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Surgical Infection

This document discusses surgical infections, including their pathogenesis, prevention, and treatment. Several factors can increase the risk of infection, such as wound hematomas, necrotic tissue, and foreign bodies. Proper wound preparation and use of perioperative antibiotics can help prevent surgical site infections. Administering antibiotics within 1 hour before incision and redosing if the procedure is long or there is significant blood loss is recommended. The appropriate antibiotic depends on the type of surgery and perceived contamination risk.

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0% found this document useful (0 votes)
127 views19 pages

Surgical Infection

This document discusses surgical infections, including their pathogenesis, prevention, and treatment. Several factors can increase the risk of infection, such as wound hematomas, necrotic tissue, and foreign bodies. Proper wound preparation and use of perioperative antibiotics can help prevent surgical site infections. Administering antibiotics within 1 hour before incision and redosing if the procedure is long or there is significant blood loss is recommended. The appropriate antibiotic depends on the type of surgery and perceived contamination risk.

Uploaded by

charoite
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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8

Surgical Infection
Ho H. Phan and Tiffany Lasky

The term surgical infection refers to infections that occur postoperatively and that are associated with the
surgical sites, as well as de novo infections that require urgent surgical evaluation and treatment. Many of these
infections are community acquired, requiring simple bedside incision and drainage; however, more complex
and invasive infections prompt exploration, operative drainage, and radical debridement. This chapter reviews
the basic principles associated with surgical infections including the risks, sources, diagnosis, and treatment for
many commonly seen diseases.

PATHOGENESIS OF INFECTION

Scheduled operations, traumatic injury, and nontraumatic local bacterial invasion can all lead to severe
infections that may require surgical intervention. Following bacterial soilage of host tissues, the body initiates
a well-defined process of host defense. There are several host factors that will affect bacterial virulence and the
cellular host response, which in turn alter the pathogenesis of the infectious disease (Table 8-1). Retained
wound hematomas provide an iron-rich environment that will potentiate bacterial growth, whereas the
hemoglobin content will inhibit the effectiveness of the neutrophil response in eradicating the
microorganisms. Blood is an excellent bacterial growth agar, and meticulous care must be given prior to
wound closure in obtaining hemostasis. Likewise, dead tissue provides a means of bacterial growth not well
penetrated by host defenses. Careful wound debridement and irrigation of all nonviable tissue is necessary for
adequate healing. Foreign bodies, such as suture, drains, urinary catheters, and intravenous catheters, provide
potential portals of bacterial entry and must be evaluated for their risk of infection versus benefit and necessity
for patient care.

TABLE 8-1 Risk Factors That Increase the Incidence of Surgical Infection

Local Wound Systemic

Wound hematoma Advanced age


Necrotic tissue Shock (hypoxia, acidosis)
Foreign body Diabetes mellitus
Obesity Protein–calorie malnutrition
Contamination Acute and chronic alcoholism
Corticosteroid therapy

160
Cancer chemotherapy
Immunosuppression (acquired and induced)
Remote site infection

Systemic factors (e.g., shock, hypovolemia, hypoxia, comorbid disease) will also affect the host response to
infection. Shock leads to tissue hypoperfusion and a metabolic acidosis that weakens host defense
mechanisms. Hypoperfusion of end-organ tissue and subsequent cellular dysfunction increases septic
complications in patients who have traumatic injury or who are postoperative from elective surgery.
Oxygenation is an essential metabolic component for phagocytosis and intracellular killing. Inadequate oxygen
delivery (related to both hypoperfusion and inadequate oxygenation) results in acidosis at the site of bacterial
contamination and will significantly increase the likelihood of subsequent infection. Patient comorbid diseases
must also be considered when assessing infection risk. Patients with diabetes have impaired neutrophil
function and microcirculatory disease, whereas obese patients frequently have poor tissue perfusion secondary
to poor blood supply in adipose tissue. Malnutrition will increase the vulnerability of the host to infection and
alcoholism impairs the host immune response. The use of systemic corticosteroids is common in many disease
states. Steroid use, cancer chemotherapy, and transplant immunosuppression will all greatly increase the host
risk for postoperative or surgical infection. A chronic disease that alters immune system function also poses
infectious risk following injury or surgery.

PREVENTION OF SURGICAL INFECTIONS

Mechanical Preparation

The prevention of surgical site infections (SSI) begins with adequate wound preparation. Most surgical
infections are due to contamination of the patient’s own endogenous flora. Therefore, appropriate preparation
of the surgical site is necessary to minimize the source of contamination. The patients should shower or bathe
with soap or antiseptic agent on the night before the day of operation. Body hair should be clipped, not
shaven, to prevent skin irritation and breakdown that can create a portal of bacterial entry into the wound bed.
Hair removal should occur immediately before the planned procedure. Skin preparation should include the
use of an alcohol-based antiseptic agent to reduce the number of endogenous flora. The sterile attire and
aseptic techniques utilized are also designed to minimize the source of intraoperative contamination.
Reducing operative time, maintaining normothermia, and controlling the glucose level during the procedure
have also been shown to significantly reduce the rate of SSI.
Good surgical technique also plays a role in the reduction of postoperative infection. Devitalized tissue and
foreign materials should be debrided to effectively remove any nidus for bacterial growth. Likewise, adequate
hemostasis and the lavage of any large blood clots from the wound will reduce the risk for SSI. Maintenance
of adequate tissue perfusion and oxygenation by intraoperative volume replacement and oxygen
supplementation may also reduce SSIs.

Perioperative Antibiotics

The use of perioperative prophylactic antibiotics relates to the magnitude of surgical intervention and the

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presumptive microbes to be encountered in the elective surgical setting. Adequate dosing of the antibiotic to
obtain maximal tissue and serum concentration at the time of making the incision is necessary for infection
prevention. In general, antibiotics administered after the contaminating event are not effective in the
prevention of surgical infections. The use of preoperative antibiotics has been shown to reduce the rate of
SSIs, leading to a reduction in intensive care unit and hospital length of stay, hospital costs, risk of
readmission, and mortality.
To insure adequate serum and tissue levels, initial antibiotics are given within 1 hour prior to the incision.
Some agents, such as fluoroquinolones and vancomycin, require administration over 1 to 2 hours; therefore,
the administration of these agents should begin 120 minutes before surgical incision. Intraoperative redosing
is needed if the duration of the procedure exceeds two half-lives of the antibiotic or if there is excessive blood
loss during the procedure. The chosen agent should be well tolerated and safe, have a long half-life, and
possess an antimicrobial spectrum appropriate for the planned procedure. The Surgical Infection Society
Guidelines for the selection of prophylactic antibiotics for some common surgical procedure types is outlined
in Table 8-2.

TABLE 8-2 Prophylactic Antibiotic Selection for Elective Surgery

Surgical Procedure Recommended Agents Agents for Patients with β-lactam Allergy

Cardiac or vascular Cefazolin, cefuroxime Clindamycin, vancomycin

Orthopedic Cefazolin Clindamycin, vancomycin

Gastroduodenal Cefazolin Clindamycin or vancomycin + aminoglycoside or


aztreonam or fluoroquinolone

Biliary tract Cefazolin, cefoxitin, cefotetan, ceftriaxone, Clindamycin or vancomycin + aminoglycoside or


ampicillin-sulbactam aztreonam or fluoroquinolone

Small intestine Cefazolin + metronidazole, cefoxitin, cefotetan Clindamycin + aminoglycoside or aztreonam or


fluoroquinolone

Colorectal Cefazolin + metronidazole, cefoxitin, cefotetan, Clindamycin + aminoglycoside or aztreonam or


ampicillin-sulbactam, ceftriaxone + metronidazole, fluoroquinolone, metronidazole + aminoglycoside or
ertapenem fluoroquinolone

Hysterectomy Cefazolin, cefotetan, cefoxitin, ampicillin-sulbactam Clindamycin or vancomycin + aminoglycoside or


aztreonam or fluoroquinolone

From Surgical Infection Society. Guidelines for antimicrobial prophylaxis in surgery. Am J Health Syst Pharm. 2013;70:195–283.

Perioperative antibiotic use requires an understanding about the type of case to be performed and the level
of contamination perceived (Table 8-3). Clean cases with little risk of contamination do not require antibiotic
coverage. However, prophylaxis is utilized in clean cases where prosthetic material (i.e., mesh, vascular graft
orthopedic device) is used as a means to reduce the likelihood of device infection. For cases in which there is a
risk of minimal endogenous contamination (clean-contaminated), the source must be considered, because the
SSI risk for these cases is three times higher than that of clean cases. Upper intestinal tract surgery requires
Gram-positive and Gram-negative coverage, whereas lower intestinal tract surgery requires the addition of
anaerobic coverage. Contaminated cases involve gross spillage from bowel perforation and polymicrobial

162
bacterial involvement. The overall risk of site infection for contaminated cases increases 5- to 10-fold over
clean cases. Dirty wounds involve existing contaminated or established infection and are at the highest risk for
infection to develop, reaching approximately 50% in most series. Antibiotics are considered therapeutic in
these cases with dirty wounds.

TABLE 8-3 Classification of Surgical Wounds Based on Level of Contamination

Bacterial Infection
Wound Contamination Source of Contamination Frequency (%) Examples

Clean Gram-positive Operating room environment, 3 Inguinal hernia, thyroidectomy,


surgical team, patient’s skin mastectomy, aortic graft

Clean Polymicrobial Endogenous colonization of the 5–15 Elective colon resection, gastric
contaminated patient resection, gastrostomy tube,
common bile duct exploration

Contaminated Polymicrobial Gross contamination 15–40 “Spill” during elective GI surgery,


perforated ulcer

Dirty Polymicrobial Established infection 40–50 Drainage of intra-abdominal


abscess, resection of infarcted bowel

GI, gastrointestinal.

Perioperative antibiotic therapy is continued in the postoperative setting for less than 24 hours. For the
majority of surgical cases, antibiotic infusion for more than 24 hours has been shown to increase bacterial
resistance and have no further improvement on SSI rates. In certain surgical interventions, such as cardiac
surgery, use may be extended to 48 hours. When antibiotics are used to treat existing infection, the empiric
agent is usually continued until specific cultures dictate a more specific agent. Should the prophylactic agent
need to be extended for treatment of established infection, such as would occur with ruptured appendicitis,
appropriate chart documentation should indicate the shift from prophylaxis to a treatment modality.

ESTABLISHED INFECTION

Surgical infections can be grouped as community acquired or hospital acquired. Community-acquired


infections are processes that were present before and, in many cases, are the reason the patient requires
treatment. Hospital-acquired infections occur as a consequence of or during treatment and are termed
nosocomial.

Nosocomial Infections

Nosocomial infection is by far the most common complication affecting hospitalized patients. It is estimated
that 5% of hospitalized patients will acquire at least one nosocomial infection during their stay. Nosocomial
infections are associated with a significant increase in morbidity and mortality and are often preventable. The
treatment of nosocomial infection is largely supportive: control the source of infection by drainage or
debridement, initiate appropriate antibiotic treatment, and support failing organs. Prevention, whenever
possible, is the best treatment.

163
Choosing the correct empiric antibiotic for the right indication can have a significant impact on the
outcome of patients with nosocomial infections. For example, up to 30% of patients with catheter-related
bloodstream infections have inadequate antimicrobial therapy. The mortality for these patients is twice that of
patients with adequate antimicrobial coverage. Similar findings have been demonstrated in patients with
ventilator-associated pneumonia. Essentially, the risk of mortality is increased when empiric antibiotic therapy
is delayed or inadequate. Therefore, early and appropriate diagnosis and treatment of infections should be a
major priority in hospitalized patients.

Postoperative Fever
Fever that occurs in the postoperative period can be an early indication of developing infection. The
traditional six “Ws” listed in Table 8-4 provide a systematic approach to help identify an etiology for the fever.
Early temperature elevation is usually due to pulmonary atelectasis, which usually responds to deep breathing
exercises and expectoration of secretions from the airway. Later in the postoperative course, fever points to the
surgical wound, urinary tract, intravenous catheter site phlebitis, or deep vein thrombophlebitis as potential
sources. The development of deep infections or abscess is usually identified as a late occurrence. Drug fever is
an unusual event and should be considered only when all other obvious causes of fever have been ruled out. A
postoperative fever should stimulate a careful patient examination and chart review to identify an etiology.
Antibiotic treatment should be initiated only when a specific infectious source has been identified.

TABLE 8-4 The Ws of Postoperative Fever

Site/Source Postoperative Timing (d)

Wind 1–2

Water 2–3

Wound 3–5

Walking 5–7

“W” abscess 7–10

Wonder drugs Any time, provided other etiologies have been ruled out

Surgical Site Infections


SSIs account for approximately 20% of all hospital-acquired infections, leading to increased cost and
prolonged hospitalization, and are divided into categories on the basis of the level of tissue penetration. The
diagnosis of superficial surgical infection is made in the majority of cases with examination of the incision and
surrounding skin demonstrating erythema and purulent drainage. For deep SSI and organ-space infection,
fever and/or leukocytosis may also be present.
Superficial SSI involves the skin and subcutaneous tissues and is the most common type of SSI. Clinically,
it ranges from simple cellulitis to overt infection of the wound bed above the fascia. Treatment includes oral
antibiotics (Gram-positive coverage) for cellulitis and reopening of the wound for those infections with
purulent drainage.
Deep SSIs extend into the muscle and fascia. Treatment of deep SSIs requires reopening of the wounds

164
and frequently sharp surgical debridement of the necrotic tissue. Deep SSI of abdominal wounds can lead to
fascial necrosis and fascial dehiscence. In some of these cases, debridement of necrotic fascia and
reapproximation is the best treatment course to prevent evisceration of abdominal contents. In more severe
cases, the infections can spread along the fascial plane, causing fascial necrosis, systemic infection, and sepsis.
Source control with radical debridement and intravenous broad-spectrum antibiotics is required for successful
treatment in these severe infections. Because of extensive tissue loss, reconstruction of the abdominal wall in
these cases can be challenging.
Organ-space SSIs are infections that involve the body cavity where the operations were performed. These
infections include secondary peritonitis, intra-abdominal abscess, and empyema. They are often related to
inadequate source control from the original bacterial contamination event. Sometimes, a subfascial collection
can manifest as wound drainage as the abscess attempts to extrude itself from the deeper space between fascial
sutures. This can be difficult to differentiate from deep SSIs without the help of imaging studies. Intra-
abdominal infections are usually polymicrobial, and broad-spectrum empiric antibiotic coverage should be
started when the diagnosis is made. Anaerobic coverage should be considered on the basis of the most likely
source and indigenous bacterial contaminants. Intrathoracic infections are less frequently polymicrobial, and
antibiotic selection should be targeted at the most commonly occurring organisms for each patient’s particular
disease state. Patients with deep-space infections can become quite ill very quickly because of systemic
extension of the infection and sepsis. Rapid diagnosis and treatment is necessary to prevent further morbidity
and mortality. Computed tomography (CT) with contrast is a helpful diagnostic tool when this type of
infection is suspected. Many isolated collections are amenable to percutaneous drainage utilizing radiographic
guidance; however, those with ongoing contamination from infected implanted devices or anastomotic
breakdown will require operative intervention.

Intra-Abdominal Infections
Intra-abdominal infections following abdominal surgery is a type of organ-space SSI. Postoperative intra-
abdominal infection generally manifests in two clinical settings. The first and less common setting is diffuse
peritonitis with florid sepsis. This is usually associated with major dehiscence of a bowel anastomosis or
perforation with gross spillage of enteric or biliary contents. In these cases, reoperation is required for source
control. Diffuse abdominal pain, peritonitis, fever, leukocytosis, and toxic septic state (rather than imaging
studies) are the most important indicators of the need for reoperation in this setting. The second and more
common setting is intra-abdominal abscess formation resulting from small anastomotic leak or intraoperative
contamination. Usually, persistent fever, leukocytosis, or ileus prompts the workup for intra-abdominal
abscess. CT with enteric and intravenous contrast is the most useful diagnostic test to evaluate for intra-
abdominal abscess, demonstrating a well-organized fluid collection with peripheral contrast enhancement.
Percutaneous drainage guided by ultrasound or CT is the initial intervention of choice for localized accessible
abscesses. Operative source control is needed when there is (1) a source of ongoing contamination such as
bowel perforation or an anastomotic leak or fistula, (2) devitalized tissue requiring debridement, (3) failure of
percutaneous drainage, or (4) progression to generalized peritonitis.
In all cases of intra-abdominal infections, primary source control is an imperative step in the treatment
plan. Systemic antibiotics alone will seldom be adequate therapy. Antibiotic therapy for intra-abdominal

165
infections should appropriately cover the organisms that are inherent in the source of contamination. After
adequate primary source control, the duration of antibiotics for intra-abdominal infections should not be
longer than 2 days after resolution of fever and leukocytosis. A recent randomized controlled trial (STOP-IT)
demonstrated similar outcome in patients with intra-abdominal infections treated with a 4-day course of
antibiotics compared with those treated with a longer course.

Empyema
Pleural effusions are common in complicated surgical patients. Most often these are caused by volume
overload, sympathetic effusions, or parapneumonic effusion. When a postoperative patient with systemic signs
of infection (fever, systemic inflammatory response syndrome, leukocytosis) develops a pleural effusion, the
composition of the fluid should be determined by thoracentesis. A transudative effusion is caused by increased
hydrostatic forces and has low protein content, whereas an exudative effusion is caused by increased
permeability and has high protein content. Determining the fluid lactate dehydrogenase (LDH), glucose, pH,
cell count, and Gram stain can help determine the type of effusion. Exudative effusions due to inflammation
have a pH <7.2, a glucose <60 mg/dL, and/or a LDH> 3× serum levels. They may be Gram stain or culture
positive, although in up to one-third of patients with empyema, organisms are not identified in the fluid. The
diagnosis can usually be confirmed by CT scan and the identification of a loculated rim-enhancing pleural
collection. In symptomatic patients or in patients with effusions associated with the characteristics of an
exudate on thoracentesis sampling, adequate drainage of the pleural space should be accomplished. Although
repeat therapeutic thoracentesis may be sufficient in some cases, surgical drainage is usually required either
with video-assisted thoracic surgery or, for more advanced cases, thoracotomy and decortication.

Hospital-and Ventilator-Associated Pneumonia


Hospital-associated pneumonia and ventilator-associated pneumonia (VAP) together account for 22% of all
hospital-acquired infections, making them the most common hospital-acquired infections. Approximately
10% of patients who require mechanical ventilation are diagnosed with VAP, and this rate has not declined
over the past decade. The duration of mechanical ventilation, hospitalization, mortality, and treatment cost in
ventilated patients diagnosed with VAP are substantially higher when compared with those without VAP.
The diagnosis of VAP is suspected when the patient has an infiltrate/consolidation on chest x-ray that is
new or progressive, along with clinical signs of fever, leukocytosis or leukopenia, new onset or increased
purulent sputum production, and worsening gas exchange. Patients with suspected VAP should be further
evaluated by bronchoscope-guided bronchial sampling (bronchoalveolar lavage, protected bronchial brushing)
or blind bronchial sampling (mini-bronchoalveolar lavage) for quantitative cultures. Alternatively, noninvasive
sampling with endotracheal aspiration for semiquantitative cultures can be done to guide antibiotic therapy. A
positive quantitative culture is defined as ≥104 colony-forming units (CFU)/mL for bronchoalveolar lavage
and ≥103 CFU/mL for protective bronchial brushing. A negative endotracheal aspirate culture has a very
strong negative predictive value.
Once VAP is suspected, empiric antibiotic(s) must be chosen. This will largely be based on the patient’s
risk of having resistant organisms. In general, patients in the hospital for less than 5 days are at low risk for
multidrug-resistant organisms. Antibiotic coverage should include Staphylococcus aureus and Gram-negative
bacteria. Patients who are immunocompromised or have been in the hospital for 5 days or more or who have

166
acute respiratory distress syndrome at the time of diagnosis are at high risk for infections with multidrug-
resistant organisms. In this setting, empiric antibiotic coverage should include methicillin-resistant
Staphylococcus aureus (MRSA) and Pseudomonas. Once the causative organism is identified by culture, empiric
antibiotics should then be tailored to the narrowest possible spectrum to cover the organism(s). Patients with
negative endotracheal aspirate cultures or patients with quantitative bronchial cultures below the diagnostic
threshold should have their empiric antibiotics discontinued. Specific antibiotic treatment for 7 days is
sufficient for most patients with VAP.
Attempts at VAP prevention have led to the development of a group of interventions that when bundled
together seems to have a great impact when compared with any individual effort. The basic principles for
VAP prevention are to (1) minimize sedation and sedation interruption daily, (2) assess readiness for
extubation daily with spontaneous breathing trials, (3) maintain and improve physical conditioning by early
mobility, (4) minimize pooling of secretions above the endotracheal tube cuff by using an endotracheal tube
with a subglottic suction device, (5) elevate the head of the bed 30° to 45°, and (6) maintain the ventilator
circuit (change only when visibly soiled or malfunctional). Adherence to these recommendations has
demonstrated a significant reduction in the length of time patients require ventilator assistance, which leads to
a reduction in VAP rates.

Urinary Tract Infections


The greatest risk factor for developing a urinary tract infection (UTI) is the presence of an indwelling bladder
catheter. The rate of catheter-related UTI is directly related to the duration catheter placement. Therefore,
the need for a urinary catheter in every patient should be evaluated daily, and catheters should be removed as
soon as they are no longer indicated. Other prevention strategies include aseptic placement, maintenance of
the closed drainage system, and daily urethral hygiene.
The diagnosis of postoperative UTI is traditionally made with a quantitative bacterial culture of more than
100,000 organisms/mL of urine. However, bacteriuria does not mean invasive urinary sepsis and is usually not
the source of fever in postsurgical patients. In most cases, positive urinary cultures with an indwelling catheter
usually clear after removal of the catheter. In the absence of a functional or anatomic obstruction to urine flow,
systemic bacteremia from the urinary tract is uncommon, and a postoperative fever should not be attributed to
the urinary tract even with positive urinary cultures. Surveillance for other sources of fever should be
undertaken in these clinical scenarios.

Community-Acquired Infections

Skin and Soft-Tissue Infections


Common soft-tissue infections are outlined in Table 8-5. Cellulitis as manifested by blanching erythema is
caused by group-A streptococci (GAS), which respond to penicillin therapy. Staphylococci may also be the
cause of cellulitis, particularly if gross suppuration (pus) is present at the affected site. Suppurative lesions
require local incision and drainage in addition to antibiotic therapy. Increasingly, the offending organism is
community-acquired MRSA, which is particularly virulent and can cause local tissue necrosis.

TABLE 8-5 Common Soft-Tissue Infections

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Typical
Infection Etiology Organism(s) Physical Findings Treatment

Cellulitis Break in skin Streptococcus Warm to touch, diffuse erythema, Systemic antibiotics and local wound
barrier tenderness care

Furuncle, Bacterial growth Staphylococcus Localized induration, erythema, Incision and drainage, systemic
carbuncle within skin glands tenderness, swelling with purulent antibiotics
and crypts drainage

Hidradenitis Bacterial growth Staphylococcus Multiple small localized Incision and drainage of small
suppurativa within apocrine subcutaneous abscesses, drainage, lesions, systemic antibiotics, large
sweat glands commonly from axilla and groin areas will require wide local excision
and skin grafting

Lymphangitis Infection within Streptococcus Diffuse swelling and erythema of Local wound care, systemic
lymphatics distal extremity with areas of antibiotics, removal of any foreign
inflamed streaks along lymphatic body, elevation of extremity
channels

Gangrene, Destruction of Synergistic: Necrotic skin/fascia, swelling and Radical debridement/amputation of


necrotizing soft- healthy tissue by Streptococcus/ induration, foul-smelling discharge, involved tissues, aggressive local
tissue infections virulent microbial Staphylococcus crepitus with subcutaneous wound care with frequent
enzymes Mixed emphysema, frequently with toxic debridement as necessary, parenteral
aerobic/anaerobic systemic signs and symptoms of broad-spectrum antibiotics
Clostridium sepsis

NSTIs, necrotizing soft-tissue infections.

Soft-tissue infections characterized by pathogen invasion, tissue necrosis, and systemic signs of sepsis are
collectively termed necrotizing soft-tissue infections (NSTIs). Necrotizing infection can be classified on the
basis of the depth of invasion (e.g., necrotizing adipositis, fasciitis, or myositis). All are surgical emergencies
requiring aggressive fluid resuscitation, intravenous broad-spectrum antimicrobials, and wide surgical
debridement of the necrotic tissue. Delay in recognition and treatment will lead to extensive tissue loss, limb
loss, and mortality. The most characteristic finding is pain out of proportion to physical appearance. Other
early clinical manifestations include edema beyond the area of erythema, skin anesthesia, epidermolysis, and
skin discoloration. Bullae, crepitus, foul-smelling drainage, and dermal gangrene are late manifestations and
are usually associated with systemic sepsis. Leukocytosis and hyponatremia, if present, can support clinical
suspicion. Radiographic imaging (x-ray and CT) may reveal asymmetric tissue inflammation and occult soft-
tissue gas. However, soft-tissue emphysema is detected only in 39% of patients, and its absence does not rule
out NSTIs. Surgical exploration of the affected area is often necessary to definitively rule in or rule out
NSTIs. Fournier gangrene is an eponym that specifically applies to NSTI of the genitalia and perineum. The
vast majority of these infections are polymicrobial. Antibiotic coverage for these patients should include
MRSA, Gram-negative organisms, and anaerobic organisms. If GAS infection is suspected, high-dose
penicillin should be included. A protein synthesis inhibitor such as clindamycin is commonly used because it
theoretically reduces toxin production.
Two monomicrobial NSTIs deserve specific attention: GAS infection and clostridial myonecrosis.
Necrotizing streptococcal gangrene rarely occurs in surgical patients. These infections are characterized by
nonblanching erythema, with blisters and frank necrosis of the skin. Nonblanching erythema indicates

168
subdermal thrombosis of the nutrient blood supply of the skin. Extensive surgical debridement of the affected
area and a combination of high-dose penicillin and clindamycin are the appropriate treatment. A Gram stain
of blister fluid or tissue obtained during the debridement is useful in differentiating this infection from other
necrotizing infections of the skin and skin structures.
Clostridial myonecrosis or clostridial cellulitis are fulminant life-threatening infections characterized by
tissue necrosis and rapidly advancing crepitus (gas gangrene). Either may occur as early as 1 day
postoperatively or after tissue injury, most commonly from puncture wounds, and carries a high mortality rate.
When Clostridium gas gangrene is diagnosed, immediate radical surgical debridement is necessary. Antibiotic
therapy should include high-dose penicillin. Clindamycin is a reasonable alternative in patients with penicillin
allergy, as is tigecycline, a glycylcycline related to tetracycline. Hyperbaric oxygen therapy to vastly increase
local O2 concentration, directly kill bacteria, and support WBC oxidative burst has also been successfully
utilized as an adjunct for NSTI in general, and clostridial myonecrosis and GAS in particular, but it is not a
substitute for aggressive surgical debridement. Adequate surgical debridement without primary wound closure
prevents clostridial myonecrosis or cellulitis in most patients with high-risk wounds.

Tetanus
Tetanus (lockjaw) is caused by the neurotoxin produced by Clostridium tetani that affects the brain, spinal
cord, and peripheral nerves. After an incubation period of 3 to 21 days, prodromal symptoms of restlessness
and headache are followed by descending muscular spasms, beginning with masseter muscle stiffness, neck
stiffness, and difficulty swallowing, and spreading to the rest of the body. Violent generalized tonic muscle
spasms usually follow within 24 hours of symptom onset, culminating in acute respiratory arrest, which may
require ventilator support. Autonomic nerve involvement may lead to episodic tachycardia and hypertension.
The diagnosis is made clinically rather than by microbiology, because the organism is isolated in only 30% of
the cases. The keystone of management is the prevention of exotoxin production by debridement and
cleansing of all wounds in which devitalized, contaminated tissue is present, coupled with an immunization
program. Tetanus immunoglobulin (TIG) is recommended for patients with tetanus. TIG can only help
remove unbound toxin and cannot affect toxin already bound to nerve endings. It is usually given
intramuscularly and infiltrated around the wound. All patients who sustain tetanus-prone wounds, as
described in Table 8-6, receive tetanus prophylaxis in accordance with the recommendations of the
Committee on Trauma of the American College of Surgeons, as outlined in Table 8-7. Patients with high-
risk wounds who have not completed the primary three-shot series of tetanus immunization should be given
TIG in addition to tetanus immunization. Tetanus in persons with a documented primary series of tetanus
toxoid is exceedingly rare.

TABLE 8-6 Tetanus Risk by Wound Type

Tetanus Prone Nontetanus Prone

Age >6 hr <6 hr

Type Crush Sharp/clean


Avulsion
Extensive abrasion

169
Burns or frostbite

Contaminants (soil, saliva) Present Absent

TABLE 8-7 Guide to Tetanus Prophylaxis in Routine Wound Management Among Adults Aged 19 to
64 Years

Clean, Minor All Other


Characteristic Wound Woundsa

History of absorbed tetanus toxoid (doses) Tdap or Tdb TIG Tdap or Tdb TIG

Unknown or <3 doses Yes No Yes Yes

≥3 doses Noc No Nod No

a
Such as, but not limited to, wounds contaminated with dirt, feces, soil, and saliva; puncture wounds; avulsions; and wounds resulting from missiles,
crushing, burns, and frostbite.
bTdap (tetanus, diphtheria, pertussis) is preferred to Td (tetanus, diphtheria) for adults who have never received Tdap. Td is preferred to TT
(tetanus toxoid) for adults who received Tdap previously or when Tdap is not available. If TT and TIG (tetanus immunoglobulin) are both used, TT
adsorbed rather than TT for booster use only (fluid vaccine) should be used.
cYes, if >10 years since the last tetanus toxoid-containing vaccine dose.

dYes, if >5 years since the last tetanus toxoid-containing vaccine dose.

Adapted from Centers for Disease Control and Prevention. Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid,
reduced diphtheria toxoid and acellular pertussis vaccine, Recommendations of the Advisory Committee on Immunization Practices (ACIP).
MMWR Recommend Rep. 2006;55(RR-17):1–33.

Breast Abscess
Breast abscess, characterized by localized severe tenderness, swelling, and redness associated with a mass, is a
common staphylococcal soft-tissue infection. Risk factors for breast abscess include breast feeding, maternal
age >30, first pregnancy, gestation age >41 weeks, smoking, and obesity. Development of breast abscess in a
nonlactating woman should alert the physician to the possibility of an underlying malignancy. The diagnosis is
made on the basis of clinical examination with confirmation by ultrasound and aspiration of purulent fluid.
Antistaphylococcal antibiotics and serial ultrasound–guided aspiration should be the initial treatment option.
Usually 2 to 3 serial aspirations separated by 2 to 3 days are required for complete resolution. In cases when
the overlying skin is compromised or when serial aspiration fails, surgical drainage is required. Surgical
drainage as the initial treatment is acceptable; however, it is associated with worse cosmetic outcome and a
higher rate of mammary duct/milk fistula. Mothers who are breastfeeding should be encouraged to continue
feeding or pumping even in the setting of breast infection. In patients at risk for malignancy, biopsy should be
performed.

Perirectal Abscess
These abscesses result from infection within the crypts of the anorectal canal and present as a tender mass in
the perianal area. Perirectal abscess can extend into the pelvis above the pelvic floor and can be fatal, especially
in diabetic or immunocompromised patients. Perirectal abscesses are exquisitely tender and usually require
general anesthesia to be examined and to establish adequate drainage. Antibiotic coverage is usually broad-
spectrum, targeting both anaerobes and aerobes, and is necessary in patients with bacteremia and patients with

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associated cellulitis. Invasive infection may result in subcutaneous tissue necrosis, which requires wide
debridement for salvage.

Hand Infections
Although generally not life-threatening, hand infections may lead to severe morbidity from loss of function as
a result of tissue loss, scar, and contracture. Paronychia is a staphylococcal infection of the proximal fingernail
that erupts at the sulcus of the nail border. Simple drainage and hot soaks usually provide adequate therapy.
Felons are deep infections of the terminal phalanx pulp space. These infections usually occur after distal
phalanx–penetrating injuries and are treated by drainage. A subungual abscess is the extension of a deep
paronychia and is diagnosed by fluctuance beneath the nail. Removal of the nail is usually necessary to permit
adequate drainage. Neglected infections of the fingers may result in tenosynovitis, an infection that extends
along the tendon sheath of the digit. Drainage requires opening the sheath along its entire length to prevent
necrosis of the tendon.
Penetrating injury or spread from a contiguous fascial compartment may lead to infection in one of three
deep-space compartments in the hand. A thenar space infection causes swelling and pain directly over the
thenar eminence. The thumb is held in abduction to reduce pain and tendon stretch. Loss of the normal
concavity as a result of tense, painful swelling of the palm is characteristic of a midpalmar space abscess.
Rarely, the hypothenar space presents in a similar fashion, with swelling and painful movement. Urgent
incision and drainage are required for these infections and empiric broad-spectrum antibiotics, later based on
culture data, are generally continued for 10 days depending on the response to therapy.
Human bites of the hand are common, and the potential infectious nature should not be underestimated.
Contamination of these wounds with polymicrobial aerobic and anaerobic oral flora contributes to invasive
deep-space infections, including tenosynovitis. Copious irrigation, debridement of devitalized tissue, hand
elevation, and broad-spectrum antibiotics are required to reduce the potential for infectious complications.
Human bites are the only penetrating injury of the hand in which primary closure is not done. Human oral
flora includes the invasive pathogen Eikenella corrodens, an organism that is known to suppurate along tendon
sheaths, leading to extensive tissue destruction. The hand and upper extremity are often injured by animal
bites as well. Debridement and irrigation are required (as for human bites), but the pathogens involved are
likely to be aerobic Pasteurella species from both dogs and cats.

Foot Infections
Foot infections result from direct injury or, more commonly, from mechanical and metabolic derangements
that occur in patients with diabetes. Trauma-related infections are best prevented by adequate wound
cleansing at the time of injury. Established infections should raise concern that a retained foreign body or
underlying osteomyelitis is present. All foreign bodies associated with infection require localization and
removal for healing to occur. Osteomyelitis requires operative debridement and long-term antibiotics.
Foot infections in patients with diabetes are a common problem because of neuropathy, the resultant bone
deformities, and the vascular compromise that occurs in this population, which leads to ischemic and
pressure-related ulceration. Ulcers on the plantar aspect of the forefoot underneath a metatarsal head are
typical for such pressure ulcers. A thorough examination of the infected foot should determine the extent of
vascular and neurologic impairment. Plantar space infections may present with dorsal cellulitis, and all cases of

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dorsal cellulitis should trigger a search for a plantar source. Osteomyelitis in a diabetic foot wound can be
present even when the wound itself does not show evidence of active infection. Wounds with exposed bone or
those that probe to bone are highly suspicious for underlying osteomyelitis, and they should be evaluated
further. Diabetic foot infections are usually polymicrobial in nature, including Pseudomonas, which is highly
prevalent in this patient population. Cultures of involved tissue (not just surface swabs) should be obtained,
followed by initial empiric broad-spectrum antibiotic therapy, debridement, and drainage. Efforts should
focus on limb salvage in these patients, because amputation is a frequent morbid consequence of these
complex infections. Such efforts may require the management of concomitant vascular disease by
revascularization procedures. Antibiotics alone may be insufficient to clear infection and allow tissue healing
without specific wound dressings, correction of pressure points by orthotic foot wear, and/or surgical
debridement and arterial inflow improvement.

Biliary Tract Infections


Biliary tract infections are usually a consequence of obstruction within the biliary tree, involving either the
cystic or the common bile duct. The bacteria most commonly involved include Escherichia coli, Klebsiella spp.,
and Enterococcus spp., whereas anaerobes are not commonly encountered. In patients with previous biliary-
enteric anastomosis, the likelihood of anaerobic organism involvement is increased. Antibiotics are utilized as
an adjunct to surgical and/or endoscopic intervention for effective drainage and infection resolution.
Acute cholecystitis is the most common inflammatory condition in the biliary tract. It begins as an
obstruction of the cystic duct by gallstone. Entrapped bacteria convert inflammation to an invasive infectious
process. Increased endoluminal pressure, combined with invasive bacterial infection into the wall, may also
compromise the blood supply of the gallbladder walls, resulting in ischemia, necrosis, and perforation.
Prevention of these complications is best achieved by operative intervention.
Infection proximal to a common duct obstruction causes ascending cholangitis. Patients present with
fulminant fever, right upper quadrant abdominal pain, and jaundice (Charcot triad); the addition of
hypotension and altered mental status is known as Reynold pentad. These patients usually manifest with
severe sepsis or septic shock, accompanied by hemodynamic instability, which require aggressive intravenous
fluid resuscitation to maintain mean arterial pressure. Prompt common bile duct drainage, together with the
administration of empiric systemic antibiotics, is imperative. The common duct can be drained by endoscopic
means (endoscopic retrograde cholangiopancreatography with stone extraction and sphincterotomy of the
sphincter of Oddi), percutaneous transhepatic cholangio-catheter placement, or surgical exploration of the
common bile duct. Cholecystectomy should be undertaken once the patient’s septic pathology has been
corrected.

Acute Peritonitis
Acute peritonitis occurs when bacteria are present within the normally sterile peritoneal cavity. Primary
peritonitis is spontaneous bacterial peritonitis that occurs without a breach of the gastrointestinal (GI) tract or
peritoneal cavity. It is usually monomicrobial and is more commonly seen in alcoholics with ascites and in
immunocompromised patients. Secondary peritonitis occurs as a result of spillage of gut organisms from the
GI tract or contamination from indwelling catheters (peritoneal dialysis catheters). It is usually polymicrobial.
Peritonitis causes acute abdominal pain, usually accompanied by fever and leukocytosis. Examination of

172
the abdomen typically demonstrates marked tenderness with voluntary guarding and percussion tenderness.
Involuntary guarding with board-like rigidity is characteristic of generalized peritonitis. An upright chest
roentgenogram commonly shows pneumoperitoneum beneath a hemidiaphragm. CT is more sensitive for
pneumoperitoneum, and a small amount of free air can be readily demonstrated by CT that may not be
initially apparent on plain radiography (Figure 8-1).

Figure 8-1 Coronal imagining of the abdomen with free intraperitoneal air under the right hemidiaphragm.

Perforated gastroduodenal ulcers usually present with acute onset abdominal pain with little or no
antecedent history of abdominal discomfort. Approximately 80% of patients have pneumoperitoneum on an
upright chest film. The perforation allows gastric acid, bile, as well as oral microflora to gain access to the
peritoneal space. Operative repair of the perforation is usually necessary for source control. All patients with
ulcer-associated perforation should be assessed for the presence of Helicobacter pylori infection. Perioperative
antibiotic therapy to address oral aerobes and anaerobes is generally indicated for acute perforations for <24
hours. Established infection with peritonitis and abscess indicates a need for longer therapeutic antibiotics
whose duration exceeds 24 hours. Importantly, perforation in patients with achlorhydria (endogenous or
medication induced) should prompt empiric antifungal therapy as well.
Acute appendicitis causes localized peritoneal irritation, and appendiceal perforation commonly causes
generalized peritonitis. In the absence of an appropriate operation, perforation may occur within 24 hours of
symptom onset. Patients typically demonstrate the characteristic findings of acute, diffuse peritoneal irritation
when the perforation is not contained, whereas a contained perforation with periappendiceal abscess
formation (Figure 8-2) may induce only right lower quadrant pain and tenderness. Antibiotic therapy is
directed against both aerobic (E. coli) and anaerobic (Bacteroides fragilis) enteric organisms. Treatment

173
depends on the hemodynamic status of the patient and the presence or absence of a localized collection that is
amenable to percutaneous drainage. Patients without a localized collection should undergo an emergent
operation for source control.

Figure 8-2 Localized psoas abscess following appendectomy for perforated, gangrenous appendicitis.

Colonic perforation with diffuse peritonitis creates the most virulent type of peritonitis, because the
colonic aerobic and anaerobic floral densities are high. Patients generally demonstrate peritonitis,
hemodynamic instability, and septic shock. After volume resuscitation and initiation of broad-spectrum
antibiotics, surgical intervention is generally required to manage the perforation, drain purulent collections,
debride nonviable tissue, and decontaminate the fecal materials. The etiology of colonic perforation may vary
(ischemia, diverticulitis, perforated colon cancer, etc.). CT findings may include thickened bowel wall,
mesenteric stranding, pneumatosis intestinalis, pericolonic fluid collections, and pneumoperitoneum. Colon
perforations usually require resection of the perforated segment and diversion of the fecal stream as part of
their management. Selected patients who present with a localized perforation (including mesocolonic
perforation) may be initially managed without immediate operation, provided the leak is adequately drained.

SUMMARY

The term surgical infections has now been expanded to encompass an entire host of disease states for which
evaluation by a surgeon and potential surgical intervention are necessary. SSI is in general an infrequent event
after elective surgery; however, emergent procedures with gross bacterial contamination are at a much higher
risk for subsequent development of postoperative infection. Many of these will require, at the very least,
opening of the surgical wound with daily local wound care. A small subset will require debridement and
drainage with the adjunctive use of antibiotics. Careful surveillance of the wound is necessary in those patients
at high risk for infection. Early identification and treatment will limit further complications related to ongoing

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infection. Numerous strategies targeted at prevention are being employed with protocols on the basis of
current evidence. Other types of surgical infections range from cellulitis to deep organ-space infections,
requiring a myriad of treatment techniques ranging from oral antibiotics to incision and drainage to radical
debridement to organ removal. A prompt diagnosis with rapid surgical treatment will limit morbidity and
mortality in many of these diseases.

SUGGESTED READINGS

Berrios-Torres SI, Umscheid CA, Bratzler DW, et al. Centers for Disease Control and Prevention guideline
for the prevention of surgical infection, 2017. JAMA Surg. 2017;152(8):784–791.
Bratzler DW, Dellinger EP, Olsen KM, et al. Clinical practice guidelines for antimicrobial prophylaxis in
surgery. Am J Health Syst Pharm. 2013;70:195–283.
Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-
associated pneumonia: 2016 Clinical Practice Guidelines by the Infectious Disease Society of America
and the American Thoracic Society. Clin Infect Dis. 2016;63(5):e61–e111.
Klomkas M, Branson R, Eichenwald EC, et al. Strategies to prevent ventilator-associated pneumonia in
acute care hospitals: 2014 update. Infect Control Hosp Epidemiol. 2014;35(8):916–936.
Sawyer RG, Claridge JA, Nathens AB, et al. Trial of short-course antimicrobial therapy for intraabdominal
infections. N Engl J Med. 2015;372(21):1996–2005.

Sample Questions

Questions
Choose the best answer for each question.

1. A 32-year-old man is seen in the emergency department 45 minutes after a motor vehicle collision.
His only injury is a long linear laceration beginning on the left temporal forehead at the hairline
and extending posteriorly for 10 cm. The edges are still bleeding briskly and the emergency
medical technicians described a large amount of blood at the scene. He did not lose consciousness.
His last tetanus booster was 4 years ago. Which of the following is required for tetanus
prophylaxis in this patient?
A. TIG only
B. Nothing further at this time
C. Tetanus toxoid only
D. TIG followed by a single tetanus toxoid booster
E. TIG followed by three tetanus boosters

2. A 48-year-old man is being evaluated in the emergency department with fevers, chills, and
abdominal pain for the past 24 hours. He has a history of hepatitis C infection following a blood
transfusion 14 years ago for a large scalp laceration and orthopedic injuries sustained in a motor
vehicle collision. He has not been to a physician for 5 years. He does not smoke or drink alcohol.

175
He takes no medications. His temperature is 39°C and vital signs are the following: blood pressure
(BP) os 90/50 mm Hg, pulse of 110/minute, and respirations of 26/minute. A CT scan shows a
single stone in the gallbladder that does not appear to be obstructing. The bile ducts are normal
caliber and the gallbladder wall is not thickened. There is a moderate amount of fluid, mild small
bowel distention, and stranding around the sigmoid colon as well as a small amount of free
intraperitoneal gas around the liver. An aspirate of the peritoneal fluid shows leukocytes and
mixed Gram-positive and Gram-negative bacteria on Gram stain. Laboratory values show a white
blood cell count of 19,000/mm3, a total bilirubin of 1.2 mg/dL, and an alkaline phosphatase of 40
U/L. In addition to fluid resuscitation and broad-spectrum antibiotics, what is the best step in
management?
A. Laparoscopic cholecystectomy
B. Long-term antibiotics only
C. Laparotomy
D. Magnetic resonance cholangiopancreatography
E. Endoscopic retrograde cholangiopancreatography

3. A 72-year-old woman underwent an operative fixation of intertrochanteric femur fracture 7 days


ago. Her urinary catheter was removed on postoperative day 5. Now, she is complaining of
burning with urination and urinary urgency. Her urinalysis is positive for leukocytes and bacteria.
Which of the following statement is NOT correct about this condition?
A. The diagnosis is made with quantitative bacterial culture.
B. The rate of infection is unrelated to the duration of the indwelling urinary catheter.
C. This condition is rarely the cause of postoperative fever.
D. This complication adds to the cost of hospital care.
E. Prevention of this condition involves maintenance of the close drainage of the urinary catheter
and aseptic placement.

4. A 30-year-old man is in the hospital recovering from splenectomy for a ruptured spleen sustained
in a motor vehicle collision. He has otherwise been healthy and was not taking medications prior
to the injury. A temperature of 102°F is noted on the second postoperative day. Vital signs are as
follows: a BP of 130/80 mm Hg, a pulse of 100/minute, and a respiration rate of 18/minute. His
pain is moderately controlled with morphine using patient-controlled analgesia. Breath sounds are
diminished at both bases, more so on the left. His abdomen is mildly distended, soft, and tender
near the incision. The incision appears to be healing without a problem. What is the most likely
cause for his fever?
A. Atelectasis and pulmonary infection
B. Peritonitis
C. UTI
D. Suppurative thrombophlebitis
E. Cardiac contusion

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5. A 25-year-old man is seen in the emergency department because of a painful swollen forearm. Two
days ago, he sustained a small laceration to his left forearm while clearing brush. It caused only
minor discomfort until about 12 hours ago when the area around the laceration became redder and
more swollen. He has otherwise been healthy. He takes no medications. His temperature is 38°C.
There is a 2-cm superficial laceration on the dorsum of his left forearm with a 15-cm diameter–
surrounding erythema that is quite tender. The edges of the erythema were marked, and 20
minutes later the erythema has extended 1 cm further beyond the mark. The most likely causative
organism is
A. MRSA
B. Group-A β-hemolytic streptococcus
C. Escherichia coli
D. Streptococcus faecalis
E. Candida albicans

Answers and Explanations

1. Answer: B
Wounds prone to the development of tetanus include those with extensive contamination with soil, deep
puncture wounds from metal objects, exposure injury complicated with frostbite, and wounds >6 hours
from the time of injury (see Table 8-6). Linear lacerations in general are not prone to tetanus. The extent
of blood loss does not affect the need for tetanus booster administration. The patient last received tetanus
toxoid <5 years ago, so nothing further is required. For more information on this topic, please see the
section on Tetanus.

2. Answer: C
This patient has secondary peritonitis. This usually involves perforation of a hollow viscus and thus
involves contamination of the peritoneal cavity with multiple organisms. Gram stain and culture of the
peritoneal fluid usually shows a single organism in patients with primary peritonitis, and this can be
treated with antibiotics without surgical intervention. In this scenario, the CT scan shows stranding
around the sigmoid and fluid and evidence of free air suggestive of a diverticulitis with fecal peritonitis.
Laparotomy with washout and correction of underlying cause is indicated. Patients with underlying liver
disease are prone to gallstones and are a common finding. There is no evidence of common bile duct
obstruction that warrants further investigation because the alkaline phosphatase is normal. For more
information on this topic, please see the section on Acute Peritonitis.

3. Answer: B
The rate of catheter-related infection is directly related to the duration of the urinary catheter being in
place. The diagnosis of UTI is usually made with a quantitative bacteria culture of more than 100,000
organisms/mL urine. UTI is rarely the cause of postoperative fever. UTI adds to the cost of care for
hospitalized patients, and prevention requires aseptic placement and maintenance of a closed drainage
system. For more information on this topic, please see the section on Urinary Tract Infections.

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4. Answer: A
Early postoperative fever is usually the result of atelectasis and subsequent pulmonary infection (see
Table 8-4). In this scenario, because of the close proximity of the left hemidiaphragm to the spleen, an
infiltrate in the left lower lobe of the lung is a high probability. An adequately drained urinary tract in a
young person seldom gives a high fever this early in the postoperative period. Although peritonitis from
injury to a surrounding structure during the splenectomy (i.e., pancreas, stomach, or bowel) is a
possibility, it is much less likely than a pulmonary source. Cardiac contusion does not elicit a febrile
response. For more information on this topic, please see the section on Postoperative Fever.

5. Answer: B
Although cellulitis may be caused by any organism, the most likely early organism would be group-A β-
hemolytic streptococcus. MRSA more commonly causes local inflammation and pus formation. The
other three species are rarely isolated from skin infections but are more commonly seen in infections
involving the GI tract. For more information on this topic, please see the sections on Urinary Tract
Infections and on Skin and Soft-Tissue Infections.

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