakdown in liver, spleen, and marrow
<1.2 mg/dl *Direct: hepatic obstruction
*Indirect: Liver disease
-Increases: Cirrhosis, acute Hepatitis

Albumin
Normal *Good indicator of hepatic health
3.6-5.2 Gm/dl

Renal Studies
Blood Urea Nitrogen (BUN)
Normal *Is an end product of protein metabolism and produced only in liver and excreted in the kidney
5-25 mg/dl -Increases: DM, kidney disease, Starvation (#1 cause is dehydration)
-Decreased: Hydration, liver disease

Creatinine
Normal *from creatine in muscle tissue and excreted by the kidneys
<1.2 mg% *not elevated until 50% of kidney function is lost
-any reduction in creatinine clearance in urine indicates kidney impairment

Cardiac Enzymes
Lactate Dehydrogenase (LDH)
Normal *Glycolytic enzyme in carbohydrate metabolism
208-378 U/L -Increases: any tissue damage, so is NOT specific

Others
Cholesterol
Normal *can be endogenously produced by liver
150-220 mg/dl *used for membranes, steroid production, bile acids

Glucose
Normal *liver produces glucose from protein (gluconeogenesis)
70-110 mg/dl -Increases: CushingYs, DM, stress, burns, obesity
-Decreases: Islet cell tumor, glucagon deficiency, AddisonYs
*glucose in urine is completely reabsorbed in proximal tubules, so if glucose is in urine when blood
glucose is <180, it may signify proximal tubule damage

Uric Acid
Normal *from Purine Metabolism
2.8-8 mg/dl *Urine pH must be close to 7.4 (when treating gout, check pH of urine)
-uric acid is poorly soluble as pH Ys causing crystals (Urine alkanization Ys uricosuric activity)
-as ketones (acetone from fat metabolism) increases, pH decreases
 Electrocardiogram

P wave Depolarization that spreads from the SA node throughout the atria (atrial depol) 0.08-0.1s
P-R interval Time for impulse to travel from SA node to ventricle 0.12-0.2s
QRS complex Ventricular depolarization 0.06-0.1s
ST segment Time at which entire ventricle is depolarized. plateau phase of ventricular action
(isoelectric period) potential
T wave Ventricular repolarization and is longer in duration than depolarization
Q-T interval Time for both ventricular depolarization and repolarization to occur. Roughly estimates 0.2-0.4s
the duration of an average ventricular action potential

Bipolar Indirect leads

*record difference between two points on the body, in electrical events by cardiac
action. Right leg is ground
I = measures voltage from Right arm to left arm
II = measures voltage from Right arm to left leg
III = measures voltage from Left arm to left leg

Augmented Unipolar leads

*Indicate electrical potentials at one point. Electrodes of the three limbs are
attached together to form one electrode (central terminal lead).
Difference in electrical potentials are recorded between the central
terminal and each of the three extremities
aVR = Right arm positive
aVL = Left arm positive
aVF = Augmented foot (Left foot) positive

Precordial Unipolar Chest leads

*Indicate the variation of electrical potentials at a given anatomical site. 6 locations (V1-V6)
 Pre-Op Note
HPI: This 55 YOF presents for an Austin Bunionectomy. She has a long history of right bunion pain and relates
conservative measures such as modified shoe gear, padding and analgesics have failed to offer her any relief and
now presents for surgical intervention

PMH: IDDM (Insulin-Dependent Diabetes Mellitus), HTN (well-controlled)

Meds: insulin, procardia

Allergies: NKDA (no known drug allergies)

PSH:

Social Hx:

Vitals:

Vasc:

Neuro:

Derm: Skin texture and turgor is WNL. Webspaces are clean and dry b/l. No open lesions, no erythema, no calor, no
signs of infection.

MS: Muscle strength is 5/5 for all groups tested. The right hallux is abducted with evidence of a dorsomedial
eminence. Decreased ROM of the 1st MTPJ in the corrected and abducted position. No sesamoid pain. Pain noted
with palpation of the medial eminence

Labs:

EKG:

Chest Xray

Foot Xrays:

A: 55 YOF with HAV right foot

Plan: Again, a long discussion was performed which included all risks, benefits, nature and alternatives to the surgery:
Austin Bunioctomy. Mrs **** again appears to understand and wishes to proceed. All questions were answered to
patient's and family's satisfaction with no guarantees given. Pt has been NPO since midnight and the consent is
signed, up to date and in chart.
PRINCIPLES OF SURGERY

Regional and Local Nerve Blocks

Common Peroneal
Diagnostic for: assessing spastic peroneal muscles (flexible flatfoot)
Steps: palpate fibular head and nerve, enter laterally 1> distal to head

Mayo Block
Deep Peroneal n.
First Proper Digital Branch of Medial Dorsal Cutaneous n.
First Proper Digital Branch of Medial Plantar n.
Second Proper Digital Branch of Medial Plantar n.

Reverse Mayo Block

Intermediate Dorsal Cutaneous Branch to Fourth Interspace and Lateral Plantar branch
Lateral Dorsal Cutaneous n. (sural)
Proper Digital Branch to 5th Digit of Lateral Plantar n.

Bone Healing
DEFINITIONS
Osteoblasts: only cell that can produce bone. Derived from precursors (mesenchyme cells) in blood vessel
walls. This means adequate blood supply must be present
Osteoclasts: dissolve bone matrix forming canals through existing bone. Responsible for bone formation
Osteoid: Non-calcified organic matrix formed by osteoblasts. 95% collagen and 5% proteoglycans
Mineralization: osteoid depositing with calcium phosphate in form of hydroxyapatite. Occurs 7-10 days after
osteoid if formed. Mineralization in lamellar bone occurs at a rate of 1um/day.
Woven Bone: forms healing bone callus. Contains a disordered three dimensional array of collagen fibrils.
Rapidly mineralizes following formation. Osteoblasts come in and extrude matrix in all directions. It
eventually remodels to lamellar bone.
Lamellar Bone: highly organized bone laid down in congruent layers with parallel collagen fibers which change
directions from one lamella to the next.

STAGES OF BONE HEALING

1) Inflammation (day 1-4)
-Initial hematoma formation around site followed
by necrosis of bone margins
2) Induction (day 1): two possibilities
1. Good oxygen, vascularity: Osteoblasts
induced
2. Poor oxygen, vascularity: Chondroblasts
induced
3) Soft Callus (day 4-week 4)
-clinical union if motion across site is eliminated
-formation of callus is noted
4) Hard Callus (week 4- month 4)
-callus converts to mature lamellar bone
-radiographic union noted
5) Remodeling (month 4- year 2)
TYPES OF BONE HEALING
Primary (Direct)
-Occurs with Rigid Immobilization between bone fragments
-Bony healing stages are undifferentiated, & callus formation is absent (not necessary w/immobilization)
-Fixation device assumes partial load applied to bone bone resorption due to biomechanical load
-2 types of Direct Bone Healing
1. Gap Healing: hematoma fills microscopic gaps, bringing in osteoblasts which form lamella
90° to long axis of fx, and are then replaced by axially oriented lamella
2. Contact healing: surfaces in direct contact. ]Cutting Cones> make concentric lamellar bone.
Cutting cones advance 70-100um/day.
Secondary (Indirect)
-Occurs when bone is NOT rigidly immobilized
-Motion causes additional hemorrhage, favoring fibrocartilage formation, which leads to callus formation
*Bone Callus: creates a layer of high tensile strength connective tissue between fragments,
followed by granulation tissue, which resists compression. This framework is eventually
replaced by fibrocartilage. Chondroclasts remove cartilage and osteoblasts begin to
produce woven bone
-Bone remodeling follows Wolff`s law: bone deposition takes place on the concave side and resorption on
the convex side

COMPLICATIONS OF BONE HEALING

Malunion: nonanatomic position of fracture fragments. Result of poor reduction and inadequate fixation
Delayed Union: prolonged casting or dynamic loading may be needed
Non-Union: generally considered non-union at least 6 months after surgery

NON-UNION
Daignosis:
*presence of sclerotic border or osseous void at fx site
*stress fluoroscopy: manipulate fx under fluoro
*Tc-99m bone scan
Week1-4: diffuse uptake
Week 4-12: biphasic pattern
Week 12-year 2: coalescence
Classification
Hypertrophic/Hypervascular (viable fragment ends)
Elephant Foot: very hypertrophic, premature weight-bearing
Horse’s Hoof: slightly hypertrophic, unstable fixation
Oligotrophic: fx displaced
Atrophic/Avascular (no biologic reaction)
Torsion Wedge: Intermediate fragment is healed to one main
fragment but not the other
Comminuted: one or more intermediate fragments
Defect: loss of fragment. Exposed ends are viable, but gap is so big bridging cannot occur
Atrophic: missing intermediate fragment, scar tissue fills void
Treatment
Electrical properties of bone:
ElectroNEGATIVE potential in areas of bone growth (see growth at negative end)
ElectroPOSITIVE potential in areas of less activity
Hypertrophic Non-unions: stabilization of fracture ends
Atrophic Non-Unions:
1. Resection of non-union and bone-graft
2. Ilizarov Technique:
a. corticotomy followed by distraction (to induce local necrosis and neovascularization)
b. compression-distraction (]accordion technique)
3. Electrical Stimulation: no correction for shortening of malposition. Gap larger than ½ the
diameter of involved bone is a contraindication to electrical stimulation.
Radiology
Radiation physics, biological effects of radiation, operator and patient protection

Radiation Physics
Radiation: energy in motion
Particulate: radiation acts primarily as a particle
Non-particulate: interacts primarily as a wave
Ionizing: formation of positive (alpha particles) or negative charged particles
-radiations exceeding ionization potential (4.3-17.4 Ev) can cause ionization
-Include those exceeding UV (x-rays, gamma rays)
-Directly: charged particles such as electrons, alpha particles. Ionize by collision
-Indirectly: gamma rays, x-rays
Non-Ionizing: UV, visible light

Dual Nature of Matter

X-rays: electromagnetic radiation (simultaneous transfer of energy through electric and magnetic fields)
-have high frequency and short wavelength

X-Ray Production
X-Ray Tube

-fast moving electrons produced by heating a tungsten filament strike a tungsten target, a small
fraction is converted into x-rays
-Filament: Cathode (- terminal)
-Target: Anode (+ terminal)
-Current (mAs = milliamperes/second): # of electrons passing from cathode to anode in 1 second
*Determines the Quantity of x-rays produced
-Voltage (kV = kilovolts): potential difference across the anode and the cathode
-kVp: maximum or peak potential difference applied across the cathode and anode.
*Determines the Quality of the x-rays
-Efficiency: ratio of energy released as x-rays to the energy deposited onto the anode by electrons
*When electrons from cathode hit the anode, most (99%) of the energy is converted into
heat and only about 1% is converted into x-rays
Are two processes by which energy of the electrons are converted into x-rays
-Bremsstrahlung: when negatively charged electrons approach the area of a positively charged nucleus,
electron may be deflected from its path. The sudden change in velocity causes electron to lose part of
its energy as x-rays. Peak energy determined by the kVp

-Characteristic X-Rays: electron may also interact with an orbiting electron, ejecting it from the atom.
Vacancy created in that orbit is filled by an electron from a higher orbit. In this process,
electromagnetic radiation is released

Heel Effect
-Beams produced by an x-ray machine have non-uniform angular
distributions, with the intensity on the cathode side being
greater than on the anode side. Effect more pronounced with
steep (decreased) anode angles
-Is more evident for large field sizes and shorter source to film
distances. One way to exploit this apparent disadvantage is to
position thicker parts being examined toward the cathode.
Thus, the thinner forefoot should be placed under the anode
and the thicker rear-foot under the cathode

Collimation
-beam striking a patient is limited to the area of clinical interest and not to exceed
the size of the film

Grids
-to cut down on the scatter that reaches the film and contributes to image
degradation, grids are used
-Grids improve contrast

Filtration
-Filters out long wavelength, lower energy (aka ^soft_)
radiation: "hardens" the beam
-There is inherent (glass, insulating oil) and added filtration
(Aluminum).
Biological Effects of Radiation
Interaction of X-rays with matter
Elastic (Coherent) Scattering:
-when photon passes near an electron, the electric field associated
w/the moving photon accelerates the electron, radiating energy.
-photon changes direction, and the atom returns to its initial state
-no energy transfer, no ionization
-unimportant in diagnostic radiology

Photoelectric Effect: (significant)

-incoming x-ray photons interacts w/one of the inner-shell
electrons, knocking it out. The void created by the inner shell
when an electron is ejected is filled by an electron from higher
shell, producing characteristic x-rays
-energy of incoming photon must exceed the binding energy of
the electron

Compton Scattering: (significant)

-photon is deflected in one direction, and electron recoils in
another direction

Pair Production:
-photon with energy >1.02 MeV interacts w/the
nucleus and disintegrates into an electron and a
positron (positively charged electron)

Photonuclear Disintegration (photodisintegration):

-x-ray photon interacts w/nucleus, resulting in the disintegration of the nucleus, w/ejection of one
or more nuclear particles
Molecular Effects
Direct Effect: lethal damage caused through direct ionization of a crucial molecule (usually DNA or
lipoproteins in nuclear or cytoplasmic membrane)
-accounts for only a small fraction of damage caused by low-LET (linear energy transfer, see
below) radiation but accounts for most of the damage caused by high-LET radiations
Indirect Effect: lethal damage to crucial molecules caused by free radicals (usually done through water)
-accounts for most damage caused by low-LET radiations

Protectors and Sensitizers [Effective with low-LET (not high-L ET) because they deal with free radicals]
Protectors: substances that radiation-induced damage (alcohol, cysteine)
-act as scavengers by soaking up free radicals
Sensitizers: substances that enhance the effects of radiation (Increases # of free radicals)
-oxygen, metronidazole: hypoxic sensitizers (sensitize hypoxic cells but not normal or oxic cells)
*Oxygen Effect: Biologic tissue is more sensitive under aerobic conditions

Dose Rate Effect and Dose Fractionation

-when radiation is delivered at low dose rates, it is less effective than when exposure is at acute dose rates
*this means a fractionated dose is less effective than the same total dose when given at one time

Linear Energy Transfer (LET)

-amount of energy transferred along the path of radiation (measured by energy lost per unit length)
-Low LETis: x-rays and gamma-rays

Effects on Tissues
-sensitivity of tissues to radiations depends on 2 factors
1. Proliferative capacity: rapidly dividing tissues are more sensitive to radiation
2. Differentiation: differentiating cells are more sensitive to radiation
-most sensitive tissues:
1. Bone Marrow
2. Lymphocytes
3. GI tract
-most resistant tissue: CNS

Somatic Effects
-primary cause of radiation-induced death is inability to fight infection
-fetus is most sensitive to radiation in the first trimester (particularly weeks 8-15)
-10 Day Rule: x-rays on women of childbearing age involving pelvis should be performed only during the
first 10 days following the onset of menstruation

Stochastic Effects
-effects in which the probability of occurrence (but NOT severity) increases with dose (e.g. Cancer)
-no threshold dose

Non-Stochastic Effects
-must exceed a threshold dose before effects become evident. When threshold is exceed, the severity of
the effect is proportional to the dose (e.g. Cataract, w/ a threshold of 2 Sv)

Probability of Causation (PC)

-estimate of the probability that a specific malignancy was caused by a specific radiation exposure
Radiation Protection
ALARA Concept: exposure should be kept ^as low as reasonably achievable_
There are 4 quantities important for radiation protection:
1) Exposure: roentgen (R)
-amount of ionization produced when radiation passes through matter
-exposure reduction
P Time Minimize
P Distance Maximize
P Shielding Employ
2) Absorbed Dose: gray (Gy)
-amount of energy absorbed in matter when radiation passes through it
3) Dose Equivalent: sievert (Sv)
-biologic damage caused by radiation
4) Effective Dose Equivalent: sievert (Sv)
-dose equivalent multiplied by weighting factor
*weighting factor: measure of the risk from exposure to that organ compared to the risk from
whole-body exposure to the same dose

Sources of radiation
-Primary beam radiation: the one directed at pt out of the tube head
-Secondary beam radiation: 2 types
l Scatter radiation A pt. major source
l Leakage radiation emanates from the tube head in all directions

Structural Barriers
Primary: 1/16" (1.6 mm) lead typical
Secondary: 1/32" (0.8 mm) lead typical

Tenth Value Layer (TVL)

-material thickness required to attenuate a radiation beam to 1/10 its original intensity
-used in radiation protection to determine the number of thicknesses required for shielding or for beam
blocks

Aprons
-dead cells on skin cuts provides 100% protection from low energy beta particles emmited by tritium
-0.5 mm lead (for 10 beam): cuts off 95% of low kVp (<70) x-rays, but ineffective for high kVp x-rays
-0.25 mm lead (for 20 beam radiation)

Principles of Radiation Protection

As Low As Reasonably Achievable (ALARA)
Below Regulatory Concern (BRC) or De Minimus
 Radiographic technique and development

X-Ray beam Intensity (Exposure): Product of number of photons & their average photonic energy
Intensity = quantity x quality (in Coulombs)
Factors effecting Quantity
p Milliamperage x Time = mAs
-Doubling mAs will double # of emitted Xrays & vice versa
p Kilovoltage (kVp)
-Doubling the kVp increases beam intensity fourfold & vice versa (Overall effect on film blackening is
approx. equal to the fourth power)
-15% rule: to maintain constant film density, with a of kVp by 15%, there should be a 50% of mAs
p Distance
-Doubling distance from X ray source decreases intensity by factor of 4
p Filtration
Factors of Attenuation (gradual loss of intensity) Half Value Layer = determined by thickness of an Aluminum
absorber that reduces the beam intensity by 50%
p Kilovoltage -A in HVL means that beam has too many low energy photons
p Density -increased filtration increases beam quality
p Atomic Number (Z) -describe the penetration of superficial x-rays
p Electrons per gram of tissue
Resolution: The ability to image two separate objects as being distinct
p Contrast resolution: The ability to distinguish anatomic structures of similar subject contrast
p Spatial resolution: The ability to image small objects that have high subject contrast (e.g. bone soft tissue
interface)
Radiographic Contrast
p Film Contrast
High contrast film = HShort gray scale" film & vice versa
Latitude: range of exposures over which the image receptor responds with optical densities (ODs) in the
diagnostically useful range
l With wider latitude, mAs can vary more and still result in diagnostic image
l Wider latitude, greater margin for error
l Inversely related to film contrast
p Subject Contrast
Thickness differences
Thicker parts = increased attenuation
Thinner parts = decreased attenuation
Density differences
Greater density (mass per unit volume) of a tissue results in greater beam attenuation
Atomic number differences
-Higher atomic numbered tissues attenuate more X rays
-Primarily results from photoelectric attenuating absorptions in patient
-Substance atomic number
FAT 5.9
MUSCLE 7.4
LUNG 7.4
AIR 7.6
BONE 13.8
BARIUM 56.0
Quality of radiation (kVp)
p in kVp Ls subject contrast & vice versa
l Lower kVp = Higher contrast
l Higher kVp = Lower contrast
p Changing mA x time (mAs) does not affect subject contrast!
Fog & Scatter
p The ultimate effect of Fog and Scatter is to reduce radiographic contrast
p Scattered radiation that reaches film produces unwanted density
p Scatter radiation increases with:
l Increasing part thickness
l Increased field size
l Increased energy (kVp) of X rays
Optical Film Density:
p Measures film blackening
p As O.D. increases, % transmittance decreases (transmittance: amount of light that passes through sample)
Image Formation
Soft X-Rays
Low voltage: speed of electrons
Low speed electrons: longer wavelength x-rays
Decreased penetrating power
Hard X-Rays
Increased voltage: increased speed of electrons
High speed electrons: shorter wavelengths
Increased penetrating power

Positions
Look at Osher packet
Normal radiographic anatomy,
 Anatomical Variations

Developmental landmarks
 Biomechanical interpretation
Angle View Normal Description Increases w/ Decreases w/
PASA AP 0-8o axis of distal 1st met articular set line to 90 HAV Rectus
DASA AP 0-8o axis of prox. phalanx & its prox. articular set HAV Rectus
line to 90
HIP Angle AP 0-10o+2 intersection of long axes of 1st proximal & distal Normal 1st MPJ Subluxed 1st MPJ
phalanges -HA -HA
IMA 1-2 AP 0-8o intersection of long axes of 1st & 2nd mets Pronation Supination
(met prime Adductus)
IMA 2-5 AP 16o + 4o intersect axis of 2nd met & med aspect of 5th met Splayfoot > 20
IMA 4-5 AP 8o + 2o intersect axis of 4th met & med aspect of 5th met Tailoris Bunion
HA Angle AP 0-16o intersection of long axes of 1st met & 1st -Pronation Supination
proximal phalanx -Met, FF Adductus
Met. Adductus Angle AP 0-15o intersect of long axis of lesser tarsal & 2nd met -FF to MF deformity
Talar Declination LAT 21o + 3-4o intersection of column tali & WB reference line -Pronation (Talus -Supination (Talus
Angle pf/adducts) DF/Abducts)
-RF eversion -RF inversion
TC Angle (Angle of AP 19o + 2o intersection of longitudinal axes of talus (column Pronation Supination
Kite) tali) & calcaneus (STJ)
Calcaneal Inclination LAT 20o + 2o intersection of longitudinal axis of calcaneus & Supination Pronation
Angle WB reference line
1st Met. Declination LAT 23o + 8o intersection of 1st met longitudinal axis & WB Supination Pronation
Angle reference line
Lateral TC Angle LAT 42o + 5o intersect long talar & calcaneal axes (CI + TD) Pronation Supination
Posterior Facet LAT 35o + 5o intersection of WB reference line & a tangent to Pronation Supination
Angle posterior facet
Cuboid Abduction AP 0-5o intersection of longitudinal axes of calcaneus & Pronation Supination
Angle cuboid (MTJ) FF adduction
Lateral Deviation AP 0-7o -proximal & distal aspects of 5th met Tailoris Bunion
Angle -evaluated in concert with IM 4-5
Met. Protrusion AP + 2mm difference in distal protrusion of 1st & 2nd mets -Long 1st met Short 1st met
from common IM vertex -HIP > 20
-Congruous 1st MPJ
FF Adduction Angle AP 0-10o longitudinal axis of talus & column tali -Supination Pronation
-FF to RF deformity
Met. Parabola Angle AP 142o + 5o lines connect distal aspects of mets 1&2 w/2&5 Long 1st met Short 1st met
TN Angle AP 70o + 10o intersection of longitudinal talar axis & Supination Pronation
transaction of lesser tarsus (MTJ)
TN Articulation AP 70% % talus articulates w/navicular Supination (100%) Pronation (<55%)
Talocuboid Angle AP 31o + 3o intersection of column tali & long axis of cuboid Pronation Supination
(MTJ + STJ)
Boehlercs Angle LAT 25-40o high points of ant. process, post. facet, & Intraarticular
posterosuperior surfaces of calcaneus calcaneal fxis
Lat. Talo-1st Met \ LAT 0-15 o -intersection of column tali with 1st met head Supination -> Pronation ->
(Mearycs Angle) Superior Inferior
Tib Sesamoid AP 1-4 -relationship of tibial sesamoid to 1st met HAV
position* longitudinal axis (4 is center)

Relationship of subchondral cortices across 1st MPJ

Parameter Positional Structural Combined
HAA > 16o > 16o > 16o
PASA &/or DASA Normal Abnormal Abnormal
PASA + DASA: HAA < 0 <
Joint Position Subluxed Congruous Deviated / Dislocated
 Systemic Diseases

Rheumatoid Arthritis
-Synovium is primary site for the inflammatory process in RA (Response to synovial ^auto-antigen_)
* Synovial membrane becomes an invasive ^pannus_
* Focal bone erosions develop at margins
between bone & cartilage
* Tissue-infiltrating T-cells (cytokine cascade)
are a consistent feature of RA synovitis
-Symmetry = hallmark

Diseases Asoociated w/ Rheumatoid Arthritis:

1. Sjogrenis
2. Amyloidosis
3. Feltyis Syndrome

Articular Manifestations
-Joint swelling and tenderness
-Local warmth over affected joint
-Limited Range of motion

Extra-Articular Manifestations
-Rheumatoid Nodules over pressure points
-Pulmonary Rheumatoid nodules
-Possible pericarditis
-Anemia of chronic disease and Feltyis syndrome (rheumatoid arthritis, splenomegaly and neutropenia)
-Achilles tendon thickening

Laboratory Findings
-RFis not specific for RA; seen in chronic bacterial infection & inflammatory disorders
*Although not always present (85%) l RFs are major lab hallmark of disease
Some Diseases Associated w/elevated serum RF:
-Bacterial Endocarditis
-Leprosy
-Liver ds
-Syphilis
-TB
-Mononucleosis

Diagnosis (need 4 of 6)
CRITERION DEFINITION
Morning Stiffness Lasting at least 1 hour
Arthritis > 3 joints Simultaneously with fluid (not bone growth)*
Arthritis hand joints At least one l wrist, MCP or PIP*
Symmetric Arthritis Bilat. acceptable without absolute symmetry
Serum RF Usually present in adults (80-85%)
Rheumatoid Nodules Non-calcified: SQ, over bony prominences, extensor surfaces, juxtaarticular
*Present for at least 6 weeks
Radiographic Signs
EARLY LATE
-ST swelling often lateral 5th MPJ (¥) -fibular deviation (i)
-periarticular osteopenia/osteoporosis -5th met osseous ^islands_ (®)
-concentric joint space narrowing -severe generalized osteoporosis
-^bare area_ erosions seen in fibular notch, -arthritis mutilans
medial lesser met meads, hallucal IPJ, sesamoids -bywateris lesions at sites 1,2 (cutaneous infarctions around nailbeds)
-subchondral cyst formation (©) -insufficiency/spontaneous fractures

Erosive Target Sites ( )

-Medial & lateral 5th met. Head (circumferential)
-Medial aspects lesser met. heads
-Medial IP joint l hallux
-Hallucal sesamoids

Midfoot/Rearfoot Involvement
-Tarsometatarsal & intertarsal joints in approx. 1/3 of patients
-Lisfrancis & T-N most common
*T-N most common @ about 40%
-Ankle joint once thought rare, probably fairly common
*Distal fibular ^notching_ or ^scalloping_ (43% of pts) (£)
-79% of them have ankles demonstrate co-existent joint
narrowing and/or marginal erosions

Treatment
Rehabilitation/ Physical Therapy
1. Improve muscle tone
2. Maintain joint mobility and function (important during perioperative setting)
Symptomatic Medical Therapy
-Aspirin, NSAIDS, Gluccocorticoids, DMARDS
-Gold salts
-DMARDS (Disease Modifying Anti-Rheumatic Drugs) -Azothioprine:oral cytotoxic purine analog
Surgical Treatment -Methotrexate: folic acid antagonist
ST procedure: Synovectomy (removal of synovial membrane) -TNF inhibitors (Infliximab, Etanercept)
Osteotomy: Arthroplasty
Arthrodesis
 Rheumatoid vs Seronegative Arthritis
Sero(-) Arthritis
-Symmetrical distribution
-Negative for rheumatoid factor (RF) -Hands, feet, knees, hips, cervical spine
-Unilateral (asymmetric) -Lack of bone proliferation & sclerosis (hardening)
-Dactylitis (sausage digit) frequently associated with periostitis -Well-defined marginal erosions; acrolysis uncommon
-Heel spurs more frequent at plantar aponeurosis attachment -Prominent cyst/synovial cyst formation
-Uniform joint space loss -Subluxations more common
-Enthesitis: Inflammation at tendon and ligament attachments to bone is pathological hallmark of sero (-) arthritis

Sero (-) Arthropathies

Ankylosing spondylitis
*90% have HLA-B27 gene
*Bamboo spine/ sacroiliitis is hallmark of ankylosing spondylitis

Reiteris disease (Reactive Arthritis)

*Most common oligoarthropathy in young males
*Triad of:
1. Non-gonococcal urethritis ( frequency and burning during urination)
2. Conjunctivitis
3. Arthritis
*Typically last symptoms to occur:
-Oligoarthritis: < 4 joints in asymmetric distribution
-Feet, ankles (49%), knees, & SI joints; U.E./hands, wrists & elbows less frequent
*Heel is involved in more than 50% of patients with Reiteris disease (heel pain)
-Attacks last 3-12 months
*Radiographic Features
-1st MTP and IP joints are especially vulnerable (50% of pts)
-Retrocalcaneal bursitis around Achilles & fluffy periostitis
of inf. tuberosity (35% of pts) ( )
*Lab shows large macrophages containing nuclear debris & engulfed
neutrophils (Reiteris cells)

Psoriatic arthritis
*Characteristics
1. Synovial inflammation w/significantly less lymphocytes and plasma cells than R.A.
2. Inflammatory synovial tissue (Pannus) only on cartilage surface (R.A. has inflammatory
synovial tissue on superficial and deep layers)
3. Bone proliferation evident in peri-articular areas and tendon and ligament insertions
4. Fibrous and bony ankylosis of articulation may be seen (fibrous only in RA)
*Radiographic Features
-Presence of bone proliferation
-Most destructive arthritis of great toe IP joint
-30% of joints fuse via Boney Ankylosis (£)
-Resorption of tufts if distal phalanges (Ivory Phalanx) (®)
-Pencil-in-Cup progression (i)
 *Nail changes on digits w/ significant distal IP joint articular abnormality
-Pitting
-Transverse ridges (Beauis lines)
-Subungual hyperkeratosis (white, waxy, greasy debris; may cause onycholysis)
*Macular or papular Psoriatic skin lesions w/grey-white scales. Bleeds on scale removal (Auspitz sign)
*Suppression of the skin disease is important in controlling arthritis. Local Ointments:
-Goeckerman regimen
-PUVA therapy
-Topical corticosteroids

Enteropathic arthritis
*Bechetis
*Whippleis disease
*Ulcerative colitis/Crohnis dx.

Radiographic Features
-Erosive & proliferative arthritis (© white lines)
*Marginal & central joint erosions (© black line)
*Periostitis: ^fluffy margins_ (¥)
-Medullary/subchondral sclerosis
-Bony ankylosis (joint stiffness)
-Acro-osteolysis (terminal tuft bony erosions) (£)

Treatment
-NSAIDS
-ROM/strengthening exercises of affected joints
-Local corticosteroid injections or topical agents
-Sulfasalazine
-Immunosuppressive therapy
Heel Pain Differential Diagnosis

Calcaneal Arthropathy Sites

R.A. Erosions sites 1 & 2
Reitercs ds E & P sites 1, 2, & 4
Psoriatic A. E & P sites 2 - 5
A. spondylitis E & P sites 2 - 5
D.I.S.H. Large, well-defined spurs 3 - 5 w/o erosions

(A) proliferative enthesopathies, DISH (diffuse idiopathic skeletal hyperostosis) with ossification within the plantar fascia;
(B) Reiter's disease with fluffy periostitis of the inferior tuberosity;
(C) Paget's disease with a ^moth-eaten_ ground glass bone density;
(D) neuropathic fracture in a patient with diabetes;
(E) malignant bone tumor in a young male with a large lytic lesion of the lateral calcaneal wall.
Osteoarthritis (DJD)
Characteristics of OA
1. Progressive loss of articular cartilage
2. Appositional new bone formation in subchondral trabeculae,
3. Formation of new cartilage and new bone at joint margins

Pathology
Early Stage: Cartilage is thicker than normal

Increase in water content and Swelling of cartilage

Rate of proteoglycan synthesis in an attempt to repair by chondrocytes

Joint surface thins and proteoglycan synthesis is

Loss of surface integrity and development of vertical clefts

Exposed bone

Pain: is the cardinal symptom of OA

*Not always present in patients with radiographic features
*Gradual or insidious onset of pain, amenable to NSAIDs initially
*Pain is present after joint use and relieved by rest
*Pain at rest or night = severe dx.

Clinical
-Age > 50 y/o
-Morning stiffness < 30 minutes
-Crepitus
-No inflammation
-Bony enlargement or tenderness (from spurs, secondary synovitis, or effusions)

Wear and tear in medial column (more than lateral) including 1st MPJ, medial Lisfrancis joint & ankle joint (uncommon
unless associated with trauma)

Pronation, 1st ray instability

*Radiographic evidence of metatarsus primus elevatus (Dorsal flag sign exostosis at MPJ)
*Meary-Tomeno line
*Absolute declination angles

Osteophytes
Marginal
Central
Capsular (®)
Periosteal
Radiographic Findings
-Minimal to absent ST changes
-Marginal bony outgrowths
-Gradual, focal joint space loss (©)
-Thickening of subchondral bone (beneath cartilage) (¥)
*Occurs after cartilage loss
*Subchondral sclerosis
*Stages
Destructive Phase - Regressive remodeling dominant in pressure
segment
Productive Phase - Progressive remodeling
Eburnation: New bone deposited on existing trabeculae &
osteophytes
-Subchondral cyst formation ( )
-Mild juxta-articular (near the joint) fragmentation (i)

Treatment and Management

General
1. Rest
2. Physical therapy: heat/ice, exercise, gait training
3. Occcupational therapy: splints, joint protection
Drug: analgesics, and anti-inflammatories
Surgery
1. Joint alignment correction
2. Debride loose bodies and spurs
3. Arthrodesis
4. Partial or total joint replacement ( )
Gout
Monosodium urate crystals from supersaturated extracellular fluids; results in:
-Gouty Arthritis -Tophi
-Gouty Nephropathy -Uric Acid Calculi in kidneyis
** (asymptomatic hyperuricemia in absence of gout is not a disease state)

Epidemiology
-Usually in men (most common inflammatory arthritis in men >30yrs)
-Donit hit women until post-menopause
*Discrepancy in serum urate levels between sexes during reproductive
years looks to stem from estrogen which promotes renal excretion of uric
acid (why women get it post-menopause; estrogen dried up)

Pathogenesis
-Gout in humans is from lack of the Uricase enzyme, which oxidizes uric acid to allantoin
-Uric acid (U.A.) is normal end-product of purine degradation
-Familial - approx. 20-25% (esp. 1st degree relatives)

Pathology
1. Urate crystallizes as monosodium salt in over-saturated joints
a. Crystals deposit in peripheral structures (toes, ears) since sodium urate solubility is at lower temps
2. Inflammatory response occurs in reaction to urate crystals in joint
a. The crystals are able to initiate and sustain intense attacks of acute inflammation due to their capacity
to stimulate the release of several inflammatory mediators
b. Consists of mononuclear cells and giant cells

Stages
1. Asymptomatic Hyperuricemia
a. Only a minority w/sustained hyperuricemia develop tophi and gouty arthritis
b. Occasionally gout develops without evidence of hyperuricemia
2. Acute Gouty Arthritis (most common early clinical manifestation)
a. 1st episode usually begins in 1 joint, often during night. Patient wakes w/intense pain & swelling
b. Pain ^crescendos_ up to peak over 8-12 hour period
c. Attack may correspond w/high grade fever & systemic symptoms (can be confused for infection)
3. Intercritical Gout
a. Previously involved joints symptom-free, but MSU crystals still often identified in synovial fluid (SF)
b. May last for years
4. Chronic Tophaceous Gout
a. Usually develops after > 10 years of acute intermittent gout
b. Clinical hallmark: intercritical periods no longer free of pain
i. Joints persistently painful & swollen
ii. Intensity less than acute attack
c. Acute attacks can occur during this time
5. Renal Disease/Gouty Nephropathy

Clinical Features
-1st MPJ involved in 75% of patients (ankle, tarsal, knee are also common)
-Affected joints are red, hot, swollen, and very tender
Classifications
Overproduction (10%)
-occurs in states where there is excessive rates of nucleic acid turnover. Examples:
*Myeloproliferative and lymphoproliferative disorders
*Hemolytic anemia
*Psoriasis Uric Acid Formation:
Hypoxanthine Xanthine Uric Acid
Diagnosis: urine Uric Acid level >600mg in 24hrs
xanthine oxidase xanthine oxidase
Treatment: Allopurinol: xanthine oxidase inhibitor
Under Secretion (90%)
-plasma urate is filtered by glomerulus, so diminished kidney function causes problem
Diagnosis: urine Uric Acid level <600mg in 24hrs
Treatment: Uricosurics (Probenecid, Sulfinpyrazone): uric acid excretion in kidneys

Radiographic Findings
-Unilateral
-Most common pedal sites are 1st MPJ, Lisfrancis joint, hallucal IPJ, heels & ankle joint
Acute Gout Findings
*Marked periarticular inflammatory ST swelling (^cloud sign_) (®)
*Typically monoarticular
*No crystals, erosions, joint space widening or osteoporosis
Chronic Gout Findings
*Eccentric ST masses, frequently periarticular (tophus calcification)
-Common sites of Tophi are base of great toe (©), Achilles tendon ( ), and knee
*Large intra/extra articular erosions
-Erosions tend to involve joint margins before extending centrally (¥)
-Early may be marginal and small 50% target capsular attachment
-Erosive changes > 5.0 mm with ^punched out_ sclerotic margins that may be concentric (£)
-Martelis ^overhanging margins_ (£)
*Normodensity- subchondral bone
*Late joint space loss (ankylosis and subluxation may occur in advanced stages)
Acute Gout Treatment
1. Colchicine:
a. Binds tubulin inhibits microtubule polymerization stops mitosis inhibits inflammation
b. GI toxicity seen in 80% of patients (N/V/D/abdominal pain may be severe) (avoid w/IV Colchicine)
c. Max dose: 8mg over 24hrs
2. NSAIDS
3. Corticosteroids:
a. Not recommended for parenteral use in acute gouty arthritis bc effects are inconsistent and rebound
attacks are frequent upon discontinuation.
b. Intra-articular injections are beneficial w/colchicine or NSAIDS, or in patients who are unable to take
colchicine or NSAIDS
4. ACTH: from pituitary gland

Chronic Gout Treatment

1. Colchicine: given as prophylactic
2. Allopurinol: blocks xanthine oxidase (used for overproducers)
3. Uricosurics (Probenecid, Sulfinpyrazone): uric acid excretion in kidneys
4. Diet change. Foods and meds that exacerbate gout:
a. Organ meat (liver, kidney, etc)
b. Lard
c. Anchovies/sardines
d. Alcohol (especially red wine)
e. Diuretics
*do NOT use Allopurinol or Uricosurics during an acute gouty attack

CPPD (Calcium pyrophosphate dihydrate disease) (pseudogout)

Inflammatory process: crystals (calcification) deposit in tendons, ligaments, articular capsules, synovium, & cartilage
Acute pseudogout is marked by inflammation in one or more joints lasting for several days or more
Knee is site of about ½ of attacks. 1st MPJ is most common site in foot
Radiographic Features
1. Punctate and linear densities in articular hyaline or fibrocartilaginous tissues
2. Subchondral bone cysts and hook like osteophytes may be seen
3. Concentric loss of joint space resembles secondary OA
Laboratory Findings
Diagnosis is made by identifying CPPD crystals in joint fluid
Needle shaped, and positively bifringent
Treatment
No effective way to remove CPPD crystals from joint
Acute attacks in large joints can be treated by aspiration alone in in combo w/injection of microcrystalline
corticosteroids (NSAIDS are helpful)
Colchicine in IV form is effective (oral is less effective)
DISH (disseminated idiopathic skeletal hyperostosis)
-Osteoproliferative enthesopathy producing large, irregular bone at tendon/ligament attachments
-Ligament calcification, ossification + para-articular osteophytes + exuberant midfoot spurring
-No direct joint space attack or joint erosions
-Typical locations are calcaneus sites 3-6, dorsal talus/MF, 5th met base, anteromedial navicular, medial
1st cuneiform, hallucal sesamoids
-Can coexist with RA, gout, sero(-)
-Frequently seen in Diabetics
-May cause asymmetrical periosteal reactions of met shafts or ankylosis via extra-articular fusion

-Virtually all soft-tissue musculoskeletal infections present with non-specific inflammatory swelling on plain-film
radiographs
-Soft Tissue Emphysema: air in the subcutaneous tissues
Osteomyelitis
-generally a disease of growing bones occurring most commonly in infants and children
Foot Ulcers
Evaluate Ulcers when they are:
-Longstanding ulcers (> 4 wks)
-Large foot ulcers (> 3 cm)
-Deep foot ulcers (> 3 mm)
-Associated with ESR > 70 mm/h
Radiology
Lags behind clinical signs
-Need 30-50% resorption to detect osseous changes (10-14 days)
Minimal cortical erosion
^Acid on bone_ lysis
Acute Changes in order of appearance:
1. ST swelling
2. Periosteal reaction (new bone formation
thickening or elevation) (©)
a. Around diaphysis (proximal
phalanges & metatarsal shafts)
3. Focal Osteopenia
Chronic cases (®)
Involucrum: (i)
Florid periosteal new bone formation (periosteum elevated)
Sub periosteal spread of pus
Sequestrum: (£)
-Avascular, necrotic, dense bone (typically segments off)
-Presents as ^segmented off_ appearance from the normal bony architecture
-Radiographic hallmark of chronic OM
Cloaca:
Defect(s) in the involucrum, may form a sinus and drain
Brodies Abscess:
-Abscess in bone surrounded by dense fibrous tissues and sclerotic bone (in
metaphysis)

Diagnosis
Bone Biopsy: Gold Standard for diagnosis
3 ways of Infection
Hematogenous: enters bone via blood stream
Direct/Contiguous Extension: spread from adjacent ST
Direct Inoculation: trauma or surgical
Treatment
Primary Goals
1. Adequate drainage
2. Thorough debridement
3. Obliteration of deadspace
4. Antimicrobial coverage
Primary Surgical
Debridement
Surgical: sharp debridement causing little or no damage to healthy tissue
Mechanical: changing wet-to-dry gauze dressings or hydrotherapy
Enzymatic: topical agents degrade eschar (dry, rough crust), & protein (Accuzyme, Santyl)
Autolytic: bodies own phagocytes are encouraged by moist occlusive dressing such as Hydrogel
Antibiotic Polymethylmethacrylate Impregnated Beads (PMMA)
Indicated for deadspcae maintenance, debridement, and closure
Gentamycin is common PMMA bc itis not heat labile (PMMA is an exothermic process)
Close wound over beads and leave 2-4 weeks
Ingress-Egress system
Closed suction irrigation
Must worry about contamination (usually pseudomonas)
Secondary Surgical (reconstructive)
Papineau bone graft: fill bone defects in which small cancelleous chips are packed into bone deficits
when wound is granular
Follow up
Goal is to prevent recurrence
Intervals:
First 6 months: every month
6 months- year 1: every 3 months
Year 1- year 2: every 5 months
Septic Arthritis
Mechanism of Septic Arhritis
1. Direct Joint Invasion by the Microbe (puncture wound, hematogenous spread)
2. Indirect Joint Infection from:
a. Immune response of the affected host
b. Microbial debris persists in joint and perpetuates inflammatory response
c. Unkown mechanism

Acute Bacterial Arthritis

-Medical Emergency requiring hospital admittance
Gonococcal Non-Gonococcal
-Accounts for > ½ of all septic arthritis in otherwise healthy -Occurs in patients w/previous joint damage or
sexually active young adults (see rash) immunocompromised patients
-Patients w/complement deficiency are at high risk
-Neisseria Gonorrhea: -Staph Aureus (70%)
*seldom isolated from synovial fluid , so all mucous -Streptococcus
membranes should be cultured -Gram (-) seen in IV drug abuse, UTIis, and post-ops
-Usually presents as migratory polyarthritis involving -In kids <2, most common pathogens are S. Aureus> H.
several joints in rapid succession then settles into 1 or 2 Influenzae > gram (-) bacilli
Synovial Cultures: 25-50% positive Synovial Cultures: 100% positive
Gram Stain smear: <25% positive Gram Stain smear: 50-75% positive

3 Stages of Destruction
1. Lysosomal enzymes from synovial lining & PMNis (polymorphonuclear leukocytes/Granulocytes) results in
loss of proteoglycan from cartilage (if resolved early, proteoglycan matrix may be restored and chondrocyte
damage will be avoided)
2. Increased mechanical stress and inadequate nutrition results in chondrocyte damage
3. Enzymes released from PMNis and synovial lining cells w/altered joint mechanics gradually destroy collagen

Clinical Features
Usually affects one joint that is red, hot, swollen, acutely painful, and ROM
Knee followed by hip and ankle are most common non-gonococcal involved joints

Route of Infection
1. Dissemination of pathogens via blood stream (most common)
2. Dissemination from an acute osteomyelitic focus
3. Dissemination from adjacent ST infection
4. Trauma
5. Iatrogenic means (joint injection)

Long Bone Vasculature (Possibility of Sepsis via Metaphysis)

Infants (0-1yr) Childhood (1-16yrs) Adult (over 16)
-Vessels penetrate growth -Vessels donit penetrate -Vessels penetrate growth
plate growth plate plate, joint
-Joint sepsis possible -Joint sepsis NOT possible -Joint sepsis possible

Lab Tests & Diagnosis

Diagnosis established by gram stain & (+) synovial fluid culture (look at synovial fluid section below)
obligatory tests if septic arthritis is suspected
Radiology
-ST swelling & joint effusion
-Periarticular osteopenia ( density)
-Rapid joint space narrowing (®)
-Marginal & central osseous erosion (®)
-Bony ankylosis (adhesion/end stage)
-Loss of subchondral cortical white line is Hallmark (©)
-Bone destruction localized to part of joint strongly suggests presence of Pannus (synovial tissue proliferation) (£)

Treatment
1. Begin treatment immediately if there is suspicion and/or confirmation of diagnosis
2. Antibiotics chosen primarily on synovial fluid & gram stain adjusted based on culture results
a. Ceftriaxone, Augmentin, Cipro
b. Parenteral (IV) antibiotics continued for 24-48 hours until symptoms resolve, then switch patient to
enteral (oral) antibiotics to complete 7-10 day course
3. Closed needle aspiration should be performed at least once daily on affected joint
a. Open surgical drainage is indicated if there is a lack of response to therapy (3-4 days)
4. Joint should be kept at rest to prevent mechanical stress
a. As symptoms resolve, passive ROM exercises should be started to prevent joint contractures
b. No weight-bearing activity until inflammation has completely resolved
Synovial Fluid Analysis
Arthrocentesis and Synovial Fluid Analysis Technique
1. Move joint through ROM to resuspend contents
2. Identify anatomic landmarks defining joint surface and outline with pen
3. Identify area of joint to be aspirated and mark with retracted ball point pen
4. Clean skin and infiltrate with local followed by brief beta-dine scrub
a. Do NOT touch skin at aspiration site after cleansing
5. Must use large gauge needle. Viscous material flows with difficulty through needles <20 gauge
6. Stretch skin slightly, penetrate skin, aspirate, and advance slowly until fluid appears in syringe
7. After removal, apply gentle compression at puncture site for several minutes

Synovial Fluid Analysis

1. Viscosity: decreased in inflammatory joint fluids
2. Color and Clarity: if newspaper print canit be read through fluid, suggest inflammatory process
3. Wet Mount: Identify cells, cartilage fragments, lipid droplets, cytoplasmic inclusions, and crystals
4. Crystal Analysis: monosodium urate (gout), etc

Rheumatic Disease Characterized by Synovial Fluid Analysis

Non-Inflammatory Inflammatory Hemorrhagic
-Osteoarthritis -Rheumatoid Ds -Post-Surgical
-Trauma -Sero (-) -Coagulation Disorders
-Hemochromatosis -Ulcerative Colitis Septic
-Acromegaly -Lupus -Bacterial Infection
-Osteochondritis Dessicans -Viral or Fungal Infection

Classification of Synovial Effusions

Exam Normal Non-Inflammatory Inflammatory Septic
Color Straw Straw/yellow Yellow Variable
WBC (mm3) <200 200-2,000 2,000-75,000 >100,000
PMN (%) <25 <25 >50 >75
Culture (-) (-) (-) Often (+)
Mucin clot firm firm friable friable
Charcot
See Diabetes Outline

Acromegaly
Metabolic Bone Disease
Stimulation of bone formation:
Enchondral bone: Thickened intervertebral discs & enlarged costochondral junctions
Periosteal bone: Skull, jaw, cortical thickening of tubular bones, phalangeal tufts
Subligamentous bone: Calcaneal spurs; excrescences on tuberosities, patella, trochanters
Stimulation of bone resorption
Acrolysis
Overtubulation of phalanges, variably metacarpals & metatarsals
Intracortical striations
Medullary widening
Cartilaginous proliferation, degeneration, & regeneration
Widening of articular spaces
Narrowing of joint spaces
Periarticular calcifications & ossifications
Osteophytosis, osteoarthritis
Connective tissue hyperplasia
Skin thickness, e.g. heel pad
Radiographic Features
-Overall enlargement with ST & bony overproliferation
-Distal ^tuft_ and heel pad thickening (©)
-Joint space widening
-Periostitis in metatarsals (®)
-Gracile phalanges
-Pseudoforamen (i)
-DISH like spurring (£)
Tarsal Coalitions
Clinical Manifestations
-Tarsal area pain -Limited STJ or MTJ motion
-Rigid/Semi rigid flatfoot deformity -Peroneal muscle spasm = w/coalition fracture or Overactivity
-Prominence of peroneal tendons -Tarsal Tunnel discomfort
-No Peroneal m. spasm = w/long standing rigid valgus foot deformities

Associations
-Flatfoot deformity -Cavus foot deformity
-Peroneal spastic flatfoot -Rigid valgus foot

Classification
Synostosis: bones are normally fused
Syndesmosis: Fibrous tissue involved
Synchondrosis: Cartilagenous tissue involved

Types
True coalition: 2 osseous segments are FUSED w/in an anatomical joint= bar/bridge ([Link])
Complete coalition: complete bridge of bone is found between fused tarsal bones w loss of involved joint motion
Incomplete coalition: 2 bony projections from tarsal bones united by intervening cartilaginous or fibrous tissue
Rudimentary coalition: bony projections impede tarsal joint motion (may be identical to true tarsal coalition)

Normal Radiograph
TALOCALCANEAL CALCANEONAVICULAR
-MOST COMMON -2nd most common
-Unilateral -B/L
-Absent middle facet -Anteater sign
(green arrow) -Lateral oblique view, lateral view, AP
-C sign(orange arrows)
-Lateral view,
-Harris Beath,
Harris Beath oski jumpp
radiographs =
-Fail to visualize middle STJ facet
-Irregular sustentaculum tali
-Rounding of lateral talar process
-angulation of middle facet by more
than 20 deg off the horizontal is
consistent with a coalition, even if
the joint space is open;

Secondary changes
-Talar Beaking
*On ANT LAT aspect of talus
*Associated w/abnormal STJ function secondary to jamming of TNJ
 -Narrowing of post talocalcaneal facet
-Narrowing of Post subtalar joint

-Flattening & widening of lat triangular process of talus

-Cortical margins= rounded, 2ry to increased compressive force on lateral
talar surface into calcaneal sulcus in assoc w loss of normal
Subtalar rotational motion
-Altered calcaneal trabecular patterns = ^Halo effect_
-Bohleris angle = decreased
-Degenerative ^Ball & socket_ ankle joint changes
-Radiographic findings assoc w flatfoot deformity noted

C SIGN
Diagnosis: Subtalar coalition/Talocalcaneal Coalition
p C shaped line formed by the medial outline of the talar
dome and the inferior outline of the sustentaculum tali.
p This is a sign of subtalar coalition.
p It is a reliable indicator of subtalar coalition on the lateral
radiograph and represents the bony bridge between the talar
dome and the sustentaculum tali.

ANTEATER NOSE SIGN

Diagnosis: Calcaneonavicular coalition
p Notice the elongated, tubular like extension of the anterior calcaneus seen on the lateral film; this imagery has
been likened to the elongated nose of an anteater.
p There is abnormal bony fusion of the calcaneus and navicular bones, with the presence of a bony bar extending
between these two bones.
 Local Diseases

Lesser Metatarsalgia
Mortoncs neuroma
- Repetative irritation of nerve by neighboring ligament (usually 3rd IM space)
-Hyperpronating individuals, obese patients, and high-heel wearers are prone to
entrapment irritation of common plantar nerve, plantar to DTIL
Symptoms
*Sharp, aching, shooting pain brought on by forefoot weight-bearing load
*Insidious onset, progressive worsening
*Relieved by sitting and massaging unshod foot for brief time
Diagnosis
*Paresthesia to direct deep palpation
*Positive Muldercs sign: palpating the affected interspace with one hand
and squeezing the entire foot at the same time with the other hand, causing a click sound
*Tinelcs sign: percussing over the nerve to elicit a sensation of tingling or "pins and needles"
Differential Diagnosis
*Bursitis, Diabetic peripheral neuropathy, neoplasm
Treatment
Non-Surgical: Met projection pad, orthoses, steroids, ultrasound w/MTPJ ROM exercises, NSAIDS, etc
Surgical: Neurolysis of plantar n. & excision of common plantar n. proximal to proximal margin of DTIL
Approaches for incision:
1. Plantar longitudinal interspace (yields optimum exposure w/o DTIL disruption)
2. Transverse plantar incision (yields exposure to adjacent interspaces)
3. Dorsal longitudinal (MC, but hematoma in dead space can be complication post op)
4. Plantar zig-zag or lazy-S
-Sectioning of DTIL readily exposes plantar nerve and its branches & makes easy to excise the
neuroma, which is typically present at distal margin of the DTIL
-Resect proximal to proximal margin of DTIL

The incision, between the two The incision deepened between The mortons neuroma (1) The nerve at the point of The neuroma being dissected
affected toes into the web the metatarsals to reveal the branching (2) where the free.
space. neuroma (1). neuroma occurs.

The proximal end of

the nerve (1), now
divided, the neuroma
(2) and the two
digital nerves (3)
into which it splits.

The neuroma excised The wound closed with The compressive dressing to be
absorbable suture worn for 2 weeks post
operatively
Capsulitis
Capsulitis is a condition in which ligaments around joint have become inflamed
Most commonly affects the second toe
*From abnormal mechanics where joint takes excessive amount of weight-bearing pressure
-Bunion deformity, long 2nd toe, structurally unstable arch (hypermobility), &
tight calf muscle
Symptoms
*Progressive disorder and usually worsens if left untreated
*It can feel like thereis a marble in the shoe or a sock is bunched up
*Swelling in the area of pain, including the base of the toe
*_Crossover Toe_ (end stage): unstable toe drifts toward big toe & crosses over & lies on top of big toe
Diagnosis
*Essential because symptoms of capsulitis can be similar to those of Mortonis neuroma
*Diagnosis based on history b/c x-ray often normal
Treatment
*Want to treat early for conservative treatment (RICE, meds, splints, stretching, shoe modification)
*Must do surgery if in end stage (may have plantar plate injury)
- For true plantar plate injury, surgery may include ST release, arthrodesis, or tendon transfer

Osteochondroses (Epiphyseal Ischemic Necrosis)

-Disease of the growth or ossification center in children (type a AVN)
-Begins as a degeneration or necrosis and is followed by regeneration or recalcification
-Idiopathic, insidious conditions and cause diffuse aching and guarded ambulation
-Treatment entails RICE and oral anti-inflammatory medication

Blountcs Disease
-Osteochondrosis of medial portion of proximal epiphyseal ossification center in the tibia
-See lateral bowing of the leg and limping

Freibergcs
Osteochondrosis of the metatarsal head (2nd met head is most frequent)
More common in girls between ages 12-15
Symptoms
*Pain on ROM of affected joint
*Local tenderness and swelling
*Generalized thickening at the MPJ
Radiographic Evaluation
*Sclerosis and fragmentation of the met head
*Flattening of articular surface (blue line)
Treatment
Conservative: met pads, short leg cast
Surgical: want to remove bony lipping from perimeter of met head (Implant needed if DJD present)

Kohler Disease
Osteochondrosis of the navicular
More common in boys from 3-6yrs presenting with midtarsal pain
Radiograph: navicular becomes sclerotic and flattened (silver dollar sign)
Treatment: self-limiting disease, recovery usually takes from 2-4yrs (much
less time for recovery if you use casting)
Legg-Calve-Perthes Disease
-Osteochondrosis of the femoral head (Most common form of osteochondrosis)
-Younger the child, the better the prognosis
-See generalized groin pain in males age 3-12

Osgood-Schlatter Disease
-Osteochondrosis of the tibial tuberosity
-In boys 10-15 who play a lot of sports
-Caused by excessive traction (pulling) of patellar tendon from underdeveloped
tibial tubercle (repeated overuse before the area has finished growing)
-Pain will be elicited with direct pressure
-Treatment: rest from activity with NSAIDS and rest and ice

Severs Disease
-Osteochondrosis of the calcaneus (apophysis)
-Caused by excessive traction of the Achilles tendon (more
common in pts w/equinus)
Treatment
*RICE, NSAIDS, elimination of sports, Heel lifts
*Achilles tendon stretch exercises

Luschkecs
-Osteochondrosis of the 5th met base

Avascular Necrosis (Osteonecrosis)

Definition: Death of bone marrow and trabecular elements secondary to interruption of the blood supply to bone
Etiology
*Atraumatic
-Alcoholism -excess steroid use/steroid therapy -others (chemo)
*Traumatic
-Fractures/Dislocations -Iatrogenic
Signs and Symptoms (from podiatry Institute)
Stage I: asymptomatic or perhaps minimal pain and stiffness
Stage II: significant pain and stiffness, occasionally asymptomatic
Stage III: pain and stiffness most typical
Radiology
*Not for early diagnosis
*Subchondral collapse/stress fracture or total joint destruction
*Radiographic Classification of AVN of 1st Met Head (from podiatry Institute)
Stage I: Pre-Collapse
Early: normal density, localized cold bone scan
Intermediate: sclerosis of dead bone due to hyperemia and disuse osteoporosis
Late: true sclerosis due to new bone accretion, hot bone scan
Stage II: Collapse
Early: mild step defect
Late: fragmentation of articular surface and metaphysis
Stage III: Arthritis
Early: joint space narrowing, subchondral cysts and sclerosis, osteophytosis
Late: sclerosis, ankylosis, articular erosion
 Differential Diagnosis
*Arthrosis (DJD)
*RSDS (Reflex sympathetic dystrophy syndrome)
*Infection
Treatment
*Early Stages (Goal: prevent subchondral collapse)
Reduced weight bearing: may involve the use of crutches or the limitation of certain activities
Core decompression: a surgery in which the inner layer of bone is removed. This surgery is most
effective for people in the earliest stages of the disease
*Late Stages (Goal: alleviate pain)
-Osteotomy: reshape bone to stress on affected area. For when AVN affects large area of bone
Bone graft: its effectiveness has not yet been proven
Arthroplasty/total joint replacement: late-stage AVN and/or when the joint is destroyed

Stress Fractures
Symptoms
-Often appear initially as simply pain over the top of the foot, sometimes l but not always l with swelling
-Is usually worse after activity or during activities that require bending of the foot
-Is very common for patients to state that they have no memory of any injury
Causes
-Decreased density of the bones (e.g.. osteoporosis)
-Abnormal foot structure or mechanics (e.g.. flatfoot)
-Increased levels of activity, especially without proper conditioning or Excessive stress (running a marathon)
-Unstable shoes

-Metatarsal fatigue -> microtrauma > ability to heal

-May see displacement l thru and thru or infraction
-Pedal swelling
-2nd digit most common
-Stress riser is an area of cortical medullary loss
-Insufficiency is a type of stress fracture
-Must be able to chronologically gauge stress fracture
Less than 4 wks 4-6 wks Greater than 6 wks
-evidence of acute trauma -amorphous callous -sharply defined callus
TAILORS BUNION DEFORMITY
Splayfoot (common in tailors bunion pts)
-IM angle 1-2 (0-8) + IM angle 4-5 (8+2) > 20
IM angle 4-5 increases when weight bearing
-Lateral Deviation angle C 2.5
-Widening of entire foot medial subluxation of 5th digit on met head
Etiology
-Uncompensated Varus deformity
-5th Ray Function
*5th ray DF and Eversion (hypermobile 1st ray) rotates plantar condyle lateral Tailors bunion (see
sub 4 lesion)
*Inadequate 5th ray ROM (see sub 5 lesion)
-Idiopathic Causes
Absence of Quadratus Plantae Muscle attachment

Cut Distal Medial to Proximal Lateral

Treatment
Locate Apex of Deformity
*Distal Apex (normal to mild increase in IM angle 4-5): exostectomy, distal metaphyseal osteotomy
*Proximal Apex (marked increase in IM angle 4-5): basal osteotomy
Never fuse 5th met (can[t get shoe on)

Lateral Exostectomy
Resect lateral prominence of met head to be flush with shaft
If you[re too aggressive, will lose cubic content on lateral side and joint will sublux medially
Indication: no structural or positional deformity, only for misshapen head
Distal Osteotomy
Indication: Distal Apex (increased LDA, normal IM)
]Reverse 1st met osteotomy^
Reverse Austin
Reverse Mitchell
Shortens
Reverse Wilson
Distal Wedge Osteotomy
Base Osteotomy
Indictaion: High IM angle, severe lateral bowing of 5th met
Moderate to Severe deformity
Trauma

Work-up of a Trauma Patient

There are three other topics that you need to address on every trauma patient for every work-up:
1. ABCDE’s of the Primary Survey
Airway: 3 common forms of airway obstruction:
1) Cervical spine injury
2) Swollen tongue
3) Facial fracture
Breathing: Different than an established airway (Someone can have an airway, but still not be breathing)
Circulation: Assess vascular status in all four extremities
Deficits (Neurological): There are two ways to assess this
AVPU: Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive
Exposure: Complete exposure of the patient to evaluate further, unknown damage
2. Tetanus Status
-Clostridium tetani: It releases an exotoxin causing a presympathetic blockade
-Triad of tetanus symptoms: Trismus (lock-jaw), Risus Sardonicus (fascial m. spasm), Aphagia (canKt swallow)
-Characteristics of a tetanus-prone wound: > 6 hours old, clinical signs of infection, deep, devitalized tissue
Basic Tetanus 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: -Toxoid: 0.5ml

-TIG (tetanus immunoglobulin): 250-300 units

3. NPO status
-Nothing by mouth after midnight the night before elective surgery
-Nothing by mouth within 6-8 hours of any type of surgery

Podiatric Surgical Emergencies

-Infection with emphysema (gas gangrene)
-Open fracture/dislocation
-Compartment syndrome
-Necrotizing Fasciitis
-General Neurovascular compromises
 General Trauma Topics
Open Fractures
-Treatment Mainstays: Aggressive incision & drainage w/copious lavage
(irrigation)
-Never primarily close an open fx until devitalized ST has demarcated
Gustilo-Anderson Classification of Open Fractures
I Clean Wound <1cm in diameter
Abx choice: 1st gen cephalosporin (Ancef)
II Wound 1.0-5.0cm in diameter w/little ST damage
Abx choice: Ancef, Clindamycin
III Wound >5cm in diameter w/extensive ST damage
Abx choice: Ancef, Clindamycin and Aminoglycoside
IIIA Adequate soft tissue coverage

IIIB Extensive ST damage w/periosteal stripping and massive

contamination
IIIC Arterial damage requiring primary repair

Fracture Blisters
Location: Subepidermal
-The fluid is sterile and are histologically similar to 2nd degree burns
Etiology: Secondary to high-energy trauma (ankle fx, calcaneus fx or
Lisfranc injury)
Types of Fracture Blisters
*Clear fluid: Most common (75%)
*Hemorrhagic: Most severe. Roof is flaccid. Takes longer to re-epithelialize
Treatment: conservative approach is to never incise through and delay surgery until re-epithelialization

Foreign Bodies/Puncture Wounds

When to remove foreign object
*Clinical signs of infection, pain, object close to NV elements, intra-articular
Foreign body imaging
*Plain film radiography (no oblique views!), US (make sure its diagnostic ultrasound)
*Glass must be >5mm to be visible
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: Order of OM in pt w/foot trauma: toeas>calcaneus>mid-foot
Puncture wound common bugs
*Most common: Staph A.
*2nd most common? Beta-hemolytic Strep
*Puncture through shoe gear? Pseudomonas
*Puncture involving soil or a farm? Clostridia
*Cat bites? Pasteurella
Mainstays of foreign body/puncture wound treatment
*Tetanus status, antibiotics, aggressive I&D with copious lavage
Shock
Signs/Symptoms: Tachycardia, delayed capillary refill, pulse P, systolic P, urine output
Types of Shock:
Hypovolemic (M.C.): acute loss of circulating blood. Treatment is aggressive fluid replacement
Cardiogenic: induced by myocardial dysfunction
Neurogenic: secondary to sympathetic tone from head and spinal cord injuries
Septic: shock secondary to infection
Goal of Treatment: restore organ perfusion

Gun Shot Wounds

High velocity GSWs: speeds >2500 ft/s. This is significant because high velocity GSWs have a tendency to yaw
and tumble leading to increased cavitation
Cavitation: Negative pressure sucks outside contaminants into the wound

Compartment Syndrome
-Look at “Postoperative Care and Complication” outline

Digital Fractures Workup

Subjective
History of trauma: Bedpost fracture describes stubbing your toe while walking at night. Also common are
injuries from dropping objects on the foot
Diagnostic Classifications
Rosenthal Classification
Zone I: Injury distal to distal aspect of the phalanx
Zone II: Injury distal to the lunula
Zone III: Injury distal to the most distal joint
Treatment
Zone I Injuries
-If no exposed bone and a total tissue loss < 1cm squared, then:
*Allow to heal in by secondary intention
-If total tissue loss > 1cm squared, then:
*Use STSG or FTSG depending on weight-bearing position (skin graft)
Zone II Injuries
-Flaps and Skin Grafts generally employed:
*Atasoy flap: plantar V Y advancement
*Kutler flap: biaxial V Y advancement
Zone III Injuries
-Usually requires distal amputation (Distal Symes amputation)
Miscellaneous Notes
-If subungual hematoma is present, thereKs a 25% incidence of underlying phalanx fx
-If a subungual hematoma covers >25% of the nail, then the nail should be removed
-Only 1mm2 of free space from onycholysis is necessary for hematoma development
-For proper nail function & adherence, should be no onycholysis w/in 5mm of lunula
-A Beau’s line is a transverse groove often associated with nail trauma

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
-Take the time for proper palpation
-Joplin’s neuroma: irritation of the medial plantar proper digital nerve
-Associated with rigidly plantarflexed first metatarsals, anterior cavus, etc
Imaging
Differentiate sesamoid fx from bipartite sesamoid:
*Jagged, irregular and uneven spacing
*Large space between fragments
*Comparison to a contra-lateral view
Also useful are:
*HISTORY of acute incident
*Bone scan (shows in osteoblastic/osteoclastic activity with acute fracture)
Jahss Classification
Type I Type II A Type II B Type II variant
Mechanism Dorsal Dorsal Dorsal Dorsal
dislocation of dislocation of dislocation of dislocation of
the hallux the hallux the hallux the hallux

Intersesamoid Intact Ruptured Ruptured Ruptured

lig.

Fracture No sesamoid No sesamoid Fracture of at Separation of a

fracture fracture least one bipartite
sesamoid sesamoid

Treatment Requires Closed Closed Closed

open reduction/ reduction/ reduction/
reduction Conservative Conservative Conservative
Care Care Care

Conservative Treatments
-Immobilization
-Dancers Pad
Surgical Treatment
-Excision of the fractured fragment or entire sesamoid
Miscellaneous Notes
IlfeldKs Disease: Agenesis (failure to develop) of the fibular sesamoid
Incidence of Bipartite Sesamoid in Population:
-As much as Kewenter: 35.5%
-As few as Inge: 10.7% with 75% of cases being unilateral
Metatarsal Fractures
Subjective and Objective
-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

Metatarsal Head/Impaction Fractures

MOI: Direct or indirect trauma
Radiographic findings: Expect a shortening mechanism
Conservative Treatment: Closed reduction generally unsuccessful
Surgical Treatment:
*ORIF with fixation of K-wire, screws or absorbable pins
*Immobilization for 4-6 weeks and NWB

Metatarsal Neck Fractures

MOI: Shearing forces or direct trauma
Radiographic findings: Expect elements of shortening, PF, and lateral displacement of the distal segment
Conservative Treatment: Closed reduction generally unsuccessful
Surgical Treatment:
ORIF effective in restoring and maintaining alignment with K-wires, IM pinning and plates
General Information:
*Metatarsal neck fractures often involve multiple metatarsals due to the mechanism of injury.
*Multiple fxKs are unstable from loss of function of DTIL, which usually prevents displacement
Vassal Principle: Adjacent fractures generally improve alignment after reduction of the initial fracture
because soft tissue structures are returned to their normal position through traction

Midshaft Metatarsal Fractures

MOI: Result of direct, blunt or torsional injuries
Radiographs: Expect oblique fracture line, but transverse, spiral and comminuted are all possible
Expect elements of shortening, plantarflexion and lateral displacement of the distal segment
Treatment: Based on displacement and fracture type:
Non-displaced fractures: NWB SLC 4-6 weeks
Fractures w/>2-3mm of displacement and >10 degrees of angulation: ORIF
Transverse displaced fractures: Consider plates, IM percutaneous pinning, crossed K-wires
Long oblique or spiral fractures: Consider screws, plates, IM pinning, cerclage wiring
Comminution: Consider screws, plates, cerclage wiring, K-wires and external fixation

Metatarsal Base Fractures

MOI: Direct trauma (MVA, fall from height, etc.) Usually associated with LisfrancKs trauma
Radiographs: Generally remain in good alignment/angulation because of surrounding stable structures

First Metatarsal Fractures

MOI: Direct trauma (MVA, fall from height, etc.) & indirect trauma (torsional, twisting, avulsions, etc.)
Radiographic findings: Variable
-Examine for distal intra-articular fractures
-Examine for avulsion-type fractures
Conservative Treatment:
-Be wary of closed reduction because extrinsic muscles may displace after apposition
Surgical
-Various ORIF techniques, Percutaneous pinning & cannulated screws are option in first met
-ORIF should be utilized if intra-articular fracture involves >20% of articular surface
5th Metatarsal Base Fractures
Subjective and Objective
-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

Stewart Classification
Type I: Extra-articular fx at metaphyseal-diaphyseal junction
*(True Jones Fracture)
MOI: FF Internal rotation while 5th met base remains fixed
Radiographs: Usually oblique or transverse fx at
metaphyseal-diaphyseal junction
Treatment: NWB SLC 4-6 weeks for non-displaced fractures, ORIF with displacement >5mm
*Very unstable fx w/ incidence of non-union/delayed union secondary to variable blood supply.
-Remember, diaphysis & metaphysis are generally supplied by 2 different arterial sources
Type II: Intra-articular avulsion fracture
MOI: Shearing force caused by internal twisting with contracture of peroneus brevis tendon
Radiographs: 1 or 2 fracture lines, Intra-articular in nature
Treatment: NWB SLC 4-6 weeks for non-displaced fractures, ORIF with displacement >5mm
Type III: Extra-articular avulsion fracture
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 for displacement >5mm
*Consider excision of fragment and reattachment of peroneus brevis tendon
Type IV: Intra-articular, Comminuted fracture
MOI: Crush injuries with base of 5th 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
Type 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)

Stress Fracture
Subjective
CC: Pt presents complaining of diffuse foot & ankle pain. Classic patient is a military recruit or athlete
HPI: Nature: Pain described as ksharp w/WBl or ksore/achingl. May have element of kshootingl pain
Location: Common areas are dorsal met or distal tib/fib
Course: Subacute onset. Usually related to an increase in patientKs physical activity
Aggravating factors: Activity
Alleviating factors: PRICE
PMH: Look for things that would weaken bone (eg. Osteoporosis)
Objective
Derm: Generalized or localized edema [Ecchymosis (subcutaneous purpura) is rare]
Ortho: Painful on localized palpation (positive pinpoint tenderness), Possible pain with tuning fork
Imaging
Plain Film Radiograph: Localized loss of bone density and bone callus formation are hallmark signs
*Must be 30-50% loss of bone mineralization (10-21 days) before bone density is seen on x-ray
Bone Scan: Increased uptake in all phases regardless of time of presentation
Stress fractures can occur via two mechanisms:
1. Chronic strain upon a normal bone
2. A chronic, normally benign strain upon a weakened bone
Treatment
Conservative treatment is mainstay:
*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)
 Lisfranc Trauma
Sagittal plane motion of the three functional columns of the Lisfranc joint:
*Med Column (1st met & med cuneiform): 4mm of motion in sagittal plane
*Central (2nd/3rd mets & central/lat cuneiforms): 1mm of motion in sagittal plane
*Lat. Column (4th/5th mets and cuboid): 10mm of motion in sagittal plane

Mechanism of Injury
*Most common in MVA and sports injuries
*Occurs by direct crushing (i.e. dropping something on the foot) or indirectly (usually a PFKed & abducted foot)

Diagnosis
Clinical
-Midfoot pain and tenderness. Exacerbated when foot pronates, abducts or PFKs (when FF is locked)
-Plantar ecchymosis
-Be wary of compartment syndrome! Always check neurovascular status
Plain Film Radiography
-Pathognomonic “fleck sign” (small fragment avulsed by the Lisfranc ligament)
representing an avulsion fx in the 1st IM space (best seen on MO view)
-Look for deviations from normal in the AP, MO and Lat views
-“Lisfranc variant”: fx damage extends proximally into cuboid-navicular region
-Consider stress radiographs with the foot in plantarflexion or abduction
-Nutcracker Fx: compression fx of cuboid between calcaneus and 4th & 5th met

Myerson Classifications (Classification is listed w/the Quenu and Kuss equivalent in parentheses)
Type A: Total incongruity in any plane (QK: Homolateral)
Type B: Partial incongruity (QK: Isolateral)
B1: 1st met 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)

Treatment
*ORIF with any displacement (>2mm between 1st and 2nd mets)
*If plain film and stress radiographs show no displacement, then NWB SLC for 6 weeks

Operative
Goal: Reduce & stabilize of medial & central columns. You must reduce the lateral column, but itKs usually left
unfixed bc of the pronating mobile adapter mechanism
Fixation: 1st met to medial cuneiform, 2nd met to central cuneiform, and 3rd met to lateral cuneiform with crossed
0.062l K-wires (removed at 8 weeks), cannulated cancellous screws (removed at ~12 weeks) or 3.5mm
corticals. Consider 4th met to cuboid and 5th met to cuboid with a single 0.062l K-wire
-Lat. column length must be restored following knutcracker fxl (Consider an H-plate or external fixation)

Complications
*ARTHRITIS! 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

Objective
*MMT (manual muscle testing) of the PT tendon is important in these cases

Relevant Anatomy
*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 DP artery supplies the dorsal and medial aspects
-The medial plantar artery supplies the plantar and lateral aspects
-The central 1/3 has variable, radially-projecting branches from anastomosis
of these arteries

Watson-Jones Classification
Type I: Navicular Tuberosity Fractures
-Occurs 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
-Treatment:
*Displacement <5mm: Conservative immobilization
*Displacement >5mm: Excision of fragment w/tendon reattachment

Type II: Dorsal Lip Avulsion Fractures

-Occurs secondary to plantarflexion/frontal plane mechanisms
-Differentiate from os supranaviculare & os supratalare accessory ossicles
-Generally treated with conservative immobilization

Type III: Navicular Body Fractures

IIIA: Coronal Plane Fracture with no angulation (100% successful reduction usually achieved)
IIIB: Dorso-lat to Plantar-med fx w/forefoot adduction (67% successful reduction usually achieved)
IIIC: Comminution with abduction of the forefoot (50% successful reduction usually achieved)

Principles of ORIF for Type III fractures:

*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 using 3.5mm Cortical Screws:

*2 screws directed lateral to medial
*2 crossed screws directed proximal to distal
*1 screw directed prox-med to distal-lat into middle cuneiform (©)
*Consider FDL transfer in the presence of a weakened PT tendon

Type IV: Stress Fracture of the Navicular

-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
 Talar Fractures
-Talar fractures are generally associated with high energy trauma
Subjective
*History of trauma w/a high incidence of MVC.
*Classic talar neck fracture description: forced DF of the foot on the ankle (kaviatorKs astragulus)

Objective
*Important to verify NV status, & rule out dislocations & compartment syndromes

Imaging:
Canale & Kelly View: Plain film radiograph taken w/foot in a PF 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

Relevant Anatomy
*An intimate knowledge of the vascular
supply to the talus is essential with regard
to avascular necrosis (AVN):
*Dorsalis Pedis: Supply the superior
aspect of the head and neck (artery of the
superior neck)
-Artery to the sinus tarsi: supplies
the lateral aspect of the talar body
*Posterior Tibial Artery:
-Deltoid branch: medial aspect of
the talar body
-Artery of the canalis tarsi:
majority of the talar body
*Peroneal/Perforating Peroneal
Artery: supplies posterior and lateral
aspects of the talar body

Hawkins Classification: (Talar NECK fractures)

Type I: Non-displaced (~13% incidence of AVN)
Type II: Displaced fx w/STJ dislocation (~50% incidence)
Type III: Displaced fx w/STJ and ankle dislocation (~95%)
Type IV: Displaced fx w/STJ/ankle/TN dislocation (>95%)
-(Type IV added by Canale and Kelly)
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

Talar Dome Lesion Location (DIAL a PIMP)

-DF, Internal rotation = Ant. Lat. lesion
-PF, Inversion = Med. Post. lesion

Sneppen: (Talar BODY fractures)

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

Modified Hawkins: (Lateral process fractures)

Type I: Simple bipartite fracture from AJ articulation to STJ
Type II: Comminuted fracture involving calcaneus and fibula articulation
Type III: Chip fracture of anteroinferior lateral process

Others:
ShepherdKs fx: acute fx of posterolateral talar process
CedellKs fx: acute fx of the posteromedial talar process
SnowboarderKs fx: lateral process fractures

Treatment
Titanium hardware may be used so MRI evaluation may be used in post-operative period to evaluate for AVN!
Hawkins sign: radiolucency of talar body noted at 6-8 weeks after fracture (is indicative of intact vascularity)
-However, the absence of this sign does not indicate that osteonecrosis and talar collapse are eminent

Calcaneal Fractures
Subjective
Common mechanisms of injury
-Vertical shear force (gravity), MVC, gastroc contraction, stress fracture, ballistics, iatrogenic surgical fx
Objective
Physical Exam:
-Pain with palpation to heel
-Inability to bear weight
-Short, wide heel
Hoffas sign: less taut Achilles tendon on involved side
Mondors Sign: characteristic ecchymosis extending into plantar medial foot
Plain film Imaging:
Bohler’s Angle: normally 25-40 degrees ( with fracture)
Critical Angle of Gissane: normally 125-140 degrees ( with fracture)
*Both demonstrate loss of calcaneal height
Broden’s View: 2 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
Sanders Classification: Uses widest view of posterior facet on semicoronal CT cut
*Type I: Non-displaced articular fx *A, B and C further describe the fx (lateral medial)
*Type II: Two-part posterior facet fx *A/B: divide posterior facet into equal 1/3Ks
*Type III: Three-part posterior facet fx *C: divides posterior facet from sus tali
*Type IV: Four-part/comminuted fx

-See page 1845 of McGlams

Rowe Classification:
Type I:
-Type IA: Plantar tuberosity fractures [medial (eversion) more common than lateral (inversion)]
-Type IB: Sust-tali fracture (remember FHL: pt will have pain with hallux PROM)
-Type IC: Anterior process fractures (bifurcate ligament avulsion fx; goes to cuboid & navicular)
-further divided into three parts by Degan Classification
Type II:
-Type IIA: Extra-articular “beak” fracture of post-sup calcaneal body (heel strikes ground w/knee
extended and foot dorsiflexed)
-Type IIB: Intra-articular “tongue-type” Achilles avulsion fx (same as IIA, but complete dislocation)
Type III: Extra-articular calcaneal body fracture (no STJ involvement; from fall)
Type IV: Intra-articular joint depression fracture (STJ involvement)
Type V: Intra-articular comminuted fracture
Essex-Lopresti Classification (Replaces Rowe Type IV & V)
-Discerns between extra-articular (~25%) & intra-articular (~75%) fxKs
Intra-articular fractures:
*Same primary force, but different secondary exit points
*Tongue-type: Axial load plantarfelxed
*Joint depression fractures: Axial load Dorsiflexed

Zwipp Classification
-Assigns 2-12 points based on: 1) Number of fragments 2) Number of involved joints

Treatment
*Appreciate the debate in the literature between cast immobilization vs. percutaneous reduction vs. ORIF vs.
primary arthrodesis [Barei DP, Fractures of the calcaneus. Orthop Clin North Am. 2002 Jan; 33(1): 263-85.]
*Goals of therapy are to restore calcaneal height, decrease calcaneal body widening (reduce lateral wall blow-
out), take it out of varus, and articular reduction
*Review the lateral extensile surgical approach [Benirschke SK, Sangeorzan BJ. Extensive intraarticular
fractures of the foot. Surgical management of calcaneal fractures. CORR. 1993 Jul; 292: 128-134.]
*Complications: Wound healing, arthritis, lateral ankle impingement, malunion, nonunion, etc.

Patient Work-up
45 Year old fell off a ladder while hanging Christmas lights and states he cannot walk on his
heel because it hurts too bad
Subjective: CC/HPI, PMH, Meds/Allergies, PSH, FAM Hx, Social, ROS,

Objective
*Vitals
*Check for Polytrauma
-DonKt forget to look proximally for associated trauma
*Must rule out L 1-2 veterbral fracture (Seen in 10% of Calc fractures)
-You evaluate this by asking about ability to have bowel movements
*Also look for other associated fractures of the foot/leg
*What do you want to order?
*Presenting where? Initial treatment? Reduced in ED or not?

Physical Exam
Vascular
-Make sure you assess pulses due to trauma
-Be suspicious of Compartment Syndrome (in 10-20% of calcaneal fxKs) (look in post-op care section)
*Clawing of the toes after calcaneal fracture = be suspicious of compartment syndrome
-This is sometimes also referred to as Volkmann’s Contracture (more for the hand)
-Due to late contracture of Quadratus Plantae muscle in calcaneal compartment which
communicates w/the post compartment of the leg & causes flexors to cause claw toe
Neuro
Any damage to the sural or large P.T. nerves that run around the ankle joint (Not common)
Derm
Mondor’s Sign: Ecchymosis to med & plant aspect along tarsal tunnel (pathopneumonic for calcaneal fx)
-Fracture blisters can arise quickly and must be properly respected
*ORIF of calcaneus must either be done immediately after injury before fracture blisters occur
*Or you must wait for fracture blisters to resolve before ORIF can be done
-Delta frame is a good idea if it is a significant calc fracture w/significant ST involvement
-Must have a positive wrinkle test in order to proceed with surgery
Musculoskeletal
-Significant pain with medial and lateral compression of the heel
Radiographic Interpretation
-Read them out loud making sure you describe the fractures as well as classification
Assessment
*Rank from most probable to least probable
*List 3 or 4 other differentials
*Calcaneal Fx: make sure to include open vs. closed, dislocated vs. non-dislocated, displaced vs. non-displaced

Plan
*To surgerize or not to surgerize?
-Worried about fracture blisters
-Do it quickly. If not, reduce and put them in a posterior splint
*With Posterior splint ice behind the knee not on top of the splint
-Plan for definitive treatment
*Soft tissues will dictate the time frame
*If fx blisters occur, consider putting patient in a delta frame to keep length & prevent contracture
-This would remain on for 1-2 weeks as dictated by the skin quality and turgor
*DonKt rule out ex fix with diabetics or those that are non-compliant

Treatment
Goals of Treatment
-Primarily to restore close to perfect anatomical alignment of the STJ and CCJ
-Secondarily to restore the calcaneus to its proper Height, Width, and Length

Conservative Treatment
-Closed Reduction (Either performed by you or the E.D. docs on initial presentation)
-Immobilize (Posterior Splint most often utilized) u Get to 90° at the AJ
-If not surgical candidate or doesnKt require surgical intervention plan for cast application
*Sometimes calcaneal fractures that are completely comminuted are better treated conservatively
so as to not add more injury to insult of the tissues and neurovascular that is already damaged.
You may make things worse by trying to fix the pieces together and would do better just to let the
pieces consolidate and plan for a STJ fusion down the road
-Cast applied in office or at the ED either way but make sure you maintain the 90° relationship of the AJ
-Cast usually indicated for 4 - 6 weeks NWB or until trabeculation across fx site is noted radiographically
*At that time patient may be transitioned into a CAM walker for another 4-6 weeks PWB and
transitioned into a shoe as tolerated

Surgical Treatment
AO principles
-Perfect Anatomic Reduction
-Rigid Fixation / Immobilization
-Atruamatic technique
-Early Range of Motion

AO Technique
1. Underdrill
2. Overdrill glide hole (If trying to provide compression with a fully cortical screw)
3. Countersink
4. Measure
5. Tap
6. Insert Screw

Typical treatment of a calcaneal fracture

-Lateral Extensile incision approach most commonly used
*Watch out for Sural nerve, peroneal tendons, and small saphenous vein
*Incision needs to be taken down to bone with the soft tissue flap with the periosteum being
reflected superiorly with atraumatic (No Touch) technique
*Place a 1 k-wire in neck of talus & 1 in lateral malleolus to hold the full thickness flap
*From this point try not to touch the flap bc every time you do you risk of complication
 -Reduce from Front-to-back
*ant process post Facet tuberosity Re-establish post Facet
height Reduce from varus
-In order to reduce the varus, a Steinman pin is placed
transversely though the calcaneus
-Once reduced in a manner that is adequate and acceptable
*Place temporary fixation (K-wires) to hold the pieces in proper
alignement
*Make sure your temporary fixation is out of the way of your
permanent fixation
-When everything is reduced and held in place you can pack the void with bone chips
-With the posterior facetKs height restored the lateral wall can be relocated
-Final fixation will be put in place (Sizes of screws depend on plate used)
*Many options are available but usually some type of lateral plate is used
-The plate is used to maintain the tuberosity position out of varus
-This must be verified with calc axial before definitive fixation is placed
-Drain can be applied but should be removed after 24 u 48 hours
-Must take extreme care in closing the flap back over the plate and such
*Modified Denotti suture technique can be utilized which obviates need of suturing through flap
-Consider using a jones compression splint post-op w/red cross cotton to provide sufficient compression
*Calcaneal fx ORIF causes significant post-op edema which needs to be controlled to prevent
complications

Ankle Fracture Evaluation

-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

Relevant Anatomy to Review (not just for this topic; think

lateral ankle instability, peroneal tendonopathy, sprains, etc.):
Ankle Ligaments:
Lateral: ATFL, CFL, PTFL
Medial: Superficial Deltoid: superficial talotibial,
naviculotibial, tibiocalcaneal ligaments
Deep Deltoid: ant. talotibial & deep posterior ligKs
Syndesmotic Ligaments:
AITFL, PITFL (and inferior transverse tibiofibular
ligament), Interosseous ligament

Ottawa Ankle Rules

[Stiell IG, et al. A study to develop clinical
decision rules for the use of radiology in acute
ankle injuries. Ann Emerg Med. 1992;21(4):
384-90.]
*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 5th met
-Bone tenderness on the navicular
-Inability to bear weight/walk 4 steps in ED
Lauge-Hansen Classification

Supination-Adduction
Stage 1: Transverse fracture of lateral malleolus, at or below the level of
anterior talo-fibular ligament or a tear of lateral collateral ligament structures
with the anterior talofibular ligament disrupted most often and frequently the
calcaneofibular ligament also being torn (Weber A)
Stage 2: Oblique fracture of medial malleolus (Muller D)

Supination-External (Eversion) Rotation

Stage 1: Rupture of ant. Inf. tibiofibular ligament
Stage 2: Oblique or spiral fx of lat. Malleolus
(Weber B)
Stage 3: Rupture of post tibiofibular lig. or fracture
of posterior malleolus of tibia
Stage 4: Transverse (sometimes oblique) fracture of
Tibial malleolus (Muller B)
*40% - 70% of all ankle fractures

Pronation-Abduction
Stage 1: Rupture of the deltoid ligament or transverse fracture
of the medial malleolus (Muller B)
Stage 2: Rupture of the anterior and posterior inferior
tibiotalofibular ligaments or bony avulsion
Stage 3: Oblique fx of fibula at level of syndesmosis (Weber B)
Less than 5% of ankle fractures

Pronation-External (Eversion) Rotation

Stage 1: Deltoid ligament rupture or transverse
fracture of the medial malleolus (Muller B)
Stage 2: Rupture of the anterior inferior
tibiotalofibular ligaments or bony avulsion
Stage 3: Spiral/Oblique fracture of the fibula
above the level of the syndesmosis (Weber C)
Stage 4: Rupture of the posterior inferior
tibiofibular ligament or fracture of the posterior
malleolus

Pronation-Dorsiflexion
Stage 1: Fracture of the medial malleolus
Stage 2: Fracture of the anterior lip of the tibia
Stage 3: Fracture of the supramalleolar aspect of the fibula
Stage 4: Rupture of the posterior inferior tibiofibular ligament or fracture of the posterior malleolus
Danis-Weber/AO Classification (for lateral malleolar fractures) (From AO Group)
Type A Infrasyndesmotic Type B Transyndesmotic Type C Suprasyndesmotic
Below level of the ankle joint At level of ankle joint, extending Above the level of the ankle joint
Tibiofibular syndesmosis intact superiorly & laterally up fibula Tibiofibular syndesmosis
Deltoid ligament intact Tibiofibular syndesmosis intact or disrupted with widening of the
Medial malleolus often fractured partially torn, but no widening of distal tibiofibular articulation
Usually stable: occasionally the distal tibiofibular articulation Medial malleolus fracture or
requires an (ORIF) Med malleolus may be fractured deltoid ligament injury present
or deltoid ligament may be torn Unstable: requires ORIF
Variable stability

Mueller Classification (for medial malleolar fractures) (From AO Group)

A B C D
Avulsion Transverse at level of mortise Oblique Near vertical

Radiology

Talocrural Angle (Mortise View) Bimalleolar Angle (Mortise View) Dime Sign (Mortise View) Shenton Line (Mortise View)
Uses the line perpendicular to the Uses the intramedullary canal of the Unbroken curve between the Small spike or fibular tubercle can
tibial plafond as the vertical line distal fibula as the vertical line the lateral talus and the peroneal be seen and should be in line with
bisector is the intermalleolar line. groove of the fibula the tibial subchondral bone
Normal = 75 - 86°
Work Up
Subjective
o CC/HPI, PMH, Meds/Allergies, PSH, FAM Hx, Social, ROS
Objective
o Vitals
o Check for Polytrauma
o What do you want to order?
o Presenting where? Initial treatment? Reduced in ED or not?
Process of reduction
3 steps of reduction:
1) Exaggerate deformity
2) Distract adequately
3) Relocate reversing MOA
For Example: SER IV ankle fracture
1. Exaggerate by supinating and externally rotating the foot
2. When in proper exaggerated location pull out
3. In one sweeping motion after pulling out relocate the foot into proper alignment by
pronating and internally rotating the foot on the leg
Hematoma block / Conscious sedation
Hematoma Block u consists of injecting the patients AJ with 10 u 20 ccKs of Lidocaine plain in
order to insufflate the joint as well as provide analgesia
Conscious Sedation u Also can be used depending on the patient
Give patient versed or other benzo along w/an inducing agent such as propofol if IV
started or possibly Ketamine in order to put the patient under while reduction takes place.
Physical Exam
V: Make sure you assess pulses due to trauma
N: Any damage to the sural or large P.T. nerves that run around the ankle joint (Not common)
D: Mostly concerned about fracture blisters or if it is open note SOI
M: will mostly be deferred due to splinting and guarding of injury
Radiographic Interpretation
Read them out loud making sure you describe the fractures as well as classification
Assessment
o Rank from most probable to least probable
o List 3 or 4 other differentials
o Ankle Fx: include open vs. closed, dislocated vs. non-dislocated, displaced vs. non displaced
Plan
o Initial treatment from ED
o To surgerize or not to surgerize?
*Worried about fracture blisters
*Do it quickly
*If not reduce and put them in a posterior splint
-With Posterior splint ice behind the knee not on top of the splint
*Plan for definitive treatment
-Soft tissues will dictate the time frame
-If fracture blisters occur consider putting patient in a delta frame to keep length and
prevent contracture
*This would remain on for 1-2 weeks as dictated by the skin quality and turgor
-DonKt rule out ex fix with diabetics or those that are non-compliant
Principles of Fixation:
Restore fibular length
*Most people agree that fibular fracture is the dominant fracture. So, if you adequately reduce the fibula, then
other fractures and dislocations more or less fall into line because of soft tissues (poor manKs definition of
the Vassal Principle). It doesnKt mean that other fractures donKt require fixation, but it means thereKs no
real sense in fixating the other fractures unless you have the dominate fracture fixated (or at least reduced)
*A fixed fibula is essentially acting as a buttress, keeping the talus within the ankle mortise
*The fibula is generally shortened in ankle fractures, so you want to get the full length back with your reduction
-[Yablon IG, et al. The key role of the lateral malleolus in displaced fractures of the ankle. JBJS-Am.]
*Restore the ankle mortise (medial clear space and the syndesmotic gap)
-Remember fibula keeps talus in ankle mortise. Ramsey and Hamilton showed a 42% decrease in the
tibiotalar contact area when the talus was displaced 1mm laterally. From this, people inferred that
if the talus isnKt perfectly reduced back into mortise, then gross instability occurs
-This is assessed by:
*Medial Clear Space (Mortise)
-E F (Normal = <4-6 mm)
-If = Deltoid insufficiency
*Tib-Fib Overlap (AP)
-B C (Normal = 6 mm to 1 cm)
-If be suspicious of syndesmotic rupture
*Tib-Fib Clear space (AP)
-A B (Normal = <6mm)
-[Park SS, et al. Stress radiographs after ankle fracture: the effect of ankle position and deltoid
status on medial clear space measurements]

Treatment

*Ring theory states that the ankle can be thought of with 3 important
stabilizing structures from most important to least important:
1. Lateral Malleolus / LCL ligaments
2. Medial Malleolus / Deltoid Ligaments
3. Tib-Fib Syndesmosis / AITFL, PITFL, IOL
*Theory suggests an ankle is stable as long as a minimum of two of the
stabilizing structures are intact
*If however 2 or more of the stabilizing structures have been altered, surgical
correction is warranted
*When any 1 of the stabilizing structures are altered drastically (ie. Major
displacement) surgical correction can also be warranted because of instability

Conservative Treatment
Closed Reduction (Either performed by you or the E.D. docs on initial presentation)
Immobilize (Posterior Splint most often utilized) u Get to 90° at the AJ to avoid contractures
If not surgical candidate or doesnKt require surgical intervention plan for cast application
o Cast applied in office or at ED either way but make sure you maintain 90° relationship of the AJ
o Cast usually indicated initially for 4 u 6 weeks or until trabeculation across fracture site is noted
radiographically
o At that time patient may be transitioned into a CAM walker for another 2-3 weeks and
transitioned into a shoe as tolerated
Surgical Treatment
*AO principles
1. Perfect Anatomic Reduction
2. Rigid Fixation / Immobilization
3. Atruamatic technique
4. Early Range of Motion

*AO Technique
1. Underdrill
2. Overdrill glide hole (If trying to provide compression with a fully cortical screw)
3. Countersink
4. Measure
5. Tap
6. Insert Screw

*Typical treatment of a fibular fracture

-Incision down to bone over Fibula
-Perfect anatomic reduction achieved with length restored verified with flouro
-Insert 2.7 Interfrag screw, partially threaded (or fully threaded with lag technique)
-1/3 tubular plate applied laterally (or postero-lateral with Anti-glide Plate with SER fractures *7*)
-3.5 fully threaded screws through holes in the plate
*You want 3 screws proximal to fracture in a bi-cortical fashion
*As many distal to fracture as you can get, note that any screws distal to AJ line should be
cancellous in a unicortical fashion

*Typical treatment for a medial malleolar fracture

-Two 0.062 K- Wires inserted in the medial malleolus from distal to proximal across the fracture site
-Two 4.0 malleolar cannulated screws inserted
-Other options would include tension band which is actually a very good fixation for this type of fracture
 General Tendon Trauma
Mechanism of Injury
*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:
-Tension overload on a passive muscle
-Eccentric overload on an actively contracting muscle
-Laceration
-Blunt Trauma

Factors which can intrinsically weaken tendons

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

Imaging in Diagnosis of Acute Tendon Injury

*Plain Film Radiograph: May see avulsions, soft tissue swelling, accessory bones/calcifications
*Tenograph: Radiopaque dye injected into tendon sheath and viewed on plain film radiograph
*Ultrasound: Tendon normally appears hyperechoic to muscle on US
-See alternating hyperechoic and hypoechoic bands w/rupture
-It is very important that the US head is held perpendicular to the long axis of the tendon
*CT: Tendon normally appears as a homogenous, well-circumscribed oval surrounded by fat on CT.
-Will be able to appreciate discontinuity on CT with injury
*MRI: -T1: Tendons normally have a uniform low-intensity (very black)
-T2: Tendons are normally low-intensity. Will light up w/high-intensity signal w/injury (from hematoma)
-Remember the 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
-[Mengiardi B, et al. Magic angle effect in MR imaging of ankle tendons: influence of foot positioning on
prevalence and site in asymptomatic patients and cadaver tendons. Eur Radiol]

Principles of Repair
*Special attention should be paid to vascular supply. Remember that the majority of a tendonKs vascularity comes
from the mesotenon, and therefore should be preserved as much as possible
*If primary repair not possible, consider using lengthening tendon slides, grafts, tendon transfers & biomaterials
such as Graft-Jacket (allograft dermal tissue matrix) or Pegasus (equine pericardium) to restore tendon integrity
*Goal of treatment: allow early PROM without gapping of the tendon
Achilles tendon Rupture Work-Up
Subjective:
CC: Typical complaint is pain, weakness & swelling in back of the leg following acute injury. The typical patient
is kweekend warriorl (30-50 y/o male participating in strenuous athletic activity after a general inactive lifestyle)
HPI:
Nature: Pain, weakness and swelling. Pain is surprisingly non-intense allowing the patient to ambulate.
Pt may relate an audible kpopl or ksnapl or feeling they were kkicked or shotl in back of the leg
Location: Distal posterior leg. The left leg is more affected. Some people theorize that this has to do with
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:
1. Unexpected dorsiflexion with triceps contraction
2. Pushing off during WB with the leg extended (tennis lunge)
3. Violent dorsiflexion on a plantarflexed ankle
-Also consider lacerations and blunt trauma
Previous History: obviously more likely to re-rupture
PMH:
Inflammatory conditions: RA, SLE, Gout
Endocrine dysfunction: DM, Renal failure w/hyperparathyroidism, hyperthyroidism, Xanthoma
Infection: Syphilis
Meds:
Corticosteroid injection
Fluoroquinolone use
SH: Smoking, Sedentary lifestyle with weekend activity

Objective:
Derm: Posterior, Medial and Lateral Ecchymosis
Open lesion associated with laceration
Vasc: Posterior, Medial and Lateral edema Hatchet strike defect: tender, palpable defect 2-6cm proximal to
Neuro: Sural Neuritis insertion site
Ortho: Thompson Test: patient lies prone on table w/foot extended
beyond the end of the table & the examiner squeezes the calf. A
-Palpable gap (Hatchet strike defect) normal non-injured response to this maneuver is slight
-Positive Thompson test plantarflexion of the ankle. Lack of ankle movement can indicate a
-Negative Jack’s test rupture of the Achilles' tendon.
Jack’s test (Hubscher's maneuver): patient weight bearing while
-Pain in the area
clinician DFKs hallux and watches for the formation of an arch.
-Increased PROM ankle dorsiflexion -Positive result (arch formation) from flatfoot being flexible
-Decreased AROM ankle plantarflexion -Negative result: (no arch formation) from flatfoot being rigid
-Retraction of proximal gastroc belly
-Apropulsive gait
Other specific tests:
*Mattles test: Foot should be in PF position w/patient prone & knee at 90°
*Simmonds’ test: Foot should be in PF position with patient prone
*Various needle tests (O’Brian, Cetti)
*Toygar’s skin angle: Normal 110-125°. Increases to 130-150° w/rupture
Imaging: (see above)
-Plain film: r/o Rowe Type IIB avulsion fracture
-Obliteration of Kagers triangle
-Soft tissue edema
Achilles Tendon Rupture Treatment
Anatomy Review
-Muscles of the Triceps Surae (origins, insertions, NV supply, action)
-Plantaris (origins, insertions, NV supply, action)
-Segmental Blood Supply of Tendon
-kTwistingl of tendon
Specific Information regarding the Watershed Area
-Lagergren and Lindholm (used human cadavers for study)
*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
-Leadbetter
*Found increased stress/strain at the watershed area regardless of vascularity

Kuwada Classification of Achilles Tendon Ruptures

Type I: Partial tear involving <50% of tendon. Note that in a partial Achilles tear, the posterior fibers are torn
first. So the direction of the tear/rupture is from posterior to anterior
Type II: Complete tear with <3cm deficit
Type III: Complete tear with a 3-6cm deficit
Type IV: Complete tear with a >6cm deficit

Puddu Classification of Chronic Achilles Pathology

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 repair

Do nothing
-Gap will eventually fill in with fibrotic scar tissue (usually requires later surgical intervention)
Cast Immobilization
-AK cast versus SLC (Schuberth is proponent 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
Surgical Repair
Surgical 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
Primary Open Repair
*Keith needles with non-absorbable suture (or fiberwire) with
absorbable sutures to reinforce
*There are three common stitches used:
A) Bunnell: Figure of 8 or weave stitch
B) Kessler: Box stitch
C) Krakow: Interlocking stitch
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
*V Y lengthening of the proximal segment with primary repair
*Reinforcement with FHL
*Graft Jacket, Pegasus, etc.
Percutaneous Primary Repair
*Ma and Griffith described a percutaneous Bunnell-type approach
*May be associated with high re-rupture rates
Post-Op Treatment
SLC in gravity equinus with gradual reduction over 6-10 weeks