WOUNDS AND INFECTION
| WOUND CARE UPDATE —Loren Crown, MD, Clinical Professor, Family and Emergency Medicine, University of Tennessee
Health Science Center College of Medicine, Memphis, TN
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| History: most important part of practice of medicine (90% of information obtained before touching patient); no “magic
window” in wound care; the longer wound open, the more skin bacteria migrate into wound; in emergency medicine, all
wounds contaminated; in chart—important to mention circumstances of injury and position of part at time of injury; also,
location of wound (pictogram), length, depth, and neurovascular tenderness (NVT; note whether normal or not); note
whether bone intact or foreign body present (must anesthetize wound and go to depth to determine presence of foreign
body)
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| General management: speaker prefers having patient lying on stretcher and having setup on side of dominant hand
when repairing wound; speaker makes sure children restrained when wound stitched; not all wounds need to be closed
immediately; closure of wound least important step; lidocaine—be careful not to administer overdose; 30 mL, ie, 300
mg, fatal dose for adult); put needle into wound, not into normal skin; inject slowly into subcutaneous tissue by increments;
tips—if patient has several cuts, close stepwise; not necessary to use sterile saline to clean wound (tap water acceptable);
do not use pure iodine, mercurochrome, or alcohol in wound; povidone iodine (Betadine)—made for intact
skin (do not put into wound); cytotoxic; dilute before use
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| Wound closure: debridement—remove devitalized tissue and irrigate; in puncture wound, pick up one corner of punctured
area and make slit with hemostat or scissors and lift back corner to remove any foreign body present; sutures—
speaker uses 4-0 nylon on FS-1 needle; problem with using too big or too little sutures is tying knot in tight corner; nylon
better for skin; silk not too good, except for mouths; nylon not good for tongue (patients play with knot and knot unties);
avoid layered closures on mouth; with needle size, bigger better as long as able to make it through tissue (pressure applied
by suture must hold wound together over largest area possible); better to avoid “railroad tracks” on skin (not from
too big size of stitch or needle); small stitch with small needle has bigger potential to leave track (crushed tissue underneath
stitch); too long or too tight sutures cause tracks; for good appearance of wound, make sure no pressure necrosis,
close all layers, and remove suture in 5 days; wound eversion—goal; have edge of wound slightly puckered externally,
so that as wound goes through healing phases, eschar forms across that area; evert wound initially, so that as scar contracture
occurs over weeks to months, it will be even; instrument tie with 2 loops effective; to keep wound from spreading—
assume that both sides like reins of buggy (one side taut, other lax); take lax side and cross over, so that both ends of suture
on one side of laceration; while doing this, make small pull with far-side loop that turns knot sideways and keeps it
from sliding; ensure that all wound layers paired up by putting suture around everything; scars contract and pull wound
margin down into body; try to go deeper than wide, not wider than deep (which makes edges of wound dip in); vertical
mattress suture—provides wound eversion (less prominent scarring, better tension release, and no tracks when removed
properly); reason for less scarring more tissue within suture as suture tied (also avoids putting retained material under
surface ); takes 30 days for suture material to dissolve in dirty wound, and suture acts as retained foreign body; horizontal
mattress suture—turn vertical mattress suture sideways; good for patients in nursing home
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| Wound healing: acute inflammatory response present in first few days (not infection); in first phase, wound weak (has
only 5% of original tension capabilities), so necessary to reinforce; after 1 or 2 wk, fibroplasia begins, achieving ≈15%
original strength; even after several months, only 80% of original skin strength regained (scars not stronger than original
skin)
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| Wound infection: decreased—if on face or scalp; slice instead of crush; occurrence in clean environment; immune status
present; properly cleaned; closed well; dead space avoided; hair removed (with scissors; do not shave); foreign bodies
removed; avoid retained layered sutures if possible; increased—if on feet or hands; crushes and bites; waiting too long
to seek care; antibiotics—no benefit if used routinely; in selected high-risk cases, speaker gives one dose of oral cephalosporin
(cephalexin [Keflex] 1000 mg); dressings and ointment—protect wound from trauma, absorb fluid, and keep
wound lubricated; ointment keeps eschar pliable, making it easier to remove; tetanus prophylaxis—ask whether patient
had tetanus series and when last tetanus booster received; must give active and passive immunizations; probability of tetanus
infection increases with same factors that increase wound-infection probability; leaving foreign body inside wound
highest rate of causation; speaker gives analgesic before and after initial repair; speaker uses splints and advises patients
to elevate wound and apply ice for 20 min periodically (every 2 hr); glue—cannot be used on face, mucous membranes,
joints, and areas where skin moves; not effective in sweaty areas; sometimes necessary to apply several layers; wound
still must be anesthetized and examined
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| MANAGEMENT OF SKIN AND SOFT TISSUE INFECTIONS IN THE ERA OF RESISTANCE —Fredrick M. Abrahamian,
DO, Assistant Professor of Medicine, David Geffen School of Medicine at the University of California, Los Angeles,
and Director of Education, Department of Emergency Medicine, Olive View-UCLA Medical Center, Los Angeles, CA
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| Cellulitis: most common type of skin infection; terms “cellulitis” and “erysipelas” often used interchangeably;
differences—anatomically, cellulitis deeper infection; erysipelas superficial and involves more lymphatics (edema); typically
affects face, ear, and lower extremities (lymphedema); affected area clearly demarcated (not as clear in cellulitis);
as condition progresses, skin changes in erysipelas (develops vesicles and crusting); often mistaken for herpes zoster
(erysipelas does not follow dermatomal pattern); both most often caused by Streptococcus; if associated with trauma or
abscess, can have coinfection with Staphylococcus; clinically, difficult to determine in patients with cellulitis whether infectin
mixed or purely streptococcal (antibiotic choices should cover both); outpatient treatment—includes first-generation
cephalosporins (eg, cephalexin) and dicloxacillin (has bitter taste); for patients allergic to penicillin, macrolides
recommended as second agent; significant Group A resistance with erythromycin; macrolides second choice because of
significant streptococcal resistance (even advanced-generation macrolides); drawback of clindamycin coverage of anaerobes
(unnecessary most of time); inpatient therapy—intravenous (IV) formulation of first-generation cephalosporins,
nafcillin, and oxacillin; for patients with penicillin allergy, use broader-spectrum antibiotics
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| Methicillin-resistant S aureus (MRSA) and cellulitis: role of MRSA not clear (no studies); cover MRSA in severe
infections or purulent cellulitis; for outpatient therapy, good choice trimethoprim–sulfamethoxazole (TMP–SMZ;
eg, Bactrim) plus first-generation cephalosporin or dicloxacillin; TMP–SMZ alone does not cover Streptococcus (only
Staphylococcus); also can use clindamycin, vancomycin, or linezolid; duration of treatment 7 to 10 days; demarcate area
of cellulitis; end of progression of infection early sign of effective treatment; do not rely on color (as condition treated,
color becomes worse, ie, deeper red); study found that 5 days of treatment just as effective as 7 days for uncomplicated
cellulitis; distinction between complicated and noncomplicated not as clear in skin and soft tissue infections (SSTIs)
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| Complicated cellulitis: include mixed infections (multiple organisms) and those that require surgical intervention; simple
abscess that requires incision and drainage (I and D) not considered complicated; consider in patients with chronic cellulitis,
lower extremity involvement, perirectal abscesses or infections, diabetes, vascular insufficiency,
immunocompromised condition, and IV drug abuse (more likely to have mixed infections); treatment—if methicillin-susceptible
S aureus (MSSA) suspected, choices include second-generation cephalosporin with anaerobic activity (cefoxitin
only one); problem significant Bacillus fragilis resistance to cefoxitin; if B fragilis suspected in patient with intra-abdominal
wound, add metronidazole (eg, Flagyl); next choice β-lactamase inhibitors (eg, ampicillin and sulbactam [Unasyn]),
but ≈30% Escherichia coli resistance; carbapenems (impenem, meropenem, and ertapenem) effective; fluoroquinolones
(levofloxacin and moxifloxacin) indicated in complicated and uncomplicated infections; not all fluoroquinolones equal,
even though within same class; moxifloxacin has good anaerobic coverage; quinopristin and dalfopristin (Synercid)—act
together to inhibit protein synthesis in bacterial cell; indicated for MSSA SSTIs and vancomycin-resistant Enterococcus
bacteremia; does not have Food and Drug Administration (FDA) indication for treatment of MRSA but bactericidal for
MRSA; drawback drug must be given through central line (cannot be given through peripheral IV line) because drug irritating;
1-hr infusion time; no gram-negative coverage; drugs of choice for MRSA—include vancomycin, clindamycin, linezolid,
and daptomycin; in complicated infections, need broader coverage (coverage of gram-negative organisms, with or
without coverage of anaerobes); tigecycline has broad gram-positive, gram-negative, and anaerobic coverage but does not
cover Pseudomonas
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| Prevalence of MRSA: multicenter study in 2004 showed prevalence 59% in presence of purulent SSTIs (range 15%-
74%); higher rates at present; often suspected by patient to be “spider bite”; no clinical predictors for MRSA; absence of
risk factors does not mean absence of MRSA; no case report of USA300 MRSA strain resistant to TMP–SMZ; penicillin
and cephalosporins ineffective; study showed in 75% of cases, patient prescribed wrong antibiotic for MRSA; I and D
treatment of choice; drugs have variable susceptibility pattern (know pattern in local hospital); erythromycin and fluoroquinolones
have low susceptibility patterns (should not be used to treat MRSA)
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| Clindamycin resistance: prevalence varies by region; increasing reports of resistance; phenomenon of inducible
resistance—organism susceptible before therapy but becomes resistant after therapy due to activation of gene; clinical
relevance unclear; potential cause of treatment failure; D test determines whether bacteria possesses gene
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| Abscess management: I and D primary mode of therapy; needle aspiration not definitive technique; keep wound open
with packing; do not pack tightly; packing material must touch walls of abscess cavity, so removal of packing becomes
form of debridement; discontinue packing if wound clean, has no purulence, and walls of abscess cavity visible;
antibiotics—not required for simple uncomplicated cases, even with MRSA; indicated in presence of major surrounding
cellulitis, signs of systemic toxicity, facial abscess (midfacial abscesses drain into cavernous sinus and have higher risk
for septic thrombophlebitis), immunocompromise (recurrent abscesses), and large abscess (>5 cm); I and D not performed
properly most common reason patients fail with just I and D; duration 7 to 10 days; use ultrasonography (US) in
equivocal cases (unsure whether cellulitis or abscess); in patient who fails therapy for cellulitis, first thought should be
deep abscess, rather than antibiotic or resistance issue
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| Antimicrobial therapy: TMP–SMZ—1 to 2 double strength (DS) tablets bid (with 1 tablet, amount of drug in abscess
cavity barely reaches concentration required to kill 90% of organisms; 2 tablets recommended); with 2 DS tablets, complaints
of nausea and vomiting reported; combination of rifampin and TMP–SMZ—thought to have synergistic effect (no
data to support); should not be used routinely due to several drug-drug interactions of rifampin, and overall benefit of adding
rifampin small; clindamycin—no gram-negative coverage and variable susceptibility pattern; doxycycline or
minocycline—low susceptibility pattern; alternative in patient with limited choices; tetracyclines have high level of Group
A streptococcal resistance (should not be used); minocycline preferred over doxycycline (has more extensive history of use
in SSTIs); side effects of minocycline dizziness and vertigo, but typically not seen with short courses; vancomycin—given
IV; traditionally used for treatment against MRSA; problem emergence of resistance; has poor tissue penetration;
linezolid—has faster action than vancomycin; inhibits release of exotoxins (important in MRSA infections);
daptomycin—indicated in complicated SSTIs, bacteremia, and right-sided endocarditis; should not be used in suspected
MRSA pneumonia because of poor activity in pneumonia (binds surfactant); tigecycline—does not cover Pseudomonas;
studies of all drugs used for MRSA, specifically SSTIs, limited (<100 participants in all studies); potential future antimicrobial
therapies—include dalbavancin (1 g IV, with next dose 1 wk later), telavancin, and oritavancin; cover gram-positive
organisms (no gram-negative and anaerobic coverage); ceftobiprole is cephalosporin with anti-MRSA activity; also
has gram-positive and gram-negative activity but poor anaerobic coverage
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| Decolonization: not routinely done in emergency department; suspect colonization in patients with recurrent infections,
in whom everything possible was done to prevent recurrence; common site of colonization nasal area; current prevalence
of MRSA colonization in general population unknown (latest data from 2001-2002 show prevalence 0.8%); newer data
from Centers for Disease Control and Prevention (CDC) for 2002 to 2004 show prevalence ≈1.5%; decolonization should
not be performed routinely; demonstrate that patient colonized (through culture) before decolonizing; no specific studies
looking at eradication of community-associated (CA) MRSA (most for hospital-acquired MRSA); best regimen mupirocin
nasal ointment with chlorhexidine body wash
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| Prevention: case reports of transmission among family members, and strain of CA-MRSA replacing hospital-acquired
MRSA; patients with highly suspected MRSA infection, need to be admitted to isolation (CDC recommendation)
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| Animal bites and human bites: in human bites, β-lactamase-producing organisms comprise good portion of ones
causing infection; antibiotic regimen should cover these organisms; antibiotics—amoxicillin–clavulanic acid (Augmentin)
or ampicillin–sulbactam (Unasyn; IV formulation) fairly effective; cefoxitin previously fairly effective drug,
but no longer (does not cover B fragilis and Bacteroides, common in animal bites); carbapenems effective; azithromycin
alternative but not best because it does not cover anaerobes (consider for children and pregnant patients); with fluoroquinolones,
moxifloxacin best choice because of better anaerobic coverage; combination antibiotics—clindamycin
and ciprofloxacin or clindamycin and TMP–SMZ effective; avoid penicillin and cephalexin for human bites (does not
cover β-lactamase–producing anaerobes and Haemophilus influenzae); take-home points—in patient with purulent
SSTI or abscess, consider MRSA; absence of risk factors does not exclude MRSA; if deep abscess suspected, use US;
consider susceptibility patterns, especially if using clindamycin; if treating cellulitis or abscess with TMP–SMZ, must
combine with another agent that covers Group A Streptococcus (eg, dicloxacillin); absence of gas does not rule out necrotizing
fasciitis
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Suggested Reading
Awad SS et al: Increasing incidence of methicillin-resistan.Staphylococcus aureus skin and soft-tissue infections: reconsideration
of empiric antimicrobial therapy. Am J Surg 194:606, 2007; Broughton G 2nd et al: Wound healing: an
overview. Plast Reconstr Surg 117:1e, 2006; Brun-Buisson C et al: Isolation of patients with MRSA infection. Lancet
365:1303; author reply 1304, 2005; Chaby G et al: Dressings for acute and chronic wounds: a systematic review. Arch
Dermatol 143:1297, 2007; Chambers HF: Community-associated MRSA--resistance and virulence converge. N Engl J
Med 352:1485, 2005; Diehr S et al: Clinical inquiries. Do topical antibiotics improve wound healing? J Fam Pract
56:140, 2007; Dufel S et al: Simple cellulitis or a more serious infection? J Fam Pract 55:396, 2006; Eaton L: Hand
washing is more important than cleaner wards in controlling MRSA. BMJ 330:922, 2005; Frazee BW et al: High prevalence
of methicillin-resistant Staphylococcus aureus in emergency department skin and soft tissue infections. Ann Emerg
Med 45:311, 2005; Grey JE et al: Wound assessment. BMJ 332:285, 2006; Hawkes M et al: Community-associated
MRSA: superbug at our doorstep. CMAJ 176:54, 2007; Headley AJ: Necrotizing soft tissue infections: a primary care review.
Am Fam Physician 68:323, 2003; Hepburn MJ et al: Comparison of short-course (5 days) and standard (10 days)
treatment for uncomplicated cellulitis. Arch Intern Med 164:1669, 2004; Jose RM et al: Mammalian bite wounds: is primary
repair safe? Plast Reconstr Surg 119:1967, 2007; Mills AM et al: Are blood cultures necessary in adults with cellulitis?
Ann Emerg Med 45:548, 2005; Moran GJ et al: Methicillin-resistant S. aureus infections among patients in the
emergency department. N Engl J Med 355:666, 2006; Schmidt AH: Are single-dose preoperative antibiotic regimens really
appropriate? Arch Surg 142:576, 2007; Sharpe JN et al: Clinical and economic outcomes of oral linezolid versus
intravenous vancomycin in the treatment of MRSA-complicated, lower-extremity skin and soft-tissue infections caused by
methicillin-resistant Staphylococcus aureus. Am J Surg 189:425, 2005; Ueeck BA: Penetrating injuries to the face: delayed
versus primary treatment--considerations for delayed treatment. J Oral Maxillofac Surg 65:1209, 2007; Weir E et
al: Invasive group A streptococcal infections. CMAJ 175:32, 2006.
Educational Objectives
| The goal of this program is to improve wound care and management of skin and soft tissue infections. After hearing and assimilating
this program, the clinician will be better able to:
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 | 1. Summarize the principles of wound care.
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| 2. Utilize appropriate techniques for wound closure.
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| 3. Distinguish between cellulitis and erysipelas.
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| 4. Prescribe appropriate antibiotic therapy for skin and soft tissue infections.
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| 5. Recognize colonization with methicillin-resistant Staphylococcus aureus.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires the planning committee and all faculty
members to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of
interest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and
not a proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Abrahamian is on
the Advisory Board of Schering-Plough and Ortho-McNeill, Inc. and is on the Speakers’ Bureau of Schering-Plough. The
planning committee reported nothing to disclose.
Acknowledgements
Dr. Crown was recorded at Symposium on Critical Care and Emergency Medicine, held March 29-31, 2007, in Hot Springs,
AR, and sponsored by the University of Arkansas for Medical Sciences College of Medicine and the University of Tennessee
Health Sciences Center College of Medicine. Dr. Abrahamian was recorded at the 20th Annual Advances in Emergency
Medicine and Primary Care, held April 18-20, 2007, in Las Vegas, NV, and sponsored by the Olive View-UCLA Department
of Emergency Medicine and the American College of Emergency Physicians, State Chapter of California, Inc. The Audio-Digest
Foundation thanks the speakers and the sponsors for their cooperation in the production of this program.
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