VARICES ESOFAGICAS

Varices appeared to be the source of bleeding in 50 to 90 percent of patients with cirrhosis

In patients with cirrhosis, any upper gastrointestinal bleeding associated with hemodynamic changes should be considered to be variceal in origin until proven otherwise.

Early rebleeding – Bleeding that occurs >120 hours but <6 weeks from time zero,

Only 50 percent of patients with variceal hemorrhage stop bleeding spontaneously

Cuando la presión portal pasa de 10 mmHg se incrementa potencialmente el desarrollo de colaterales.

Se define como hipertensión portal un gradiente de presión venosa hepática mayor a 5 mmHg, y el valor de 12 mmHg es un factor de riesgo para predecir hemorragia variceal.

a hepatic venous pressure gradient >20 mmHg is associated with a greater risk of continued or recurrent bleeding

50 percent of all early rebleeding episodes occur within the first 10 days

The risk of bleeding and of death in patients who survive six weeks is similar to that in patients with cirrhosis of equivalent severity who have never bled

Acute bleeding from varices is associated with approximately 15 to 20 percent 30-day mortality

Platelet counts often drop within the first 48 hours after a bleed and may necessitate platelet transfusions if values below 50,000/mm3

Bacterial infections are present in up to 20 percent of patients with cirrhosis who are hospitalized with gastrointestinal bleeding

effectiveness of prophylactic antibiotics in patients with cirrhosis hospitalized for bleeding suggest an overall reduction in infectious complications and decreased mortality

A systematic review that included eight placebo-controlled trials with a total of 864 patients found the antibiotics were associated with a significant reduction in mortality (RR 0.75, 95% CI 0.55 to 0.95) and bacterial infections (RR 0.40, 95% CI 0.32 to 0.51) including bacteremia, pneumonia, spontaneous bacterial peritonitis, and urinary tract infections

patients with cirrhosis who present with upper GI bleeding (from varices or other causes) should be given prophylactic antibiotics, preferably before endoscopy

fOR PREVENTION OF INFECTIONS, intravenous ceftriaxone (1 g/day for seven days), which was superior to norfloxacin in a randomized controlled trial [

Short-term (maximum seven days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and GI hemorrhage.

Among patients with cirrhosis, varices form at a rate of 5 to 15 percent per year, and one-third of patients with varices will develop variceal hemorrhage

Treatment with endoscopic variceal ligation decreases the risk of rebleeding to approximately 30 percent, and the risk of death to approximately 25 percent.

Endoscopic sclerotherapy is associated with a decrease in the risk of rebleeding to 40 to 50 percent, and a decrease in the risk of death to 30 to 60 percent

Pharmacologic therapy should not be delayed pending confirmation that the source of bleeding is indeed from varices

pharmacologic therapy typically consists of an octreotide bolus (50 mcg intravenous [IV]) followed by a continuous infusion (50 mcg IV per hour).

Terlipressin is administered at an initial dose of 2 mg IV every four hours and can be titrated down to 1 mg IV every four hours once hemorrhage is controlled

Pharmacologic therapy is typically continued for three to five days following cessation of bleeding

The goal should be to perform an upper endoscopy after fluid resuscitation and within 12 hours of presentation

If the bleeding cannot be controlled endoscopically, treatment options include transjugular intrahepatic portosystemic shunt (TIPS) placement or surgical shunting

terlipressin is the only agent individually shown to reduce mortality

— Vasopressin can achieve initial hemostasis in 60 to 80 percent of patients, but has only marginal effects on early rebleeding episodes and does not improve survival from active variceal hemorrhage [12].

terlipressin is released in a slow and sustained manner, permitting its administration via intermittent injections.

terlipressin has been associated with hyponatremia,

A study comparing the acute hemodynamic effects of terlipressin to octreotide in stable patients with cirrhosis found a sustained effect of terlipressin on portal pressure and blood flow compared with only a transient effect from octreotide

Somatostatin inhibits the release of vasodilator hormones such as glucagon [20], indirectly causing splanchnic vasoconstriction and decreased portal inflow.

the most consistently delocteotride observed is the decrease in collateral flow (azygos flow)

While somatostatin and octreotide help achieve hemostasis and prevent rebleeding, neither has a clearly established benefit on mortality [

A systematic review found that combination therapy with somatostatin or octreotide and endoscopic variceal ligation improved the five-day success rate compared with endoscopic variceal ligation alone