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Acs0818 Intra Abdominal Infection
- 1. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 1
18 INTRA-ABDOMINAL INFECTION
Robert G. Sawyer, M.D., F.A.C.S., Jeffrey S. Barkun, M.D., F.A.C.S., Robert Smith, M.D.,T Chong, M.D., and George Tzimas, M.D.
ae
Recognition and Management of Intra-abdominal Infection
The basic principles of rapid diagnosis, timely physiologic sup- whereas a stable patient presenting with a chronic complaint can
port, and definitive intervention for intra-abdominal infections be evaluated in a more deliberate fashion.The specifics of the pre-
have remained unchanged over the past century. Specific manage- senting episode (e.g., the onset, location, and nature of the pain
ment of these conditions, however, has been transformed of late as and any changes in bowel habits) are undeniably crucial, but the
a result of numerous advances in technology. Improved radiologic patient’s medical and surgical histories, as well as any previous
and laboratory techniques have led to more precise preoperative similar illnesses, are equally critical. Many medical problems and
diagnoses, and newer procedures have led to treatment algorithms therapies are associated with abdominal pain or discomfort, and
that cause less morbidity and permit faster recovery. Whereas the an accurate accounting of previous surgical manipulation of the
pathophysiology of these infections remains largely unchanged, abdomen is vital for refining the differential diagnosis, as well as
their management is now marked by an ever-growing complexity. for prioritizing further tests.The question of whether a patient has
It is no longer true that the diagnosis of intra-abdominal infection, presented with similar symptoms before (particularly if those
even in association with a perforated viscus, necessitates urgent symptoms led to a diagnosis) may be important for determining
exploration, but it remains the case that decisions regarding the the timing of any intervention, as well as for putting the current
ultimate course of action for any individual patient are solely the complaint in the context of an ongoing condition. In fact, many
responsibility of the surgeon. patients arrive for medical treatment with a strong (and frequent-
ly correct) concept of the nature of their disease.
Clinical Evaluation PHYSICAL EXAMINATION
Once the history has been obtained, a thorough physical assess-
HISTORY
ment is performed, with the emphasis on the abdomen, the pelvis
The general approach to a patient sus- (including the vagina), and the rectum. The usual sequence—
pected of having an intra-abdominal inspection, auscultation, percussion, and palpation—should be
infection is much like that to a patient followed as traditionally taught.This sequence need not be exten-
with any other acute surgical condition. sively reviewed here; however, certain points should be empha-
Specific approaches to various intra- sized. With the advent of laparoscopy, inspection must include a
abdominal infections are addressed in more detail elsewhere [see careful search for scars indicating previous operations, given that
Infections of the Upper Abdomen and Infections of the Lower any laparoscopic procedure can be undertaken by way of a variety
Abdomen, below]. of trocar sites. Auscultation, though occasionally helpful, is also
The first step is an accurate history.To begin with, cases of peri- probably the least specific form of examination. Percussion is valu-
tonitis are broadly classified as primary, secondary, or tertiary; this able for assessing tenderness, as well as for differentiating abdom-
classification provides a useful framework for suggesting general inal distention caused by intraluminal gas or free air (signaled by
approaches to treatment. Primary peritonitis arises spontaneously, tympany) from that caused by fluid in the peritoneum, such as
without a demonstrable source of contamination, and is generally ascitic fluid or blood (signaled by dullness).
treated with antibiotics alone; an example is spontaneous bacteri- Proper and humane assessment of the abdomen for tenderness
al peritonitis in the setting of ascites. Secondary peritonitis is via palpation can be learned only through extensive experience.
caused by a breach in the GI tract that leads to contamination of Gaining the patient’s trust is fundamental: an anxious or dis-
a normally sterile space. Control of the source of infection via tressed examinee may respond in a hypersensitive manner, there-
drainage, resection, diversion, or some combination thereof is by hindering the acquisition of information. An individualized
imperative for optimizing outcome. Tertiary peritonitis is a poorly approach is essential as well. Palpation should not be performed in
defined entity associated with recurrence of intra-abdominal infec- a uniform manner from patient to patient; rather, the amount of
tion after the treatment of secondary peritonitis. It frequently fea- tenderness present ought to be judged by the degree of pressure
tures a diffuse infection in a critically ill patient and may be caused or indentation required to cause a given patient significant dis-
by any of a long list of nosocomial pathogens (e.g., Pseudomonas comfort. In the setting of severe abdominal pain, elicitation of
aeruginosa, Staphylococcus aureus, and Candida albicans). Manage- rebound tenderness by means of deep palpation followed by rapid
ment of tertiary peritonitis is complex and must be individualized release of pressure usually does not improve diagnostic accuracy
for each patient. or alter subsequent evaluation and should therefore be discour-
The acuteness and severity of the presenting symptoms may aged. Finally, administration of small doses of narcotics to patients
help localize the origin of the infection. More important, however, with abdominal pain is unlikely to alter an experienced examiner’s
they allow appropriate triage of these patients, who are frequently diagnostic ability for the worse.
seen in a crowded emergency department. For example, a patient Occasionally, a young patient whose history and physical exam-
with sudden onset of severe abdominal pain and physiologic ination (including vital signs) fit the classic clinical picture of
derangement must take precedence over almost all other patients, appendicitis may be taken to the OR without further assessment.
- 2. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 2
Recognition and Management of
Intra-abdominal Infection
Patient has suspected intra-abdominal
infection
Obtain history, including previous surgical
manipulation of abdomen.
Perform physical examination, focusing on
abdomen, pelvis and vagina, and rectum
(inspection, auscultation, percussion, palpation).
Order blood tests as appropriate.
• General tests of systemic response to
infection
• Specific tests to localize source or focus
of infection
On occasion, a young patient with classic
presentation of appendicitis may be taken to
OR without blood tests or imaging.
Order diagnostic imaging as appropriate.
Patient has “certain“ History and physical exam warrant Patient has upper abdominal All other patients
appendicitis exploration of abdomen for peritonitis, pain, elevated bilirubin level
but confirmation (free air) is needed or liver function test results, Order abdominal and pelvic
first; or index of suspicion for or history of biliary tract CT scans.
Resuscitate, give antibiotics,
peritonitis is very low disease Treat specific infection as
and take to OR.
appropriate [see Figure 9].
Order upper abdominal US.
Obtain plain abdominal films, including
upright chest film. Treat specific infection as
appropriate [see Figure 1].
Free peritoneal air is present No free peritoneal air is present, No free peritoneal air is present,
and index of suspicion for but index of suspicion for
Resuscitate, give antibiotics, peritonitis is low peritonitis is high
and take to OR.
Discharge from surgical care. Order abdominal and pelvic CT
scans (see above, right).
- 3. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 3
Practically speaking, however, almost all patients with significant abnormalities, and inflammatory changes. Now that significant
intra-abdominal infections undergo blood tests, and most also intra-abdominal infections—perhaps even in the setting of a per-
undergo some sort of radiologic evaluation. forated viscus—are no longer automatically considered to man-
date operative intervention, the ability of CT scanning to identify
the source and assess the chronicity of an infection is critical to
Investigative Studies effective modern management. Multiple common conditions have
now been defined for which an adequate CT scan allows nonop-
LABORATORY TESTS
erative management either as definitive therapy (e.g., expectant
Blood work can be divided into two treatment of a simple perforated duodenal ulcer) or as a means of
categories: (1) general tests designed to temporizing (e.g., percutaneous drainage of a periappendiceal or
assess the systemic response to infection peridiverticular abscess). In addition, in experienced hands, a neg-
and (2) specific tests designed to localize ative CT scan of the abdomen and the pelvis virtually excludes
the source or site of infection.The former any significant acute surgical illness.
category includes serum chemistries and hematology studies. The It must be noted, however, that a CT scan is not necessary in
latter category commonly includes amylase and lipase concentra- all patients with abdominal pain, and the decision whether to
tions (in patients suspected of having pancreatitis), bilirubin levels obtain one should be made on the basis of predefined guidelines
and liver function tests (to evaluate hepatic or biliary tract disease), or with the input of a general surgeon. When the need for opera-
and lactate levels (when an ischemic bowel is suspected). These tive intervention has already been determined, as in a classic case
tests are discussed further elsewhere, in connection with specific of appendicitis, imaging is unnecessary. In addition, some patients
infections (see below). Urinalysis, of course, is necessary whenever with an intra-abdominal infection amenable to nonoperative man-
urinary tract infection or urolithiasis is a possibility. agement (e.g., simple, mild diverticular disease that can be treat-
ed with oral antibiotics on an outpatient basis) do not necessarily
DIAGNOSTIC IMAGING
benefit from CT scanning.
The use of various radiologic studies In selected cases, other forms of imaging may be used.
in the diagnosis of intra-abdominal infec- Magnetic resonance imaging, though usually more difficult to
tion continues to evolve rapidly. Outside obtain in an emergency and logistically more complicated than
the setting of trauma, it is now very rare CT scanning, yields excellent tomographic images and has the
for patients to undergo operations or added benefit of imaging vascular structures and the pancreatico-
other major interventions without first biliary tree more precisely. Nonetheless, MRI has no significant
undergoing imaging. At one time, plain role in the evaluation of acute peritonitis. Nuclear medicine scans
films of the abdomen (including an and fluoroscopic studies, though occasionally useful adjuncts for
upright chest film) were routinely obtained whenever a significant evaluating biliary tract and upper GI disorders, also play no role
intra-abdominal infection was suspected, principally to detect free in the assessment of acute peritonitis.
peritoneal air, bowel obstruction, or fecaliths. Abdominal plain
films proved to lack sensitivity, specificity, and anatomic definition
in this setting and consequently have, in many cases, been sup- Options for Intervention
planted by abdominal and pelvic computed tomographic scanning. Once an intra-abdominal infection is diagnosed, there are mul-
There are, however, two circumstances in which plain films of the tiple options for intervention. Not infrequently, an approach com-
abdomen remain a reasonable first study for a patient with sus- bining several modalities is warranted. Occasionally, administration
pected peritonitis: (1) when the surgeon has almost decided, on the of systemic antibiotics is all that is necessary (or practical), as in
basis of the history and physical examination, to explore the patient cases of spontaneous primary bacterial peritonitis or of multiple
yet needs confirming evidence of perforation (i.e., free air), and (2) infected fluid collections that are small but too numerous to drain.
when the index of suspicion for peritonitis is so low that the plain Single abscesses, particularly those without thick or particulate
film studies are intended to rule out an unexpected positive finding contents, can be adequately treated with simple aspiration and a
and will not be followed by an abdominal CT scan if negative. short course of antibiotics. For discrete infected fluid collections in
Ultrasonography for intra-abdominal infection is useful only for almost any setting, placement of a percutaneous indwelling drain
focused examination of specific organ systems; it is inferior to CT (most commonly under radiologic guidance) is currently the treat-
scanning for generalized surveillance of the abdomen because of ment of choice. Operative management, either open or laparo-
the inability of sound waves to penetrate gas in the bowel. By far scopic, is employed for resection of damaged or inflamed and
the best-delineated use of ultrasonography is in the diagnosis of unsalvageable organs, diversion of enteric contents, or drainage of
liver and biliary tract disease, for which its ability to demonstrate collections that are too thick or numerous for percutaneous
cholelithiasis makes it superior to CT and for which it should drainage. Beyond these general guidelines, therapy for specific
almost always be the first radiologic test in the appropriate cir- intra-abdominal infections must be individualized (see below).
cumstances (e.g., a classic history of biliary colic or an elevated
serum bilirubin level). Ultrasonography also visualizes the spleen,
the kidneys, and the gynecologic pelvic organs well and has the Infections of the Upper Abdomen
additional benefit of using no ionizing radiation. Biliary tract and pancreatic infections present as a systemic sep-
The abdominal and pelvic CT scan, appropriately, has become tic response or as infections localized in the upper abdomen [see
the key diagnostic test for evaluating patients with suspected peri- Figure 1].Typical findings include abdominal pain, a tender upper
tonitis. This modality is widely available throughout much of the abdominal mass, fever and leukocytosis, and jaundice. Various
world, and newer scanners yield significantly higher resolution combinations of these symptoms may occur, but it is convenient
than older ones, with reduced scanning times and radiation expo- to consider three common clinical presentations. In each of the
sure. CT is highly sensitive for free air, fluid collections, bowel wall presentations, one or two symptoms dominate: (1) upper abdom-
- 4. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 4
Patient has clinical signs of upper abdominal infection,
or serum bilirubin or liver function tests are suggestive
Order abdominal US.
Upper abdominal pain and Fever and jaundice are Fever and abdominal
fever are dominant findings dominant findings mass are dominant
findings
US is normal Stones are seen in Evidence of acute Patient has choledocholithiasis
gallbladder without cholecystitis is apparent or biliary dilation consistent
evidence of with cholangitis
Consider nonbiliary
cholecystitis or If US is equivocal,
disease, especially Resuscitate, and give antibiotics.
choledocholithiasis consider nuclear
acute pancreatitis.
medicine scanning. Consider emergency
Consider abdominal Consider other endoscopic, radiologic, or
Resuscitate; take to OR
and pelvic CT scans. diagnoses. operative biliary drainage.
for urgent cholecystec-
Evaluate for elective tomy if patient is medi-
cholecystectomy. cally fit, or perform
percutaneous drainage
if not.
Patient has liver mass, with Patient has signs of Patient has splenic mass,
or without abscess pancreatic infection with or without abscess
Obtain travel history and Confirm diagnosis via abdominal Confirm diagnosis via abdominal
serologic tests to rule out amebic CT scan. CT scan.
and echinococcal abscesses. Resuscitate, and give antibiotics if Resuscitate, and give antibiotics.
For bacterial abscesses, infection is probable or necrosis Treat with splenectomy or
resuscitate, give antibiotics, is noted on CT. percutaneous drainage.
seek sources, and perform Discrete fluid collection: Aspirate
percutaneous drainage. or drain.
Phlegmon: Attempt medical
management. If unsuccessful and
percutaneous aspirate positive
for bacteria, perform open
Figure 1 Algorithm outlines approach to patient with drainage.
suspected upper abdominal infection.
inal pain and fever, (2) fever and jaundice, and (3) an upper abdominal ultrasound examination: an abnormal image of the
abdominal mass and fever. These clinical findings signal the need gallbladder or bile ducts supports a biliary etiology [see Figure 2].
for a battery of screening tests, including a complete blood count The differential diagnosis should include acute cholecystitis,
(CBC); routine blood tests of liver function; determination of biliary colic, acute pancreatitis, and acute cholangitis, each of
serum amylase level, prothrombin time (PT), and partial throm- which requires specific management [see Table 1]. For example, ini-
boplastin time (PTT); blood culture; chest and abdominal x-rays; tial management of biliary colic and mild acute pancreatitis is usu-
and abdominal ultrasonography. When considered together, the ally nonoperative, whereas severe acute cholangitis and acute
clinical findings and the test results allow early differentiation of cholecystitis are treated by means of surgical, endoscopic, or radi-
the three most common disease entities: acute cholecystitis, acute ologic intervention (see below). Clinical features and blood test
cholangitis, and acute pancreatitis. results, though helpful, may be inconclusive.The abdominal ultra-
sonogram may provide specific clues. Stones appear in biliary colic
UPPER ABDOMINAL PAIN AND FEVER
[see Figure 2]; stones and thickening of the gallbladder wall, in
Patients with upper abdominal sepsis may present with epigas- acute cholecystitis; gallstones and dilatation of the common bile
tric or right upper quadrant pain and fever. Only two thirds of duct (CBD), in acute cholangitis; and pancreatic enlargement and
these patients admitted with a working diagnosis of acute chole- sonolucency, in pancreatitis.
cystitis have acute biliary inflammation.1 In some patients, non-
surgical conditions (e.g., pneumonia, acute hepatitis, familial Pancreatitis
Mediterranean fever, herpes zoster of the intercostal nerves, and Diagnosis Differentiating acute pancreatitis from acute
gastroenteritis) can be distinguished clinically from biliary disease. cholecystitis may be difficult.The serum amylase level lacks speci-
The most important screening test for acute biliary infection is the ficity, but if the clinical findings suggest acute pancreatitis, an ele-
- 5. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 5
Table 2—Ranson’s Early Objective Signs
of Severity of Acute Pancreatitis2
On Admission After Initial 48 Hours
Age > 55 yr Serum Ca2+ < 8 mg/dl
Glucose > 200 mg/dl Arterial PO2 < 60 mm Hg
WBC > 16,000/mm3 Base deficit > 4 mEq/L
LDH > 350 IU/L BUN increase > 5 mg/dl
Hematocrit fall > 10%
AST > 250 Sigma Frankel U/dl
Fluid sequestration > 6,000 ml
Note: < 3 signs = mild pancreatitis; ≥ 3 signs = severe pancreatitis.
AST—aspartate aminotransferase—BUN—blood urea nitrogen—PO2—oxygen tension—
WBC—white blood cell
acute pancreatitis.5,6 Unless clinical findings and the results of bio-
chemical tests and ultrasonography are unequivocal, a contrast-
enhanced spiral abdominal CT scan is usually performed to estab-
lish the diagnosis and stage acute pancreatitis. It has been sug-
gested, however, that CT scanning should be reserved for patients
with clinically suspected severe acute gallstone pancreatitis, on the
grounds that the results would not change the recommended
course of action in other patients.7 Occasionally, a very mild pan-
creatitis may give rise to no findings on a CT scan, and a normal
technetium-99m (99mTc)–labeled HIDA (lidofenin) scan may help
differentiate this condition from acute cholecystitis.
Figure 2 Abnormal abdominal ultrasound examination shows Treatment Given that pancreatitis encompasses a wide
calculi in gallbladder casting shadows on underlying liver tissue. range of diseases with varying degrees of severity, treatment must
be individualized for each patient. Possible therapeutic strategies
range from outpatient management with temporary dietary mod-
vated level of serum amylase clinches the diagnosis. In one study, ification (for very mild cases) to open debridement and complex
the initial laboratory results in 100 patients with acute pancreati- intensive care (for severe cases). It is therefore useful to base pos-
tis were compared with those in 100 patients with acute abdomi- sible treatment approaches in particular cases on the cause and
nal pain caused by acute cholecystitis, perforated peptic ulcer, or severity of the pancreatitis.
acute appendicitis.2 The serum amylase concentrations were ele- Gallstone pancreatitis. Standard therapy for gallstone pancreatitis
vated in 95% of patients with acute pancreatitis but were normal includes I.V. fluids and narcotic analgesics. Nasogastric suction is
in 95% of patients with acute abdominal pain from other causes. useful in patients with significant ileus but need not be used rou-
These concentrations peak within the first 48 hours and are tinely.8 The use of systemic antibiotics is controversial; they are of
almost always elevated in biliary pancreatitis3; in fact, a serum benefit in the 10% to 34% of patients who have concomitant
amylase concentration above 1,000 U/L strongly suggests a biliary cholangitis.9 Other treatments suggested previously—including
origin of the pancreatitis.4 In addition, determination of serum total parenteral nutrition (TPN) and various pharmacologic agents
lipase levels has been shown to be more specific than and at least (e.g., cimetidine, somatostatin, glucagon, and insulin)—have not
as sensitive as determination of amylase levels for the detection of proved useful in all cases of gallstone pancreatitis.10 Continuous
intraduodenal infusion of an elemental diet has reduced exocrine
pancreatic secretions in animal experiments.11 Furthermore, enter-
Table 1—Diagnostic Indicators of al feeding has been shown to be beneficial and to decrease disease
Upper Abdominal Pain and Fever severity in patients with acute pancreatitis.12-14
In clinical practice, the need for further treatment depends on
Acute Acute the severity of the acute pancreatitis. Severity determines both the
Biliary Colic
Cholecystitis Pancreatitis risk of sepsis, which governs outcome, and the risk associated
with early cholecystectomy [see 5:21 Cholecystectomy and Bile Duct].
Short: 40%
Duration
< 1 hr
Persistent Persistent The most commonly used clinical prognostic index in North
America was developed by Ranson and reliably defines the sever-
Pathogenesis Visceral Somatic Retroperitoneal
ity of pancreatitis [see Table 2].2 In mild pancreatitis, one or two
Guarding and Guarding and Ranson signs are present; in more severe pancreatitis, three to five
Signs Tender
spasm spasm signs are present; and in very severe pancreatitis, more than five
Laboratory tests signs are present. This distinction serves to stratify further treat-
Liver function tests Occasionally Abnormal Abnormal ment. Other clinical prognostic scores, such as the APACHE-II
abnormal (Acute Physiology and Chronic Health Evaluation II) and
Serum amylase Normal Normal or slightly Increased APACHE-III scores and the Balthazar score, have been shown to
increased
Leukocyte counts Often normal Increased Increased
possess discriminatory value in identifying patients at high risk for
complications.15,16
- 6. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 6
Mild pancreatitis usually subsides within 1 week of onset. Most cholecystectomy has facilitated this approach safely without pro-
surgeons defer cholecystectomy until then; urgent operation should longing hospital stay.
be reserved for cases complicated by biliary sepsis, and it may Severe pancreatitis. Patients with three or more Ranson signs are
reveal acute cholecystitis in as many as 31% of patients.17 at particular risk for pancreatic sepsis.28 Repeated clinical and
An attack of acute gallstone pancreatitis is initiated by obstruc- radiologic evaluation is required in these patients to ensure early
tion at the confluence of the lower end of the CBD and the pan- detection of complications, because the outcome of an episode of
creatic duct by a stone or by edema at the ampulla of Vater result- pancreatitis depends on whether sepsis supervenes. When infec-
ing from stone migration. These stones may be found and tion occurs, operative debridement and drainage are required [see
removed in 63% to 78% of patients who undergo operation with- Fever and Abdominal Mass, below]. Some surgeons have attempt-
in 72 hours of admission17-19 [see 5:22 Biliary Tract Disease]; by ed to alter the course of severe disease by early operation; howev-
contrast, they are present in only 3% to 33% of patients explored er, urgent operation is associated with a high mortality in patients
after the first week.18-22 A randomized trial exploring the optimal with more than three Ranson signs.19,21,23,29 To avoid the mortali-
timing of surgery for gallstone pancreatitis showed that early ty associated with early operative intervention, some clinicians
surgery (within 48 hours after admission) was not associated with advocate early diagnosis by ERCP [see Figure 3], followed by bil-
a significant increase in morbidity or mortality in patients with iary decompression by means of endoscopic sphincterotomy and
mild pancreatitis but did not change prognosis.23 stone extraction. In a randomized trial comparing early ERCP and
Endoscopic retrograde cholangiopancreatography (ERCP). Early sphincterotomy with conservative therapy in patients with severe
ERCP and sphincterotomy [see 5:18 Gastrointestinal Endoscopy] has acute pancreatitis, ERCP and sphincterotomy decreased morbid-
been suggested as an alternative to surgery of the CBD in patients ity from 61% to 24% and lowered mortality from 18% to 4%.24
with mild pancreatitis. However, randomized trials comparing The results of this trial, however, have been the subject of debate,
endoscopic treatment with conservative treatment within the first and the success of this approach has been attributed by some
72 hours in patients with mild pancreatitis did not find that urgent authors to the treatment of a concomitant cholangitis rather than
endoscopic sphincterotomy improved outcome in this group of of the actual pancreatitis.25 A well-conducted trial that excluded
patients.24,25 Other studies showed that delaying surgery beyond 6 patients with concomitant cholangitis was published in 1997;
weeks may lead to a 32% to 57% risk of recurrent pancreatitis.26,27 unfortunately, this trial was unable to answer the question defini-
Therefore, cholecystectomy and cholangiography should be tively, because too few patients with severe pancreatitis had been
delayed only until just before patients are discharged from the hos- recruited.30 It appears that ERCP is warranted mainly in cases of
pital, 5 to 15 days after the onset of symptoms. Laparoscopic acute pancreatitis complicated by cholangitis and biliary sepsis.31,32
Use of peritoneal lavage in early severe pancreatitis was advo-
cated in one study to decrease morbidity and mortality.33 Use of
standard lavage over a 2-day period did not improve patient out-
come, but use of peritoneal lavage for 7 days (long peritoneal
lavage) yielded some improvement in outcome.34 Early use of
antibiotics and selective decontamination have been proposed as a
means of reducing septic complications, but neither has convinc-
ingly or reproducibly been shown to improve prognosis.35,36
Although prophylactic antibiotics have been shown to decrease the
rate of infectious complications in severe acute pancreatitis, they
have not clearly been shown to reduce overall disease mortali-
ty.35,37-40 Attempts have been made to modulate the initial systemic
inflammatory response seen in early severe acute pancreatitis to
reduce the risk of subsequent infection and improve overall prog-
nosis; somatostatin has exhibited limited success in this regard.41,42
Another drug in this category, the platelet-aggregating factor
(PAF) inhibitor lexipafant, initially yielded promising results in
animal models43,44 and in phase II trials45; however, a 2001 trial
using the same drug did not find it efficacious for treating severe
acute pancreatitis.46
Acute Cholecystitis
Diagnosis Acute cholecystitis is the most common diagnosis
in patients presenting with upper abdominal pain and fever and is
characterized by the clinical finding of a midinspiratory arrest on
palpation of the right upper quadrant (Murphy’s sign). As noted
(see above), with the widespread availability of ultrasonography,
acute cholecystitis can usually be diagnosed rapidly on the basis of
the findings of gallbladder wall thickening, pericholecystic fluid,
and stones. Occasionally, more complex cases must be evaluated
Figure 3 Endoscopic retrograde cholangiopancreatography with nuclear medicine scanning to look for cystic duct obstruc-
shows distal CBD stone in acute pancreatitis. Papillotome has tion. Concurrent acute obstructive cholangitis must also be con-
been placed through sphincter of Oddi in preparation for endo- sidered in all patients with acute cholecystitis. Supportive labora-
scopic sphincterotomy. tory data include a high serum bilirubin level and an increased
- 7. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 7
Table 3—Comparison of Acute Cholecystitis
and Emphysematous Cholecystitis
Emphysematous
Acute Cholecystitis
Cholecystitis
Gender 70% male 70% female
Stones 70% 90%
Bile culture positive 95% 66%
Clostridia found 46% 1.2%
Gangrenous gallbladder 75% 2.5%
Perforation of gallbladder 20% 4%
Mortality at age < 60 yr 15% 1.5%
Pathogenesis Ischemia, obstruction Obstruction
sustained narcotics therapy). In addition, focal inflammation may
cause biliary colonization or may activate coagulation factor XII,
thereby causing severe injury to the blood vessels in the gallblad-
der muscularis and serosa. A high index of suspicion is necessary.
Acute acalculous cholecystitis should be considered in any post-
operative or acutely ill patient with upper abdominal pain and
Figure 4 Air outlines gallbladder and bile ducts in emphysema-
fever or with unexplained fever and leukocytosis. It is particularly
tous cholecystitis.
common 2 to 4 weeks after injury. The diagnosis is confirmed by
findings on abdominal ultrasound examination [see Figure 5] and
99m
alkaline phosphatase level. Positive blood cultures and dilated Tc-labeled HIDA scanning coupled with infusion of cholecys-
biliary ducts on abdominal ultrasonography usually confirm the tokinin and morphine.52-54
diagnosis.
Emphysematous cholecystitis. An uncommon and insidious vari- Treatment Standard treatment of acute cholecystitis consists
ant of acute cholecystitis, emphysematous cholecystitis is charac- of I.V. fluid administration, analgesics, and cholecystectomy.
terized by gas in the gallbladder lumen or wall or in the perichole- Although the timing of operation is somewhat controversial in
cystic soft tissue and biliary ducts secondary to gas-forming bac- ordinary acute cholecystitis, cholecystectomy should be per-
teria.The key to the diagnosis is the presence of air on abdominal formed at the earliest opportunity [see 5:21 Cholecystecomy/Bile
x-ray [see Figure 4] or ultrasound examination. Three stages of Duct]. This approach has been confirmed by at least one ran-
emphysematous cholecystitis have been defined: (1) gas is seen domized trial comparing early with late laparoscopic cholecystec-
only in the lumen of the gallbladder, (2) a ring of gas is identified tomy.55 The delayed-surgery group had a greater need for conver-
in the wall of the gallbladder, and (3) gas is seen in the tissues adja- sion to open cholecystectomy (23% versus 11%), as well as a longer
cent to the wall. Compared with ordinary acute cholecystitis,
emphysematous cholecystitis is associated with a fivefold increase
in the risk of gallbladder perforation, as well as a 10-fold increase
in mortality in patients younger than 60 years [see Table 3].47
Studies from the 1960s noted an increased risk of gangrene and
perforation of the acutely inflamed gallbladder in patients with
diabetes mellitus.48,49 The mortality for acute cholecystitis was also
shown to be five to 10 times higher in patients with diabetes than
in other patients. Later studies, however, did not show an in-
creased mortality in patients with both diabetes and acute chole-
cystitis.50,51 Nevertheless, one third of patients with emphysema-
tous cholecystitis also have diabetes.This factor, coupled with the
current tendency to perform cholecystectomy early in most pa-
tients with acute cholecystitis, may account for the disparity be-
tween previous studies and later reports.
Acute acalculous cholecystitis. Another variant of acute cholecys-
titis is acalculous cholecystitis; though still rare, it became more
common from the 1950s through the 1990s.This disease was orig-
inally described as occurring after surgical treatment of unrelated
disease but was subsequently identified in patients with multiple Figure 5 Abnormal abdominal ultrasound examination con-
trauma, prolonged critical illness, and sepsis. Predisposing factors firms diagnosis of acute acalculous cholecystitis. When image is
include gallbladder ischemia (in patients with shock or trauma) compared with that in Figure 2, thickening of gallbladder wall
and biliary stasis (in prolonged fasting, hyperalimentation, and and intraluminal debris are obvious.
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 8
average total hospital stay and convalescence. Administration of jaundice, with pain a less marked component. Jaundice is almost
systemic antibiotics is not required; however, single-dose antibiot- always associated with obstruction of the biliary tree, either intra-
ic prophylaxis (e.g., cefazolin, 2 g I.V.) can be given at the start of hepatic or extrahepatic. The combination of fever with jaundice
the operation [see 1:1 Prevention of Postoperative Infection].56-58 always suggests acute cholangitis, a condition that can have a ful-
Some patients with acute cholecystitis are at high risk for gan- minant and fatal course if not treated promptly.
grene and perforation of the gallbladder. It is crucial to identify
these patients and perform cholecystectomy promptly because Acute Cholangitis
delay increases morbidity and mortality. Clinically, gangrene and Diagnosis If a patient presents with a temperature higher
perforation of the gallbladder in this high-risk population are sug- than 38.5º C (101.3º F) in conjunction with jaundice [see 5:3
gested by marked systemic toxicity or by the radiologic demon- Jaundice], the possibility of acute cholangitis should always be
stration of either emphysematous cholecystitis or acute acalculous investigated. If cholangitis is present, laboratory studies will reveal
cholecystitis. leukocytosis, and blood cultures will often be positive. A finding of
With ordinary acute cholecystitis, body temperature is slightly gallstones and dilated biliary ducts on abdominal ultrasound exam-
increased in most patients—averaging 37.8º C (100.04º F)—but ination supports the diagnosis. Reynolds’ pentad is present in the
is normal in 20% of patients. By comparison, the risk of gangrene full-blown syndrome.66 This syndrome includes upper abdominal
and perforation is reportedly higher in patients with marked sys- pain, fever and chills, jaundice, hypotension, and mental status
temic toxicity, manifested by a pulse rate greater than 120 changes. Acute cholangitis is usually related to choledocholithiasis,
beats/min, a body temperature higher than 39º C (102.2º F), and recent biliary manipulation, or biliary stenting performed for chron-
a left shift in the differential white blood cell count, showing more ic obstruction.
than 90% polymorphonuclear leukocytes. Unfortunately, findings Gallbladder infections. Gallbladder empyema can duplicate most
of systemic toxicity are frequently absent in elderly patients. of the findings associated with acute cholangitis. In this condition,
Patients with acute cholecystitis who have signs of systemic tox- acute cholecystitis is complicated by suppuration within the gall-
icity, emphysematous cholecystitis, or acalculous cholecystitis are bladder, which then becomes the focus of generalized sepsis. The
at high risk for gallbladder gangrene and perforation and therefore distended gallbladder may be palpable and tender.When jaundice
require prompt and aggressive treatment. I.V. antibiotic therapy is associated with empyema of the gallbladder, it is less likely to be
with a single agent (e.g., ceftriaxone, piperacillin, or a quinolone obstructive than when it is associated with acute cholangitis.True
such as ciprofloxacin or ofloxacin) can be given.59,60 Early chole- empyema of the gallbladder is rare. Treatment includes adminis-
cystectomy is the treatment of choice. Unfortunately, mortality tration of I.V. fluids, systemic antibiotic therapy, analgesics, and
may be as high as 20% to 30% with the traditional surgical ap- early cholecystectomy.
proach.61 If perforation and gangrene are not suspected but med- In some patients with jaundice and inflammation, a stone
ical illness poses a high risk of mortality from operation, nonoper- impacted in the cystic duct or in Hartmann’s pouch may suggest
ative supportive therapy may suffice. If this fails, another treatment choledocholithiasis, but preoperative diagnosis by ERCP shows an
option is cholecystostomy. extrinsic compression of the duct known as Mirizzi syndrome.Two
Percutaneous transhepatic cholecystostomy has been recom- types of Mirizzi syndrome exist. In type I, a stone impacted in the
mended for these high-risk patients,62 particularly where there is a cystic duct or Hartmann’s pouch compresses the common hepatic
low risk for perforation of the gallbladder.63 To determine the risk duct and causes inflammation, thereby leading to jaundice.
of gallbladder perforation, a risk score can be assigned to each of Treatment of this type consists of obliteration of the cystic duct and
seven findings that may be present on the preoperative abdominal careful partial cholecystectomy, with the neck of the gallbladder left
ultrasound examination: pericholecystic fluid, 7 points; distention in place. In type II, protrusion of the stone into the hepatic duct
of the gallbladder, 4 points; intraluminal membrane, 4 points; erodes the septum between the cystic duct and the hepatic duct
intraluminal debris, 3 points; round gallbladder, 3 points; sonolu- and causes a cholecystocholedochal fistula. Treatment of this type
cent zone in the gallbladder wall, 2 points; and a thick gallbladder involves internal biliary drainage to the wall of the cholecysto-
wall (> 3.5 mm), 1 point.63 A patient with a total risk score of 12 choledochal defect, usually with a choledochojejunostomy [see 5:22
or more points requires urgent cholecystectomy; one with a lower Biliary Tract Disease], in addition to cholecystectomy.67
score who does not respond to conservative treatment may be Primary sclerosing cholangitis. Patients with primary sclerosing
treated with percutaneous transhepatic cholecystostomy. cholangitis, especially those who have undergone internal or exter-
A 1997 review of 59 patients exhibiting the septic response who nal biliary drainage, are at high risk for recurrent bouts of ascend-
underwent successful percutaneous radiologic cholecystostomy ing cholangitis. Primary sclerosing cholangitis predominantly affects
defined predictors of a successful clinical outcome: localized right young males, particularly those with chronic ulcerative colitis.The
upper quadrant tenderness and gallstones, as well as gallstones diagnosis is suggested by the dominant cholestatic biochemical
and pericholecystic fluid on ultrasound examination.64 Patients profile—that is, elevation of the serum bilirubin concentration, the
with more equivocal findings may derive greater benefit from serum alkaline phosphatase level, and aspartate aminotransferase
more invasive techniques that can simultaneously be used for activity. Because of the concomitant hepatic scarring, ultrasonog-
diagnostic purposes (e.g., laparoscopy, which can even be per- raphy may not reveal the presence of dilated intrahepatic ducts.
formed at the ICU bedside65). Definitive diagnosis requires visualization of the beaded appear-
A few patients with acute cholecystitis will have concurrent ance of the biliary tree by means of cholangiography. Cholangio-
acute cholangitis. Cholecystostomy is contraindicated in these carcinoma and secondary sclerosing cholangitis in patients with
patients because of its high mortality; adequate drainage of the Caroli disease or choledochal cysts may mimic these clinical, bio-
CBD is required in such cases [see Fever and Jaundice, below]. chemical, and radiologic features, but this is an unusual occur-
rence and can be distinguished by careful follow-up of patients.
FEVER AND JAUNDICE
Currently, magnetic resonance cholangiopancreatography
An alternative presentation of upper abdominal infection (MRCP) is the imaging modality of choice for elective manage-
includes patients whose predominant symptoms are fever and ment of patients with primary sclerosing cholangitis, in that it yields
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 9
results comparable to those of ERCP without being invasive.68-71 decompression in these critically ill patients can result in a mor-
Other causes of cholangitis. An uncommon cause of recurrent tality of 30% to 40%.82-85 Furthermore, reoperation is required in
cholangitis in North America is Oriental cholangiohepatitis, which one third of survivors because important diagnostic information is
is characterized by intrahepatic duct scarring, biliary strictures, not available at the initial laparotomy. As a result, nonoperative
and hepatolithiasis, as demonstrated by cholangiography. Irrever- methods of biliary decompression, including percutaneous trans-
sible intrahepatic and extrahepatic liver damage may result be- hepatic biliary drainage (PTBD) and endoscopic sphincterotomy
cause of the overwhelming propensity of these patients to form at ERCP, have gained favor. PTBD was originally developed for
calcium bilirubinate stones. preoperative management of biliary obstruction without cholangi-
A few patients with cholangiocarcinoma causing bile duct ob- tis but has not been found to be beneficial in that setting. At pres-
struction or liver metastases causing intrahepatic bile duct obstruc- ent, it is mainly used for the management of proximal bile duct
tion may also present with a clinical picture suggestive of cholan- strictures or for the treatment of cases not amenable to ERCP; its
gitis. CT followed by MRCP can delineate the diagnosis in most complication rate is less than 10%.86
such cases.Treatment consists of I.V. antibiotics and biliary drain- Although PTBD can reduce the mortality associated with ini-
age by radiographic or surgical means. tial biliary decompression, many patients still require a definitive
operation. Consequently, endoscopic sphincterotomy [see 5:18 Gas-
Treatment Once acute cholangitis is diagnosed, resuscita- trointestinal Endoscopy] has been proposed for decompression of
tion is started with I.V. fluids and antibiotics, such as fluoro- the biliary tree in patients with acute cholangitis from choledo-
quinolones, mezlocillin, cefoperazone, or piperacillin,59,72-75 partic- cholithiasis [see Figure 6]. In a study of 82 patients with acute
ularly in patients with marked hyperbilirubinemia, in whom treat- cholangitis caused by CBD calculi, early operation was employed
ment with aminoglycosides may contribute to renal toxicity in up in 28 patients, endoscopic sphincterotomy in 43, and antibiotic
to 33% of cases [see 8:6 Renal Failure].76 These antibiotics are therapy alone in 11.87 Surgical mortality was 21% and morbidity
required to deal with the various aerobic bacteria, of which 57%; by comparison, mortality for endoscopic sphincterotomy
Escherichia coli, Klebsiella species, and enterococci are the most fre- was 5% and morbidity 28%. Others confirmed these findings.81 In
quently encountered in this setting. Anaerobes may be isolated in patients whose gallbladder is still in place, endoscopic sphincter-
15% to 30% of patients and are particularly likely to be present in otomy alone, without cholecystectomy, may even be a reasonable
diabetics, the elderly, and patients who have previously undergone long-term option. Of 23 patients whose gallbladders were left in
biliary manipulation. In patients with indwelling catheters, situ,87 only two required cholecystectomy in the 1- to 7-year fol-
Enterobacter, Pseudomonas, and Candida organisms are being isolat- low-up period: one for empyema of the gallbladder and one for
ed with increasing frequency. Indications of high risk include a recurrent cholangitis.
serum bilirubin concentration higher than 3 mg/dl. An increasingly recognized cause of cholangitis is biliary sepsis
Approximately 75% of patients with acute cholangitis respond after manipulation of the biliary tree with ERCP or PTBD.
to conservative measures,77 and supportive treatment is contin- Treatment includes I.V. fluids and antibiotics. To prevent this
ued. Subsequent investigations usually include CT followed by complication, prophylactic antibiotics should be administered be-
MRCP.78,79 Because of their invasive nature, ERCP and needle fore every biliary manipulation.88
percutaneous transhepatic cholangiography (PTC) are reserved
FEVER AND ABDOMINAL MASS
for cases in which a drainage procedure is anticipated or the infor-
mation from the MRCP is deemed inadequate. A third group of patients with upper abdominal infection pre-
For the 25% of patients who do not respond to conservative sent with fever and an upper abdominal mass identified either by
treatment, early recognition may improve their prognosis. In one clinical signs or through diagnostic imaging. Even if the mass is
study, patients who did not respond immediately to antibiotics only vaguely palpable, the mass effect is demonstrable on ultra-
had a mortality of 62%, compared with a mortality of 1.5% in sound examination of the abdomen. If the abdominal ultrasound
those who improved.80 In another study, indicators of high risk examination is technically unsatisfactory because of intestinal gas,
were an arterial blood pH less than 7.4, a serum bilirubin con- contrast-enhanced CT of the abdomen will facilitate the diagnosis.
centration above 9 mmol/L, a blood platelet count below The differential diagnosis is aided by the location of the mass.
150,000/mm3, and a serum albumin concentration lower than 3 A mass in the right upper quadrant usually indicates acute chole-
g/dl.102 These high-risk patients often have systemic hypotension, cystitis, though the possibility of a liver abscess must also be con-
mental confusion, a temperature higher than 39º C (102.2º F), or sidered. A mass in the epigastrium or in the left upper quadrant
hypothermia. Occasionally, acute cholangitis is complicated by dis- usually signals a pancreatic infection; in rare instances, a solitary
seminated intravascular coagulation (DIC), which manifests itself splenic abscess is found. Patients with an intra-abdominal abscess
as a tendency to bruise and bleed or merely as prolongation of the in the subphrenic space or an interloop abscess may also present
PT and the PTT, together with a fall in the blood platelet count in this manner.
[see 1:4 Bleeding and Transfusion]. If DIC is suspected, the diagno-
sis should be confirmed and treatment started before biliary Liver Abscess
decompression. Diagnosis In the setting of acute upper abdominal sepsis, a
Patients with refractory cholangitis who do not improve within tender mass in the right upper quadrant is most likely an enlarged,
24 hours require urgent biliary decompression. Urgent biliary inflamed gallbladder, possibly wrapped with omentum [see Upper
decompression had traditionally been accomplished via surgical Abdominal Pain and Fever, Acute Cholecystitis, above]. The next
exploration of the CBD and T-tube drainage [see 5:22 Biliary Tract most common cause of fever and abdominal mass in the right
Disease]. Cholecystostomy is an inadequate and often fatal upper quadrant, however, is liver abscess.
option in this context. Rarely, T-tube insertion alone may be life- Pyogenic abscess. Today, pyogenic liver abscess is most common-
saving in a desperately ill patient; generally, however, definitive ly related to biliary tract obstruction from gallstones or malignant
internal decompression is preferable. Unfortunately, any surgical disorders (35% of cases), and the ultrasound examination may
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 10
Figure 6 Endoscopic sphincterotomy for acute biliary decompression in acute obstructive cholangitis is shown.
At left, stone is visible in common hepatic duct, and papillotome has been passed through sphincter of Oddi. At
right, stone is held within a Dormia basket before extraction.
reveal both the abscess and the dilated biliary ducts. Previously, isoenzyme analysis, Entamoeba histolytica–specific antigen detec-
portal pyemia from diverticulitis, inflammatory bowel disease tion, or even polymerase chain reaction (PCR) is preferred to con-
(IBD), or perforated appendicitis had been the most common firm the diagnosis of amebiasis.91
cause; it now accounts for 20% of cases. Even less common is Echinococcal abscess. The diagnosis of echinococcal liver abscess
hematogenous spread via the hepatic artery. Approximately 20% can be confirmed by means of elevated indirect hemagglutination
of hepatic abscesses are cryptogenic. Ultrasonographic imaging of (IHA) titers (> 250). In the late 1980s, a combination of tests that
the liver may demonstrate lesions as small as 2 cm in the liver sub- included IHA for Echinococcus granulosus and enzyme-linked im-
stance. CT scanning, however, is superior to ultrasonography for munosorbent assay (ELISA) using E. multilocularis antigen yielded
evaluating the presence of air and abscesses as small as 0.5 cm in an 89% species-specific diagnosis of echinococcal disease.92 Later
diameter, especially near the hemidiaphragms.89 Abdominal CT is work indicated that IgG ELISA and IHA were the best tests for
also the diagnostic modality of choice in the postoperative follow-up after resection of the abscess. In patients with a favor-
patient.90 ERCP and PTC are indicated only when gallstone dis- able clinical outcome, the specific IgG level decreased toward the
ease or a biliary malignancy is the potential source of the abscess. end of the first year, though in some cases, a positive serologic
Most liver abscesses occur in the right lobe: 40% are 1.5 to 5 cm result persisted beyond 6 years.93 Diagnostic aspiration is indicat-
in diameter, 40% are 5 to 8 cm in diameter, and 20% are greater ed when a diagnosis of pyogenic or amebic abscess is in doubt, but
than 8 cm in diameter. not in echinococcal disease. Aspiration may also be beneficial in
Amebic abscess. Although pyogenic abscesses are commonly patients with left-side abscesses and abscesses greater than 10 cm
multiple, no imaging technique can reliably differentiate them in diameter. The chest x-ray is abnormal in as many as 50% of
from amebic abscesses.The best indication of a parasitic infection cases of amebic abscess, and the plain abdominal x-ray may show
is a history of travel to an endemic area (e.g., Mexico, Central calcification of an echinococcal cyst with secondary pyogenic
America, or Southeast Asia). However, when a hepatic abscess is infection.
detected by an imaging technique, serologic tests should be per- It is essential to differentiate infected echinococcal cysts from
formed to rule out active amebiasis or echinococcal infection. pyogenic abscess: special precautions are required for drainage of
Examination of stool for amebae is insensitive; consequently, echinococcal cysts because of the risk of spillage and anaphylaxis.
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 11
Blood cultures are positive in as many as 50% of patients with a decrease in the size of the abscess is apparent within 1 week on
pyogenic abscess, particularly in those with multiple abscesses; in ultrasonographic examination, though a small residual cavity may
fact, the presence of Streptococcus milleri in the blood suggests a vis- persist for as long as 2 years. If the patient’s condition does not
ceral abscess. improve, needle aspiration and culture are indicated. Secondary
infection is treated as a pyogenic abscess. Otherwise, oral emetine,
Treatment Pyogenic abscess. The preferred treatment of pyo- 65 mg/day, is added for up to 10 days.
genic abscess is closed continuous percutaneous drainage guided Echinococcal abscess. Symptomatic or secondarily infected echi-
by CT or ultrasonography, provided that it is technically feasible nococcal cysts are best treated by means of surgical excision or
and no other indication for laparotomy exists.94 More than one marsupialization. The use of oral anthelmintics (e.g., albendazole
catheter may be required for complete drainage. An alternative and mebendazole) has met with limited success. Nevertheless, pre-
treatment is repeated percutaneous needle aspiration, the results operative treatment with albendazole or mebendazole for 1 month,
of which are comparable to those of continuous drainage.95 One combined with postoperative treatment, is indicated to reduce the
advantage to repeated needle aspiration is the elimination of cum- risk of intraoperative seeding or postoperative recurrence.109,110
bersome, painful drainage tubes, which are prone to dislodgment.
Although initial studies showed a good response rate with repeat- Pancreatic Infection
ed needle aspiration,96 the results were not duplicated in a subse- Diagnosis When the mass is located in the epigastrium or the
quent randomized trial.97 left upper quadrant, a pancreatic source is most likely. Prompt and
The abscess cavity dimensions are followed by serial imaging accurate diagnosis is crucial because severe pancreatic infection is
until the cavity collapses, and the catheter can usually be removed fatal if left untreated.The key to successful treatment is early diag-
2 to 3 weeks later. Continuous percutaneous drainage has been nosis of infected pancreatic necrosis, infected pseudocyst, and pan-
associated with a complication rate of 4% and a failure rate of creatic abscess. A high index of suspicion is required to diagnose
15%.98 However, operative drainage is the treatment of choice in these three infectious processes and to differentiate them from a
patients with an identified intra-abdominal focus of infection and pancreatic inflammatory mass or phlegmon,28 in which pancreatic
in patients in whom percutaneous drainage is not feasible or has edema and inflammation are present without necrosis or infection.
failed.99 Operative drainage, especially via a laparoscopic approach, Correct diagnosis and treatment of infected pancreatic necrosis,
is a highly effective treatment option that is associated with low infected pseudocyst, and pancreatic abscess require an under-
mortality and morbidity.100 In some patients, a limited hepatic standing of their pathophysiology. It is generally assumed that
resection [see 5:23 Hepatic Resection] may be required to eliminate infected pancreatic necrosis develops as a transmural, transductal,
multiple abscesses, particularly when an underlying intrahepatic lymphatic, or hematogenous infection of a necrotic region of the
stricture is the source.101 pancreas. Infection develops in 40% of cases of pancreatic necro-
Treatment of pyogenic liver abscess should include systemic sis, usually in week 2 or 3 after development of the acute pancre-
antibiotic therapy. Approximately 70% of pyogenic liver abscesses atitis.111 Surgical debridement is required in these cases to prevent
yield polymicrobial isolates,102 and 25% to 45% of the organisms death. Pancreatic abscesses form by liquefaction of infected necro-
are anaerobic.103 Multiple anaerobic isolates suggest the colon as a sis.They usually occur after week 5 of pancreatitis, when the acute
source, whereas a single isolate of E. coli suggests a nidus in the bil- phase of the disease has subsided.112 Pancreatic abscesses are asso-
iary tree. Antibiotic treatment should include initial coverage of ciated with a lower mortality than infected pancreatic necrosis.
both aerobes and anaerobes with either a single agent or multiple Like pancreatic abscesses, infected pancreatic collections and
agents.The need to cover enterococci has been debated, but these pseudocysts present late in the course of pancreatitis. They are
organisms clearly are increasingly important nosocomial patho- associated with a lower mortality than pancreatic abscesses.
gens. An acceptable initial treatment regimen consists of a single Caused by infection in 13% of localized collections resulting from
broad-spectrum agent (e.g., ticarcillin-clavulanate or meropenem). ductal blowout, infected pancreatic collections and pseudocysts
It should be noted that significant changes have occurred in the eti- may occur in the pancreas itself, in contiguous peripancreatic tis-
ology, bacteriology, and treatment of liver abscesses. There is a sue, or in remote (extrapancreatic) tissue.
trend toward a higher incidence of pseudomonal and streptococcal Clinical evaluation alone is generally insufficient to diagnose
infections, and the frequency of fungal infection is increasing as pancreatic infection. A clearly defined upper abdominal mass is
well.104 The mortality from this disease remains high, and appropri- palpable in only 50% to 75% of cases.28 In most patients, the
ate antibiotic coverage with drainage is of paramount importance. screening battery of tests reveals leukocytosis with leukocyte
The duration of antibiotic therapy is controversial105; according counts greater than 15,000/mm3. Blood cultures are positive in
to one set of guidelines, antibiotics should be continued for 3 to 4 50% of cases. CT-guided percutaneous aspiration with Gram stain
weeks when the abscess has been excised, 4 to 8 weeks when a soli- and culture provides the best method of diagnosing pancreatic
tary abscess has been drained, and 6 to 8 weeks when multiple infection. In one study of 75 patients with clinical toxicity sugges-
macroscopic abscesses have been drained.106 Multiple microscopic tive of pancreatic sepsis, infection was confirmed in only 40%.113
abscesses usually require that a biliary source also be treated.85 The In another study of 21 patients with pancreatic infection, only five
overall prognosis for multiple small hepatic abscesses is not as good had specific signs on abdominal CT scan.114 CT-guided diagnos-
as that for solitary abscesses, and the development of a pyogenic tic needle aspiration leads to a correct diagnosis within 72 hours
abscess in a patient with an underlying hepatobiliary or pancreatic in two thirds of patients, and the mortality associated with opera-
malignancy has been identified as a preterminal event associated with tive intervention is 19%; however, CT-guided needle aspiration is
a hospital mortality of 28% and survival of less than 6 months.107 beneficial only if pancreatic infection is suspected and if the tech-
Amebic abscess. Medical treatment is now the standard approach nique is used early in the course of disease.
to management of amebic liver abscesses. Metronidazole, 750 mg Several laboratory markers of pancreatic necrosis have been
orally three times a day for 10 days, is a highly effective regimen.108 investigated, such as serum methemalbumin, serum ribonuclease,
A favorable response to treatment occurs within 4 to 5 days, and and C-reactive protein. Most of these markers are too insensitive
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 12
for routine clinical practice. However, serum levels of C-reactive pseudocysts can usually be treated nonoperatively. In one prospec-
protein above 10 mg/dl have been reported to be 95% accurate in tive study, percutaneous and surgical drainage were equally suc-
predicting necrosis.115 cessful in treating infected pancreatic fluid collections and pseudo-
Currently, the best indicators of infected pancreatic necrosis or cysts.124 Clinical signs of progress rather than CT findings are the
abscess are a combination of Ranson’s objective prognostic signs best indicators of the need for intervention, and nonoperative
[see Table 2] and dynamic abdominal CT scan findings. In Ranson’s methods should be attempted before open surgery is planned.
series, the pancreatic findings on CT were graded in five categories Adjunctive procedures. In the past, debridement and sump
[see Figure 7]116: (a) normal, (b) pancreatic enlargement alone, (c) drainage were accompanied by the so-called triple ostomy tech-
inflammation of the pancreas and peripancreatic fat, (d) one peri- nique, which involved cholecystostomy, gastrostomy, and jejunos-
pancreatic fluid collection, and (e) two or more peripancreatic fluid tomy. The role of these ancillary procedures, however, is contro-
collections. Only category e was associated with a high (61%) inci- versial at best, and currently, cholecystostomy is employed only if
dence of pancreatic abscess. The number of objective prognostic gallstones are detected.
signs present also predicted the subsequent development of an Other operative procedures may be required to manage gastric
abscess: fewer than three signs, 12.5%; three to five signs, 31.8%; or colonic complications. Gastric bleeding, gastric outlet obstruc-
and more than five signs, 80%. However, the value of this method tion, and gastric fistula necessitating reoperation are relatively
was limited because only five of the 83 patients evaluated had more infrequent in this setting. By contrast, colonic necrosis and fistula
than five prognostic signs. By combining the objective prognostic formation are relatively common and occur either spontaneously
signs with positive abdominal CT findings, the investigators identi- or as complications of treatment. The usual site of involvement is
fied 30 patients who had three or more objective signs and were the splenic flexure or upper descending colon.Treatment consists
graded as category c, d, or e on abdominal CT scan; in these of colonic resection or a diverting colostomy [see 5:34 Laparo-
patients, the incidence of pancreatic abscess was 56.7%. By con- scopic Coloctomy].
trast, no patient with fewer than three prognostic signs and graded Antibiotic therapy.The role of systemic antibiotic therapy in the
as category a or b on abdominal CT scan had a pancreatic abscess. prophylaxis of pancreatic abscess is controversial. Experimental
evidence suggests that antibiotics may sometimes decrease the
Treatment Once pancreatic infection is diagnosed, support- severity of pancreatitis,125 and endoscopic cannulation of the
ive measures are initiated, including nasogastric suction, with- pancreatic duct has yielded bacteria in pancreatic secretions of
holding of oral feedings, meticulous attention to respiratory care patients with acute pancreatitis.126 In patients with pancreatic
and fluid and electrolyte balance, systemic antibiotic therapy, and abscess, bacteriologic cultures are usually polymicrobial, the
nutritional support. The key to successful treatment, however, is most common organisms being E. coli, enterococci, Klebsiella
surgical, radiologic, or endoscopic drainage. pneumoniae, P aeruginosa, S. aureus, Bacteroides fragilis, and Clos-
.
Pancreatic necrosis. Sterile pancreatic necrosis alone is not an tridium perfringens. There is a growing trend toward early use of
indication for surgical debridement. In one prospective study, 11 prophylactic antibiotics in cases of pancreatic necrosis, even
patients with sterile pancreatic necrosis were all followed success- though there are no data that convincingly demonstrate a clini-
fully with conservative treatment.117 However, once infected pan- cal benefit. This trend may be partly responsible for the increas-
creatic necrosis is confirmed by Gram stain or culture, surgical ing prevalence of Candida species in pancreatitis-related sepsis; a
debridement is required to remove the characteristically thick 1996 report stated that Candida infection was detected in 21%
necrotic material; radiologic or endoscopic methods alone are not of patients.127
as effective for this purpose. Nutrition. Nutritional support of patients with pancreatic abs-
The choice of drainage technique is nevertheless controversial. cesses usually consists of TPN, though small bowel feeding may
Many clinicians prefer operative debridement and sump drainage. be attempted occasionally.These patients have high metabolic de-
The mortality associated with extensive operative debridement (so- mands and may experience glucose intolerance or hyperlipi-
called necrosectomy) and sump drainage may range from 30% to demia. Nevertheless, they generally tolerate I.V. feeding well. A
40%,118 and this technique may be associated with a 30% to 40% 10-fold increase in mortality (from 2.5% to 21%) was reported
reoperation rate because of sepsis or GI complications.28,119 in patients in whom a positive nitrogen balance could not be
Open drainage. To reduce the frequency of reoperation and to achieved.128
lower mortality, some clinicians opt for open drainage or marsu-
pialization of the infected pancreas. One modification involves the Splenic Abscess
use of a prosthetic mesh and a zipper to facilitate reexploration in Diagnosis A splenic abscess should be considered in patients
patients with severe intra-abdominal abscess.120 A 1991 meta- who present with fever and a left upper quadrant mass, though it
analysis of published surgical studies on infected pancreatic necro- remains a rare cause of these symptoms. Most splenic abscesses
sis found statistically better results with debridement and lavage or encountered in clinical practice are solitary; multiple abscesses are
debridement and open packing than with extensive debridement usually covert and are typically found at autopsy in patients with
and sump drainage.121 However, surgical treatment should be cus- disseminated malignancy, collagen vascular disease, or chronic
tomized for each patient. In one study, open packing was used for debility.
massive necrosis (more than 100 g removed by debridement at Because splenic abscess is rare, correct diagnosis requires a high
operation or CT evidence of at least 50% pancreatic necrosis) or index of suspicion.The main clue is the clinical setting: both bactere-
for extrapancreatic necrosis, whereas conventional debridement mia and local splenic disease are required to produce splenic abscess.
and sump drainage were used in other cases; the overall mortality In the preantibiotic period, this combination was seen most frequent-
in this study was only 14%.122 ly in patients with bacterial endocarditis and typhoid. Even today,
Pancreatic abscess. Pancreatic abscess resulting from liquefaction more than three quarters of splenic abscesses occur in patients who
of necrosis is also best treated by surgical drainage because resid- already have an infection elsewhere in the body; splenic abscesses
ual necrosis may cause failure of treatment by percutaneous meth- can also occur in patients with splenic infarcts, splenic hematomas,
ods.123 On the other hand, infected pancreatic fluid collections and or local splenic disease caused by hemoglobinopathies.
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8 CRITICAL CARE 18 Intra-Abdominal Infection — 13
a Pancreas b Pancreas
c Pancreas d
Pancreas
Fluid
e Fluid Pancreas f Abscess
Fluid
Figure 7 Pancreatic findings on CT scan have been graded by Ranson into five categories: grade A—normal pancreas
(a); grade B—diffuse enlargement of pancreas and nonhomogeneous density of gland (b); grade C—diffuse enlargement
of pancreas associated with peripancreatic inflammation (c); grade D—high-density fluid collection in left anterior
pararenal space (only head of pancreas is visualized at this level) (d); and grade E—diffuse enlargement of pancreas
with several intrapancreatic small fluid collections and poorly defined fluid collections adjacent to tail and head of pan-
creas (e). In final CT scan (f), pancreatic abscess is demonstrated; partially encapsulated fluid collection containing
bubbles of air represents large abscess.
The diagnosis of splenic abscess may be supported by indirect tion or abdominal CT scan is required. The abdominal CT scan,
radiologic signs, such as an elevated left hemidiaphragm or the enhanced with I.V. or oral contrast material, is preferred [see Figure
finding of a left upper quadrant air-fluid level (mimicking the stom- 8].129 This technique provides a direct image of the spleen, on
ach). To clinch the diagnosis, an abdominal ultrasound examina- which abscesses appear as low-density areas that may contain gas.
- 14. © 2004 WebMD Inc. All rights reserved. ACS Surgery: Principles and Practice
8 CRITICAL CARE 18 Intra-Abdominal Infection — 14
Mass
Figure 8 Abdominal CT scan, enhanced by contrast material, confirms diagnosis of splenic abscess.
Infections of the Lower Abdomen
Treatment Treatment of splenic abscess includes I.V. admin-
istration of antibiotics and splenectomy [see 5:25 Although enteric perforations, like pancreatitis and cholecystitis,
Splenectomy].The usual pathogenic organisms found are staphylo- present most commonly with pain and fever, their diagnosis differs
cocci and streptococci, though gram-negative bacilli and anaer- from that of upper abdominal infections of the solid organs.The pain
obes may also be present.When splenic abscesses are not drained, associated with enteric perforation frequently is not well localized;
mortality approaches 100%. At one time, splenotomy was the pre- consequently, CT scanning is used more frequently than ultra-
ferred operative treatment, but splenectomy is currently the pre- sonography because it is superior for evaluating the entire abdomen
ferred approach. Percutaneous catheter drainage is being per- [see Figure 9]. Moreover, a perforated viscus may present more acute-
formed with increasing frequency and appears to be as effective as ly than other forms of infection do, and it is a common indication
operative drainage.8,130.131 for emergency exploration. Thus, in the setting of a possible lower
Patient does not have "certain" appendicitis, signs of
upper abdominal infection are not present, and abdominal
plain films are not indicated
Order abdominal and pelvic CT scans.
Diffuse infection is Free peritoneal air is Evidence of duodenal Localized infection
Scans are normal
observed; infection seen without evidence perforation is seen, with or is seen
is uncontrolled, and of controlled leak without free peritoneal air
Consider nonsurgical
source is unclear (duodenal ulcer,
diagnoses. Treat operatively; if upper GI
periappendiceal or
Consider esophago- diverticular abscess) study shows perforation is
Resuscitate, give
gastroduodenoscopy. sealed, consider nonoperative
antibiotics, and take
to OR. Resuscitate, give treatment.
antibiotics, and take
to OR.
No discrete fluid collection is Discrete fluid collection is
present (pancreatitis, present (periappendiceal or
diverticulitis) diverticular abscess)
Provide nonoperative management, Resuscitate and give antibiotics.
including resuscitation and Treatment options:
antibiotic therapy (antibiotics are • percutaneous drainage with
unnecessary for bland pancreatitis delayed resection
Figure 9 Algorithm outlines approach to patient with without necrosis). • immediate open resection and
suspected lower abdominal infection. drainage
• diversion and drainage only