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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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ligation is superior. Sclerotherapy has more complications, such as stricture formation and
scarring. It is important to stabilize the patient before any procedure and to try to correct
coagulopathy as well. The risk of recurrent bleeding from varices is very high and ranges from
40–80%. Risk of recurrent variceal bleeding can be reduced with the use of nonselective beta-
blockers (e.g., propranolol) once the patient is stable.
If bleeding cannot be controlled with banding, the next line of treatment includes TIPS, or
transjugular intrahepatic portosystemic shunting. Somatostatin/octreotide causes splanchnic
vasoconstriction and should be used as adjuncts to endoscopic therapy to control bleeding and
prevent further bleeding. If the above measures fail, shunt operations can be considered to
decrease portal hypertension. A Blakemore tube is rarely used and only as a bridge to surgery.
Platelet transfusions are used as needed if the platelet count drops. Fresh frozen plasma is used
to correct the elevation in PT/PTT. This elevation is common in alcoholics and can be
secondary to nutritional deficiency or liver disease with poor synthetic function.
Given the history of recent alcohol use and severe bleeding, this patient should also be
monitored in an intensive care setting for signs of delirium tremens. Gastric varices can regress
in alcoholic patients who abstain from alcohol. Once this patient recovers, he should be
advised to stop alcohol consumption and seek professional treatment regarding this.
Vasopressin is no longer used with variceal bleeding. It has no additional efficacy when
compared with octreotide and has more potential cardiac adverse effects.
Follow-up Management and Prevention
Surveillance for varices every 2 years after initial presentation
If varices are present on subsequent endoscopies, band ligation is the most appropriate
therapy
To prevent further variceal bleeds, use a nonselective beta blocker (propranolol or nadolol)
491
Final Diagnosis
Bleeding esophageal varices
492
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Case 3
Chief Complaint
“My gut hurts, but it feels better after I eat.”
History and Physical Examination
A 52-year-old man presents with a 2-month history of epigastric pain. The pain wakes him
up from his sleep. Eating and over-the-counter antacids relieve it. He has no significant
weight loss and no nausea or vomiting. He has no known history of pancreatic or ulcer
disease. He does not drink alcohol. He occasionally smokes and takes aspirin for back
pain.
He is a healthy-appearing man in very mild distress. His vital signs are stable.
Examination of his heart and lungs is WNL. His abdomen is soft, nontender, nondistended,
and there are no palpable masses. Rectal examination is without any masses and is guaiac
negative.
Differential Diagnosis
Duodenal ulcer1.
Epigastric pain that is long-standing and awakens someone from sleep can be gastric
or duodenal, but classically pain that is better with eating is duodenal in nature
—
Gastric ulcer2.
More common when patient has pain that is worsened with eating—
493
Initial Management
Setting: outpatient
Diagnostic/Therapeutic Plan
Test Results
Assessment
Esophagitis
3.
Commonly found in patients with GERD; would have complaints of chest pain
—
Gastric cancer
4.
Does have dull epigastric pain that is unrelated to eating; would be associated with
early satiety
—
Cholelithiasis
5.
Would have post-prandial pain; would localize to right upper quadrant
—
CBC
Liver function tests
U/S of the gallbladder
Amylase/lipase
CBC: normal
LFTs: normal
U/S: negative for cholelithiasis
Amylase/lipase: normal
494
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The patient presents with epigastric pain relieved partially with antacids. This is suggestive of
peptic ulcer disease, specifically, duodenal ulceration. Pain is classically described as burning
or gnawing and is most severe in early morning and 2–3 hrs after eating. Gastric ulceration can
be associated with a worsening pain on eating. Complications of peptic ulcer disease include
bleeding, perforation, and gastric outlet obstruction, which may present as protracted vomiting
immediately after eating.
Cholelithiasis may also present with postprandial epigastric pain and may be excluded with
U/S of the gallbladder. Initial diagnostic assessment should exclude evidence of chronic blood
loss. A young patient with classic presentation for peptic ulcer disease can be treated
empirically with H2-blockers or proton pump inhibitors. If symptoms persist, then an
evaluation should be pursued.
If ulcers recur, an underlying disorder such as Zollinger-Ellison syndrome should be excluded.
A patient age >50 is at greater risk for a malignant ulcer, and should be evaluated initially with
endoscopy.
CLINICAL PEARL
Testing for eradication for H. pylori can be with either urea breath testing or stool
antigen testing. Both are equivalent but stool testing is more cost effective.
Further Management Plan/Results
Upper
endoscopy with
biopsy
Nondilated stomach with 1-cm ulceration in the first portion of the
duodenum; no bleeding or evidence of gastric outlet obstruction
Biopsy with Warthin–Starry stain is positive for H. pylori
495
CLINICAL PEARL
If a patient has a duodenal ulcer and is H. pylori-negative, the likely cause is NSAID-
induced peptic ulcer disease. The chance of getting peptic ulcer disease and bleeding
with NSAIDs increases with advanced age, comorbid conditions, and concomitant use
of corticosteroids and high-dose NSAIDs.
Basic Science Correlate
Discussion
This patient has a duodenal ulcer secondary to H. pylori. The initial medical management of
peptic ulcer disease is antisecretory therapy with proton pump inhibitors (e.g., omeprazole,
lansoprazole). There is no difference between the different medications within a class;
however, the proton pump inhibitors produce more rapid healing of duodenal ulcers because of
their sustained antacid secretory effect compared with H2 blockers.
Sucralfate is an inert orally ingested medicine that topically coats the ulcer, forming a
protective layer. Sucralfate is equal in ulcer-healing efficacy to H2 blockers. Antacids are
composed of aluminum and magnesium hydroxide and act by neutralizing gastric acid and
H. pylori is a microaerophilic helix-shaped gram-negative bacterium
H. pylori produces oxidase, catalase and urease
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protecting gastric mucosa. Antacids at high doses also demonstrate healing rates comparable
with H2 blockers, but the ulcers will recur without eradicating H. pylori.
H. pylori infection is associated with 90% of duodenal ulcers and 70% of gastric ulcers.
Therapy for H. pylori dramatically reduces the recurrence of ulcer disease (75–90% reduction
in peptic ulcer). Almost 50–60% of patients will have a recurrence after treatment with H2
blockers or PPIs alone if H. pylori is not eradicated with antibiotics.
Unfortunately, the therapeutic regimen for H. pylori has not been sufficiently standardized to
offer a single recommendation. Combination therapy with a PPI and 2 of 4 antibiotics
(clarithromycin, amoxicillin, tetracycline, or metronidazole) is most commonly used. Other
therapeutic regimens include bismuth subsalicylate combined with 2 antibiotics. The urease
test, breath test, and H. pylori serum antibody all have a sensitivity of >96% and a specificity
of 99%. When duodenal ulcers occur in young patients with typical features, an upper
endoscopy is not always necessary to confirm the diagnosis.
Follow-up Management and Prevention
H. pylori therapy for 2 wks with an oral PPI (such as omeprazole, pantoprazole, or
rabeprazole), combined with amoxicillin/clarithromycin or metronidazole/clarithromycin.
Alternatives include tetracycline/metronidazole/bismuth subsalicylate or
tetracycline/clarithromycin/bismuth subsalicylate. Any PPI with amoxicillin/clarithromycin
is the single best answer.
Surgery for severe complications such as severe bleeding not responsive to local therapy,
perforation, or obstruction; although duodenal ulcers are not associated with malignancy,
refractory cases may rarely require surgery
Counseling of patients:
Avoid excess use of NSAIDs—
Smoking and alcohol use prevent the healing of ulcers but do not cause them—
Bland (nonspicy) diets do not help, nor does removing spicy food from diets—
497
CLINICAL PEARL
H. pylori is not associated with GERD.
Final Diagnosis
Duodenal ulcer
498
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Case 4
Chief Complaint
Confusion
History and Physical Examination
A 45-year-old man was admitted 2 days ago for an acute upper GI bleed. The patient is an
alcoholic with a long history of alcoholic liver disease. He underwent endoscopy on
admission and was found to have a bleeding duodenal ulcer that responded to treatment
with omeprazole. The patient appeared to be stabilizing. This morning, however, the nurse
noted that the patient was becoming increasingly confused. He appeared agitated and was
oriented to his name, but thought the current year was 1972 and that Nixon was president.
The patient has become increasingly lethargic over the last few hours. He has been on
thiamine since admission.
He is afebrile; BP is 130/80 mm Hg, pulse 80/min, and respirations 16/min. The neck is
supple, lungs are clear, and heart has RRR. His abdomen is soft, nontender, liver edge not
palpated, splenic tip 3 cm below the left costal margin. He is lethargic and uncooperative,
withdraws to pain, and is hyperreflexic bilaterally. Asterixis is present, while nystagmus
is not. Cranial nerve examination reveals no overt opthalmoplegia.
Differential Diagnosis
Hepatic encephalopathy1.
Confusion in liver disease is highly suspicious for hepatic encephalopathy,—
499
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Test Results
compounded by the fact that the patient recently had an upper GI bleed (a known
trigger for worsening hepatic encephalopathy)
Alcohol withdrawal/delirium tremens
2.
Liver disease can be secondary to alcoholism and so a concurrent syndrome could
be seen. However the finding of asterixis and normal vital signs make it less likely.
—
Infection: meningitis, bacterial peritonitis if patient has ascites
3.
Any infection has the potential to cause sepsis and lead to end-organ damage (AMS,
confusion, low urine output, etc.)
—
CBC
BUN/creatinine
AST/ALT
Lactate dehydrogenase
Bilirubin
Glucose
Ammonia
WBC 5,000/mm
3
(normal 4,000–11,000/mm
3
), hemoglobin 10 mg/dL (normal 13–17mg/dL),
platelets 110,000/mm
3
(normal 150,000–350,000/mm
3
); MCV 92 μm
3
BUN 20 mg/dL; creatinine 1.1 mg/dL
AST 60 U/L (normal 8–30 U/L); ALT 48 U/L (normal 8–30 U/L)
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