Varices esophagus
post variceal banding

Video Endoscopic Sequence 1 of 10.

Endoscopy of status post variceal banding

This is a 54 year-old female, with liver cirrhosis as a complication of long-standing type 2 diabetes mellitus.
Esophageal varices were banded, four days later showed a slight fainting with little bleeding in the mouth. An emergency endoscopy was performed. Finding a status of post variceal ligation.
There was no active bleeding, apparently the site of a banding came off, and had a little bleeding. It only was alarm of bleeding.

Endoscopy of status post variceal banding


For more endoscopic details, download the video clip by clicking on the endoscopic image. Wait to be downloaded complete then Press Alt and Enter for full screen. All endoscopic images shown in this Atlas contain video clips. We recommend seeing the video clips in full screen mode.

 

Esophageal Varices

Video Endoscopic Sequence 2 of 10.

There are multiple fresh scars.

In this image as well as the video clip display, the status of variceal banding at the gastroesophageal junction.

The varices are in the process of necrosis were observed. No active bleeding was found.

This case after variceal ligation gives us an important follow up what happens normally as a subsequent treatment.

Elective esophageal variceal ligation (EVL) is performed to decrease the risk of variceal hemorrhage. Side effects of EVL include hemorrhage, chest pain, dysphagia, and odynophagia. Because gastric acid may exacerbate postbanding ulcers and delay healing, proton pump inhibition may decrease side effects associated with EVL.





Esophageal Varices

Video Endoscopic Sequence 3 of 10.

Table 1. Liver Disease and Diabetes Mellitus

1. Liver disease occurring as a consequence of diabetes mellitus
  • Glycogen deposition
  • Steatosis and nonalcoholic steatohepatitis (NASH)
  • Fibrosis and cirrhosis
  • Biliary disease, cholelithiasis, cholecystitis
  • Complications of  therapy of  diabetes (cholestatic and necroinflammatory)

2 . Diabetes mellitus and abnormalities of glucose homeostasis occurring as a complication of liver disease

  • Hepatitis
  • Cirrhosis
  • Hepatocellular carcinoma
  • Fulminant hepatic failure
  • Postorthotopic liver transplantation

3 . Liver disease occurring coincidentally with diabetes mellitus and abnormalities of glucose homeostasis

  • Hemochromatosis
  • Glycogen storage diseases
  • Autoimmunebiliary disease

 

Esophageal Varices

Video Endoscopic Sequence 4 of 10.

The varix that has been ligated, there is no active bleeding.

The image as well as the video clip display the subsequent appearance after of four days of banding was two apparently linked varices, which were up from the first three that were ligated into the gastroesophageal junction.

The liver plays a central and crucial role in the regulation of carbohydrate metabolism. Its normal functioning is essential for the maintenance of blood glucose levels and of a continued supply to organs that require a glucose energy source. This central role for the liver in glucose homeostasis offers a clue to the pathogenesis of glucose intolerance in liver diseases but little insight into the mechanisms of liver disease in diabetes mellitus.


Esophageal Varices

Video Endoscopic Sequence 5 of 10.

There are two rubber bands impacted with fibrin

Liver Disease Occurring as a Consequence of Diabetes Mellitus

Excess glycogen accumulation in the liver is seen in 80% of diabetic patients. Glycogen synthesis in the liver is impaired in diabetes due to defective activation of glycogen synthase. However, studies attesting to this were usually performed on animals with recently induced diabetes. In patients with chronic diabetes, glycogen accumulation is seen, and it is postulated that long-standing insulin deficiency may actually facilitate synthase activity. This and enhanced gluconeogenesis may account for the net accumulation of glycogen in diabetes.



Esophageal Varices

Video Endoscopic Sequence 6 of 10.

The acoustic effect of water

Fatty Liver, Steatohepatitis:
Hepatic fat accumulation is a well-recognized complication of diabetes with a reported frequency of 40–70%. Unfortunately, associated obesity is a frequently occurring confounding variable. Type 1 diabetes is not associated with fat accumulation if glycemia is well controlled, but type 2 diabetes may have a 70% correlation regardless of blood glucose control.

Fat is stored in the form of triglyceride and may be a manifestation of increased fat transport to the liver, enhanced hepatic fat synthesis, and decreased oxidation or removal of fat from the liver. The steatosis may be microvesicular or macrovesicular and may progress to fibrosis and cirrhosis. The degree of glycemic control does not correlate with the presence or absence of fat. The most common clinical presentation is hepatomegaly, and most patients have normal or only mildly abnormal transaminases and normal bilirubin.



Esophageal Varices

Video Endoscopic Sequence 7 of 10.

In the cardia, necrotic appearance of varices, after four days that has been ligated.

CT scan and ultrasound are claimed to be sensitive tests for detecting hepatic fat accumulation. A negative ultrasound, however, does not exclude the presence of microscopic fatty infiltration. A liver biopsy is obviously the best method for detecting hepatic fat accumulation. It is unclear at this time whether a biopsy is always necessary in patients with suspected steatohepatitis. Biopsy probably should be performed when the diagnosis is unclear, although some authors suggest that it is necessary in all cases to confirm the diagnosis and assess the degree of fibrosis.

Excessive fat accumulation is seen in alcoholic liver disease, obesity, prolonged parenteral nutrition, protein malnutrition, jejunoileal bypass, and chronic illnesses complicated by impaired nutrition, such as ulcerative colitis and chronic pancreatitis. It can also occur as a result of hepatotoxins, such as carbon tetrachloride, and can be seen in association with abetalipoproteinemia, Weber-Christian disease, the HIV virus, cholesterol ester storage disease, and Wilson's disease, in addition to diabetes mellitus. A number of drugs, such as amiodarone, perhexilene, glucocorticoids, estrogens, and tamoxifen, may cause macrovesicular steatosis. The amount of fat frequently diminishes with improvement of the underlying condition



 

Esophageal Varices

Video Endoscopic Sequence 8 of 10.

The image and the video clip show water floodedr.The varices that have been previousloy strangled with bands.

Nonalcoholic steatohepatitis (NASH) is a variant of fatty liver in which fat in the hepatocytes is accompanied by lobular inflammation and steatonecrosis. The diagnosis can only be made in the absence of alcohol abuse or other causes of liver disease, particularly hepatitis C. In patients with diabetes and steatohepatitis, Mallory bodies such as those seen in alcoholic liver disease may be seen. Nonalcoholic steatohepatitis has been associated most commonly with obese women with diabetes, but the disease is certainly not limited to patients with this clinical profile. There is certainly a higher prevalence in type 2 diabetic patients on insulin.

Esophageal Varices

Video Endoscopic Sequence 9 of 10.

In the image and video clip the two varices that have been strangled with bands (four days before).

The spectrum of clinical disease in fatty liver with steatohepatitis varies from the asymptomatic elevation of liver enzymes to severe liver disease with fibrosis and nodular regeneration. Patients with nonalcoholic steatohepatitis can develop progressive liver disease and complications to the point that they may need liver transplantation.

Nonalcoholic steatohepatitis should be considered as a cause for chronically elevated liver enzymes in asymptomatic diabetic patients particularly if they are obese and have hyperlipidemia. In type 2 diabetic patients with or without obesity, up to 30% have fat with inflammation, 25% have associated fibrosis, and 1–8% have cirrhosis.

Esophageal Varices

Video Endoscopic Sequence 10 of 10.

Another aspect in water immersion

The morphological pattern of diabetic steatohepatitis resembles that seen in alcoholic hepatitis. However, the histopathological changes in diabetes tend to be periportal (situated in zone I), while those in alcoholic hepatitis are predominantly pericentral (in zone III). It is not clear whether the diabetes is causally related to the steatohepatitis. In an animal model of type 1 diabetes, there is a high incidence of perisinusoidal hepatic fibrosis, while in humans perisinusoidal fibrosis often parallels with diabetic microangiopathy.

Cirrhosis
There is an increased incidence of cirrhosis in diabetic patients, and, conversely, at least 80% of patients with cirrhosis have glucose intolerance. The reported prevalence of cirrhosis in diabetes varies widely. Diabetes increases the risk of steatohepatitis, which can progress to cirrhosis. Obesity is a significant confounding variable in determining the prevalence of cirrhosis in diabetes. Even with normal glucose tolerance, obesity can cause steatohepatitis and cirrhosis. Likewise, the lack of a clear definition of diabetes in the past somewhat confounds these statistics.

Biliary Disease, Cholelithiasis, Cholecystitis
There is a reported increased incidence of cholelithiasis in diabetes mellitus, but obesity and hyperlipidemia may again be confounding variables. Several articles have reported a two- to threefold increased incidence of gallstones in diabetic patients, whereas others have failed to demonstrate a significant association. Gallbladder emptying abnormalities found in diabetic patients may predispose patients to cholelithiasis. Secretion of lithogenic bile by the liver in patients with type 2 diabetes probably predisposes them to forming gallstones, but this is likely a result of concomitant obesity rather than a result of the diabetes itself. Increased biliary cholesterol saturation has not been demonstrated in insulin-dependent diabetic patients.

There is no indication in the literature that the natural history of gallstones is different in diabetic and nondiabetic individuals. The relative risk of mortality following acute cholecystitis is not significantly greater in diabetic patients than in the general population, and neither is the risk for serious complications. For that reason, prophylactic cholecystectomy cannot routinely be recommended for asymptomatic gallstones in patients with diabetes.55 Any increase in mortality may be attributed to underlying renal or vascular disease. Patients with diabetes have comparable survival outcomes from laparoscopic or open cholecystectomy.

 

Endoscopic rubber band ligation in treatment of esophageal varices bleeding

Video Endoscopic Sequence 1 of 17.

Endoscopic rubber band ligation in treatment of esophageal varices bleeding

This Sequence displays banding of esophageal varices. Endoscopic variceal ligation, a less invasive procedure than endoscopic sclerotherapy.







rubber band ligation

Video Endoscopic Sequence 2 of 17.

Endoscopic rubber band ligation in treatment of esophageal varices bleeding

The esophageal varices are seen in retroflexed view.

Esophageal varices eventually develop in most patients with cirrhosis, but variceal bleeding occurs in only one third of them. Treatment of patients at highest risk for bleeding is critical because of the high risk of death with each episode of variceal hemorrhage. The goal of treatment of portal hypertension is decreased variceal flow, which is achieved by reducing either portal venous inflow or resistance to portal outflow.



Endoscopic rubber band ligation in treatment of esophageal varices bleeding

Video Endoscopic Sequence 3 of 17.

Endoscopic rubber band ligation in treatment of esophageal varices bleeding

Suction is applied through the endoscope, and the band is released over the entrapped varix.

The clear plastic cylinder of the variceal ligation device is seen attached to the end of the endoscope.

The portal venous system, formed by the confluence of the superior mesenteric vein and the splenic vein drains the stomach, the large and small intestine, the pancreas, and the spleen. An important feature of this system is that a number of its tributaries also communicate with the systemic circulation. These include the intrinsic and extrinsic veins of the gastroesophageal junction; hemorrhoidal veins of the anal canal; paraumbilical veins and the recanalized falciform ligament; the splenic venous bed and the left renal vein; and the retroperitoneum. In portal hypertension, these venous collaterals dilate and allow portal venous blood to return to the systemic circulation. Clinically, the most significant collaterals are the intrinsic veins of the gastroesophageal junction, which are located close to the mucosal surface. They are the collaterals most likely to bleed when dilated because of increased blood flow.



Endoscopic rubber band ligation in treatment of esophageal varices bleeding

Video Endoscopic Sequence 4 of 17.

Endoscopic rubber band ligation in treatment of esophageal varices bleeding

More bands have been placed on the varices, resulting in spherical blebs.
Note the colored elastic bands strangulating each varix at the base.

A typical appearance after a band has been placed at its base. Below the small circular band, which failed to deliver properly is observed.

rubber band ligation

Video Endoscopic Sequence 5 of 17.

As seen through the banding apparatus attached to the tip of the endoscope.
Ligation therapy has been used for years as the treatment of hemorrhoids, and the technique was modified for the treatment of esophageal varices.


rubber band ligation

Video Endoscopic Sequence 6 of 17.

The video clip displays two varices with typical appearance after a band has been placed at its base.

Variceal hemorrhage accounts for one third of all deaths related to cirrhosis. To date, many modalities of treating variceal bleeding have been devised, including pharmacological therapy. Treatment of variceal hemorrhage includes resuscitation, initial hemostasis, and prevention of complications and recurrent bleeding. Intravenous vasoactive agents such as terlipressin, somatostatin, octreotide, or vapreotide should be administered in patients with suspected variceal bleeding. Endoscopic treatment remains the mainstay of treatment



Esophageal Varix

Video Endoscopic Sequence  7 of 17.

A varix has been ligated at the cardias.


Esophageal Banding due to varices.

Video Endoscopic Sequence 8 of 17.

Endoscopic view of Esophageal Banding due to varices.

Retroflexed view of cardias, the video clip display four varices that have been banding.


Esophageal Varices

Video Endoscopic Sequence 9 of 17.

The video clip displays two varices that have been banding. Note the raised mucosal bleb (the varix) with a black band at the base.

Esophageal Varices

Video Endoscopic Sequence 10 of 17.

Follow up endospy, 5 days after the banding.

An endoscopy was performed to follow up the banding treatment; the four varices were with necrotic appearance. similar of the treatment for hemorrhoids with banding.

 

Esophageal Varices

Video Endoscopic Sequence 11 of 17.

Another image and video clip of the follow up endoscopy, some varices are seen with white color due to necrosis exerted by the bands.

 


Esophageal Varices

Video Endoscopic Sequence 12 of 17.

Two necrotic varices are seen at the cardias.

Esophageal Varices

Video Endoscopic Sequence 13 of 17.

Retroflexed image, an ulceration is observed where the band was come off, attach to the endoscope a fibrin fragment is observed which recently has been fallen from this ulceration.

 

Esophageal Varices

Video Endoscopic Sequence 14 of 17.

A new follow up after two weeks of the variceal band treatment. Status post treatment was observed, some ulcers where the varices were found. The rubber band has already fallen off, leaving behind an oozing ulcer.

 

Esophageal Varices

Video Endoscopic Sequence 15 of 17.

The image and the video show multiple oozing ulcer.


Esophageal Varices

Video Endoscopic Sequence 16 of 17.

Another post ligation ulcer is observed retroflexed image. See the video clip.

Esophageal Varices

Video Endoscopic Sequence 17 of 17.

This image shows status post variceal banding.

The scope is retroflexed in the stomach to check for gastric varices, none are seen.
The ulcer is seen at the gastric cardias. Because varices tend to recur over time, surveillance endoscopy must be performed every 6 to 12 months so that banding can be reinstituted as needed. Repeated endoscopic treatment eradicates esophageal varices in most patients, and provided that follow up is adequate serious recurrent variceal bleeding is uncommon. Because the underlying portal hypertension persists, patients remain at risk of developing recurrent varices and therefore require lifelong regular surveillance endoscopy.

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 1 of 25.

Sequences of images and videos of a case on hemorrhage due status post rubber band ligation of esophageal varices.

A 77 year-old female, one month previously she started with her first hematemesis, was hospitalized in a National Hospital called “ Hospital Rosales”. She was stabilized with intavenous liquid and blood transfusion. The hemorrhage was stopped with the Minnesota balloon. After that, 4 rubber bands were placed in the middle third of the esophagus.

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 2 of 25.

Status post rubber band ligation of esophageal varices.

Some ulcers are observed, one of them with vessel and blood clots. “Stigmata of Bleeding”.

Ligation therapy has been used for years as treatment of hemorrhoids, and the technique was modified for the treatment of esophageal varices.


Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 3 of 25.

Sclerotherapy Versus Banding for Variceal Bleeding. Endoscopic sclerotherapy also reduces the rate of rebleeding, although overall mortality is not affected.

The main disadvantage of endoscopic sclerotherapy is the variable incidence of local and systemic complications, with serious complications occurring in 10-20% of patients, leading to a 2-5% procedure-related mortality. Multiple studies have demonstrated that variceal ligation has a remarkably low complication rate.

A number of studies have been completed to compare the efficacy and safety of endoscopic sclerotherapy versus endoscopic variceal ligation. These studies demonstrate that ligation is equally as effective as sclerotherapy in achieving control of acute variceal bleeding. On the basis of the results of a number of trials comparing sclerotherapy with band ligation, endoscopic variceal ligation has evolved to be the preferred first line modality for the endoscopic treatment of esophageal variceal bleeding.



Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 4 of 25.

Retroflexed view in the esophagus some ulcers are observed to the left side.

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 5 of 25.

Status post Minnesota tube insertion. Necrosis and ulceration are appreciated. Retroflexed view of the cardias. 

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 6 of 25.

Frontal view of the cardias.

There are some ulceration at this level due to a Minnesota tube.

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 7 of 25.

Endoscopy of Variceal Sclerotherapy.
Polydocanol 0.75% was used.

Sclerotherapy injection of the bleeding area of the status post rubber band ligation.


Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 8 of 25.

Endoscopy Image of Variceal Sclerotherapy

Successfully injected, bleeding did not recur.
This sclerotherapy proved to be a life-saving procedure. The patient was discharged from the hospital on the next day.

Variceal Sclerotherapy

Video Endoscopic Sequence  9 of 25.

Endoscopy Appearance of Variceal Sclerotherapy.

12 days after the first sclerotherapy, we performed a second elective session of variceal injection.
The sequences of images and video clips display this procedure. We planned to inject four further varices on this day, Note the scar tissue on the right side of the image above due to status post variceal ligation.



Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence  10 of 25.

1.5 ml of Polydocanol at 1.5% was injected with a 4.15 minute time delay before the injector was retracted.

Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence  11 of 25.

The image and video display the retraction caused by the injector as well as a slight hemorrhage which originates in the variceal wall.

Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 12 of 25.

This image and the video show the third sclerotherapy applied on a large vein which presented with various red signs.

Variceal appearance on endoscopy ("red signs") Red wale marks (longitudinal red streaks on varices) Cherry-red spots (red, discrete, flat spots on varices) Hematocystic spots (red, discrete, raised spots) Diffuse erythema.  

Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 13 of 25.

Maintaining a certain force on the injector during 4 minutes Polydocanol was injected.



Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 14 of 25.

Endoscopy of Variceal Sclerotherapy.

The injector is retracted and a small ulcer is observed as a result of the injection.






Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 15 of 25.

The fourth sclerotherapy is displayed in this image as well as the video clip.

Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence  16 of 25.

Some bleeding is observed as a consequence of the sclerotherapy.

The bleeding, which originated in the variceal wall, stopped spontaneously


Endoscopy Image of Variceal Sclerotherapy

Video Endoscopic Sequence 17 of 25.

In sequence to the images presented above, you can see and blood clots, consequence of the last injection.

The endoscopist needs to develop a certain degree of self-confidence
.

hypertensive portal gastropathy

Video Endoscopic Sequence  18 of 25.

This post-procedure control image shows no active bleeding. After a period of observation the procedure was considered complete.
The patient was discharged from the hospital the next day. The image above displays some degree of hypertensive portal gastropathy.


the cirrhosis

Video Endoscopic Sequence 19 of 25.

Two years later the patient re-bleeds, She had not taken a suitable medical control, the cirrhosis has progressed, now with ascitis. The hemoglobin was 6.0 gr/dl.


bleeding from esophageal varix.

Video Endoscopic Sequence 20 of 25.

The image and the video display bleeding from esophageal varix.

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 21 of 25. 

Many varices are displayed with “the red sign”

Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 22 of 25.

The exactly site of bleeding was located at the anterior wall of the esophagus near two cm. of the gastroesophageal junction.


Sclerotherapy for Variceal Bleeding

Video Endoscopic Sequence 23 of 25.

Another image and the video clip of the site of bleed.

banding the varix

Video Endoscopic Sequence 24 of 25.

We beging with the procedure to banding the varix.

varix were ligated

Video Endoscopic Sequence  25 of 25.

The bleeding has been stopped, tree varix were ligated. Patient was discharged from the hospital with an appointment to eradicate the varices with the same method.



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