Diagrama de Von
Diagrama de Von
Diagrama de Von
a b,
Gina R. Shirah, MD , Patrick J. O’Neill, PhD, MD *
KEYWORDS
Antibiotics Complicated intra-abdominal infections Damage control surgery
Resuscitation Source control Systemic inflammatory response syndrome
Uncomplicated intra-abdominal infections
KEY POINTS
Intra-abdominal infections (IAI) should be suspected in a patient manifesting a systemic
inflammatory response syndrome (SIRS) and gastrointestinal dysfunction.
Uncomplicated IAI are predominantly isolated to an organ and do not involve gastrointes-
tinal disruption, whereas complicated IAI are usually diffuse peritoneal processes that may
include disruption of the gastrointestinal tract.
Adequate treatment of IAI requires early diagnosis combined with resuscitation, appro-
priate antibiotic therapy, and adequate drainage/debridement of on-going infection or
leaking gastrointestinal contents (ie, source control, SC).
Appropriate and timely empiric antibiotic coverage is imperative because inappropriate or
delayed coverage increases morbidity and mortality that cannot be reversed if subse-
quent appropriate antibiotics are added later.
In general, b-lactam/b-lactamase antibiotics will provide adequate empiric coverage for
low-risk patients; however, high-risk patients are at risk for more resistant microbiologic
flora, and empiric coverage should be driven by individual hospital or unit antibiograms.
Percutaneous drainage is preferred in stable patients with an isolated, anatomically
amenable source; surgical debridement (open or laparoscopically) remains the mainstay
for failed SC.
INTRODUCTION
Disclosure: G.R. Shirah has nothing to disclose. P.J. O’Neill has served as a consultant on the Sur-
gical Review Panel for Cubist Pharmaceuticals.
a
Division of Trauma & Critical Care Surgery, Department of Surgery, Maricopa Medical Center,
2601 East Roosevelt Street, Phoenix, AZ 85008, USA; b Trauma Department, West Valley Hospi-
tal, 13677 W McDowell Road, Goodyear, AZ 85395, USA
* Corresponding author. Trauma Department, West Valley Hospital, Goodyear, AZ.
E-mail address: pjoneill@abrazohealth.com
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1320 Shirah & O’Neill
IAI are divided into uncomplicated and complicated types. Uncomplicated IAI affect
a single organ and do not spread to the peritoneum. In these cases, there is no
anatomic disruption of the gastrointestinal tract. Complicated IAI describes an exten-
sion of the infection into the peritoneal space. It may be localized, as in the case of an
intra-abdominal abscess. For the insult that is not contained, diffuse peritonitis may
ensue.1,2 The resultant physiologic response may develop into a systemic inflamma-
tory response syndrome (SIRS) (Table 1).3,4
In addition to defining type of infection, patient stratification serves as an important
guide for treatment and will assist with initial resuscitation, treatment options, and spe-
cifically, antimicrobial therapy. Patients are divided into low-risk and high-risk cate-
gories that take into account the patient’s history, the type of infection, and the
resulting physiologic derangements.
Low-risk patients typically have community-acquired infections of mild to moderate
severity (perforated appendicitis or diverticulitis). The underlying physiologic status in
these patients is not compromised. High-risk patients, on the other hand, are used to
define patients who are at risk for multi-drug-resistant organisms,5–7 failure of source
control (SC),8 and ultimately, increased mortality.1,5,8–10 Predetermined patient-
specific and disease-specific factors act together to determine patient morbidity
and mortality (Box 1).6,8,10
PATHOPHYSIOLOGY
The inner abdomen is lined with a layer of tissue (peritoneum) innervated by the so-
matic nervous system. Infection begins, followed by inflammation by mast cell
degranulation with subsequent increased vascular permeability. This increased
vascular permeability causes an influx of complement factors and neutrophils that
are responsible for both direct bacterial opsonization and release of cytokines to
propagate the host response. This process may be localized to an abscess when
the inflammation, chemotaxis, and fibrin formation may form sufficient physical
barriers.10
Intra-abdominal inflammation may lead to a diffuse paralytic ileus, distention, obsti-
pation, and vomiting.4 When the host ability to contain the infection is overcome, the
infection progresses to diffuse peritonitis. Systemic response to the release of cyto-
kines will lead to a pro-inflammatory state, systemic vasodilation, hypotension, and
myocardial depression, manifested clinically as severe sepsis and subsequently as
septic shock.3,10
DIAGNOSIS
Table 1
Systemic inflammatory response syndrome criteriaa
Finding Value
Temperature <36 C or >38 C
Heart rate >90/min
Respiratory rate >20/min or PaCO2 <32 mm Hg
WBC <4 109/L, >12 109/L, or 10% bands
Abbreviations: PaCO2, partial pressure of carbon dioxide; WBC, white blood cell count.
a
Defined as having at least 2 of the above.
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Intra-abdominal Infections 1321
Box 1
Characteristics of high-risk intra-abdominal infection patients
Patient-specific factors
Advanced age (>70 y)
Immunosuppression
Poor nutritional status
Corticosteroid therapy
Organ transplantation
Presence of malignancy
Pre-existing chronic conditions
Liver disease
Renal disease
Disease-specific factors
High APACHE II score (>15)
Health care–associated infection
Delay in initial intervention (>24 h)
Inability to obtain source control
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1322 Shirah & O’Neill
One of the most urgent clinical circumstances is the patient who presents with peri-
tonitis (abdominal rigidity, guarding, and rebound tenderness). These signs are con-
cerning for pending hemodynamic collapse, and urgent evaluation and disposition
are necessary. Early hemodynamic assessment is a priority; if adequate (systolic
blood pressure >90 mm Hg), there may be time for further workup. On the other
hand, unstable patients (systolic blood pressure <90 mm Hg) and the need for vaso-
pressor support indicate the need emergent laparotomy for diagnostic and therapeu-
tic purposes with the understanding that the risk of mortality is higher than in a stable
patient.3
TREATMENT
Resuscitation
Intravascular volume depletion should be expected in patients with IAI. A thorough
history and physical examination may aid with guiding resuscitation. Severe nausea
and vomiting will cause metabolic alkalosis with relative hypokalemia, whereas a
high-volume diarrhea will cause a nonanion gap metabolic acidosis. With peritonitis,
the cytokine inflammation causes fluid sequestration both locally and systemically,
which may be profound, further contributing to intravascular volume depletion. Fluid
accumulation is noted with an ileus by both bowel wall edema and ascites. In addition,
patients with fever and tachypnea have more than 700 mL/d of excess fluid loss.10
These abnormal fluid shifts place patients at risk for intravascular volume depletion,
hypotension, and decreased end-organ perfusion. With an increasing severity of
illness, more invasive hemodynamic monitoring is indicated (central venous and arte-
rial pressure catheter placement and monitoring).
It has been learned from the Surviving Sepsis Campaign (SSC) that fluid re-
suscitation should be initiated immediately after the diagnosis of sepsis is suspec-
ted.3 The strategy of early goal-directed therapy has been shown to decrease
mortality.14
Source Control
SC is a fundamental surgical principle and is defined as the ability to effectively erad-
icate infection (ie, purulent fluid or tissue) and control leakage (ie, drainage of
on-going enteric contamination) by whatever means necessary.4,6,10 Although resus-
citation and treatment with antibiotics are central to the treatment of IAI, SC is para-
mount. It may be accomplished in a variety of ways, ranging from percutaneous
drainage to repeat operations. Timing of SC is generally undertaken as early as safely
possible. Although the goal is to remove the driver of the inflammatory response, pa-
tients may be in a delicate physiologic state that puts them at high risk for immediate
intervention. Nonetheless, SC is directly related to outcome, and inability to provide
adequate SC is associated with increased mortality.8,9 The exception to this rule is
acute pancreatitis and pancreatic necrosis, which does not benefit from early SC
(see later discussion).
In general, the least invasive procedure that is safely able to eradicate the infec-
tion is preferred. Percutaneous image-guided drainage is preferred for isolated IAI
that are anatomically amenable to drainage. Surgical debridement, whether laparo-
scopic or open, remains the mainstay of therapy for failed percutaneous control.
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Intra-abdominal Infections 1323
Antibiotics
Although secondary to adequate SC, appropriate and timely empiric antibiotic
coverage is imperative. Inappropriate coverage increases hospital stay, postoperative
abscesses,10 and mortality that cannot be reversed if subsequent appropriate antibi-
otics are added later in the clinical course.2,4 In severe sepsis, appropriate coverage
should be started within 1 hour as recommended by the SSC.3,10 Just as important is
the appropriate discontinuation of antibiotics (Antibiotic Stewardship). Unnecessary
antibiotic use has contributed to the emergence and spread of drug-resistant
microorganisms.
Box 2
Clinical indications for damage control surgery
Hemodynamic instability
On-going contamination or need for further debridement
Tissue/organ ischemia
Loss of abdominal domain
Development of/risk for abdominal compartment syndrome
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1324 Shirah & O’Neill
Initial empiric antibiotic coverage requires both knowledge of normal enteric flora
and assessment of potential risk factors. In general, proximal small bowel contains
enteric gram-positive streptococcus and gram-negative bacteria, whereas anaerobic
bacteria populate the distal ileum and colon (Table 2).8,10,12
To help guide the clinician, guidelines have been published that standardize the
diagnosis and management of IAI.8,12 The first guideline represents a consensus be-
tween the Surgical Infection Society and the Infectious Disease Society of America.
Second, worldwide guidelines have been published by the World Society of Emer-
gency Surgery. As previously mentioned, patients with IAI are divided into low-risk
and high-risk categories to stratify their risk for developing complicated infections.
In general, b-lactam/b-lactamase (penicillin, cephalosporins, carbapenems, mono-
bactams) antibiotics will provide adequate empiric coverage for low-risk patients
(Table 3).8,12
High-risk patients, on the other hand, are at risk for more resistant microbiologic
flora. Specifically, this includes gram-negative Pseudomonas aeruginosa and Acineto-
bacter species, extended spectrum b-lactamase producing Klebsiella species,
Escherichia coli, Enterobacter species, Proteus species, methicillin-resistant Staphy-
lococcus aureus (MRSA), enterococci, and Candida species. Empiric therapies are
institution-specific and should be adjusted for individual hospital/unit antibiograms
(Table 4).
Routine coverage for Enterococcus faecalis is only recommended if IAI is health
care–associated, if the patient had previously received cephalosporins, if the patient
has a history of valvular heart disease/prosthetics, or if the patient is elderly or critically
ill. E faecalis is seen with frequency in patients with liver disease and infections with a
hepatobiliary source.7 Antibiotics that will provide adequate coverage include ampi-
cillin, piperacillin-tazobactam, and vancomycin. Fungal coverage is necessary in the
presence of a nosocomial infection, a critically ill community-acquired infection, a pa-
tient on pharmacologic immunosuppression, or isolation of fungi from normally sterile
sites. Also, coverage should be considered if there was recent exposure to broad-
spectrum antimicrobials. Fluconazole is recommended unless critically ill; then echi-
nocandin is recommended as first-line treatment. MRSA coverage is recommended
Table 2
Normal enteric flora by gastrointestinal region
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Intra-abdominal Infections 1325
Table 3
Empiric antibiotic recommendations for low-risk intra-abdominal infection patients
Table 4
Empiric antibiotic recommendations for high-risk IAI patients
Ceftazidime
Local Piperacillin- or Cefepime
Organism Carbapenems Tazobactam (DMetronidazole) Aminoglycoside Vancomycin
<20% resistant 1 1 1
P aeruginosa
ESBL-producing
Enterobacter
sp.
Acinetobacter
sp.
or other MDR
GNR
ESBL-producing 1 1 1
Enterobacter
sp.
>20% of P 1 1 1
aeruginosa
resistant to
ceftazidime
MRSA 1
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1326 Shirah & O’Neill
patients show clinical response because longer treatment has not been associated
with improved outcome.8 Historically, studies have suggested antibiotics should be
continued until the patient has resolved their leukocytosis or fever and is tolerating
oral diet, but that may not be necessary.10 Transition to oral antibiotics may be initiated
when the patient is taking oral diet without an increased risk of treatment failure.8,17
If the patient continues to show signs of fever, leukocytosis, or delayed gastrointes-
tinal function after 7 days, a persistent infection should be suspected and reimaging
should be completed to search for on-going infection.8 In this situation, it is recom-
mended to continue antibiotics and strongly consider a change in covering
antibiotic-resistant microorganisms.
Source Control
In acute appendicitis, nonoperative management has been suggested as an alterna-
tive to traditional treatment of appendectomy. Meta-analyses demonstrate antibiotic
treatment alone was associated with decreased complications, less pain, and a
shorter sick leave. Ultimately, antibiotics were found to have only a treatment success
rate of 63% at 1 year and thus remain inferior to surgical management.10,18,19
Both the open laparoscopic approach and the laparoscopic approach to appendec-
tomy continue to be accepted treatment modalities and have been extensively
compared in the literature. The open approach has been associated with less cost,
shorter operative times, and decreased risk of IAI in multiple studies. Alternatively,
the laparoscopic approach has been found to have fewer surgical site infections,
less pain, shorter hospital stays, and more rapid return to normal activity. For compli-
cated or perforated appendicitis, the laparoscopic approach has been shown to
reduce overall mortality.10,20–22
Patients who present with a phlegmon or periappendiceal abscess had traditionally
required an operation for SC. When patients present during the peak of intra-
abdominal inflammation, the safety of surgical intervention comes into question.
Treatment with antibiotics and percutaneous drainage, if amenable, have been found
to be associated with fewer complications and shorter hospital stay when compared
with immediate appendectomy.10,23 Treatment of periappendiceal abscesses with an-
tibiotics alone has also been suggested but compared with percutaneous drainage
has a significant recurrence rate and is therefore not recommended.24
For those patients who were treated with percutaneous drainage and antibiotics,
generally an interval appendectomy was recommended owing to the variable rates
of recurrence (5%–37%).10,23,25 There is not enough evidence to firmly support inter-
val appendectomy and, in fact, interval appendectomy may be unnecessary in 75% to
90% of cases.12 Advocates for interval appendectomy argue that there is a significant
risk of recurrence and, if no surgical intervention is undertaken, there is a risk of
missing a diagnosis of cancer or Crohn disease. A systematic meta-analysis reviewed
61 studies from 1964 to 2005 and found a recurrence rate of only 7.4% and a 1.2% risk
of malignancy.26 Patients who underwent interval appendectomy were found to have a
prolonged hospital stay.26 Interval appendectomy is not strongly supported in the
literature.
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Intra-abdominal Infections 1327
Acute Cholangitis
Acute cholangitis is defined as a biliary obstruction complicated by infection. The
obstruction may be due to calculi, stricture, or a blocked biliary stent. The clinical pre-
sentation and subsequent decompensation of a patient may be quite rapid so prompt
diagnosis is essential. Rates of mortality have improved over time but remain 11% to
27%.27 Classic diagnosis is described by Charcot triad: fever, abdominal pain, and
jaundice. The complicated form of cholangitis includes septic shock and mental status
change (ie, Reynold pentad). The Tokyo Guidelines clarified the diagnostic criteria and
in addition graded the severity of cholangitis (Box 3).28
The severity of disease increases with the presence of organ dysfunction and nonre-
sponse to initial medical treatment. Severe acute cholangitis requires urgent biliary
compression with endoscopic retrograde cholangiopancreatography (ERCP).27
Source control
No randomized trials have been completed that compare treatment options, but in
accordance with the theme of least invasive treatment that may safely provide SC,
ERCP-directed internal drainage is the first-line therapy. Recent data suggest that
early ERCP (24 hours) leads to significantly shorter hospitalization without a signifi-
cant increase in intervention-related complications.29 Percutaneous transhepatic
drainage is available as a second-line therapy. Operative drainage may be indicated.
Recently, endoscopic ultrasound-guided biliary drainage has emerged as an option
for biliary decompression.30
Antibiotics
Coverage of microorganisms from the proximal bowel is usually sufficient for initial
empiric treatment in biliary disease. Anaerobic therapy is added in the case of acute
cholangitis and, when there is a biliary-enteric anastomosis, severe physiologic distur-
bance, or an immunocompromised state. Enterococcus species coverage is only
necessary if the patient has undergone an extensive hepatic procedure or has other
risk factors for enterococcus, such as immunocompromisation.8
Box 3
Diagnostic criteria for acute cholangitis
A. Systemic inflammation
1. Fever and/or chills
2. Elevated WBC or CRP
B. Cholestasis
1. Jaundice
2. Elevated transaminases
C. Imaging
1. Biliary dilatation
2. Evidence of cause on imaging (stricture, stone, stent)
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1328 Shirah & O’Neill
Pancreatitis
Pancreatitis has a variable presentation and if not recognized and treated may
result in rapid and severe patient decompensation. Ninety percent of acute
pancreatitis is caused by alcohol and gallstones. Simultaneous evaluation of
cause should be delineated. Ultrasound and serum alcohol level should be per-
formed in all patients. If these are negative, less common causes should be
pursued.31
Given the severe inflammatory response seen in these patients, resuscitation is
paramount. Worsening hemoconcentration 24 hours after admission is associated
with increased morbidity. Lactated Ringer solution should be run at 250 to 500 mL/h
within the first 12 to 24 hours of admission, and urine output should be closely
monitored.31,32
Many scoring systems have been proposed to predict which patients are at risk
for complicated pancreatitis. The classic Ranson’s criteria on admission and at
48 hours may delay recognizing severe pancreatitis. The Bedside Index for Severe
Acute Pancreatitis has been described as easier to use, whereas The Revised
Atlanta Classification incorporates both physiologic and radiologic findings. Unfor-
tunately, no system has proven to be all inclusive and therefore the close evalua-
tion of fluid losses, SIRS, and presence of organ dysfunction is absolutely
imperative.31 Radiologic evaluation of pancreatitis is best if performed at least
72 hours after presentation to get a complete evaluation of pancreatic inflamma-
tion and necrosis.32
Source control
In the setting of gallstone pancreatitis, clearance of CBD with ERCP is strongly recom-
mended within 24 hours. Although the evidence is not as strong as it is in the presence
of cholangitis, most recommendations include ERCP.31,33 If on-going signs of
obstruction are present, surgical exploration of the common bile duct may be indi-
cated. Early cholecystectomy (within 48 hours) is recommended in mild gallstone
pancreatitis because waiting until complete symptoms and chemical resolution is un-
necessary. Aboulian and colleagues34 found in their randomized study that early cho-
lecystectomy was not associated with increased technical difficulty or complications
but resulted in a shorter hospital length of stay. In addition, offering an interval chole-
cystectomy was associated with a significant increase in biliary readmissions (18%)
and is therefore not recommended.35
Antibiotics
Unlike other intra-abdominal infectious processes, this disease is not initially second-
ary to bacterial infection. Unless signs of cholangitis are present, routine use of anti-
biotics in pancreatitis is not recommended. Prophylactic antibiotics, even in severe
necrotizing pancreatitis, do not prevent progression of sterile necrosis to infected ne-
crosis and are therefore not recommended.8 Ten percent of patients with pancreatitis
will ultimately become infected. This number increases to between 30% and 70% if
necrosis is present.1,32
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Intra-abdominal Infections 1329
Source control
With a diagnosis of infected pancreatitis, traditionally this was an indication for oper-
ative intervention. Clearly, there is a need for intervention, but image-guided catheter
placement with upsizing as necessary has proven to be effective and safe and may be
able to successfully avoid surgery in 50% of patients. Multiple approaches have been
successfully attempted, including laparoscopic anterior/retroperitoneal or percuta-
neous radiologic-guided catheter placement followed by endoscopy through the tract.
Ultimately, surgical debridement may be needed to remove infected, necrotic tissue
if catheter drainage does not appear to be providing adequate SC. Delayed interven-
tion in pancreatitis, unlike other acute IAI, is associated with improved morbidity. Rec-
ommended surgical approach is midline or subcostal and approaches the lesser sac
through the gastrocolic ligament. The initial goal of surgery is to obtain aggressive SC
and close the abdomen with closed suction drains. Open packing and planned rela-
parotomies are associated with significant mortality.32
Antibiotics
If infection is suspected, broad-spectrum antibiotics should be initiated and CT or
US-guided fine-needle aspiration should be obtained for culture material. Carbape-
nems, fluoroquinolones, metronidazole, and high-dose cephalosporins have best
penetrance into pancreatic tissue.31
Diverticulitis
The frequency of diverticulosis within the Western population increases with age. Thir-
ty percent of people have diverticulosis by the age of 60. Ten to 25% of these patients
will ultimately develop diverticulitis.36 Diverticulitis is an inflammation and ultimately a
microperforation of a diverticula-containing segment of colon. With the great variation
in presentation and clinical course, it is imperative to appropriately classify patients.
CT scan of the abdomen and pelvis with oral, IV, and rectal contrast is the examination
of choice for patients with suspected diverticulitis.36 The traditional classification was
based on clinical and operative findings but, with the widespread use of CT scanning,
a modified classification has been proposed (Table 5).
Table 5
Hinchey classification with modification
Hinchey Modified
Classification Hinchey
Uncomplicated I Pericolic abscess or Ia Confined pericolonic
phlegmon inflammation,
phlegmon
Ib Confined pericolonic
abscess
Complicated II Pelvic, intra- II Pelvic, distant intra-
abdominal or abdominal or
retroperitoneal retroperitoneal
abscess abscess
III Generalized purulent III Generalized purulent
peritonitis peritonitis
IV Generalized fecal IV Fecal peritonitis
peritonitis
Data from Sartelli M, Viale P, Catena F, et al. 2013 WSES guidelines for management of intra-
abdominal infections. World J Emerg Surg 2013;8:3; and Moore LJ, Moore FA, Jones SL, et al. Sepsis
in general surgery: a deadly complication. Am J Surg 2009;198:868–74.
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1330 Shirah & O’Neill
Source control
The ideal approach of SC in complicated diverticulitis has been widely debated
intensely studied, and ultimately, undergone significant changes in management.
Traditional treatment of complicated diverticulitis was managed by surgical interven-
tion up until the 1990s.37 Current treatment paradigm has shifted to aggressive med-
ical support and, if necessary, nonurgent surgical intervention. Approximately 15% of
patients with acute diverticulitis will develop a pericolonic or intramesenteric ab-
scess.36 Abscesses less than 3 cm have been found to safely resolve with antibiotics
alone. Percutaneous drainage is recommended for accessible abscesses greater than
4 cm.10,38 The ultimate goal for those who are amenable to drainage with percuta-
neous catheters is to avoid emergency surgery.36 In fact, nonoperative management
has been found successful in 91% of patients with complicated diverticulitis, including
patients with large pneumoperitoneum and large abscesses.37,39 Failure of nonoper-
ative management ultimately requires segmental colectomy. Laparoscopic approach,
even for complicated diverticulitis, has been shown as safe even in the setting of
longer operative times, demonstrating fewer complications, less pain, and shorter
hospital stay.40,41
What is not debated is that emergency operative intervention is required for free
perforation with peritonitis (Hinchey III or IV) or the presence of hemodynamic insta-
bility. Immunocompromised patients are more likely to present with perforation and
failed medical management necessitating a lower threshold for urgent surgery. Histor-
ically, a Hartmann procedure was standard and necessary. In certain clinical sce-
narios, primary resection and anastomosis have been proven safe even with diffuse
peritonitis.12 A recent randomized trial compared the Hartmann procedure to resec-
tion and primary anastomosis (PA). The PA group was found to have less risk of
serious complications, lower in-hospital costs, decreased operating times, and ulti-
mately, decreased hospital length of stay.42 Another less invasive treatment option
that has been proposed is laparoscopic lavage. Laparoscopic lavage has also been
proven safe and will be compared with conventional management in the upcoming
“LADIES” trial.43
Antibiotics
Uncomplicated diverticulitis has a standard treatment with bowel rest and antibiotics
for 7 to 10 days, which is successful in 70% to 100% of patients.10,36,44 Classically, a
combination of quinolone and metronidazole are used, but recently Ertapenem, a
carbapenem, has been increasingly used and may provide a well-tolerated
monotherapy.44
The length of treatment has come into question in the literature. A recent study ran-
domized patients with uncomplicated sigmoid diverticulitis to a 4-day versus the tradi-
tional 7-day course of antibiotics and found no significant differences in recurrence
rate at 1 month and at 1 year. The 4-day group had a significantly shorter hospital
length of stay.44 In the face of increased antibiotic resistance, Chabok and col-
leagues45 took the next step and questioned the need for antibiotics at all in uncom-
plicated acute diverticulitis. In an interesting multicenter randomized trial, patients with
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Intra-abdominal Infections 1331
SUMMARY
IAI arise from many sites and range from a moderate nuisance to life-threatening.
Prompt identification, diagnosis, and treatment allow optimal patient outcomes.
Resuscitation from shock, early appropriate antibiotic administration, and control of
the source of infection are necessary components of a 3-pronged approach. Initial
antibiotic administration should be broad spectrum and tailored to the most likely
pathogen and then narrowed to the best agent for the appropriate duration. SC may
be obtained using radiographically placed percutaneous or traditional operative
drains; the choice depends on the anatomic site, site accessibility, and the patient’s
clinical condition. Patient-specific factors (advanced age and chronic medical condi-
tions) as well as disease-specific factors (health care–associated infections and
inability to obtain SC) combine to affect patient morbidity and mortality.
REFERENCES
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13. Moore LJ, Moore FA, Jones SL, et al. Sepsis in general surgery: a deadly compli-
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14. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment
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2018. Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2018. Elsevier Inc. Todos los derechos
reservados.