material used for final exam preparation *at own risk

1. Diabetic foot
1. History
a. Affect propioception 1st
b. Why current admission?
c. Trauma → infection (sequence) → gangrene
d. Diabetic neuropathy → pain is late symptom d/t pain occur when deep structure is involve
e. Symptoms
i. Polyuria, polydipsia, nocturia, weakness (hypoglycemia), hx of candidia infection
f. Diabetic control
i. Poor control → infection
ii. Eating habit
g. Duration of DM
i. Systemic ds
ii. BOV → cataract
iii. Heart → chest pain
iv. Sympathetic neuropathy
v. Parasympathetic neuropathy → dry eye, periodic diarrhea
vi. Urinary problem
vii. Neuropathy → loss of sensation → gait
h. Fever → uncommon d/t immunocompromise pt
i. Amputated feet → can walk / climb → any CVS problem (d/t use more energy to walk)
j. Occupationhx → footactivity,eatingtime,regularmeal?Type of meal?Outside food?Amount of food?
k. Lifestyle
l. Medications: regular? Type?
m. Monitoring of DM
n. Previous admission
o. Diet hx → type of food, where the food from
p. Pt knowledge about DM, taught how to care foot? Know early symptoms of diabetic foot problem?
q. Compliance to medication, what type of medication, any measure machine at home
r. Hx of fracture
i. Non-union
ii. Tissue dead → bone no growth
iii. ↑ osteoclastic activity → osteopenia
2. Physical examination
a. General
i. Metabolism syndrome: obesity, Body built
ii. BP
iii. AV fistula
iv. Hygiene
v. Injection scar at abdomen
b. Head
i. Eye (fundoscopy)
● Premature Cataract (change in water content)
● Diabetic retinopathy
c. Neck
i. Carotid → bruit
● Microembolism
● TIA secondary to embolism
ii. JVP
d. Heart
i. Chest pain → IHD (coronary ds)
ii. Cardiomegaly
e. Renal
i. Early nephropathy → polyuria, ascites, anuria, nocturia, tiredness
f. Limb
i. Hypoaesthesia (distal to proximal not according to dermatome; at level of distal tibial?)
ii. Peripheral pulse

2. iii. Ankle-brachial index (0.5-1.0 Dr Azani)
● Ratio of the blood pressure in the lower legs to the blood pressure in the arms.
● Comparedto the arm, lowerbloodpressure inthe legisan indicationof blockedarteries
(peripheral vascular disease).
ABPI value Interpretation Action Nature of ulcers, if present
above 1.2 Abnormal
Vessel hardeningfromPVD
Referroutinely Venousulcer
use full compressionbandaging
1.0 - 1.2 Normal range None
0.9 - 1.0 Acceptable
0.8 - 0.9 Some arterial disease Manage riskfactors
0.5 - 0.8 Moderate arterial disease Routine specialist
referral
Mixedulcers
use reducedcompression
bandaging. Claudication maybe presentatvalues
lessthan0.6.[13]
under0.5 Severe arterial disease Urgent specialist
referral
Arterial ulcers
no compressionbandagingused.Painatrestmay
be presentat valueslessthan0.25.[13]
g. Skin to bone
i. Look
● Multiple scar, recently heal scar (dry skin, edema heal → wrinkle of skin),
hyperpigmentation (conseque of inflammation), hypopigmentation (heal scar), loss of
hair, shiny & thin, thinning subcutaneous tissue, muscle wasting
● Bony prominent → any swelling
● Bunion
o Enlargement of bone or tissue around the joint at the base of the big toe
(metatarsophalangeal joint)
o Bump is the swollen bursal sac and/or an osseous (bony) anomaly on the
mesophalangeal joint (where the first metatarsal bone and hallux meet)
o Hallus valgus (abnormal angulation of the great toe)
o Hammer toe: pressure on volar side of metatarsal → hyperextension pull
metartasal down (2nd
toe)
o Pressure of medial side of big toe → weight bearing callosities
● Interdigital wear
o Fissure fungal infection
o Infection scar
o Skin changes
ii. Palpation
● Dosalis pedis & posterior tibial artery
● Sensory different → which level? (distal to proximal with pin)
3. Principle of treatment
a. Control blood sugar
i. Hypocount monitoring
ii. Diabetic chart
iii. Sliding scale treatment
● With K+ in drip because K+ will go into cell with insulin (to prevent hypokalaemia)
iv. Diet control
b. Infection treatment
i. Broadspectrum AB
ii. Swab & culture → adjust AB
c. Manage wound
i. Debridement necrotic matter
ii. Drain pus, loculation
iii. Dress wound
d. Patient education & compliant
i. Understanding
ii. Diet control

3. iii. Leg care
iv. Eye care (ophthalmo refer)
v. Comorbid management
4. Damage to the nervoussystem→ may not be able to feel hisor her feetproperly+ Normal sweatsecretionand
oil productionthat lubricatesthe skinof the foot is impaired→ abnormal pressure onthe skin,bones,andjoints
of the foot during walking → breakdown of the skin of the foot → sores
5. Damage to bloodvessels+impairmentof the immune system→ difficulttoheal wounds→ Bacterial infectionof
the skin, connective tissues, muscles, and bones → gangrene.
6. Poor blood flow → AB cannot get to the site of the infection easily → amputation of the foot or leg.
7. Etiology
a. Peripheral neuropathy (Affects sensory, motor, and autonomic pathways)
i. Sensoryneuropathydeprivesthe patientof earlywarningsignsofpainor pressurefromfootwear,
from inadequate soft-tissue padding, or from infection. This neuropathy appears in a stocking-
glove distribution, with many patients complaining of burning or searing pain.
ii. Optimal control of bloodglucoselevelsdecreasestheincidence ofmostdiabetes-associatedorgan
system morbidity. The primary risk factor for the development of diabetic foot ulcers (DFUs) is
lossof protective sensation,bestmeasuredbyinsensitivitytothe Semmes-Weinstein5.07 (10 g)
monofilament.
iii. Abnormal white bloodcell (WBC) functionandthe presence of peripheral vasculardisease allow
wounds to become contaminated and infected by organisms that normally are nonpathogenic.
Thisexplainsthe identification of unusual bacteria from the wounds of patients with diabetes.
iv. Autonomic neuropathy produces chronic venous swelling.
v. Motor peripheral neuropathy or Charcot arthropathy can produce bony deformity, which,
combinedwiththe lossof protectivesensation,canresultinskinulcerationfrompressureorfrom
shear forces.
vi. Associatedfactorsare a historyof foot infectionorulcerationandpreviouspartial orwhole-foot
amputation.
vii. Motor neuropathyleadstomuscle weaknessandintrinsicmuscle atrophyinthe handsand feet.
Patientswithmotor neuropathycan developbunion,claw toe,and hammertoe deformitiesasa
result of muscle imbalance. They lose normal vascular tone and thermal regulation, often
developing severe venous swelling that can be managed only with compression hose.
viii. Severe tissue swellingcanleadtoulcerationandinfection.The patientsdevelopdry,crackedskin
as aresultof autonomicdysfunction,withthe cracks allowingtheentryof bacteria.Naildeformity
or pathologic proliferation may make the areas adjacent to the nails foci for skin breaks or for
infection.
b. Vascular disease
i. Ischemic peripheral vascular disease is the second risk factor for developing diabetic foot ulcer
and infection.
ii. Thisdisorderusedtobe consideredasmall vesseldisease,butcurrentresearchlinksthe vascular
pathology to the basement membrane of the arterial wall.
iii. The characteristicsof the disease are similarinpersonswhoare diabeticandthose who are not,
except that its distribution is somewhat more scattered and geographic in persons who are not
diabetic, as opposed to being progressive in a distal direction in persons who are diabetic.
c. Immune deficiency
i. Glycosylated immune proteins lose efficiency, and granulocytes do not perform adequately,
leaving these patients prone to infection with organisms that would not affect a healthy host.
ii. Each of these potentialabnormalitiesmake the diabeticfootsusceptible toabnormal mechanical
stresses that can lead to a break in the normal soft-tissue envelope. This can initiate a foot
infection that cannot be resolved easily.
8. Pathophysiology
a. Pressure overabonyprominenceorskinbreakdownoccursatfarlesserloadswhenthepressure isapplied
by shear forces + loss of protective sensation → no warning sign to patient→ blister formation and full-
thickness skin loss → process is heightened in the presence of severe venous swelling, which further
lowers the injury threshold.
b. Shoes become tight due to swelling → ↑ the direct pressure and shear forces applied to skin overlying
the bony prominence.

4. c. Thickened, hypertrophic nails increase pressure on the soft tissues surrounding the nails. The common
result is tissue failure and ulcer formation.
d. Once the skin barrier is broken, wound healing can be impaired by abnormally functioning WBCs.
Moreover, patients often are malnourished. Many have a marginal vascular supply, with less ability to
achieve resolution of infection and wound healing.
9. Type of neuropathy
a. Autonomicneuropathy-trophicskinchanges(brittle nail,losshair,dry/scalyskin) ,postural hypotension,
warm footwithboundingpulses,tachycardiaatrestand lossof sinusarrhythmia
b. proximal asymmetrical neuropathy(diabetesamyotrophy)
c. radiculopathy
d. mononeuritismultiplex
e. distal symmetrical polyneuropathy-ddx->dm,vit<,alcoholic
i. glove orstockingdistributionratherthanmapaffectednerve inmononeuropathy
● stocking&glove sensoryloss→unrecognizedtrauma→blister→ulcer
ii. involve of small muscleof feet→wastingof interosseousmuscle→unbalance traction bylong
flexormuscles→footdeformity(higharchand clawingof toes)→abnormal pressure distribution
on walking→callusformat1st
MT head/tipof toes&perforatingneuropathiculcer&charcot’s
joint
iii. trophicskinchanges
iv. ataxiadue to lossof propioception
10. Charcot’s disease(neuropathic arthritis)
a. Rapid progressive degenerationjoint(OA) due to lack of positionof sense(propioception) and protective
pain sensation
b. Symptoms: instability(ligament & capsule lax), swelling(joint effusion), deformity but patient happy,
painless, non tender and warm (paradox is dx)
c. Causes: upper limb-syringomyelia, lower limb-cauda equine, tabes dorsalis, diabetic neuropathy
d. Investigation
i. X-ray-jointsubluxatedordislocated,bone destruction(OA),irregularcalcifiedmassesincapsule(dt
new bone form at peripheral of joint)
ii. WBC,ESR,biopsy→to differentiate OMwhen presence of concomitant ulcer
e. Complication: Rocker bottom deformities,ulceration
f. Treatment: immobilization and rest by wheelchair,crutches,cast
i. Protected weight bearing and operation when cx
11. Risk factor
a. Poor foot wear
b. Peripheral neuropathy
c. Poor circulation
d. Trauma
e. Infection: athletic foot
f. Smoking → damage b.v & disrupt healing process
12. Symptoms
a. Pain
b. Redness
c. Swelling
d. Sign of poor circulation
i. Claudication
ii. Loss of hair
iii. Hard shiny skin
e. Warm
f. Callus (tyloma) & corns (heloma) (sign of chronic trauma to foot)
i. Calluses
● Thickening of skin without distinct borders
● Most commonly on feet and hands over bony spots
● Vary in color from white to gray-yellow, brown, or red
● May be painless or tender
● May throb or burn
ii. Corns

5. ● Texture varies from dry, waxy, transparent to a horny mass
● Distinct borders
● Most common on feet
● May be hard or soft
● Usually painful
g. Toenail fungus, athlete foot
h. Pus
i. Ulcer
j. Fever
k. Skip lesion
l. Numbness
m. Difficulty in walking (Charcot’s joint)
n. Constant itching due to fungal infection
13. Investigation
a. HBA1C
b. X-ray of leg
c. Blood culture
d. ECG
e. CXR
f. FBC: to check for infection (WBC)
g. FBS
h. USG: blood flow
14. Treatment
a. Patient education
i. Wash feeteverydaywithmildsoapandwarmwater.Testthe watertemperature withyourhand
first.Don't soakyour feet.Whendryingthem, pateachfootwitha towel andbe careful between
your toes.
ii. Use qualitylotionto keepthe skin of your feetsoftand moist,but don't put any lotionbetween
your toes.
iii. Trim yourtoenailsstraightacross.Avoidcuttingthe corners.Use anail file oremeryboard.If you
find an ingrown toenail, see your doctor.
iv. Don't use antisepticsolutions,drugstore medications,heatingpads,orsharpinstrumentsonyour
feet. Don't put your feet on radiators or in front of the fireplace.

6. v. Always keep your feet warm. Wear loose socks to bed. Don't get your feet wet in snow or rain.
Wear warm socks and shoes in winter.
vi. Don't smoke or sit cross-legged. Both decrease blood supply to your feet.
vii. Never walk barefoot or in sandals or thongs.
viii. Choose and wear your shoes carefully. Buy new shoes late in the day whenyour feet are larger.
Buy shoesthatare comfortable withouta"breakingin"period.Checkhow yourshoe fitsinwidth,
length, back, bottom of heel, and sole. Avoidpointed-toe styles and high heels. Try to get shoes
made withleatheruppermaterial anddeeptoe boxes.Wearnew shoesforonly2hoursor lessat
a time.Don't wearthe same paireveryday. Inspectthe inside of eachshoe before puttingiton.
Don't lace your shoes too tightly or loosely.
ix. Choose socksand stockingscarefully.Wearclean,dry socks everyday.Avoidsocks withholesor
wrinkles. Thin cotton socks are more absorbent for summer wear. Square-toe socks will not
squeeze your toes. Avoid stockings with elastic tops.
b. All foot lesions
i. Reduce pressure on foot lesion
● Crutches
● Cam-walker
● Surgical shoe with cushioned insert
● Dressings: Foam or felted foam
ii. Optimize comorbid conditions
● Control Hypertension
● Improve glycemic control
● Maximize nutritional status
c. Closed foot sores
i. Warm water soaks (not hot) for 15 minutes twice daily
● Epson salts added to water may be soothing
ii. Hypoallergenic lotion to affected area bid
iii. Cotton socks
d. Ulcerated wounds
i. Wound Cleansing
ii. Wound Debridement (debride necrotic tissue)
iii. Choose dressing to maintain warm, moist environment
● Wound Dressing (inc. Pressure Sore Dressings)
● Hydrocolloid Dressing (avoid if wound infected)
● Transparent Film Dressing (avoid if wound infected)
● Foam Dressing
● Calcium Alginate Dressing
iv. Consider adjuncts to promote Wound Healing
● Growth factors (e.g. Becaplermin)
● Bioengineered skin grafts (Apligraf, Dermagraft)
e. Ischemic wounds
i. Revascularization or Angioplasty
ii. Hyperbaric oxygen therapy
● Reduces amputations due to Diabetic Foot Ulcers
iii. Vasodilator drugs have not been efficacious
f. Infected wounds
i. Cellulitis for infected diabetic wound management
ii. Findings suggestive of serious infection
● Cellulitis involves >2 cm of skin
● Deep ulcer
● Purulent drainage
● Fever
● Probe-to-Bone Test positive
15. Prognosis: Foot ulcer healing in Diabetes Mellitus
a. Healing prediction based on 3 criteria (one point each)
i. Foot wound present >2 months
ii. Foot wound >2 cm

7. iii. Grade 3 or more on Wagner Ulcer Classification
b. Interpretation: Score of 2 or more
i. Wound not healed in 79% of patients by 20 weeks
16. Ulcer-breakina continuityof epithelial surface
17. Gangrene- deathtissue,oftenwithputrefactionof macroscopicportionof tissue
a. Causes:
i. neuropathy-leadto->ulcer,trophicchanges,lossjointpositionsense andpredispose to
progressive jointdetruction(neuropathicjointds)
ii. Coz:
● vasculopathy-microvascularocclusion
● Hyperglycaemialeadtoincrease formationof sorbitolandfructose inSchwanncells,
accumulate these sugarsmaydisruptfunctionandstructure->delaynerve conduction(dt
demyelinationandaxonal degeneration)
iii. vascular-leadto->ischemicchanges
iv. Immunocompromise-neutrophil malfunction->followingminortraumaorulcer(infection)
v. Osteoporosis and risk of #
WagnerUlcer ClassificationSystem
Grade Lesion
0 No openlesions;mayhave deformityorcellulitis
1 Superficial diabeticulcer(partial orfull thickness)
2 Ulcer extensiontoligament,tendon,jointcapsule,ordeepfasciawithoutabscessorosteomyelitis
3 Deepulcerwithabscess,osteomyelitis,orjointsepsis
4 Gangrene localizedtoportionof forefootorheel
5 Extensive gangrenousinvolvementof the entire foot
UniversityofTexas Diabetic WoundClassification
A. Stages
a. Stage A: Noinfectionorischemia
b. Stage B: Infectionpresent
c. Stage C: Ischemiapresent
d. Stage D: Infectionandischemiapresent
B. Grading
a. Grade 0: Epithelializedwound
b. Grade 1: Superficial wound
c. Grade 2: Wound penetratestotendonorcapsule
d. Grade 3: Wound penetratestobone orjoint
Amputation

8. 1. Indication of amputation (3 D’s)
a. Dead
i. Peripheral vascular disease
ii. Severe trauma
iii. Burns
iv. Frost-bite
b. Dangerous
i. Trauma: crush syndrome
ii. Infection: Gas gangrene, lethal sepsis
iii. Neoplasm: malignant tumour
c. Damn nuisance
i. Pain
ii. Recurrent sepsis
iii. Gross malformation
iv. Severe loss of function
2. Level of amputation
a. The higher the level of a lower-limb amputation,the greater the energy expenditure that is required for
walking.
b. Muscles are divided distal to proposed site of bone section
c. Nerves are divided proximal to bone cut
d. Upper limb & transfemoral (above knee): ant & post flaps of equal length
e. Below knee: long posterior flap
f. Below knee
i. Posterior myoplastic flap (Burgess technique)
● Skinandmuscle fromthe calf are broughtforwardtocoverthe shinbonesaftertheyhave
been divided.
ii. Skew flap (Kingsley Robinson technique)
● Musclesof the calf are broughtforwardinthe same wayasinthe posteriortechnique but
the skin flaps are skewed in relation to the muscle.
g. Transfemoral: 12cm from knee
h. Below knee: 14cm from knee
i. Below elbow: 18cm from elbow
j. Above elbow: 20cm from shoulder to stump
k. Type
i. Terminalization
ii. Disarticulation (until joint)
iii. Ray amputation (until metatarsal) V shape
iv. Fore foot amputation
v. Midfoot amputation
vi. Sims amputation

10. 3. Complication of amputation

11. a. Early
i. Hemorrhage
ii. Infection
iii. Wound breakdown (due to vascular disease)
iv. Gas gangrene
v. Thrombosis
vi. Hematoma
vii. Swelling, edema,
viii. Pain
b. Late
i. Skin problem: eczema, ulceration
ii. Poor circulation
iii. Nerve: neuroma
iv. Muscle atrophy
v. Phantom limb sensation.
vi. Joint contractures
vii. Chest infection
viii. Pressure sore
4. Management of amputation stump
a. Acute immediate post-op:
i. Compressive drainage
ii. Adequate dressing
iii. Keep joint straight (flexion → contracture)
iv. Prevent pressure on wound (pressure necrosis)
b. General principles for amputation surgery involve appropriate management of skin, bone, nerves, and
vessels, as follows:
i. The greatest skin length possible should be maintained for muscle coverage and a tension-free
closure.
ii. Muscle is placedoverthe cut endof bonesvia a myodesis(ie,muscle suturedthroughdrill holes
in bone), a long posterior flap sutured anteriorly, or a well-balanced myoplasty(ie,antagonistic
muscle and fascia groups sutured together).
iii. Nervesare transectedundertension,proximal tothe cutendof bonesina scar- and tension-free
environment.Thisreducesthe chance neuromaswillformandbe asource of pain.Placingthe cut
nervesinamore proximalscar-freeenvironmentassistsindecreasingpotential irritationandpain.
Ligation of large nerves can be performed when an associated vessel is present.
iv. The largerarteriesandveinsare dissectedandseparatelyligated.Thispreventsthe development
of arteriovenous fistulas and aneurysms.
v. Bony prominencesarounddisarticulationsare removedwithasaw and filedsmooth.Diaphyseal
transections can be covered with a local flexible osteoperiosteal graft. Maintaining the maximal
extremity length possible is desirable. However, below-knee amputations are best performed
12.5-17.5 cm below the joint line for nonischemic limbs.
vi. One applicationguide istomake a limb2.5 cm longfor every30 cm of bodyheight.Forischemic
limbs,a higherlevel of 10-12.5 cm below the jointline isusedbecause makinglimbslongerthan
this can interfere with prosthetic use and design.
5. Rehabilitation of amputation
6. Indication for prosthetic limb
7. Contraindication for prosthetic limb
Gangrene

12. 1. Types
a. Dry gangrene
i. Reduction of blood flow through the arteries.
ii. Appears gradually and progresses slowly.
iii. In most people, the affected part does not become infected.
iv. Tissue becomes cold and black, begins to dry, and eventually sloughs off.
v. Commonly seen in people with blockage of arteries (arteriosclerosis) resulting from increased
cholesterol levels, diabetes, cigarette smoking, and genetic and other factors.
b. Wet or moist gangrene
i. A complication of an untreated infected wound.
ii. Swelling resulting from the bacterial infection causes a sudden stoppage of blood flow.
iii. Cessation of blood flow facilitates invasion of the muscles by the bacteria and multiplicationof
the bacteria because disease-fighting cells (white blood cells) cannot reach the affected part.
c. Gas gangrene isa type of wet gangrene causedby the bacteriaknownas Clostridia.Clostridiaare a type
of infection-causing bacteria that grow only in the absence of oxygen. As Clostridia grow, they produce
poisonous toxins and gas; therefore, the condition is called gas gangrene.
Cellulitis
1. The wordcellulitisliterallymeansinflammationof the cells.It generallyindicatesanacute spreadinginfectionof
the dermis and subcutaneous tissues resulting in pain, erythema, edema, and warmth.
2. Risk factors
a. Group A Streptococcus Cellulitis (Erysipelas)
b. Trauma
i. Laceration
ii. Puncture Wound
iii. Post-operative infection at incision site
c. Underlying skin lesion
i. Furuncle
ii. Skin Ulcer
iii. Fungal Dermatoses
iv. Non-Group A Streptococcus Cellulitis related lesions
● Coronary artery bypass with saphenous vein graft
● Radical pelvic surgery or radiation
d. Neoplasms
i. Lymphatic Cutaneous metastases from neoplasms
ii. Inflammatory Breast Cancer
iii. Carcinoma Erysipeloides
e. Extremity Stasis or Edema
i. Chronic Dependent edema (may progress rapidly)
ii. Peripheral Vascular Disease
f. Perianal Streptococcal Cellulitis (in children)
g. Diabetes Mellitus
h. Immunocompromised patients
3. Causes: Streptococcal and Staphylococcal Cellulitis
a. Common (most cellulitis cases)
i. Staphylococcal Cellulitis
ii. Group A Streptococcus Cellulitis (Erysipelas)
b. Less common Streptococcal infections
i. Pneumococcus
ii. Non-Group A Streptococcus Cellulitis
● Group C or G Streptococcus Cellulitis
● Group B Streptococcus Cellulitis in newborns
c. Rapidly progressive cellulitis
i. Necrotizing Fasciitis
ii. Vibrio Cellulitis (Vibrio vulnificus)
iii. Clostridium perfringens
iv. Pasteurella multocida

13. v. Aeromonas Hydrophila
4. Causes: Exposure
a. Fish Handlers or water exposure (See Marine Trauma)
i. Erysipelothrix rhusiopathiae (Erysipeloid)
ii. Mycobacterium marinum (Fish tank exposure)
iii. Aeromonas Hydrophila
iv. Vibrio Cellulitis
b. Animal Bites
i. Cat Bites: Pasteurella multocida
ii. Dog Bites: Staphylococcus intermedius
c. Envenomation spines of stonefish (South Pacific): Risk of serious systemic toxicity, pulmonary edema
d. Human Bites
e. Miscellaneous
i. Pseudomonas aeruginosa
● Sweaty Tennis Shoe Syndrome
ii. Eosinophilic Cellulitis
5. Immunocompromised Patients
a. Serratia
b. Proteus
c. Enterobacteriaceae
d. Cryptococcus
e. Legionella pneumophila
i. Associated with Legionella pneumonia
f. Legionella micdadei
i. Seen in renal transplant patients
g. Escherichia coli
i. Seen in children with relapsing Nephrotic Syndrome
6. Symptoms
a. Inflamed skin wound develops rapidly days after injury
i. Local tenderness
ii. Pain
iii. Very red, hot, swollen an painful
b. Associated symptoms
i. Malaise, fever, chills
7. Signs
a. Draw margins of erythema with marker
i. Follow course of infection on antibiotics
b. Wound with contiguous inflammation
i. Erythema (Rubor)
ii. Swelling (Tumor)
iii. Local tenderness (Dolor)
iv. Warm to touch (Calor)
c. Contrast with findings in Erysipelas
i. Not elevated
ii. No sharp demarcation
d. Regional Lymphadenopathy
e. Local abscesses
f. Small patches of necrosis
g. Gram Negative superinfection may also be present
h. Hemorrhagic and necrotic bullae (specific conditions)
i. Group A Streptococcal Cellulitis
ii. Pseudomonas Cellulitis
iii. Vibrio Cellulitis (Vibrio vulnificus)
iv. Clostridium perfringens
v. Aeromonas Hydrophila
8. Differential Diagnosis: Non-infectious Conditions
a. Vascular Conditions

14. i. Superficial thrombophlebitis
ii. Deep Vein Thrombosis
b. Dermatologic Conditions
i. Contact Dermatitis
ii. Insect Bites
iii. Acute Drug Reaction
iv. Eosinophilic Cellulitis
v. Sweet Syndrome
c. Rheumatologic Conditions
i. Gouty Arthritis
ii. Relapsing Polychondritis
d. Miscellaneous
i. Erythromelalgia
ii. Inflammatory Carcinoma (metastatic cancer to skin)
iii. Foreign body reaction (mesh, metal, silicone implant)
iv. Familial Mediterranean fever
9. Labs
a. Fine Needle Aspiration
i. Technique
● Leading edge injection and aspiration with saline
ii. Efficacy
● May assist diagnosis with cellulitis
● Not useful in Erysipelas
● 30% sensitivity from closed lesions
iii. Indication
● Unusual pathogens suspected
● Cellulitis refractory to current antibiotics
b. Blood Culture (25% sensitivity)
c. Skin biopsy (25% sensitivity)
10. Management: General Care
a. Tetanus prophylaxis
b. Immobilization and elevation of involved limb
i. Splint in a position of function
ii. Decreases swelling
c. Clean wound site
i. Copious irrigation
ii. Debride devitalized tissue
iii. Incision and Drainage if deep fluctuant pocket
d. Compresses
i. Cool sterile saline dressings decrease pain
ii. Later, moist heat helps localize infection
11. Management: Extremity Cellulitis
a. Precaution
i. MRSA is becoming more common and more resistant
● Consider Septra or Doxycycline if MRSA is suspected
ii. Avoid Fluoroquinolones in cellulitis due to high resistance
b. Mild to Moderate Infection (uncomplicated)
i. Course
● Standard course has been 10 days of antibiotics
● New: 5 day as effective as 10 day if uncomplicated
ii. Agents
● Dicloxacillin 500 mg PO every 6 hours or
● Augmentin 875 mg PO bid or
● Cefazolin 1 g IV every 8 hours
c. Severe Infection
i. Nafcillin 2 g IV every 4 hours or
ii. Oxacillin 2 g IV every 4 hours

15. d. Penicillin Allergy
i. Erythromycin or
ii. Azithromycin or
iii. Clarithromycin or
e. Outpatient parenteral (moderate to severe cellulitis)
i. Efficacy
● As effective as daily Rocephin
ii. Protocol (adults): 7-10 day course
● Cefazolin 2 gram IV q24 hours
● Probenacid 1 gram PO q24 hours
o Decreases Cefazolin excretion
iii. Benefits
● Lower cost
● More narrow spectrum
12. Management: Facial Cellulitis (Erysipelas)
a. Mild to Moderate Infection
i. Augmentin 875 mg PO bid
ii. Cefazolin (Ancef) 1 g IV every 8 hours
b. Severe Infection
i. Nafcillin 2 g IV every 4 hours
ii. Oxacillin 2 g IV every 4 hours
iii. Vancomycin 1.0-1.5 g IV qd
13. Prevention: Recurrent episodes
a. Reduce peripheral edema (support stockings)
b. Good skin hygiene
c. Prophylactic antibiotics:
i. Efficacy
● Not useful if underlying predisposing condition
ii. No Penicillin Allergy
● Penicillin G 1.2 MU IMq4 weeks
● Penicillin V 250 mg PO bid
iii. Penicillin Allergic
● Erythromycin 500 mg PO qd
● Azithromycin 250 mg PO qd
● Clarithromycin 500 mg PO qd
14. Complications:
a. Thrombophlebitis in older patients
b. Necrotizing Fasciitis
Incision Vs laceration wound

16. 1. Incision is iatrogenic & wound border straight
2. Laceration is not iatrogenic & wound border zig-zag
National Pressure Ulcer Advisory Panel (NPUAP) grading system
1. Stage 1
● Nonblanchable erythema of intact skin
2. Stage 2
● Superficial or partial thickness skin loss
● Ulcer involves Epidermis or Dermis
o Skin abrasion
o Blister
3. Stage 3
● Full thickness skin loss with Subcutaneous damage
● Ulcer extends down to underlying fascia
● Presents as deep crater
4. Stage 4
● Full thickness skin loss with extensive destruction
● Tissue necrosis
● Damage to muscle, bone, tendon or joint capsule