CCFP Topic: Gastrointestinal Bleeds

First and foremost, upper and lower GI bleed.  What’s the difference? Why do we care?

If you recall the early anatomy days of med school, the bottom part (aka pylorus) of the stomach drains into the duodenum, which itself is comprised of a few segments – four to be specific. The names of these segments aren’t really important, but you should know that the duodenum is kind of shaped like a lower-case u, and that the little vertical dangly part at the end of the u (aka the duodenojejunal flexure) is held up by a suspensory ligament referred to as the ligament of treitz.

It is this ligament that divides the terminal duodenum and the end of the upper GI tract…  from the beginning of the jejunum… and the start of the lower GI tract.

So why do we care? Well, although this division point is somewhat arbitrary, we care because the causes, workup, and treatment for upper and lower GI bleeds are quite different from each other.

Thankfully, a good history will almost always tell us where the bleed is coming from. And with that, let’s talk about the approach to the undifferentiated GI bleed.

First off, this will seem obvious, but where is the blood coming from, what does it look like, how much is there, and how often is it occurring? Upper GI bleeds will present with hematemesis (often described with a classic coffee ground appearance) and/or melena stools. Think of hematemesis as red/maroon in colour and sometimes containing clots. Coffee ground emesis tells us the blood has been in the stomach for longer, whereas red or maroon hematemesis would indicate fresher blood without prolonged gastric acid exposure.

LGIBs, on the other hand, will present with hematochezia, AKA bright red or maroon stools, aka bright red blood per rectum. Rarely, hematochezia in an unstable patient could also represent a brisk UGIB – but they’re that sick you’ll probably know. Other features of LGIB on history could include streaking blood on stools or blood on the toilet paper.

For all patients, you should also try and quantify the volume and frequency of bleeding to get an idea of the severity, which will help guide treatment and disposition. Take it with a grain of salt, however, because when it comes to estimating blood loss – patients are almost as bad as surgeons.

If you think you’ll be calling GI, they love if you can rattle off the patient’s Glasgow-Blatchford score – which is a risk score that objectively stratifies upper GI bleed patients based on their overall risk profile, ranging from 0 (the lowest risk) to 23 (the highest risk). It uses a few objective measurements like hemoglobin and systolic BP, as well as clinical features like presence of melena and recent syncope. Check it out on MDCalc or your favourite online risk calculator.

Step 1 is, as always, look at the patient and decide: sick or not sick? Stable or unstable? If unstable, your sole objective is to stabilize them. Regardless of UGIB or LGIB, this is our standard resuscitation stuff, and will look fairly similar, with the caveat being that upper GI bleeds causing massive hematemesis are obviously going to be higher risk airway cases than LGIBs, so you may need to jump to intubation more quickly.

In either case, start with ABCs, and throw on a MOVIE. And of course by movie I am referring to monitors, oxygen, vitals, IV access (2 large bores if you’re worried), and an ECG. Don’t actually start watching a movie while your patient crashes in front of you, as this could be seen as unprofessional and lead to regulatory action from the college.

Other things to consider on a case-by-case basis are massive transfusion protocol, anticoagulant reversal, and calling the consult for definitive management. Generally speaking, this will be GI for the unstable UGIBs, gen surg +/- interventional radiology for the unstable LGIBs, though this is site-dependent.  That’s all we’ll say about unstable bleeds, since they’re actually not a part of the CCFP objectives – but it’s important to have that general approach nonetheless. 

As part of your initial assessment, you should also be doing a quick cardiac review of systems, particularly in the setting of a big hemorrhage. So ask about orthostatic dizziness, confusion, anginal chest pain, heart palpitations, and cold/clammy extremities, and have a low threshold to grab an ECG. Rosen’s actually recommends it for all patients above 40 with a GI bleed, but, as always, use your clinical judgement.

We should also be mindful that there are certain things that can look just like a GI bleed, but are in fact not GI bleeds at all. For melena stools, ask about bismuth medications like Pepto Bismol or iron supplements. In these cases, patients should theoretically have a negative guaiac stool test, which are those little cards you can put a small stool sample on and turn blue when exposed to blood. I say theoretically because they are notoriously non-sensitive and non-specific for these purposes – so you shouldn’t be using them to help diagnose a GI bleed.

For Hematochezia, common mimics include vaginal bleeding, gross hematuria, or even partially digested red foods, so ask about them beets. Now that we’ve identified that it is, in fact, a GI bleed, we’ll go through the rest of our standard history, which will take a particular focus on comorbidities, bleeding risk factors, and medications.

When comparing between upper and lower GIBs, over 75% of cases of GI hemorrhage will be due to an upper GI source. Not only that, but the UGIB mortality rate is also higher than LGIB mortality, around 15% versus around 4%.

Most of this mortality is coming from esophageal variceal bleeds (which have a nearly 1 in 3 mortality rate), AND their management differs from other causes, and so the best first step in approaching your UGIB differential diagnosis is ask one key question: variceal or non-variceal. This is going to be largely guided by the good old history and physical.

On history, the most obvious clue would be a history of known alcoholic liver disease – especially if its required past hospitalization, ICU admission, or they’ve had prior variceal bleeds. On the spectrum of disease, cirrhosis is the most severe and carries with it the highest chance of portal hypertension and, consequently, variceal bleeds, due to the backflow of all that hepatic portal blood into the systemic circulation, also known as portosystemic anastomoses.

The way I remember some of the physical exam findings is by recalling that underlying pathophysiology.

• First off, Blood is getting shunted to places it shouldn’t be:
  • Look for variceal bleeds, caput medusae, transudative ascites, splenomegaly
• and the liver isn’t doing its job very well, which normally includes things like protein synthesis:
• this also contributes to ascites from loss of oncotic pressure, you may also expect petechiae or purpura from a loss of coagulation factors
• the liver also performs toxic metabolite breakdown, particularly ammonia, look for altered mental status from hepatic encephalopathy
• It also plays a role in sex hormone metabolism, so you may see gynecomastia or testicular atrophy
• And bilirubin drainage. So look for jaundice

Management of variceal bleeds is outside the scope of this podcast, but very quickly – because its important – in addition to supportive care, you’ll need:

•  antibiotic prophylaxis with something like ceftriaxone,
• administration of a vasoactive agent such as octreotide,
• reversal of any coagulopathy – typically with vitamin K, and
• calling GI – because ultimately, these patients will likely require emergent upper endoscopy for variceal banding.
• They’ll almost always be getting high dose PPIs as well, since you often won’t know whether the bleed is GI.

That said, the emphasis is on stabilization and calling GI

Peptic Ulcer Disease

I’m thinking about someone in their mid-40s with daily NSAID use and/or history of H Pylori infection who presents with a few days of coffee-ground emesis, dark/tarry, stools, and intermittent epigastric pain, and its typically relieved by food and antacids. For these cases, PPI is the mainstay of therapy, generally oral PPIs, or IV PPI if severe enough to bring them to the ER. This is quite nuanced, however, and will often involve a discussion with GI, particularly when it comes to disposition and length of treatment.

You’ll also eventually want to consider H Pylori testing, which would then step-up management to the infamous quadruple therapy, though this will have reduced sensitivity and specificity during an acute bleed – so the ideal time to test would be once the patient has come off their PPI and the GI bleed has settled. No firm timeline – but typically the endoscopist will be the one to recommend empiric treatment in this scenario.

As another quick pearl, for patients taking regular NSAIDs, consider co-prescription of a PPI, or use of a combination product, if they have risk factors for a GI bleed or are above the age of 60 or so. This is actually one of the very few indications for longterm PPI use. RxFiles has a nice chart called “NSAIDs and other analgesics comparison chart” that covers this in detail, which can often be accessed for free from hospital computers, as a little FYI

Jumping back a step, what if that same person we just described (the lady in her mid-40s with daily NSAID use who presents with coffee-ground emesis) was an active smoker?

I’d still keep peptic ulcers on the top of my differential, but this also starts to raise my suspicion for malignancy, particularly for older patients. For malignancy specifically, I’d also be looking for things like dysphagia, early satiety, involuntary weight loss, and cachexia.

So for the patient with the query PUD, when is it appropriate to start with PPIs alone and when should we also be referring them onward for endoscopy?

If they’re above the age of 50, have a family history of GI malignancy, previously diagnosed PUD, or have any red flag symptoms

• vomiting,
• any evidence of bleeding or anemia,
• an abdominal mass,
• weight loss,
• dysphagia, or
• early satiety
  you’ll want to jump to endoscopy.

So for this 40 year old smoker with coffee ground emesis, it’s actually the coffee ground emesis that tips us off for needing an upper scope referral – the smoking history, while it does place her at higher risk for malignancy, does not actually change her risk category in and of itself. So either of those scenarios will need a scope referral.

Otherwise, in the absence of any of the above, we can start with PPIs and can consider grabbing a CBC to check for anemia as well.  If things aren’t improving in the next 4 to 8 weeks, that’s another good reason to consider endoscopy, which we could then refer to as a failure to respond to treatment.

Mallory-Weiss tears

This is another common cause of upper GI bleed. Look for recurrent retching and multiple non-bloody episodes of vomiting followed by hematemesis. Commonly, this can be in the context of alcohol intoxication and is therefore quite important to distinguish from variceal bleeds. Really though, anything that causes recurrent emesis can lead to M-W tears – so your main job will be to figure out what that source could be.

What about kids, any big changes to our differential?

With the caveat that UBIGs are more common in adult patients overall, the differential is in nearly the same order, again with peptic ulcers, esophagitis, and gastritis leading the way, with esophageal varices and Mallory Weiss tears also on the differential, but more rare.

. I like to use the classic mnemonic: CHAND (or C-HAND). For this, we’re thinking of Colitis, Hemorrhoids/anal fissures, Angiodysplasia, Neoplasm, and Diverticular disease. Now of course there are many other causes, including upper GI bleeds, but the C-HAND causes are the biggest offenders.

Unlike the UGIB differential, peds is a bit different in this case: we’ll again think of things like anorectal fissures and infectious colitis. Particularly in toddlers, we also need to keep intussusception and Meckel’s diverticulum in mind. Inflammatory bowel disease is another lower GI bleed presentation that typically presents in childhood or adolescence, with a smaller incidence peak in later adulthood.

That’s a lot of stuff, so let’s go through the important ones for adults and kids and the key stuff you should know.

Like we said, anorectal sources, such as hemorrhoids or anal fissures, are going to be the most common causes of LGIB in all age groups. How might this present?

So first I’ll clarify that we’re mostly talking about internal hemorrhoids. Generally speaking, the internal ones bleed and the external ones hurt. With that said, I’m looking for the patient with a history of chronic constipation and straining who present   s with painless small volume bright red rectal bleeding at the end of their bowel movement, with small red drops in the toilet bowl, and often having scant blood on the toilet paper as well. There could be some dull aching pain in some cases. They might also endorse anal pruritis, or a perianal mass in the event of a prolapsed hemorrhoid. External hemorrhoids can bleed as well of course, but these will be more painful and will, by definition, have a visible perianal mass, often severely painful with bowel movements.

Now, although hemorrhoids are a clinical diagnosis, as patients get older, so increases their risk of more serious causes of LGIB, particularly malignancy. In those higher risk patients (age over 50, colorectal CA risk factors, family history, or red flags), you’ll need a colonoscopy to fully confirm nothing else is going on. Lower risk patients will not need this whole workup if the diagnosis is clear, but you should be performing perianal and digital rectal examinations at the very least. Anal fissures are a similar story, with the difference being that bowel movements will be very painful, and so will DRE. This can similarly be caused by constipation, and can also actually make it worse, over fear of bowel movements on account of the severe accompanying pain.

For both hemorrhoids and anal fissures, initial management is optimizing bowel habits and avoiding constipation at all costs, using dietary and supplemental fibre if needed. You’ll also want to consider a short trial of topical treatments for symptom relief, of which there are several available over the counter, usually containing some combination of topical anasthetics, corticosteroids, or vasoactive agents like phenylephrine. These are the Preparation Hs and the Anusols… they don’t alter the disease course, but they provide analgesia.. Moving down the list, we just mentioned malignancy risk factors and red flags as important components of the approach to LGIB. What are some of those?

Aside from our classic constitutional symptoms like unintentional weight loss, fevers, and night sweats, we’re looking at progressive general weakness or malaise, change in bowel habits – particularly with hematochezia or blood-streaked stools, decreased stool calibre (aka thin stools), abdominal discomfort, signs of obstruction, and tenesmus. The biggest risk factor for colorectal cancer is age, while other risks include family history, low-fibre/high meat diets, obesity, smoking, and alcohol consumption. These patients need referral to GI and a colonoscopy, in addition to standard bloodwork.

Moving our way further down the list, we see colonic diverticula – which are one of the most common causes of lower GI bleeds in adults, particularly older adults. What’s the classic story with these patients?

I’m thinking of the 60-year old patient presenting with painless bright red blood per rectum and chronic constipation, who consumes a low-fibre diet. Be careful not to confuse this with its higher acuity counterpart, diverticulitis, which is an inflammatory and infectious complication of diverticulosis that we are all undoubtedly quite familiar with.

Diverticulosis is often picked up incidentally on colonoscopy, either as part of routine colon cancer screening programs or as a workup for an undifferentiated lower GI bleed. Management is preventative, and includes high fibre diet, weight loss, and physical activity. The goal is to stop the progression and reduce the chance of diverticulitis. Further down this list, another common cause of hematochezia is angiodysplasia. These are vascular malformations of the GI tract, typically affecting the right-colon, that can cause fairly brisk GI bleeding – or can simply just hang out in the GI tract without bleeding at all. Diagnosis is by endoscopy.

The biggest risk factor is age, with most cases diagnosed in adults over 60, and other risk factors include End stage renal disease, von Willebrand disease, and aortic stenosis. Clinically, they can range from asymptomatic to frank bleed – though the latter is far less common. Treatment for the bleeders is endoscopic, while the incidentally found ones are generally left alone, though you typically won’t be the one making this call. 

Finishing off our differential is colitis. When it comes to colitis, I like to think about the “icky I’s” – ischemia, infection, and inflammatory. Of these, infection is the most common, particularly bacterial infections, as those viral gastros usually don’t bleed. This is an acute presentation, and will often be accompanied by other signs of infection. Check out the diarrhea episode for a deeper dive.

Intestinal ischemia, AKA ischemic colitis, also tends to be acute but can also be chronic, and can affect many places along the lower GI tract.For this, think about the older patient, classically the vasculopath, who has some some acute trigger (often some form of dehydration) leading to a low-flow state and manifesting clinically with abdominal pain and bloody stools. It typically resolves with rehydration and supportive care.

Don’t confuse ischemic colitis for the life-threatening acute mesenteric ischemia, which essentially the STEMI of the gut, caused from some acute occlusion of the mesenteric vasculature, typically embolic or thrombotic. This is always acute and these patients will look very sick with abdominal pain out of proportion to their clinical exam.

Finishing things off, we have the inflammatory causes of colitis, encompassing the IBDs: ulcerative colitis and Crohn’s. Age distribution is bimodal, affecting the young and old, and they present with chronic diarrhea, cramping, weight loss, fever, hematochezia, and possibly systemic features of uveitis, myalgias, arthritis, rash, and oral ulcers in the case of Crohn’s. In addition to our basic bloodwork, consider fecal calprotectin and colonoscopy, and of course, referral to GI if your suspicion is high enough.  Non-IBD related colitis can also be a consequence of radiation, so be aware of the patients with a history of significant radiation exposure.

I would want to rule out PUD, and GERD is also on the list. I’d look for NSAID use, grab a CBC to rule out anemia, grab an H Pylori test  – typically a stool or breath test (based on local practice pattern). I’d also make sure there weren’t any red flags that would warrant endoscopy, and start a trial of PPIs in addition to lifestyle counseling, particularly around diet.

This is very suspicious for a variceal bleed. Before anything, I’d be grabbing ABCs and starting a MOVIE (monitors, o2, vitals, IV, ecg). Ultimately, this is someone who needs emergent GI consultation as their disposition. Interim steps would involve supportive care with fluids or blood transfusion if needed, reversing any coagulopathy, and starting octreotide and ceftriaxone. This person needs a close eye on them.

This sounds a lot like hemorrhoids, especially with the clear risk factor of having recently been pregnant – which of course increases intra-abdominal pressure and increases the risk of hemorrhoids. It sounds more like an internal hemorrhoid, but I’d do an anorectal exam and DRE (and anoscopy if I had access to it) to see if I can confirm that. No red flags so I won’t order any investigations. First steps will be conservative, so I’d recommend stool softeners, increased dietary fibre, sitz baths, and a topical steroid cream could be helpful if they are painful or prolapsing internal hemorrhoids.

The differential is fairly broad at this point, I’m thinking primarily about angiodysplasia, but given his age and out of date screening, I’d want to keep colorectal cancer on my differential as well. I’ll start by grabbing a CBC to check for anemia. FIT would not be appropriate at this point, as we’re no longer in screening territory. We’ll be jumping straight to colonoscopy. Treatment depends on what the colonoscopy shows, at which point you’ll have GI or gen surg following along to help make these decisions. Iron supplementation can be considered in the anemic patients. Let’s say the scope comes back showing diverticulosis, there’s nothing that can be done to reverse this, we’ll simply counsel on increased dietary fiber to prevent the progression.

–          This sounds a lot like a bacterial gastroenteritis, given the presence of blood in the diarrhea. Aside from supportive care and ensuring he stays well-hydrated, I’d want stool studies, so leukocytes, blood, and, most importantly, stool culture. Depending on how sick he looks, I’d also consider CBC and possibly a hemolytic workup if I were worried about HUS.

Common things being common, we’re thinking about non-typhoidal salmonella, shigella, and campylobacter as our main bacterial causes, with less common causes including E coli, yersinia, and C. Diff. I’d want to ask about food, antibiotic, animal, and environmental exposures, sick contacts, travel history… the routine stuff.

Generally speaking, antibiotics are not indicated for suspected bacterial enteritis and can actually increase the risk of HUS in some cases. I’d also counsel against antidiarrheal agents like loperamide.  Stay hydrated, practice good hygiene, and you’re good to go.

 Rosen’s Emergency Medicine, 9th Edition

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ACG and CAG Clinical Guideline: Management of Dyspepsia. Am J Gastroenterol 2017; 112:988–1013; doi: 10.1038/ajg.2017.154; published online 20 June 2017

Gastrointestinal Bleeding. Amboss. Gastrointestinal bleeding – AMBOSS

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Katz, Philip O. MD, MACG1; Dunbar, Kerry B. MD, PhD2,3; Schnoll-Sussman, Felice H. MD, FACG1; Greer, Katarina B. MD, MS, FACG4; Yadlapati, Rena MD, MSHS5; Spechler, Stuart Jon MD, FACG6,7 ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease, The American Journal of Gastroenterology: January 2022 – Volume 117 – Issue 1 – p 27-56 doi: 10.14309/ajg.0000000000001538

  **but almost always continue