Upper GI Bleeding: Upper GI Bleeding: Varices and Hidden Sources

0:00Welcome to Board Pearls. This is episode two of two of the Upper GI Bleeding chapter, in the Stomach and Small Bowel Disorders module. This episode covers variceal bleeding, then the bleeding sources the standard approach misses unless someone suspects them. A man with cirrhosis vomiting blood shows why varices bleed, what starts before the endoscope, why transfusion is restricted and clotting tests aren't corrected, and who needs a transjugular intrahepatic portosystemic shunt, TIPS, within seventy-two hours. A man whose two endoscopies were normal has a Dieulafoy lesion. A man with an aortic graft shows why a small first bleed is a warning. A woman with scleroderma has watermelon stomach and shows why it isn't portal hypertension, and why a hiatal hernia needs a second look. A man with aortic stenosis shows small bowel angiodysplasia. And a man with lifelong nosebleeds shows hereditary hemorrhagic telangiectasia.

0:56Here's the first patient. A fifty-four-year-old man with alcohol-associated cirrhosis vomits a large amount of bright red blood at home. In the emergency department his blood pressure is ninety-two over fifty-four, and his pulse one hundred eighteen. He's confused and drowsy, with asterixis. He has ascites. His bilirubin is four point one, albumin two point six, international normalized ratio, INR, one point nine, and platelets sixty-eight thousand. His hemoglobin is seven point two. He's Child-Pugh class C, with eleven points.

1:33Upper GI bleeding in a patient with cirrhosis is variceal until proven otherwise, and his care is built on that assumption from the first minute. Why varices bleed explains every part of the treatment. Portal hypertension raises wall tension in thin-walled submucosal collaterals at the gastroesophageal junction, in the gastric fundus, in the rectum, and at sites of prior surgery. Varices form when the hepatic venous pressure gradient exceeds ten millimeters of mercury, and they bleed when it exceeds twelve.

2:03The most dangerous collaterals are in the esophagus. They lie in the last five centimeters, where submucosal veins normally drain through the left gastric vein into the portal system. In portal hypertension that flow reverses, the veins balloon, and rising wall tension eventually ruptures them. The risk is highest with large varices, red wale marks, and severe liver disease, Child C most of all, and he has severe disease.

2:27So everything in his treatment lowers portal pressure, keeps it from rising, or closes the ruptured vein. It's a bundle, each part with its own survival benefit: a vasoactive drug, antibiotics, band ligation, and an early TIPS in high-risk patients, most of it started before the endoscope.

2:46The bundle starts with his airway, because he could aspirate before anything else is done. He's confused, with active hematemesis, so his aspiration risk is high. A patient with grade three or four encephalopathy and active bleeding is intubated electively before endoscopy, and so is he.

3:05His transfusion is restrictive, to a hemoglobin of about seven, because extra blood worsens variceal bleeding. Liberal transfusion expands blood volume, raises portal pressure, and makes varices rebleed, and the survival benefit of the restrictive threshold was largest in exactly these patients.

3:24His clotting tests aren't corrected just because they're abnormal, so he gets no routine plasma, platelets, or cryoprecipitate. Clotting in cirrhosis is rebalanced rather than truly hypocoagulable, and overcorrection raises portal pressure. During active bleeding, reasonable targets are a hematocrit over about twenty-five percent, platelets over fifty thousand, and fibrinogen over one hundred twenty. His platelets are sixty-eight thousand, so he gets red cells only.

3:50The vasoactive drug is started immediately, before endoscopy confirms varices. In the United States that's octreotide, a fifty-microgram intravenous bolus, then fifty micrograms per hour for two to five days, usually five. It constricts the splanchnic arteries through somatostatin receptors, lowering portal inflow and variceal pressure. It's started on suspicion because it reduces active bleeding and doesn't harm a patient whose bleeding turns out not to be variceal. Terlipressin is preferred in Europe, but in the United States it's approved only for hepatorenal syndrome.

4:26Antibiotics are given at the same time, because infection drives decompensation after a bleed. They go to every patient with cirrhosis and gastrointestinal, GI, bleeding, with or without ascites, whatever the Child class, and whether or not infection is evident. A meta-analysis of randomized trials showed prophylaxis raises the share of patients free of infection and improves short-term survival by about nine percentage points.

4:52His antibiotic is chosen around resistance. It's ceftriaxone, one gram intravenously daily for up to seven days, rather than a fluoroquinolone, because fluoroquinolone resistance is common in these patients. Ceftriaxone covers the gram-negative rods that translocate from the gut, such as E. coli and Klebsiella.

5:12Endoscopy, done within twelve hours, confirms the source and treats it. Band ligation is the treatment. The bleeding varix, or the one with a red wale or fibrin clot, is suctioned into a cap on the scope, and a rubber band is released around it, so the strangled column clots and sloughs over one to two weeks. Banding stops the bleeding in eighty to ninety percent and is preferred over sclerotherapy, with less rebleeding and fewer ulcers and strictures.

5:38Banding is a course, not a single session. Several bands go on at the first session, and more sessions follow every one to four weeks until the varices are obliterated. About thirty percent rebleed within seventy-two hours, which is why octreotide continues for five days and antibiotics for seven. His endoscopy shows large esophageal varices, one with a spurting point. Four bands are placed, and the bleeding stops.

6:03With the bleeding stopped, the decision that changes his survival is whether he needs an early TIPS. A TIPS is a covered stent placed through the liver between a hepatic vein and the portal vein, which drops portal pressure directly. In patients at high risk of rebleeding, placing it within seventy-two hours of admission, even after banding has controlled the bleeding, sharply reduces rebleeding and improves one-year survival. The indications are Child-Pugh class C with ten to thirteen points, or Child-Pugh class B with active bleeding seen at endoscopy. Covered stents have less thrombosis and stay open longer than bare metal ones.

6:39He's Child C with eleven points, so he meets the criteria even though his bleeding has stopped, and he gets a covered TIPS on day two. Early TIPS is for high-risk patients whose bleeding is controlled, not only for those who keep bleeding. Salvage TIPS is used for bleeding endoscopy can't control, regardless of those criteria. The contraindications are severe right heart failure, severe pulmonary hypertension, polycystic liver disease that obscures the portal anatomy, biliary obstruction, and uncontrolled infection.

7:09A patient whose bleeding nothing stops, before a TIPS is available, needs a bridge. Balloon tamponade uses a Sengstaken-Blakemore tube, with gastric and esophageal balloons and aspiration ports, or the Minnesota tube, a four-lumen version with separate esophageal aspiration. The gastric balloon, inflated with two hundred fifty to four hundred milliliters of air, presses on the junction. The esophageal balloon is inflated to thirty to forty-five millimeters of mercury if esophageal bleeding continues. The Linton-Nachlas tube has a single large gastric balloon for gastric varices.

7:44Tamponade has strict limits, and a stent has partly replaced it. The patient must be intubated, and the balloon stays no more than twenty-four hours, because longer causes pressure necrosis and perforation. A self-expanding covered esophageal stent can stay up to seven days without the same pressure injury and has replaced tamponade in some centers. Both are bridges to a TIPS, repeat banding, or a surgical shunt, not treatments on their own.

8:10Had his varices been in the stomach, the treatment would differ, because gastric varices are harder to band. Gastroesophageal varices type one extend from the esophagus along the lesser curvature and are banded like esophageal varices. Type two extend into the fundus. Isolated gastric varices type one sit in the fundus with no esophageal varices, and type two sit elsewhere in the stomach.

8:34Fundal varices get a different treatment and a different question. They're treated with cyanoacrylate glue injection, used off label in the United States, or ultrasound-guided coil and glue, with a low threshold for TIPS. Isolated fundal varices should always prompt a search for splenic vein thrombosis, often from pancreatic disease. That's left-sided portal hypertension, and splenectomy cures it, because the problem is the splenic vein, not the liver.

9:01Preventing his next bleed is the last part of his plan. A patient without a TIPS gets secondary prophylaxis: a non-selective beta-blocker, propranolol, nadolol, or carvedilol, plus repeated banding until the varices are eradicated, with endoscopy every one to three months and then surveillance every six to twelve. Carvedilol is increasingly favored because it lowers the hepatic venous pressure gradient more and may improve transplant-free survival in compensated cirrhosis.

9:29Two cautions shape that prophylaxis. Refractory ascites and spontaneous bacterial peritonitis aren't absolute contraindications to a beta-blocker, though the dose is titrated to blood pressure and sodium. And for his alcohol-associated disease, abstinence is the treatment at every stage.

9:48The second patient's bleeding has hidden from two endoscopies. A seventy-one-year-old man has had three episodes of sudden, large hematemesis over two weeks, each requiring transfusion. He takes no nonsteroidal anti-inflammatory drugs, NSAIDs, or anticoagulants, and his H. pylori test was negative. Two endoscopies, each done a day after a bleed had stopped, showed old blood in the stomach and nothing else. Tonight he's vomiting bright red blood again. His blood pressure is ninety-eight over sixty, and his pulse one hundred ten.

10:24Two normal endoscopies after heavy bleeding are themselves the clue. Recurrent heavy bleeding with no lesion to account for it suggests a source that's invisible between bleeds, and the leading candidate is a Dieulafoy lesion. It's an abnormally large submucosal artery, one to three millimeters across, that doesn't taper as it approaches the mucosa. Its pulsation erodes a tiny hole in the mucosa above it, and then it bleeds massively, with no ulcer around it.

10:51Its location and behavior explain the missed scopes. The classic location is the upper stomach, within about six centimeters of the gastroesophageal junction along the lesser curvature, but it can occur anywhere in the gut, including the duodenum, small bowel, and colon. Between bleeds, the tiny defect is almost invisible and the surrounding mucosa is normal, which is why his scopes, done after the bleeding stopped, looked normal.

11:17Confirming it means setting up the next endoscopy so it succeeds. He's resuscitated with large-bore lines, crystalloid, and transfusion, which he needs sooner than the restrictive threshold because he's unstable and actively bleeding, and he gets an intravenous proton pump inhibitor, PPI. Intravenous erythromycin, two hundred fifty milligrams thirty to ninety minutes before the scope, clears blood and clot from the stomach, which matters in heavy bleeding.

11:45The timing and target of his scope are chosen for this lesion. Because it's hardest to see between bleeds, he's scoped once resuscitated, while he's still bleeding, with a careful look at the upper stomach near the junction along the lesser curvature. If the view stays obscured, hemostatic powder can buy time as a bridge. If the upper stomach is clean, Dieulafoy lesions also occur further down, out of reach of a standard upper endoscopy. This time, the endoscopist sees a pulsatile jet of blood from a pinpoint spot high on the lesser curvature, with normal mucosa all around it.

12:18He has a Dieulafoy lesion, and it has to be treated so it stays treated. Rebleeding is high when the lesion is missed or undertreated, so durable mechanical or thermal therapy is preferred over epinephrine alone. Treatment is dual therapy, hemoclips plus injection or thermal coagulation, with high success when the lesion is found. If standard clips fail, an over-the-scope clip is the rescue, and in a randomized trial in ulcer and Dieulafoy bleeding, it lowered rebleeding and transfusion needs.

12:48One more step makes the lesion findable again. The endoscopist tattoos the spot with India ink, so it can be found at a second-look procedure or at surgery if needed. He gets epinephrine injection, three hemoclips, a tattoo, and seventy-two hours of high-dose intravenous PPI. He doesn't rebleed and goes home four days later.

13:08The third patient has the warning that's easiest to dismiss. A sixty-nine-year-old man had an open repair of an abdominal aortic aneurysm with a synthetic graft five years ago. This morning he vomited a cup of blood, and then it stopped. He's stable, with a hemoglobin of eleven. He's had low-grade fevers for two weeks.

13:29Any GI bleed after an aortic graft is an aortoenteric fistula until proven otherwise. The graft becomes infected, and the infection erodes it into the adjacent bowel. The third part of the duodenum lies directly in front of the aorta, so up to seventy-five percent of fistulas connect there, and the rest connect to the jejunum, stomach, or colon. A primary fistula without prior surgery is rare, usually from an infected aneurysm or trauma.

13:55His small bleed and his fevers are both part of the picture. His small, self-limited bleed is a herald bleed, which precedes an exsanguinating hemorrhage by hours to weeks and is the warning. His fevers point to graft infection. Patients may also have bacteremia with several gut organisms at once, and abdominal, back, or groin pain.

14:16His workup has a specific order. An endoscopy, if done, must be an extended exam reaching the third part of the duodenum. Endoscopy often misses the fistula because it hides behind clot, so in a stable graft patient, computed tomography, CT, angiography is the next step. It can show gas around the graft, a pseudoaneurysm, loss of the fat plane between graft and bowel, or contrast leaking into the bowel. When suspicion is high, surgical exploration goes ahead regardless of imaging.

14:46His CT angiogram shows gas around the graft and loss of the fat plane next to the third part of the duodenum, and he goes for emergency repair. Mortality from aortoenteric fistula exceeds fifty percent, and emergency surgical or endovascular repair is the only definitive treatment.

15:03The fourth patient's bleeding is slow, and it comes from the stomach's own vessels. A sixty-eight-year-old woman with systemic sclerosis and Raynaud phenomenon has needed transfusions every few months for a year for iron deficiency anemia. Her stools are guaiac positive but never black. She has no liver disease. She has a moderate hiatal hernia. Endoscopy shows red stripes running lengthwise along the antrum, converging on the pylorus like the stripes of a watermelon. The body and fundus look normal.

15:33She has gastric antral vascular ectasia, GAVE, the watermelon stomach. It's a collection of dilated small veins in the antral mucosa, and on biopsy those vessels contain small clots, with thickened fibromuscular tissue and spindle cells. It causes chronic slow bleeding, sometimes overt, and iron deficiency. The typical patient is an older woman with scleroderma, autoimmune hepatitis, or Raynaud phenomenon and transfusion-dependent iron deficiency. A punctate or diffuse form, without stripes, occurs more often in men with cirrhosis.

16:09Before treating it, GAVE must be separated from portal hypertensive gastropathy, because the two are treated in opposite ways. GAVE is in the antrum, while portal hypertensive gastropathy is in the body and fundus. GAVE shows red stripes or spots without a mosaic, while portal hypertensive gastropathy shows a mosaic, snakeskin pattern. GAVE biopsies show clots and spindle cells, while portal hypertensive gastropathy shows only mildly dilated vessels.

16:37The cause decides the treatment. Portal hypertensive gastropathy is caused by portal pressure and responds to a non-selective beta-blocker or a TIPS. GAVE is a disease of the mucosal vessels themselves, so beta-blockers and TIPS don't help it, even when the patient also has cirrhosis. A biopsy settles an unclear pattern.

16:58Her GAVE is treated endoscopically. The options are argon plasma coagulation in repeated sessions, radiofrequency ablation, cryotherapy, or band ligation, which is increasingly favored because randomized data show it needs fewer sessions than argon plasma coagulation. Antrectomy is the historical rescue for disease that won't respond, and beta-blockers have no role. Iron, oral or intravenous, rebuilds her stores while the lesions are treated.

17:25Her hiatal hernia means one more lesion to look for while the scope is in. Cameron lesions are linear erosions on the crests of the gastric folds where they pass through the diaphragm. They come from the diaphragm rubbing the herniated stomach as it slides with breathing, and from intermittent ischemia of the trapped mucosa. They sit at the fold crests at the level of the hiatus and are best seen in retroflexion, so a quick look can call the exam normal.

17:52Cameron lesions are treated mostly mechanically. Treatment is iron and a PPI, though the PPI's benefit is uncertain because the cause is mechanical, and surgical hernia repair is the only definitive treatment when bleeding continues. Her endoscopist looks in retroflexion and sees no Cameron lesions. She has band ligation of the antral lesions in two sessions with intravenous iron, her transfusion needs stop, and her hemoglobin stays stable.

18:20The fifth patient's slow bleeding is out of reach of the upper scope. A seventy-nine-year-old man with severe aortic stenosis has recurrent iron deficiency and occasional melena. Endoscopy and colonoscopy are normal. A capsule endoscopy shows several flat, bright red, fern-like lesions in the jejunum. They're angiodysplasias, the most common cause of small bowel bleeding in older people.

18:45His heart valve is part of the cause. As blood forces through the narrowed valve, shear stress breaks apart the largest multimers of von Willebrand factor, producing an acquired von Willebrand deficiency in which angiodysplasias bleed. That's Heyde syndrome, and aortic valve replacement corrects it. A left ventricular assist device does the same, and fifteen to twenty percent of patients with one develop GI bleeding, often from acquired von Willebrand deficiency and angiodysplasia. Angiodysplasia is also associated with end-stage kidney disease.

19:17His lesions are treated by reach. Reachable lesions are treated with argon plasma coagulation. For diffuse or unreachable lesions, thalidomide, fifty to one hundred milligrams daily, reduces bleeding episodes by blocking vascular endothelial growth factor, VEGF. Long-acting octreotide, forty milligrams intramuscularly monthly, reduces transfusion needs through splanchnic vasoconstriction. Bevacizumab, an anti-VEGF antibody, is used for refractory cases. For him, aortic valve replacement, which his valve needs anyway, should end the bleeding.

19:51The last patient's clue is in his history. A forty-five-year-old man has had nosebleeds since childhood and now has iron deficiency. He has small red spots on his lips, tongue, and fingertips, and his mother had the same nosebleeds. That's hereditary hemorrhagic telangiectasia, an autosomal dominant disorder of vessel development.

20:11Its diagnosis uses four criteria. They're spontaneous recurrent nosebleeds; multiple mucocutaneous telangiectasias at characteristic sites, such as the lips and mouth; visceral involvement, such as GI telangiectasias or arteriovenous malformations in the lungs, brain, or liver; and a first-degree relative with the disease. Three or more is definite, two is suspected, and fewer than two makes it unlikely. He has all four.

20:39Its genetics change his surveillance. Mutations in endoglin cause type one, and mutations in ALK1, also called ACVRL1, cause type two, both in the transforming growth factor beta pathway of the vessel lining. Mutations in SMAD4 cause an overlap with juvenile polyposis, so those patients need colon polyp surveillance as well as screening for vascular malformations.

21:04His bleeding is treated in steps. His GI bleeding comes from telangiectasias throughout the gut, though nosebleeds are usually the biggest source of iron loss. Treatment is iron, argon plasma coagulation of reachable GI lesions, octreotide for refractory bleeding, and bevacizumab for refractory disease, with high response rates in randomized data. Liver transplantation is rarely needed, for heart failure from large liver malformations.

21:30His lungs and his family need attention too. He needs screening for lung arteriovenous malformations with contrast echocardiography or chest CT, and embolization when they cause symptoms, because they let clots and bacteria bypass the lungs and cause strokes and brain abscesses. His first-degree relatives should be offered evaluation and genetic testing.

21:50Each of these last lesions escapes the standard approach of resuscitate, give a PPI, scope, and treat what's found. A Dieulafoy lesion looks normal between bleeds. An aortoenteric fistula announces itself only with a herald bleed. GAVE doesn't respond to lowering portal pressure. Cameron lesions hide at the hiatus. Small bowel angiodysplasia is out of reach of both scopes. And hereditary hemorrhagic telangiectasia needs the family history.

22:19Here are the traps the boards set in these patients. Octreotide doesn't wait for endoscopy. Antibiotics aren't skipped in a patient with cirrhosis without ascites, and the choice is ceftriaxone, not a fluoroquinolone. Transfusion doesn't aim for nine or ten, and plasma isn't given to correct the INR. An encephalopathic, vomiting patient is intubated before the scope. Early TIPS isn't skipped in a Child C or actively bleeding Child B patient because the bleeding stopped. A balloon doesn't stay in more than a day. Fundal varices aren't banded, and splenic vein thrombosis isn't missed behind isolated fundal varices.

22:57The hidden source traps follow. A normal endoscopy after recurrent heavy bleeding isn't accepted, and the next scope is done during active bleeding. A Dieulafoy lesion isn't treated with epinephrine alone, and it's tattooed. A graft patient isn't discharged after a small bleed that stopped, the endoscopy doesn't end at the second part of the duodenum, and surgery doesn't wait for imaging certainty when suspicion is high.

23:21The slow bleeding traps close the list. GAVE isn't treated with beta-blockers or a TIPS, and it isn't confused with portal hypertensive gastropathy. Cameron lesions are missed without retroflexion at the hiatus. Aortic stenosis or an assist device isn't missed behind angiodysplasia. And hereditary hemorrhagic telangiectasia needs lung malformation screening and, with SMAD4, polyp surveillance.

23:47So, start to finish. Variceal bleeding is a bundle started before the scope. Intubate the encephalopathic patient, transfuse restrictively to about seven, don't routinely correct laboratory coagulopathy, start octreotide immediately, and give ceftriaxone to every bleeding patient with cirrhosis. Band within twelve hours.

24:08Give an early covered TIPS within seventy-two hours to Child C patients with ten to thirteen points or actively bleeding Child B patients, and a salvage TIPS when endoscopy fails, with tamponade or a stent as a short bridge. Fundal varices get glue or coils, and isolated fundal varices mean looking for splenic vein thrombosis.

24:30A Dieulafoy lesion is a large submucosal artery under a tiny defect, usually high on the lesser curvature. Give erythromycin, scope during active bleeding, treat with clips plus injection or thermal therapy, and tattoo it. Any GI bleed after an aortic graft is an aortoenteric fistula until proven otherwise, so do an extended endoscopy, CT angiography in the stable patient, and surgery when suspicion is high.

24:54GAVE is antral stripes treated endoscopically, not with beta-blockers or TIPS. Cameron lesions need retroflexion at the hiatus. Angiodysplasia is the main small bowel source, linked to aortic stenosis, assist devices, and kidney failure. Hereditary hemorrhagic telangiectasia is nosebleeds, telangiectasias, visceral malformations, and family history, with lung malformation screening and family evaluation.

25:22The next chapter is celiac disease, from its biology and diagnosis through the gluten-free diet, refractory disease, and its complications.

25:32For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode two of two of chapter nine, and I'll see you in the next one.