TRIPASS XR تري باس

 

93

Varices can only be visualized during a diagnostic endoscopy. Esophageal varices

are graded as small or large (>5 mm). The presence or absence of red signs (red

wale marks or red spots) on varices is also noted.

92

Despite improvement in the management of portal hypertension, massive bleeding

from esophageal or gastric varices is the leading cause of death in patients with

cirrhosis.

94 Prevention of variceal bleeding is critical because the mortality rate

remains at 32% in Child–Turcotte–Pugh class C patients.

94 New varices develop at a

rate of 5% to 10% per year in cirrhotic patients. Once varices develop, they enlarge

by 4% to 10% each year.

95 Acute variceal bleeding is considered a medical

emergency and should be treated immediately. Treatment goals include volume

resuscitation, acute treatment of bleeding, and prevention of recurrence of variceal

bleeding. Approximately 10% to 20% of patients are refractory to endoscopic and

medical intervention and may require life-saving portal decompressive shunt surgery

or TIPS.

24

p. 546

p. 547

GENERAL MANAGEMENT

Resuscitation is the first priority in patients with acute bleeding episodes. An

indwelling nasogastric tube (NG) should be placed, then saline or tap-water lavage

of the stomach, with suctioning of the gastric contents, should be initiated promptly to

prevent airway complications such as aspiration pneumonia.

83,96 Obtunded or

unconscious patients should be intubated to maintain and protect the airway.

Pharmacologic treatment should be initiated immediately to reduce bleeding and the

risk of hypotension-induced renal failure. The patient should also be monitored for

any abnormal electrolyte and metabolic chemistries (e.g., potassium, sodium,

bicarbonate), hypoxia (e.g., Po2

, pH), serum creatinine, and decreased urinary

output.

96

Re-bleeding is most likely to occur within the first 2 to 5 days in patients with

large varices and in patients with advanced liver disease (i.e., Child–Turcotte–Pugh

class C, Table 25-1).

24,97 Factors associated with early re-bleeding include age

greater than 60 years, acute renal failure, and severe initial bleeding defined by

hemoglobin less than 8 g/dL at presentation. Risk factors for late re-bleeding are

severe liver failure, continued alcohol abuse, large variceal size, renal failure, and

hepatocellular carcinoma.

97

HYPOVOLEMIA/BLOOD LOSS

Care should be taken when correcting hypovolemia so as not to increase the degree

of portal hypertension by over-transfusion, which can increase the risk of further

bleeding. Hypovolemia should be immediately managed to maintain a systolic blood

pressure of 90 to 100 mm Hg and the hemoglobin at approximately 8 g/dL.

24,98 C.V.’s

pallor, cold and clammy skin, rapid pulse, and a systolic BP less than 80 mm Hg

suggest significant hypotension and hypovolemia needing correction with whole

blood or packed red cell transfusion along with fresh frozen plasma.

92,97

Patients with liver disease and elevated bilirubin frequently develop some level of

vitamin K deficiency. Prolongation of the PT because of vitamin K deficiency usually

improves within 24 hours after a 10 mg subcutaneous or oral dose of vitamin K

(although evidence suggests parenteral repletion may be more reliable).

27

In contrast,

a prolonged PT caused by poor liver function is not responsive to the administration

of vitamin K. If the INR requires rapid correction because of bleeding or a planned

invasive procedure, fresh frozen plasma should be transfused. Although vitamin K is

often administered in the treatment of acute variceal bleeding, there is no data to

support this practice.

99

CASE 25-2, QUESTION 2: Three units of whole blood and two units of fresh frozen plasma were transfused

initially. C.V.’s stomach was lavaged with saline, and the gastric aspirate from the NG tube continued to be

strongly positive for blood. Four hours later, her bleeding still persisted. What other pharmacologic interventions

can be used to control C.V.’s bleeding esophageal varices?

OCTREOTIDE

Octreotide is a synthetic analog of somatostatin, with similar pharmacologic

properties and a slightly longer half-life. Somatostatin is available in Europe, but is

substituted with octreotide or vapreotide (orphan drug status) in the United States

(Table 25-2).

100–103 Octreotide is shown to be effective for controlling acute variceal

bleeding and appears comparable in efficacy to vasopressin and balloon tamponade,

with fewer side effects. Octreotide is administered as a 50 mcg bolus followed by an

infusion of 50 mcg/hour for 3 to 5 days.

24

In one study, complete bleeding control

was achieved in all patients receiving octreotide after 48 hours of therapy compared

with 64% of vasopressin-treated patients, and 59% in the omeprazole groups (p <

0.005). Patients receiving vasopressin also experienced more side effects

(abdominal cramps, nausea, tremor, decreased cardiac output, myocardial ischemia,

and bronchial constriction) than those receiving octreotide or omeprazole (p < 0.01).

In the patients with bleeding not controlled within 48 hours in the vasopressin and

omeprazole groups, complete bleeding control was subsequently achieved by

octreotide.

104

In a meta-analysis of octreotide and somatostatin versus vasopressin in

the management of acute esophageal variceal bleeds, octreotide and somatostatin

appeared to be more effective in controlling acute bleeding (82% vs. 55%; p = NS)

and had fewer adverse effects requiring discontinuation than vasopressin (0% vs.

10%; p = 0.00007).

105

In general, octreotide is fairly well tolerated.

104 Although some

centers may still initiate therapy with vasopressin, most will use octreotide as firstline therapy and reserve vasopressin for treatment failures.

VASOPRESSIN

Vasopressin, a naturally occurring hormone (also known as 8-arginine vasopressin,

ADH), is produced by the posterior pituitary and was originally derived for the

treatment of diabetes insipidus in persons with pituitary insufficiency.

100,101

Its use to

control variceal bleeding is a non-FDA-labeled use that takes advantage of its

intense smooth muscle vasoconstrictive properties. Vasopressin (Table 25-2) is

effective in reducing or terminating bleeding in approximately 60% of patients with

variceal hemorrhage.

100,101 Of concern are reports of patients developing

hypertension, angina, arrhythmias, and, rarely, myocardial infarction while receiving

vasopressin. Vasopressin is given as a continuous IV infusion because of its short

half-life. To minimize dose-related adverse effects, the lowest effective dosage

should be used. Vasopressin may be administered by peripheral IV infusion, but use

of a central vein is preferred because of the risk of tissue necrosis if extravasation

occurs. Most commonly, vasopressin is initiated as a continuous IV infusion of 0.2 to

0.4 units/minute, and increased every hour by 0.2 units/minute until control of

bleeding is obtained (maximal dose 0.8 units/minute).

92 Approximately 12 hours after

the control of bleeding, the infusion rate can be decreased by half. Higher doses

should be avoided because dosages exceeding 1 unit/minute fail to control

hemorrhage in patients who are unresponsive to lower dosages.