Aa
Do espohageal varices reverse without intervention
I am cirrhotic........A year and a half ago: stage 2 varices- 2 weeks ago stage 1. No testing variables: same hepa/endoscopy specialist, same environment, same person reading the results......And no intervention of any type between the two tests....No changes in lifestyle or exercise patterns? Thanks. d
Mucho gratitude for all the responses that my question catalyzed. I'm looking to start treatment while I have an insurance granting temp (12 months) R.N. job: Triple treatment for a double failure....Appropriately I am a professional blues musician by night. p.s. I am way too stage vain to ever stop exercising. Neither cirrhosis, antivirals, or depression shall have victories over my resolution to stay on stage and work out....d
Dee, I too have portal hyptertension n started tx. I've posted a lot the last few days n may have already posted this. But like Hector, I'm down to 20 mg Nadolol n doing fine. The exercise helps. I had to quit totally, start again light, and am now lifting 35 lbs n doing yoga. No outdoor walking in this heat.
AND... I take my 3rd shot tomorrow. I had a Dopplar sonography done in the morning before they wrote the script. I was SO relieved the blood flowed through the liver n did not reflux. I saw it myself on color radar! We're gonna do fine girl...
Hope springs eternal, Karen
AND... I take my 3rd shot tomorrow. I had a Dopplar sonography done in the morning before they wrote the script. I was SO relieved the blood flowed through the liver n did not reflux. I saw it myself on color radar! We're gonna do fine girl...
Hope springs eternal, Karen
Thank you all for your posts. I have been wondering about the EGD and how often you should get it done. I had EGD 2 years ago and am glad to know I can wait a year to recheck especially since I will be starting tx in the next month or so
D
D
Did anyone mention the TIPS procedure as an approach to managing varices?
TIPS = transjugular intrahepatic portosystemic shunt. Basically it connects the incoming portal vein with the outgoing hepatic vein and allows blood to bypass the liver. This decreases portal hypertension. There are side effects to this procedure - onset of or worsening of hepatic encephalopathy is a main one. But when varices cannot be managed TIPS is an option. I believe that TIPS is primarily used as a bridge to liver transplantation.
Anecdotally: I had two major bleeds in the first quarter of 1995. I lost approximately 4 units of blood each bleed. My varices were not banded which I believe is the preferred approach. Mine were injected with a sclerosing drug. After my second bleed a new GI told me he was going to do a series of the endoscopic sclerosing treatments to "obliterate" the varices (vessels?). I had 6 or 7 treatments which I assume did obliterate the varices and was then monitored monthly or very 6 weeks. I never had another bleed and was transplanted in June of 2000. And I maintained a healthy and active lifestyle for 5 years with not a single problem.
Good luck,
Mike
Mike
TIPS = transjugular intrahepatic portosystemic shunt. Basically it connects the incoming portal vein with the outgoing hepatic vein and allows blood to bypass the liver. This decreases portal hypertension. There are side effects to this procedure - onset of or worsening of hepatic encephalopathy is a main one. But when varices cannot be managed TIPS is an option. I believe that TIPS is primarily used as a bridge to liver transplantation.
Anecdotally: I had two major bleeds in the first quarter of 1995. I lost approximately 4 units of blood each bleed. My varices were not banded which I believe is the preferred approach. Mine were injected with a sclerosing drug. After my second bleed a new GI told me he was going to do a series of the endoscopic sclerosing treatments to "obliterate" the varices (vessels?). I had 6 or 7 treatments which I assume did obliterate the varices and was then monitored monthly or very 6 weeks. I never had another bleed and was transplanted in June of 2000. And I maintained a healthy and active lifestyle for 5 years with not a single problem.
Good luck,
Mike
Mike
Hey there! WOW! Thanks for all the information, really nice of you to share so much, this is very helpful
D
D
For your late night reading....
The most important point is if you have developed varices due to portal hypertension, it is standard treatment to take a beta-blocker to prevent the first bleed. Once you have that first bleed. Re-bleeding becomes common and potentially fatal. The toughest part I from is that if you take too high of a dose it is possible to have some serious lightheadedness, fatigue, and shortness of breath to the point where I felt like I was going to past out and end up in ER. Once the dose was reduced (I take 20mg of Nadolol) I notice no side effects.
-----------------------------------------------------------------------------------------------------------------------
AASLD
Prevention and Management of Gastroesophageal
Varices and Variceal Hemorrhage in Cirrhosis
http://www.aasld.org/practiceguidelines/Documents/Bookmarked%20Practice%20Guidelines/Prevention%20and%20Management%20of%20Gastro%20Varices%20and%20Hemorrhage.pdf
Pathophysiology of Portal Hypertension in Cirrhosis
Cirrhosis, the end stage of any chronic liver disease, can lead to portal hypertension. Portal pressure increases initially as a consequence of an increased resistance to flow
mostly due to an architectural distortion of the liver secondary to fibrous tissue and regenerative nodules. In addition to this structural resistance to blood flow, there is
an active intrahepatic vasoconstriction that accounts for 20%-30% of the increased intrahepatic resistance, and that is mostly due to a decrease in the endogenous production of nitric oxide. Portal hypertension leads to the formation of porto-systemic collaterals. However, portal hypertension persists despite the development of
these collaterals for 2 reasons: (1) an increase in portal venous inflow that results from splanchnic arteriolar vasodilatation occurring concomitant with the formation of collaterals.
; and (2) insufficient portal decompression through collaterals as these have a higher resistance than that of the normal liver.
Therefore, an increased portal pressure gradient results from both an increase in resistance to portal flow (intrahepatic and collateral) and an increase in portal blood inflow.
....Natural History of Varices
Gastroesophageal varices are the most relevant portosystemic collaterals because their rupture results in variceal hemorrhage, the most common lethal complication of cirrhosis. Varices and variceal hemorrhage are the complications of cirrhosis that result most directly from portal hypertension. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm Hg. Gastroesophageal varices are present in approximately
50% of patients with cirrhosis. Their presence correlates with the severity of liver disease (Table 2); while only 40% of Child A patients have varices, they are present in 85%
of Child C patients....It has also been shown that 16% of patients with hepatitis C and bridging fibrosis have esophageal varices. Patients without varices develop them at a rate of 8% per year, and the strongest predictor for development of varices in those with cirrhosis who have no varices at the time of initial endoscopic screening is an HVPG 10
mmHg. Patients with small varices develop large varices at a rate of 8% per year. Decompensated cirrhosis (Child B/C), alcoholic cirrhosis, and presence of red wale marks
(defined as longitudinal dilated venules resembling whip marks on the variceal surface) at the time of baseline endoscopy are the main factors associated with the progression from small to large varices. Variceal hemorrhage occurs at a yearly rate of 5%-15%, and the most important predictor of hemorrhage is the size of varices, with the highest risk of first hemorrhage (15% per year) occurring in patients with large varices. Other predictors of hemorrhage are decompensated cirrhosis (Child B/C) and the endoscopic presence of red
wale marks. Although bleeding from esophageal varices ceases spontaneously in up to 40% of patients, and despite improvements in therapy over the last decade, it is
associated with a mortality of at least 20% at 6 weeks.Patients with an HVPG 20 mmHg (measured within 24 hours of variceal hemorrhage) have been identified as
being at a higher risk for early rebleeding (recurrent bleeding within the first week of admission) or failure to control bleeding (83% vs. 29%) and a higher 1-year mortality
(64% vs. 20%) compared to those with lower pressure. Late rebleeding occurs in approximately 60% of untreated patients, mostly within 1-2 years of the index
hemorrhage. Variceal wall tension is probably the main factor that determines variceal rupture. Vessel diameter is one of the determinants of variceal tension. At an equal pressure, a large diameter vessel will rupture while a small diameter vessel will not rupture.
Besides vessel diameter, one of the determinants of variceal wall tension is the pressure
within the varix, which is directly related to the HVPG. Therefore, a reduction in HVPG should lead to a decrease in variceal wall tension, thereby decreasing the risk of
rupture. Indeed, variceal hemorrhage does not occur when the HVPG is reduced to 12 mmHg. It has also been shown that the risk of rebleeding decreases significantly with reductions in HVPG greater than 20% from baseline. Patients whose HVPG decreases to 12 mmHg or at least 20% from baseline levels (“HVPG responders”) not only have a lower probability of developing recurrent variceal hemorrhage, but also have a lower risk of developing ascites, spontaneous bacterial peritonitis, and death.
Recommendations
1. Screening esophagogastroduodenoscopy (EGD) for the diagnosis of esophageal and gastric varices is recommended when the diagnosis of cirrhosis is made.
2. On EGD, esophageal varices should be graded as small or large (>5 mm) with the latter classification encompassing medium-sized varices when 3 grades are used (small, medium, large). The presence or absence of red signs (red wale marks or red spots) on varices should be noted.
Recommendations
4. In patients who have compensated cirrhosis and no varices on the initial EGD, it should be repeated in 3 years. If there is evidence of hemorrhage (Child B/C or presence of red wale marks on varices), nonselective -blockers should be used for the prevention of first variceal hemorrhage.
6. In patients with cirrhosis and small varices that have not bled and have no criteria for increased risk of bleeding, beta-blockers can be used, although their long-term benefit has not been established.
7. In patients with small varices that have not bled and who are not receiving -blockers, EGD should be repeated in 2 years. If there is evidence of hepatic decompensation, EGD should be done at that time and repeated annually. In patients with small varices who receive beta-blockers, a follow-up EGD is not necessary.
C. Patients with Cirrhosis and Medium/Large Varices That Have Not Bled
A meta-analysis of 11 trials that included 1,189 patients evaluating nonselective -blockers (i.e., propranolol, nadolol) versus non-active treatment or placebo in the prevention of first variceal hemorrhage shows that the risk of first variceal bleeding in patients with large- or mediumsized varices is significantly reduced by -blockers (30% in controls vs. 14% in -blocker-treated patients), and indicates that 1 bleeding episode is avoided for every 10
patients treated with -blockers. Mortality is also lower in the -blocker group compared with the control group and this difference has recently been shown to be statistically significant.
Additionally, a cost-effectiveness study comparing nonselective -blockers, sclerotherapy, and shunt surgery shows that beta-blockers were the only cost effective form of prophylactic therapy.
---------------------------------------------------------------------------------------------------------------------------
Cheers!
Hector
The most important point is if you have developed varices due to portal hypertension, it is standard treatment to take a beta-blocker to prevent the first bleed. Once you have that first bleed. Re-bleeding becomes common and potentially fatal. The toughest part I from is that if you take too high of a dose it is possible to have some serious lightheadedness, fatigue, and shortness of breath to the point where I felt like I was going to past out and end up in ER. Once the dose was reduced (I take 20mg of Nadolol) I notice no side effects.
-----------------------------------------------------------------------------------------------------------------------
AASLD
Prevention and Management of Gastroesophageal
Varices and Variceal Hemorrhage in Cirrhosis
http://www.aasld.org/practiceguidelines/Documents/Bookmarked%20Practice%20Guidelines/Prevention%20and%20Management%20of%20Gastro%20Varices%20and%20Hemorrhage.pdf
Pathophysiology of Portal Hypertension in Cirrhosis
Cirrhosis, the end stage of any chronic liver disease, can lead to portal hypertension. Portal pressure increases initially as a consequence of an increased resistance to flow
mostly due to an architectural distortion of the liver secondary to fibrous tissue and regenerative nodules. In addition to this structural resistance to blood flow, there is
an active intrahepatic vasoconstriction that accounts for 20%-30% of the increased intrahepatic resistance, and that is mostly due to a decrease in the endogenous production of nitric oxide. Portal hypertension leads to the formation of porto-systemic collaterals. However, portal hypertension persists despite the development of
these collaterals for 2 reasons: (1) an increase in portal venous inflow that results from splanchnic arteriolar vasodilatation occurring concomitant with the formation of collaterals.
; and (2) insufficient portal decompression through collaterals as these have a higher resistance than that of the normal liver.
Therefore, an increased portal pressure gradient results from both an increase in resistance to portal flow (intrahepatic and collateral) and an increase in portal blood inflow.
....Natural History of Varices
Gastroesophageal varices are the most relevant portosystemic collaterals because their rupture results in variceal hemorrhage, the most common lethal complication of cirrhosis. Varices and variceal hemorrhage are the complications of cirrhosis that result most directly from portal hypertension. Patients with cirrhosis and gastroesophageal varices have an HVPG of at least 10-12 mm Hg. Gastroesophageal varices are present in approximately
50% of patients with cirrhosis. Their presence correlates with the severity of liver disease (Table 2); while only 40% of Child A patients have varices, they are present in 85%
of Child C patients....It has also been shown that 16% of patients with hepatitis C and bridging fibrosis have esophageal varices. Patients without varices develop them at a rate of 8% per year, and the strongest predictor for development of varices in those with cirrhosis who have no varices at the time of initial endoscopic screening is an HVPG 10
mmHg. Patients with small varices develop large varices at a rate of 8% per year. Decompensated cirrhosis (Child B/C), alcoholic cirrhosis, and presence of red wale marks
(defined as longitudinal dilated venules resembling whip marks on the variceal surface) at the time of baseline endoscopy are the main factors associated with the progression from small to large varices. Variceal hemorrhage occurs at a yearly rate of 5%-15%, and the most important predictor of hemorrhage is the size of varices, with the highest risk of first hemorrhage (15% per year) occurring in patients with large varices. Other predictors of hemorrhage are decompensated cirrhosis (Child B/C) and the endoscopic presence of red
wale marks. Although bleeding from esophageal varices ceases spontaneously in up to 40% of patients, and despite improvements in therapy over the last decade, it is
associated with a mortality of at least 20% at 6 weeks.Patients with an HVPG 20 mmHg (measured within 24 hours of variceal hemorrhage) have been identified as
being at a higher risk for early rebleeding (recurrent bleeding within the first week of admission) or failure to control bleeding (83% vs. 29%) and a higher 1-year mortality
(64% vs. 20%) compared to those with lower pressure. Late rebleeding occurs in approximately 60% of untreated patients, mostly within 1-2 years of the index
hemorrhage. Variceal wall tension is probably the main factor that determines variceal rupture. Vessel diameter is one of the determinants of variceal tension. At an equal pressure, a large diameter vessel will rupture while a small diameter vessel will not rupture.
Besides vessel diameter, one of the determinants of variceal wall tension is the pressure
within the varix, which is directly related to the HVPG. Therefore, a reduction in HVPG should lead to a decrease in variceal wall tension, thereby decreasing the risk of
rupture. Indeed, variceal hemorrhage does not occur when the HVPG is reduced to 12 mmHg. It has also been shown that the risk of rebleeding decreases significantly with reductions in HVPG greater than 20% from baseline. Patients whose HVPG decreases to 12 mmHg or at least 20% from baseline levels (“HVPG responders”) not only have a lower probability of developing recurrent variceal hemorrhage, but also have a lower risk of developing ascites, spontaneous bacterial peritonitis, and death.
Recommendations
1. Screening esophagogastroduodenoscopy (EGD) for the diagnosis of esophageal and gastric varices is recommended when the diagnosis of cirrhosis is made.
2. On EGD, esophageal varices should be graded as small or large (>5 mm) with the latter classification encompassing medium-sized varices when 3 grades are used (small, medium, large). The presence or absence of red signs (red wale marks or red spots) on varices should be noted.
Recommendations
4. In patients who have compensated cirrhosis and no varices on the initial EGD, it should be repeated in 3 years. If there is evidence of hemorrhage (Child B/C or presence of red wale marks on varices), nonselective -blockers should be used for the prevention of first variceal hemorrhage.
6. In patients with cirrhosis and small varices that have not bled and have no criteria for increased risk of bleeding, beta-blockers can be used, although their long-term benefit has not been established.
7. In patients with small varices that have not bled and who are not receiving -blockers, EGD should be repeated in 2 years. If there is evidence of hepatic decompensation, EGD should be done at that time and repeated annually. In patients with small varices who receive beta-blockers, a follow-up EGD is not necessary.
C. Patients with Cirrhosis and Medium/Large Varices That Have Not Bled
A meta-analysis of 11 trials that included 1,189 patients evaluating nonselective -blockers (i.e., propranolol, nadolol) versus non-active treatment or placebo in the prevention of first variceal hemorrhage shows that the risk of first variceal bleeding in patients with large- or mediumsized varices is significantly reduced by -blockers (30% in controls vs. 14% in -blocker-treated patients), and indicates that 1 bleeding episode is avoided for every 10
patients treated with -blockers. Mortality is also lower in the -blocker group compared with the control group and this difference has recently been shown to be statistically significant.
Additionally, a cost-effectiveness study comparing nonselective -blockers, sclerotherapy, and shunt surgery shows that beta-blockers were the only cost effective form of prophylactic therapy.
---------------------------------------------------------------------------------------------------------------------------
Cheers!
Hector
since portal hypertension causes varices can you reverse varices by reversing portal hypertension
Angiogenesis is a biological process where new blood vessels grow from ones already in place
CONCLUSIONS: Our results provide new insights into how angiogenesis regulates portal hypertension by demonstrating that the maintenance of increased portal pressure, hyperkinetic circulation, splanchnic neovascularization, and portosystemic collateralization is regulated by VEGF and PDGF in portal hypertensive rats. Importantly, these findings also suggest that an extended antiangiogenic strategy (that is, targeting VEGF/endothelium and PDGF/pericytes) may be a novel approach to the treatment of portal hypertension.
Angiogenesis is a biological process where new blood vessels grow from ones already in place
CONCLUSIONS: Our results provide new insights into how angiogenesis regulates portal hypertension by demonstrating that the maintenance of increased portal pressure, hyperkinetic circulation, splanchnic neovascularization, and portosystemic collateralization is regulated by VEGF and PDGF in portal hypertensive rats. Importantly, these findings also suggest that an extended antiangiogenic strategy (that is, targeting VEGF/endothelium and PDGF/pericytes) may be a novel approach to the treatment of portal hypertension.
Thank you so much for sharing your information regarding varices
I really appreciate your thoughts, I have learned so much from you.
I haven't read Dante's Inferno, don't think I will :)
I had an endoscopy 2 years ago. Hoping (not hoping) to start tx in the next few of months and was thinking maybe I should get that checked first. I see the Hep Doc later this month, not sure if it is something that is checked on a scheduled basis or not.
Thanks again for all that you share with us, I have your mantra, one day at a time, one day at a time...running through my head :)
D
I really appreciate your thoughts, I have learned so much from you.
I haven't read Dante's Inferno, don't think I will :)
I had an endoscopy 2 years ago. Hoping (not hoping) to start tx in the next few of months and was thinking maybe I should get that checked first. I see the Hep Doc later this month, not sure if it is something that is checked on a scheduled basis or not.
Thanks again for all that you share with us, I have your mantra, one day at a time, one day at a time...running through my head :)
D
I'm no doctor but did have Verices banding twice. If they would have reversed on their own, I'm sure the doctor would have said "let's wait and see what happens". I would not ignore this potentially serious problem. Banding takes about 30 minutes. It's no big deal. You will possibly experience some esophagus pain for a few days. No bread or meat for three days and I’m sure the doctor will explain all to you. Don't ignore this!
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Varices, portal hypertension change all the time. But the trajectory for End Stage Liver Disease is always the same over time. At some point our livers will fail given enough time unfortunately. But before failure certain complication will come and go more often and become more severe. Think about our MELD scores. Why are we tested every 6 months, 3 months, 1 month, 2 weeks, weekly? Because depending how ill we are our MELD is constantly in flux.
Mine have gone from 2 to 3 in the last year. (bad) But my MELD has gone from 18 to 12. (good). But I also have developed HCC ($%&$^&%%!!!) "Ever changing, ever living..." (Oopps flashed back to a Bob Marley song). Maybe cause I haven't slept in 2 days? "Jah Rastafari! Just can't live that negative way...make way for the positive day!"
whew I'm losin' it mon. Give me another hit of the lactulose!
So how can varices reduce their severity? One obvious way is that other veins in other parts of the body are now taking more of the back pressure that was building in your esophagus or where ever you had them before. Is this a good this? It depends how you look at it. It is good because the pressure has been reduced in the varices you already have. So it makes it more unlikely that those particular vein will rupture any time soon. On the other hand there are now other veins that are under pressure that they weren't designed to handle.
I'm afraid that once we become too ill to treat the cause of our liver disease all we can do is try to stay as healthy and active as possible and hope a donated liver will be available with our livers can no longer function. You are I are in the two regions with the longest wait lists for a donated liver in the entire country. I don't know the MELD score they are transplanting at in NYC but here it is in the upper 30s. Which could be called "livin' on the edge" of life.
Hang in there. Keep taking your meds to moderate your symptoms. Are you taking Nadolol for your portal hypertension? I've been put on a light exercise program (walking, yoga & light weights) and I can't tell you how much more stamina I have now. I am doing thing physically I never would have imaged I could just 6 months ago. I wish all this would go away. I really do. But for some reason I can't comprehend this is my life now. I feel pretty good physically. My biggest issue is these crazy nightmares I've been having about dying and still being conscious as they start cutting me into pieces. I guess it is a phase I am going through because of my diagnoses of HCC, liver cancer. I knew I had an imagination, but nothing this graphic and macabre. I guess I read Dante's Inferno too many times that it is in my unconscious. haha Thanks Durante degli Alighieri.
Hang in there. We are gonna make it somehow. Take it one day at a time and live in the moment. We have the same as everyone else on this planet this moment that is all there is or ever will be.
Hector