Compared to untreated controls, prophylactic VBL reduces the risks of variceal bleeding and mortality [ 32 ]. Several studies compared endoscopic VBL with propranolol for primary prophylaxis of variceal bleeding [ 28 — 31 ]. Three studies found no difference between beta blockers and VBL concerning prophylaxis of bleeding [ 28 , 30 , 31 ]. One study that is controversially discussed because of some methodological flaws found a significant benefit for endoscopic VBL [ 30 ]. A recently published Cochrane analysis that included 19 randomized trials found a slight beneficial effect for VBL, but that effect was not present when only full-published paper articles were analyzed [ 33 ].
In terms of efficacy, VBL and nonselective beta blocker therapy are considered to be equivalent. Because of the low costs, ease of administration with no need of special endoscopic expertise, and the absence of procedure-related mortality, nonselective beta blockers are recommended as first-line treatment for the primary prophylaxis of esophageal variceal bleeding [ 15 ].
Variceal band ligation is recommended in patients with serious side effects or intolerability of beta blocker therapy as well as in patients with contraindications for drug therapy. Figure 3 shows a flow chart for the prophylactic treatment of esophageal varices. More than two-thirds of all bleeding episodes in patients with liver cirrhosis are caused by esophageal variceal hemorrhage [ 34 ].
Hence, every patient with liver cirrhosis and signs of gastrointestinal bleeding should be treated as having variceal hemorrhage until a definite diagnosis is made. Six weeks after the bleeding episode the risk of bleeding equals the initial risk before the bleeding [ 37 ].
Rebleeding within the first five days is associated with a high mortality and was analyzed in most studies as a composite endpoint referred to as 5d failure. Acute bleeding from esophageal varices is a medical emergency and often a dramatic event. Most patients vomit blood, but hematochezia and melena might be the only symptoms.
Dependent on the amount of lost blood, patients might be hemodynamic instable and present in hemorrhagic shock. Patients should be managed on an intensive care unit by a multidisciplinary team consisting of endoscopists, hepatologists, and specially trained nurses as well as interventional radiologists and surgeons if necessary.
The outcome of patients is directly correlated to the extent of organ failure. Most deaths are caused by complications of bleeding like liver failure, infections, and hepatorenal syndrome [ 34 , 36 ].
Risk factors for an adverse course are the degree of liver dysfunction, creatinine, hypovolemic shock, active bleeding on endoscopy, and presence of hepatocellular carcinoma [ 7 , 34 , 36 , 37 , 39 , 44 ]. Thus, the management of patients with acute variceal bleeding includes not only treatment and control of active bleeding but also the prevention of rebleeding, infections, and renal failure [ 45 ].
If variceal bleeding is suspected, patients should be hemodynamically stabilized and receive medical treatment with vasopressors and antibiotic therapy [ 46 — 50 ]. In uncomplicated patients antibiotic therapy is done using quinolones [ 51 ]. High-risk patients with advanced liver disease ascites, encephalopathy, jaundice, and malnutrition or previous treatment with quinolones should receive ceftriaxone [ 48 ].
Antibiotic therapy of patients with acute variceal bleeding does not only decrease mortality but also decrease the probability of rebleeding [ 49 ]. Patients with variceal bleeding are at high risk of bronchial aspiration.
Extreme care of the airways is therefore mandatory. Another concern in cirrhotic patients is the often impaired blood coagulation due to a low platelet count and impaired plasmatic coagulation. These factors have long been considered as risk factors in variceal hemorrhage, but in reality these factors are only poorly correlated with variceal bleeding [ 55 ].
Available therapy options include pharmacologic and endoscopic treatment, balloon tamponade, placement of fully covered self-expandable metallic stents, transjugular intrahepatic shunt TIPS , and surgical shunts. Nowadays, the initial approach is a combination of vasoactive drugs, antibiotics, and endoscopic therapy [ 56 ]. Figure 4 shows a treatment algorithm for acute esophageal variceal bleeding.
The aim of pharmacological therapy is to reduce splanchnic blood flow and portal pressure and thereby control of active bleeding [ 57 , 58 ].
Vasoactive drugs currently in use are vasopressin, somatostatin, and, most important in Europe, terlipressin. Moreover, active bleeding during endoscopy is reduced when vasoactive drugs are given before endoscopy, and thereby the success rate of endoscopic therapeutic procedures is higher [ 61 — 63 ]. Vasopressin is the most potent splanchnic vasoconstrictor. Due to its short half-life, vasopressin has to be given as a continuous i.
Relevant adverse effects include systemic vasoconstriction with serious implications like mesenteric or myocardial ischemia [ 64 ]. Application of vasopressin in combination with nitrates reduces the side effects associated with vasoconstriction [ 65 , 66 ]. Several studies have shown that treatment with vasopressin is effective in terms of bleeding control but does not affect mortality [ 64 , 67 — 69 ].
Terlipressin is a synthetic vasopressin analogue with a longer half-life and less adverse effects. Its effect is still significant 4 hours after administration [ 70 — 72 ].
Several studies have shown that terlipressin is effective in bleeding control and has a positive impact on survival [ 61 , 73 — 75 ]. Therefore, serum sodium should be monitored in patients receiving terlipressin.
Compared to vasopressin, terlipressin is more effective in control of esophageal bleeding [ 73 , 78 ], and compared to vasopressin plus nitrate [ 79 ] as well as compared to somatostatin it is comparably effective [ 80 , 81 ]. Terlipressin has to be used with caution in patients with ischemic heart disease and in patients with peripheral vascular disease as it may cause ischemic complications as well as relevant dysrhythmias. Somatostatin causes splanchnic vasoconstriction as well as a reduction in portal pressure and HVPG [ 82 — 84 ].
Furthermore, it inhibits the postprandial increase in portal blood flow and portal pressure. The efficacy of somatostatin in variceal bleeding was shown in several trials. The effect on HVPG seems to be dose related [ 82 ], and higher doses might therefore be more effective in severe bleeding [ 86 ]. Somatostatin is as effective as vasopressin in control of variceal bleeding; the safety profile is superior to vasopressin [ 87 ].
Octreotide is a synthetic analogue of somatostatin with a longer half-life. The longer half-life, however, is not reflected by longer hemodynamic effects [ 88 , 89 ], what might be caused by rapid desensitization or tachyphylaxis [ 90 ]. Since convincing studies are lacking [ 91 ], octreotide is not recommended as a single therapy in acute variceal hemorrhage.
The combination of terlipressin and octreotide is not superior to a monotherapy with terlipressin [ 92 ]. One meta-analysis has shown that octreotide is effective in the prevention of rebleeding when it is given in addition to endoscopic therapy [ 93 ]. Both somatostatin and octreotide have a good safety profile. Possible adverse effects include mild hyperglycemia and abdominal cramps. In summary, the available data is most convincing for terlipressin; however, the direct comparison of terlipressin and octreotide revealed no superiority of terlipressin [ 91 , 95 ].
Nowadays, most important is endoscopic VBL. Injection therapy using sclerosing agents like ethoxysklerol or cyanoacrylate is less commonly used. Aethoxysklerol is injected next to—not into—the varix. It causes local inflammation and scaring and thereby thrombosis and obliteration of the vessel. On the other hand, cyanoacrylate is injected directly into the varix, causing immediate obliteration of the vessel. Endoscopic band ligation is done using a transparent cap that is attached to the tip of the endoscope.
By applying suction, the varix is then pulled into the cap and a rubber ring is thrown over the varix causing thrombosis and scaring of the vessel. Before the introduction of VBL, aethoxysklerol injection was widely used in the treatment of acute esophageal variceal bleeding.
Studies have shown that sclerotherapy was at least as effective as balloon tamponade [ 98 , 99 ]. The injection of cyanoacrylate is used as a second-line therapy when VBL of variceal bleeding fails. Endoscopic VBL was first carried out in [ ]. The method is now widely available, and complications are—compared to sclerotherapy—less common [ ].
The most frequent complications are superficial ulcerations and esophageal strictures. Bleeding after the rubber rings have fallen off is less common. A disadvantage of the method is the impaired sight that is caused by the ligation system.
Costs are—compared to sclerotherapy—higher. Mortality rates after VBL are lower as compared to sclerotherapy [ , ]. Several randomized controlled trials as well as meta-analyses of these trials have shown that the combination of endoscopic treatment and vasoactive drugs is superior to either treatment alone.
Another trial using combination therapy of endoscopic treatment either sclerotherapy or VBL and pharmacologic treatment with vapreotide a somatostatin analogue found the combination treatment to be superior to endoscopic treatment alone in the control of bleeding, but a difference in mortality was not evident [ 63 ]. However, when pooling the patients from the above-mentioned studies who underwent VBL, a reduction in early mortality is evident [ 54 ].
Only one full-published paper compared combination therapy sclerotherapy and somatostatin with somatostatin treatment alone [ ]. The authors found combination therapy more effective than somatostatin alone with therapeutic failure occurring in 21 patients of the somatostatin group and in 7 patients of the combined therapy group. One trial compared VBL in combination with terlipressin versus terlipressin alone in patients with no active bleeding on endoscopy.
In summary, the combination of endoscopic VBL and vasoactive drugs preferably terlipressin is clearly more effective in the control of active bleeding and in the prevention of rebleeding than endoscopic or pharmacologic treatment alone. The effect on mortality was less clearly shown in the available studies, but this might be related to an insufficient number of patients included in the studies.
The use of balloon tamponade for the treatment of acute esophageal variceal bleeding was introduced by Sengstaken and Blakemore in [ ]. The Minnesota tube is a modified version with an aspiration channel above the esophageal balloon.
For uncontrolled bleeding from gastric varices, the Linton-Nachlas tube is preferred [ ]. In the hand of the experienced user the method allows control of bleeding in most patients [ ]. Deflating of the balloon after six hours reduces the risk of complications. Due to the serious risks, balloon tamponade should only be applied by an experienced physician under fluoroscopic control.
After all, balloon tamponade is only a bridging procedure until other definite therapy options are available. The placement of fully covered self-expandable metal stents SEMS is an alternative to balloon tamponade. The SEMS is inserted over an endoscopic placed guide wire using a stent delivery device without the need of fluoroscopy [ ]. SEMS controls bleeding by compression of the bleeding varices [ ]. The stent can be left in place for up to two weeks and can be easily removed by endoscopy.
The effectiveness in the control of refractory esophageal variceal bleeding has been shown in four case series [ — ]. The procedure is safe with minor complications like esophageal ulcerations, compression of the bronchial system, and stent migration into the stomach being described [ — ]. Like balloon tamponade, the procedure is reserved for patients with bleeding refractory to medical and endoscopic treatment. It does not allow definite treatment of variceal bleeding due to the high percentage of patients with rebleeding after the SEMS has been removed but has to be considered as an effective and safe bridging procedure that allows stabilization of the patient until definite treatment is possible.
By TIPS placement a functional portacaval side-to-side shunt is established. After TIPS insertion, bleeding is stopped in almost all of the affected patients [ — ]. Disadvantages of the procedure are the risk of hepatic encephalopathy as well as TIPS dysfunction with the risk of recurrent bleeding [ , ].
A major improvement was the introduction of polytetrafluoroethylene PTFE covered stents. These stents have higher rates of patency over time, and mortality rates are lower [ ]. A recently published trial has investigated the role of early TIPS in high-risk patients [ , ]. These results are very promising and make the early insertion of a PTFE covered TIPS in high-risk patients an alternative to the combination of pharmacologic and endoscopic treatment.
Possible procedures are portosystemic shunt operations [ ] or staple transection of the esophagus [ ]. Prevention of rebleeding is therefore a major goal in patients in whom the initial bleeding episode has been successfully controlled. Figure 5 shows an algorithm for the secondary prophylaxis of esophageal variceal bleeding. Several studies are available that compared the nonselective beta blockers propranolol or nadolol with no prophylaxis after initial bleeding [ — ].
Most of the studies found a reduction of the rebleeding risk as well as a reduction in mortality. Addition of nitrates further increased this positive effect [ ]. Several groups studied the effect of sclerotherapy for secondary prophylaxis of variceal bleeding [ , — ].
The comparison of sclerotherapy to medical therapy with a nonselective beta blocker found a benefit for patients treated with sclerotherapy in two studies [ , ] and a slight but statistically not significant benefit for beta blocker therapy [ , , ]. Three more studies did not find a difference between the two treatment modalities [ , , ]. For prophylaxis of recurrent bleeding, sclerotherapy is now replaced widely by VBL. Several studies have shown the superiority of VBL over sclerotherapy [ , , — ].
Comparing VBL to medical therapy with nonselective beta blockers in combination with nitrates, two studies found medical therapy to be as effective [ ] as or more effective [ ] than VBL. In contrast, one study found VBL to be advantageous over medical therapy [ ]. From the pathophysiological point of view, the combination of VBL and medical therapy is an even more promising approach for secondary prophylaxis.
This has been investigated in five studies [ , — ]. Whereas two studies found combination therapy to be more effective than VBL alone [ , ], two more recent studies that compared nadolol plus nitrates with the combination treatment of drugs and VBL, failed to demonstrate superiority of combination treatment [ , ]. Therefore, it seems that a clear recommendation of medial treatment alone, VBL alone, or combination treatment of drugs and VBL cannot be made at the moment.
In all but two studies [ , ] patients treated with TIPS had lower rates of recurrent bleeding. Three meta-analyses [ — ] summarized the available studies and found a significant lower probability of rebleeding in the TIPS treated patients.
The incidence of hepatic encephalopathy was higher in the TIPS group. A difference in mortality was not evident. Shunt surgery has been shown to be effective in the prophylaxis of rebleeding from esophageal varices. This has been shown for nonselective as well as for selective shunts e. As in TIPS, the most important side effect was the incidence of hepatic encephalopathy. Both shunts led to an adequate reduction in portal pressure, but patency rates of the operative shunts were higher over time.
This led to a lower rate of rebleeding as well as to a decrease in mortality in patients with the surgical shunt. A meta-analysis compared different portosystemic shunts TIPS, diverse surgical shunts with endoscopic treatment [ ]. All shunts were equally effective in reducing the risk of rebleeding. The incidence of hepatic encephalopathy was higher in patients who received a shunt procedure.
TIPS was complicated by a high incidence of shunt dysfunction. Comparing the different shunt procedures, there was no difference in survival. A reasonable approach for secondary prophylaxis Figure 5 is to perform VBL alone in patients with contraindications for beta blocker therapy or in patients who suffer from side effects of beta blocker therapy.
Patients who tolerate drug treatment well should be placed on a combination therapy. Patients with decompensated liver disease who are not suitable for TIPS should undergo evaluation for liver transplantation and repeated endoscopic treatment in combination with beta blocker therapy.
In contrast to esophageal variceal bleeding, prevention and treatment of bleeding from gastric varices and from portal gastropathy are less well evaluated in controlled clinical studies. According to Sarin et al. The diagnosis of gastric varices is made by endoscopy. In case of doubt of the diagnosis, endosonography with Doppler sonography allows further differentiation. If only isolated gastric varices are present, the exclusion of portal or splenic vein thrombosis as the underlying cause is mandatory.
About one-fifth of the patients with portal hypertension develop gastric varices [ ]. The prophylactic treatment of esophageal varices by VBL does not increase the risk of secondary gastric varices compared to propranolol [ ].
Almost no data is available on whether medical treatment for the primary prophylaxis of bleeding from gastric varices is effective. Pathophysiological considerations warrant the use of nonselective beta blockers for this indication [ ]. One trial including 27 patients with gastric varices studied the injection of cyanoacrylate for primary prophylaxis of bleeding from large gastric varices and found the injection of cyanoacrylate to be safe and effective in primary prophylaxis [ ].
However, before recommending cyanoacrylate injection as prophylactic therapy, more studies are necessary. Data for the treatment of acute bleeding from gastric varices is sparse. Therapy with terlipressin or somatostatin is recommended although controlled studies are lacking. The endoscopic treatment of choice is injection with cyanoacrylate [ — ]. Known complications of cyanoacrylate injection include mucosal ulcerations as well as thromboembolism.
The use of nonselective beta blockers and nitrates for prophylaxis of rebleeding was shown in one study to be ineffective [ ]. The comparison of cyanoacrylate with propranolol for secondary prophylaxis has shown no difference between the two treatment modalities in terms of rebleeding or mortality but found more complications in the cyanoacrylate group [ ]. Another study compared TIPS with cyanoacrylate in patients with bleeding from gastric varices.
TIPS was shown to be more effective for prevention of recurrent bleeding, with no difference in mortality [ ]. These results are in contrast to a retrospective analysis that found TIPS and cyanoacrylate to be equally effective in controlling and preventing gastric variceal hemorrhage with no significant differences in survival [ ]. Patients who received TIPS experienced significantly more long-term morbidity [ ]. Nevertheless, the above-mentioned studies have to be interpreted with caution, since they included patients with different types of gastric varices.
The diagnosis of portal hypertensive gastropathy is made by endoscopy. These signs are mostly found not only in the fundus and body but also in the gastric antrum [ , ].
Several attempts to classify portal hypertensive gastropathy have been made, with the classification of the NIEC North Italian Endoscopic Club for the study and treatment of esophageal varices being widely accepted [ — ]. The classification system of the NIEC is a two-category system mild or severe and describes two types of lesions: the mosaic-like pattern as a marker of mild disease and red marks as a marker of severe gastropathy [ ].
Histopathological features of portal hypertensive gastropathy are vascular ectasia of the mucosal and submucosal veins and capillaries [ ]. The exact pathogenesis of portal hypertensive gastropathy is unknown. Important factors in the pathogenesis are the presence of portal hypertension as well as hyperemia of the gastric mucosa.
One study found portal hypertensive gastropathy more common in patients with gastroesophageal varices than in patients with esophageal varices alone [ ]. Several authors assumed that the endoscopic treatment of esophageal varices aggravates portal hypertensive gastropathy [ ].
One study that evaluated the cause of GI bleeding in patients found bleeding from portal hypertensive gastropathy to be the cause in 0.
There is only one small trial that studied the effect of nonselective beta blockers on portal hypertensive gastropathy [ ]. Endoscopic grading of portal hypertensive gastropathy improved after propranolol in nine patients compared to three after placebo [ ].
The therapy of acute bleeding from portal hypertensive gastropathy is mainly based on drugs that decrease portal pressure. Since the study did not have a control group of untreated patients, the results have to be interpreted with caution.
A small study compared octreotide, vasopressin, and omeprazole for therapy of acute bleeding. In this setting, octreotide was more effective than omeprazole or vasopressin [ ]. Terlipressin was also shown to be effective in acute bleeding from portal hypertensive gastropathy [ ].
No studies that investigated the role of endoscopic treatment using argon-plasma coagulation in acute or recurrent bleeding from portal hypertensive gastropathy are available. If medical therapy fails, TIPS insertion or surgical shunt is an option [ 13 , , ].
In the secondary prophylaxis of bleeding from portal hypertensive gastropathy, one study including 54 patients showed that propranolol is effective in the prevention of rebleeding [ ]. In summary, the risk of bleeding from portal hypertensive gastropathy is low, and primary prophylaxis is therefore not necessary. In patients with recurrent bleeding from portal hypertensive gastropathy, propranolol should be considered for secondary prophylaxis.
In the majority of cases, portal hypertension as a complication of liver cirrhosis or an extrahepatic obliteration of the portal vein is the cause for the development of ectopic varices. Gastroesophageal varices are the most common portosystemic collaterals that develop in patients with portal hypertension.
In comparison, ectopic varices are less often found. In one case series including patients with varices due to portal hypertension, 43 3.
They are predominantly located in the duodenum, jejunum, ileum, colon, and the rectum [ ]. Other sides like the urinary bladder or gallbladder bed have been described.
By definition, ectopic varices are dilated portovenous vessels of the gastrointestinal mucosa that are located outside the esophagus or the stomach. They have their origin from preexisting small veins of the gastrointestinal mucosa that are portosystemic collaterals between the portal vein and the inferior vena cava. Under normal conditions, the small size and the high vascular resistance in these vascular beds restrain blood flow through the collaterals [ ].
In portal hypertension, the deep mucosal veins of the GI tract become enlarged [ ], and the number and size of the vessels are increased [ ]. A large retrospective analysis of endoscopic procedures revealed 13 patients with duodenal varices. Sixty-nine percent of these patients had also esophageal varices [ ]. The reported prevalence of varices of the jejunum and ileum is in the range of 1.
Varices and angiodysplasia of the colon in patients with portal hypertension are termed portal hypertensive colopathy [ ]. Rectal varices are a frequent complication of portal hypertension and liver cirrhosis. Stomal varices are a common complication in patients with surgical stoma and chronic liver disease. Bleeding from ectopic varices Figure 10 is a rare event. Endoscopy is the most important diagnostic tool. In patients with portal hypertension, acute bleeding, and negative findings on upper endoscopy, bleeding from ectopic varices has to be considered.
In these patients, accurate examination of the duodenum is mandatory. Examination of the jejunum makes double-balloon enteroscopy or capsule endoscopy necessary. Colonoscopy is the principal method for the diagnosis of colonic varices. In patients in whom bleeding from ectopic varices is suspected but endoscopy was negative, NMR with NMR angiography is the diagnostic tool of choice and allows the identification of ectopic varices in most patients.
There are no randomized trials that compared the different treatment modalities that are available for the therapy of bleeding from ectopic varices.
In patients with liver disease and portal hypertension, it seems reasonable to extrapolate the supportive treatment guidelines of acute esophageal variceal hemorrhage cautious transfusion regimens, vasoactive drugs, and antibiotics to patients with bleeding from ectopic varices. Endoscopic therapy of ectopic varices is mainly based on sclerotherapy or injection therapy.
Controlled studies for which method is the best are not available, but case reports showed that both sclerotherapy with aethoxysklerol and injection of the varix with cyanoacrylate are feasible [ — ]. Band ligation may be useful for temporary hemostasis of bleeding duodenal varices [ , ], but rebleeding is a problem with ligation therapy. Additional treatment following band ligation for duodenal varices is therefore mandatory.
Furthermore, it might be technically difficult to obtain visualization of the bleeding side in the duodenum with the banding device in place. The choice of endoscopic therapy is therefore mainly based on personal expertise and location of the bleeding site.
Portacaval shunts are effective therapy measures in patients with uncontrolled or recurrent bleeding from ectopic varices [ , , ]. Another option in patients without portal vein thrombosis is TIPS insertion. Several case reports that show that TIPS is an effective option in the treatment of ectopic varices have been published [ — ].
Angiography is not only a diagnostic tool but allows therapeutic interventions. Angiography of ectopic varices is performed by either a direct access of the portal system through transhepatic portography or indirect by visualization of the venous phase after mesenteric or splenic arteriography. Ectopic varices are displayed as atypical splanchnic vessels that are fed from the superior or inferior mesenteric vein showing a hepatofugal flow [ ]. Balloon-occluded retrograde transvenous obliteration B-RTO was successfully performed for patients with duodenal varices [ , ].
B-RTO can obliterate not only varices but also the afferent and efferent veins and should be considered for treating duodenal varices. Bleeding from varices is a common and often life-threatening complication of portal hypertension.
The best modalities for prophylaxis and treatment of acute bleeding from esophageal varices were investigated in numerous clinical studies, and evidence based clinical guidelines are available. Only few studies investigated the prophylaxis and treatment of bleeding from gastric varices, and almost no controlled studies investigating prophylaxis and treatment of bleeding from portal hypertensive gastropathy and from ectopic varices have been conducted. A trained interdisciplinary team consisting of endoscopists, hepatologists, and specialized nurses as well as interventional radiologist if appropriate should administer treatment of acute bleeding related to portal hypertension.
Treatment is done according to the current guidelines. Endoscopic therapy is a key aspect, but pharmacologic treatment with vasopressors and antibiotic treatment are also important components of successful patient care. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Academic Editor: A. Received 30 May Accepted 29 Jun Published 22 Jul Abstract Gastrointestinal bleeding related to portal hypertension is a serious complication in patients with liver cirrhosis. Introduction One of the main complications of liver cirrhosis is portal hypertension. Primary Prophylaxis of Esophageal Variceal Bleeding The identification and prophylactic treatment of patients at risk of esophageal variceal bleeding is a major goal [ 13 ]. Figure 1. Esophageal varices in a patient with liver cirrhosis, second grade.
Figure 2. Endoscopic view through the transparent cap mounted at the tip of the endoscope at a ligated varix in the lower esophagus. Figure 3. Flow chart showing the options for primary prevention of esophageal variceal bleeding.
Patients at high risk of bleeding are those with medium or large varices, small varices, and red whale signs and patients in a Child class C state.
Though small varices may not require treatment, medium or large varices should be treated with beta blockers first, and EVL should be used an alternate therapy. Secondary prophylaxis is intended to prevent re-bleeding, which Therapondos said is also common in liver failure. EVL and beta-blockers should be used, though TIPS is considered to be rescue therapy, as it can precipitate cardiac failure and may lead to further decompensation and death. Portal hypertensive gastropathy usually affects the proximal stomach and responds to reduction in portal pressure.
Ascites formation results from renal arterial vasoconstriction that causes retention of sodium and water. If the condition persists, hepatorenal syndrome develops, which can result in refractory ascites with either acute renal failure or stable renal failure. Model for end-stage liver disease MELD for predicting mortality in patients with acute variceal bleeding. Hepatology ; 35 5 : — 4. Comparison of clinical outcomes between variceal and non-variceal gastrointestinal bleeding in patients with cirrhosis.
J Gastroenterol Hepatol ; 33 10 : — 9. Hepatology ; 61 3 : — Prospective validation of Baveno V definitions and criteria for failure to control bleeding in portal hypertension. R Core Team. Google Preview. Am J Gastroenterol ; 99 7 : — Predictive factors of mortality from nonvariceal upper gastrointestinal hemorrhage: a multicenter study. Am J Gastroenterol ; 7 : — 47; quiz A risk scoring system to predict in-hospital mortality in patients with cirrhosis presenting with upper gastrointestinal bleeding.
J Clin Gastroenterol ; 48 8 : — Improving prognosis following a first variceal haemorrhage over four decades. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.
Sign In or Create an Account. Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume 3. Article Contents Abstract. Oxford Academic. Parul Tandon, DO. Stacey Fisher, MSc. Ian Carrigan.
These authors contributed equally to this study. Select Format Select format. Permissions Icon Permissions. Abstract Background. Cirrhosis , ICU , Upper gastrointestinal bleed. Table 1. Baseline characteristics of study population. P value.
Open in new tab. Table 2. Table 3. Table 4. SD, standard deviation; IQR, interquartile range. Table 5. Table 6. Age per year 1. Open in new tab Download slide. This is the main cause of the bleedings observed in patients with cirrhosis.
Portal hypertension can also cause what is called portal hypertensive gastropathy. This includes changes in the blood vessels of the stomach which can cause bleeding in the stomach.
Why is gastrointestinal bleeding a complication of cirrhosis? Sep 20, Because cirrhosis causes hypertension in the veins of the gastrointestinal tract. Explanation: Cirrhosis is a disease in which healthy tissue of the liver is replaced with scar tissue. Related questions In what organ is the waste from the digestion process collected for eventual disposal?
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