SURGICAL INFECTIONS POS LECTURE 4
Abd, biliary, soft tissue, S aureus, tetanus, bites, Actino, TB, OPSI
JMA Bohnen January 2012
ABDOMINAL INFECTIONS
CID 2010;50:133
Importance: 1) the most common lethal surgical infections 2) huge inocula of pathogens and
adjuvants infect deep sites over large areas, needing cuts and tubes which contaminate and injure
unaffected tissues, a model for all infections 3) you will all face them.
Definitions: primary peritonitis: unimicrobial; spont bact peritonitis (infected ascites often
E.coli, S pneumo), perit dial-assoc (usu staph, Gm neg), TB. Secondary peritonitis: GI leak 2° to
ischemia/infla/perf. Local peritonitis: limited to organ region (eg appx, GB); generalized
peritonitis involves entire perit cavity; abd abscess: intraperit, retroperit or visceral
Pathology: Bacteria: number crucial, fecal peritonitis worst. Gm neg facultative rods +
anaerobes, esp E. coli, B. fragilis. Recurrent/persistent infection: bugs often resist antibiotics =
“3°peritonitis.” Local environment: subdiaphragm lymphatics absorb bugs to bloodstream,
RES → systemic effects; peritoneal inflammation kills bugs but decreases O2 and pH, digests
tissues, deposits fibrin, traps bugs → abscesses. Host defenses: small response if localized,
massive local infla and SIRS if generalized. Duration of infection: treatment delay ↑mortality:
Good outcome depends on early diagnosis and treatment!
Clinical Features and Diagnosis: Gm stain/cult can sort unimicrobial from 2° polymicrob. Typical
dx easy – tend, rebound, guarding; atypical (↑↓ age, postop, ↓immun, ↓CNS) dx tricky, delay
common in pts already sick, may present with MODS → ↑M. Mortality: generalized perit:
~25%, abd abscess ~10%, from MODS, underlying disease, GI fistula or 2° pneumonia, MI etc
Treatment : 1) resuscitate 2) give antibiotics 3) operate, drain or watch closely
1) Resuscitate with fluids, add nutrients if nil per GI for 7d
2) Antibiotics: Use single dose pre-op prophylaxis before operation to excise locally infected
organ (eg GB, appx) with primary skin closure. Continue as therapy for generalized or severe
infection, compromised host, till pt better, usually ≤ 7d. If still sick at 5-7d, don’t just extend
antibiotics, find source: GI leak, ischemia, abscesses, lines, pneumonia, fungus, DVT/PE. Value
of changing antibiotics based on cultures is controversial. Antibiotic regimens: cover community
acquired E. coli/B. frag; if nosocomial, hit broader spectrum. Many regimens ok eg single
agents: pip/tazo, ticar/clav, cefox, moxi, tigecyc, carbapenem; combinations: ceph³ or cipro or
levo + metro. Heed local prevalence and resistance patterns.
3) Operate, drain, watch: Sometimes use antibiotics alone for mild or early local peritonitis eg
some perf DU, colonosc perf, appendicitis, diverticulitis, acute cholecystitis. Watch closely if no
operation. Generalized, worsening, severe, potentially severe peritonitis or compromised pt
mandate prompt laparotomy, laparoscopy, perc drain and/or endoscopy to repair, remove,
divert or drain the source and peritoneum. Goals are to remove and prevent further contam,
treat cause (eg excise cancer), try to preserve abd wall. Avoid colon-colon anast (leak risk). Value
of intra-op C+S debated. NS lavage as good as antibiotic wash. Abd wall, wound: may leave skin,
subcut open to prevent spfcl incision ssi; fascial defect: may need mesh. Abdominal Abscess:
CT>U/S. Usually perc drain; operate if GI leak or ischemia, mult interloop absc, resection
otherwise needed eg cancer. Percut drain can turn leak into controlled fistula while boosting
patient for planned resection operation (eg divertic local perf with abscess)
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BILIARY TRACT INFECTIONS
(Usually stones, less often tumor; parasites)
Bacteria: coliforms (E. coli, Klebsiella, etc.), streptococci, enterococci. Anaerobes unusual,
clostridia in diabetics (may cause emphysematous cholecystitis); anaerobes present in suppurative
cholangitis, more likely in elderly
Acute cholecystitis: calculous: cystic duct obstr’n; bactibilia; value of antibiotics unclear other
than to prevent wound infection; acalculous (uncomm, sick, NPO). Rx: Cholecystectomy, perc
cholecystostomy if too sick; Acute cholangitis without suppuration: Charcot’s triad (abdominal
pain, jaundice, fever/chills). CBD stone usually. Not immediately life threatening, but mandates
biliary decompression within hours. Acute suppurative cholangitis (dying): Charcot’s triad: PLUS
hypotension, confusion = Reynolds’s pentad. Needs immed CBD decompression (ERCP or OR).
Pip-tazo, amp-sulbactam, carbapenem; Ceph³/4 or quin plus anti-anerobe if old, sick, or
cholangitis
SPREADING SOFT TISSUE INFECTIONS SSTI CID 2007;44:705
Confusing names eg anaerobic cellulitis, nonclostridial crepitant cellulitis, necrotizing fasciitis,
streptococcal hemolytic gangrene describe similar syndromes. Avoid confusion The names come
from 5 descriptors: level, necrosis, bugs, gas, microb synergy. Only level and necrosis matter:
At risk: Diabetes, trauma, obesity, unresolved contiguous infection, abdominal operation,
vascular insufficiency, perianal/rectal abscess: esp if  blood supply
Pathology/microbial
:
LEVEL
 cellulitis: subcut tissue ; erysipelas: dermis, distinct border
 fasciitis
 myositis or myonecrosis: muscle
NECROSIS – if so, it is
‘necrotizing’ and ‘gangrene’
(gangrene = ischemic necrosis)
See below, under
“diagnosis” and
“treatment”: level
and presence of
necrosis are the
important
descriptors
ORGANISM: Usually polymicrobial, fecal flora eg coliforms and Bacteroides.
Sometimes unimicrobial, especially Group A strep, Clostridia, S. aureus.
CREPITUS: physical or radiologic finding of gas in tissue; cues microbial etiology:
anaerobes or facultative coliforms
SYNERGY: polymicrobial eg Meleney’s progressive synergistic gangrene (S. aureus and
microaerophilic strep)
Authors use many combinations of those descriptors, hence the confusion; but dx + rx do not
require knowledge of those names or combinations.
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Diagnosis of SSTI
Viable
Type 1 
Cellul/erysip
Fasciitis
Myositis
Necrosis
Cellulitis/erysip
Fasciitis
 Type 2
Myonecrosis
Type 1: Treat with antibiotics
Type 2: Treat with operation
and antibiotics
Clinical diagnosis guides main treatment decision (operate or not); determine the level and
whether necrosis is present to distinguish simple cellulitis or erysipelas (type 1) from
necrotizing cellulitis, fasciitis, or myonecrosis (type 2). Treat type 1 with antibiotics only,
operate + antibiotics for “deep or dead”. Don’t miss type 2 SSTI.
Local findings of type 2 infection: discolouration other than pink (blue, brown, black, crimson);
excruciating pain or tenderness, hypesthesia, anesthesia, paresis, paralysis; discharge; putrid
odour; extreme swelling, woody induration. Crepitus occurs in type 1 but suggests type 2.
Advancing erythema despite adequate antibiotics suggests type 2. MARK BORDERS with
waterproof marker, followed closely over minutes then hours.
Systemic findings of type 2 infection: Confusion, lethargy, renal insufficiency possibly with
myoglobinuria, shock, hypoxemia, DIC. Get XRs if you suspect more than simple cellulitis, for
FB, gas or osteomyelitis. Hi fever may occur with type 1 or 2. If in doubt, explore under local
anaesthesia, look for fascia involvement (probe slides without resistance), dead fascia or muscle
(°contraction, °bleeding, stinky etc).
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Micro dx: gm stain and culture of infected tissue may influence antibiotic rx and
epidemiology, especially if unimicrobial. Type 1 usually is unimicrobial, often strep, staph,
other Gm pos, Gm neg; anaerobes in ischemic tissue, resistant bugs in hosp setting. Erysipelas
+ lymph obstr usually strep. Type 2 are uni- and poly-microbial. Culture result permits
narrowing antibiotic spectrum. Aspiration of injected saline has ~20% yield.
Antibiotics for type 1 cellulitis and erysipelas: clox, pen+clox, cefazolin, amox/clav, clinda,
clarithro, tigecyc etc and close observation NEJM 2004;350:904. If not improving in 24 hr add
Gm neg and anaerobe coverage, consider Type 2 infection.
Treat type 2 infections the same regardless of microbial etiology or tissue level: debride
aggressively, amputate if nec. Exception: TSS below. Resusc with O2 and fluids. Usually spare
sphincters in perineal SSTI (“Fournier’s gangrene”) and testicles and because of independent
blood supply, unless internal spermatic artery thrombosed.
Antibiotics for type 2: Unless unimicrobial (eg strep or clostrid), cover Gm pos cocci, Gm neg
rods and anerobes eg pen+quin+clinda, imipenem/meropenem/ertapenem.
Hyperbaric O2 WJS 2011;35:535 recommended for clostridial myonecrosis, limited to centres (eg
TGH) where available - clinical efficacy unproven, but strong theoretical and anecdotal support.
DON’T DELAY OPERATION FOR HYPERBARIC O2. Hyperbaric O2 may help resid infection
if excision not practical eg head + neck or pt refuses amput
Three common clinical syndromes :
1) Clostridical myonecrosis = “gas gangrene”
Microbiology: C. perfringens, other clostridia; at risk: 1) trauma 2) abdominal surgery 3)
spontaneous – diabetes, vascular insufficiency, perirectal abscess: esp if  blood supply
Pathogenesis: Bact toxins and hemolysins → shock, ARF assoc with muscle necrosis
Clinical: Severe pain, crepitus usually, sepsis; vascular collapse
2) Necrotizing fasciitis + necrotizing cellulitis
Microbiology: Single organism (less common): strep, clostridia, gm negs, others. Usually
polymicrobial coliforms + gm neg anaerobes ie GI flora; at risk: diabetes, obesity
Clinical: Most common type 2 infection; skin discolouration, blisters, “dishwater pus”
3) Meleney’s gangrene = “progressive synergistic gangrene” Uncommon, except books, exams
Microbiology: microaerophilic nonhemolytic strep + S. aureus
Clinical: Tender circular cellulitis. Black centre, then purple, red on outside. Burrowing tracts.
Treat: antibiotics +/- wide excision
S. AUREUS INFECTIONS
Source: blood: native or prosthetic valve, metastastatic from anywhere esp line; contiguous:
anywhere (eg skin to bone to joint); aspiration; airborne/fomite eg OR, trauma. Community
MRSA incidence continually ↑
Pathol: Toxin: food poisoning, toxic shock. Local invasion: 1) abscess incl surgical site,
traumatic wounds; skin incl furuncle, carbuncle (coalescence of furuncles); brain; lung; LKKS;
bone (osteo); muscle (pyomyositis, incl “tropical,” HIV) 2) regional spread eg cellulitis, fasciitis
3) FB/implant –assoc
Dx: Get cardiac echo for persistent/unexplained S. aureus bacteremia esp if intra-cardiac
device CID 2011;53:1.
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Treat: Drain, debride, remove FB as nec. Antibiotics for bacteremia, infection deep to skin,
regional spread, critically ill, immunocomp, to preserve infected FB. Bacteremia is serious! If
remove focus eg line, rx 2 wks clox IV. Deep (eg pneumonia): 3 wks clox IV to prevent
metastatic inf’n. For persistent S. aureus bacteremia, get cardiac echo, give 4-6 weeks IV clox.
MRSA needs vanco, clinda, linezolid, TMP/SMZ, doxy CID 2011;52:285; maybe rifampin.
VRSA exists. Under treatment is common Arch Intern Med 2002;162:25. Late (>48h) rx of
bacteremia → 4x mort CID 2003;36:1418
TOXIC SHOCK SYNDROME (TSS)
Micro/clinical: Toxin-mediated shock and MODS assoc with S. aureus or S. pyogenes infections.
Origin vagina (S. aureus, tampons), surgical wound (especially S. aureus), SSTI (especially S.
pyogenes) or obscure. Mortality ~15%.
Rx: hi dose clox or pen plus clinda ( toxin production). Add IVIG, especially for Strep; IVIG
neutralizes superantigen and has trend to ↓ mortality CID 2003;37:333, 2010;51:58 used in
Toronto, controversial. Invasive S. pyogenes infections (ie nec fasciitis + TSS) routine
screening/proph of household contacts not indicated, but consider for hi risk (chickenpox, HIV,
diab, cancer, hrt dis, IV drugs, steroids: CID 2002;35:950). MSH has expertise and database.
TETANUS
Micro/at risk: Clostridium tetani. Trauma, severe contamination especially fecal, dead tissue or
decreased blood supply (it’s an anaerobe), heroin addiction, bites, neonatal oomphalitis LACK
OF PREVIOUS IMMUNIZATION! Full immunization prevents tetanus.
Pathogenesis: C. tetani spores become vegetative in local anoxia  tetanospasmin (neurotoxin)
travels in blood, along axons (days to weeks, dep how close to CNS) inhibits inhibitory
neurotransmitters  spasm, irritability.
Clinical forms: Local: Mild, but may become generalized. Cephalic: Rare, head injury a cause,
involves VII n, may become generalized Generalized – 80% of cases. Local tingling at first, then
muscle rigidity,  T 2-4ºC, seizures,autonomic:  HR,   BP, arrhythmia
Prevention is crucial Bull ACS 1996;81:42; elderly less likely immune – confirm immun hx
Immunization HX
“uncertain” to 2
three or more
Clean, minor wounds under 6 hr:
Toxoid
yes
no
(unless  10 yr since last dose)
TIG
no
no
All other wounds (i.e. tetanus-prone), including burns, frostbite:
Immunization HX
Toxoid
TIG
“uncertain” to 2
yes
yes
three or more
no
no
(unless  5 yr sincce last dose
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Post-exposure prophylaxis:Passive: 500u human immune globulin TIG; active: immunize with
toxoid at a site remote from TIG; penicillin for dirty wounds; DEBRIDE (may liberate toxin,
give TIG 1st if indicated) Tetanus does NOT confer immunity; patients require immunization
Treat established tetanus: ICU, early airway; quiet room, diazepam, barbiturates, curare, 
blockade for  HR; phentolamine, guanethidine for  BP; TIG, immunization, penicillin or metro
Prognosis: 18% mortality, increases with age
ANTIBIOTIC PROPHYLAXIS FOR BITES
Debride, prevent tetanus and rabies as above and below: “amox/clav, rabies, tetanus”
Animal
Bugs
Drugs
Comments
Bat, raccoon, skunk
Unknown
amox/clav
rabies!
Cat
Pasteurella multocida
and S. aureus
amox/clav
80% become inf’d; switch
to pen if P multocida;
clox, cephalexin do not
cover P. multo
Dog
Same as cat plus some
anerobes
amox/clav
Only 5% become infected,
antibiotics controversial
Human
Streps, staphs,
anerobes, Eikenella
amox/clav
Tooth puncture on fist =
bite
Rat
Spirillum and strep
amox/clav
don’t worry about rabies
RABIES
1. Infection fatal; only survivors received prophylaxis before symptoms.
2. 11th most common infection killer in the world (but only ~3 cases/yr in USA).
3. Only 22 deaths in Canada since 1925 but infected animals probably increasing.
4. Most deaths now 2° to bat exposure without bite (CID 2002;35:738 CMAJ 2002;167:781
NEJM 2004;351:2626 MMWR 2011;60:437
PREVENTION (NEJM 351:2626, 2004)
(Wound care important too):
Animal
Wild
Skunk, bat
fox, coyote
raccoon
Status of Animal
Rx
regard as rabid
human rabies immune
globulin (HRIG) + vaccine
(D/C if brain neg)
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Domestic
dog/cat
healthy (quarantine, observe)
nil unless pet devel rabies
dog/cat
escaped (unknown)
HRIG + vaccine
dog/cat
rabies confirmed
HRIG + vaccine
dog/cat
rabies suspected
HRIG + vaccine (D/C if brain
neg for virus)
Other
rodents
rabbit
None unless v aggressive
Incubation period usually 20-90 days, shorter for bite on head, ranges 4 days to years.
Prophylaxis: use if bat in room, sleeping unattended or incapacitated (eg drunk), test bat if
possible if exposure can’t be ruled out; squirrels, chipmunks, rabbits: 0.1% infected; never cause
human rabies in US, treat only if aggressive. Domestic dog or cat, unprovoked – observe 10 days.
Vaccine: in deltoid; don’t use same syringe as HRIG. HRIG: ½ in wound area, ½ in ant thigh;
wash wound thoroughly with virucide (eg povidone-iodine) HRIG + vaccine safe, effective.
Give pre-exposure proph in those at risk (eg vets). Post-exposure prophylaxis is urgent ASAP
– delay affects outcome.
Treatment: 1st case survival multimodality rx without immune prophylax NEJM 2005;352:2508;
before, all fatal exc 5 survivors who had proph before symptoms
SOME POINTS ABOUT ABSCESSES
S. aureus causes abscesses everywhere. Antibiotics DO penetrate abscesses in most cases, but
may be inactivated. Treat most abscesses with drainage and antibiotics.
Exceptions good access from circulation:
brain abscess
lung abscess
Antibiotics alone often
amebic abscess
enough
multiple small liver abscesses
tubo–ovarian abscess
ACTINOMYCOSIS
Micro: Actinomyces are Gm pos branching anaerobic rods. A. israelii most common, NOT
opportunistic, NOT a fungus. Humans naturally colonized but does not transfer person to person.
Pathology: Enters thru break in GI mucosa 2° to disease/trauma. Sinus tracts and fistulae
typical. Sulfur granules, mineralized masses of bacteria up to 2mm in diameter, sometimes
visible to the naked eye, also found in Nocardia and other infections. Granulomas with
neutrophil infiltrate. Any unexpected “granuloma” on path report think TB, actino, FB, Crohns.
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Clinical: Four types, usually present chronically:
Cervicofacial: (half of cases) 2 types: a) painless, indolent b) painful, spreading, invasive
Thoracic: dental disease plus aspiration; lung actino may be diffuse, with small cavities. Pleura
and heart may be involved.
Abdominal: suspectwith any unexpected fistula formation or persistence; occurs 2° to any GI
operation/condition esp ileocecal, anorectal, adnexal.
CNS: abscess anywhere in CNS 2 to hematog spread; brain 75%.
Treat: Hi dose, long-term pen or amp/amox (10-20 million u pen G or 3 g amp IV daily for 4-6
wks, followed by po pen or amox 3-6 mo. Operate to drain abscess, resect, debride.
TUBERCULOSIS
Mycobacterium tuberculosis, spreads by aerosols. After inhalation organisms spread, become
dormant but viable, reactivate when host defenses ↓ (esp cell-mediated immunity age, malnut,
AIDS, lymphoma). Positive skin test shows previous exposure. Dx: acid-fast bacilli confirmed by
TB culture. “Scrofula,” peripheral lymphadenitis, may need excis bx (80%, sensitivity FNA
useful too CID 2011;53:555). Clinical: multisystem: pleuropulmonary, meningitis, pericarditis,
renal, osteomyelitis, lymph nodes, peritonitis. Consider TB in chronic or subacute undiagnosed
syndrome in patient with altered immunity. Rx: combo antibiotics, resistance problem.
OVERWHELMING POST – SPLENECTOMY INFECTION (OPSI)
Micro: Uncommon, lethal infection < 2% of kids post-splenectomy; also functional asplenia eg
sickle disease. S. pneumoniae most common, other encapsulated bugs (meningococci, H.
influenzae). Nausea, vomiting, confusion progress rapidly to death within hours despite hi dose
pen. Source usually obscure. Blood cultures are positive, bacteria often seen on blood film.
Prevent: Prophylaxis includes spleen preservation esp in kids. Give pneumococcal,
meningococcal and “H flu” vaccines (per CPS) before elective or after emergency splenectomy
though do not cover all bacterial strains. Repeat pneumococcal vaccine q 6 yrs. Vaccines have
few side effects. Give kid pen daily for 3 yrs after splenectomy. Asplenic patients should carry
amox or amox/clav always, take if fever.
Treatment: Ceftriaxone or cefotaxime IV. If Gm stain, cultures grow S. pneumoniae, use pen
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