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11 Abdominal Exploration: Finding What Is Wrong 93
continue to be a common source of preventable morbidity. The praticalities of
systemic abdominal exploration are described in a separate section.
Intraperitoneal Contamination or Infection
First, you register the offensive fecal smell or fecal-looking fluid that denotes
abundance of anaerobic bacteria and usually an infective source in the bowel.
Note, however, that neglected infections from any source can be pseudofeculant
due to the predominance of anaerobes. When, on opening the peritoneum, gas
escapes with a hiss, be aware that a viscus has perforated. In the nontrauma situation, this usually implies perforated peptic ulcer or sigmoid diverticulitis. Bile
staining of the exudate points to pathology in the biliary tract, gastroduodenum,
or proximal small bowel. Dark, stout-beer fluid and fat necrosis hint at pancreatic
necrosis or infection in the lesser sac. John Hunter (1728–1793) observed that “the
gastric juice is a fluid somewhat transparent, and a little saltish or brackish to the
taste,” but we would not suggest you go that far. Whatever the nature of contamina-
tion or pus, suck and mop it away as soon as possible.
Generally, bile directs you proximally and feces distally, but “simple” pus
can come from anywhere. When its source remains elusive, start a systematic
search, keeping in mind all potential intra- and retroperitoneal sources “from the
esophagus to the rectum.” Be persistent with your search. We recall a case of spontaneous perforation of the rectum in a young male, twice explored by experienced
surgeons who failed to appreciate the minute hole deep in the rectovesical pouch.
It was found during a third operation.
Occasionally, however, the origin of contamination or secondary peritonitis
is not found. A Gram stain disclosing a solitary b acte rium—as o ppo sed to a fe w—
would support the diagnosis of primary peritonitis since secondary peritonitis
(e.g., secondary to a visceral pathology) is always polymicrobial. More about this
in > Chap. 12.
The Direction and Practicalities of Exploration
The direction and practicalities of exploration depend on the reason for the
laparotomy; let us start with a general plan.
The peritoneal cavity comprises two compartments: the supracolic and the
infracolic. The dividing line is the transverse (meso)colon, which in a xiphopubic
midline incision is located approximately in the center of the incision. It is important to develop and adhere to a fixed routine of abdominal exploration, which
94 Moshe Schein
will include both compartments. Our preference is to begin with the infracolic
compartment: The transverse colon is retracted upward, the small bowel eviscerated, and the rectosigmoid identified. Exploration begins with the pelvic reproductive organs in the female and then attention is turned to a systematic
inspection and palpation of the rectosigmoid, progressing in a retrograde fashion
to the left, transverse, and then right colon and cecum, including inspection of
the mesocolon. The assistant follows the exploration with successive movements
of a handheld retractor to retract the edge of the surgical incision and to enable
good visualization of whichever abdominal structure is the focus of attention.
Exploration then proceeds in a retrograde fashion from the ileocecal valve to the
ligament of Treitz, with special care taken to inspect both “anterior” and “posterior” aspects of each loop of bowel as well as its mesentery.
Attention is then turned to the supracolic compartment. The transverse colon is pulled down, and the surgeon inspects and palpates the liver, gallbladder,
stomach (including the proper placement of a nasogastric tube), and spleen. Special
care should be taken to avoid iatrogenic damage to the spleen caused by pulling
hard on the body of the stomach or the greater omentum. A complete abdominal
exploration also includes entry into the lesser peritoneal sac, which is best undertaken through the gastrocolic omentum. This omentum is usually only a thin avascular membrane on the left side, and this should therefore be the preferred entry
route into the lesser sac. Take care to avoid injury to the transverse mesocolon,
which may be adherent to the gastrocolic omentum. A misdirected surgeon can be
convinced that he or she is entering the lesser sac when in fact he or she is cutting
a hole in the transverse mesocolon. If “vascular,” the gastrocolic omentum is divided between ligatures, bringing the body and tail of the pancreas into full view.
Exploration of retroperitoneal structures involves two key mobilization
maneuvers, which should be employed whenever access to the retroperitoneum
is deemed necessary:
Kocher’s maneuver is mobilization of the duodenal loop and the head of
the pancreas by incising the thin peritoneal membrane (posterior peritoneum)
overlying the lateral aspect of the duodenum and gradually lifting the duodenum
and pancreatic head medially. This maneuver is also the key to surgical exposure
of the right kidney and its hilum and the right adrenal gland. Kocher’s maneuver
may be extended further caudad along the “white line” on the lateral aspect of the
right colon all the way to the cecum. This extension allows medial rotation of the
right colon and affords good exposure of the right-sided retroperitoneal, structures such as the inferior vena cava, iliac vessels, and the right ureter. Further extension of this incision angles around the cecum and continues in a superomedial
direction along the line of fusion of the small bowel mesentery to the posterior abdominal wall. Thus, it is possible to mobilize and reflect the small bowel upward,
the so-called Catell-Braasch maneuver. This affords optimal exposure of the entire
inframesocolic retroperitoneum, including the aorta and its infrarenal branches.
11 Abdominal Exploration: Finding What Is Wrong 95
The second key mobilization maneuver is called the left-sided Kocher or
medial visceral rotation (also called by some the Mattox maneuver) and is used
especially to gain access to the entire length of the abdominal aorta and to the
left-sided retroperitoneal viscera. Depending on the structures to be exposed,
this maneuver begins either lateral to the spleen (splenophrenic and splenorenal
ligament), working caudally or in the white line of Toldt lateral to the junction of
the descending and sigmoid colon, working upward. The peritoneum is incised,
and the viscera, including the left colon, spleen, and tail of pancreas are gradually
mobilized medially. The left kidney can either be mobilized or left in situ, depending on the surgical target of the exploration.
In cases of spontaneous hemoperitoneum, you will have to look for a ruptured aortic, iliac, or visceral arterial aneurysm, ectopic pregnancy, bleeding
hepatic tumor, spontaneous rupture of an enlarged spleen, or any of the other
causes listed in >Tab le 11.1. In penetrating trauma, you will follow the entry–exit
tract, taking into consideration the missile’s energy, velocity, and potential to fragment. Wherever there i s an ent ry wound i n a v isc us or blood ves sel, look for t he exit
one. The latter may lie concealed on the lesser sac wall of the stomach, the retro-
peritoneal surface of the duodenum, or the mesenteric edge of the small bowel.
Missing an exit wound is often a death sentence to your patient. It is the blunt
abdominal injury, however, that requires the most extensive and less-directed
search, from the surface of both hemidiaphragms to the pelvis, from gutter to gutter, on all solid organs, along the whole length of the gastrointestinal tract, and on
the retroperitoneum (the retroperitoneum selectively, as discussed in > Chap. 39).
The exact sequence of exploration is less important than its thoroughness.
Comment: Because this book is aimed also at trainees, we had to be complete and describe the “classical abdominal exploration.” Frankly, if the patient is
bleeding from a ruptured liver, we would explore the upper abdomen, but if the
infracolic compartment looks pristine and dry, we would leave it alone. So, use
your common sense: do not look for ovarian cysts in a patient with a bleeding
spleen. Like Dr. Leo Gordon said: “When common sense interferes with a protocol, follow common sense.”
What about retractors? Use whatever is available at your institution. In
most circumstances, we prefer one of the handheld retractors in the hand of the
assistant. But, not all assistants are as passive or active as you wish them to be. As
Arthur E. Hertzler (1870–1946) wrote: “If I ever deliberately commit murder I
shall select an inattentive and awkward assistant as my victim. I shall select one
who has assisted enough to delude himself into thinking he could himself do the
work better than the surgeon who is operating. This usually reaches the high
point at about the third week of the intern’s experiences.”
96 Moshe Schein
In some situations, a “passive” fixed “retractor” should be used—especially
when operating in the pelvis or upper abdomen. The good old Balfour retractor is
useful when doing a midline laparotomy. Of course, your hospital may have one of
those fancy multiarm retractors (called omni or whatever) or the ingenious
Bookwalter ring retractor; some surgeons like to use them, particularly those who
do not have residents but have to rely on sleepy nurses. We try to avoid those types
of mechanical retractors: often, the time needed to place them is longer than the
operation, and we hate operating with a sharp metal frame piercing our paunch.
Additional Points: Grading the Severity of Injury
Abdominal exploration for trauma ends with a strategic decision about the
subsequent steps. Forget at this stage the many available organ injury scales, which
are of only academic value; from the operating surgeon’s point of view, there are
essentially two patterns of visceral damage: minor and major trouble.
Minor trouble involves easily fixable injuries, either because the injured
organ is accessible or the surgical solution is straightforward (e.g., splenectomy,
suture of mesenteric bleeders, or a colon perforation). There is no immediate
danger of exsanguination or loss of surgical control. Under these circumstances,
you can immediately proceed with definitive repair.
Major trouble is when the spontaneous condition or injury is not easily rec-
tified because of complexity or inaccessibility (e.g., a high-grade liver injury, a
major retroperitoneal vascular injury in the supracolic compartment, or destruction of the pancreatoduodenal complex). Here, the secret of success is to stop the
operation when temporary (usually digital or manual) control of bleeding is
achieved. Take time to optimize the surgical attack on the injured organ. Update
all members of the operating and anesthesia teams on the operative plan. Allow
your anesthesiologist to use the time to stabilize the patient hemodynamically
and to obtain more blood products. (Often, you have to think for your anesthetist;
do not assume that the anesthetist is awake. However, bear in mind that just as
you are a “modern” surgeon, there are now “modern” anesthetists, and they are
an invaluable resource in the management of such patients. Take care not to
alienate these excellent practitioners.) Order an autotransfusion device and a full
range of vascular and thoracotomy instruments to be brought to the surgical
suite. This is also the appropriate time to seek more competent help and to plan
the operative attack, including additional exposure and mobilization. Such preparations are crucial for the survival of your patient.
Remember: very often the initial exploration of the abdomen in the trauma
patient is incomplete because the patient’s critical condition creates a situation in
which every minute counts, and injuries are simply repaired as they are encountered.
11 Abdominal Exploration: Finding What Is Wrong 97
Under these circumstances, you must complete the exploration before terminating
the procedure.
Finally, first do no harm. This applies everywhere in medicine but is of
paramount importance during abdominal exploration. The injured or infected
contents of the peritoneal cavity may be inflamed, swollen, adherent, friable, and
brittle. Careless and sloppy manipulation and separation of viscera during exploration commonly induce additional bleeding and may produce additional
bowel defects or enlarge the existing ones. And as usual, new problems translate
into additional therapies and morbidity.
This is what makes emergency abdominal surgery so exciting and demanding:
the ever-looming catastrophe and the anxiety about whether you are able, or not, to
tackle it competently.
Peritonitis: Contamination and
Infection—Principles of Treatment
Moshe Schein · Roger Saadia
In peritonitis—source control is above all.
“The mechanical control of the source of infection, while itself nonbiologic, determines
the extent of the host biologic response to the disease.” (Ronald V. Maier)
The finding of inflammation, bowel contents, or pus localized or dispersed
throughout the peritoneal cavity is common at emergency laparotomy. How is
this scenario best handled? This chapter discusses semantic distinctions and
general aspects of the surgical treatment. For the management of individual
causes of peritonitis, refer to the specific chapters.
Nomenclature
Inflammation of the peritoneum is termed peritonitis. It is generally caused
by a bacterial inoculum. This explains why peritonitis and intra-abdominal infec-
tion (IAI) are mistakenly used interchangeably. It is important to note though, that
these two terms are not synonymous because peritonitis may also be sterile, as
with the chemical peritonitis of early perforation of a peptic ulcer or inadvertent
infusion of enteral feeding through a misplaced jejunostomy tube.
IAI. For a condition to be labeled IAI, both the intraperitoneal presence of
micro-organisms (or their toxins) and the inflammatory response of the peritoneum are required. At laparotomy, a purulent exudate is often found.
Peritoneal contamination is different. It consists merely of the soiling of the
peritoneal cavity by a fluid rich in micro-organisms, as in the immediate aftermath of a penetrating intestinal injury, before an inflammatory response has taken
place. Peritoneal contamination occurs commonly in the course of routine elective
surgery of the gastrointestinal tract.
IAI can be diffuse, as in generalized peritonitis, or localized, as in intra-
abdominal abscesses. Many surgical texts still erroneously use the term intra-
abdominal abscess as a variant of peritonitis. This is not entirely correct since
abscesses develop as a result of effective host defenses and represent a relatively
successful outcome of peritonitis. The mainstay of treatment is drainage. For
how and by which route, find out in > Chap. 49.
12
Moshe Schein
Marshfield Clinic Ladysmith Center, 906 College Avenue, Ladysmith, WI 54848, USA
M. Schein et al. (eds.), Schein’s Common Sense Emergency Abdominal Surger y,
DOI: 10.1007/978-3-540-74821-2_12, © Springer-Verlag Berlin Heidelberg 2010
99
100 Moshe Schein · Roger Saadia
We like to refer to IAI as resectable when not only the source of infection is
amenable to surgical removal but also when the remaining locoregional conditions
of the peritoneal cavity are such that prolonged postoperative antibiotic therapy is
not required (e.g., gangrenous appendicitis). Nonresectable IAI, in contrast, is an
infection that has spread beyond the confines of the source organ; in perforated
appendicitis, for instance, you may resect the appendix, but residual peritoneal
infection persists, requiring extended antibiotic coverage (> Chap. 47).
Abdominal sepsis is still a term used very commonly, but we, semantic
nudniks, do not like it. According to modern consensus, sepsis means the host’s
response to infection (systemic inflammatory response syndrome [SIRS] plus a
source of infection) (> Chap. 54). Thus, the use of “sepsis,” in the abdominal con-
text, would not take into account the important initial local inflammation within
the peritoneal cavity. This peritoneal response is analogous, at a local level, with
SIRS at the systemic level because it represents, likewise, a nonspecific inflammatory response of the host to a variety of noxious stimuli, not necessarily infectious. Strictly speaking, therefore, local contamination, infection, and sepsis
refer to different processes. Yet, they may coexist in the same patient, developing
simultaneously or consecutively—a continuum. Untreated or neglected abdominal contamination progresses to IAI, which is invariably associated with a systemic
inflammatory response. More significantly, abdominal inflammation or indeed the
systemic response (fever, leukocytosis) may even persist after the intraperitoneal
infection has been eradicated.
Classification of Peritonitis
Secondary peritonitis. It is caused by the perforation or transmural necrosis
of a hollow viscus. It is usually characterized by an aerobic and anaerobic polymicrobial inoculum, reflecting the flora of the gastrointestinal tract. This condition’s
management is the “bread and butter” of the general surgeon. Examples include
perforated appendicitis, perforated diverticular disease of the colon, strangulation obstruction of the small bowel, and ruptured tubo-ovarian abscess.
Primary peritonitis, in contrast to secondary peritonitis, is not caused by a loss
of gastrointestinal wall integrity and is not associated with leakage of intestinal contents into the peritoneal cavity. It is also referred to as spontaneous bacterial peritoni-
tis. The responsible micro-organisms originate from a source outside the abdomen.
In young girls, it is usually a Streptococcus gaining access via the genital tract. In cir-
rhotics, Escherichia coli is thought to be a blood-borne agent infecting the ascites. In
patients receiving peritoneal dialysis, Staphylococcus migrates from the skin along the
dialysis catheter (> Chap. 32). Primary peritonitis in patients without a predisposing
factor, such as ascites or a dialysis catheter, is extremely rare. It is usually diagnosed
when laparotomy performed for an “acute abdomen” reveals odorless fluid without
an apparent source. The diagnosis is reached by exclusion after a thorough abdominal
12 Peritonitis: Contamination and Infection—Principles of Treatment 101
exploration and is confirmed by a Gram stain and culture, which usually isolates a
solitary aerobic organism: it is a “single-bug disease.” In patients with a known
predisposing factor (e.g., ascites associated with chronic liver disease), suspected primary peritonitis can be diagnosed by paracentesis (polymorphonuclear count in
the ascitic fluid greater than 250 cells/mm3); a positive culture confirms the diagnosis,
but even with a negative culture, antibiotic treatment should be instituted. Whenever
possible, a diagnostic exploratory laparotomy should be avoided because of its prohibitive mortality; in a patient with advanced cirrhosis, it often amounts to an autopsy in
vivo. Initial antibiotic treatment is empiric until results of bacteriological sensitivities
become available.
Tertiary peritonitis is associated with multiple-organ failure and reflects
the host’s global immunodepression. The microbial inoculum consists mainly of
organisms of low pathogenicity, such as Staphylococcus epidermidis, Enterococcus,
and Candida albicans (> Chap. 54). Some surgeons include “postoperative perito-
nitis” (e.g., due to a leaking anastomosis) in this category. Others, more correctly,
consider this a more morbid variant of secondary peritonitis (> Chap. 52).
Management
The outcome of IAI depends on the virulence of the infection, the patient’s premorbid reserves, and the patient’s current physiological compromise. Your goal here
is to assist the patient’s own local and systemic defenses. The philosophy of manage-
ment in a typical case of secondary peritonitis is simple, comprising two steps: source
control followed by peritoneal toilet. More aggressive methods are also discussed.
Source Control
The key to success is timely surgical intervention to interrupt the delivery of
bacteria and adjuvants of inflammation (bile, blood, fecal matter, barium) into the
peritoneal cavity. All other measures are of little use if the operation does not successfully eradicate the infective source and reduce the inoculum to an amount that
can be handled effectively by the patient’s defenses, supported by antibiotic
therapy. This is not controversial—all the rest may be. Source control frequently
involves a simple procedure such as appendectomy (> Chap. 28) or patch closure
of a perforated ulcer (> Chap. 18). Occasionally, a major resection to remove the
infective focus is indicated, such as gastrectomy for perforated gastric carcinoma
(> Chap. 18) or a colectomy for perforated diverticulitis (> Chap. 26). Generally,
the choice of the procedure, and whether the ends of resected bowel are anastomosed or exteriorized (creation of a stoma), depends on the anatomical source of
infection, the degree of peritoneal inflammation and SIRS, and the patient’s premorbid reserves, as discussed in the individual chapters.
102 Moshe Schein · Roger Saadia
Note that situations exist when the source cannot be eradicated or the expected price to pay for its removal is deemed too high. Less-radical options may
then be used, such as diversion (e.g., colostomy proximal to a rectal injury) or
drainage (of a leaking duodenum).
Peritoneal Toilet
Once the source of infection is eradicated, cleaning the peritoneal cavity is
aimed at minimizing the intraperitoneal bacterial load. Several maneuvers deserve discussion. Liquid contaminants and infected exudates should be aspirated
and particulate matter removed by swabbing or mopping the peritoneal surfaces
with moist laparotomy pads. Although cosmetically appealing and popular with
surgeons, there is no scientific evidence that intraoperative peritoneal lavage re-
duces mortality or infectious complications in patients receiving adequate systemic antibiotics. Similarly, peritoneal irrigation with antibiotics is not
advantageous, and the addition of antiseptics may produce local toxic effects.
Irrigate copiously (to use a term popular among American surgeons) if you wish,
but know that, beyond wetting your own underwear and shoes, you will not accomplish much. Should you choose to remain a dedicated irrigator, try to confine
the irrigation to the contaminated area—to avoid spreading s**t all around—and
do remember to suck out all the lavage fluid before you close; there is evidence that
leaving irrigation fluids behind interferes with peritoneal defenses by “diluting the
macrophages.” Bacteria swim perhaps better than macrophages.
The concept of radical debridement of the peritoneal cavity is based on the
premise that fibrin is a nidus for microbial implantation, hence the recommendation
to peel off every bit of fibrin coating peritoneal surfaces and viscera. The procedure
is tedious, results in excessive bleeding from the denuded peritoneal surfaces, and
endangers the integrity of an already friable intestine. It did not withstand the test
of a prospective randomized study comparing it to a more conservative approach.
Despite the dictum that it is impossible to effectively drain the free perito-
neal cavity, drains are still used (and often misused). Their aim must be re-
stricted to the evacuation of an “established” abscess (when the residual cavity
will not collapse or cannot be filled with omentum or adjacent structures), to
allowing escape of potential secretions (e.g., bile, pancreatic juice), or, rarely, to
establishing a controlled intestinal fistula when exteriorization is not possible.
To prevent intestinal erosion, soft drains should be left in place for the shortest
duration possible and well away from bowel wall. In general, active suction
drainage may be more effective than the passive kind, and infectious complica-
tions can be reduced by choosing “closed” systems. Drains provide a false sense
of security and reassurance. We have all seen a moribund postoperative patient
with an abdomen “crying” to be re-explored and a surgeon in denial because the
12 Peritonitis: Contamination and Infection—Principles of Treatment 103
Fig. 12.1. “Which of the drains is draining?”
tiny four-quadrant drains are dry and nonproductive. This is particularly true
of drains inserted to deal with postoperative hemorrhage (> Chap. 56); a tiny
trickle of blood from a drain may hide a huge intra-abdominal clot. Drains inserted close to an anastomosis “just in case it leaks” are more likely to cause an
anastomotic dehiscence than to establish a controlled fistula. For more on
drains, refer to > Chap. 42.
The role of postoperative peritoneal lavage through tube drains left in place
for this purpose is at best questionable. Is it really possible to irrigate the whole
abdominal cavity? In our experience, such tubes are rapidly walled off by adhesions and adjacent tissues. At the end of the day, you will be irrigating nothing
more than the drains’ tracks (> Fig. 12.1).
Aggressive Modalities of Management
“In doubtful cases do not wait too long
Before exploring, for it is quite wrong
To act upon the slogan Wait and See,
When looking may provide the remedy” (Zachary Cope, 1881–1974)
Most IAI patients respond to the combination of adequate source control,
appropriate antibiotics, and competent supportive management. Might a few
others need more? In the 1980s, it was believed that failure of the initial standard
operation could be accounted for by either persisting or recurring infection
diagnosed too late. Waiting for overt signs of infection or organ failure as the
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