GI Emergencies: GI Emergencies: Lower Bleeding and Ischemia

0:00Welcome to Board Pearls. This is episode two of four of the GI Emergencies chapter, in the Special Populations and Acute or Supportive Care module. This episode is blood from below and the bowel that's losing its blood supply. The first patient is a woman with painless maroon stools, and her case shows how to exclude an upper source in lower gastrointestinal bleeding, the bedside test that comes first, who goes to computed tomography angiography and who goes to colonoscopy and how soon, and why a bleeding diverticulum is clipped rather than burned. A man whose cramping came before his bleeding shows what pain first means, and why ischemia of the right colon sends the workup to the mesenteric arteries. The second patient is a woman in agony with a soft abdomen, and her case shows acute mesenteric ischemia: why it still kills, the one test and why the lactate can't be trusted, what's done before the cause is known, and what makes a surgeon operate regardless. Short cases then show the other three causes of mesenteric ischemia and their three different treatments.

1:02Here's the first patient. A seventy-nine-year-old woman has passed three large, painless, maroon and red stools since this morning. She has diverticulosis and aortic stenosis and takes no anticoagulants. Her heart rate is ninety-six, her blood pressure one hundred twenty-four over seventy, and her hemoglobin nine point four, down from twelve last year. Her blood urea nitrogen, BUN, is twenty-two and her creatinine one point two.

1:29She has acute lower gastrointestinal bleeding, and with painless bleeding and known diverticulosis, a diverticular source is most likely. Acute lower gastrointestinal bleeding is hematochezia, or hemodynamically significant melena, from a source beyond the ligament of Treitz. Before anything else, the blood has to be confirmed as coming from below, because about fifteen percent of presumed lower bleeds turn out to be brisk upper sources. A BUN to creatinine ratio above thirty favors an upper source, because blood digested higher in the gut is broken down and absorbed as protein, raising the BUN out of proportion to the creatinine. Hers is about eighteen, which favors a lower source. A ratio of forty with a fast pulse would have put upper endoscopy first.

2:12Whatever the source, she's stabilized the same way as an upper bleed, covered in episode one and chapter nine: two large-bore intravenous lines, type and crossmatch, restrictive transfusion for a hemoglobin below seven grams per deciliter, and reversal of any anticoagulant. The Oakland score stratifies severity in lower bleeding, and a score of eight or below identifies low-risk patients who can be managed as outpatients. At seventy-nine, with a hemoglobin of nine point four and visible ongoing bleeding, she's admitted.

2:43Bedside anoscopy comes before any referral for colonoscopy, because an anorectal source changes everything that follows. It excludes hemorrhoids or a fissure, and bright blood from a fissure doesn't need a colonoscopy at all. Hers shows small, non-bleeding hemorrhoids, so her blood is coming from higher up.

3:02Her next test depends on whether she's hemodynamically stable, not on the suspected cause. A stable patient goes to colonoscopy first. A randomized trial comparing colonoscopy within twenty-four hours with colonoscopy at twenty-four to ninety-six hours found no difference in finding stigmata of recent bleeding, rebleeding, mortality, transfusion, or length of stay. So the standard is colonoscopy twelve to twenty-four hours after rapid bowel preparation, rather than an emergency examination, because an unprepared colon hides lesions and emergency colonoscopy has more complications. Rapid preparation is four liters of polyethylene glycol over three to four hours, with prokinetic and antiemetic support if needed. She's stable, so she drinks her preparation over the afternoon for colonoscopy the next morning, trading a few hours for a colon clean enough to find and treat the bleeding vessel.

3:55Had she been unstable, with a blood pressure of eighty-four, a heart rate of one hundred thirty, and continued bleeding, she'd have gone first to computed tomography, CT, angiography. It's preferred over a tagged red blood cell scan in active bleeding because it shows contrast leaking in real time during a single arterial pass and gives three-dimensional vascular anatomy that guides embolization, while a tagged scan shows when bleeding happens but not the anatomy interventional radiology needs. CT angiography needs a bleeding rate of about zero point three milliliters per minute or more, which corresponds to a clinically active bleed rather than an intermittent ooze. A positive scan triggers superselective embolization of the feeding vessel with microcoils, gel foam, or particles. Surgery is rarely needed and is reserved for an unstable patient with a localized source in whom both endoscopic and radiologic approaches have failed. The tagged red cell scan still has a role in intermittent or obscure overt bleeding, because a single injection can detect bleeding that happens hours later, which CT angiography would miss.

5:02Her colonoscopy confirms what her history suggested. Diverticular bleeding is the most common cause of brisk lower bleeding, classically painless and abrupt. More than half of bleeding diverticula are in the right colon, even though diverticulosis itself is mostly left-sided, because right-sided diverticula have wider necks and thinner walls that expose the vasa recta to more shear stress. Diverticular bleeding stops on its own in about seventy-five percent of cases, and it rebleeds in about fifteen percent after a first episode and twenty-five to fifty percent after a second. Her prepared colonoscopy shows blood in the right colon and an ascending colon diverticulum with a visible vessel at its dome.

5:41Her vessel is treated mechanically, not with heat. Endoscopic hemostasis in the colon uses the same tools as in upper bleeding, but diverticular stigmata, meaning active bleeding, a visible vessel, or adherent clot, are treated with clips or band ligation rather than deep thermal therapy. The diverticular wall has no serosal layer, so coagulation deep enough to seal the vessel risks transmural injury and perforation, while clips and bands close the dome mechanically without that depth. Her dome is clipped and the bleeding stops. The thin wall that let her vessel bleed is the same wall heat would have perforated.

6:17The same reasoning applies if her bleeding had followed a polypectomy. Post-polypectomy bleeding appears one to fourteen days after the procedure, classically when antiplatelet therapy is restarted too early or after removal of a pedunculated polyp with a thick stalk whose feeding artery wasn't controlled. It's treated with through-the-scope clips on the visible vessel at the resection site, because thermal therapy on the thinned wall there risks delayed perforation. That mechanical advantage is also why prophylactic clips placed at the time of resecting large or pedunculated polyps reduce delayed bleeding.

6:51Her aortic stenosis keeps one more cause in view. Angiodysplasia favors the right colon and bleeds intermittently or chronically more often than torrentially. It's associated with aortic stenosis in Heyde syndrome, where shear across the stenotic valve unfolds large von Willebrand multimers, which are then cleaved, producing an acquired type two A von Willebrand disease that bleeds from the angiodysplastic lesions. Her bleed was diverticular, but recurrent intermittent bleeding without a diverticular source would put angiodysplasia high on her list, with her valve as part of the reason. Hemorrhoids, fissure, neoplasm, inflammatory bowel disease, and radiation proctitis are the other causes her colonoscopy would have looked for.

7:35Her bleeding was painless, and pain before the blood points somewhere else. A sixty-four-year-old man had sudden cramping left lower abdominal pain this morning, then four hours later urgency and a bloody stool. His heart rate is ninety and his blood pressure normal. He most likely has colon ischemia, which presents with sudden cramping pain, usually in the left lower quadrant, followed within twenty-four hours by urgency and hematochezia. The pain is what separates it from painless diverticular bleeding. CT with oral and intravenous contrast shows segmental wall thickening with a thumbprinting pattern, and his shows thickening of the descending and sigmoid colon.

8:14His severity decides whether he needs antibiotics. Mild disease is treated with intravenous fluids and bowel rest, because the mucosal barrier is still intact and the segment heals once perfusion returns. Antibiotics are added in moderate to severe disease, defined by a white count above fifteen thousand, a BUN above twenty, or severe ulceration, because deeper ischemia has breached the mucosa and bacteria are translocating, turning a self-limited insult into a sepsis risk. With a white count of eleven thousand and a BUN of sixteen, he gets fluids and bowel rest without antibiotics.

8:47His ischemia is on the left, which is the usual pattern. Isolated right colon ischemia carries the worst prognosis, with the longest hospital stays and the highest rates of surgery and death. The right colon is supplied by the superior mesenteric artery, SMA, so isolated right-sided ischemia can herald a silent SMA occlusion, and mesenteric vessel imaging is mandatory in that presentation. That leads directly to the second patient.

9:13A seventy-four-year-old woman with atrial fibrillation stopped her anticoagulant two months ago because of nosebleeds. Two hours ago she developed sudden severe periumbilical pain, then a forceful non-bloody bowel movement. She's writhing and rates her pain ten out of ten, but her abdomen is soft, with mild tenderness and no guarding. Her heart rate is one hundred eighteen and irregular, her white count fifteen thousand, and her lactate one point six, which is normal.

9:41She has acute mesenteric ischemia until CT angiography says otherwise: a sudden loss of blood supply to the bowel. The findings that point to it are pain out of proportion to her examination, a sudden onset, a forceful bowel movement, and atrial fibrillation without anticoagulation. Mortality is about fifty to eighty percent and has changed little despite better imaging, because the presentation is non-specific, bowel infarcts within hours, and severe pain with a soft abdomen doesn't look like an emergency until the lactate rises or the bowel dies. So the recognition rule is pain out of proportion to the physical findings, and her soft abdomen is the clue, not a reassurance.

10:21Her normal lactate can't slow anything down. Lactate often rises only late and isn't sensitive for early ischemia, so a normal value doesn't exclude the diagnosis, and waiting for it to rise loses the window in which bowel can be saved. The test is CT angiography, with a sensitivity of about ninety-six percent, using intravenous contrast in arterial and portal venous phases. A plain CT without arterial contrast doesn't show the occlusion and isn't adequate. Early findings, such as wall thickening, abnormal mucosal enhancement, and ileus, are non-specific. Late findings, pneumatosis intestinalis, portomesenteric venous gas, and a paper-thin bowel wall, are highly specific but mean infarction has already happened and the options have narrowed to resection. Her CT angiogram shows an abrupt SMA cutoff a few centimeters from its origin, beyond the middle colic branch, with normal enhancement of the proximal jejunum and reduced enhancement of the distal small bowel, without pneumatosis.

11:25Her treatment starts while the cause is still being worked out, because it's the same for every cause. She gets isotonic crystalloid resuscitation; broad-spectrum antibiotics covering enteric flora, because mucosal permeability rises and bacterial translocation risks sepsis; serial electrolyte and acid-base checks; and optimization of her cardiac output. Vasopressors are avoided where possible, because they worsen splanchnic perfusion, so she's supported with volume rather than pressors.

11:53Then her cause decides her intervention, because the wrong intervention for the cause fails. The four causes differ in history, speed of onset, and the site of the blockage. An SMA embolus, about half of cases, is a discrete clot lodged in an otherwise normal artery, classically from atrial fibrillation or a left ventricular thrombus after a recent infarction. It lodges beyond the origin of the middle colic artery, so the proximal jejunum is spared while the mid-jejunum to ileum infarcts, and it presents abruptly, with severe periumbilical pain and often a rapid, forceful, non-bloody bowel movement. She has every feature. Because the artery underneath is normal, treatment removes the clot. Surgical embolectomy with resection of any infarcted bowel is the historical standard, and intra-arterial thrombolysis with mechanical thrombectomy is the endovascular alternative in selected stable patients without peritoneal signs. Her team considers thrombectomy, but over the next hour she develops tenderness with guarding.

12:54Her new peritoneal signs change the plan. Rebound, guarding, or rigidity trigger urgent laparotomy regardless of the cause, because they mean infarcted bowel with peritonitis. The operation is resection with a planned second-look laparotomy at twenty-four to forty-eight hours, to reassess segments that looked marginal. She goes to the operating room, her embolus is removed, forty centimeters of ileum that doesn't recover is resected, and the second look finds the rest of her bowel viable.

13:25Had her CT shown the occlusion right at the origin of the SMA instead, the cause would be thrombosis, and removing the clot alone would fail. SMA thrombosis, about a quarter of cases, is acute thrombosis on an atherosclerotic plaque at the origin of the artery, in a patient with diffuse atherosclerosis, often after a history of chronic mesenteric ischemia, with pain after meals, fear of eating, and weight loss. Because the plaque sits at the origin, the occlusion is more proximal than an embolus, and a longer length of bowel infarcts. A sixty-eight-year-old man who smokes heavily, with peripheral vascular disease, months of pain twenty minutes after eating, and eight kilograms of weight loss, most likely has thrombosis. Embolectomy alone would fail him, because the plaque left behind re-occludes immediately. He needs revascularization of the stenosis itself, by surgical bypass or by angioplasty and stenting.

14:22In some patients the vessels are open and there's nothing to remove at all. Nonocclusive mesenteric ischemia, about a fifth of cases, is splanchnic vasospasm without an occlusion in a low-flow state. The classic patient is elderly and in the intensive care unit, on vasopressors after a cardiac arrest, in cardiogenic or septic shock, or hypotensive during dialysis. Picture a man on vasopressors two days after a cardiac arrest whose abdomen distends and whose lactate rises, with patent mesenteric vessels on CT angiography. There's no clot to remove and no plaque to bypass, because the arterioles are constricted in response to his failing circulation. Treatment is intra-arterial papaverine, a smooth-muscle vasodilator, at thirty to sixty milligrams an hour through a catheter placed selectively in the SMA, plus aggressive correction of the low-flow state: reducing vasopressors where possible, optimizing cardiac output, and correcting the volume deficit. The vasopressors keeping him alive are part of the problem.

15:25The last cause is on the venous side, and it's slower. Mesenteric venous thrombosis, about five percent of cases, is venous occlusion in a hypercoagulable state: factor V Leiden, the prothrombin gene mutation, a JAK2-positive myeloproliferative neoplasm, antiphospholipid syndrome, oral contraceptives, recent abdominal surgery, or intra-abdominal sepsis. It's more indolent than the arterial causes, because the arterial supply stays open and venous collaterals form over days, so the pain develops over days rather than hours, and the venous phase of CT shows thrombus in the superior mesenteric vein. Treatment is systemic anticoagulation, not surgery or endovascular therapy, along with a workup for the underlying hypercoagulable disorder, which often decides whether anticoagulation is lifelong. A thirty-eight-year-old woman on an oral contraceptive with five days of worsening pain and a superior mesenteric vein thrombus gets anticoagulation, stops her contraceptive, and has a thrombophilia workup.

16:32Here are the traps the boards set in lower gastrointestinal bleeding. A BUN to creatinine ratio over thirty raises an upper source. Anoscopy comes before colonoscopy. A low Oakland score means the patient can go home. A stable patient gets a prepared colonoscopy at twelve to twenty-four hours, not an emergency unprepared one. An unstable patient goes to CT angiography before colonoscopy. A tagged red cell scan is for intermittent bleeding, and CT angiography for active bleeding. A bleeding diverticulum is clipped or banded, not treated with deep thermal therapy, and most bleeding diverticula are on the right. Bleeding that follows cramping pain is ischemia, not diverticular bleeding. And isolated right colon ischemia needs mesenteric imaging.

17:18For mesenteric ischemia, the traps are these. A soft abdomen in a patient in severe pain is the warning, not the reassurance. A normal lactate doesn't exclude it. A plain CT can't make the diagnosis; CT angiography can. Fluids and antibiotics come first, and vasopressors are avoided. Thrombosis needs revascularization, not embolectomy alone. Nonocclusive ischemia has no clot and is treated with papaverine and better perfusion. Venous thrombosis is anticoagulated, not operated on. Peritoneal signs mean laparotomy without delay. And resection is followed by a second look.

17:55So, start to finish. In lower gastrointestinal bleeding, consider an upper source when the BUN to creatinine ratio is over thirty, do anoscopy, stabilize with restrictive transfusion and reversal, and send home patients with an Oakland score of eight or below. Unstable patients get CT angiography and then embolization, and tagged scans are for intermittent bleeding. Stable patients get a prepared colonoscopy at twelve to twenty-four hours, and diverticular stigmata are clipped or banded. Painful bleeding suggests colon ischemia, treated supportively, with antibiotics for a white count over fifteen thousand or a BUN over twenty, and isolated right-sided ischemia needs mesenteric imaging.

18:38Pain out of proportion to the examination is mesenteric ischemia until CT angiography says otherwise, without waiting for the lactate. Resuscitate with fluids, give broad antibiotics, and avoid vasopressors. An embolus, about half of cases, is abrupt, comes with atrial fibrillation, and spares the proximal jejunum, and the clot is removed surgically or endovascularly. Thrombosis, about a quarter, comes with atherosclerosis and prior pain after meals, and the plaque is revascularized. Nonocclusive ischemia, about a fifth, comes in shock and is treated with intra-arterial papaverine and better perfusion. Venous thrombosis, about five percent, is subacute and hypercoagulable, and it's anticoagulated with a thrombophilia workup. Peritoneal signs mean laparotomy with a second look.

19:29Episode three is the injured esophagus: foreign bodies, food impaction, perforation, and caustic ingestion.

19:37For 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 four of chapter thirty-one, and I'll see you in the next one.