chapter 4d podiatric infectious diseases

8/2/2019 Chapter 4d Podiatric Infectious Diseases

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4.4 Podiatric Infectious DiseasesMark Kosinski, DPM

Assessment of the Patient with InfectionIn addition to performing the requisite history, review of systems and physical examination, it may be helpful

include the following questions and observations when assessing a patient with infection.

History

When did the infection begin? Where and how was it acquired ? Distinguish between community and noso-

comial (hospital acquired) infections.

Past Treatment

What previous treatment if any, has the patient received? Has the patient been taking antibiotics?

Drug Allergies/Sensitivities

Does the have an allergy to penicillin or another antimicrobial agent? What form did the allergy take? Was it

an anaphylactic reaction or delayed hypersensitivity ? How long ago did it occur and with what drug?

Review of Systems

Inquire about the presence of fever, chills, nausea, vomiting, diarrhea, weakness, malaise, and diaphoresis

Past Medical History

Including diabetes, HIV, IVDA, tuberculosis, STDs , sickle cell anemia, renal or hepatic disease, and risk fac-

tors for infective endocarditis

Medications

Is the patient currently receiving antibiotic therapy or taking any medication which could affect immune

response or mask the signs of infection (e.g., corticosteroids, cyclosporine)

Past Surgical History Does the patient have implanted biomaterials, prosthetic joints, heart valves or shunts that might become

secondarily infected ? Has the patient recently been hospitalized, putting them at risk for MRSA?

Social History

Ask about travel, jobs and pets

Physical Examination

Vital Signs

Include oral temperature, blood pressure, pulse and respiration

Area of Chief Complaint

Note the presence and extent of cellulitis, lymphangitis, and regional lymphadenopathy (inguinal and

popliteal). Note the odor and appearance of exudate and the extent and depth of the wound or ulcer.

Lab Tests

Appropriate lab tests for a patient with infection include a CBC with differential, renal and hepatic functiontests, ESR, blood glucose with glycosylated hemoglobin, urinalysis, X-rays, wound cultures and Grams stain.

Consultations

Consult other medical services (eg., infectious diseases, internal medicine, vascular surgery) as needed

Medicine | Podiatric Infectious Diseases 283


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Five Basic Principles of Antibiotic Selection and Empiric Treatment

1. Your antibiotic choice should be governed by the organisms you expect to find in agiven situation

2. Distinguish between community and hospital acquired infections3. Use an antibiotic with proven efficacy to the suspected or known organism(s)4. Change or continue antibiotics based on culture results as soon as possible. Avoid

prolonged empiric therapy5. When sensitivities are known, choose the narrowest spectrum agent with the highest

efficacy and the lowest toxicity

Odor, Color and Appearance as Clues to the Infecting Organism

Yellow pus S. aureus (coagulase positive Staph.)

White pus S. epidermidis (coagulase negative Staph.)

Green pus/exudate P. aeruginosa

Dishwater pus Strep. group A (necrotizing fasciitis)

Draining sinuses /granules* Actinomyces, Nocardia

Fruity odor P. aeruginosa

Foul, fetid odor Anaerobes (B.fragilis in diabetic foot)

Woods Light flourescence Coral red C. minitissimum

Green P. aeruginosa

Red Bacteroides melaninogenicus

Yellow Pityriasis versicolor

* sulfur granules are composed of colonies of Actinomyces or Nocardia surrounded by inflammatory cells.

Distinguish actinomycosis from nocardiosis by culture and biopsy.

When you hear Think Paronychia S. aureus Diabetic foot infection Polymicrobial (Staph., Strep.,B. fragilis) Sickle cell disease OM Salmonella Puncture wound OM P. aeruginosa Post op infection S. aureus (MSSA/MRSA) Post op infection (implant) S. aureus (MSSA/MRSA), S. epidermidis Human bites Eikenella corrodens. HIV, syphillis, hepatitis Cat bites Pasturella multocida, Bartonella henselae Dog bites DF-2 (Capnocytophaga canimorsus) Burn wounds (acute) nitially sterile, then S. aureus Burn wounds (chronic) P. aeruginosa IVDA MRSA, P.aeruginosa, human oral flora (Eikenella corrodens)

Florists/Rose bushes Sporothrix schenkii

Fish tanks, pools Mycobacterium marinum Salt / brackish water Vibrio vulnificus Superficial Impetigo Group A Beta hemolytic Streptococci (Strep. Pyogenes) Bullous Impetigo S. aureus Erysipelas Group A Beta hemolytic Streptococci (Strep. Pyogenes)

Occasionally streptococci group C and G Web spaces T. mentagrophytes, T. rubrum, C. minitissimum, Gram negative

bacteria (e.g., pseudomonas, klebsiella, proteus) Scaulded Skin Syndrome S. aureus

284 The 2005 Podiatry Study Guide


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Empiric Therapy

Empiric Therapy for Diabetic Foot Infections

Your empiric antibiotic(s) should cover S. aureus, Group B Strep and in more serious infections, Gram negativebacteria and anaerobes (B. fragilis).

It is therefore useful to choose an antibiotic based on the severity of infection

Mild Infection:

Local cellulitis (< 2 cm) No proximal spread No systemic S & S

Normal labs

Contrary to previous belief that ALL diabetic infections werepolymicrobial; these (mild infections) frequently

are not.

Cover for: Staphylococcus aureus(MSSA/MRSA) Increasing community-acquired MRSA

Group B Streptococcus

Drugs used to kill S. aureus will almost always kill Strep.

MRSA

TMP/SMX

Minocycline

MSSA

Cephalosporins (cephalexin, cefdinir) Amoxicillin/clavulanate Levofloxacin

Clindamycin

Moderate to Severe Infection Significant cellulitis (> 2 cm)

Gas Proximal spread - lymphangitis Constitutional S & S Laboratory changes

Elevated WBC, left shift

Although moderate to severe infections are commonly polymicrobial, S.aureus and Strep still predominate.

Organisms Found in Moderate to Severe Diabetic Infections:

Staphylococcus aureus(MSSA/MRSA) Group B Streptococcus

Gram-negatives Pseudomonasstill uncommon as a pathogen Anaerobes B. fragillis

Peptococcus, Peptostreptococcus



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Some Antibiotic Choices to Treat Moderate to Severe Infections:

b-lactamase inhibitor compounds Ampicillin/sulbactam Ticarcillin/clavulanate Piperacillin/tazobactam

Imipenem/cilistatin, ertapenem

Clindamycin + a gram-negative agentFor MRSA

Linezolid ( plus gram negative agent + anaerobic agent)

Vancomycin ( plus gram negative agent + anaerobic agent)

Empiric Therapy for Mammalian Bite Wounds

Ampicillin/sulbactam (Unasyn). Amoxicillin/ clavulante (Augmentin).

Ciprofloxacin/Clindamycin (Cipro/Cleocin) *

*for pcn allergic patients

Empiric Therapy for Post-Operative Wound Infections

S. aureus is the most commonly isolated organism in post operative wound infections.In addition, S. epidermidis is a common organism in post operative infections involving implants.

MRSA

TMP/SMX Minocycline For more sever infections, vancomycin or linezolid

MSSA

Cephalosporins (cefazolin, cephalexin, cefdinir) Amoxicillin/clavulanate Levofloxacin

Clindamycin

Antibiotic Therapy for Methicillin Resistant Staph. aureus (MRSA)

Differentiate Community Acquired MRSA (CA-MRSA) from Hospital Acquired MRSA

(MA-MRSA)

In general, CA-MRSA retains susceptibility to TMP/SMX and Tetracycline.HA-MRSA is resistant to TMP/SMX and tetracycline and like CA-MRSA is sensitive to vancomycin and

linezolid.

What both CA-MRSA and HA-MRSA have in common is the mec-A gene, making them resistant to all beta-

lactam drugs.

MRSA Risk Factors

Patients in acute care and nursing facilities. Individuals who have undergone previous antibiotic therapy

Those in proximity to patients infected or colonized with MRSA

Patients with CA-MRSA may have no known risk factors.



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Antimicrobial Therapy for MRSA

Vancomycin Tetracycline (minocycline/doxycycline) TMP/SMX Quinupristin/Dalfopristin Linezolid

Vancomycin (Vancocin)

Drug of Choice (DOC) for MRSA Use parenterally for systemic infections. Use orally for C. difficile colitis Concomitant use with an aminoglycoside can lead to additive nephrotoxicity Monitor serum concentration (peak and trough levels) and renal function (serum creatinine) Hemodialysis removes little or no vancomycin. Use 1g Q7-10 days in functionally anephric adults If red-man/red neck (anaphylactoid) reaction occurs, infuse slowly(over 60 minutes ) and pre-medicate with

Benedryl. Administration of vancomycin 500mg q6h as opposed to 1g q12h will also minimize reaction Poor bone penetration. Combine with rifampin for additive effect

Trimethoprim/Sulfamethoxazole (TMP/SMX) (Bactrim/Septra)

Do not use in patients with an allergy to sulfa drugs Most common adverse effect is skin rash which may limit its use Hematologic adverse reactions and bone marrow toxicity / neutropenia have also been reported Commonly used in the treatment of urinary tract infections and by patients with HIV disease for

Pneumocystis carinii pneumonia (PCP) prophylaxis Combine with Rifampin for additive effect.

Quinupristin/Dalfopristin (Synercid):

Active against MRSA/VRE. Parenteral only.

Use within 30 minutes of reconstitution to prevent crystallization.

Linezolid (Zyvox)

Active against MRSA/VRE. Oral and parenteral forms available. High bioavailability after oral administration . In terms of blood levels; 600mg BID P.O. = 600mg BID I.V.



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OralAntibiotics

(+)good

(+/-)fair

(-)noactivity

Generic

UsualDose

TradeName

MRSA

Gram

+

Gram-

P.aeruginosa

Anaerobes

Cephalexin

250mg-500mg

Q6h

Keflex

(-)

(+)

(+)

(-)

(-)

Dicloxacillin

500mgQ6h

Dynapen

(-)

(+)

(-)

(-)

(-)

Clindamycin

150mg-450mg

Q6h

Cleocin

(-/+)

(+)

(-)

(-)

(+)

Ciprofloxacin

500mgQ12h

750mgQ12h

Cipro

(-)

(+/-)

(+)

(+)

(-)

Azithromycin

500mgday1then

250mgday2-5

Zithromax

(-)

(+)

(-)

(-)

(-)

TMP/SMX

1DSQ12h

Bactrim

(+)

(+)

(+)

(-)

(-)

Amoxicillin/Clav

500mgQ12h

875mgQ12h

Augmentin

(-)

(+)

(+)

(-)

(+)

Metronidazole

500mgQ8H

Flagyl

(-)

(-)

(-)

(-)

(+)

Theabovetablesareintendedonlyasastudyguideandarebasedonpodiatricallyreleva

ntpathogenswithinagivenclass.Definitivean

tibi-

otictherapyshouldbebasedoncultureresults

andMICs.


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ParentalAntibiotics

(+)g

ood

(+/-)fair

(-)noactivity


Generic

UsualDose

TradeName

MRSA

Gram

Positive

Gram

Negative

P.aerugoinosa

A

naerobes

Cefazolin

1g

Q6-8H

Ancef

(-)

(+)

(+)

(-)

(-)

Clindamycin

15

0mg-900mg

Q6-8H

Cleocin

(-)

(+)

(-)

(-)

(+)

Vancomycin

1g

Q12H

Vancocin

(+)

(+)

(-)

(-)

(-)

(exceptC.

difficile

(+))

Nafcillin

500mg-1.5mg

Q

4-6H

Unipen

(-)

(+)

(-)

(-)

(-)

Aztreonem

1gQ8H

Azactam

(-)

(-)

(+)

(+)

(-)

Ampicillin/

Sulbactam

3gQ6H

Unasyn

(-)

(+)

(+)

(-)

(+)

Ticarcillin/

Clavulanate

3.1gQ6H

Timentin

(-)

(+)

(+)

(-)

(+)

Piperacillin/

Tazobactam

3.375gQ6H

Zosyn

(-)

(+)

(+)

(-)

(+)

Imipenem/

Cilistatin

50

0mgQ6H

Primaxin

(-)

(+)

(+)

(+)

(+)

Cefipime

2g

Q12H

Maxipime

(-)

(+/-)

(+)

(+)

(-)

(exceptC.perfringens(+/-))

Thea

bovetablesareintendedonlyasastudyguideandarebasedonpodiatricallyrelevantpathoge

nswithinagivenclass.Definitiveantibi-

otictherap

yshouldbebasedoncultureresultsandMICs

.


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Antibiotic Caveats and Facts

Ticarcillin/ Clavulanate

High sodium load (avoid in patients with CHF).

Imipenem/Cilistatin

Associated with dose-related seizures (use with caution in patients with seizure history). Cross

reativity in patients with anaphylaxis to penicillin

Quinolones

Associated with tendinitis and tendon rupture. Studies involving the use ofciprofloxacin in children with cyctic fibrosis have shown that quinolones can be used

with relative safety in this age group Ciprofloxacin: Most active quinolone against P. aeruginosa Levofloxacin : More active against gram positive aerobic cocci than ciprofloxacin

Clindamycin

Associated with C. difficile colitis. Active against Gram positive aerobes and anaerobes.Combine with a quinolone for gram negative coverage

Metronidazole

Has no aerobic coverage (do not use it as single agent therapy in foot infections) Metronidazole has been shown to be more active against B. fragilis bloodstream isolates

than clindamycin. Mild disulfuram reaction. Drug of choice for C. difficile colitis

Rifampin

An anti-tuberculous drug with activity against S. aureus. Rifampin should not be usedalone since rapid resistance can develop. Use in combination with vancomycin forMRSA. May impart an orange color to the urine and cause a pink staining of soft contactlenses. May interfere with activity of oral contraceptives

Aminoglycosides

Nephrotoxic and ototoxic. Monitor serum levels with peaks and troughs. Try not to use

for diabetic patients. There are better, albeit more expensive ways to cover gram negatives(e.g., quinolones, aztreonam)

Piperacillin/Tazobactam

Not recommended for monotherapy of P.aeruginosa at3.375g q6h. (Med Lett Drugs Ther 1994 Nov 25;36(936):110). Many strains of P. aerugionsa have becomeresistant to the anti-pseudomonal penicillins by virtue of their hyperproduction of beta-lactamase

Cefepime

Fourth generation cephalosporin. Good activity against P.aeruginosa

Bactrim

Good bioavailability after oral administration. Can cause neutropenia. No anaerobic coverage



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Antibiotic Selection in Pregnant Patients / FDA Risk Categories

Base your antibiotic choice on the FDA assigned risk category. Choose the drug from the safest category that

will cover the infecting organism. A= safest / D= least safe.

FDA Category A

NONE

FDA Category B

penicillins, cephalosporins clindamycin aztreonam meropenem erythromycin/azithromycin metronidazole terbinifine

FDA Category C

imipenem/cilistatin quinolones trimethoprim/sulfamethoxazole vancomycin rifampin itraconazole

FDA Category D

aminoglycosides

tetracyclines

Ordering Lab Tests

CBC/ Differential

Acute infection is characterized by an elevated WBC count (absolute leukocytosis), as well as a shift to the left

(increased number of immature or band cells)

Renal Function Tests

Evaluate renal function and dose adjust antibiotics accordingly BUN largely dependant on the hydration status of the patient and therefore of limited use. Serum Creatinine - a more sensitive indicator of renal function than BUN. Serum creatinine may not

accurately reflect the patients renal function in the elderly who may have decreased creatinine production.Creatinine clearance is a better measure.

Creatinine Clearance most useful for antibiotic dose adjustment. Can either be had via a 24 hour urine

collection or derived using the patients serum creatinine and the equation ofCockroft and Gault



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Estimating creatinine clearance using serum creatinine

Modified equation of Cockroft and Gault

Intended for ages 18-110, serum creatinine 0.6-7 mg/dl

NOTE: This is the more popularly used version of the Cockroft-Gault formula at present. See literature for

supporting data (e.g., Hutson P et al. Carboplatin Dosing in Obese Patients. Proc Am Soc Clin Oncol 2000, abstract

725). Ccr = (140-age) (weight in kg) For females multiply result by 0.8572 X serum creatinine (1kg = 2.2 lbs)

Note: the following antibiotics do not need dose adjustment for patients with renal impairment: amphoterecin B,

azithromycin, ceftriaxone, clindamycin, nafcillin, trovafloxacin

ESR

Non-specific. Although elevated in any inflammatory process, a patient with a non-healing foot ulcer and a sig-

nificantly elevated ESR is suspicious for underlying osteomyelitis.

Wound, Bone and Blood Cultures

Order aerobic, anaerobic, acid-fast and fungal cultures where clinically indicated.

Principles of Wound Cultures

Prep wound site to remove surface bacteria Take a deep culture. Avoid contact with surrounding skin Include tissue if possible (pus is a sub-optimal culture source since it contains mainly WBCs and phagocy-

tized bacteria) Use proper transport media with respect to the organism being cultured Rapid transport to lab

Principles of Bone Cultures

With the possible exception of S. aureus, sinus tract cultures are rarely helpful in establishing the causative

organism in osteomyelitis. The diagnosis of osteomyelitis rests with the isolation of the organism from bone Sinus tract cultures are unreliable in predicting the infecting organism in bone Bone biopsy is diagnostic If possible, approach bone through uninfected tissue Send bone for microscopic diagnosis. Send bone for Grams stain Order aerobic and anaerobic cultures If clinically indicated, also order acid fast and fungal cultures and stains

Principles of Blood Cultures

Draw 2 sets 15 minutes apart (from different sites) If an organism grows from only one bottle, suspectcontamination.

Drawing blood cultures on a fever spike may be of benefit



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Ordering Stains

Results of cultures and MICs can take days (bacterial) to weeks (fungal and mycobacterial) to return. Ordering

the appropriate stain/smear can provide a clue to the infecting organism in the interim.

Bacteria Grams stain

Fungi KOH prep., PAS stain

Mycobacteria Acid fast stain Virus Tzanck smear

Grams Stain

Terminology relates to appearance

Staphlococcus = cluster of berries Streptococcus = twisted chain of berries

A Grams Stain That Reveals Would be

Gram positive cocci in clusters Staphlococcus

Gram positive cocci in chains Streptcoccus

Coagulase Positive vs. Coagulase Negative Staph

Coagulase positive (invasive) Staph aureus

Coagulase negative (non-invasive) Staph. epidermidis

Soft Tissue Infections

Necrotizing Fasciitis

Infection characterized by rapidly progressing necrosis and edema of subcutaneous fat and fascia.

Patient is acutely ill with fever, tachycardia and leukocytosis with bandemia Extremity is initially hot, erythematous, edematous and exquisitely tender Edema is hard and non-pitting and may extend beyond erythema Skin becomes dusky with vesicles and bullae filled with deep purple fluid

Process spreads rapidly along subcutaneous tissue and undermines superficial fasciaproducing cutaneous anesthesia and eventually skin gangrene and slough

Grey, stringy, subcutaneous fascia, liquefaction necrosis and the presence of a thin, watery, foul smelling exu-date (dishwater pus) are characteristic

Rapid progression may result in loss of limb or death Bacteriology varies widely. No single organism is pathogneumonic. Aerobic and anaerobic bacteria have been

identified including Streptococci group A, Clostridia spp. and Bacteroides spp. Treatment is directed toward aggressive surgical debridement, broad spectrum antibiotics and stabilization of

the patient medically

Common Cutaneous Viral Infections

Herpes Zoster (Shingles)

Painful vesicles on an erythematous base in a dermatomal distribution.Etiology: reactivation of Varicella Zoster (chickenpox) virus (VZV).

More common in elderly and immunocompromised patients.

Herpes simplex (HSV)

Painful vesicles or pustules on an erythematous base, but no dermatomal distribution as in Herpes Zoster.

HSV-1 typically affects above the waist, HSV-2 typically below

Molluscum Contagiosum

Painless 3-6mm pearly papules with central umbilication. Etiology: Molluscum contagiosum virus

(poxvirus). Spread by person to person contact



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Verruca

Etiology: Human Papilloma Virus (HPV). Distinguishing features include the presence of punctate black dots(thrombosed capillaries) and interruption of skin lines

Joint Infections

Infectious ArthritisAny warm, swollen joint should be considered infected until proven otherwise.Antibiotic therapy should be guided by the patients age, the results of the synovial fluid analysis, culture and

Grams stain.

Commonly Isolated Organisms

Infants and young children (


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Gonococcal Arthritis (GCA)

Usually develops within 3 weeks of onset of genitourinary infection Patient may be otherwise asymptomatic Migratory polyarthralgia with periarticular inflammation is typical in the early phase of GCA.

Vesiculopustular skin lesions may be present As the disease progresses, skin lesions resolve. Arthritis settles into one or two joints. The arthritis of dissemi-

nated GCA is asymmetrical The diagnosis of gonococcal arthritis depends on culture and identification of the organism. Obtain cultures

of blood, joint fluid and skin lesions

HIV-related Arthropathy

More than half of all patients infected with HIV will experience some bone or joint symptom during thecourse of their disease

Reiters syndrome and reactive arthritis are the most common etiologies followed by Psoriatic arthritis and Septic arthritis (Candida species, C. neoformans, H. capsulatum, Salmonella, S. schenkii, M. avium intracel-

lulare, M. tuberculosis)

Infectious Causes of Heel Pain

Heel pain accompanied by inflammatory signs should raise the suspicion of osteomyelitis.

Although the most common pyogenic organism responsible for puncture wound osteomyelitis is P. aeruginosa,virtually any organism implanted into soft tissue or bone has the potential to cause osteomyelitis. Foreign body pen-etration may inoculate not only pyogenic bacteria, but fungi and mycobacteria as well. Lymphocutaneous sporotri-chosis, chromoblastomycosis, phaeohyphomycosis and mycetoma are among the more common mycotic syndromesarising from puncture wounds associated with soil, thorns and wooden splinters.

Routine bacterial culture and Grams stain may not demonstrate the presence of these organisms. Negative bac-terial cultures of clinically infected areas should raise suspicion. It is therefore prudent to perform biopsy of boneand soft tissue as well as aerobic, anaerobic, acid-fast and fungal cultures when clinically indicated.

Reactive arthritis, including Reiters syndrome must be considered in any evaluation of heel pain. Reactivearthritis is an aseptic synovitis arising from a previous non-articular infection.. Reiters syndrome requires host pre-disposition, which is thought to be linked to human leukocyte antigen HLA-B27.Reactive arthritis can be triggeredby various organisms, including species of Campylobacter, chlamydia, Salmonella, Shigella and Yersinia.

Bone Infections

Diagnosis of Osteomyelitis

X-ray changes lag 10-14 days behind bone changes 99Tc-HMPAO(Ceretec) Scansand the gadolinium enhanced-fat suppressed MRIare the 2 most sensitive

imaging modalities. They are particularly useful in differentiating chronic osteomyelitis from Charcotosteoarthropathy

Biopsy, culture and Grams stain of bone are the gold standards of diagnosis

Treatment

Acute osteomyelitis can be cured by antibiotics alone. Chronic osteomyelitis requires surgical debridement of

the infected bone for cure. Antibiotics directed against the causative organism are adjunctive.

General Principles

Debride area clean of infected and devitalized bone. Be certain arterial supply to area is adequate to supporthealing



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Remove implanted biomaterials and fixation devices unless such device is providing osseous stability to afracture site or osteotomy

Obliterate dead space with appropriate packing material If there is any question as to whether infected bone remains, follow debridement by 4-6 weeks of antibiotic

therapy directed against the causative organism. If possible, administer antibiotics parenterally

Assessing Efficacy of Treatment After Debridement

Monitor for signs of clinical improvement Compare plain x-rays at 7-10 day intervals against post-debridement films.

Monitor WBC and differential, ESR and oral temperature

Osteomyelitis: Classification Systems

Waldvogel Classification System

hematogenous direct extension vascular insufficiency

Cierney - Mader Classification System

Anatomic Type Stage 1: Medullary osteomyelitis Stage 2 : Superficial osteomyelitis Stage 3: Localized osteomyelitis Stage 4 Diffuse osteomyelitis

Physiologic Class

A Host: Normal host B Host: Systemic compromise (Bs)

Local compromise (Bl)Systemic and local compromise (Bls)

C Host: Treatment worse than the disease

Systemic or Local Factors That Effect Immune Surveillance, Metabolism and Local Vascularity

Systemic (Bs) Local (Bl) Malnutrition Chronic lymphedema Renal, hepatic failure Major vessel compromise Diabetes mellitus Small vessel disease Chronic hypoxia Vasculitis Immune disease Venous stasis Malignancy Extensive scarring Extremes of age Radiation fibrosis Imunosupression or immune deficiency Neuropathy

Tobacco abuse

Osteomyelitis: Commonly Isolated OrganismsCierney-Mader Stage 1 (Monomicrobic Infection)

Infant Childhood Adults

< 1 year 1-16 years > 16 yearsGroup B Strep S. aureus S. aureusStaph. aureus Strep. Pyogenes S. epidermidisE. coli H. influenzae Gram positive bacilli

P. aeruginosaS. marcescensE. coli



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Cierney-Mader Stages 2,3 and 4 (Polymicrobic Infection)

S. aureus Diabetic Foot Osteomyelitis S. epidermidis S. aureus Strep pyogenes Streptococcus species Enterococcus species Enterococcus species Gram negative bacilli Proteus mirabilis

Anaerobes P. aeruginosaAnaerobes (B. fragilis)

Update on the diagnosis and management of osteomyelitis

Mader J, Ortiz M, Calhoun J. Clinics in Podiatric Medicine and Surgery Vol 13, No 4 October 1996

Infections in the Surgical Patient

Surgical Wound Prophylaxis

The goal of an effective prophylactic regimen is to decrease the numbers of pathogenic organisms below levelsnecessary to cause infection.

Surgical Wound Prophylaxis Has Been advocated in four clinical situations

Implant usage

Trauma surgery Prolonged operating time (>2-3 hours) The immunocompromised patient

To be effective, a prophylactic regimen must satisfy two criteria. First, the antibiotic must be active against thepathogen most likely to be encountered in a given situation and second, peak serum concentrations should beachieved at the time of inoculation.

S. aureus is the most commonly isolated organism in post operative wound infections.For orthopedic procedures therefore, cefazolin (Ancef) has proven effective. In settings where MRSA is an

important pathogen, vancomycin (Vancocin) should be used.

Trauma

The severity of the fracture is the major determining factor as to whether or not infection will occur.Infection following fracture varies with the degree of injury

Grade I fracture 0 - 9% Grade II fracture 1% - 12% Grade III Fracture 9% - 55%

In the case of open fractures the length of antibiotic administration is proportional to the severity of the infection.

Prophylactic antibiotics for Type 1 and II fracture is maximally effective if given for no more than 24 hoursafter surgery.

For type III fractures continuation of antibiotics for 48 hours appears warranted assuming adequate soft tis-sue coverage after surgery.

The length of antibiotic administration should be extended if there appear to be signs and symptoms ofinfection.

Although statistically S. aureus is the most common infecting organism in traumatic fractures, one must becognizant of organisms which inhabit the environment in which the trauma was sustained . Antibiotic choicesshould be made accordingly.

When instituting antibiotic prophylaxis for patients with distant prosthetic joints who undergo incision anddrainage of infected tissue, base antibiotic selection on preoperative Grams stain and culture results or the antici-pated organism. It is not necessary to use antibiotic prophylaxis to protect distant prosthetic joints who are under-going clean orthopedic surgery, since bacteremia is unlikely to occur.



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Lower Extremity Surgery and Patients with HIV

Regardless of their CD4 lymphocyte count, HIV-infected patients undergoing surgery have not been demon-strated to have a greater than usual rate of complication or a greater than usual rate of post-operative wound infec-tion.

T-cell mediated immunity is severely impaired in HIV infected patients, which is reflected by an increase in thenumber of intracellular pathogens such as viruses and non-pyogenic organisms as well as some extra-cellular organ-

isms such as fungi and Pneumocystis, for which T-cell mediated immunity is the primary defense. Neutrophil medi-ated immunity on the other hand remains largely intact in HIV-infected patients.

Infections for which the bodys primary defense is the T-cell mediated immunity (TB, parasites, mycobacteria)are thus more common in the HIV infected population. However, those infections for which the primary defense isthe white blood cell or neutrophil (pyogenic bacteria such as Staph and Strep) are not significantly more common

in non-neutropenic HIV patients.

Recommendations for perioperative surgical prophylaxis remain identical for HIVpositive and HIV negative patients

The choice of antibiotic and dosage for a given infection is identical whether a patientis HIV positive or HIV negative and regardless of CD4 lymphocyte count

The use of markers such as viral load and CD4 lymphocyte count as an arbitraryqualification for surgery (e.g., CD4 cutoff lines as a criterion) is both unwarrantedand unsubstantiated in the literature

Common Causes of CD4 Lymphocytopenia (CD4 Count Less Than 300)

Human immunodeficiency virus infection Mycobacterium tuberculosis infection Granulomatous disease (e.g., sarcoid) Malignancy Acute viral infection Immunosuppressive medication (corticosteroids, cyclophosphamide, cyclosporine)

Pregnancy

Malnutrition

Aging

CD4 Counts at which Opportunistic Infections Occur

< 200/mm3


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Moderate Risk Category (endocarditis prophylaxis recommended)

Acquired valvular dysfunction Hypertrophic cardiomyopathy

Mitral valve prolapse with valvular regurgitation and/or thickened leaflets

Negligible Risk Category (endocarditis prophylaxis NOT recommended)

Previous coronary bypass surgery (CABG) Mitral valve prolapse withoutregurgitation Physiologic, functional or innocent heart murmurs Previous rheumatic fever w/o valvar dysfunction Cardiac pacemakers and implanted defibrillators

Endocarditis prophylaxis regimen for patients undergoing lower extremity surgery

Based on AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations

bythe American Heart Association. JAMA 1997;277:1794-801.

Oral

No Penicillin allergy

Cephalexin 2g PO 1 hour before surgery

Penicillin allergy

Clindamycin 600mg PO 1 hour before surgery

Parenteral

No Penicillin allergy

Cefazolin 1g IV 30 minutes before surgery

Penicillin allergy

Clindamycin 600mg 30 minutes before surgery

C. difficile Colitis

Consider C. difficile colitis in any patient who develops diarrhea while on antibiotics.C. difficile colitis can also occur after antibiotics are stopped. Although it is most commonly associated withclindamycin, it can occur with most any antibiotic. Symptoms can range from mild diarrhea to crampy abdominal

pain, fever, leukocytosis and watery diarrheal stools > 4 /day.

Diagnosis is by C. difficile toxin titers (from stool sample). Definitive diagnosis is by colonoscopy (visualizingthe pseudomembranes on the bowel wall).

Treatment of C. difficile colitis:

Orally administered Metronidazole. Parenteral metronidazole can also be used if patients cannot use oral route Orally administered vancomycin (for patients fail metronidazole therapy) Vancomycin is poorly absorbed

from the gastrointestinal tract resulting in high intraluminal concentrations. Nephrotoxicity from orally

administered vancomycin can occur.

Tetanus

Symptoms of tetanus usually appear within of 3-21 days after inoculation but can occur between 1 day toseveral months

Localized tetanus- muscle spasm and rigidity begin local to the area of injury. May progress to generalized form Generalized tetanus- muscle spasm begins with masseter and spreads to affect entire body Clostridium tetani is an obligate anaerobe. Treat with metronidazole 500mg q6h or 1g q12h IV Diazepam can be used to control muscle spasms.



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Prevention of Tetanus

Categorize wound as being either low or high risk If wound is tetanus prone, begin prophylaxis

Clean (Low Risk)

Clean incised wound Superficial graze

Scald

Tetanus Prone (High Risk)

Wounds neglected > 24 hours Any wound with one or more of the following:

Contact with soil, manure, compost Open fracture Puncture type wound Large amount of devitalized tissue Gunshot wound Animal or human bite Infected wound Foreign bodies

*TIG-tetanus immune globulin.Unless more than 10 years since last dose.Unless more than 5 years since last dose.

Note: Tetanus immune globulin and Td may be given simultaneously but in different sites. Substitute DTP orDTaP vaccine for children under 7 years of age.

New York State Dept. of HealthImmunization Guidelines for Health Care Providers 2001


History of tetanus Immunization (doses) Clean, minor wounds

Td (Adult) TIG*All other woundsTd (Adult) TIG

Uncertain or


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References

1. Antrum R, Solomkin J. A review of Antibiotic Prophylaxis For Open Fractures. Orthop review. 16: 246-254,1987.

2. AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterialendocarditis (Recommendations by The American Heart Association.) JAMA

1997; 277:1794-801.

2. Gilbert D, Moellering R, Sande M. The Sandford Guide to Antimicrobial Therapy. Antimicrobial Therapy

Inc. pub.30th edition. 2000

3. Armstrong D, Cohen J. Infectious Diseases, eds. Mosby ed. 1999.

4. Joseph W, Kosinski M.Prophylaxis in Lower Extremity Infectious Diseases.Clinics in Podiatric Medicine and Surgery, Vol 13, No 4. October 1966.

5. Kosinski, MA, Lilja E. Infectious causes of heel pain.J Am Podiatr Med Assoc.January; 89(1): 20-3. 1999.

6. Kosinski M, Rodriguez A. Bone and Joint Manifestations of Systemic Infectious Diseases. Clinics inPodiatric Medicine and Surgery, Vol 1,5 No 4. October 1996.

7. Mader J, Ortiz M, Calhoun J. Update on the Diagnosis and Management of Osteomyelitis.Clinics in Podiatric Medicine and Surgery, Vol 13, No 4. October 1996.

8. Med Lett Drugs Ther 1994 Nov 25;36(936):110

9. Saxon A, Adelman DC. Imipenem cross-reactivity with penicillin in humans.

J Allergy Clin Immunol. 1988. Aug; 82(2): 213-7.



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chapter 4d podiatric infectious diseases

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