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27 Massive Lower Gastrointestinal Bleeding 291
powerful tools to help you: the patient’s history and the rectoscope. First, find out
whether the blood is pink-fresh blood or maroon-almost-fresh blood. These two
represent hematochezia (bloody stools) and signify a colonic (common) or small
bowel (rare) source. We need not remind you that tarry black stools of melena
signify an upper gastrointestinal (UGI) source above the ligament of Treitz
(> Chap. 17). Remember that with massive UGI hemorrhage and rapid intestinal
transit, unaltered fresh blood may appear in the rectum. Insertion of a nasogastric
tube followed by gastric irrigation may quickly direct you to a gastric bleed but
always remember that bleeding duodenal ulcers may not show blood in the stomach (> Chap. 17).
Rectoscopy
For all cases of hematochezia, rectoscopy is the mandatory first step. It is
amazing how often this step is omitted in “modern” practice—how often we see
patients immediately referred instead for a “panendoscopy.” Use a rigid rectoscope because the flexible instrument will be coated rapidly with blood, and you
will see nothing. Have a good suction device available. It is not unusual to discover that there is simply too much blood to really see anything (> Fig. 27.1). If
blood can be aspirated and you do get to see the rectum, simple things like a
rectal cancer or proctitis should be obvious. Do not decide on a diagnosis of
proctitis too lightly because the mucosa may look all red from the fresh blood.
The mucosa should be swollen, and there should be no visible mucosal blood
vessels. The proctitis is often so distal that the margin between inflamed and
Fig. 27.1. “Hey, are you sure that all of this is coming from above?”
292 Per-Olof Nyström
normal mucosa can be seen. The redder the blood is, the closer to the anus the
source. Bleeding from the upper anal canal and lower rectum will reflux at least
to the rectosigmoid junction, so do not be fooled by finding fresh blood at that
level. If you have a good view, when there is not too much bleeding, fresh blood
may be seen flowing on the wall or dripping from above, in which case bleeding
from a more proximal source is likely. Quite frankly, in most patients with active
bleeding you will not be able to see much at rectoscopy. But, at least you have the
opportunity to exclude an anal source and to observe personally the character
and magnitude of the bleeding.
Let us forget, at this stage, the majority of patients in whom the bleeding
stops spontaneously. They will be further investigated with a colonoscopy performed in a well-prepared bowel. Let us concentrate instead on that problematic
minority of patients—those bleeding massively or continuing to bleed. In such
patients, more aggressive measures will be needed.
The “Sophisticated” Means of Diagnosis
There are two “sophisticated” means of diagnosis in this situation: technetiumlabeled erythrocyte scan and mesenteric angiography. Which of the two should be
chosen roughly depends on the intensity of the bleeding and the availability of either
test. The more profuse the bleeding, the better it is to start with angiography. Not only
will it define the site of the bleeding, but also the bleeding vessel may be treated by
embolization through the angiographic catheter. Both investigations require active
bleeding at the time of the procedure; do not waste the radiologist’s time with a nonbleeding patient. In angiography, the “window” for detecting active bleeding is just a
few seconds; in scintigraphy, it is substantially longer. Many sources bleed intermittently, and the site may be “quiet” at the time of angiography. Remain vigilant after a
negative study because it does not signify that the bleeding episode is over.
Emergency Colonoscopy
To be of any diagnostic help, the colon must be cleaned as for an elective
endoscopy. Oral cleansing solution in excess of 4 L is required and often mandates
a nasogastric tube to make the patient ingest the volumes needed to produce a
“clean” distal effluent. This investigation will identify the bleeding site with certainty in less than half the instances, but if seen the site can be treated with adrenalin injection or a Hemoclip. Endoscopy is probably more valuable in sigmoid
diverticular bleeding than more proximal sites. However, few hospitals have an
27 Massive Lower Gastrointestinal Bleeding 293
endoscopy service experienced in dealing with massive colon bleeding out of
hours. What about your hospital?
The Operation
This is how to proceed if you elect to perform a laparotomy on a patient who
fails to settle: make a quick examination of the colon to exclude obvious pathology. Then, inspect the small bowel, which may contain blood even if the bleeding
comes from the right colon, although it would be unusual for the blood to regurgitate throughout the entire small bowel. If you find blood in the upper small
bowel, direct your investigation to the UGI tract. Blood in the right colon, but not
small bowel, does not definitely identify the bleeding as being in the right colon
because blood will reflux long distances in the colon. Make your guess based on
what you find because now comes the really difficult part. Are you going to take a
chance on a right or left colectomy? Do you trust the preoperative localizing studies—if performed? Or, can you identify the bleeding spot with certainty? Not even
if you open and clean the colon can you be sure to see the bleeding site. It is messy
and takes time, which is a reason why traditional teaching proposed the “blind”
right hemicolectomy (assuming angiodysplasia as the cause).
There are instances when the colon is so full of blood that a total or subtotal
colectomy is the reasonable procedure. Temporary clamping of the three main
vessels to the colon will reduce the bleeding while you mobilize the colon. What
few statistics there are suggest that segmental resection is associated with higher
rebleeding rate (no surprise), while subtotal colectomy has higher mortality. It is
a delicate balance of judgment.
A recent case of mine
A healthy, 32-year-old woman presented repeatedly with significant maroon
rectal bleeding; sometimes she had a hemoglobin around 6 g/dL. The bleeding
episodes always stopped spontaneously. All attempts to visualize the bleeding
site with certainty failed. The only positive finding was angiodysplasia of the
right colon and terminal small bowel, so she was subjected to elective exploration with intraoperative endoscopy; right ileocolic resection was performed. A
few months later, she was again admitted with a significant LGIB. This time,
however, the bleeding did not stop completely, but it was observed that she
passed normal-colored stools together with fresh blood, strongly suggesting
a bleeding site at the anus, possibly hemorrhoids. Always think outside the
box—everything is possible—and do not forget the humble hemorrhoid.
294 Per-Olof Nyström
A Pathway to Reason
The experience with, and perception of, LGIB differs slightly from one surgeon to another. This is understandable if one realizes that all published data on
this topic are retrospective studies on poorly stratified patients. So, this is what we
think:
Let’s face it—in nine-tenths of patients with LGIB, the bleeding stops spon-
taneously. Emergency localizing tests are unnecessary in this group; elective
colonoscopy is indicated. Hysterical MDs tend, however, to overinvestigate this
group—jumping on them with isotope scans and angiograms, all useless when
the hemorrhage is not active.
Each of us operates perhaps once or twice a year on “massive” lower LGIB
(>4–6 units of blood over 24 hrs), which continues. Therefore, the collective experience of each hospital is small, not allowing any meaningful prospective studies. All that is published on this subject is therefore retrospective and biased by
local dogma and facilities.
Reports by radiologists boasting about high accuracy rates of isotope scans
and angiography are often meaningless because such reports do not discuss the
clinical benefit of such accuracy; that is, did it change the management and
how?
Most massive LGIB in elderly patients is either from colonic diverticula (in
the left or, less commonly, the right colon) and angiodysplasia (usually of the
right colon). True, angiodysplastic lesions are common, but we do not know how
often they bleed. It is our impression that colonoscopists often overdiagnose
these lesions as the source after the hemorrhage has ceased, whereas the true
source of bleeding was elsewhere (e.g., diverticular).
[The Editors]
Based on these considerations, this is how we would approach a LGIB:
Start with supportive care. Exclude UGI bleeding. There is no need for a rou-
tine UGI endoscopy as fresh blood per rectum in a stable patient means that the
source is not in the UGI tract. Do a rectoscopy to rule out an anorectal source.
When the patient requires the second and third unit of blood, it is time
to get a little excited. Angiography at this stage is indicated; if it localizes the
source of bleeding in the left or right colon, so much the better. If it fails, it is not
a big deal. An isotope scan requires time and anyway is clinically almost useless
in actively bleeding patients. Blood migrates within the lumen of the colon and
so does the extravasated isotope. We do not value this investigation. (Nuclear
medicine = unclear medicine.)
When the patient is on the fifth or sixth unit and blood is still dripping
from the patient’s rectum, it is time to take the patient to the operating room.
If angiography has localized the source in either the left or right colon, we do a
segmental colectomy—either right or left hemicolectomy. If angiography is not
27 Massive Lower Gastrointestinal Bleeding 295
available or is nonlocalizing, we do a subtotal colectomy with ileorectal anastomosis. “Blind” segmental colectomy may produce a rebleeding patient who will
not tolerate a major reoperation.
A few authors have described intraoperative colonoscopy after “on-table”
colonic lavage. Theoretically, it appears attractive, but practically it is messy and
time consuming. If the hemorrhage has stopped, it will not show much; try it and
see what angiodysplasia is and what just some old clotted blood looks like.
There is no doubt that in practice we are overinvestigating these patients
and often waiting too long prior to operation. The bleeding either stops or continues; when it continues, you must operate—on a well-resuscitated patient who
has not been allowed to deteriorate in a medical ward. A fast subtotal colectomy
is a safe, definitive, and lifesaving procedure.
Whether we are right or wrong depends on which articles you read, on what
you believe, your local facilities, and your own philosophy. We hope you will
adopt ours.
Beware: in lower gastrointestinal bleeding, removing the wrong side of the colon
is embarrassing. Removing any segment of the colon while the bleeding source is in the
anorectum is shameful.
Acute Appendicitis
Moshe Schein · Ahmad Assalia
Theoretically it would seem to be much better if we would cut down upon the
appendix as soon as the diagnosis was tolerably certain, tie it above the seat of
perforation, and remove from its neighborhood any concretion or decomposing
material that might be the cause of irritation. (Samuel Fenwick, 1821–1902)
We all know: “Whatever the clinical presentation, whatever the abdominal
findings, always keep acute appendicitis at the back of your mind.”
Acute appendicitis (AA) is discussed in any surgical text dating from the
turn of the nineteenth century. Looking at the lengthy chapters devoted to this
subject, we often wonder what there is to chat so much about. Knowing that you
have been fed on AA ad nauseum since the early days of medical school, we do
not intend to repeat here the whole “spiel” again. Instead, we promise to be brief
and not to bore and perhaps teach a few things that have previously escaped
you.
Diagnosis
28
Acute appendicitis is an inflammation and subsequent infection of the
appendix. This rudimentary structure varies in length and position, making matters complicated. Even a dentist (but not a gynecologist) can diagnose a case of
classical AA (> Fi g. 28.1); the history of midabdominal visceral discomfort, shift-
ing to the right lower quadrant (RLQ) and becoming a somatic, localized pain
speaks for itself. Add to it the clinical and laboratory evidence of systemic inflammation/infection and, most important, the localized physical findings of peritoneal
irritation. Unfortunately (or fortunately, otherwise dentists would be treating AA),
for each classical case you will see two atypical cases. Sure, you know by now that
the diagnosis of AA tends to be missed at the extremes of age, that in fertile females
it is often confused with gynecological conditions (> Chap. 33), that retrocecal and
pelvic appendices tend to be more “silent,” and that it should be “always on your
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_28, © Springer-Verlag Berlin Heidelberg 2010
297
298 Moshe Schein · Ahmad Assalia
mind”—at least second on your list of differential diagnosis. So, what can we add
that you do not know? Perhaps nothing, but let us emphasize a few points:
Never confirm or exclude the diagnosis of AA on the presence or absence
of one or another symptom, sign, or finding “that must be there” because such
an obligatory variable does not exist. Instead, suspect AA from a synthesis of the
whole clinical picture and the various laboratory tests.
New “diagnostic scores” for AA are popping up in the literature almost ev-
ery year. But to us, what they describe is intuitive and thus clinically useless. We
know that obvious RLQ peritonitis in a male teenager, accompanied by nausea
and vomiting, fever, and elevated white cell count means AA. And of course, AA
is much, much less likely in the fertile woman, presenting with minimal RLQ
tenderness, preserved appetite, no fever, and normal white cell count—but can
we absolutely rule out the possibility of AA in such a lady? No. So, those scoring
systems are a good justification for writing papers—that is all.
Every budding surgeon feels compelled to design a personal screening test
for AA: the “cough test,” the “jump sign,” the “please bring your tummy to my finger
test,” and many others. They are all fun, but none approaches a sensitivity or specificity of 90% (oops, sorry, we promised not to use percentages). The truth is that it
is impossible to be completely accurate in the clinical diagnosis of AA. Should your
policy to operate be based only on clinical assessment and basic laboratory values,
then one or two out of ten removed appendixes will be a normal, “white” appendix
(in fertile females, this proportion will be much higher). More than that implies
that you are a cowboy; fewer suggests that you are dangerously conservative.
Fig. 28.1. Even a dentist can diagnose classic appendicitis
28 Acute Appendicitis 299
So, you seriously suspect AA after having excluded, or at least you believe
so, a gynecological complaint, urological pathology, gastroenteritis, the nebulous
“mesenteric lymphadenitis,” or the trash bin called “nonspecific abdominal
pain.” Should you now proceed directly to the operating theater or order fancy
imaging?
“Mesenteric adenitis” is code for “I thought it was appendicitis, but the appendix
was normal.” (David Dent)
Caveat
The management of patients with suspected appendicitis has traditionally
focused on the prevention of perforation by early operation at the expense of a
high proportion of unnecessary operations. But, despite an increase in use of modern diagnostic modalities, the rate of perforation has not declined. Furthermore,
population-based studies document that diagnostic accuracy decreases as the rate
of appendectomy increases, but the incidence of perforation does not change. This
teaches us that perforation is a different disease. Patients come to the hospital with
perforation; they do not perforate while we investigate them or observe them.
Sure, sometimes we miss a “masked” perforation, but that is another story.
The proportion of perforated appendicitis is not a good measure of quality. The
proportion of perforations may increase because you operate on fewer patients with
nonperforated appendicitis. A high proportion of perforations may in fact be a good
thing because it means you operate only on those patients who need surgical
treatment. (Roland Andersson)
Abdominal Imaging in Acute Appendicitis
While it is clear that we cannot modify the rate of perforated appendicitis
(one in four will be perforated), we can decrease the number of unnecessary, negative appendectomies. It has been said that “a fool with a tool is still a fool.”
Indiscriminate and nonselective usage of modern diagnostic technology is not
going to change this observation. What is needed is common sense and rational
deployment of available investigations. Frankly, managing at least one case of AA
per week, I do not recall when last I [MS] removed a normal appendix or missed
an abnormal one. But then again, don’t all my patients do well? ☺
300 Moshe Schein · Ahmad Assalia
And, this is how I [MS] do it:
1. Male patients with typical presentation: operate immediately or the next
morning.
2. Male patients with atypical presentation: serial re-examinations; if not better
or still atypical, order a computed tomographic (CT) scan (see >Chap. 5).
3. Females in the reproductive age with typical presentation: start with transvagi-
nal ultrasound (US), which frequently detects ovarian pathology (>Chap. 33)
and fluid in the pouch of Douglas to explain the clinical picture. If US is not
helpful, they are sent for a CT.
4. Females with atypical presentation: see points 2 and 3.
5. As these approaches differentiate between those who need an operation and
those who do not, I see no sense in using laparoscopy as a purely diagnostic tool.
Diagnostic laparoscopy per se is a costly and invasive operation (some call it
“controlled penetrating abdominal trauma”) and despite assertions that normal
appendices discovered during laparoscopy should be left alone, most surgeons
still feel uncomfortable with this approach. Thus, commonly, “negative laparoscopy” means “negative appendectomy.” And in fact, studies of laparoscopic
appendectomy (LA) report a much higher rate of negative appendectomies.
In good hands, US has been reported to be accurate in the diagnosis of AA
and is useful in excluding other diagnoses, which may require a different therapy
(e.g., hydronephrosis), incision (e.g., acute cholecystitis), or indeed no therapy at
all (e.g., ovarian cyst). Most of us do not work in an institution where we can be so
confident of the radiologist’s diagnosis of appendicitis on the basis of US. The
value of CT in diagnosing conditions that mimic AA but may not need operative
>
treatment (e.g., cecal diverticulitis;
Chap. 26) is emphasized in > Chap. 5.
Periodic Re-evaluation
Many of you, however (in developing countries or in some “bush,” for example), do not have a CT scanner readily available and thus cannot follow the advice
given. This does not mean that you should have a high rate of negative appendectomies. Periodic reevaluation is a time-honored and proven diagnostic modality in
the doubtful case. Unfortunately, the art of periodic re-examination and the virtue
of patience are disappearing from the scene of modern practice, in which the
emphasis is on obsessive activity and to prove oneself one has always to “do something.” In the absence of clear peritonitis and toxicity, very rarely are attacks of AA
a true emergency requiring an immediate operation. If undecided, admit the
patient and periodically re-examine him or her over the day or night. In most
instances, AA will declare itself, and if it is not AA, the “attack” will resolve. Patients
28 Acute Appendicitis 301
do not perforate under surgical observation; but occasionally they lie with neglected
perforations in the emergency room or pediatric wards.
(Note: if you decide to observe the patient, do not administer antibiotics as they
may mask the findings or “partially treat.” However, they may cure the AA in most
nonperforated cases, which in some specific circumstances could be a good idea.)
So, we order imaging selectively. Unfortunately, on our side of the Atlantic the
diagnostic algorithm is increasingly driven by dogmatic emergency room personnel
who perform CT scans in lieu of clinical evaluation. Such indiscriminate use of CT
scanning leads to a new syndrome we call “CT appendicitis”: you admit for observation a patient with RLQ pain and ambiguous clinical findings. Meanwhile, the emergency room doctor orders a CT, which is reported by the radiologist the following
morning. At this stage, the patient feels much better, his or her abdomen is benign,
and the patient wants to go home, but the radiologist claims that the appendix is
inflamed (“cannot exclude …” or “suggestive of …”—these are the ambiguous terms
they like to use to cover their ass). But, s hould we treat the CT image or the patient?
Classification
Let us bring here a simple classification of AA to facilitate the discussion of
management. In essence, AA is either simple or complicated. “Simple” AA implies
inflammation of the appendix of any extent in the absence of appendiceal gan-
grene, perforation, or peri-appendicular pus formation. Define AA as “complicated” whenever any of these changes is present.
Another entity you should be familiar with is the appendiceal mass, developing late in the natural history of AA. The “mass” is an inflammatory phlegmon
made of omentum or adjacent viscera, walling off a complicated appendicitis. A
mass containing a variable amount of pus is an appendiceal abscess.
Management
Antibiotics
Judicious administration of antibiotics, to cover Gram-negative and anaerobic bacteria, will minimize the incidence of postoperative wound (common) and
intra-abdominal (rare) infective complications. In simple AA, the antibiotics are
considered prophylactic, while in complicated AA they are therapeutic. We encourage
you to administer the first dose of antibiotics preoperatively just before you
scrub. If at surgery the AA proves to be simple, no postoperative administration
is necessary. Should you, on the other hand, discover complicated AA, additional
postoperative doses are indicated. We suggest that you tailor the duration of
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