Prism Flashcards
acronym for wound descrption
Acronym 3D MOBB (depth, diameter, drainage, measure, odor, base, border
Periwound skin DFu
Consider normal, erythematic (document/draw extent), streaking, stasis changes, trophic changes
ABIs for DFU
- Values >0.9 associated with good healing potential
- Values 0.5-0.9 associated with PVD and delayed healing
- Values <0.5 associated with ischemia and problematic healing
- Be wary of elevated values secondary to vessel calcification
TcPO2 for DFU
-TcPO2: -Values >30mmHg associated with good healing potential [Mars M. Transcutaneous oxygen tension as a predictor of success
after an amputation. JBJS-Am. 1988; 70(9): 1429-30.]
-Values <20mmHg associated with microcirculatory problems and delayed/problematic healing.
absolute pressures and absolute relative skin temp
- Absolute Pressures: -Should have 40mmHg at ankle and 20mmHg at the digits for healing potential.
- Absolute/Relative skin temperature: compare B/L (normal around 94° F)
vascular things to look for for DFU
pulses CFT, pedal hair ABI TcPO2 absolute pressures Absolute/relative skin temperatures
neurological things for DFU
- Sensory testing:
- Posterior column: Vibratory, Proprioception
- Anterior column: Light touch (5.07 SWMF)
- Lateral column: Pain and temperature
- Motor testing:
- Expect intrinsic weakness with advanced neuropathy
- Manual Muscle Testing
- Spinal Reflexes (Achilles, Patellar, Babinski)
- Autonomic:
- Increase in skin temperature
- Lack of sweating leading to xerosis
- Any other relevant neurologic tests (you should have an awareness of Dellon’s work and the PSSD).
MSK for DFu
- Document any/all foot deformities, especially osseous prominences.
- Expect intrinsic muscle weakness leading to digital deformities.
- Overall foot type
- Equinus
wagner
[Wagner FW: The dysvascular foot: a system of diagnosis and treatment. Foot Ankle 2: 64–122, 1981]
0: Pre-ulcerative area without open lesion
1: Superficial ulcer (partial/full thickness)
2: Ulcer deep to tendon, capsule, bone
3: Stage 2 with abscess, osteomyelitis or joint sepsis
4: Localized gangrene
5: Global foot gangrene
Modified with the following risk factors:
A: Neuropathic
B: Ischemic
C: Neuroischemic
-So an infected ulcer with localized gangrene and bone exposure on a fully sensate, ischemic foot is: Wagner 4B
-University of Texas: [Lavery LA, Armstrong DG, Harkless LB: Classification of diabetic foot wounds. J Foot Ankle Surg 35:528–531, 1996
0: no open lesion
1: superficial
2: Tendon capsule
3: Bone Joint
A: no ischmia/infection
B: infection
c: ischemia
D: both
PEDIS system
-Recommended by the Infectious Disease Society of America.
-PEDIS is an acronym standing for perfusion (measure of vascular supply), extent/size, depth/tissue loss, infection,
and sensation.
-Each of the 5 categories is graded from 0 (minimal) to 2 (severe).
-Based ona 10-point scale with 10 being most serious ulcer with greatest difficulty in treatment
-Liverpool Classification System: Dfu
- Primary:
- Neuropathic
- Ischemic
- Neuroischemic
- Modified with:
- Uncomplicated
- Complicated (cellulitis, abscess, OM, etc.)
LABS FOR DFU
CBC CHEM 7 Minerals Glucose (HA1c) ESR CRP Albumin Pre-Albumin Wound culture and sens: -gram stain -preliminary -final Blood Cultures Bone Biopsy If surg candidate get: -CXR -EKG
WBC for DFU
-Total Leukocyte Count (~4-10 x 10^3 leukocytes/ul)
-Leukocyte is a generalized term for any WBC including neutrophils/granulocytes, monocytes,
lymphocytes, eosinophils and basophils. So an increased leukocyte count can indicate a rise in any or all of
these. This is the reason why a differential is so important.
PMN/granulocytes in DFU
- Neutrophils/Granulocytes (Usually ~54%; increased >85%)
- Part of the humoral system.
- Phagocytic cells in the inflammatory process.
- Normally take 8-14 days to mature. Functionally last 1-2 days. Half-life 6 hours.
- Would be increased in an inflammatory state.
- PMNs: Mature neutrophils that you would expect to see in an infection.
- Band cells: Immature neutrophils. Presence indicates active, ongoing infection.
- A left shift is an increased neutrophil percentage in the presence of band cells
Monocytes in DFU
- Monocytes (Usually ~6%)
- Phagocytic, bacteriocidal macrophages in the humoral system.
- Accumulate after neutrophils in acute infection.
- Presence indicates post-inflammatory state or chronic infection
Lymphocytes in DFU
- Part of the cellular system.
- Produce immunoglobulins and express cellular immunity (T and B cells).
- Not normally increased in bone/soft tissue infections.
- Possibly increased in a foreign body reaction.
Eosinophils in DFU
- Part of the cellular system.
- Generally involved in allergic and immune responses.
- Develop in the same line as lymphocytes.
- Increased with acronym NAACP
- (Neoplasm, Allergy, Addison’s, Collagen vascular disorder, Parasites
basophils in DFU
- Part of cellular immunity.
- Involved with acute allergic responses and histamine release
Glucose and Ha1c
DFU
- HbA1C: Measure of glycosylated hemoglobin and long-term glucose control:
- 1% equals approximately 20 glucose points (7% equals ~140ug/ul)
- Note that the stress of infection will probably cause a hyperglycemic state
ESR for DFu
Normal: 60mm/hr
-Analyzed using the Westergren method, which measures the distance erythrocytes fall in one hour in a vertical
column of anti-coagulated blood under the influence of gravity (even though gravity is just a theory).
-Sensitive, but not specific for infection as it is increased in any inflammatory state with increased fibrinogen.
-Also elevated in: Pregnancy, DM, ESRD, CAD, CVD, Malignancy, Age, etc.
-[Karr JC. The diagnosis of osteomyelitis in diabetes using ESR. JAPMA 2002 May; 95(5): 314.]
-[Lipsky BA. Bone of contention: diagnosing diabetic foot osteomyelitis. Clin Infect Dis. 2008 Aug; 47(4): 528-30.]
CRP in DFU
-Normal: 0-0.6mg/dl
-Measures a liver protein only present in acute inflammation (not normally found at all).
-Sensitive, but not specific for infection.
-Also elevated in: RA, Malignancy, MI, SLE, Pregnancy, etc.
-More expensive and technically difficult to perform compared to the ESR.
-[Jeandrot A. Serum procalcitonin and CRP concentrations to distinguish mildly infected from non-infected diabetic foot ulcers: a pilot study.
Diabetologia. 2008 Feb; 51(2): 347-52.]
wound culture swabs can be easily contaminated.
What is ideal situation to swab
The ideal situation is a deep wound specimen of tissue (not just a swab)
following incision and drainage with pulse lavage before beginning antibiotic therapy
blood cultures and biopsy consideration for dfu
- Blood Cultures
- Should be drawn from 2 sites; 20 minutes apart.
- Indicates bacteremia/septicemia
- Bone Biopsy
- Gold standard for diagnosis of osteomyelitis (discussed further later)
aerobic gram pos cocci
Staph Aureus MRSA Staph Epi MRSE Enterococci VRE Strept pyogenes (A) Strept agalactia (B) Strept Bovis (D) Strept viridans
Anaerobic gram pos cocci
peptostreptococcus
aerobic gram pos rods
Bacillus anthracis
Corynebacterium diphtheriae
Listeria Monocytogene
Anaerobic Gram Positive Rods
Clostridium perfringens
Clostridium difficile
Clostridium tetani
aerobic gram neg rods
pseudomonas e coli enterobacter proteus vibrio Y. pestis shigella salmonella klebsiella serratia e. corrodens paturella multicide
morganella morganii(?)
anaerogic gram neg rods
bacteroides fragilis
aerobic gram neg cocci
neisseria
spirochetes
Treponium pallidum
Borrelia burgdorferi
Imaging for DFU
xray mri bone scan wbc scan CT PET scan
xrays for dfu
-Soft Tissue: Infection characterized by radiolucent area. One should be able to see a soft tissue deficit if an ulcer is present. It is very important
to rule out emphysema (gas in the tissues) with a plain film. Can also appreciate soft tissue edema.
-Osseous Tissue:
-Early Osteomyelitis (OM) signs: No reliable ones. Rarefaction and periostitis are possible.
-Subacute OM signs: Brodie’s abscess (lytic lesion surrounded by sclerotic rim).
-Chronic OM: Lysis, Malformation, Involucrum, Cloaca, Sequestra.
-Plain film radiographs are 67% specific, 60% sensitive for OM [Termaat, JBJS 2005]
-MRI
mri for dfu
-Cellulitis:
T1: Diffuse and infiltrative decreased signal intensity as inflammation replaces fat.
T2 and STIR: Increased signal intensity.
-Abscess:
T1/T2/STIR: Homogeneous increased signal intensity.
-Note that pus/necrotic tissue has a decreased intensity compared to inflammatory fluid.
-OM:
T1: Decreased signal intensity, cortical lysis and intramedullary changes.
-Increased signal intensity in known OM indicates healing as fat infiltrates.
T2: Increased signal intensity, cortical lysis, and intramedullary changes.
-Rim sign: thin layer of active infection surrounding normal bone.
-60% Specificity, 85% sensitivity per Termaat.
bone scans for dfu
-A radio-isotope is injected into the patient and imaged at specific intervals.
- Phases:
- Immediate Angiogram (1-3sec): Essentially an arteriogram.
- Blood Pool (3-5min): Demonstrates blood pooling in capillaries and veins.
- Delayed (2-4 hours): Increasingly specific to activity patterns and pathology.
- 4th Phase (varying times): Increasingly specific to activity patterns and pathology
technitium 99 bone scan for dfu
- Binds to calcium hydroxyapatite and measures osteoblast/osteoclast activity.
- Half-life: 6 hours
- Excreted through kidneys which will show homogenous control signal.
- Mucomyst 600mg PO q12 day before and of surgery as renal ppx.
- Cellulitis: Focal uptake in blood pool; Negative in delayed phase.
- OM: Diffuse uptake in blood pool; Hot increased uptake in delayed phases.
- 45% Specificity; 86% sensitivity per Termaat
types of wbc scans for dfu
gallium 67 citrate
indium 111 oxime
technetium 99m HMPAO
technetium 99m sulfur colloid marrow scan
Combination Sequential Technitium-Gallium scans
explain combo sequential technetium gallium scans
- Scan at 4 hours, then at 48-72 hours. Based on half-lives.
- Increased specificity for infection if gallium has higher uptake then technetium.
- Can use any other combination
explain technetium 99 m sulfur colloid marrow scan for dfu
- Specific for bone marrow and neutrophil production
- Has shown promise in differentiating OM from Charco
technetium 99m HMPAO for dfu
- WBCs isolated from blood samples, tagged and re-injected. Scan at 3 hours.
- Tagged molecule is HMPAO (hexamethylpropyleneamine oxime) ->you will get asked this!)
- Technically easier with less radiation than indium
indium 111 oxime for dfu
- WBCs isolated from blood sample, labeled and re-injected.
- Scan at 24 hours. Half life: 67 hours.
- Predominantly uptaken by neutrophils, so it demonstrates acute infections better than chronic infections
gallium 67 citrate
- Uptake by siderophore complex (direct bacteria) and lactoferrin (protein-released by bacteria)
- Scan taken 48-72 hours after injection or done in triphasic manner.
- Has longer half-life
- 42% Specificity; 80% Sensitivity per Termaat
ct scans for dfu
Radiograph altered by computer to highlight specific “windows”. You can isolate soft tissue or different aspects of bone, for example.
- Soft tissue infection: Exact locations and anatomy of abnormal soft tissue density.
- OM: Increased density in the marrow.
- CT scans can be combined with contrast
explain PET scan
- A tracer is injected/inhaled into the patient which releases radioactive positrons. The positrons collide with electrons and produce gamma rays.
- > 90% Sensitivity and Specificity per Termaat (best in study
High sens,spec
3 pathogenesis of dfu
neuropathy
trauma leading to ulcer
impaired wound healing
pathogenesis of dfu
explain neuropathy
- 30-50% of diabetics have some form of sensory, motor and/or autonomic neuropathy.
- Sorbitol accumulation in Schwann cells leads to hyperosmolarity of the nerve cells in turn leading to swelling and cellular lysis. This leads to decreased nerve signal conduction. Microvascular damage to the nerve (described later) also impairs healing of the damaged nerve.
- Sensory Neuropathy
- Loss of light touch/protective sensation (anterior spinothalamic tract)
- Loss of vibratory/proprioception mechanisms (posterior tract)
- Loss of pain/temperature sensation (lateral tracts)
- The patient has no warning of current, developing or impending trauma.
- Motor Neuropathy
- “Intrinsic Minus” foot-type with wasting of the intrinsic muscles and extensor substitution.
- Undetected excess plantar pressures develop.
- Autonomic Neuropathy
- Damage occurs in the sympathetic ganglion
- AV shunting occurs with global LE edema not relieved by diuretics or elevation.
- Increased skin temperature predisposes to ulceration (Armstrong)
- Decreased sweating leads to xerosis and fissuring (portal for infection)
pathogenesis dfu
explain traum leading to ucleration
-Abnormal anatomy: extrinsic and intrinsic abnormalities secondary to motor neuropathy and tendon glycosylation.
-Decreased joint mobility: secondary to non-enzymatic glycosylation and excess collagen cross-linking of tendons,
ligaments, joint capsules (especially at the STJ and the MTPJ).
-Equinus: Increased cross-linking of collagen in the Achilles tendon (leads to increased forefoot pressures).
-Skin stiffness: secondary to glycosylation of keratin.
-Intrinsic skin weakness: trophic changes associated with PVD.
-All lead to increased plantar pressures, which is the driving force behind ulceration.
explain impaired wound healing for dfu pathogenesis
-Can be thought of as increased inflammation, decreased vasculature and decreased catabolism.
-Increased Inflammation
-The inflammatory phase of the healing process actually lasts longer than necessary.
-Inflammation initially not as effective due to decreased leukocyte adhesion and morphologic changes to
the macrophages.
-Prolongation occurs due to decreased chemotaxis of growth factors and cytokines.
-MMPs increase their activity and continue to produce an “inflammatory soup.”
-All contribute to a wound “stuck” in the inflammatory phase.
-Decreased Vasculature
-Macroangiopathy: Atherosclerotic obstructive disease of large vessels due to LDL oxidation.
-Microangiopathy: Thickened basement membrane decreases diffusion at capillary level.
-Mechanism behind neuropathy, nephropathy and retinopathy
-Think of it in terms of a decreased TcPO2
-Endothelial dysfunction:
-Decreased nitric oxide (NO) and prostaglandin to promote vasodilation
-Decreased smooth muscle cell relaxation to promote vasodilation
-AV shunting secondary to autonomic neuropathy
-Decreased vasodilation and membrane permeability in response to trauma/damage/inflammation:
-Usually regulated by substance P and vasomodulators from damaged cells and nociceptors.
-Overall leads to a “sluggish” vasculature with decreased inflow, diffusion, outflow and angiogenesis.
-Decreased Catabolism
-Decreased collagen synthesis, both in peptide production and post-translational modification
-Morphologic changes to keratinocytes
-Decreased angiogenesis
surgical layers of dissestion used for dfu depth measurement
Skin Superficial Fascia -First Dissection Interval containing superficial neurovascular structures Deep Fascia -Second Dissection Interval containing muscular and deep neurovascular structures Periosteum -Third Dissection Interval Bone
OM definitions per Resnick:
Periostitis Osteiotis OM Sequestrum Involcrum Cloaca Brodies Abscess Sclerosing OM of Garre
- Periostitis: Inflammation of the periosteum
- Osteitis: Inflammation of the cortex
- Osteomyelitis: Inflammation of the medullary canal
- Sequestrum: piece of dead bone floating in pus/inflammation
- Involucrum: sheath of bone surrounding pus/inflammation
- Cloaca: tract through an involucrum
- Brodie’s Abscess (1832): Chronic abscess in bone surrounded by sclerosis
- Sclerosing OM of Garre: low grade inflammatory condition
waldvogel and lew article on definitions
acute OM chronic OM Contiguos/Direct extension Hematogenous spread vascular impairment
-Acute Osteomyelitis: Systemic clinical signs of infection
-Chronic Osteomyelitis: Subacute clinical signs of infection
-Contiguous/Direct Extension: spread of infection to bone from exogenous source or adjacent tissue.
This can be described as an “outside-in” spread invading the cortex and proceeding to the medullary canal.
-Hematogenous Spread: Infective agent reaches medullary canal of bone from the vascular supply. This
can be described as an “inside-out” infection invading the medullary canal first and spreading to the cortex.
-Vascular Impairment: Decreases the effectiveness of the inflammatory response and Abx delivery.
Other people who differnetiate acute vs chronic OM
Weiland: Describes chronic OM as lasting > 6months.
-Schauwecker: Describes chronic OM as lasting > 6 weeks and one failed episode of tx.
AJM classification for OM
- Acute Osteomyelitis
- Contiguous/Direct Extension
- No PVD
- PVD
- Hematogenous Spread
- No PVD
- PVD
- Chronic Osteomyelitis
- Contiguous/Direct Extension
- No PVD
- PVD
- Hematogenous Spread
- No PVD
- PVD
-Cierny-Mader-Penninck Classification [A clinical staging system for adult osteomyelitis. CORR. 2003; (414): 7-24.
-Anatomic Stage
Stage 1: Medullary: infection of only the medullary canal
Stage 2: Superficial: infection of only the superficial cortex
Stage 3: Localized: infection of only the cortex
Stage 4: Diffuse: infection of both the cortex and medullary canal
-Physiologic Stage
A: Normal Host
Bs: Compromised Host with systemic risk factors (eg DM)
Bl: Compromised Host with local risk factors (eg smoking)
C: Treatment worse than the disease
- So a smoking DM patient with infection of only the superficial portion of the cortex is: 2Bs
- Obviously much more work needs to be done on the topic of osteomyelitis classification.
OM diagnosis
- Subjective Findings (See Diabetic Infection Work-up)
- Objective Findings (Diabetic Infection Work-up)
- Probing to bone 89% positive predictive value (Grayson JAMA 1995).
- Gold Standard: Bone biopsy. This is ideally performed when the patient has been free of antibiotics for 2 weeks.
- Imaging Studies:
- Review plain films, MRI, Bone Scans, WBC scans, CT, PET in Diabetic Infection Imaging Sheet.
- These all add evidence, but are rarely exclusively diagnostic.
- Blood Cultures: Hematogenous OM diagnosed with positive BCx and positive bone scan.
general OM treatment
- There is much controversy regarding long-term Abx (PO vs. IV vs. PMMA) vs. Surgical Debridement.
- The Cierny-Mader Classification makes some general recommendations:
- CM Stage 1: 2 weeks IV + 2-4 weeks PO Abx
- CM Stage 2: Surgical Debridement + 2 weeks IV
- CM Stage 3&4: Surgical Debridement + 4-6 weeks IV Abx
OM abx administration options
-Long-term Abx (4-8 weeks) is a conservative option because many people believe you can never cure OM and that
it can reactivate at any time for years to come.
OM abx PO
- Doxycycline and Ciprofloxacin are reputed to have the best bone penetration.
- Keep in mind that most ID docs would never substitute coverage for bone penetration.
- Your Abx choices should be culture driven.
OM abx IV
- Culture driven
- Access options: IV, PICC, Infusion pump, etc.
OM PMMA beads
- PMMA: polymethylmethacrylate
- PMMA is a combination of monomer (liquid) and polymer (powder).
- Comes in 20, 40 and 60g packets.
- 7% elusion in the first 24 hours with activity noted for 14 days.
- Demonstrates exponential release.
- Cierny proposes a 1:5 ratio of Abx:PMMA. Another common standard is 4-8g:40-60g.
- Increased Abx means increased elution, but decreased bead hardening.
- Smaller beads means increased overall surface area and increased elution.
- The Abx must be heat-labile
- Gentamycin, Tobramycin, Vancomycin, Ticarcillin, Cefazolin, Moxalactam, Cefotaxime
IDSA General Treatment Recommendations
Soft Tissue
[Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections.
IDSA Guidelines. CID 2004; 39: 885-910.]
Soft Tissue Only
Mild
Topical or oral 1-2 weeks up to 4 weeks
Moderate
Oral 2-4 weeks
Severe
Initial parenteral, then switch to oral 2-4 weeks
IDSA General Treatment Recommendations
‘bone or joint
[Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections.
IDSA Guidelines. CID 2004; 39: 885-910.]
No residual infection Parenteral or oral 2-5 days
Residual infected soft tissue
Parenteral or oral 2-4 weeks
Residual infected (but viable) bone initial parenteral, then switch to oral 4-6 weeks
Residual dead bone post-operatively
Initial parenteral, then switch to oral >3 months
charcot defintion
Neuropathic osteoarthropathy first described by Musgrave in 1703 and named for JM Charcot in 1868
NV/french/theory of charcot pathogenesis
- Trophic centers in the anterior horn of the spinal cord maintain nutrition to joints.
- Trauma to these trophic centers leads to increased blood flow and osteoclastic activity.
- Evidence for the Neurovascular Theory:
- Autonomic neuropathy in DM leads to increased AV shunting, edema and skin temperature.
- Boulton: Increased PO2 in venous system of Charcot pts (63mmHg vs. 46mmHg)
- Shows increased perfusion in neuropathic diabetics
- Edmonds: Increased blood velocity in neuropathic diabetics
- Young: Decreased bone density in patients with decreased nerve conduction velocities
- Cundy: Decreased bone density in Charcot patients
- Gough: Increased osteoclastic activity in Charcot patients
Neurotraumatic/German/Theory of Virchow and Volkmann
-Repeated trauma from biomechanical stresses during ambulation on an insensate foot.
-Evidence for the Neurotraumatic Theory:
-Eloesser and Johnson: Trauma is the necessary predisposing factor, and not underlying bone weakness, to
create Charcot changes in a neuropathic limb.
-Common sense
-Two opposing, fighting theories (with two opining blowhards on either side getting red-faced)? Probably a little bit of both.
etiology of charcot
-First described: Tabes Dorsalis (Charcot 1868)
-Most common: DM
-3 most common: DM, Syringomyelia (longitudinal cavities lined by dense tissue), and Tabes Dorsalis
-C: Myelomeningocele, Spina Bifida, CMT, MS, CP, Syringomyelia, Congenital insensitivity
M: DM, Alcoholic neuropathy, Uremia, Pernicous Anemia
I: Tabes Dorsalis, Polio, Leprosy, TB
N: Tumors in brain, spinal cord, peripheral nerve
T: Trauma to brain, spinal cord, peripheral nerve
D: Indomethacin, Intra-articular corticosteroids, phenylbutazone
ddx of charcot
OM AVN Inflammatory arthritis PVS septic arthritis CPPD Neoplasm
charcot clinical findings
- Presents similar to infection
- Red, hot, swollen, deformed foot +/- pain
- Neuropathic
- Readily available pulses (often described as bounding)
radiograhpic findings in charcot
- Atrophic:
- With osteopenia, pencil&cup deformities, resorption of bone ends
- Without osteophytes, sclerosis, fragmentation, soft tissue debris
- Hypertrophic:
- With joint space narrowing, fractures, fragmentation, ST debris, periosteal rxn, subluxation
- Without osteoporosis
- Be aware of both types
classifications for charcot
- Eichenholtz Classification
- Brodsky Classification
- Schon Classification
treatment for charcot
- Acute:
- Strict and immediate NWB and immobilization for 12-16 weeks.
- Edema control (Jones cast, ACE inhibitors, Diuretics, Posterior splint, Elevation, Ex Fix, etc.)
- Education and family support
- FXR every 4-6 weeks with relatively few cast changes
- Transition:
- Transition to WB (CAM walker, CROW, Bracing, MAFO, Shoes, etc.)
- Permanent:
- Surgical correction of underlying deformity
- Consider TAL, Arthrodesis, Wedging osteotomies, Amputation
- Adjunctive:
- Bone stimulators
- Bisphosphonates: -Pamidronate (Aredia): 60-90mg over 24h. 3 doses in 2 weeks.
- Alendronate (Fosamax): 5mg PO q24h
eichenoholtz 1966 classification of charcot
- Based on plain film radiographic findings
- Originally described Stages 1Æ3, but Stage 0 added later (Yu given credit, but really Schon).
- [Yu GV, Hudson JR. Evaluation and treatment of stage 0 Charcot’s neuroarthropathy of the foot and ankle. JAPMA. 2002; 92(4): 210-20.]
-Stage 0:
High risk pre-Charcot
-Radiograph: Unremarkable. Maybe increased ST density, bone flecks or change in foot architecture.
-Clinical: Sudden onset of non-pitting edema, erythema, calor, +/- pain, bounding pulses, intrinsic atrophy.
-Normal skin temp: 94°F; can increase by 12°
-Uptake in all three phases of Tc-99 bone scan
- Stage 1: Acute/Developmental
- Radiograph: Capsular distention, fragmentation, debris, subluxation
- Clinical: Red, hot, swollen foot with joint laxity
- Stage 2: Coalescence
- Radiograph: Sclerosis, resorption of debris, fusion
- Clinical: Subjectively decreased red, hot, swollen
- Stage 3: Reconstruction
- Radiograph: Decreased sclerosis (with increased vascularity) and remodeling
- Clinical: Decreased joint mobility with increased stabilization
Brodsky Classification (1992) [Brodsky JW. The diabetic foot. In: Coughlin and Mann’s 1992 edition.
of charcot
- Type 1: Lisfranc joint (27-60% incidence)
- Type 2: Chopart’s joint and STJ (30-35% incidence)
- Type 3A: Ankle joint (9% incidence)
- Type 3B: Posterior calcaneus
- Type 4: Multiple combinations of above
- Type 5: The forefoot
-Schon Classification
[Charcot neuroarthropathy of the foot and ankle. CORR. 1998; 349: 116-131.
I: Lisfranc Pattern
-AÆC with increasing deformity to medial rockerbottom and ulceration.
II: Naviculocunieform Pattern
-AÆC with increasing deformity to lateral rockerbottom and ulceration.
III: Perinavicular Pattern
-AÆC with lateral rockerbottom, Talar AVN and ulceration.
IV: Transverse Tarsal Pattern
-AÆC with increasing deformity to central rockerbottom and ulceration.
Differentiate charcot of OM General
- Please keep in mind that these are not mutually exclusive and both can be present!
- These are just general guidelines and many people will vehemently argue about them.
- The gold standard is a bone biopsy which would show infection in OM and not in Charcot.
OM vs charcot subjective and objective
Subjective
- OM: Constitutional signs and symptoms of infection, infectious risk factors, history of infection.
- Charcot: Uncontrolled DM, history of Charcot, history of recent trauma.
Objective
- OM: Necrosis, purulent drainage, elevated white count, cultures, positive bone biopsy.
- Charcot: Increased joint laxity, non-pitting edema, bounding pulses, rockerbottom deformity, negative bone biopsy.
OM vs charcot imaging
Imaging
-Not enough evidence yet, but some believe that OM is positive on bone scans and WBC scans for greater than 24 hours
whereas Charcot neuroarthropathy is only positive during the first 24 hours.
-The Tc99 Sulfur Colloid scan would also theoretically be positive for infection, but not for Charcot.
keys to describing plain films
-Increased or Decreased
-Radiolucency or Radiodensity
-Everything that you see on a radiograph can be described using these terms. So while you may not be able
to “see” a fracture, you can describe an area of radiolucency within bone consistent with a fracture. And
while you may not be able to “see” an infection, you can describe an area of radiolucency within the soft
tissue consistent with emphysema.
reading MRI
bone scans
ultrasound
MRI:
- Increased or Decreased
- Signal intensity
- Bone scans:
- Increased or Decreased
- Signal uptake
- Ultrasound:
- Hyperechoic or Hypoechoic
bugs- cellulitis with an open wound
- Staph Aureus (SA) (if no streaking present)
- Strept (with streaking and palpable border)
- Usually monomicrobial
Infected ulcer in abx naive pateint
Staph Au
Strep
polymicrobial
chronically infected ulcer in abx naive pt
Staph Au
Strep
Enterobacter
usually polymicrobial
macerated infected ulcer
pseudomonas
poly
Chronic, non-healing ulcer with prolonged Abx therapy:
- SA -MRSA
- Staph epi
- Enterococci -VRE
- Diptheroids (Corynebacterium)
- Enterobacter
- Pseudomonas
- Extended GNR
- Usually polymicrobia
Fetid Foot with necrosis and gangrene
- Resistant Gram positive cocci
- Mixed GNR
- Anaerobes
- Polymicrobia
OM with hemodialysis
SA
enterobacter
pseudomonas
OM with IVDA
SA
enterobacter
pseudomonas
OM with decubitus
gram negatives
OM with hemoglobulinopathy
salmonella
Human mouth pathogens
haemophilus actinobacillus cardiobacterium hominis eikenella corrodens kingella kingae
water exposure
vibrio
aeromonas hyprophilia
mycobacterium
Puncture through a shoe
pseudomonas
any dirt or soil
clostridium
Cat bite
pasteurella multocida
dog bit
strep virdans
capnocytophaga canimorsus
immunocompromised pt
gram negatives
septic burisitis
Staph aureus
gas gangrene
clostridium
post op infection following implant
staph epi
fruity odor/green hue
pseudomonas
foul smelling discharge
anaerobes
creamy yellow discharge
SA
White discharge
Staph epi
generalized gram pos coverage
- 2ndGeneration PCN -2ndGeneration Quinolones
- Synercid
- 4thGeneration PCN -Macrolides
- Rifampin
- 1stGeneration Cephs -Bactrim
- 2ndGeneration Cephs
- Vancomycin
- Carbapenems -Clindamycin
- Tetracyclines
- Zyvox
generalizd MRSA coverage
- Vancomycin -Synercid
- Clindamycin
- Bactrim/Rifampin
- Zyvox
- Cubicin
gram neg coverage
3/4 PCN 2/3/4 quinolones carbapenems tetracycline aztronam bactrim
Generalized Pseudomonas Coverage
- Cephalosporins x 3 (Fortaz, Cefobid, Maxipime)
- PCN x 2 (Zosyn, Timentin)
- Aminoglycosides
- Primaxin
- Quinolones
- Aztreonam
- ACRONYM: FAT CIAZ (Fortaz, Aztreonam, Timentin, Cefobid, Imipenin, Aminoglycosides, Zosyn)
Anaerobes
4PCN 1/2/3/4 Ceph Aminoglycosides Carbapenems 4Quinolones Clindamycin Flagyl
IDSA source citation
-from Lipsky BA, et al. Diagnosis and Treatment of Diabetic Foot Infections. IDSA Guidelines. CID 2004; 39: 885-910.
IDSA uninfected wound
- Definition: No purulence, inflammatory manifestations, or systemic manifestations
- Empiric Therapy: None
IDSA Mildly infected wound
- Definition:
- 2+ Manifestations of Infection (purulence, induration or erythema/pain/warmth)
- <2cm of erythema
- Limited to skin and subcutaneous tissue
- No systemic complaints
- Empiric Therapy Recommendations:
- 2-PCN -Bactrim
- Clinda -Augmentin
- Keflex -Levo
IDSA Moderately Infected Wound
- Definition:
- As above, in a systemically/metabolically stable patient PLUS
- > 2cm cellulitis OR streaking OR involvement of deep tissue
-Empiric Therapy Recommendations:
- Bactrim -Invanz
- Augmentin -Ceftin + Flagyl
- Levo -Timentin
- 2-Ceph -Zosyn
- 3-Ceph -Levo + Clinda
- Daptomycin + Aztreonam -Cipro + Clinda
- Zyvox + Aztreonam
IDSA Severely Infected Wound
- Definition: -Infection as above in a patient with systemic toxicity and metabolic instability
- Empiric Therapy Recommendations:
- Primaxin
- Vanco + Fortaz
- Zosyn
- Vanco + Fortaz + Flagyl
- Cipro + Clinda
- Levo + Clinda
empiric therapy if MRSA is likely
- Zyvox
- Vanco + Fortaz
- Zyvox + Aztreonam
- Vanco + Fortaz + Flagyl
- Daptomycin
- Daptomycin + Aztreonam
empiric therapy to cover all bases
Vanco + Aztreonam + Flagyl
DOC Staph aureus
alternatives
1-ceph
vanco
clinda
azithromycin
DOC MRSA
Vanco
DOC Staph Epi
2-PCN
MRSE dOC
Vanco
DOC Enterococci
3-PCN
VRE DOC
Linezolid
Strep pyogenes Group A Strep DOC
Strep agalactiae (B)
Strep bovis (D)
Strep Viridans
3-PCN
Peptostreptococcous DOC
Clinda
bacillus antracis doc
cipro
conynebacerium diptheriae doc
macrolide
liseria monocytogenes
3-pcn
clostridium perfringens doc
ertapenam
c diff doc
flagyl
clostridium tetani doc
clindamycine
pseudomonas doc
zosyn
e coli doc
3 cep
enterobacter doc
bacrim
proteus doc
3-pcn
vibrio doc
tetracyclines
y. pestis doc
aminoglycosides
shigella doc
cipro
salmonella doc
cipro
klebsiella doc
3-ceph
serratia doc
3-ceph
e. corrodens doc
augmentin
p. multocida doc
doxycycline
bacteroides fagilis doc
ertapenem
neisseria doc
rocephin
spirochetes doc
t. pallidum
borrelia burgdorferi
1-pcn
staph aureus
po/iv dosing
-PO:
Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid
Zithromycin -500mg PO day 1, 250mg PO days 2-5
-IV:
Ancef -1g IV q8
Vancomycin -1g IV q12
Clindamycin -600mg IV q8
streptococcus
po and iv dosing
-PO:
Keflex -500mg PO tid or 750mg PO bid
Clindamycin -300mg PO qid
-IV: Ancef -1g IV q8 Vancomycin -1g IV q12 Clindamycin -600mg IV q8 3.
MRSA
po and iv dosing
-IV:
Vancomycin -1g IV q12
-PO: Bactrim -1 tablet PO bid Rifampin 300mg \+Minocycline -100mg PO bid
enterococcus dosing chart
-PO:
Amoxicillin -250-500mg tid
Augmentin -875mg bid or 500mg tid (or bid)
Zyvox -600mg PO bid
-IV:
Vancomycin -1g IV q12
Zyvox -600mg IVq12
VRA/VRE dosing iv and po
-PO:
Zyvox -600mg PO bid
-IV:
Zyvox -600mg IV q12
Synercid -7.5mg/kg/hr over 1 hour q12
pseudomonas dosing iva nd po
-PO:
Ciprofloxacin -250-750mg PO bid
-IV:
Ciprofloxacin -400mg IV q12
Fortaz -2g IV q12
Aztreonam -1g IV q8
e coli, proteus dosing iv and po
-PO: Keflex -500mg PO tid or 750mg PO bid
Cipro -250-750mg PO bid
Levaquin -500mg PO qday
Tequin -400mg PO qday
-IV: Ancef -1g IV q8
Cipro -400mg IV q12
Levaquin -500mg IV qday
Tequin -400mg IV qday
dosing of penicilliins
1st Generation:
- Pen V: 500mg q6 PO
- Pen G: 250,000 units/kg/day IV
2nd Generation: -Dicloxacillin: 250mg q6 PO
- Oxacillin: 1-2g q4 IV
- Nafcillin: 1-2g q4 IV
3rd Generation: -Amoxicillin: 500mg q8 PO
-Ampicillin: 1g q4-6 IV
4th Generation: -Augmentin: 875mg q12 PO
- Unasyn: 3g q6 IV
- Zosyn: 4.5g q6 IV
- Timentin: 3.1g q6 IV
cephalosporins dosing
1stGeneration: -Keflex: 500mg q8 PO or 750mg PO bid
- Duricef : 2g q24 PO
- Ancef: 1g q8 IV
2ndGeneration: -Ceftin: 500mg q12 PO
- Zinacef: 1.5g q8 IV
- Mefoxin: 1g q6 IV
3rd Generation: -Omnicef: 300mg q12 PO
- Vantin: 400mg q12 PO
- Rocephin: 1g q24 IV
- Fortaz: 1g q8 IV
- Cefobid: 2g q12 IV
4th Generation: -Maxipime: 2g q12 IV
quinolones dosing
2ndGeneration: -Ciprofloxacin: 750mg q12 PO/400mg q12 IV
3rdGeneration: -Levofloxacin: 500mg q24 PO/IV
4thGeneration: -Tequin: 400 q12 PO/IV
-Avelox: 400 q24 PO
Macrolines dosing
- Biaxin: 500mg q12 PO
- Ketek: 800mg q24 PO
- Zithromax: 500 q12 IV/ 500mg PO Day 1; 250 mg PO Day2-5
- Erythromycin 500mg q6 PO
carbapenems dosing
- Invanz: 1g q24 IV
- Primaxin: 500mg q8 IV
- Merrem 1g q8 IV
Aminoglycosyides dosing
- Amikacin: 1500mg/day
- Tobramycin: 3-5mg/kg/day
- Gentamycin: 3-5mg/kg/day
tetracyhclines dosing
- Minocycline: 100mg q12 PO/IV
- Doxycycline: 100mg q24 PO
- Tetracycline: 500mg q6 PO
bactrim dosing
160/800mg q24 PO
vanco dosing
1g q12 iv
clindamycin dosing
600mg q8 IV
300 mg q6 PO
Zyvox dosing
600 mg q12 PO/IV
Synercid dosing
7.5mg/kg q8 IV
Flagyl dosing
500mg q8 PO
Trauma Work-up
CC HPI PMH PSH Meds Allergies FH ROS ABCDEs of primary survey Tetanus Status NPO Status
ABCDES of Primary survey
-Airway: Three common forms of airway obstruction are cervical spine injury, swollen tongue and facial fracture.
-Breathing: Note how this is different than an established airway. Someone can have an airway, but still not be
breathing.
-Circulation: Assess vascular status in all four extremities. Two large-bore (18-gauge) IV’s should be started
immediately if fluid replacement is considered necessary.
-Deficits (Neurological): There are two ways to assess this.
–AVPU
—Alert, responds to Verbal stimuli, responds to Painful stimuli, or Unresponsive
—Glasgow Coma Scale
—-Based upon three criteria: eye opening, verbal response, motor response.
-Based on scale of 0-15 with a higher score indicating a better prognosis.
-13+ associated with a good prognosis; 7- associated with a poor prognosis.
-Exposure: Complete exposure of the patient to evaluate further, unknown damage
trauma secondary survery
HPI, PMH, etc and physical exam
Racquet-shpaed gram positive bacillis
Releases exotoxin causing a pre-sympathetic blockade
Clostridium Tetani
Triad of tetanus symptoms
trismus - Lockjaw
Risus Sardonicus - spasms causing smiling
Aphagia - can’t swallow
Charateristic of a tetanus prone wound
greater than 6 hours old, clinical signs of infection, deep, devitalized tissue, contamination, traumatic mechanism of injury, etc
Tatanus algorithm
- Unknown tetanus status:
- Clean wound: Give the toxoid; Hold the TIG
- Tetanus-prone wound: Give the toxoid; Give the TIG
-Incomplete tetanus status:
-Clean wound: Give the toxoid; Hold the TIG
(No booster within 5 years) -Tetanus-prone wound: Give the toxoid; Give the TIG
-Complete tetanus status:
-Clean wound: Hold the toxoid; Hold the TIG
(Booster within 5 years) -Tetanus-prone wound: Hold the toxoid; Hold the TIG
dosages of tetanus treatments
toxoid 0.5ml
TIG (tetanus immunoglobulin) 250 to 300 units
NPO status considerations
-All trauma patients are potential surgical candidates, so get this information for the weenie anesthesiologists
-Traditional guidelines recommend:
-Nothing by mouth after midnight the night before elective surgery
-Nothing by mouth within 6-8 hours of any type of surgery
-These strict guidelines are in the process of changing however, particularly with regard to allowing the ingestion
of small amounts of clear liquids up to the time of surgery
What are considered podiatric surgical emergencies
- Infection with emphysema (gas gangrene)
- Open fracture/dislocation
- Compartment syndrome
- Necrotizing Fasciitis
- General Neurovascular compromises
Mangled Extremity Severity Score MESS
- Based on 4 criteria: Skeletal/Soft Tissue Injury, Limb Ischemia, Age, and Shock
- Based on a scale from 1-11 with a higher score leading to an increased incidence of amputation.
- A score of 7+ has an increased likelihood of amputation.
Open fractures generally
-Note that 30% of lower extremity open fractures are associated with polytrauma.
-Mainstays of treatment: Aggressive incision and drainage with copious lavage.
-It is generally recommended to never primarily close an open fracture until devitalized soft tissue has demarcated,
but this certainly isn’t always the case in practice. In fact, the Ortho Trauma service at Inova routinely primarily
closes open fractures following I&D with ORIF.
guistillo anderson classification of open fractures
I. Clean Wound 5cm in diameter with extensive soft tissue damage
- Abx choice: Ancef (or high dose PCN), Clindamycin and Aminoglycoside
- IIIA: Adequate soft tissue coverage
- IIIB: Extensive soft tissue damage with periosteal stripping and massive contamination
- IIIC: Arterial damage requiring primary repair
fracture blisters general
-Location: Subepidermal
-Note that the fluid is sterile. Fracture blisters are histologically similar to 2nd degree burns.
-Most common LE etiology? Secondary to high-energy trauma such as ankle fx, calcaneus fx or Lisfranc injury.
-2 Common Types of Fracture Blisters
-Clear fluid: Most common (75%). Very tense in appearance.
-Hemorrhagic: Most severe. Roof is flaccid. Takes longer to re-epithelialize.
-Treatment is controversial, but the conservative approach is to never incise through a fracture blister and to delay
surgery until re-epithelialization
signs and symptoms of shock
Tachycardia, Tachypnea, delayed capillary refill, decreased pulse pressure, change in mental status, decreased systolic pressure, decreased urinary output decreased H&H
Types o f shock
-Hypovolemic: most common; defined as the acute loss of circulating blood. Treatment is aggressive fluid
replacement.
-Cardiogenic: induced by myocardial dysfunction.
-Neurogenic: secondary to decreased sympathetic tone from head and spinal cord injuries.
-Septic: shock secondary to infection
goal of treating shock
Restore organ perfusion
When should a foreign body be removed?
-Clinical signs of infection, known contaminated object, pain, object close to NV elements, intra-articular
-Recommended imaging studies for a foreign body?
-Plain film radiography (no oblique views!), fluoroscopy, CT, MRI, US
-How will wooden objects appear on US
-Hyperechoic with a hypoechoic dark shadow
-How large must a glass foreign body be to be visible on plain film radiography? Does leaden matter
A piece of glass, regardless of whether it is leaden, must be >5mm to be visibl
-Classification for foreign bodies?
- Resnick Classification
- Patzakis Classification
-Resnick Classification
- I. Superficial/cutaneous: usually visible without signs of infection.
- II. Subcutaneous or articular without signs of infection.
- IIIA. Subcutaneous or articular with signs of infection.
- IIIB. Bone penetration without signs of infection.
- IV. Bone penetration with known osteomyelitis.
-Patzakis Classification
Wound site as a predictore of complications following deep nail puctures of foot.
- Zone 1: Toe to met head (50% incidence of osteomyelitis in this limited study.)
- Zone 2: Midfoot (17% incidence of osteomyelitis in this limited study.)
- Zone 3: Calcaneus (33% incidence of osteomyelitis in this limited study.
puncture wound most common bug
Staph Aureus
Beta Hemolyitc strept
puncture thru shoe
pseudomonas
puncture on farm
Clostridia
Human bite
Eikenella corrodens
cat bites
pasteurella multocida
dog bites
enterobacter
pseudomonas
Staph
Bacillis
mainstay of foreign body punture/wound treatment
Tetanus status
abx
aggressive I& D
lavage
Gunshot wounds genreral
-High velocity GSWs are characterized by speeds >2500 ft/s. This is significant because high velocity GSWs have a tendency
to yaw and tumble leading to increased cavitation.
describe cavitation
GSW
Large wound is created under a situation of negative pressure. This negative pressure “sucks” outside
contaminants into the wound
Compartment syndrome
-Results when interstitial pressure exceeds capillary hydrostatic pressure, so the microcirculation shuts down
symptoms of compartment syndrome
- P’s of Compartment Syndrome (These are very generalized)
- Pain out of proportion and not controlled by analgesics -Paralysis
- Pain with passive dorsiflexion of the toes -Pulselessness
- Paresthesia -Pressure
- Pallor
normal compartment pressures
0 to 5 mmHg
treatment of compartment syndrome
- Decompression via fasciotomy, debridement of necrotic tissue, copious lavage and delayed closure
- Incision approaches: Consider dorsal vs. medial approaches
how is compartment syndrome dx made
wick or slit catheter to measure pressures
complications of compartment syndrome
-Complications: permanent loss of function with structural deformity (Volkmann contractures), myoneural necrosis, sensory
loss, chronic pain
comparmtents
-Intermetatarsal Compartments X 4: Contains the interossei muscles
-Medial Compartment: Abductor Hallucis
-Lateral Compartment: Abductor digiti minimi
-Superficial Central Compartment: FDB
-Deep Central Compartment: Adductor Hallucis
-Calcaneal Compartment: Quadratus Plantae and late
Dorsal: EHB and EDB
comparmtent syndrome suspected but why still have DP andPT pulses
lie above fascial compartments so they are the last to go.
Digital fx, subjective
-History of trauma. “Bedpost” fracture describes stubbing your toe while walking at night. Also common are injuries from
dropping objects on the foot
Objective for digital fractures
- Edema, erythema, ecchymosis, open lesions, subungual hematoma, and onycholysis should all be expected.
- Any rotational/angulation deformities should be identified on plain film radiograph.
digital fx classification
- Rosenthal Classification [Rosenthal EA. Treatment of fingertip and nail bed injuries. Orthop Clin North Am. 1983; 14: 675-697.]
- Zone I: Injury occurs with damaged tissue completely distal to the distal aspect of the phalanx.
- Zone II: Injury occurs with damaged tissue completely distal to the lunula.
- Zone III: Injury occurs with damaged tissue completely distal to the most distal joint (IPJ in hallux; DIPJ in
lesser) .
digital fractures treatment by zone
- Zone I Injuries
- If injury involves no exposed bone and a total tissue loss less than 1cm squared, then:
- Allow to heal in by secondary intention.
- If injury involves a total tissue loss greater than 1cm squared, then:
- A STSG or FTSG should be used depending on weight-bearing position.
- Zone II Injuries
- Flaps and Skin Grafts generally employed:
- Atasoy flap: plantar V to Y advancement
-Kutler flap: biaxial V to Y advancement
- Zone III Injuries
- Usually requires distal amputation (Distal Symes amputation)
Most common forefoot fracture
hallus
digital fracture without nail involvement or displacement tx
immobilization
if subungal hematoma is present than there is a what chance of what
25% incidienc of underlying phalanx fracture
if subungal hematoma is greater than 25% then
remove nail
for proper nail function and adherence there should be no onyholysis within what of what
5mm of lunula
Transverse groove often associated with trauma
beau’s line
