GI Emergencies: Lower GI Bleeding and Mesenteric 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. In this episode we cover the lower GI and ischemic emergencies: acute lower GI bleeding with its risk-stratified workup and CT angiography for active bleeding, colon ischemia recognized by pain before bleeding, and acute mesenteric ischemia where lactate out of proportion to exam and CT angiography drive the door-to-revascularization clock.

0:30The last episode stayed with the upper GI hemorrhage bundle. This one moves below the ligament of Treitz and then to the mesenteric vessels, and the same time-sensitive logic carries over: pick the imaging that feeds the next intervention, and recognize the pattern that flips the algorithm.

0:48Acute lower GI bleeding is hematochezia or hemodynamically significant melena from a source distal to the ligament of Treitz, and the workup branches sharply on hemodynamic stability rather than on the suspected etiology. The first rule worth naming is that about fifteen percent of presumed lower GI bleeding episodes turn out to be brisk upper GI sources. A blood urea nitrogen-to-creatinine ratio above thirty favors an upper source, because protein breakdown in the small bowel raises BUN out of proportion to creatinine when blood is digested upstream.

1:21Initial stabilization mirrors upper GI bleeding. Two large-bore peripheral IV lines, type and crossmatch, restrictive transfusion to a hemoglobin trigger of seven, and the same anticoagulation reversal algorithm. Anoscopy at the bedside excludes anorectal sources before colonoscopy referral, because a pile of bright blood in the toilet bowl from a fissure does not need a colonoscopy at all.

1:47The hemodynamic split is the central decision. The unstable patient with severe ongoing bleeding goes first to CT angiography. The mechanistic reason is that CT angiography images contrast extravasation in real time during a single arterial-phase pass and produces three-dimensional vascular anatomy that the embolization plan is built directly from. Tagged red blood cell scintigraphy detects bleeding only when labeled cells reach the lumen and lacks the anatomic resolution that interventional radiology needs to guide a microcatheter.

2:22CT angiography requires a bleeding rate of about zero point three milliliters per minute or greater for reliable detection. That corresponds to a clinically active bleed rather than an intermittent ooze. A positive CT angiogram triggers IR embolization by superselective catheterization with microcoils, gel foam, or particle embolization. Tagged red cell scintigraphy still has a role, but its role is intermittent or obscure overt bleeding, where its temporal sensitivity over hours after a single injection captures bleeding that CT angiography would miss.

2:55The hemodynamically stable patient goes to colonoscopy. A randomized trial in acute lower GI bleeding compared early colonoscopy within twenty-four hours against elective colonoscopy at twenty-four to ninety-six hours and found no significant difference in identification of stigmata, thirty-day rebleeding, mortality, transfusion requirement, or length of stay. The current standard is colonoscopy at twelve to twenty-four hours after rapid bowel preparation, not emergent. Emergent colonoscopy in an unprepped colon misses lesions through poor visualization and carries higher complication rates. Rapid preparation uses four liters of polyethylene glycol over three to four hours, with prokinetic and antiemetic support as needed.

3:41The etiologies of brisk lower GI bleeding divide by anatomy and by pattern. Diverticular bleeding is the most common cause, classically painless and abrupt. The boards-favorite anatomic fact is that over half of bleeding diverticula sit in the right colon, even though diverticulosis itself is left-sided. Right-sided diverticula have wider necks and thinner walls that expose the vasa recta to greater shear stress, which is why they bleed disproportionately. Diverticular bleeding stops spontaneously in roughly three-quarters of cases, with rebleeding rates of fifteen percent after a first episode and twenty-five to fifty percent after a second.

4:20Angiodysplasia favors the right colon and presents with intermittent or chronic bleeding more often than torrential hemorrhage. The high-yield association is Heyde syndrome. Shear-induced unfolding of high-molecular-weight von Willebrand multimers across a stenotic aortic valve produces an acquired type two A von Willebrand disease that bleeds from angiodysplastic lesions. The aortic stenosis is the upstream lesion, and valve replacement often resolves the bleeding.

4:48Post-polypectomy bleeding presents one to fourteen days after the index colonoscopy. The classic patient is on antiplatelet therapy resumed too early, or had a pedunculated polyp with a thick stalk whose feeding submucosal artery was not adequately controlled at resection. The interval matters because the bleed declares well after the patient has gone home.

5:07Endoscopic hemostasis at colonoscopy uses the same modalities as upper GI bleeding, with two important differences in mechanism that drive modality choice. Diverticular bleeding stigmata are managed with endoscopic clipping or band ligation rather than deep thermal therapy, because the diverticular wall lacks a serosal layer. Thermal coagulation deep enough to seal the underlying vessel risks transmural injury and perforation. Clips and bands close the dome mechanically without depth, which is why they are preferred.

5:41Post-polypectomy bleeding within fourteen days is identified by stigmata at the polypectomy site and treated with through-the-scope clips that close the visible vessel directly. The mechanism is the same. The bleeding originates from a feeding submucosal artery at the resection base, and thermal therapy on the thinned post-resection wall risks delayed perforation. The same mechanical-versus-thermal logic explains why prophylactic clip placement at the time of large or pedunculated polyp resection reduces delayed post-polypectomy bleeding.

6:11Colon ischemia is the recognition stem worth distinguishing from diverticular bleeding, because the two share hematochezia but separate cleanly on pain. Colon ischemia presents with sudden cramping abdominal pain, typically left lower quadrant, followed within twenty-four hours by an urgent desire to defecate and hematochezia. Pain before bleeding is the key feature. Diverticular bleeding is painless.

6:35CT abdomen and pelvis with oral and intravenous contrast shows segmental bowel wall thickening, the thumbprinting pattern. Treatment is supportive with intravenous fluids and bowel rest in mild disease, because the mucosal barrier remains intact and the ischemic segment heals once perfusion is restored. Antibiotics are added in moderate-to-severe disease, defined by a white blood cell count over fifteen thousand, BUN over twenty, or severe ulceration. The mechanistic reason for the antibiotic threshold is that deeper ischemia has breached the mucosal barrier and bacterial translocation is occurring, which converts a self-limited ischemic insult into a sepsis risk.

7:15Isolated right colon ischemia is the variant that flips the algorithm. It carries the worst prognosis, with the longest hospitalization and the highest surgery and mortality rates, and it can herald clinically silent SMA occlusion. The right colon is a watershed-equivalent territory of the SMA, so isolated right-sided ischemia implies SMA-side flow compromise rather than the typical left-sided watershed pattern between SMA and IMA. Mesenteric vessel imaging becomes mandatory in this presentation, and that link is what connects acute lower GI bleeding to acute mesenteric ischemia.

7:50Move to acute mesenteric ischemia. The mortality remains approximately fifty to eighty percent despite advances in imaging. The reason mortality has not budged is that the clinical presentation is non-specific, bowel infarction occurs within hours of vascular compromise, and the diagnostic instinct is often the wrong one.

8:09The patient with severe abdominal pain and a soft abdomen looks like a non-emergent presentation until the lactate rises or the bowel infarcts. The recognition rule is pain out of proportion to physical findings. The diagnostic anchor is CT angiography. And the mechanism-driven point is that there are four distinct etiologies, each with a characteristic patient profile and an etiology-specific intervention. Applying the wrong intervention to the wrong etiology fails.

8:40SMA embolus accounts for about half of cases. The mechanism is a discrete clot lodged in an otherwise normal SMA, classically in a patient with atrial fibrillation or with a recent myocardial infarction and a left ventricular thrombus. The embolus typically lodges distal to the origin of the middle colic artery, which spares the proximal jejunum and infarcts the mid-jejunum to ileum. The presentation is abrupt. Sudden severe periumbilical pain, often with rapid forceful non-bloody bowel evacuation, in a patient with the cardiac history.

9:13The intervention follows the mechanism. Because the underlying artery is normal, the answer is removal of the clot rather than repair of an underlying lesion. Surgical embolectomy with concurrent bowel resection of any infarcted segment is the historical standard. Intra-arterial thrombolysis with mechanical thrombectomy by interventional radiology is the endovascular alternative in selected stable patients without peritoneal signs.

9:37SMA thrombosis accounts for about a quarter of cases. The mechanism is acute thrombosis on top of pre-existing atherosclerotic plaque at the SMA origin, classically in a patient with diffuse atherosclerotic disease and often with a history of chronic mesenteric ischemia. That history is its own recognition stem. Postprandial pain, food fear or sitophobia, and weight loss preceding the acute event tell you the chronic lesion was there before the acute thrombosis lit it up.

10:07The occlusion is more proximal than embolic disease because the plaque sits at the vessel origin, so a longer length of bowel infarcts. The intervention is not embolectomy. Removing the clot leaves the plaque to re-occlude immediately. The answer is surgical revascularization with bypass or endovascular angioplasty and stenting that addresses the underlying stenosis itself.

10:34Nonocclusive mesenteric ischemia, NOMI, accounts for about a fifth of cases. The mechanism is splanchnic vasospasm without organic occlusion in a low-flow state. The classic patient is elderly, in the ICU on vasopressors after cardiac arrest, in cardiogenic or septic shock, or on hemodialysis with intradialytic hypotension. There is no clot to remove and no plaque to bypass. The bowel is hypoperfused because the arterioles are constricted in response to systemic hemodynamic compromise.

11:08Treatment is intra-arterial papaverine thirty to sixty milligrams per hour through a catheter selectively positioned in the SMA. Papaverine is a smooth-muscle vasodilator that reverses the spasm. The second half of treatment is aggressive correction of the underlying low-flow state, by reducing vasopressor doses where possible, optimizing cardiac output, and resuscitating the volume deficit. The vasopressors that are keeping the patient alive are also constricting the bowel that is dying.

11:37Mesenteric venous thrombosis accounts for about five percent of cases. The mechanism is venous occlusion in a hypercoagulable state. Factor five Leiden, prothrombin gene mutation, JAK two-positive myeloproliferative neoplasm, antiphospholipid syndrome, oral contraceptives, recent abdominal surgery, intra-abdominal sepsis. The clinical course is more indolent than the arterial causes, because the arterial supply remains patent and collateral venous drainage develops over days.

12:09The presentation is subacute abdominal pain over days rather than hours, with thrombus in the superior mesenteric vein on CT venous phase. Treatment is systemic anticoagulation, not surgical or endovascular intervention, with workup for an underlying hypercoagulable disorder that drove the venous thrombosis. That workup often dictates lifelong anticoagulation.

12:32CT angiography is the imaging modality of choice with sensitivity approximately ninety-six percent for acute mesenteric ischemia. Plain CT without arterial-phase contrast is not adequate because it does not visualize the arterial occlusion. A bowel-targeted protocol with IV contrast in the arterial and portal venous phases is required.

12:54The early CT findings are non-specific. Bowel wall thickening, abnormal mucosal enhancement, ileus. The late findings of necrotic bowel are highly specific but signal that the operative window has narrowed to bowel resection rather than revascularization. Pneumatosis intestinalis, portomesenteric venous gas, paper-thin bowel wall. By the time those findings appear, infarction has already happened.

13:20This is where the lactate trap matters. Lactate is often elevated only in late disease and is not sensitive for early ischemia. A normal lactate does not exclude the diagnosis. The candidate who waits for lactate to rise before ordering CT angiography misses the early window. The recognition rule is pain out of proportion to exam plus a vascular risk profile, and the answer is CT angiography now, not lactate first.

13:47Initial management for any suspected acute mesenteric ischemia is a small bundle. Fluid resuscitation with isotonic crystalloid. Broad-spectrum antibiotics covering enteric flora, because mucosal permeability is rising and bacterial translocation is a sepsis risk. Serial electrolyte and acid-base monitoring. Optimization of cardiac output. And avoidance of vasopressors when possible, because they worsen splanchnic perfusion.

14:16Peritoneal signs change the answer for everyone. Rebound, guarding, or a rigid abdomen triggers urgent laparotomy regardless of etiology, because peritoneal signs mean bowel infarction with peritonitis. The operation is bowel resection with a planned second-look laparotomy at twenty-four to forty-eight hours to assess marginal segments that were borderline at the first operation.

14:38So pull the lower GI and ischemic threads together. Acute lower GI bleeding branches on hemodynamic stability, CT angiography for the unstable patient because it gives interventional radiology the anatomy and colonoscopy at twelve to twenty-four hours for the stable one, and the etiologies read by pattern, painless diverticular bleeding against painful colon ischemia. Isolated right colon ischemia flips the algorithm toward mesenteric imaging. And acute mesenteric ischemia turns on recognizing pain out of proportion to exam and reaching for CT angiography before lactate rises, then matching the intervention to the etiology, embolectomy for the embolus, revascularization for the thrombosis, papaverine and low-flow correction for NOMI, and anticoagulation for venous thrombosis, with peritoneal signs sending everyone to laparotomy.

15:29The next episode picks up the mechanical and structural GI emergencies. Foreign body and food bolus impaction with EGD timing driven by object type. Caustic ingestion graded by the Zargar endoscopic scale. Esophageal perforation and Boerhaave syndrome with imaging-guided management. And acute colonic pseudo-obstruction with Ogilvie syndrome and neostigmine.

15:52For 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.