Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3860_Библиотеки_им_академика_М_И_Перельмана
.pdf
354
https://t.me/med1917
M. J. Hallisey and S. G. Meranze
the Hurst or Maloney dilators); however, the use of endoscopic techniques has encouraged the development of
types of bougies that pass over guidewires, reducing the
likelihood of perforation. The most popular of these
models are the Celestine and Eder-Puestow devices.
Although effective, these devices have one major disadvantage: They provide a significant radial force on the
stricture but also exert longitudinal force on the adjacent, normal esophagus. This additional stress can lead
to perforation or mucosal tears.
3
Angioplasty balloons
passed over a wire and placed directly across the lesion
may overcome the shortcomings of bougienage. These
balloons can be introduced on a small catheter that then
can be inflated to a large outer diameter, thus maximizing the radial force on the lesion while reducing the
longitudinal force on the adjacent esophagus.
General intubation techniques
Before esophageal dilation, an esophagram is required to
help delineate the anatomy of the stricture. Stricture
dilation generally does not require analgesics, and sedation with intravenous midazolam hydrochloride (Versed)
is usually adequate. Atropine may be helpful if the patient
develops signs of increased vagal tone (e.g., bradycardia)
or if secretions are copious. The use of topical analgesia
such as anesthetic gels or oral sprays are recommended
to avoid patient discomfort and to reduce the gag reflex.
A soft nasogastric tube is passed transorally and placed
just above the level of the stricture. The transoral intubation approach usually is employed for esophageal stricture dilation. This transoral route is easier and better
tolerated, and it will permit passage of catheters larger
than those used in the transnasal approach. Moreover,
this route must be used for the placement of stents. The
transnasal approach is preferred if a feeding tube is to be
placed over the same guidewire. By enlarging the side
hole in the nasogastric tube, the rounded tip of the tube
can be maintained while still allowing guidewires to be
inserted through the tube. After the tube is in position, a
small amount of contrast is injected to define the proximal aspect of the stricture. In patients at risk for aspiration, dilute barium or oily contrast may be used.
A flexible-tipped standard 0.035-inch guidewire then is
passed through either the endhole or sidehole of the
nasogastric tube, which then is exchanged for a 5 Fr selective angiographic catheter. Although the stricture often
can be traversed using a flexible guidewire, a torque-control guidewire or hydrophilic guidewire may be used to
cross the lesion if the stricture is particularly tight or irregular. Great care must be exercised to minimize the risk
of esophageal perforation, particularly in patients who
have malignant strictures. Once the guidewire and catheter are through the lesion, the guidewire is removed and
replaced with a long exchange wire (⬎ 180 cm), which is
advanced well into the stomach or small bowel. At this
point, the catheter can be exchanged for the balloon
dilating catheter, which is placed across the stricture.
A diameter of 20 mm in the esophagus is recommended to permit normal oral intake. With extremely
tight strictures (i.e., ⱕ 3 mm) a 6- to 8-mm predilating
balloon is used and then exchanged for larger-diameter
sizes as needed. If no “waist” persists with the small balloon, it is exchanged for one with a larger diameter (i.e.,
12, 15, or 20 mm) until the 20-mm diameter is achieved.
Whereas most patients experience some discomfort, a
significant degree of discomfort during dilation should
signal the interventional radiologist to limit the increase
in balloon size, at least for the current session. In patients
with achalasia, overdistention of the esophagus may be
desired, and multiple balloons may be used to achieve the
desired lumen diameter. In patients who have strictures
resulting from caustic ingestion, great care must be taken
to avoid perforation.
An esophagram should be performed after the dilation
procedure to evaluate for possible esophageal tears. The
appearance of the lesion at this point is not predictive of
clinical success, however. A postprocedural success rate of
90 to 95% in the esophageal lesions, with approximately
70% of benign lesions remaining asymptomatic 2 years
following dilation, should be expected.
4
Although long-term relief is unlikely, dilation of malignant lesions can be used to assist in the placement of
enteric feeding tubes, and some degree of palliation can
occur, if only for a short time. The use of stents has greatly
changed the ability to palliate these patients.
Stents
Plastic stents have largely been replaced by metallic stents
because of problems with food impaction and perforation. In one review, the complication rate was 36% the
dislodgment rate 20%, and the morbidity rate 16% during endoscopic placement of these plastic stents.
other locations, the use of metallic stents in the esophagus
is intended to maintain a stable lumen diameter, with a
small and well-tolerated introducing system. Currently,
three metallic stents are available that have been approved for use in the esophagus. The Cook Gianturco
(Cook Inc., Bloomington, IN) stent and the Schneider
Wallstent (Schneider USA, Minneapolis MN) are covered. The third, the Ultraflex nitinol stent (Medi-tech,
Boston Scientific, Watertown, MA), is a tightly woven metal mesh. All three stents were designed to provide a largelumen diameter while preventing ingrowth of tumor at
the ends or through the body of the stent.
The procedure for placing these stents is similar to
performing a balloon dilation (Fig. 29-1). It is necessary
5
As in
BA C
https://t.me/med1917
D E
FIGURE 29-1. Transluminal stent placement for the relief of esophageal obstruction. A: A 55-year-old man with esophageal
carcinoma originating just above the gastroesophageal junction. Note the “bird’s beak” appearance of the stenotic segment and
the proximal esophageal dilation. B: The stenotic area was dilated with a 15-mm balloon before the stent was placed. C: An
18-mm diameter by 6 cm Wallstent is deployed under fluoroscopic guidance across the stenotic segment by releasing the
constraining membrane. D: The stent fully expands after balloon dilation, which provides the patient with a large enough lumen
for passage of the food bolus. E: After stent placement, contrast empties from the esophagus into the stomach. The stent
terminates just above the gastroesophageal junction in an attempt to avoid reflux.
356
https://t.me/med1917
M. J. Hallisey and S. G. Meranze
to extend the neck fully to insert these stents because of
size and rigidity of introducer device. It is important to
predilate the lesions to at least 12 to 14 mm to allow the
device to be inserted and withdrawn without difficulty.
The results obtained with these stents have been encouraging. In most series, with properly selected patients,
no problem with initial insertion has been encountered.
Most patients have had prompt relief of dysphagia (within
24 hr). Complications can include migration, perforation, tumor overgrowth (all types), and tumor ingrowth
(uncovered stents). Erosion with hemorrhage (some fatal) has occurred, particularly in patients who have previously undergone radiation therapy. Tracheoesophageal
fistulas that occur as a consequence of malignancy
infection
7
also have been treated by placing covered
6
or
stents.
Because of their short life expectancy, long-term follow-up is a relative concept in these patients. Complications or tumor overgrowth have been treated either by
redilating or repeat stenting. In cases of tumor ingrowth,
laser cauterization or restenting is usually adequate to
reestablish patency. Treatment of benign stenoses with
stents is still controversial. Long-term sequelae from
these stents may be esophageal erosion or intense tissue
hyperplasia.
8
■ Gastric and Duodenal Strictures
Strictures of the antral and pyloric regions as well as the
body of the stomach and duodenum also may be dilated.
Balloons larger than 20 mm may be required. If balloons
larger than 20 mm are not readily available, multiple
balloons are necessar y to achieve a diameter this large.
The use of two balloons will result in an oblong-shaped
dilation surface. Therefore, three balloons are recommended to create a shape more closely approximating a
round dilation surface.
9
Compared with the esophagus, the stenotic antrum,
pylorus, or duodenum may require more skill in intubation. The stomach may be fluid filled and distended,
making the use of standard angiographic techniques difficult. In these patients, stiffer tubes such as those used
for duodenal intubation or cooperation with the endoscopist may be necessary during the initial stricture passage. Although the endoscope may not pass through the
stricture, it can be used to support the angiographic
catheters and to assist in the direction of the guidewire.
Once the lesion has been traversed, the techniques are
similar to those used in the esophagus, with exchanges
made over a stiff exchange-length guidewire. A final
lumen size of approximately 12 mm is ideal. In our series, long-term follow-up has demonstrated that approximately 75% of patients developed some degree of relief
following dilation.
4
■ Postoperative and Anastomotic
Strictures
Postoperative and anastomotic strictures also can be
treated with balloon dilation, particularly if the patients
are poor surgical candidates. Moreover, conventional endoscopic techniques can be difficult in these patients.
The techniques for dilating anastomotic strictures are
similar to those in other areas; however, the challenge
with anastomotic strictures is due more to difficulties in
the intubation technique than that of the dilation procedure itself. Endoscopic assistance can be used to access
and treat these strictures, using the endoscope to assist in
finding the lumen. Balloons of 12 to 15 mm are generally
adequate. To our knowledge, balloon rupture of an esophagogastric anastomosis has not occurred.
Postoperative pyloric stenosis can develop following
vagotomy and pyloroplasty. The stenosis can be secondary
to pylorospasm (in the immediate postoperative period
related to an incomplete pyloromyotomy) or surrounding
fibrosis (which can occur many years after surgery). Recently, Denys et al.
channel with a 30-mm balloon as the initial treatment
procedure to reduce the likelihood of repeat dilation. Because the pylorus has a relatively smaller normal diameter
than the esophagus or stomach, many interventional radiologists previously had approached these stenoses with a
10-mm or smaller diameter angioplasty balloon, but when
balloons this size are used to treat these pyloric stenoses,
multiple repeat dilations may become necessary because
of recurrence of the stenosis.
■ Colonic Strictures
Large, expandable metallic stents are now available for
the palliative treatment of colonic obstruction. They have
not been approved for the treatment of benign strictures.
Interventional management of malignant strictures has
several advantages: (a) prompt relief of obstructive symptoms, (b) elimination of the need for emergent colostomy in the presence of unprepped bowel, (c) a less
invasive procedure compared with surgery, and (d) in
some cases, an outpatient procedure. The stents reach a
maximum diameter of 22 mm and a maximum length of
11
9 cm.
The treatment procedure (Fig. 29-2) is similar to stent
placement in other locations within the GI tract. The
lesion is localized and measured using standard barium
techniques. A small catheter is used to cross the lesion. A
stiff wire is placed across the lesion. The stent is placed
across the lesion under fluoroscopic guidance and expanded by withdrawing the constraining membrane. Decompression of the obstructed segment is immediate, but
10
advocated overdilation of the pyloric
FIGURE 29-2. A 60-year-old patient presenting with colonic
https://t.me/med1917
obstruction secondary to a malignancy. Following stent placement across the transverse colon, the large bowel obstruction
is relieved.
luminal size can be increased by balloon dilation of the
stent.
Although these larger-diameter stents are now available
for the palliative decompression of colonic obstruction,
there are emerging indications for which the stents are
proving beneficial. These indications include (a) poor
Gastrointestinal Strictures 357
surgical or medical risk, (b) no potential cure of a malignancy with resection, (c) repeat dilation of recurrent
stenoses, and (d) postoperative strictures. More research
in these newer areas will be necessar y before widespread
use and clinical approval are achieved.
■ Summary
Gastrointestinal strictures are amenable to transluminal
balloon dilation and stent placement. Newer catheters,
wires, and stent materials are now making these procedures easier to perform by interventional radiologists.
REFERENCES
1. Sons Hu, Borchard F. Cancer of the distal esophagus and cardia:
incidence, tumorous infiltration and metastatic spread. Ann Surg
1986;203:188–195.
2. Muller JM, Erasmi H, Stelzner M, et al. Surgical therapy of oesophagel carcinoma. Br J Surg 1990;77:845–857.
3. McLean GK, LeVeen RF. Shear stress in the performance of esophageal dilation: comparison of balloon dilation and bougienage. Ra-
diology 1989;172:983–986.
4. McLean GK, Cooper GS, Hartz WH, et al. Radiologically guided
balloon dilation of gastrointestinal strictures. Radiology 1987;165:
35–43.
5. Fugger R, Niederle B, Jantsch H, et al. Endoscopic tube implantation for the palliation of malignant esophageal stenosis. Endoscopy
1990;22:101–104.
6. Song H-Y, Young-Soo D, Young-Min H, et al. Covered, expandable
esophageal metallic stent tubes: experiences in 119 patients. Radi-
ology 1994;193:689–695.
7. Nelson DB, Silvis SE, Ansel HJ. Management of a tracheoesophageal fistula with a silicone-covered self-expanding metal stent.
Gastrointest Endosc 1994;40:497–499.
8. Cwikiel W, Willen R, Stridbeck H, et al. Self-expanding stent in the
treatment of benign esophageal strictures: experimental study in
pigs and presentation of clinical cases. Radiology 1993;187:667– 671.
9. Gaylord GM, Pritchard WF, Chuang VP, et al. The geometry of
triple-balloon dilation. Radiology 1988;166:541–555.
10. Denys A, De Baere T, Lasser P, et al. Single-step balloon dilation of
postoperative pyloric stenosis: benefit of large-balloon technique. J
Vasc Inter v Radiology 1994;5:781–782.
11. Mainar A, Tejero E, Maynar M, et al: Colorectal obstruction: treatment with metallic stents. Radiology 1996;198:761–764.
https://t.me/med1917
S.SprayregenNonvaricealUpper GI Bleeding
https://t.me/med1917
30
■■■
Nonvariceal Upper GI Bleeding
SEYMOUR SPRAYREGEN
Upper gastrointestinal (UGI) bleeding refers to a bleeding site proximal to the ligament of Treitz and accounts for
80% of all gastrointestinal bleeding.
entity must be recognized as potentially lethal, so diagnosis, resuscitation, and definitive treatment should be undertaken concomitantly. The mortality from acute nonvariceal UGI bleeding is approximately 10% and has
remained fairly constant over the past 50 years;
been postulated that, despite advances in pharmacologic
and endoscopic therapy, the mortality rate has remained
the same because older, sicker patients have made up an
increasing proportion of patients with gastrointestinal
bleeding.
that there is some evidence of a decline in mortality over
the past 10 years, endoscopic advances and the wider availability and increased effectiveness of treatment in intensive care units are credited with the improved survival.
The epidemiology of UGI bleeding is not static. The
number of hospitalizations for gastric ulcers increased by
20% and the frequency of bleeding gastric ulcers increased by 100% between 1980 and 1985; during the
same period, however, hospital admissions for nonbleeding duodenal ulcers decreased dramatically.
crease in bleeding gastric ulcers has been attributed to
the frequent use of nonsteroidal antiinflammatory drugs
(NSAIDs), and the lower incidence of duodenal ulcers
has been attributed to the availability of histamine 2-receptor antagonists (H
UGI bleeding from a wide variety of sources stops spontaneously in approximately 80% of patients. Recurrent
bleeding, however, occurs in as many as 25% of cases. In
patients who have continued bleeding or rebleeding,
mortality rates may be as high as 30 to 40%.
3
On the other hand, in one article suggesting
6
RAs).
2
1
From its onset, this
2
it has
5
The in-
7
Patients
4
must receive prompt, effective treatment to preclude the
onset of hemorrhagic shock and coagulopathy. Even
when bleeding rapidly ceases spontaneously, identifying
the source of the hemorrhage will facilitate rapid treatment if rebleeding occurs.
■ Clinical Approach to UGI Bleeding
History and physical examination
A careful history and physical examination often will
direct the physician to the cause of the bleeding and yield
information regarding coexisting diseases and medications that may impact diagnosis and treatment. A history
of pain preceding presentation or a histor y of peptic
ulcer disease suggests peptic ulcer disease. The use of
aspirin or other NSAIDs should raise the suspicion of
peptic ulcer. A history of retching or vomiting before
bleeding is classic for a Mallory-Weiss tear. Alcohol use or
a history of blood transfusions increases the likelihood of
liver disease with congestive gastropathy or varices. A
previous history of pancreatitis should lead the physician
to consider hemorrhage resulting from a pseudoaneurysm or pancreatic pseudocyst. Renal disease often is
associated with GI bleeding.
tients with acute renal failure have GI bleeding, often
from peptic ulcer disease. Aortoduodenal fistula must be
the primary consideration in patients with an aortic graft
for aneur ysm or occlusive disease, but it may occur with
abdominal aortic aneurysms without previous surgery. A
history of epistaxis, especially with skin telangiectasias,
should raise the possibility of Osler-Weber-Rendu disease.
8
Approximately 50% of pa-
359
360 S. Sprayregen
https://t.me/med1917
Physical evaluation should include evaluating for stigmata of cirrhosis, abdominal tenderness, and a rectal
examination. Inspection of nasogastric and rectal contents may provide information regarding the prediction
of mortality; with bleeding from peptic ulcers, mortality
rates of 30% when there was a red nasogastric aspirate
and red stool and 9% when the nasogastric aspirate and
stool were black have been reported.
9
Hematemesis generally indicates a more severe bleeding episode than melena.
Orthostatic hypotension (an increase in pulse rate by more
than 20 beats per minute, a decrease in systolic blood
pressure by more than 20 mm, and a decrease in diastolic
blood pressure by more than 10 mm) may be the only
physical finding and this usually occurs when there is a
loss of 20% of intravascular volume or 1500 mL. Frank
shock with supine hypotension and tachycardia indicates
a volume loss approaching 40% or 2500 mL. Hypotension
may result in transient hemostasis, and bleeding may recur when the blood pressure is restored to normal levels.
Resuscitation and management
An algorithm for the management of UGI bleeding is
shown in Figure 30-1.
Nasogastric tube and gastric lavage
A nasogastric tube should be passed. Black coffee-ground
material (due to gastric acid acting on hemoglobin to
form acid hematin) that tests positive for blood is indicative of recent hemorrhage, and bright red unclotted
blood suggests continued rapid bleeding. If the nasogastric aspirate does not show evidence of blood, it is important to note the presence or absence of bile; if bile is
present, it is likely that the bleeding is from the lower GI
tract or that a UGI source has stopped. If neither blood
nor bile is present, the bleeding may still be from a duodenal ulcer with no reflux of duodenal contents into the
stomach (one large survey showed that 12% of patients
with no blood on nasogastric aspirate demonstrated active UGI bleeding on endoscopy).
showed a higher correlation between nasogastric return
and endoscopy with gastric lavage and more prolonged
nasogastric monitoring. Although melena (black tarlike
stool) typically is seen with UGI or small bowel bleeding,
it occasionally is seen with colonic bleeding. Frankly
bloody bowel movements also can be due to bleeding
from the stomach or duodenum and in these latter cases
indicates rapid loss of more than 500 mL of blood.
airway should be protected in patients with a reduced
level of consciousness or repeated episodes of vomiting.
Gastric lavage has been used since the late 1950s, when
Wangensteen and colleagues introduced the principle of
gastric hypothermia for control of UGI bleeding.
sequent studies showed that lavage with saline at room
temperature works as well as with ice solutions; indeed,
cold-fluid lavage may impair coagulation, which occurs
optimally at room temperature. Gastric lavage with a
large-bore tube, regardless of the temperature and type of
solution (saline, water, epinephrine), is a mainstay of
treatment of UGI bleeding in most centers. Decreased
gastric distension results in decreased gastrin release (and
therefore decreased acid secretion). Although hemoglobin in the stomach helps to buffer acid, the fibrinolytic
activity of retained blood outweighs the acid neutralizing
action of blood.
10
This same study
11
10
The
Sub-
FIGURE 30-1. Algorithm for management of upper gastrointestinal bleeding.
Venous access lines
Large-bore (at least 16 gauge) peripheral or central venous access lines and (often) a urinar y catheter should
be placed. A Swan-Ganz catheter should be placed in
patients who have underlying cardiac or renal disease or
in patients in shock. Blood should be analyzed for type
and cross-match for packed red blood cells. Blood should
be drawn for hemoglobin, hematocrit, platelet count,
prothrombin time, partial thromboplastin time, blood
urea nitrogen (BUN), creatinine, calcium, and glucose.
The hematocrit and hemoglobin do not change for the
first few hours after hemorrhage because proportional
Nonvariceal Upper GI Bleeding 361
https://t.me/med1917
amounts of plasma and red blood cells are lost; only as
extracellular fluid enters the vascular space do these values fall, and this equilibration process may take from 24
to 72 hours. An elevated BUN with normal creatinine
suggests a UGI source of bleeding. Oxygen should be
administered because oxygen-carrying capacity is lost
due to the loss of red blood cells (RBCs). The patient
must receive appropriate blood and fluid replacement to
maintain adequate intravascular volume and red cell
mass, and coagulation defects must be corrected (usually
with vitamin K or fresh frozen plasma). A hematocrit of
30% is a reasonable goal for most patients and provides
a buffer should bleeding recur.
Histamine 2-receptor antagonists (H2RAs)
H2RAs reduce gastric acid secretion and are useful for
ulcer healing, but they have not been shown to stop
active bleeding or to definitely prevent rebleeding.
H2RAs are extremely effective in preventing the formation of, and bleeding from, stress ulcers;
13,14
their use in
intensive care unit (ICU) patients accounts for the
marked reduction in stress ulcers seen in ICU patients in
recent years.
Endoscopy
Emergency endoscopy should be the first diagnostic test
in patients with continued bleeding or if esophageal
varices are suspected to be the source of bleeding. It
should be noted that 20 to 30% of bleeding patients with
varices will be bleeding from a source other than
varices.
all melenic material and clots have been evacuated by
lavage. Endoscopy should be performed when bleeding
persists after lavage, because endoscopy usually will be
successful even in the presence of persistent bleeding. It
is likely that hemorrhage from lesions bleeding so rapidly as to preclude endoscopic diagnosis most likely will
not be stopped by further lavage.
UGI bleeding ranges from 74 to 96%.
that endoscopy be performed as close to the bleeding
episode as possible, because the longer the delay between cessation of bleeding and endoscopy, the less revealing will endoscopy be. In one study, the diagnostic
accuracy decreased from 90% when endoscopy was performed within 48 hr of a bleeding episode to 33% when
endoscopy was performed more than 48 hr from the
cessation of the bleeding episode.
rate for emergency endoscopy has been reported to
range from 0.1 to 8%, which contrasts with a complication rate of only 0.01% when elective endoscopy is
used.
emergently should have elective endoscopy within 24 hr
15,16
Endoscopy should be performed as soon as
The accuracy of endoscopy in identifying the cause of
17
It is important
18
The complication
19
All patients who do not undergo endoscopy
of the initial bleed. This timing is important because (a)
endoscopic signs (especially seeing pulsatile arterial
blood) can be used to predict the risk for continued or
recurrent hemorrhage with peptic ulcer,
20
(b) multiple
lesions are present in about 25% of cases and early endoscopy can identify the lesion actually responsible for
the bleeding, (c) superficial lesions can heal in a short
time, and (d) identification of the lesion responsible for
bleeding makes it possible to direct therapy appropriately.
■ Causes of UGI Bleeding
Endoscopic surveys
10,21
show that acid peptic diseases
account for up to 75% of cases of UGI bleeding, with
equal numbers caused by gastritis, gastric ulcer, and duodenal ulcer; varices, esophagitis, duodenitis, and Mal-
12
lory-Weiss tears account for most of the remaining cases.
The following is a brief description of some of the major
causes of nonvariceal UGI bleeding.
Peptic ulcer disease (PUD)
Whereas the number of hospitalizations, operations, and
deaths from PUD have decreased in recent years, hospitalizations for bleeding ulcers have not decreased.
is particularly a problem of the elderly: the incidence of
PUD increases with age. Of patients hospitalized for PUD
complications, 70% are 60 years of age or older, approximately 80% of ulcer deaths occur in patients over 65
years, and the average mortality from complicated PUD
in the elderly is 30%.
PUD is approximately 6%. Clinical risk factors that are
correlated with an adverse outcome from bleeding PUD
are hematemesis, red nasogastric aspirate that does not
clear, clinical shock, age greater than 60 years, and associated illnesses. Endoscopic features associated with a
poor outcome are location (high gastric ulcer, posterior
duodenal ulcer), large size, and endoscopic stigmata of
recent hemorrhage.
Gastric ulcers penetrate the muscularis mucosa, which
distinguishes them from superficial erosions. Although
ulcers can occur anywhere in the stomach, the most frequent location is on the lesser curvature near the angu-
23
laris.
In 2 to 8% of cases, ulcers are multiple.24Gastric
ulcers are one fourth as common as duodenal ulcers.
There are many theories regarding the pathogenesis
of gastric ulcers.
develop gastric ulcers, and the risk of bleeding is twice
that of gastric ulcers in patients who do not take
NSAIDs.
9
NSAID-induced duodenal ulcers occur slightly
less frequently.
acute mucosal lesions and chronic ulcers.
also has been associated with gastric ulcers.
22
Overall mortality from bleeding
20
25
Of patients who take NSAIDs, 25%
26
The use of aspirin is associated with
25,27
25
22
PUD
Smoking
362
https://t.me/med1917
S. Sprayregen
Helicobacter pylori is a gram-negative bacterium that was
first isolated in 1982 and is believed to have a dominant
causal role in chronic superficial gastritis.
28
Because only
a small percentage of patients with H. pylori develop ulcerations and because of the lack of strong evidence from
animal models, it has been difficult to prove that H. pylori
directly causes PUD; however, it is believed that infection
with the organism may be a prerequisite for the occurrence of almost all duodenal ulcers in the absence of
other specific precipitating factors.
28
As mentioned, the
prevalence of H. pylori is much higher than the incidence
of peptic ulcers; however, almost all patients with duodenal ulcer and a somewhat smaller percentage of patients
with gastric ulcer have H. pylori colonization of the stom-
29
ach.
Additional strong evidence that H. pylori causes
peptic ulcers is the marked decrease in the recurrence
rate of ulcers following eradication of the organism.
28
is not clear whether H. pylori and NSAIDs act synergistically to cause ulcers.
Acute hemorrhagic gastritis
This term describes superficial gastric mucosal lesions
(which do not penetrate the muscularis mucosa) that
result in bleeding. The erosions are found primarily in
the body and fundus of the stomach. Hemorrhagic gastritis is associated with physiologic stress (related to trauma,
surgery, burns, or severe medical problems), NSAIDs,
alcohol abuse, and portal hypertension. Less frequent
causes are gastric irradiation, ingestion of caustic substances, bile reflux, and long-distance running. In only
20% of cases is a predisposing cause absent.
erosions and gastric or duodenal ulcers may coexist with
hemorrhagic gastritis.
30
Duodenal
major physiologic stress, with a mortality rate approaching 50%.
31,33
Mallory-Weiss tear
The Mallory-Weiss syndrome, a mucosal tear at the esophagogastric junction, was first described in 1929.
proximately two thirds of patients have an antecedent history of retching or vomiting, and 70% of patients are
35
men.
Alcohol ingestion traditionally is associated with
Mallory-Weiss tears and is present in 40 to 75% of patients.
Recent use of aspirin or NSAIDs (30%), blunt trauma,
straining at stool, coughing, seizures, heavy lifting, primal
scream therapy,cardiopulmonary resuscitation,increased
intracranial pressure, pregnancy, and endoscopy are also
associated with this lesion.
It
the gastric side of the esophagogastric junction, and the
36,37
80 to 90% of tears are on
remaining 10 to 20% are in the esophagus.
authors state that although tears may extend to the
esophagus, they usually do not involve the esophagus
37
alone.
Hematemesis occurs in 85% of cases; 10% of patients present only with melena. Abdominal pain is rare.
The diagnosis is made at endoscopy with visualization of a
single linear mucosal tearin 80to 90% of cases, with two or
three tears seen in the remainder. Transfusions are required in only 40% of patients, and bleeding stops spontaneously in more than 90% of cases. Management is usually
supportive. When intervention is necessary, electrocoagulation, compression with the gastric balloon of a Sengstaken-Blakemore or Minnesota tube, vasopressin (systemic or into the celiac or left gastric artery), and left
gastric artery embolization all have been effective.
Esophageal causes of UGI bleeding
38
34
Other
37,39
Ap-
Stress-related mucosal disease (SRMD)
This is a common cause of acute hemorrhagic gastritis
and also a cause of duodenal mucosal bleeding. The formation of stress ulcers is multifactorial; factors that have
been implicated are coagulopathy, reduced mucosal
blood flow, inhibition of prostaglandin synthesis, bile reflux, reduced secretion of mucus and bicarbonate, and
possibly increased gastric acidity.
physiologic stress, nearly all patients show evidence of
acute mucosal injury. Although SRMD occurs in most
critically ill patients, it is particularly common with major
trauma, severe burns, sepsis, and respiratory, renal, and
hepatic failure. Endoscopic studies have shown that the
incidence of gastroduodenal damage within 18 to 24
hours of admission to an ICU is between 52 and 100%.
Before the use of H2RAs, clinically significant bleeding
occurred in 5 to 20% of patients who had experienced a
12,31,32
Following a major
Hemorrhage is an infrequent complication of peptic esophagitis and is more likely related to an inflamed hiatus
hernia or Barrett’s esophagus. Hemorrhage in these
cases may be the presenting symptom or may be superimposed on other symptoms of esophagitis. Hemorrhage
usually is associated endoscopically with a discrete
esophageal ulcer and less frequently by diffuse ulcerative
esophagitis.
40
Other esophageal diseases that may cause
melena and hematemesis are fungal and viral infections
and aortoesophageal fistula (as a result of foreign bodies,
lung and esophageal cancer, aortic aneurysm, or perforation of an esophageal ulcer).
41
Bleeding is usually fatal
with aortoenteric fistulas.
Gastric tumors
30
Overt bleeding, more frequently melena than hematemesis, infrequently may be the presenting symptom of
Nonvariceal Upper GI Bleeding 363
https://t.me/med1917
gastric cancer,42or it may occur in patients with known
tumors.
43
Bleeding also can be the presenting symptom
with gastric polyps, carcinoid, leiomyoma and leiomyosarcoma, lipoma, and liposarcoma. Bleeding also occurs with lymphoma, metastatic disease to the stomach,
and pancreatic rests.
Dieulafoy’s disease
Dieulafoy’s disease is bleeding that occurs from a defect
in an unusually large but histologically normal submucosal artery, through a minute mucosal erosion, usually
in the proximal stomach; 75 to 95% of lesions occur
within 6 cm of the gastroesophageal junction.
44
Lesions
also have been described in the gastric antrum, duodenum, jejunum, colon, and rectum.
44
Whereas Dieulafoy’s
disease is uncommon, it has been reported to account for
1.7 to 5.8% of cases of nonvariceal UGI bleeding.
44,45
Although alcohol, aspirin, NSAIDs, and PUD have been
45
reported to be associated with Dieulafoy’s,
ciations remain controversial.
37
these asso-
It is not known why the enlarged submucosal artery is
present or what causes the mucosal erosion or defect over
the artery. The two main theories are that a normal artery
becomes elongated with aging, and that a large submucosal artery is congenitally abnormally close to the mucosa. In either case, the tortuous artery may cause pressure on the mucosa, leading to mucosal ischemia and
erosion, which are followed by arterial rupture.
44
Dieulafoy’s disease can cause massive bleeding and can be difficult to see endoscopically because of the small mucosal
defect. The Dieulafoy lesion is identified endoscopically
in 82% of cases (49% were identified on initial endoscopy,
33% during a second examination, and 18% were seen
only at surgery).
46
The typical presentation is a middleaged or elderly man (the male-to-female ratio is 2:1) with
sudden massive hematemesis, melena, and hemodynamic
instability. Angiography can identify extravasation when
bleeding is active, but Dieulafoy’s lesions have no specific
angiographic signs.
47
A review of endoscopic treatment of
Dieulafoy’s disease in 1991 showed that permanent hemostasis was achieved in 85% of cases and that 15% rebled,
requiring a second therapeutic endoscopic procedure.
46
Aneurysms and pseudoaneurysms
Chronic pancreatitis causes pseudoaneurysms by enzymes eroding arterial walls and by pseudocysts eroding
into arteries (variceal bleeding resulting from splenic
vein occlusion also may occur). These problems are unusual but life-threatening complications of chronic pancreatitis. Pseudoaneurysms of pancreatitis rupture and
bleed more frequently than true splenic artery aneu-
rysms. Hemorrhage from these pseudoaneurysms tends
to be intermittent, repetitive, and sometimes massive.
Pseudoaneurysms can bleed into the pancreatic parenchyma or the GI tract through the pancreatic duct; presentation usually is associated with bleeding into the lumen of the GI tract, but patients may present with pain
resulting from pancreatitis or the pseudocyst. The
splenic, gastroduodenal, and pancreaticoduodenal arteries most frequently are involved, but pseudoaneurysms
can originate from any branch of the celiac or superior
mesenteric arteries. Ten percent of patients with chronic
pancreatitis will demonstrate pseudoaneurysms on arteriography.
48
Of pseudocysts, 2 to 10% have been re-
ported to hemorrhage with a mortality rate of 40 to
49
80%.
Hemobilia
Hemobilia refers to bleeding originating in the liver,
biliary tree, or pancreas and passing through the ampulla
of Vater. Trauma, both iatrogenic (40%) or accidental
(20%), is the most common cause; less frequent causes
are hepatic artery aneurysms, gallstones eroding the cystic artery, metastatic disease to the liver, and invasion of
the biliary or pancreatic ducts by tumor or parasitic infection, particularly with ascaris.
Percutaneous biliary drainage (PBD) is a commonly
performed procedure; the incidence of vascular complications requiring therapy is 4 to 6.6%.
may come from a communication of a side hole of the
catheter with the vascular system of the liver or from
vascular trauma.
53
If bleeding is not related to a side hole
of the catheter communicating with hepatic vessels, selective hepatic arteriography is performed.
identified on the arteriogram, selective hepatic venography has been advocated.
tween a hepatic vein and the biliary tract. Hemobilia has
been reported to occur from 1 day to 1 year following
51
PBD.
Asymptomatic hemobilia occurs in 8% of patients
and usually responds to either repositioning the catheter
or catheter upsizing.
reported;
54
thus, diagnosis and treatment should be ag-
51
gressive. The classic triad of biliary colic, jaundice, and GI
bleeding is present in approximately 40% of cases. Endoscopy shows blood or clots at the ampulla in 40% of
cases; it has been suggested that clots favor hepatic hemobilia (because blood remains in the biliary system for
longer periods), and oozing blood favors a pancreatic
55
origin.
Confirmation of hemobilia requires celiac or
hepatic arteriography; isolated case reports of diagnosis
by computed tomography (CT) scanning
netium-99m scintigraphy
scatheter embolization with particles of Gelfoam or
37
50–52
Hemorrhage
53
If no lesion is
53
to detect the rate fistula be-
A mortality rate of 22% has been
56
57
have been reported. Tran-
and by tech-
Соседние файлы в папке Библиотека им академика М.И. Перельмана