This 65 year-old, diabetic lady, 3 days previously has been hospitalized in another institution because of her first upper GI bleeding manifesting with hematemesis and melena an upper endoscopy displays esophageal varices; patient was discharged from the hospital without specific therapeutical treatment. She was referred to us to evaluate this condition The patient was continued with intermittent episodes of melena. A procedure of banding was planning, at endoscopy a varix with an ulcer in the tip was found (the white nipple sign). The site of bleeding was identified.
White ball appearance was a characteristic finding that appeared after ligation of a varix at the site of bleeding. This finding may be useful in the confirmation of successful ligation of a varix at its bleeding site. (Gastrointest Endosc 1998;47:254-6.).
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.
Video Endoscopic Sequence 2 of 15.
Two angiectasias were found at the gastric body.
Video Endoscopic Sequence 3 of 15.
Endoscopic Image of bleeding of Esophageal Varix
At the at the time of being exploring the stomach, the patient present a cough reflex, causing rebleeding of the varix.
The white nipple sign correlated positively with severity of bleeding (patients required more blood transfusion), hematemesis, and signs of shock. Patients with the white nipple sign also tended to undergo emergency endoscopy and have active bleeding at the time of endoscopy. There was no correlation between rebleeding rate after endoscopic therapy and presence of the white nipple sign.
Video Endoscopic Sequence 4 of 15.
Endoscopic View of Spurting Esophageal Varix
Mortality due to variceal bleeding secondary to portal hypertension has decreased significantly in the past 2 decades. Endoscopic therapy has been the mainstay of treatment for acute variceal bleeding. Variceal banding ligation has superceded injection sclerotherapy as the most popular treatment modality for acute bleeding. Multiple banding ligators are widely used with high success in restoring hemostasis. The combination of banding and sclerotherapy may be useful in preventing the early recurrence of varices and rebleeding after initial obliteration of varices. Selective vasoactive agents such as somatostatin analogs also improve the outcome of patients.
Video Endoscopic Sequence 5 of 15.
Immediately; a therapeutically approach was carry out with banding to the bleeding varix.
Video Endoscopic Sequence 6 of 15.
Two rubber bands were applied to the bleeding varix.
Endoscopic variceal ligation (EVL) was developed in an effort to find an effective means of treating esophageal varices endoscopically with fewer complications than sclerotherapy.
The concept was based upon many years of experience treating hemorrhoids with rubber band ligation in patients with and without portal hypertension.
Video Endoscopic Sequence 7 of 15.
More varices were ligated.
The first patient was treated with EVL in 1986. Since then, advances in the technique have led to its routine use in the care of patients with esophageal varices. One of the biggest advances was the development of the multiple band ligator, which has simplified and improved the safety of EVL.
Video Endoscopic Sequence 8 of 15.
EVL works by capturing all or part of a varix resulting in occlusion from thrombosis. The tissue then necroses and sloughs off in a few days to weeks, leaving a superficial mucosal ulceration, which rapidly heals. EVL avoids the use of sclerosant and thus eliminates the deep damage to the esophageal wall that occurs after ES. Collateral vessels near the cardia decrease after EVL, which may be another reason that EVL is effective for preventing further variceal bleeding.
Video Endoscopic Sequence 9 of 15.
Endoscopic Image of ligation of Esophageal Varices
Another interesting finding is that during acute variceal bleeding the hepatic venous pressure gradient (which correlates with the risk of variceal bleeding) increases after ES, but not after EVL.
Video Endoscopic Sequence 10 of 15.
Patient with Cirrhosis of the liver with Ascites
Two years after, the patient present with severe ascites
The mechanism by which ascites develops in cirrhosis is multifactorial Severe sinusoidal portal hypertension and hepatic insufficiency are the initial factors. They lead to a circulatory dysfunction characterized by arterial vasodilation, arterial hypotension, high cardiac output and hypervolemia and to renal sodium and water retention.
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Video Endoscopic Sequence 11 of 15.
Cirrhosis of the liver with Ascites
There are evidences that arterial vasodilation in cirrhosis occurs in the splanchnic circulation and is related to anincreased synthesis of local vasodilators. Vascular resistance is normal or increased in the remaining major vascular territories (kidney, muscle and skin and brain). Splanchnic arterial vasodilation not only impairs systemic hemodynamics and renal function but also alters hemodynamics in the splanchnic microcirculation.
Video Endoscopic Sequence 12 of 15.
The rapid and high inflow of arterial blood into the splanchnic microcirculation is the main factor increasing hydrostatic pressure in the splanchnic capillaries leading to an excessive production of splanchnic lymph over lymphatic return. Lymph leakage from the liver and other splanchnic organs is the mechanism of fluid accumulation in the abdominal cavity. Continuous renal sodium and water retention perpetuates ascites formation. Large volume paracentesis associated with albumin infusion is the treatment of choice of tense ascites because it is very effective and rapid and is associated with fewer complications that the traditional treatment (sodium restrictionand diuretics).
Video Endoscopic Sequence 13 of 15.
Umbilical Hernia with Ascites
Umbilical hernia is a common finding in cirrhotic patients with ascites. Spontaneous disruption of the hernia and attendant discharge of ascitic fluid is an unusual and rarely reported complication in these patients and is associated with an overall mortality rate of nearly 30%.
Video Endoscopic Sequence 14 of 15.
Pathogenesis of ascites in cirrhosis
Renal function abnormalities
Sodium Retention
The impairment in the renal ability to excrete sodium is the earliest renal dysfunction in cirrhosis. Before the development of ascites, when patients are still compensated (compensated cirrhosis is a term commonly used to define patients prior to the development of any of the major complications of the disease: i.e. ascites, hemorrhage or hepatic encephalopathy), they present subtle abnormalities in renal sodium metabolism. For example they may not escape to the sodium retaining effect of mineralcorticoids or may be unable to excrete a sodium overload. However, as the disease progresses, patients became unable to excrete their regular sodium intake and develop sodium retention.
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Video Endoscopic Sequence 15 of 15.
Cirrhosis of the liver with Ascites
Water Retention
The kidney is continuously generating free water in the ascending limb of the loop of Hente by a mechanism consisting in an active reabsorption of sodium chloride without a concomitant reabsorption of water. The final volume free water excretion, therefore, depends on the amount of free water reabsorbed in the more distal segments of the nephron, the convoluted distal tubule and the collectingtubule. This process is mediated by antidiuretic hormone (ADH). When ADH is completely inhibited, for example following a water load of 20 mL/kg of body weigh, the distal nephron is almost completely impermeable to water, leading to the excretion of a high urine volume (10 mL/min or more) with low urine osmolality.
Video Endoscopic Sequence 1 of 10.
Upper GI bleeding due to Esophageal Varices
This 42 year-old male, was admitted for massive hematemesis resulted in hypotension, history of alcoholic abuse, after promptly resuscitate and restore circulating blood volume of patientan emergency upper gastrointestinal endoscopy was performed on the first hospital day, It was carried out in the operation room with Endotracheal intubation under general anesthesia.
Video Endoscopic Sequence 2 of 10.
Mandates aggressive lavage and thorough endoscopy of the stomach to include a retroflexed view of the cardiac portion of the stomach, fresh blood at the gastric fundus is observed.
Video Endoscopic Sequence 3 of 10.
A yellowish fibrin plug is visible in the 1 o'clock varix indicating the site of recent bleeding.
The exact site of the bleeding has been identify in the Gi Junction, white point of above.
Video Endoscopic Sequence 4 of 10.
More images and video clips of the exact site of the bleeding. Close-up view of the fibrin plug.
Video Endoscopic Sequence 5 of 10.
By retrofletion the gastric cardia is inspected observing the exact site of the bleeding.
One of the most ominous complications of portal hypertension is hemorrhage from esophageal or gastric varices. Patients who bleed from varices have a poor long-term prognosis, irrespective of treatment and few survive more than 5 years. In view of the prognosis of portal hypertensive bleeding, it is clear that poorurgent treatment of acute variceal bleeding and interval management to prevent rebleeding is essential.
Video Endoscopic Sequence 6 of 10.
Endoscopic ligation of esophageal varices requires placement of an opaque cylinder over the end of the endoscope.
The exact site of the hemorrhage is ligated
Variceal bleeding is one of the complications of cirrhosis that leads to significant morbidity and mortality. It is recommended that all patients with cirrhosis be screened for gastroesophageal varices and those with large varices should be offered primary prophylaxis. Nonselective beta-blockers (nadolol or propranolol) are the treatment of choice for primary prophylaxis but there are a number of limitations to their use. A number of studies have evaluated the efficacy of variceal band ligation (VBL) in providing primary prophylaxis, either in comparison to no treatment or to beta-blockers. VBL is very effective in preventing the initial bleed when compared to no treatment, but it is not superior to beta-blockers. In this issue of the journal the effect of beta-blockers on bleeding in patients undergoing VBL is examined and no benefit compared to VBL alone is shown. Thus, patients with large varices should be treated with beta-blockers and VBL should be offered to those cirrhotics who are unable to take beta-blockers. Further study is required to determine if VBL in combination with beta-blockers is more effective than the beta-blockers alone.
Video Endoscopic Sequence 7 of 10.
Two rubber band have been applied at the site of the bleeding.
Video Endoscopic Sequence 8 of 10.
The gastric cardias at the retroflexed, observing the varix with beginnings of necrosis.
Video Endoscopic Sequence 9 of 10.
More bands were applied to several varices.
Video Endoscopic Sequence 10 of 10.
More varices have been ligated.
Video Endoscopic Sequence 1 of 26.
This 68 year old man, has a history of long standing alcohol abuse, had two episodes of gastrointestinal bleeding. Multiple red spot are seen.
One of the most ominous complications of portal hypertension is hemorrhage from esophageal or gastric varices. Patients who bleed from varices have a poor long -term prognosis, irrespective of treatment and few survive more than 5 years.
The intraluminal varices are being compressed by the water-filled balloon, and are hardly visible on the endosonographic image.
Varices are identified as multiple, well-circumscribed, hypoechoic or anechoic structures that have a tubular or serpinginous appearance; they are located in the submucosal layer.
Download the video clip by clicking on the endosonographic image. Medline.
Video Endoscopic Sequence 3 of 26.
Radial Endosonography.
Endoluminal US demonstrated the varices as anechoic areas with communications in the submucosal, periesophageal, and perigastric regions.
Fitted with a suction cap adapter and passed back down to the level of the GE junction. The varix with the red spot at the GE junction is identified, then gently sucked up into the cap and the band deployed around the varix. A second site just proximal to the first is next selected and this is banded. This process is continued until all the bands are deployed.
In view of the prognosis of portal hypertensive bleeding, it is clear that poorurgent treatment of acute variceal bleeding and interval management to prevent rebleeding is essential. Medline
Video Endoscopic Sequence 5 of 26.
The video clip and the image display one varix is banding. The varix is suctioned into the banding apparatus.
The role of endoscopic band ligation in secondary prophylaxis is now indisputable, especially in comparison with sclerotherapy. In the primary prevention of variceal bleeding, band ligation is beginning to have a competitive edge over pharmacological therapy.
The video displays multiple varices that have been banding.
The technique is an adaptation of that applied to banding ligation of internal hemorrhoids.
Video Endoscopic Sequence 8 of 26.
Magnifying view.
A large varix was ligated as is seen with magnifying endoscope.
Video Endoscopic Sequence 9 of 26.
The portal vein carries approximately 1500 mL/min of blood from the small and large bowel, the spleen, and the stomach to the liver. Obstruction of portal venous flow, whatever the etiology, results in a rise in portal venous pressure. The response to increased venous pressure is the development of a collateral circulation diverting the obstructed blood flow to the systemic veins. These portosystemic collaterals form by the opening and dilatation of preexisting vascular channels connecting the portal venous system and the superior and inferior vena cava. High portal pressure is the main cause of the development of portosystemic collaterals; however, other factors such as active angiogenesis also may be involved. The most important portosystemic anastomoses are the gastroesophageal collaterals. Draining into the azygos vein, these collaterals include esophageal varices, which are responsible for the main complication of portal hypertension and massive upper GI hemorrhage.
Video Endoscopic Sequence 10 of 26.
Status post rubber band ligation
One week after the banding a new endoscopy was performed.
There are multiple fresh scars. Banding of esophageal varices is an effective method. Showing minor or no complications, it can be performed as the preferred method for prophylactic or therapeutical management of esophageal varices, especially when bleeding occurs.
Video Endoscopic Sequence 11 of 26.
Shallow ulcers at the site of each ligation are the rule and rarely bleed.
Video Endoscopic Sequence 12 of 26.
Chromoendoscopy using Lugol's solution.
Chromoendoscopy involves the application of vital dyes that enhance the visibility of dysplastic mucosa. Vital dyes that have been studied include those that preferentially stain normal squamous mucosa (such as Lugol's iodine).
Video Endoscopic Sequence 13 of 26.
One ulceration post varix ligation is appreciated (normal status).
Video Endoscopic Sequence 14 of 26.
More images and video clip of post banding status.
Video Endoscopic Sequence 15 of 26.
A follow up Endoscopy after one month.
Status post banding
Multiple scars are seen.
Banding ligation sessions are repeated at 7- to 14-day intervals until obliteration of varices is achieved. Eradication of varices usually requires two to four band ligation sessions.
Video Endoscopic Sequence 16 of 26.
Multiple scars are seen in this image as well as the video clip.
Video Endoscopic Sequence 17 of 26.
A retroflexed view of the esophagus is observed, the multiple scars of the status post banding are seen.
Video Endoscopic Sequence 18 of 26.
Spurting esophageal varix.
Due to the retroflexed maneuver, the tip of the endoscope touched causing this bleeding that was resolved easily with argon plasma coagulator.
Video Endoscopic Sequence 19 of 26.
In the video clip, you can see a bleeding from a small fissure at the gastroesophageal junction.
Video Endoscopic Sequence 20 of 26.
In this image and the video clip, the Probe of the argon plasma coagulator is observed that will initiate the therapeutical approach.
Endoscopic variceal ligation is an established procedure for eradication of esophageal varices. However, varices frequently recur after endoscopic variceal ligation. Argon plasma coagulation has been used as supplemental treatment for eradication of varices and for prevention of variceal recurrence.
Video Endoscopic Sequence 21 of 26.
To overcome this bleeding the argon plasma coagulator was used. Endoscopic ligation of esophageal varices combined with APC is superior to ligation alone. Since APC is theoretically well suited for mucosal fibrosis therapy, it can be used for the complete elimination of esophageal varices and for fibrosis of the distal esophageal mucosa.
Video Endoscopic Sequence 22 of 26.
The bleeding was overcome easily with this therapeutical resource.
Use of argon plasma coagulation (APC) to promote mucosal fibrosis has been described in some clinical setting.
Argon Plasma Coagulator is a new device that allows for non-contact monopolar coagulation of bleeding surfaces, and devitalization of tissue in the gastrointestinal tract. It is safer and much less expensive than lasers, more effective than bipolar cauterization techniques.
Video Endoscopic Sequence 23 of 26.
One month after the previous images.
Six varices were ligated in this session of therapy.
Video Endoscopic Sequence 24 of 26.
Some fundic varices are observed.
Video Endoscopic Sequence 25 of 26.
Some varices are banding above of the multiple scars.
Video Endoscopic Sequence 26 of 26.
There are some ligated varices at the mid esophagus. The evolution of the patient has been satisfactory to date.
Video Endoscopic Sequence 1 of 6.
42 year- old male, 15 days earlier, had been hospitalized for esophageal variceal bleeding was referred to our endoscopic unit for specific treatment placing six bands.
Video Endoscopic Sequence 2 of 6.
Note the chains of varices, retroflexed maneuver into the esophagus.
Video Endoscopic Sequence 3 of 6.
Within the gastroesophageal junction are seen several varices with the red sign.
Video Endoscopic Sequence 4 of 6.
Therapy is initiated with bands
Endoscopic variceal ligation is based on the widely used technique of rubber-band ligation of hemorrhoids. The esophageal mucosa and the submucosa containing varices are ensnared, causing subsequent strangulation, sloughing, and eventual fibrosis, resulting in obliteration of the varices Rebleeding occurs less frequently with endoscopic varicea ligation (26%) than with endoscopic sclerotherapy (45%).
Video Endoscopic Sequence 5 of 6.
In this video clip can observe the placement of some bands.
Endoscopic ligation requires placement of an opaque cylinder over the end of the endoscope. This decreases the endoscopic field of view and may allow pooling of blood. Thus, in patients with active bleeding, visualization may be impaired more with ligation than with sclerotherapy.
Video Endoscopic Sequence 6 of 6.
In total there were six varices that were ligated a new session will be programmed shortly.
Thrombocytopenia, presence of encephalopathy, low hemoglobin on admission, and endoscopic findings large varices, presence of red color sign, fundal varix and portal gastropathy are predictors of esophageal variceal bleeding. This stratification may help clinicians identify cirrhotic patients who will need aggressive pharmacologic and endoscopic intervention for variceal bleeding.
Video Endoscopic Sequence 1 of 15.
Severe bleeding of the upper digestive system after two days of band ligation.
This 57 year-old male with chronic alcoholism and cirrhosis of the liver with esophageal varices, had been previously hospitalized in two occasions due to a severe upper gastrointestinal bleeding. He did not received specific treatment for these varices, so he was referred to a specific therapeutic procedure.
Video Endoscopic Sequence 2 of 15.
In this first session six varices were ligated.
Video Endoscopic Sequence 3 of 15.
Continuing with the process of ligation
Video Endoscopic Sequence 4 of 15.
Image and video clip, immediately after performing therapy with bands.
Apparently this was the varix, which subsequently caused the hemorrhage, despite having been ligated. Bleeding is observed in some of the next video clips.
Video Endoscopic Sequence 5 of 15.
Another image and video clip, in hindsight, this varix was the cause of bleeding after the ligation with bands. Note redness and edema slight bleeding, and the strangulation of the varix was adequate.
Video Endoscopic Sequence 6 of 15.
Two days after the therapeutic treatment with bands, he started with severe bleeding in the upper digestive system which is expressed with hematemesis and melena.
Video Endoscopic Sequence 7 of 15.
This image, and in the video clip shows the varix that causes this severe episode of bleeding. Enough water was used to clear and wash the bleeding.
Video Endoscopic Sequence 8 of 15.
This endoscopy shows suctioning and washing the bleeding
Video Endoscopic Sequence 9 of 15.
To perform hemostasis using argon plasma coagulator which must be worn without making contact.
Video Endoscopic Sequence 10 of 15.
Carefully argon plasma was used to perform hemostasis
Video Endoscopic Sequence 11 of 15.
It continues to monitor the variceal bleeding caused after two days, after having placed the banding. At this time it was necessary to decide the next step which would place another band on this, sclerotherapy, or leave it alone. I think that with this observation it would have been better to place another band, however we use the argon plasma.
Note: in another clinical case a patient, after having multiple sessions with rubber bands ligations by fibrosis caused by cicatrization (which is normal in the healing of the ligated varices), the patient begins with several episodes of bleeding. The exact site was located in the middle of fibrosis, which was only a blood clot in the middle of the one third of the esophagus. We proceeded to evaluate the hemostatic procedures and decided to place two bands. We were not really sure if the bands could play a role, and that hemostatic because the fibrosis could slip the bands one-by-one, and effectively reintroduce the endoscope with the air of the bands that were slipped. Caused severe bleeding which was successfully managed using a dual-channel endoscope and argon plasma coagulation. In this former case because the fibrosis we would recomended to use sclerotherapy.
I'm locating the video clip to process and place in this atlas.
Video Endoscopic Sequence 12 of 15.
There are multiple varices without being ligated, coagulation process is continuous with argon wich coagulates the surface of the varix.
Video Endoscopic Sequence 13 of 15.
This video clip shows that the argon plasma is used too close sticking the tissue and removing it. Causing a severe bleeding. A bleeding hole is observed.
At this moment, we were analyzing if it had used hemoclips or injected histoacryl.
Video Endoscopic Sequence 14 of 15.
It follows using argon plasma coagulation
Video Endoscopic Sequence 15 of 15.
To stop the bleeding after argon plasma is used sclerotherapy is carry out
