Upper GI Bleeding: Variceal and Unusual

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 is acute variceal hemorrhage and the unusual non-variceal causes: the variceal bundle with early TIPS for high-risk patients, and the recognition cues for the lesions a routine scope misses.

0:21Variceal hemorrhage is portal hypertension finding the lowest-resistance escape route through the collateral veins and rupturing through it, and the work in the first hour doesn't start with endoscopy. It starts with three things delivered together, each of which independently improves mortality, and together they're the bundle to name reflexively: a splanchnic vasoconstrictor to lower portal pressure, an antibiotic to prevent the gut-translocation infection that drives decompensation and rebleeding, and band ligation to physically stop the bleed. Each is started before the diagnosis is even confirmed endoscopically.

0:54The vasoactive drug in the US is octreotide, a somatostatin analogue given as a bolus then an infusion for five days, and the mechanism is why it's safe to give empirically: it shuts down the splanchnic vasodilators, so arterial inflow to the gut falls, portal inflow falls behind it, portal pressure drops, and the clot at the rupture stabilizes. So you start it the moment variceal bleeding is suspected, because it's harmless if the source turns out to be non-variceal and time-critical if it's a varix, and "wait for endoscopy to confirm the source" loses points. The antibiotic is ceftriaxone daily for a week, indicated for any cirrhotic with GI bleeding whether or not varices are confirmed and whether or not there's ascites, because preventing infection improves survival and reduces rebleeding, since infection itself drives further decompensation and portal pressure rise; ceftriaxone is favored over a fluoroquinolone because cirrhotic populations carry high quinolone resistance. And band ligation, within twelve hours, sucks the varix into a cap and drops a rubber band on its base so the tissue thromboses and sloughs, done over multiple sessions until the varices are obliterated; it replaced sclerotherapy because rebleeding and complications are lower. The early rebleed risk stays high in the first few days, which is exactly why the octreotide runs five days and the ceftriaxone seven even after a successful endoscopic stop.

2:17Two resuscitation modifiers in cirrhosis. First, restrictive transfusion to a hemoglobin of seven, with the cirrhotic getting the largest benefit, because liberal transfusion expands portal volume, raises portal pressure, and worsens variceal rebleeding, so "transfuse to nine in a stable cirrhotic" is reading the number backwards. And coagulopathy correction is selective, not routine, because the cirrhotic clotting system is rebalanced rather than truly deficient and overcorrecting raises portal pressure, so you transfuse toward active-bleeding thresholds rather than to normalize a lab: a hematocrit above twenty-five, platelets above fifty thousand, fibrinogen above one hundred twenty. Second, airway protection: a patient with advanced encephalopathy and active hematemesis is one breath from aspirating, and elective intubation before endoscopy is the favored answer, because the airway is the leading preventable cause of death and the cirrhotic concentrates that risk.

3:19Balloon tamponade is the bridge when endoscopy can't control the bleed and definitive therapy isn't immediately available: a tube with a gastric and esophageal balloon, or the single large gastric balloon favored for gastric varices, with the gastric balloon inflated to tamponade the junction, a maximum dwell of about a day because longer causes pressure necrosis and perforation, and the patient must be intubated. A covered esophageal stent is an alternative with a longer dwell that's replaced tamponade in some centers. Both are bridges, not endpoints.

3:46The definitive therapy in the high-risk patient is early TIPS, and this is examined in detail. In a cirrhotic with variceal bleeding who's been initially controlled with the bundle, pre-emptive TIPS within seventy-two hours of admission substantially reduces rebleeding and mortality compared with continued medical therapy, and the entry criteria are the point: Child-Pugh class C, or Child-Pugh class B with active bleeding seen at the index endoscopy. The shunt is a covered stent, because covered shunts stay patent longer. So pick early TIPS for Child C variceal bleeding or Child B with active bleeding on the index scope, and know the seventy-two-hour window; salvage TIPS for refractory bleeding after failed endoscopy is separately indicated. Contraindications are severe right heart failure, severe pulmonary hypertension, polycystic liver disease, biliary obstruction, and uncontrolled infection.

4:40Gastric varices behave differently from esophageal ones, and the Sarin classification organizes them: the ones extending along the lesser curve or into the fundus that are contiguous with esophageal varices, versus the isolated gastric varices in the fundus or elsewhere without esophageal involvement. The management split is clean: the lesser-curve type contiguous with esophageal varices is banded like esophageal varices, while the fundal varices are treated with cyanoacrylate glue injection or ultrasound-guided coil-and-glue, with a low threshold for TIPS as salvage. And the key recognition cue inside this is the isolated fundal varix without esophageal involvement, which should always prompt evaluation for splenic vein thrombosis, because pancreatic disease can cause a left-sided portal hypertension that splenectomy cures, and missing it means treating the wrong disease entirely. Secondary prevention after a controlled bleed is a non-selective beta-blocker, increasingly carvedilol because it lowers the portal gradient more, plus serial banding to obliteration and then surveillance, with the full portal hypertension framework in chapter twenty-three.

5:44So the variceal section: octreotide, ceftriaxone, and band ligation are the bundle; restrictive transfusion to seven is the rule; early TIPS within seventy-two hours is the high-risk intervention defined by Child C or Child B with active index bleeding; the Sarin classification routes the gastric varices; and isolated fundal varices always trigger a splenic vein thrombosis workup.

6:09Now the unusual non-variceal causes, and the unifying feature is that each one is missed by the standard scope-plus-acid-suppression approach unless its recognition cue is in your mind from the start. The lesion isn't hard to manage once named; the trick is naming it.

6:26Dieulafoy is an abnormally large submucosal artery that pokes through a tiny mucosal defect and bleeds massively, and its defining feature is that it doesn't taper as it nears the surface the way a normal vessel does. It's classically in the proximal stomach near the junction but occurs throughout the gut, and the recognition cue is recurrent or massive bleeding out of proportion to any visible lesion, in a stomach that otherwise looks normal, which is why it's easy to miss between bleeds, since there's no ulcer crater marking the spot. Treatment is dual therapy, a clip plus injection or thermal, because epinephrine alone fails, with the over-the-scope clip as rescue and a tattoo at the site to relocate it later.

7:06Mallory-Weiss is a longitudinal tear at the gastroesophageal junction from forceful retching, classically the binge drinker, the hyperemesis patient, or a severe coughing fit, and the cue is small-volume bright-red hematemesis after retching in a non-cirrhotic with no preceding melena and no portal hypertension. The natural history does the work, since most stop on their own, so a non-bleeding tear gets antiemetics, fluids, acid suppression, and observation, while an actively bleeding one gets endoscopic therapy. The favored trap is giving octreotide because the patient drinks: octreotide treats portal pressure, but this mechanism is mechanical, so the two diseases share a risk factor and nothing else.

7:45GAVE, the watermelon stomach, is linear stripes of dilated vessels in the antrum causing chronic bleeding and iron-deficiency anemia, classically in an older woman with an autoimmune disease like scleroderma, or a diffuse variant in cirrhotic men. The board trick is telling it from portal hypertensive gastropathy, because both occur in cirrhotics and both look vascular: GAVE is distal, in the antrum, with linear stripes, while portal hypertensive gastropathy is proximal, in the body and fundus, with a snake-skin mosaic. And the therapeutic distinction matters more, because portal hypertensive gastropathy is portal-pressure-driven and responds to beta-blockade and TIPS, while GAVE is a mucosal-vascular lesion that does not respond to TIPS, so reaching for TIPS in GAVE is the wrong move; GAVE is treated with argon plasma coagulation over serial sessions, or ablation or banding.

8:37Cameron lesions are linear erosions on the gastric folds right at the diaphragmatic hiatus in a patient with a large hiatal hernia, from mechanical rubbing and intermittent ischemia as the hernia slides through the hiatus with breathing, and the cue is chronic occult bleeding with iron-deficiency anemia in an older patient with a large hiatal hernia and an otherwise unrevealing workup, with the lesions easily missed without careful retroflexed inspection. Treatment is iron and acid suppression, though the acid-suppression benefit is uncertain since the injury is mechanical, and refractory bleeding needs surgical hernia repair, the only definitive fix.

9:12Angiodysplasia is the most common cause of small-bowel obscure bleeding, especially in the elderly, and its associations are the cues. Heyde syndrome is aortic stenosis plus angiodysplasia bleeding, where the stenotic valve shears von Willebrand factor into an acquired deficiency that bleeds from pre-existing angiodysplasias, and valve replacement reverses it. The other associations are end-stage renal disease through uremic platelet dysfunction, hereditary hemorrhagic telangiectasia, and left ventricular assist devices, again through acquired von Willebrand disease. Accessible lesions get argon plasma coagulation, and refractory diffuse small-bowel disease goes to systemic therapy, thalidomide for its anti-VEGF effect, long-acting octreotide to cut transfusions, and bevacizumab reserved for the telangiectasia syndrome.

10:03That syndrome, hereditary hemorrhagic telangiectasia, is an autosomal dominant disorder of blood-vessel development with telangiectasias on the lips and through the gut plus visceral arteriovenous malformations in lung, brain, and liver. The Curacao criteria are four: recurrent spontaneous nosebleeds, mucocutaneous telangiectasias, visceral involvement, and a first-degree relative, with three making it definite. Epistaxis is usually the first sign and the main cause of iron-deficiency anemia. Treatment is iron, endoscopic coagulation of accessible lesions, octreotide, and bevacizumab for refractory disease, and importantly, pulmonary AVMs are screened for and embolized when symptomatic because of stroke and brain-abscess risk from paradoxical emboli, and relatives are screened.

10:54Hemobilia is bleeding into the biliary tree, and the cue is the triad of right-upper-quadrant pain, jaundice, and upper GI bleeding in a patient with a recent hepatobiliary procedure or liver trauma, with blood seen coming from the major papilla at endoscopy. The source is usually a hepatic artery pseudoaneurysm, and the definitive therapy is transcatheter embolization. Hemosuccus pancreaticus is the pancreatic counterpart, and the cue is sentinel bleeding plus a pseudocyst: a pseudoaneurysm, usually of the splenic artery, communicating with a pancreatic pseudocyst in a patient with chronic pancreatitis, who has a self-limited bleed that signals a vessel which has temporarily sealed. Endoscopy may again show blood at the papilla, but the source is pancreatic, and because massive hemorrhage tends to follow within hours to days, that sentinel bleed is the window for embolization or surgery.

11:46Aortoenteric fistula is the herald-bleed-then-exsanguination vignette: an infected aortic graft eroding into the adjacent bowel, usually the third portion of the duodenum which lies against the graft, typically after prior aneurysm graft surgery. The signature is a herald bleed, a self-limited, sometimes small hematemesis or melena that precedes a catastrophic bleed by hours to weeks, often with fever, enteric bacteremia, and back or abdominal pain. The scope should be extended to reach the third part of the duodenum, but its sensitivity is poor because the fistula is often hidden behind clot, so the move in a stable graft patient with hematemesis is CT angiography looking for gas around the graft, a pseudoaneurysm, or extravasation, with surgical exploration when suspicion stays high regardless of the imaging. The definitive therapy is emergent repair, and the herald bleed after aneurysm graft surgery is the pattern never to let pass.

12:41So the unusual causes, each defined by its cue: Dieulafoy is recurrent massive bleeding from a normal-looking stomach; Mallory-Weiss is hematemesis after retching with stable hemodynamics; GAVE is antral watermelon stripes that don't respond to TIPS; Cameron lesions are iron-deficiency anemia in a large hiatal hernia; angiodysplasia is small-bowel obscure bleeding with its four associations; the telangiectasia syndrome is the Curacao criteria; hemobilia is the triad after a hepatobiliary procedure; hemosuccus is sentinel bleeding plus a pseudocyst; and aortoenteric fistula is the herald bleed after aneurysm graft surgery. Each cue triggers a specific move and a specific therapy, and none of them announces itself on a routine scope report, so the recognition comes from the history.

13:20The two halves of this episode share a logic even though they look like different chapters. In variceal disease the recognition is fast because the cirrhosis is obvious and the management is a bundle delivered together, with the high-risk patient flagged for early TIPS. In the unusual causes the management is straightforward once the lesion is named, but the recognition has to come from a history cue rather than the image. In both, the wrong reading is the one that treats the bleeding as a generic ulcer.

13:49The next chapter pivots from bleeding to malabsorption, with celiac disease. The question there is how you confirm it when the suspicion is clinical: the genetic prerequisite, the screening antibody, and the graded duodenal biopsy taken while the patient is still eating gluten, with strict gluten-free diet as treatment and the refractory-disease split when symptoms persist despite adherence.

14:23For 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.