Lower Extremity Infections
Mark A. Kosinski
Warren S. Joseph
Infections of the lower extremity, especially postoperative ones, account for a disproportionate amount of patient morbidity and medicolegal actions against podiatric surgeons. It is a complex and ever-changing topic. It seems that almost monthly a new study is published that introduces a new antibiotic with activity against skin or skin structure infections or challenges a previously sacrosanct tenet of practice. For example, the widely held notion that “probing to bone” diagnoses osteomyelitis, a concept that is less than 15 years old, has now been shown to be less than fully reliable. The long-held belief that osteomyelitis must be treated with a minimum of 6 weeks of intravenous therapy is now being shown to be incorrect. New classifications of old infections are being introduced. This is far from a static area of practice. This is what makes it challenging to write a chapter on infectious diseases. When written, the information below was as up to date as humanly possible. Unfortunately, by the time a finished book makes it into the hands of the reader, much may have changed. To this end, the authors of this section urge the reader to keep abreast of what is happening to change current medical evidence not only in the field of foot and ankle surgery but also in the infectious diseases literature. Peruse a copy of Clinical Infectious Diseases in the hospital’s library. Regularly check the website of the Infectious Diseases Society of America (IDSA) (www.idsociety.org) where evidence-based clinical practice guideline for any imaginable human infection can be downloaded free of charge. The combination of the material in this chapter and new treatments and concepts that arise in the literature published subsequent to this book should then benefit the readers and, more importantly, their patients.
DIAGNOSIS
ASSESSMENT
Since your empiric antibiotic choice is governed largely by the organisms you expect to find in a given situation (Table 85.1), treatment of infection begins with a thorough history and review of systems. Careful documentation is important not only from a treatment standpoint but from a medicolegal standpoint as well. It may be helpful to include the following questions when assessing a patient with infection:
History of chief complaint
When did the infection begin? Where and how was it acquired? Distinguish between community and nosocomial (hospital-acquired) infections. In cases of surgical wound infection, how long after the procedure did the first signs develop?
Past treatment
What previous treatment, if any, has the patient received? Has the patient been taking antibiotics prescribed for this or another condition?
Drug allergies/sensitivities
Does the patient 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
Include diabetes, human immunodeficiency virus (HIV), tuberculosis, sexually transmitted diseases, sickle cell anemia, renal or hepatic disease, and risk factors for infective endocarditis (IE).
Medications
Is the patient currently receiving antibiotic therapy or taking any medication that could affect immune response, mask the signs of infection, or delay healing (e.g., corticosteroids, cyclosporine, etanercept)?
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 him or her at risk for methicillinresistant Staphylococcus aureus (MRSA), or has he or she had a previous MRSA infection?
Social history
Ask about travel, occupation, and pets.
PHYSICAL EXAMINATION
Assess vital signs, including oral temperature, blood pressure, pulse, and respiration when appropriate.
In the case of open wounds or ulcers, note and document diameter, depth, and extent. Note the presence or absence of sinus tracts and undermining as well as the color, consistency, and quantity of any exudate (Table 85.2). Serous drainage from an open wound may be an entirely benign finding, whereas the presence of frank purulence is highly suggestive, although not necessarily diagnostic, of an infectious process.
Note and document the presence and extent of cellulitis, lymphangitis (streaking), and regional lymphadenopathy (both inguinal and popliteal). Palpate both inguinal and popliteal lymph nodes. Popliteal nodes are often more difficult to detect.
Examine the entire foot. Check for pain and fullness of the plantar arch that may signal plantar space involvement. Interspace infections may extend to the bursa of the lumbrical tendons, spread to the lumbrical muscles, and advance into the central plantar compartment. Likewise, infection of the plantar aspect of the toes may spread along the flexor tendon sheath into the central plantar compartment. Infection of the deep plantar compartments can extend along flexor tendon sheaths and involve the lower leg (1).
TABLE 85.1 Patient Factors and Environmental Influences as Clues to the Infecting Organism | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Consult other medical services (e.g., infectious diseases, internal medicine, vascular surgery) as needed.
LABORATORY TESTING
The question often arises as to what tests are appropriate for evaluating a patient with a lower extremity infection. Depending on the severity, diagnostic tests should include complete blood count (CBC) and differential, blood glucose, renal and hepatic function tests, and cultures of wound, bone, and blood. If indicated, order x-rays to rule out bone involvement and the presence of soft tissue gas.
CBC and Differential
Acute infection is characterized by an elevated white blood cell (WBC) count (absolute leukocytosis) and a shift to the left (increased number of immature or “band” cells), although it should be noted that this may not be found in a localized lower extremity infection. An increased number of band cells is often referred to as “bandemia.” An elevated number of eosinophils (eosinophilia) is suggestive of allergy.
Renal and Hepatic Function Tests and Dose Adjustments
Virtually any antibiotic, oral or parenteral, can be used for any patient regardless of their renal function; however, the antibiotic may need to be dose adjusted. A particularly useful internet resource for renal dosing can be found at www.globalrph.com.
TABLE 85.2 Odor, Color, and Appearance as Clues to the Infecting Organism | ||||||||||||||||||||||||||||||||||||||||||||||||||
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TABLE 85.3 Estimating Creatinine Clearance Using Serum Creatinine: The Equation of Cockroft and Gault | |||
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Some antibiotics do not need dose adjustment. They include ceftriaxone, clindamycin, azithromycin, linezolid, minocycline, nafcillin, and dicloxacillin. These can be given to renally impaired patients at their usual dose (2).
For antibiotics that require adjustment, renal function tests are needed. The two most easily obtainable renal function tests are blood urea nitrogen (BUN) and serum creatinine. Both can be obtained from routine blood chemistry. Since BUN is largely dependent on the hydration status of the patient, it is of limited use for determining dose adjustment.
Using the patient’s serum creatinine, one can derive the creatinine clearance by using the equation of Cockroft and Gault (Table 85.3).
Once a value for creatinine clearance is obtained, it is a simple matter to determine the appropriate antibiotic dose using the information contained in the manufacturer’s package insert.
When using serum creatinine to determine creatinine clearance, it should be remembered that serum creatinine may not accurately reflect the patient’s renal function in the elderly who may have decreased creatinine production. In these patients, creatinine clearance may be a more accurate measure. Creatinine clearance in these cases requires a 24-hour urine collection.
It is actually easier to adjust the dose for dialysis patients since standard dose adjustments exist. It is important to remember that not all antibiotics are removed during dialysis. Factors influencing dialyzability include type of dialysis membrane, blood flow rate, dialysate flow rate, and ultrafiltration rate. Drug-related factors include molecular weight, protein binding, and water solubility. Table 85.4 lists renal dose adjustment for some commonly prescribed antibiotics. As a general rule of thumb, antibiotics should be dosed after, rather than before, a dialysis treatment.
Hepatic function tests can also influence antibiotic choice. Antibiotics that are known to be dependent on the liver for metabolism or excretion should be used with caution in patients with a history of liver disease. These drugs include erythromycin, clindamycin, tetracycline, and trimethoprim/sulfamethoxazole (TMP/SMX).
Erythrocyte Sedimentation Rate and C-Reactive Protein
Erythrocyte sedimentation rate (ESR) and C-reactive protein are both nonspecific indicators of inflammation. Although elevated in any inflammatory process, a patient with a nonhealing foot ulcer and significantly elevated ESR values (>70) may arouse suspicion for underlying osteomyelitis (3,4). A downward trend can be useful as a measure of therapeutic success.
TABLE 85.4 Renal Dosing for Commonly Prescribed Antibiotics | |||||||||||||||||||||||||||||
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WOUND, BONE, AND BLOOD CULTURES
A properly taken wound culture forms a solid basis for directed therapy. Cultures, whether wound, bone, or blood, should be taken before antibiotics are started whenever practical. Order aerobic, anaerobic, acid-fast, and fungal cultures when clinically indicated. Use proper transport media with respect to the organism being cultured and transport the specimen expeditiously. When in doubt, contact the lab.
Results of cultures can take days (bacterial) to weeks (fungal and mycobacterial) to return. Ordering the appropriate stain can provide a clue to the infecting organism in the interim. Gram stain can be ordered for bacteria, potassium hydroxide wet mount and periodic acid-Schiff stains for fungi, acid-fast stains for mycobacteria, and Tzanck stains for virus.
Gram stains can be done in a matter of minutes and provide important information as to the organisms present. The Gram stain can also help differentiate colonization or contamination from true infection by looking for evidence of WBCs. Gram stain terminology relates to the appearance of the organism. Staphylococcus from the Greek literally means “cluster of berries”; streptococcus means “twisted chain of berries.” Grampositive cocci in grape-like clusters imply Staphylococcus species, whereas gram-positive cocci in chains imply streptococci.
Preliminary reports may note a particular strain of Staphylococcus as being coagulase positive or coagulase negative. Coagulase positive generally implies the more invasive S. aureus, whereas coagulase negative implies the less invasive Staphylococcus epidermidis.
Principles of Wound Cultures
Infection must be differentiated clinically from colonization and contamination. Contamination can be defined as the presence of bacteria without multiplication, colonization as the presence of bacteria with multiplication, and infection as the presence of bacteria with both multiplication and a host response. Clinically, there are five cardinal signs of infection: rubor (redness), calor (heat), dolor (pain), tumor (swelling), and functio laesa (loss
of function). Patients with infection may exhibit all or some of these signs. Not all patients who present with these signs are infected. Other inflammatory conditions (i.e., gout) may mimic some or all of the classic signs of infection Only wounds that appear clinically infected need be cultured.
of function). Patients with infection may exhibit all or some of these signs. Not all patients who present with these signs are infected. Other inflammatory conditions (i.e., gout) may mimic some or all of the classic signs of infection Only wounds that appear clinically infected need be cultured.
Before taking a culture, the wound should be thoroughly prepared to remove surface bacteria. This can be achieved by using an antibacterial scrub followed by lavage with nonbacteriostatic sterile saline or sterile water. Local débridement is also useful in removing these contaminants. Sacrifice drainage at the opening of the wound in favor of deeper culture material. If possible, include a piece of infected tissue. Infected tissue is actually preferable over pus, since pus contains mostly WBCs and phagocytized bacteria. Avoid contact with surrounding skin. Avoid superficial swab cultures.
Principles of Bone Cultures
The microbiology of soft tissue and bone can be very different. With the possible exception of S. aureus, sinus tract cultures are rarely helpful in establishing the causative organism in osteomyelitis. The best odds for diagnosis and successful treatment of osteomyelitis rest with the isolation of the organism from bone. In a study of oral therapy for diabetic foot osteomyelitis by Senneville, 81% versus 50% of diabetic patients with and without bone culture-directed antibiotic therapy were cured at the end of follow-up (5).
Bone biopsy is a safe procedure rarely associated with complications. Ideally, approach bone through uninfected tissue. Because osteomyelitis can be a focal disease, two or three specimens may be needed. Specimens should be sent for microscopic diagnosis as well as culture and sensitivity. Culture bone for aerobic and anaerobic bacteria. Acid-fast and fungal organisms should be sought, especially in refractory or chronic cases. Bone can also be sent for acid-fast and fungal and Gram stains.
Principles of Blood Cultures
Patients who are febrile or systemically ill should have blood cultures drawn. One useful protocol is to draw two sets 15 minutes apart (15 minutes is an arbitrary period of time used to force each set to be taken from a different site). A “set” is defined as one aerobic and one anaerobic bottle. If an organism grows from only one set, then suspect contamination. Drawing blood cultures on a fever spike may be of benefit. Like bone, soft tissue, and pus, blood can be Gram stained.
CHOOSING AN APPROPRIATE ANTIBIOTIC
Antibiotic therapy is based on five simple rules:
Your empiric antibiotic choice should be governed by the organisms you expect to find in a given situation.
Noninfected wounds do not need to be cultured.
Use an antibiotic with proven efficacy against the suspected or known organism(s).
Change or continue antibiotics based on culture results and clinical response as soon as possible. Avoid prolonged empiric therapy.
When sensitivities are known, choose the narrowest spectrum agent with the highest efficacy, the lowest toxicity, and the lowest cost.
Far and away, the most common organism encountered in lower extremity bone and soft tissue infections is S. aureus. Today, virtually all strains of S. aureus found in lower extremity infections produce beta-lactamase. Beta-lactamase (also known as penicillinase) is an enzyme that cleaves the beta-lactam ring and inactivates the antibiotic. Since greater than 90% of S. aureus found in skin and bone infections of the lower extremities produce beta-lactamase, empiric therapy of suspected staphylococcal infections should always include a beta-lactamase-stable antibiotic. For this reason, it is useful to categorize antibiotics as being either beta-lactamase stable or beta-lactamase susceptible.
Drugs such as amoxicillin and ampicillin are beta-lactamase susceptible and as such should not be relied upon to treat lower extremity staphylococcus infections.
To overcome bacterial resistance, some drugs combine a beta-lactam antibiotic and a beta-lactamase inhibitor, thus creating a stable, new compound effective against staphylococcus, such as amoxicillin/clavulanate, ampicillin/sulbactam, piperacillin/tazobactam, and ticarcillin/clavulanate. Addition of the beta-lactamase inhibitor also extends the drug’s spectrum to include Bacteroides fragilis, thus making them attractive choices when anaerobic bacteria are an issue.
Nafcillin, oxacillin, dicloxacillin, and methicillin are all betalactamase stable, as are the cephalosporins and carbapenems. Historically, methicillin was one of the first drugs developed to combat the growing number of beta-lactamase-producing S. aureus infections. Today, it is really of historic importance only and is not clinically used.
Other antibiotics are beta-lactamase stable by virtue of the fact that they do not contain a beta-lactam ring. Although they have varying degrees of activity against S. aureus, they are often called upon for use in patients with a history of a penicillin allergy.
METHICILLIN-RESISTANT S. AUREUS AND THE PROBLEM OF MULTIDRUG-RESISTANT ORGANISMS
Shortly after the introduction of methicillin, strains of S. aureus resistant to the drug (MRSA) began to emerge. Currently, rates of nosocomial MRSA are greater than 60% in many ICUs. Rates of MRSA in the community have likewise been increasing.
In early reports, community isolates of MRSA had largely affected persons with known risk factors for colonization. These risk factors included patients who have been in acute or longterm care facilities, individuals who have recently undergone antibiotic therapy, and those in proximity to patients infected or colonized with MRSA. This picture has changed dramatically over the last several years.
MRSA is now being seen in patients without any of the above risk factors.
Methicillin resistance is associated with the presence of penicillin-binding protein 2a (PBP2a). Encoded by the mec a gene, PBP2a has low binding affinity for beta-lactam antibiotics. By definition, therefore, MRSA is resistant to all currently available beta-lactam antibiotics.
Over the years, oxacillin has replaced methicillin on culture and sensitivity reports as the antibiotic to which one looks to identify MRSA. Oxacillin is a more stable drug and is more resistant to degradation in storage and causes fewer adverse events. Oxacillin is also more likely to detect heteroresistant strains. Methicillin has therefore fallen out of use and is no
longer commercially available in the United States. The acronym MRSA is still used to describe these isolates because of its historic role.
longer commercially available in the United States. The acronym MRSA is still used to describe these isolates because of its historic role.
Oxacillin resistance therefore implies methicillin resistance. With the exception of ceftaroline, a newly available “fifth-generation” cephalosporin, MRSA is resistant to all currently available antibiotics that contain a beta-lactam group.
One can differentiate two major types of methicillin resistance in staphylococci: community associated (CA-MRSA) and health care associated (HA-MRSA). These are two genetically distinct organisms with the CA strains containing the SCC mec IV type gene not found in HA strains. Furthermore, a virulence factor known as Panton-Valentine leukocidin (PVL) is more commonly found in CA strains and is sometimes used to differentiate the two types of MRSA. There are tests for the SCC mec IV gene, to look for PVLs, and to speciate the USA300 strain, the most common genotype of CA-MRSA. None are currently widely used in the clinical setting.
Because the mec IV gene is a “short-segment gene,” it has little space for many resistance factors. This makes CA-MRSA susceptible to a greater range of antibiotics. CA-MRSA is susceptible to non-beta-lactam antibiotics including TMP/SMX, minocycline, doxycycline, or clindamycin. HA-MRSA tends to exhibit multidrug resistance. HA-MRSA is resistant to TMP/SMX, minocycline, doxycycline, and clindamycin. It is susceptible only to drugs such as vancomycin, quinupristin/dalfopristin, daptomycin, tigecycline, ceftaroline, and linezolid.
In rare instances, some strains of S. aureus hyperproduce beta-lactamase, thereby exhibiting a sensitivity pattern similar to MRSA. Beta-lactam/beta-lactamase inhibitor compounds such as amoxicillin/clavulanate may show activity against these isolates.
There appears to be a hierarchy of virulence when dealing with staphylococcal infections. Of the MRSA, the CA strains are more virulent than the HA strains. The reason for the increased virulence of the CA strains may be linked to the production of various virulence factors not produced by HA strains. The aforementioned PVL may be an important virulence factor in some systemic bloodstream infections and in necrotizing pneumonias, but its role as a virulence factor in skin and skin structure infections has been questioned. Recently, new work suggests that CA-MRSA is capable of producing cytolytic peptides known as phenol-soluble modulins that actually “burst” WBCs, thereby rendering them unable to fight infection (6).
Table 85.5 lists commonly prescribed antibiotics and their activity against S. aureus including MRSA and anaerobes.
INDUCIBLE CLINDAMYCIN RESISTANCE
During laboratory testing, some strains of S. aureus appear to be resistant to erythromycin and susceptible to clindamycin; however, once the patient is exposed to clindamycin, they quickly develop resistance. Bacterial strains that possess the erm gene prevent erythromycin and clindamycin from binding to their target site. Clindamycin is a slow inducer of the erm gene compared with erythromycin and therefore may appear sensitive on lab testing, but when used clinically, the patient may fail to respond. Since the vast majority of MRSA is resistant to erythromycin, clindamycin may have limited utility. That being said, clindamycin, by its relatively unique mechanism of action as a protein synthesis inhibitor, may lessen the morbidity of the infection by inhibiting protein-based virulence factors produced by some strains of S. aureus including CA-MRSA.
TABLE 85.5 Commonly Prescribed Antibiotics and Their Activity against S. aureus and Anaerobes | ||||||||||||||||||||||||||||||||||||||||||||||
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Inducible clindamycin resistance (ICR) can be tested for in the lab by use of the D test. The D test is a double disc diffusion test whereby an erythromycin disc placed 15 mm away from clindamycin disc on agar plate. If S. aureus possesses ICR, there will be a flattening of the zone of inhibition around the clindamycin disc resembling the letter D. Some labs routinely perform the D test before reporting C&S results, other labs do so only on request by the clinician. As a rule of thumb, use clindamycin with caution if erythromycin resistance is present.
Since a similar phenomenon has been described with quinupristin/dalfopristin (dalfopristin is a type A streptogramin and quinupristin is a type B streptogramin), ICR is also referred to as MLSb resistance (macrolide, lincosamide, streptogramin b resistance).
EXTENDED-SPECTRUM BETA-LACTAMASE
The other multidrug-resistant organism with an increasing incidence is extended-spectrum beta-lactamase (ESBL)-producing gram-negative bacilli (including Klebsiella, Escherichia coli, Proteus, and Pseudomonas aeruginosa). ESBLs are named for their ability to hydrolyze the extended-spectrum cephalosporins. If ESBL is detected, all penicillins, cephalosporins, and aztreonam should be reported as resistant. This increase in ESBL-producing
strains jeopardizes the usefulness of beta-lactam agents, leading to increases in hospital costs, longer hospital stays, and greater treatment failures. Treatment options are limited and usually include only the carbapenems or tigecycline.
strains jeopardizes the usefulness of beta-lactam agents, leading to increases in hospital costs, longer hospital stays, and greater treatment failures. Treatment options are limited and usually include only the carbapenems or tigecycline.
TABLE 85.6 Chemical Structures of 7-Position Side Chains of Penicillins and Cephalosporins | |||||||||||||||||||||||||||||||||||||||
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PENICILLIN ALLERGY AND CEPHALOSPORINS
The cross-reactivity between penicillin and cephalosporins is often a concern, especially if patient has a history of anaphylaxis. Package inserts suggest a 10% cross-reactivity between penicillins and cephalosporins. It was once thought that the beta-lactam ring shared by penicillins and cephalosporins was proof enough of cross sensitivity. In reality, this high number was probably due to the fact that until 1982, penicillin compounds were produced using Cephalosporium mold, thereby contaminating the penicillin with cephalosporin. In addition, although both penicillin and cephalosporins do indeed possess a beta-lactam ring, both drugs act quite differently after metabolism. Penicillins form a stable ring, while cephalosporins undergo rapid fragmentation during metabolism (7).
Primary cephalosporin allergy is actually quite low and has been estimated to be between 1% and 3%. These numbers refer to an allergy to the cephalosporin itself and not to penicillin cross-reactivity. Even when primary allergy to a cephalosporin does occur, anaphylaxis is extremely rare and is estimated to be between 0.0001% and 0.1% (7).
There are data to suggest that the rate of cross-reactivity between cephalosporins and penicillins is low or even nonexistent and is dependent on the similarity of the side chain of the cephalosporin (independent of the generation) relative to that of the penicillin.
A recent body of work published by Pichichero (8,9 and 10) categorizes penicillins and cephalosporins based on the similarity of the side chains at the 3 and 7 position. Using Tables 85.6 and 85.7, one can predict the probability of cross-reactivity.
For example, a patient who reports an allergy to penicillin G could safely be given cephalexin since both drugs are dissimilar at both the 3- and 7-position side chains. An allergic reaction to cephalexin would be coincidental and would represent a primary allergy to the cephalosporin, not cross sensitivity. On the other hand, if the patient reported an allergy to amoxicillin, cephalexin should be avoided since cephalexin and amoxicillin are similar at the 7-position side chain and the chance for cross-reactivity would exist. Antibiotics that do not contain a beta-lactam ring do not show cross-reactivity to patients allergic to penicillins.
TABLE 85.7 Chemical Structures of 3-Position Side Chains of Penicillins and Cephalosporins | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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WHEN TO HOSPITALIZE
The face of infectious diseases is constantly changing due in large part to the availability of new drugs. Parenteral antibiotics with long half-lives may obviate the need for extended hospital stays in favor of home intravenous therapy. Indeed, even infections that once required parenteral antibiotics can now be treated effectively with highly bioavailable oral agents. The days when a patient is admitted to the hospital “for IV antibiotics” may be coming to an end.
Although mitigated by the severity of the infection and clinical judgment, the decision to hospitalize may be prudent under the following circumstances: sepsis, or “systemic inflammatory response syndrome,” patient noncompliance, fever, leukocytosis, uncontrolled blood glucose, peripheral vascular disease, and the necessity for aggressive incision, drainage, and débridement.
One of the most important orders may well be for the patient to remain NPO if there is any possibility that emergency surgery is in the offing. Once the patient is stable medically, is afebrile, and the infection is under control, the decision to discharge and treat as an outpatient can be entertained.
DIABETIC FOOT INFECTIONS
The IDSA Practice Guidelines for the Diagnosis and Treatment of Diabetic Foot Infections has been validated as a useful tool for grading foot infections (11). This system is particularly useful for predicting what organisms one can expect to find in a given situation, allowing one to institute appropriate empirical treatment. Under these guidelines, diabetic wound infections are classified as being mild, moderate, or severe (12). Table 85.8 lists antibiotics that are useful for treating these infections based on category.
CLEAN AND NONINFECTED ULCERATIONS
Noninfected wounds do not require antibiotic therapy. Routine culturing of these lesions should be avoided since even noninfected ulcerations are colonized, usually with multiple organisms. The use of “precautionary” antibiotics to prevent infection is not supported by currently available medical evidence and may lead to the development of resistant organisms, which may make subsequent infections more difficult to treat.
Clinical signs and symptoms of infection, such as erythema, edema, and heat, are absent. Because infection is primarily diagnosed by the clinical evidence of these signs of inflammation, their absence precludes the diagnosis. A common misconception is that patients with diabetes do not respond with cellulitis. Although there may be an altered response that mutes some of the symptoms, it is extremely unlikely that there would be no evidence of cellulitis at all; therefore, cellulitis is a reliable indicator of infection in all but the most arterially compromised patients.
MILD INFECTION
Ulcers with a mild infection show at least two of the signs and symptoms of a host response. There is usually localized cellulitis around the wound that, by definition, extends less than 2 cm from the periphery of the ulcer. Pus may be present and, by itself, is indicative of infection in these cases; however, the infection remains localized with no proximal spread.
TABLE 85.8 Antibiotics for Diabetic Foot Infections | ||||||||||||||||||||||||||||||||||||||||||||||||||
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