|
Lab Studies:
- Complete blood count: Results may show
anemia, leucopenia, and thrombocytopenia in patients with cirrhosis.
Anemia may be secondary to bleeding, nutritional deficiencies, or bone
marrow suppression secondary to alcoholism. Many patients with portal
hypertension have some degree of hypersplenism. The hematocrit value may
be low in patients with upper abdominal bleeding.
- Type and crossmatch blood and order 6
units of packed red blood cells.
- Prothrombin time: Because the coagulation
factors involved in this test are synthesized by the liver, impairment of
the liver function may result in a prolonged prothrombin time.
- Liver function tests: A mild elevation of
the plasma activity of aspartate aminotransferase (AST) and alanine
aminotransferase (ALT) may occur in cirrhosis, although activity may be
normal.
- Blood urea, creatinine, and electrolytes:
Blood urea and creatinine levels may be elevated in patients with
esophageal bleeding. Drug treatment, cirrhosis, ascites, and blood loss
may contribute to changes in the serum electrolytes of these patients.
- Arterial blood gas and pH measurements
- Hepatic serology helps in the assessment
of the cause of cirrhosis.
Imaging Studies:
- Ultrasound of the upper abdomen may be
indicated, especially if biliary obstruction or liver cancer is suspected.
Other Tests:
- Rectal examination: Obtain a stool sample
for visual inspection. A black, soft, tarry stool on the gloved examining
finger suggests upper GI bleeding.
Procedures:
- Endoscopy is required at an early stage to
formulate the management plan. If active variceal bleeding or an adherent
clot is observed, variceal hemorrhage can be diagnosed confidently. The
presence of variceal red color signs (eg, cherry red spots, red whale
markings, blue varices) indicates an increased risk of further bleeding.
Medical Care:
- Esophageal varices with no history of
bleeding
- Patients with esophageal varices and no
prior history of variceal hemorrhage should be treated with nonselective
beta-adrenergic blockers (eg, propranolol, nadolol, timolol), provided
that the use of beta-blockers is not contraindicated (eg, because of
insulin-dependent diabetes mellitus, severe chronic obstructive lung
disease, congestive heart failure).
- The dose of nonselective beta-blockers
is determined by a 25% decrease in resting heart rate or a decrease in
heart rate to 55 beats per minute or the development of adverse effects.
- The use of beta-blockers decreases the
risk of initial variceal bleeding by approximately 45%.
- If contraindications to using
beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate)
are alternatives.
- Treatment with beta-blockers should be
continued indefinitely.
- The role of endoscopic sclerotherapy or
variceal ligation for prevention of esophageal variceal hemorrhage is
still controversial.
- Combined sclerotherapy and treatment
with nonselective beta-blockers offer no advantages over the use of
beta-blockers alone for prevention of esophageal varices hemorrhage.
- Bleeding esophageal varices
- Assess the rate and volume of bleeding.
Check blood pressure and pulse with the patient in the supine position
and with the patient in a sitting position.
- Gain venous access and obtain blood for
immediate hematocrit. Obtain a type and crossmatch. Measure the platelet
count and prothrombin time. Send blood for renal and liver function
tests and measure serum electrolytes.
- Provide emergency treatment as outlined
below.
- Emergency treatment
- Promptly resuscitate and restore
circulating blood volume of patients with suspected cirrhosis and
variceal hemorrhage
- Establish intravenous access for blood
transfusion. While the blood is being crossmatched, start rapid infusion
of 5% dextrose and colloid solution until blood pressure is restored and
urine output is adequate.
- Establish airway protection in patients
with massive upper GI tract bleeding, especially if the patient is not
fully conscious.
- If indicated, correct clotting factor
deficiencies with fresh frozen plasma, fresh blood, and vitamin K-1.
- Insert a nasogastric tube to assess the
severity of bleeding and to lavage gastric contents before endoscopy.
- Consider pharmacologic therapy (octreotide
or somatostatin) and endoscopy as soon as the patient has been
resuscitated. The aim is to establish the cause and to control the
bleeding.
- Endoscopic therapy probably has replaced
balloon tamponade as the initial therapy for variceal bleeding. Balloon
tamponade now rarely is necessary, and, when it is used, it must be
performed by experienced personnel because it is potentially dangerous.
- Endoscopic therapy
- Sclerotherapy
- Sclerotherapy is successful in
controlling acute esophageal variceal bleeding in 80-90% of patients.
Control should be obtained with 1-2 sessions. Patients continuing to
bleed after 2 sessions should be considered for alternative methods to
control their bleeding.
- In the United States, sodium
tetradecyl sulfate or sodium morrhuate generally has been used as a
sclerosant, while polidocanol or ethanolamine has been more popular in
Europe. Variations in the technique or the sclerosant used have not
been shown to influence the outcome.
- Serious complications related to
sclerotherapy have been reported in 15-20% of patients, with an
associated mortality rate of 2%.
- Complications of sclerotherapy may
include mucosal ulceration, bleeding, esophageal perforation,
mediastinitis, and pulmonary complications. Long-term complications,
such as esophageal stricture formation, also may occur.
- Endoscopic variceal ligation (banding)
- Endoscopic variceal ligation is based
on the widely used technique of rubber-band ligation of hemorrhoids.
The esophageal mucosa and the submucosa containing varices are
ensnared, causing subsequent strangulation, sloughing, and eventual
fibrosis, resulting in obliteration of the varices.
- Endoscopic ligation requires placement
of an opaque cylinder over the end of the endoscope. This decreases
the endoscopic field of view and may allow pooling of blood. Thus, in
patients with active bleeding, visualization may be impaired more with
ligation than with sclerotherapy.
- Recent trials have demonstrated that
ligation and sclerotherapy achieved similar rates of initial
hemostasis in patients whose varices were actively bleeding at the
time of treatment.
- Local complications are less common
with ligation compared to sclerotherapy. For example, esophageal
strictures were found to be less common with ligation compared to
sclerotherapy. Systemic complications, such as pulmonary infections
and bacterial peritonitis, were not significantly different in the 2
groups. However, a trend was observed toward a decrease in these 2
complications in patients treated with ligation.
Surgical Care:
Surgical care and therapeutic radiologic procedures for variceal
hemorrhage
Approximately 5-10% of patients with
esophageal variceal hemorrhage have conditions that cannot be controlled by
endoscopic and/or pharmacologic treatment. Balloon tamponade (eg, Minnesota
tube, Sengstaken-Blakemore tube, Linton-Nachlas tube) may be used as a
temporary option in their management. Definitive salvage options may include
the following:
- Surgical interventions include the
following:
- Devascularization (transabdominal
devascularization of the lower 5 cm of the esophagus and the upper two
thirds of the stomach, with staple gun transection of the lower
esophagus) rarely is performed but may have a role in patients with
portal and splenic vein thrombosis who are not suitable candidates for
shunt procedures and who continue to have variceal bleeding despite
endoscopic and pharmacologic treatment.
- Orthotopic liver transplantation is the
treatment of choice in patients with advanced liver disease.
- Therapeutic radiologic procedures include
the following:
- Percutaneous transhepatic embolization
of gastroesophageal varices (PTE) involves catheterization of the
gastric collaterals that supply blood to varices via the transhepatic
route. A variety of agents had been used, with varying degrees of
success in controlling acute bleeding. Generally, this procedure is less
effective than endoscopic sclerotherapy for treatment of variceal
hemorrhage and is much less effective compared to medical and surgical
options. Thus, it should be reserved for situations in which acute
variceal bleeding is not controlled by pharmaceutical treatment,
endoscopic sclerotherapy, or endoscopic variceal ligation and in which
contraindications for surgical management are present.
- Transjugular intrahepatic portosystemic
shunts (TIPS) are an effective salvage procedure for stopping acute
variceal hemorrhage after failure of medical and endoscopic treatment.
However, this procedure is associated with a number of complications;
20% of patients develop encephalopathy, and 50% may occlude their shunt
in 1 year. Thus, it should be considered as a bridge to subsequent liver
transplantation.
Consultations: Consider
early consultation with a gastroenterologist and a surgeon, particularly for
patients with active bleeding from esophageal varices.
Diet: In patients with
hemodynamically significant upper GI tract bleeding, a nasogastric tube
should be in place for 24 hours to assist in identifying any rebleeding.
Gastric lavage may be performed frequently through the nasogastric tube, and
the volume and appearance of material aspirated from the stomach should be
recorded. Do not allow any food by mouth.
Two major categories of drugs
(vasoconstrictors and vasodilators) are used to treat acute bleeding related
to portal hypertension.
The main advantages to using vasoactive
agents include the ability to treat variceal bleeding in the emergency
department, lowering of the portal pressure, and offering the endoscopist a
clearer view of varices because of less active bleeding. They represent an
ideal treatment for sources of portal hypertensive bleeding other than
esophageal varices (eg, gastric varices >2 cm below the gastroesophageal
junction or portal hypertensive gastropathy).
In the treatment of acute variceal bleeding,
somatostatin or octreotide is now the preferred therapy prior to endoscopy.
Drug Category:
Vasoconstrictors -- Reduce portal blood flow and, therefore, the
flow of blood in the gastroesophageal collaterals because of their
vasoconstrictor effects on the splanchnic vascular system.
Drug Name
|
Vasopressin (Pitressin) -- Has vasopressor and antidiuretic hormone (ADH)
activity. Increases water resorption at distal renal tubular epithelium
(ADH effect) and promotes smooth muscle contraction throughout the
vascular bed of the renal tubular epithelium (vasopressor effects).
However, vasoconstriction also is increased in splanchnic, portal,
coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels.
Decreases portal pressure in portal hypertension.
Notable adverse effect is coronary artery constriction that may dispose
patients with coronary artery disease to cardiac ischemia. This can be
prevented with concurrent use of nitrates.
Rarely used.
|
| Adult Dose |
0.2-0.4
U/min IV; after bleeding stops, continue at same dose for 12 h and taper
off over 24-48 h |
| Pediatric Dose |
Initial: 0.002-0.005 U/kg/min, titrate dose prn; not to exceed 0.01
U/kg/min; after bleeding stops, continue at same dose for 12 h and taper
off over 24-48 h |
| Contraindications |
Documented hypersensitivity; coronary artery disease; severe
arrhythmias; MI; respiratory failure; stroke |
| Interactions |
Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease
effects; chlorpropamide, urea, fludrocortisone, clofibrate, and
carbamazepine may potentiate effects |
| Pregnancy |
C -
Safety for use during pregnancy has not been established. |
| Precautions |
Caution
in cardiovascular disease, seizure disorders, nitrogen retention,
asthma, or migraine; excessive doses may result in hyponatremia;
complications (eg, MI, arrhythmia, mesenteric ischemia, heart failure,
pulmonary edema, stroke, vertigo, fever, headache) may occur during
infusion; adverse reactions include tremor, wheezing,
bronchoconstriction, abdominal cramps, nausea, and vomiting;
hyponatremia due to antidiuresis may occur; should be administered as an
infusion in a peripheral vein and not by central venous line because it
can cause severe coronary artery vasospasm; combined use with
nitroglycerin allows enhancement of reduction of portal blood pressure
and a decrease in the systemic adverse effects of vasopressin therapy
(decrease in mortality is not significant); nitroglycerin usually is
administered SL/IV/TD |
Drug Name
|
Terlipressin (Glypressin) -- Synthetic analog of vasopressin. Only
pharmacologic agent shown to reduce mortality from variceal bleeding.
Widely used in Europe. In the United States, has orphan drug status to
treat bleeding esophageal varices.
Has longer biological activity compared to vasopressin.
|
| Adult Dose |
2 mg
q4-6h IV for up to 48 h |
| Pediatric Dose |
Not
established |
| Contraindications |
Documented hypersensitivity; coronary artery disease |
| Interactions |
Drugs
known to potentiate the effects include chlorpropamide, clofibrate, and
carbamazepine |
| Pregnancy |
C -
Safety for use during pregnancy has not been established. |
| Precautions |
Compared to vasopressin, adverse effects are less severe |
Drug Category:
Antisecretory agents -- Used as adjunct to nonoperative
management of secreting cutaneous fistulas of the stomach, duodenum, small
intestine (jejunum and ileum), or pancreas.
Drug Name
|
Somatostatin (Zecnil) -- Naturally occurring tetradecapeptide isolated
from the hypothalamus and pancreatic and enteric epithelial cells.
Diminishes blood flow to portal system due to vasoconstriction, thus
decreasing variceal bleeding. Has similar effects as vasopressin but
does not cause coronary vasoconstriction. Rapidly cleared from the
circulation, with an initial half-life of 1-3 min. |
| Adult Dose |
250 mcg
bolus, followed by a 250-500 mcg/h continuous infusion; maintain for 2-5
d if successful |
| Pediatric Dose |
Not
established |
| Contraindications |
Documented hypersensitivity |
| Interactions |
Epinephrine, demeclocycline, and thyroid hormone supplementation may
decrease effects |
| Pregnancy |
C -
Safety for use during pregnancy has not been established. |
| Precautions |
May
exacerbate or cause gall bladder disease; alters balance in
counter-regulatory hormones and may cause hypothyroidism and cardiac
conduction defects; modest effect on systemic circulation—mild reduction
of cardiac output and bradycardia; may adversely affect renal function
in patients with cirrhosis |
Drug Name
|
Octreotide (Sandostatin) -- Synthetic octapeptide. Compared to
somatostatin, has similar pharmacological actions with greater potency
and longer duration of action. |
| Adult Dose |
25-50
mcg/h IV continuous infusion; may be followed by initial IV boluses of
50 mcg; treat for up to 5 d |
| Pediatric Dose |
1-10
mcg/kg IV q12h; dilute in 50-100 mL NS or D5W |
| Contraindications |
Documented hypersensitivity |
| Interactions |
May
reduce effects of cyclosporine; patients on insulin, oral hypoglycemics,
beta-blockers, and calcium channel blockers may need dose adjustments
|
| Pregnancy |
B -
Usually safe but benefits must outweigh the risks. |
| Precautions |
Tachyphylaxis may develop on repeated IV bolus injections; adverse
effects primarily related to altered GI motility and include nausea,
abdominal pain, diarrhea, and increased incidence of gallstones and
biliary sludge; because of alteration in counter-regulatory hormones
(insulin, glucagon, and GH), hypoglycemia or hyperglycemia may be
observed; bradycardia, cardiac conduction abnormalities, and arrhythmias
have been reported; due to inhibition of TSH secretion, hypothyroidism
also may occur; caution in renal impairment; cholelithiasis may occur |
Drug Category:
Beta-adrenergic blockers -- May block effect of vasodilators,
decrease platelet adhesiveness and aggregation, and increase release of
oxygen to tissues.
Drug Name
|
Propranolol (Inderal) -- Competitive nonselective beta-adrenergic
receptor antagonist without intrinsic sympathomimetic activity. Competes
with adrenergic neurotransmitters (eg, catecholamines) for binding at
sympathetic receptor sites. Similar to atenolol and metoprolol,
propranolol blocks sympathetic stimulation mediated by beta1-adrenergic
receptors in the heart and vascular smooth muscles. |
| Adult Dose |
40 mg
PO bid initially, titrate to achieve heart rate reduction of 25%
|
| Pediatric Dose |
0.5-1
mg/kg/d divided q6-8h, titrate q3-5d; usual dose 2-4 mg/kg/d (higher
doses may be needed); not to exceed 16 mg/kg/d or 60 mg/d |
| Contraindications |
Documented hypersensitivity; uncompensated congestive heart failure;
bradycardia; cardiogenic shock; AV conduction abnormalities |
| Interactions |
Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins,
calcium salts, cholestyramine, and rifampin may decrease effects;
calcium channel blockers, cimetidine, loop diuretics, and MAOIs may
increase toxicity; toxicity of hydralazine, haloperidol,
benzodiazepines, and phenothiazines may increase with propranolol
|
| Pregnancy |
C -
Safety for use during pregnancy has not been established. |
| Precautions |
Beta-adrenergic blockade may decrease signs of acute hypoglycemia and
hyperthyroidism; abrupt withdrawal may exacerbate symptoms of
hyperthyroidism, including thyroid storm; withdraw drug slowly and
monitor closely |
Drug Category:
Vasodilators -- Reduce the intrahepatic vascular resistance
without decreasing peripheral or portal-collateral resistance.
Drug Name
|
Nitroglycerin (Nitro-Bid, Nitrostat, Deponit) -- Causes relaxation of
vascular smooth muscle by stimulating intracellular cyclic guanosine
monophosphate production. Result is a decrease in blood pressure.
|
| Adult Dose |
2.5-9
mg PO q8-12h; 2.5-15 mg/24h TD patch |
| Pediatric Dose |
Not
established |
| Contraindications |
Documented hypersensitivity; severe anemia; shock; postural hypotension;
head trauma; closed-angle glaucoma; cerebral hemorrhage |
| Interactions |
Aspirin
may increase nitrate serum concentrations; marked symptomatic
orthostatic hypotension may occur with coadministration of calcium
channel blockers (dose adjustment of either agent may be necessary);
beta-blockers may enhance hypotensive effects |
| Pregnancy |
C -
Safety for use during pregnancy has not been established. |
| Precautions |
Caution
in coronary artery disease and low systolic blood pressure; tolerance
may develop after chronic use; patients with cirrhosis are less likely
to develop full tolerance compared to patients with coronary artery
disease |
| |
FOLLOW-UP |
Section 8 of 10
 |
|
|
Further Inpatient Care:
- Because of the frequency and severity of
recurrent variceal bleeding, effective preventive treatment is mandatory
in patients surviving an episode of acute variceal bleeding. This may
include one of the following options:
- Elective portocaval shunt
- Devascularization procedures
- Endoscopic variceal banding ligation
Further Outpatient Care:
- The administration of propranolol and
other nonselective beta-blockers in patients with cirrhosis reduces the
portal pressure by reducing the portal collateral flow. This results from
splanchnic vasoconstriction promoted by the blockade of vasodilating
beta2-adrenoceptors in the splanchnic circulation and by decreasing heart
rate and cardiac output due to blockade of cardiac beta1-adrenoceptors.
- Beta-blocker therapy is indicated in
patients with esophageal varices and in patients treated for variceal
hemorrhage with sclerotherapy or banding. Patients selected for
beta-blocker therapy should have no contraindications to beta-blockers.
In/Out Patient Meds:
- Adjust the dose of beta-blockers.
- If therapy with beta-blockers is not
successful, addition of a second drug (eg, nitroglycerin, a long-acting
nitrate) should be considered in an attempt to further decrease HVPG.
Transfer:
- Patients with acute esophageal bleeding
require urgent treatment in a hospital setting.
Complications:
- Severe and persistent upper GI hemorrhage
(ie, requiring >5-U transfusion)
- High morbidity and mortality (30-40% of
the group with severe persistent GI hemorrhage) - Factors such as
underlying liver disease and associated abnormalities of the renal,
cardiovascular, and immune systems contribute to the high morbidity and
mortality.
- Complications associated with GI bleeding
- Vascular collapse; the sequelae of hypotension, cardiomyopathy,
arrhythmias, aspiration pneumonia, sepsis, spontaneous bacterial
peritonitis, overtransfusion, and rebound rebleeding of varices; and
encephalopathy
- Complications related to blood transfusion
- Complications related to therapeutic
procedures used in management of bleeding esophageal varices
- Balloon tamponade - Aspiration
pneumonia, esophageal perforation, superficial lesions of the gastric
mucosa, pressure necrosis to the nasal passages, mouth, or lips
- Sclerotherapy - Perforation of the
esophagus (2-6%), esophageal ulceration and bleeding (2-13%), pleural
effusion (16-48%), fever (30%), chest pain (40%), and esophageal
stricture (7%)
- Variceal banding - Rebleeding during the
course of banding
- Surgical procedures - For example,
distal splenorenal shunt surgery is associated with an increased
incidence of hepatic encephalopathy.
- Liver transplantation - Rejection,
infection, sepsis, and complications related to immunosuppressive drugs
used postoperatively.
- Complications related to pharmacotherapy
Prognosis:
- Patients with HVPG of 20 mm Hg measured 48
hours after esophageal varices bleeding have a higher 1-year mortality
rate.
- Other factors that can affect prognosis of
patients with esophageal varices include the following:
- Child classification, especially the
presence of ascites
- Active alcohol intake in patients with
chronic alcohol-related liver diseases
- Occurrence of complications (eg,
bacteremia and/or endotoxemia, spontaneous bacterial peritonitis,
portosystemic encephalopathy, hepatorenal syndrome)
- Several factors are known to influence the
prognosis of esophageal bleeding. These include the following:
- The natural course of the disease
causing portal hypertension
- The severity of portal hypertension
- The location and number of the bleeding
varices
- The functional status of the liver and
the severity of liver disease (early rebleeding, within 5 d of
admission, occurred in 21% of patients classified as Pugh grade A, 40%
of patients classified as grade B, and 63% of patients classified as
grade C)
- Presence of associated systemic
disorders
- Continued alcohol abuse
- Response to emergency treatment
Patient Education:
- All patients with esophageal varices
should take beta-blockers to reduce the risk of bleeding unless
beta-blockers are contraindicated by coexisting medical conditions.
Patients also should be educated about the adverse effects of
beta-blockers and the possible risks of their abrupt discontinuation.
- Educate patients about the benefits and
disadvantages of available treatment options.
- For excellent patient education resources,
visit eMedicine's
Esophagus, Stomach, and Intestine Center,
Liver, Gallbladder, and Pancreas Center, and
Heartburn/GERD/Reflux Center. Also, see eMedicine's patient education
articles,
Gastrointestinal Bleeding,
Cirrhosis, and
Gastritis.
| |
MISCELLANEOUS
|
Section 9 of 10
 |
|
|
Medical/Legal Pitfalls:
- Vasopressin should not be administered via
a central line, especially in elderly patients.
- Initiating therapy to prevent recurrent
bleeding as soon as the acute bleeding episode is controlled adequately is
critical.
- Liver transplantation should be considered
for patients with end-stage liver disease. The selection of candidates is
dictated by the patient's clinical status, etiology of cirrhosis,
abstinence from alcohol, and availability of a donor organ.
Special Concerns:
- Patients with massive acute bleeding from
esophageal varices who refuse blood transfusions because of their
religious beliefs may constitute a challenge to the treating team.
| |
BIBLIOGRAPHY
|
Section 10 of
10
|
|
|
- Bornman PC, Krige JE, Terblanche J:
Management of oesophageal varices. Lancet 1994 Apr 30; 343(8905): 1079-84[Medline].
- Garcia-Tsao G: Portal hypertension. Curr
Opin Gastroenterol 2000; 16: 282-289.
- Garcia-Tsao G: Angiotensin II receptor
antagonists in the pharmacological therapy of portal hypertension: a
caution. Gastroenterology 1999 Sep; 117(3): 740-2[Medline].
- Gotzsche PC, Gjorup I, Bonnen H, et al:
Somatostatin v placebo in bleeding oesophageal varices: randomised trial
and meta-analysis. BMJ 1995 Jun 10; 310(6993): 1495-8[Medline].
- Gupta TK, Toruner M, Chung MK, Groszmann
RJ: Endothelial dysfunction and decreased production of nitric oxide in
the intrahepatic microcirculation of cirrhotic rats. Hepatology 1998 Oct;
28(4): 926-31[Medline].
- Hanisch E, Doertenbach J, Usadel KH:
Somatostatin in acute bleeding oesophageal varices. Pharmacology and
rationale for use. Drugs 1992; 44 Suppl 2: 24-35; discussion 70-2[Medline].
- Patch D, Armonis A, Sabin C, et al: Single
portal pressure measurement predicts survival in cirrhotic patients with
recent bleeding. Gut 1999 Feb; 44(2): 264-9[Medline].
- Poo JL, Jimenez W, Maria Munoz R, et al:
Chronic blockade of endothelin receptors in cirrhotic rats: hepatic and
hemodynamic effects. Gastroenterology 1999 Jan; 116(1): 161-7[Medline].
- Shulkes A, Wilson JS: Somatostatin in
gastroenterology. BMJ 1994 May 28; 308(6941): 1381-2[Medline].
- Williams SG, Westaby D: Management of
variceal haemorrhage. BMJ 1994 May 7; 308(6938): 1213-7[Medline].
| NOTE:
|
| Medicine is a constantly
changing science and not all therapies are clearly established. New
research changes drug and treatment therapies daily. The authors,
editors, and publisher of this journal have used their best efforts to
provide information that is up-to-date and accurate and is generally
accepted within medical standards at the time of publication. However,
as medical science is constantly changing and human error is always
possible, the authors, editors, and publisher or any other party
involved with the publication of this article do not warrant the
information in this article is accurate or complete, nor are they
responsible for omissions or errors in the article or for the results of
using this information. The reader should confirm the information in
this article from other sources prior to use. In particular, all drug
doses, indications, and contraindications should be confirmed in the
package insert. FULL
DISCLAIMER |
Esophageal Varices excerpt
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