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17 Upper Gastrointestinal Hemorrhage (and Portal Hypertension) 147
After repeated endoscopic maneuvers, not much will be left of the first part of the
duodenum when you eventually operate. A colleague said this:
“Why are gastroenterologists more imaginative and courageous than we surgeons
in employing new and bizarre invasive therapeutic modalities? Because they have
somebody (us) to bail them out!” (Eli Mavor)
But, whatever you do, remember that old and chronically ill patients poorly
tolerate repeated episodes of bleeding; do not mess around with them. As a rough
guide, when the transfusion requirement exceeds four units of blood in a patient
over 65 years of age, consider surgery.
Operative Management
Repeat Endoscopy
It is crucial that you know the exact location in the UGI tract from which the
patient is bleeding. If the initial endoscopy was not done by you, or in your presence, do it again. In an anesthetized patient, it will not take you more than 5 min
to insert and remove the endoscope. Do not trust the scribbled, 2-day-old endoscopy report that the “source of hemorrhage appeared to be in the duodenum.” This
could lead you to start with an unnecessary duodenotomy while the source lies
high in the stomach.
Exploration
An upper midline incision, supplemented with a paraxyphoid extension and
forceful upward sternal retraction, lets you deal with anything in the foregut. In
obese patients with a wide costal angle, however, a transverse, chevron-type incision may take a few more minutes but affords a more comfortable exposure. In
addition, a generous reverse-Trendelenburg tilt of the patient will bring the upper
stomach almost to your nose.
Start by searching for external visual or palpable features of chronic ulceration. The latter are invariably associated with serosal inflammatory changes.
Look for evidence of chronic ulcers from the duodenum to the gastric cardia.
Duodenal “Kocherization” (Theodor Kocher is perhaps the only surgeon in history to have his name used as a verb) will be necessary to reveal the sporadic
148 Moshe Schein
postbulbar ulcer in the second portion of the duodenum. Occasionally, a posterior or lesser-curvature GU will become palpable only through the lesser sac.
Acute superficial mucosal lesions are unfortunately not identifiable from the outside, although a Mallory-Weiss lesion may be tattooed by bluish serosal staining
at the gastroesophageal junction.
The finding of a chronic ulcer in accordance with the preoperative endoscopic finding tells you where the trouble is, but what is to be done in the absence
of any external evidence of pathology? You have a few options:
Proceed according to the endoscopist’s findings, if you trust them, but they
will not always be correct
Surgical exploration
Intraoperative endoscopy
Intraoperative Endoscopy
Having endoscopically visualized, with your own eyes, an actively bleeding
DU, you should not have any doubts. A doubtful endoscopic report, however, may
promote a negative duodenotomy, extending it—piecemeal—proximally until the
high gastric lesion is found. All that was needed was a small gastrotomy and suture
ligation of the lesion; instead, you are left with a very long, messy, and unnecessary
duodenogastrotomy to repair. To obviate such a mini-disaster, we would unscrub for
a moment and shove in an endoscope. Sometimes, when the stomach is distended
with huge clots, we would place a purse-string suture at the anterior wall of the
antrum, perform a small gastrotomy, and with a large sucker remove and irrigate all
clots. An endoscope is then inserted through the gastrotomy with the purse string
tightened to allow gastric insufflation; this offers an excellent and controlled view of
the stomach and duodenum. We call it “intraoperative retrograde gastroscopy.”
Philosophy of Surgical Management
A friend of ours, Asher Hirshberg, aptly stated that, “In the era of Helico-
bacter pylori, doing a gastrectomy for peptic ulcer is like doing a lobectomy for
pneumonia.” Clearly, where potent antiulcer drugs are available elective ulcer
surgery has disappeared, and definitive antiulcer procedures during emergency
surgery for complications of ulcer are disappearing as well. Why do a surgical
vagotomy when PPIs offer a “medical vagotomy”?
The general philosophy is that saving lives, that is, stopping the bleeding,
comes first. This is the main consideration in severely ill patients. In the less-
compromised subjects, the secondary issue of long-term cure of disease may be
considered. But now, when such a goal can be achieved by medical means, the
role of definitive antiulcer procedures is limited and should be considered only
17 Upper Gastrointestinal Hemorrhage (and Portal Hypertension) 149
in well-selected patients: those expected to be noncompliant with medication
and in situations where such medication is not readily available. This applies also
to the management of perforated ulcers (> Chap. 18).
Our current operative approach in the vast majority of cases is thus limited
to hemostasis only. In a few selected and good-risk (e.g., APACHE II < 10) patients,
we may consider a definitive antiulcer procedure tailored to the patient and the
type of ulcer.
Specific Sources of Bleeding
Duodenal Ulcer
For a duodenal ulcer, the source of bleeding is always the gastroduodenal
artery at the base of a posterior ulcer. Hemostasis is accomplished through an
anterior, longitudinal, duodenotomy, underrunning the base (and bleeding vessel)
with two or three (2–0 monofilament) deeply placed sutures—each placed on a
different axis. When bleeding is active, successful ligation of the vessel will be evident; in its absence, you may want to abrade the ulcer’s base, dislodging the clot
and inducing bleeding. Otherwise, just underrun the base, deeply, and in a few
directions. The theoretical danger of underrunning a nearby common bile duct has
been mentioned, but we are unaware of even a single report of such a case. Others
have described ligating the gastroduodenal artery from the outside, above, and
behind the duodenum. However, we have no experience with this and would be
anxious fishing for the artery at the base of the gastrohepatic omentum, which
would be inflamed by the adjacent ulcerating process.
After achieving hemostasis, you are left with a few options. In the compromised patient—and most such patients are compromised—all you want is to stop
the ble eding , close t he duodenotom y wit hout c onstricting the lumen, and get out .
The eventual cure of the ulcer is left to acid—or Helicobacter-reducing drugs.
If the patient is in good shape and requires a definitive procedure (an extremely rare situation in our current practice), you may choose to prolong the
operation by 30 min, adding a truncal vagotomy (TV), extending the duodenotomy across the pylorus, and closing it to form a Heinke–Mikulicz pyloroplasty.
In a fit and stable patient, only 10 years ago we would close the duodenotomy and
perform a highly selective vagotomy (HSV), adding an hour to the procedure.
But today, we do not find suitable candidates for this procedure, and I bet that
you have never learned how to do it.
Local hemostasis can be achieved even in the base of giant ulcers or when the
duodenum is extremely inflamed or scarred. When simple closure of the duodenotomy appears to compromise the lumen or pyloroplasty is deemed otherwise
unsatisfactory, just close the duodenum and do a posterior gastroenterostomy
150 Moshe Schein
Fig. 17.2. Gastroduodenostomy: note that the posterior aspect of the anastomosis is
performed with interrupted sutures, taking “big bites” of the duodenum (which is adherent
to the pancreas)—well into the scar tissue at the base of the (now-excluded) ulcer
(GE), alone or added to the TV. The proponents of antrectomy plus vagotomy for
bleeding DUs claim an increased incidence of rehemorrhage when gastric resection is avoided. In over 100 emergency operations for bleeding DUs, this has not
been our experience, and we believe that there is no sense in removing a healthy
stomach, producing a gastric cripple, for benign duodenal disease, which in any
case can be subsequently cured with medications.
When, however, the duodenum is virtually replaced by a huge ulcer involving the anterior and posterior wall of the duodenal cap (“kissing ulcer”), one
essentially is forced to perform an antrectomy (with a TV). In this situation, to
avoid creating a duodenal stump that can be difficult to close and can leak, we
prefer a Billroth I gastroduodenostomy (
>
Fig. 17. 2).
Postbulbar DU
For unknown reasons, the postbulbar DU has almost disappeared from the
Western world. Although extensive resective procedures (including an emergency
Whipple) are mentioned in the old literature, all you need to do is to mobilize the
duodenum, underrun the ulcer through a duodenotomy, and—perhaps—add a GE,
with or without TV (in the previous editions, we mentioned HSV as another option,
but again, this has become a procedure known only to the old surgical farts).
Gastric Ulcer
Traditionally, for most surgeons a bleeding GU mandated a partial gastrectomy. Gastric resection is indeed effective in controlling the hemorrhage but in most
17 Upper Gastrointestinal Hemorrhage (and Portal Hypertension) 151
instances represents a superfluous ritual. For acute superficial ulcers, all that is
required is simple underrunning of the lesion through a small gastrotomy. Even in
patients who bleed from a chronic GU, simple underrunning of the ulcer from within,
through a gastrotomy, usually suffices. In large chronic ulcers, we first underrun the
bleeding point with an absorbable suture; with a heavy absorbable suture, we then
obliterate the ulcer’s base. UGI-H from a malignant ulcer very rarely requires an
emergency operation. We would, however, take tissue from the ulcer’s edges for histology. Partial gastrectomy becomes necessary only in cases of a giant GU on the
lesser curvature with direct involvement of the left gastric or splenic arteries.
Definitive Procedure?
After hemostasis, in selected patients, as discussed, a definitive ulcer procedure may be considered. Chronic GU is not “one disease” to be managed by a ritual
gastrectomy; instead, it is comprised of different types, which should be managed
selectively. But frankly, in our part of the world this has become useless information; perhaps it is still valuable in yours?
Ty pe I is the classical lesser-curvature GU. Billroth I partial gastrectomy is
the textbook recommendation. An HSV (from the ulcer proximally) plus
the excision of the ulcer (from inside the stomach) is the alternative that we
would recommend instead.
Ty pe I I is a prepyloric ulcer. Although antrectomy plus vagotomy are pop-
ular for this “hybrid”—between DU and GU—ulcer, excellent results are
achieved with HSV plus pyloroplasty. This is what we would do.
Type III is a combination of a GU and a DU; it should be treated as type II.
Ty pe I V implies a high, juxtacardial, lesser-curvature GU. Prior to the
days of effective antiulcer medication, partial gastrectomy—distal to the
ulcer—was the procedure of choice. Since the entire lesser curvature may
be obliterated, HSV is usually impossible, making TV plus a drainage pro-
cedure a reasonable alternative.
“Riding” GU is a variant of a high GU associated with sliding hiatal hernia,
produced by injury to the herniated stomach “riding” against the diaphragm.
Surgical therapy involves reduction of the stomach by pinching the ulcer
away from the adherent diaphragm, local hemostasis, and crural repair. This
may be easier said than done since occasionally the huge riding ulcer adheres
to mediastinal structures and may require major resective surgery.
Stomal Ulcer
The stomal ulcer develops on the jejunal side of the gastrojejunal anastomosis
following a previous vagotomy and GE or Billroth II gastrectomy. Because stomal
152 Moshe Schein
ulcers almost never involve a large blood vessel, hemorrhage is usually self-limiting
or amenable to endoscopic therapy. Remember also that all stomal ulcers will heal
on modern acid-suppressing medications. Persisting or recurrent hemorrhage,
however, will force you, rarely, to operate. In the high-risk patient, do the minimum:
through a small gastrotomy, perpendicular to the anastomosis, examine the stoma
and ulcer; underrun the latter with a few deeply placed absorbable sutures; close
the gastrotomy and put the patient on H2 antagonists or PPIs for life. In selected
patients, you can opt for a more definitive procedure. If the previous operation was
a vagotomy plus GE, look for a missed vagal nerve or add an antrectomy. In the case
of a previous Billroth II gastrectomy, add TV or consider a higher gastrectomy (do
not forget to rule out Zollinger-Ellison syndrome later). Remember: hemorrhage
from a stomal ulcer can be arrested with a simple surgical maneuver (underrunning); try to stay out of trouble by not escalating the emergency procedure into
complicated reconstructive gastric surgery, which may kill your bleeding patient.
Dieulafoy’s Lesion
The small, solitary, and difficult to diagnose gastric vascular malformation
termed a Dieulafoy’s lesion typically causes a recurrent “obscure” massive UGI-H.
It is best managed by transgastric local excision or underrunning.
Acute Superficial Mucosal Lesions
With effective antiulcer prophylaxis in critically ill patients, you will be called
to operate on acute superficial mucosal lesions only a few times in your surgical life.
When massive hemorrhage necessitating an operation occurs, however, the involved
stomach may look and behave like a blood-soaked and dripping sponge. Surgical
options mentioned by the standard textbooks include TV and drainage or total
gastrectomy. The former is associated with a very high rate of rebleeding and the
latter with a prohibitive mortality rate. In this situation, we advocate gastric
devascularization by ligating the two gastroepiploic and left and right gastric
arteries near the stomach’s wall. In our experience, this relatively simple and
well-tolerated procedure results in an immediate drying of the gastric sponge.
UGI-H from an Unknown Source
You will not encounter many UGI-H from an unknown source if the management plan has been followed, including—if necessary—the resort to intraoperative
endoscopy. Angiography is an option and an excuse exercised by those looking
17 Upper Gastrointestinal Hemorrhage (and Portal Hypertension) 153
for a pretext to delay surgery. It is useless if performed when bleeding is not active.
When talking about angiography, we have to mention another management
option: angiographic embolization of the bleeding vessel. We would consider this
option as an alternative to an operation in special circumstances, for example,
bleeding DU when the risk of operative intervention would be prohibitive (e.g.,
after myocardial infarction) or an UGI-H from a pseudoaneurysm of the splenic
artery associated with chronic or acute pancreatitis. Obviously, you have to have
immediate access to a skilled invasive radiologist.
Conclusions
Admit patients with UGI-H to your surgical service. Do not leave them to the
internists, who will call you when the patient is almost dead. After resuscitation,
diagnose the source of hemorrhage and stage it. Give endoscopic treatment a
chance but do not delay an indicated operation. At surgery, the goal is to stop the
bleeding—remembering that most ulcers can be cured later by medication. Life
comes first. Perhaps this rhyme will help you to remember:
When the blood is fresh and pink and the patient is old
It is time to be active and bold.
When the patient is young and the blood is dark and old
You can relax and put your knife on hold.
Esophageal Varices, Portal Hypertension, and Cirrhosis
Luckily, abdominal surgery plays almost no role in the modern management
of bleeding from esophageal or gastric varices. Luckily because some of us still
remember the old days when we spent the night inflicting on these patients all
sorts of emergency portocaval shunts or devascularization procedures, which
were effective in arresting the hemorrhage but led to tremendous mortality from
postoperative liver failure and its complications. (The operation was successful,
but the patient died.) In this section, I briefly touch on the nonsurgical approach
to variceal bleeding and the cirrhotic patient in general.
Stratification
Remember that anything you plan to do in a cirrhotic patient, with or without varices, depends on his or her hepatic reserves, which are best assessed by the
modified Child-Pugh classification presented in > Table 17.3.
154 Moshe Schein
Table 17.3. The Child-Pugh classification
Bilirubin (mg%) <2 2–3 >3
Albumin (g%) >3.5 2.8–3..5 <2.8
INR <1.7 1.7–2.3 >2.3
Encephalopathy None Mild Marked
Ascites None Mild Marked
a
Charles Gardner Child III (1908–1991) was a professor of surgery at the University of
Michigan. Pugh published his classification in 1973 (Pugh et al. 1973)
b
The individual scores are summed and then grouped as: <7 = Child A; 7–9 = Child B;
>9 = Child C (a Child C classification forecasts a survival of less than 12 months)
a
b
Score
1 2 3
Child A patients have good hepatic reserves. They will tolerate variceal
bleeding and its management fairly well. They are also reasonable candidates for
any indicated emergency abdominal procedures. Essentially, you can treat them
as you treat noncirrhotic patients. But, bear in mind that the chronically diseased liver may decompensate when burdened with the metabolic consequences
of severe surgical complications.
Child C patients (some call them “yellow balloons”) have no hepatic re-
serves whatsoever, and in the absence of successful hepatic transplantation they
are doomed to die within a year or so. Child C patients tolerate surgical procedures and their complications poorly. Consequently, operate on them only for
lifesaving indications, in the absence of non-operative alternatives, and expect
very high mortality and morbidity, depending of course on the specific problem
and the magnitude of the operation.
Child B patients fall in between groups A and C; do the minimum neces-
sary and be very careful.
Bleeding Varices
Patients presenting with UGI-H from varices will usually provide a history
of chronic liver disease or cirrhosis (alcoholic, viral) or previous episodes of
bleeding. On examination, most of them will have features of portal hypertension
and liver dysfunction listed in > Fig. 17.3. The variceal source of the hemorrhage
will be diagnosed or confirmed during the emergency endoscopy—not forgetting the cliché that one-third of UGI-H’s in portal hypertension patients are not
17 Upper Gastrointestinal Hemorrhage (and Portal Hypertension) 155
Fig. 17.3. Clinical features of cirrhosis
variceal but from other sources such as peptic ulcers. While portal hypertensive
gastropathy can be a source for minor and chronic blood loss, it is probably not
a cause for severe UGI-H. It is a classic and unforgivable error to attribute bleed-
ing in a cirrhotic patient to varices while overlooking the responsible DU.
How best to manage an episode of esophageal variceal hemorrhage depends
on the local facilities and expertise in your hospital and the tertiary care available in your environment. The essential options of management are outlined in
>
Fig. 17.4).
Summary
The surgeon’s role in variceal hemorrhage is limited. Resuscitate, exclude
nonvariceal causes of hemorrhage, tamponade bleeding with a balloon tube, and
then send for help from the gastrointestinal specialists. For once, you get to go
home at night.
156 Moshe Schein
Fig. 17.4. Variceal bleeding: options in management. TIPPS Transjugular intrahe-
patic portal systemic shunt
Reference
Pugh RN, Murray-Lyon IM, Dawson JL, Pietroni MC, Williams R. (1973) Transection of the
oesophagus for bleeding oesophageal varices. Br J Surg 60:649–690.
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