This chapter deals with the investigations and resuscitation of massive gastrointestinal bleeding. For the purposes of having a firm definition, anything below the ligament of Treitz is taken as the "lower" tract.
In terms of relevance for the CICM fellowship, massive GI bleeding is probably not a high-yield subject matter (even though it forms a major part of our daily workload). Historically, it has appeared in several SAQs:
Question 1 from the first paper of 2017 asked for four causes of massive GI haemorrhage. There is a long possible list of such causes. The list offered here was generated mainly using Oh's Manual, but contains conditions which are not listed in the canonic Chapter 42 (pp. 487, "Acute gastrointestinal bleeding" by Joseph JY Sung).
Endoscopy is best. Barium investigations are useless. Why?
Generally, postero-inferior duodenal wall ulcers and high lesser curve of stomach ulcers tend to rebleed most vigorously, owing to the presence of large arteries nearby.
In order to catch an upper GI bleeder on an angiogram, the rate of bleeding should be greater than 0.5ml/min.
Identifying the high risk patient, whom to cart away to the endoscopy suite:
If endoscopy fails, or there is evidence of perforation, the next move is surgery.
Nobody seems to agree precisely when to make this call. In general, if you are taking a patient to theatre for an emergency salvage surgery after an upper GI bleed, their mortality will be around 15-20%.
All these methods seem roughly equivalent in their effectiveness.
It is generally thought that the use of all three methods on the same lesion gives the greatest reduction in rebleeding risk.
Question 1 from the first paper of 2017 asked specifically for "clinical indicators for risk of re-bleeding", which is a fancy way of asking for a list of risk factors. A good paper by Augustine et al (2010) actually presents an entire table of studies which investigated the various prognostic indicators which predict rebleeding in acute variceal haemorrhage. Re-bleeding in the case of many of these was rolled together into "5-day failure", a sort of composite endpoint together with mortality, which it obviously has some sort of effect upon. This was remixed into the following list of predictive features:
Tranexamic acid plays no role - there is good evidence that it is ineffective.
In general, drugs can prevent rebleeding post endoscopy, but they usually play little role in massive haematemesis, and on their own are ineffective.
Endoscopy is useless. You will never find the bleeder in that mess of blood and stool. Colonoscopy in acute gastrointestinal bleeding seems to be a waste of time.
Tc-99 Red Cell Scan is a way of radiolabelling RBCs and observing where they go. Apparently, it is identifies a GI bleeder 80% of the time.
Angiography is the gold standard, as it can identify a bleeder 85% of the time, and allows one to launch a bunch of Gelfoam into the offending artery, thus putting an end to the bleeding.
In order to see the characteristic "blush" of contrast, you need to be bleeding at a rate of at least 0.5ml/minute.
Colonoscopy is the ideal treatment option for patients in whom the bleeding is minor, and who have been prepped sufficiently. It is probably the least invasive treatment option.
Angioembolisation is the best option for patients who are bleeding too rapidly to wait for bowel prep. In these people, the rate of bleeding - which makes endoscopy futile - also makes angiography more accurate.
Surgery is the option of choice for diverticular disease, unmanageable polyps and malignancies, and in situations where AVMs or inflammatory bowel disease lesions are not amenable to endoscopic management.
Balloon-occluded retrograde transverse obliteration (BRTO) is mentioned by the college in their answer to Question 1 from the first paper of 2017 as a "new technique and still undergoing evaluation", which is weird because we have been doing this since 1996 (Haruta et al). It is basically a technique whereby the interventional radiologist accesses a portosystemic shunt vein and inflates a balloon in it. Usually the gastric fundus varices drain into the left renal vein via a gastrorenal shunt, and that makes it all very convenient. With the balloon inflated, the radiologist can then inject sclerosant in a retrograde fashion into the the varix. Unfortunately, the usual sclerosant (ethanolamine oleate again) can cause anaphylaxis, renal failure and pulmonary oedema. Once the balloon is released, some sclerosant may make its way into the systemic circulation. This does not seem to impact much on outcomes, as Park et al (2015) reviewed the evidence and had found this technique "safe and efficacious".
Factor VIIa is also mentioned by the college in their answer to Question 1 from the first paper of 2017, though they themselves moderate their enthusiasm by pointing out that it has "questionable efficacy". If one reads the papers (eg. Bosch et al, 2008) this would certainly seem correct (there was no effect on any primary endpoints). The mention of this option in the college answer is itself questionable, as it is promoted as an option for controlling a re-bleed even when trial results "do not support the routine use of rFVIIa in this setting"