I am Rahul Manchal. I'm an intensivist at the Medical College of Wisconsin, and I am going to be talking about acute GI bleeds. In the context of GI bleeds, we will discuss presentation, etiology, necessitated strategies, varicial and non-varicial upper GI bleeds, lower GI bleeds, and small bowel GI bleeds, also called middle GI bleeds. GI bleeds can present in one of four ways. Hematemesis, which is vomiting fresh red blood and usually indicates an upper GI source. Coffee-brown emesis, which is vomiting of altered black blood and again indicates an upper GI source. Melanoma, or passing black, tarry stools, which is usually an upper GI source, but also depends on transit time, and therefore can be a source from the proximal colon. And hematokesia, which is bright red blood per rectum and usually indicates a lower GI source, but in 10% of the cases, when GI bleeding is really brisk, it can also be from an upper GI source. Hematokesia, with hemodynamic instability, often indicates that the bleeding is coming from the upper GI tract. The first question for the audience is the most common cause for an upper GI bleed is one varices, two peptic ulcer disease, three malarie-wise tear, and four esophagitis, with the correct answer being two peptic ulcer disease. This slide demonstrates ideologies of both upper GI bleeds and lower GI bleeds. The most common cause of an upper GI bleed is peptic ulcer disease, which occurs in about 35 to 50% of cases. Other causes of upper GI bleeds include gastrointestinal erosions, esophagitis, varices, malarie-wise tears, and so on. The most common cause for lower GI bleeds is diverticulosis, occurring in about 30 to 65% of cases. Other common causes of lower GI bleeds include ischemic colitis, hemorrhoids, polyps, post-polypectomy, and inflammatory bowel disease. The substations for GI bleeds includes ensuring adequate IV access. Two large-bore, short-peripheral IVs should be placed. Since the speed of infusion of loads of blood products depends on the diameter and length of the IV catheter, large-bore, short-peripheral IVs work better than central lines. Resuscitation should initially comprise of crystalloids, but rapidly switch to blood products. Extrapolating from the trauma literature, massive resuscitation should be performed in a balanced fashion with adequate replenishment of plasma, coagulation factors, and platelets. In case patients are taking anticoagulants, vitamin K and other reversal agents should be administered. NG tubes are usually not required, but they may help empty the stomach prior to intubation. Bloody aspirates indicates an upper GI source and is an independent risk factor for mortality. Transfusion of red blood cells in GI bleeds is truly a double-edged sword. Restrictive transfusion strategies have been shown to be safer except in massive or exaggerating GI bleeds. In massive or exaggerating GI bleeds, initially hemoglobin values may be unchanged because of plasma equilibrium times. Transfusions in these cases are dictated by predicted drop in hemoglobin and clinical status. Transfusion thresholds are also likely dictated by underlying comorbid conditions such as cardiac disease. Patients with heart disease and GI bleeds may warrant higher transfusion targets. Crystalloids aren't benign. They are associated with dilutional coagulatory, acidemia, and hypothermia. For massive bleeds, warm bladder products should be used. Balanced transfusion should be given consideration. That is, transfusion of red blood cells, plasma, and platelets in a one-to-one-to-one ratio. Permissive hypotension should also be given consideration till the source of GI bleed can be controlled. This study by Villanueva et al., now published in the New England Journal of Medicine in 2013, showed that restrictive transfusion strategy, as compared to a liberal strategy, was associated with better survival. 80% of upper GI bleeds stop spontaneously without re-bleeding. Several scores have been developed for risk stratification of patients with upper GI bleeds. For example, the Glasgow-Blatchford score. The Blatchford score predicts transfusion, intervention, re-bleeding, and death. The main use of the score is to identify patients at low risk who don't need hospitalization or endoscopy. Other risk stratification scores are the Rockoll score, which takes into account age, shock, comorbidities, and endoscopic diagnosis. Another score is the AIM-65 score, which incorporates albumin, INR, mental status, blood pressure, and age. Risk factors for mortality in both upper GI and lower GI bleeds include advanced age, greater than 60 years, hemodynamic instability, severe comorbidities, such as end-stage renal disease, cirrhosis, cancer, congestive heart failure, the ongoing need for blood transfusion, emergency surgery, onset of bleeding in the hospital, and renal failure. We will now discuss variceal upper GI bleeds. The pictures in the slide demonstrate varicea at the gastroesophageal junction. Varicea is developed as a result of portal hypertension. There is an increased pressure gradient between the portal vein and the inferior vena cava. The normal pressure is about 1 to 5 millimeters of mercury. Pressure is given as the product of resistance and flow. And portal hypertension results from both increased resistance and or an increased portal venous flow. As can be seen from this cartoon, both an increased flow and distorted sinusoidal architecture, which leads to increased resistance, maintains portal hypertension. And variceal wall tension is a major determinant of variceal rupture. The second question for the audience, which of the following have been shown to decrease mortality in variceal upper GI bleeds? One octotype, two antibiotics, three telluric resin, four proton pump inhibitors. And the correct answer is two antibiotics. The initial management of variceal GI bleeds includes establishment of large-bore IV access, intubation electively, especially those with hepatic encephalopathy, correct ventilator management with low tidal volumes and peeps to minimize post-sinusoidal hypertension, cautious volume resuscitation, and restrictive transfusion. There is no current evidence for management of coagulopathy. It should likely be guided by viscoelastic testing and consideration of platelet counts of over 50,000, at which thrombin generation has shown to be normal and never diseased, and hepatic Doppler ultrasound to assess for total vein thrombosis. Further management of variceal GI bleeds involves the administration of sphenotic mesoconstrictors, antibiotics, and proton pump inhibitors. Sphenotic mesoconstrictors consist of either octotide or telluric resin. Telluric resin is not available in the United States. And what is used in the United States is octotide alone. The efficacy of sphenotic mesoconstrictors has been shown in multiple trials. Telluric resin was associated with a mortality benefit. The duration of therapy is five days, and drug and endoscopic therapy is superior to either of them. Antibiotics have been shown to decrease mortality and prevent pre-period in multiple trials and meta-analyses. Usually, ceftriaxone is used at the dose of 2 grams for 24 hours in advanced services. The utility of proton pump inhibitors in the acute setting in variceal GI bleeds is questionable. There is a possible benefit in decreasing post-banding ulceration. In terms of endoscopy for variceal GI bleeds, a pre-endoscopy promethality agent, such as erythromycin or metopropamide, may be administered. Varices are divided into either gastroesophageal varices or isolated gastric varices. Band ligation is superior to sclerotherapy with regard to hemostasis and re-bleeding and complications for esophageal varices. For predominantly gastric varices, sinoacrylate injection is superior to endoscopic band ligation with respect to re-bleeding. Esophageal balloon tamponade in variceal bleeds is a temporizing measure for a maximum of 24 to 48 hours to buy time for definitive interventions. Patients must be intubated and sometimes require heavy sedation and paralysis. The risks include esophageal necrosis and rupture. This requires familiarity and practice, and one should not attempt to wing this in an emergency. TIPS, or transjugular intrahepatic photosystemic shunt, is the creation of a shunt between the portal system and the systemic vein. It decompresses the portal venous system and prevents variceal bleeding. It is usually performed for refractory or recurrent variceal bleeding with failure of endoscopic hemostatic therapy. It may also be performed preemptively in patients with child's B cirrhosis and variceal bleeding or child's C cirrhosis with a score less than 14. Some contraindications include portal and mesenteric vein thrombosis, pulmonary hypertension, and RV dysfunction, and a high MED score, which portends increased mortality. Complications of TIPS include bleeding, shunt malposition, RV failure, hepatic decompensation, and worsening hepatic encephalopathy. In this study, on preemptive TIPS in patients with child's B cirrhosis and bleeding or child's C cirrhosis, early TIPS was associated with better survival and less re-bleeding. BRTO, or balloon occluded retrograde transvenous obliteration is a minimally invasive technique that is used to treat gastric variceal bleeding. The procedure involves blocking dilated vessels, reducing the risk for rupture. It can be used in addition or as an alternative to TIPS, which is the primary treatment for gastric varices. Some additional therapies for variceal bleeding include esophageal stents and hemostatic powders. Esophageal stents are self-expanding metal stents that are increasingly gaining use instead of balloon tamponade. The initial findings suggest improved efficacy and safety compared to balloon tamponade. Hemostatic powders are non-contact sprayable powders that have demonstrated preliminary benefit in variceal bleeding prior to banned ligation and in the treatment of banned ulcers. Here is an algorithmic approach to variceal bleeding. In case of suspected variceal bleeding, the initial approach includes airway protection, volume resuscitation, and preferably a restrictive transfusion strategy if possible. Splanctic vasoconstrictors, antibiotics, and early endoscopy within 12 hours should be prioritized. Endoscopic banned ligation for esophageal varices and sinoacrylate lube for variceal bleeding and sinoacrylate lube for gastric varices should be performed. Vasoactive drugs should be maintained for three to five days and consideration given to early tests. In cases of re-bleeding, depending on severity, therapies such as tips, esophageal stents, and balloon tamponade should be considered. If bleeding is controlled, secondary prophylaxis should be considered. We will now switch to talking about non-variceal bleeding, that is, peptic ulcer disease. The endoscopic classification of peptic ulcer disease has a direct correlation with re-bleeding rate without therapy. Type 1a, which is an active arterial bleed, or active squirting, has a 100% re-bleeding rate without therapy. Type 2a, which is a non-bleeding visible vessel, has up to a 50% re-bleeding rate. The lowest re-bleeding rate is type 3, which is a clean ulcer base and has a re-bleeding rate of less than 3%. Early endoscopy should be facilitated in peptic ulcer disease, that is, endoscopy within 24 hours of presentation. It is safe and facilitates early discharge. It also decreases length of stay and decreases transfusion requirements. Peptic ulcers with low-risk stigmata, i.e., those with clean bases and pigmented spots, don't benefit from endoscopic therapy. Endoscopic therapy benefits mostly high-risk lesions. Endoscopic therapy versus medical management in high-risk lesions is associated with decreased re-bleeding, decreased need for surgery, and decreased mortality. Dual therapy, that is, injection of epinephrine and either clipping or coagulation is better than monotherapy for high-risk lesions. Should a repeat endoscopy be performed in recurrent peptic ulcer bleeding? In a randomized controlled trial of a second endoscopic look versus surgery in patients who re-bled, only 13 out of 48 of the endoscopic group ended up needing salvage surgery. There were decreased complications in the endoscopic group, seven versus 16 patients. However, there were no differences in mortality, ICU length of stay, or transfusion. It was less successful if patients were hypotensive and the ulcer was greater than two centimeters. Surgery of transcatheter arterial embolization is needed in peptic ulcer disease in those who fail endoscopic therapy when there are large ulcers or there are posterior duodenal bulb ulcers. The third question for the audience. Pre-endoscopy acid suppression with proton pump inhibitor in non-vericial upper GI bleed is associated with which one of the following benefits? And the choices are, one, reduction of blood transfusion, two, improvement in mortality, three, reduction in need for endoscopic therapy for bleeding, and four, reduction in overall length of stay. And the correct answer being reduction in need for endoscopic therapy for bleeding. In a randomized controlled trial of non-vericial upper GI bleeding, acid suppression with an omeprazole infusion pre-endoscopy accelerated the resolution of signs of bleeding and ulcers and reduced the need for endoscopic therapy. In endoscopically treated peptic ulcer disease with high-risk stigmata, meta-analyses of either intravenous borus proton pump inhibitor or continuous infusions of proton pump inhibitor as compared to placebo reduce mortality, re-bleeding, surgery, and urgent intervention. However, meta-analysis of continuous versus intermittent therapy in high-risk bleeding ulcers show no difference in recurrent bleeding, mortality, surgery, or urgent intervention. We now switch to talking about lower GI bleeding. The picture on the left shows a blush on an arterial angiogram, and the picture on the right shows the same angiogram after coil embolization. In terms of diagnostic evaluation for lower GI bleeds, colonoscopy is the initial procedure of choice if the colon can be reasonably prepped. Colonoscopy is diagnostic and therapeutic, and it is usually performed within 24 hours after colon cleansing. Radiographic imaging is performed if there's ongoing bleeding with hemodynamic instability or if there is a negative colonoscopy or unsuccessful hemostasis. Nuclear RBC scans detect bleeding rates at 0.1 ml per minute. CT angiography is preferred, but detects bleeding rates at about 0.3 per minute. If CT angiography is positive, conventional angiography should be performed as soon as possible because lower GI bleeds are intermittent by nature. Randomized control trials for therapy in lower GI bleeds are lacking. Usually, endoscopic therapy consists of injection of epinephrine plus mechanical or thermal coterie. The evidence of efficacy is largely from observational studies and case series of diverticular bleeds. Diverticulosis, angiodysplasia, and post-polypectomy bleeds are most likely to benefit. Angiography and intervention have a high rate of success in case series. Bowel ischemia remains a complication, and its incidence is about one to four percent. Surgery is usually reserved for failed endoscopic and radiographic treatment. Small bowel bleeds were known as obscured GI bleeds in the past. They are uncommon and comprise of about five to 10% of all GI bleeds. The most common etiology is angiodysplasia. Risk factors include age, aortic stenosis, the presence of left ventricular assist devices, and comorbid conditions. Usually, evaluation begins after a second look for a lower endoscopy. Video capsule endoscopy remains the first line for evaluation of small bowel bleeds. One can use push endoscopy for proximal lesions. However, there are lower rates of detection for lesions in the duodenum and proximal genitals. Deep endoscopy is performed if video capsule is positive or there is a strong suspicion. Brisk bleeds or hemodynamically unstable bleeds are usually localized by CT angiography. Therapy for small bowel bleeds usually involves either endoscopy, angiography, or surgery. The choice of therapy is dictated by the amount of bleed, hemodynamic instability, and ability to localize lesions. In conclusion, the priorities for upper and lower GI bleeds remain hemodynamic stabilization, avoidance of over-resuscitation, expeditious endoscopy. Risk stratification scores may be helpful, especially in selecting patients for early discharge. Proton pump inhibitors should be used in high-risk stigmata in upper GI bleeds. And please do not forget antibiotics and the resale bleeds.

acute GI bleeds

upper GI bleeds

lower GI bleeds

variceal GI bleeds

treatment strategies