TRAUMATIC INFECTIONS
From the 36th Annual Phoenix Surgical Symposium, sponsored by Banner Health and The Phoenix Surgical Society
Educational Objectives
| The goal of this program is to improve the management of surgical wound infections and necrotizing soft-tissue infections.
After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Recognize risk factors for surgical wound infections.
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| 2. Apply current management practices for surgical wound infections.
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| 3. Diagnose necrotizing soft-tissue infections based on risk factors, examination findings, and laboratory results.
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| 4. Prescribe appropriate antibiotic therapy for necrotizing soft-tissue infections.
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| 5. Diagnose and treat soft-tissue infections caused by community-acquired methicillin-resistant Staphylococcus
aureus and clostridia.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the
planning committee 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 faculty and planning
committee reported nothing to disclose.
Acknowledgments
Drs. Billingham and Jurkovich were recorded at the 36th Annual Phoenix Surgical Symposium, held February 13-16,
2008, in Phoenix, AZ, and sponsored by Banner Health and the Phoenix Surgical Society. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
| PREVENTION AND MANAGEMENT OF SURGICAL WOUND INFECTIONS —Richard P. Billingham, MD, Clinical
Professor, Department of Surgery, University of Washington School of Medicine, Seattle
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| Epidemiology: postoperative wound infections—occur in 44% of ≈23 million patients who have surgery each year; in
“clean” cases, rate 3% (4% in clean contaminated cases, eg, gastrointestinal [GI] surgery); rate 9% in grossly contaminated
cases; represent ≈14% of all adverse events occurring in hospitals; direct cost $1.5 billion; wide discrepancy in reported
incidence of incisional surgical site infections (SSIs) after colorectal surgery; no clear consensus of risk factors;
adverse events after surgical procedures most frequently drug-related; among surgical complications, wound infections
highest in frequency (13%-15%)
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| Risk factors for wound infections: longer operations; malignant disease; older patients; obesity; smoking; impaired
host defenses; hypoalbuminemia; steroid therapy; diabetes; poor preoperative bowel preparation; bacterial contamination
of surgical wound
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| Major pathogens in SSIs: Staphylococcus aureus number one (accounts for 20%); 15% from coagulase-negative staphylococci;
35% of SSIs not GI flora; study by Foley (2002)—found rate of SSIs 26%; ≈50% detected after patient left
hospital; median time for diagnosis, 9 days; 10% detected after 30 days; risk factors include increasing body mass index
(BMI) and intraoperative hypotension; other factors include length of operation, severity of patient’s illness, and American
Society of Anesthesiologists (ASA) score >2; no increase in length of stay if patient developed wound infection (patient
received home health care instead, which generated additional $6200 per patient); after 2004, study incorporated
Surgical Care Improvement Project (SCIP) guidelines and looked at additional 132 participants; 91% had antibiotics
given properly and stopped early; normothermia better controlled; incidence of SSIs still 16%
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| Summary of evidence-based literature: only one study (from Netherlands); 65 participants with acute and chronic
wounds; randomized to wound vacuum-assisted closure (VAC) or modern dressings (utilizing hydrocolloid, alginate, acetic
acid, and Dakin’s solution); found time to wound healing exactly same, except in diabetics (slightly better with wound
VAC) and those with significant cardiovascular disease; wound VAC did not result in faster granulation tissue and wound
surface reduction or better bacterial clearance; overall cost same
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| Wound healing: normal response to injury; 4 phases; hemostasis—bleeding generally stops in ≈3 hr; inflammation—
lasts for few days; proliferation phase—starts on day 3 and lasts for ≈3 wk; remodeling phase—lasts ≈1.5 yr; in hemostasis
and inflammation, vasodilatation, infiltration with appropriate cells, and phagocytosis; macrophages kill bacteria;
in proliferation phase, migration of fibroblasts, angiogenesis, and contraction of wound edges toward each other, and
ultimately, epithelialization; maturation and remodeling (collagen fibers rearrange themselves, increasing strength and
development of scar tissue)
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| Types of wounds: acute—result from trauma or surgery; easy to heal; require limited local care; progress naturally and
quickly through phases of healing; wounds infected postoperatively still considered acute; chronic wounds—due to
poor nutrition and poor circulation, eg, decubitus ulcers, diabetic foot ulcers; require extensive care; slow to heal;
progress slowly or stall through phases of healing
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| Wound healing: optimum wound-healing goals—eliminate pain and suffering; diminish risk for infection; reduce
healing time; reduce disability; reduce frequency of wound care; factors patient-, environment-, and wound-related; patient-related
factors—circulatory impairment; immobility; pressure (not problem in abdominal wound); malnutrition
and immunosuppression; environmental factors—not applicable to surgical wounds; wound-related factors—
moisture and exudate; ability of base of wound to be irrigated or treated to promote healing; keep wound moist (moisture
prevents cell death and supports epidermal migration); if too moist, exudate and edema present, macerating surrounding
tissue, and preventing proper elimination of bacterial toxins; issue of colonization vs infection (particularly in burn
wounds); all wounds colonized and have bacteria; when colonization deep into tissues, bacterial load, virulence, and inadequate
host defenses combine to cause actual infection (overgrowth or invasion of tissues); takes 104 to 106 bacteria/g
of tissue to cause wound infection; debridement sometimes helpful in removing necrotic tissues and senescent cells; International
Advisory Board on Surgical Wound Management—acronym TIME, defined as removal of nonviable tissue,
control of infection, keeping wound moist (but not too moist), and advancing wound edge; local signs of
infection—edema; erythema; pain; induration of wound edge; fever; malodorous wound; copious exudate; purulence;
systemic signs commonly associated with infections anywhere else in body; necrotic debris media for bacterial growth
and delayed wound healing
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| Management: apply evidence-based practices to diminish risk for wound infection and minimize number of infections;
SCIP objectives for prevention of SSIs—necessary to give antibiotic ≤1 hr before incision; ideally, use antibiotic recommended
by SCIP guidelines; stop antibiotic ≤24 hr after completion of surgery; in cardiac surgery patients and diabetics,
address glucose control; proper hair removal; maintain normothermia; not all SSIs preventable; period of maximum
influence on SSI risk begins and ends in operating room (OR)
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| Wound infection survey: assessment of current preferred methods for treating surgical wound infections; respondents
practicing colorectal surgeons (15% response rate [334 responses]); incidence of SSIs after colon and rectal surgery—
majority tended to underestimate own SSI risk; if surgical site infection present, timing of when incision opened—
most done at bedside; whether culture performed—slightly >50% of respondents cultured wound; reason for
culturing—to help direct selection of antibiotic (70% of respondents); hospital protocol (30%); antibiotics—90% did
not usually give antibiotics, unless extensive cellulitis present; 56% gave antibiotics in immunocompromised patient and
34% when patient febrile; choice of antibiotic—77% gave broad-spectrum antibiotics, 8% covered gram-positive organisms,
7% covered gram-negative organisms, and 5% covered anaerobes; only 5% of respondents waited for results of
culture and sensitivity test before giving antibiotics; whether antibiotics given to routinely cover for methicillin-resistant
S aureus (MRSA)—92% did not; management of physical wound—75% used wet-to-dry packing, 20% used dry
packing, and 10% did not use packing; 13% provided hydrotherapy; 50% use wound VAC; whether enterostomal therapist
or wound ostomy incontinence nurses involved in wound care—7% always; 23% most of time; 21% rarely or
never; patient disposition—36% felt skilled nursing facility sometimes indicated (most did not feel need); home health
nursing—63% recommended either always or majority of time; delay in discharge caused by surgical wound
infection—12% no delay; 29% extra day; 40% extra 2 days; 20% 3 days; most important criteria for hospital
discharge—44% stated availability of home health or wound care device; when to stop home health nursing—30%
when nurse determines no longer necessary; 56% based on appearance of wound; delayed primary closure—72% almost
never; 8% would perform; timing of primary closure—40% after 3 to 5 days; 32% after 5 to 7 days; 10% after 7
days; where primary closure performed—two-thirds at bedside; most important in surgical wound management—
45% packing; 33% wound VAC; 5% hydrotherapy
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| Adjuncts to wound care: include absorptive dressings, alginates, hydrocolloids, transparent films, wound cleansers,
protectants, hyperbaric O2 or O2 tent, and wound VAC; chronic wounds begin as acute wounds and fail to progress;
debridement—not necessary in most patients; types include 1) surgical debridement; 2) autolytic, using proteolytic enzymes;
3) enzymatic, using collagenase; 4) biologic, using maggots; 5) mechanical, using wet and dry dressings; no evidence-based
medicine about management of surgical wound infections, resulting in wide variations in treatment methods;
no studies showing that adjunctive measures work any better
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| Current practices: infected portion of wound should be opened; correct obvious impediments to healing, eg, avoiding
smoking, hypoxia, nutrition (hypoalbuminemia), hypovitaminemia; antibiotics if infection present; goal to keep skin
from healing prematurely (ie, before healing of deeper portions of wound); daily shower or irrigation; dressing to prevent
wound exudate from getting into patient’s clothes; no benefit in giving antibiotics to uninfected patient; no benefit to
packing, unless using wet-to-dry dressings for debridement; no benefit to hyperbaric O2 , adjunctive wound products,
wound VAC, and home health
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| NECROTIZING SOFT-TISSUE INFECTIONS —Gregory J. Jurkovich, MD, Professor of Surgery, University of Washington
School of Medicine, and Chief of Trauma Services, Harborview Medical Center, Seattle
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| History: first described during Civil War; at that time, combination of S aureus and group A β-hemolytic Streptococcus;
streptococci release toxin that causes thrombosis of blood supplies; leads to ischemic environment and necrosis, allowing
staphylococci to spread along ischemic environment (called “hospital gangrene” at time); involvement of perineum
(Fournier’s gangrene)—combination of β-hemolytic streptococci, staphylococci, and other organisms; particularly
characteristic, initial ulcer that spreads
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| Definition: diffuse soft-tissue infection particularly prone to occur in certain populations (eg, intravenous [IV] drug users,
morbidly obese) and particularly problematic due to emerging drug resistance; 2 fascial layers of skin—epidermis and
dermis; superficial fascia and subcutaneous tissue; deeper subcutaneous tissue before fascia investing muscle; most common
presentation in superficial fascia; almost never penetrates deep fascia into muscle; involvement of deep muscle-investing
fascia and muscle itself only in very late stages
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| Causes: depend on population; IV drug use—increasingly severe problem; in part, due to clostridial contamination of
black tar heroin; occurs in case clusters; if individual “skin-popping,” infection in subcutaneous tissue; if injecting heroin
into muscle, clostridial myonecrosis (mortality rate 38%, amputation rate 45%)
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| Diagnosis: problematic and judgment-oriented; hallmark that pain out of proportion to physical findings; if patient systemically
ill, late finding; local hard signs; white blood cell (WBC) count and serum sodium hastens decision to operate;
consider populations at risk; air in soft tissue from gas-forming organisms classic sign (only ≈6% clostridia; other gas-
forming organisms include Escherichia coli); bulging tense edema, with thin watery discharge on exploratory incision;
purple discolorations and cutaneous gangrene; bullae worrisome sign; study—31 patients with necrotizing fasciitis compared
to 238 patients who recovered with IV antibiotics only (control group); key signs included cellulitis, tense edema,
bullae, purplish discoloration, sensory defect (pain out of proportion to findings on examination), cutaneous necrosis, gas,
and any combination of signs; if any signs present, treated like necrotizing soft-tissue infection; if not present, necrotizing
soft-tissue infection not ruled out; serum sodium <135 mEq/L and WBC count >15 000/µL—best predictor; combined
with hard signs, indicates early serious systemic toxicity due to cellulitis unresponsive to antibiotics (necrotizing
soft-tissue infection) and requires treatment in OR; high sensitivity and specificity, with good negative predictive value;
laboratory risk indicators—scoring system; criteria include serum sodium, C-reactive protein, hemoglobin, WBC
count, blood glucose, and creatinine; >8 points, 75% likelihood of having necrotizing soft-tissue infection; cutoff 6
points; excellent negative and positive predictive values; imaging—no role if it delays surgical intervention; presence of
visible gas helps in diagnosis; computed tomography (CT) and magnetic resonance imaging (MRI) useful in identifying
deep abscesses; fat stranding in superficial fascia or even muscle-investing fascia nonspecific (not helpful in diagnosis);
technique—infiltrate affected area with local anesthesia and make small incision; insert finger and determine whether
able to go below superficial fascia and onto deep fascia and whether able to move finger freely (pathognomonic); implication
that infection has caused thrombosis of vessels and disruption of connective planes between fascial layers, allowing
egress along fascial planes (easily, without them being attached; pathognomonic sign); delaying diagnosis
problematic; study showed delaying surgical intervention by 24 hr resulted in 4-fold increase in mortality (25% vs 6%);
any delay increases mortality; look for constellation of risk factors, hard signs on examination, and laboratory results to
make diagnosis (requires high index of suspicion); if in doubt, go to OR and look for spreading of fascial plane
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| Management: in OR, necessary to debride necrotic tissues (may require amputation); plan for return to OR (q12-24h) to
ensure no spread and that some granulation tissue started; antimicrobial therapy—should be broad-based; initial treatment
should cover Streptococcus, Clostridium, and gram-negative organisms; penicillin and clindamycin commonly
used (synergistic); for anaerobic coverage, speaker favors gentamicin, if possible (if not, eg, elevated creatinine, use fluoroquinoline
[ciprofloxacin]); add vancomycin or linezolid if considering MRSA; in mixed infection in diabetic foot, infectious
disease guidelines suggest combination of β-lactamase inhibitors and penicillin (piperacillin and tazobactam
[Zosyn], ticarcillin and clavulanate [Timentin], ampicillin and sulbactam [Unasyn]), or any of imipenems
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| Community-acquired MRSA (CA-MRSA): increasing concern; according to Centers for Disease Control and Prevention
(CDC), as many as 60% of isolates from random carriers of S aureus methicillin-resistant; worth knowing prevalence
of CA-MRSA in community; causes pneumonia and skin and soft-tissue infections; individuals at risk—IV drug
users; sport team contacts; prisoners; military recruits; institutional residents; spread by skin contact; previous antimicrobial
therapy increases risk; oral therapy—effective if patient not septic; trimethoprim-sulfamethoxazole (TMP/SMZ;
eg, Bactrim) first-line; tetracyclines (particularly doxycycline) and fluoroquinolones (moxifloxacin most potent against
MRSA); erythromycin also useful; IV therapy—vancomycin, clindamycin, and linezolid; rifampin (synergistic)
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| Clostridial infection: typically deeper; from injecting clostridia deep into anaerobic space; ≈80% Clostridium perfringens
; germination time 8 min; invades and destroys healthy muscle tissue and releases toxins; causes hemolysis, microvascular
thrombosis, and muscle necrosis, increasing anaerobic environment; destroys polymorphonuclear leukocytes
and impairs migration; typical smear shows “tennis racket” appearance of organism (gram-positive rod), with no WBCs;
clindamycin best first-line therapy; penicillin added, due to 5% resistance to clindamycin; in laboratory studies, high
doses of clindamycin bind released toxins, reducing toxin concentrations
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| Adjunctive treatment: plasmapheresis; hyperbaric O2 ; IV immunoglobulin (IVIG); activated protein C (APC; Xigris);
no good studies on plasmapheresis (possibly beneficial [based on one study], but speaker unable to recommend); hyperbaric
O2 —limited evidence for humans and animals; recently published data from retrospective series; prospective randomized
controlled studies needed; IVIG—binds T cells; has role in streptococcal shock syndrome; difficult to use, due
to large volume needed; if used in conjunction with plasmapheresis, use afterwards; APC—problem of increased bleeding
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| Speaker’s experience: looked at 166 patients over 5 yr; mortality rate 17%; incidence of limb loss 15%; nonsurvivors
dominant in IV drug users; wide variety of organisms found; clostridia dominant in nonsurvivors; exponential increase in
mortality if WBC count >25,000/µL; extremely low WBC count, representing sepsis, predictor of poor outcome; hard
signs, WBC count and serum sodium dramatic predictors of outcome; challenges include difficult population and difficult
diagnosis, leading to delays; other major public health problem increasing role of IV and contaminated drug use
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Suggested Reading
Anaya DA et al: Predictors of mortality and limb loss in necrotizing soft tissue infections. Arch Surg 140:151,
2005; Barie PS et al: Surgical site infections. Surg Clin North Am 85:1115, 2005; Baugh N et al: Wound wise:
wounds in surgical patients who are obese. Am J Nurs 107:40, 2007; Blumetti J et al: Surgical site infections after
colorectal surgery: do risk factors vary depending on the type of infection considered? Surgery 142:704, 2007;
Fletcher N et al: Prevention of perioperative infection. J Bone Joint Surg Am 89:1605, 2007; Gillespie SH: New
tricks from an old dog: streptococcal necrotising soft-tissue infections. Lancet 363:672, 2004; Headley AJ: Necrotizing
soft tissue infections: a primary care review. Am Fam Physician 68:323, 2003; Hedrick TL et al: The appropriate
use of antibiotics in surgery: a review of surgical infections. Curr Probl Surg 44:635, 2007; Jallali N et al:
Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis. Am J Surg 189:462, 2005; Kowalski
TJ et al: Epidemiology, treatment, and prevention of community-acquired methicillin-resistant Staphylococcus
aureus infections. Mayo Clin Proc 80:1201, 2005; Majeski JA et al: Necrotizing soft tissue infections: a guide
to early diagnosis and initial therapy. South Med J 96:900, 2003; Neumayer L et al: Multivariable predictors of
postoperative surgical site infection after general and vascular surgery: results from the patient safety in surgery
study. J Am Coll Surg 204:1178, 2007; Schmidt AH: Are single-dose preoperative antibiotic regimens really appropriate?
Arch Surg 142:576, 2007; Ueno C et al: Using physiology to improve surgical wound outcomes. Plast Reconstr
Surg 117:59S, 2006; Wilkinson D et al: Hyperbaric oxygen treatment and survival from necrotizing soft
tissue infection. Arch Surg 139:1339, 2004; Wilson AP et al: Reduction in wound infection rates by wound surveillance
with postdischarge follow-up and feedback. Br J Surg 93:630, 2006.
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