Note: The following is an educational resource only, intended for use by medical and physician associate (PA) students for exam preparation. It is not a clinical guideline or substitute for medical training.
This was the first acute emergency I had to deal with as a junior doctor - I was all alone on an unfamiliar ward, my second ever day as a doctor, this in the morning and sepsis in the afternoon. It’s very frightening too - many medical emergencies can be somewhat occult, but upper GI bleeds are fairly bombastic and when someone is vomiting fresh, red blood in front of you it freaks you out. But we still have to deal with it.
GI bleeds do not necessarily fit our typical structure of these videos very well, because there are only really two key signs that you’ll see. More commonly I have seen melaena, that is the dark black, tarry looking stools associated with digested haemoglobin if blood has passed through into the lower digestive tract, or haematemesis, that is the vomiting of blood. This may be in small or large amounts too - the person may be retching small amounts into a sick bowl, or hosing large amounts all over the bed.
This raises an obvious question - why might this happen? What might predispose someone to a sudden upper GI bleed? While there are many causes, I think there are a few that it’s good to be aware of specifically for finals. The first is peptic ulcers - classically linked to either overuse of NSAIDS such as ibuprofen or naproxen, or infection with Helicobacter pylori. These ulcers are basically a sore that develops in the mucosa of the stomach, or the first parts of the duodenum, and they can erode through blood vessels causing significant bleeding - especially with duodenal ulcers, they can lie essentially on top of the gastroduodenal artery which is a classic exam question.
The second major cause of upper GI bleeding to know is oesophageal varices. These are enlarged submucosal veins that sit in the inferior third of the oesophagus, which most often appear due to portal hypertension, in settings such as chronic liver disease like cirrhosis or chronic right sided heart failure. When the pressure becomes too much, these veins simply burst open and start haemorrhaging enormous amounts of blood.
So what do we do in cases of upper GI bleeding? The main focus is really simple, which is firstly to stop the bleeding, and secondly to replace losses and maintain volume in the circulation. Let’s take a look at an exam scenario and work our way through it.
WORKED SCENARIO
You are a Foundation Year 1 doctor who has just arrived at work on the hepatobiliary surgery ward. The Charge Nurse appears and asks you to hurry to see one of the patients, Mr Sorinola. Mr Sorinola was admitted for management of his ascites secondary to severe cirrhosis and is awaiting an ascitic drain procedure. The nurse tells you that he has just vomited 1.5 litres of fresh blood into a vomit bowl and is continuing to retch.
We seek Mr Sorinola very quickly and examine him using an A-E approach.
A: Airway patent, patient maintaining own
B: RR 24, O2 sats 98% OA, symmetrical chest expansion, good inspiratory effort
C: BP 88/58, HR 120. Pulse weak and regular, HS I+II+0
D: Temp 37.4, PERL, BM 7.8
E: Vomit bowl full of bright red blood.
So what we have here is a man who is vomiting large amounts of blood and is haemodynamically unstable, as we can tell from his systolic blood pressure of less than 90 and his tachycardia.
What are we going to do? It makes sense to call for help as soon as possible here. Specifically we’re going to activate the massive haemorrhage protocol - your local trust may have specific guidelines on this so follow those - the JPAC, one of the advisory committees for blood transfusion, suggests that a pragmatic definition of when to activate this may include the loss of 70ml/lg within 24 hours, 50% of total volume in less than 3 hours, or indeed a systolic BP of less than 90 or a heart rate of 110 or more. We’ll cover the MHP in more detail in another video, but for the sake of this context, it’s going to get us the blood products we need to appropriately transfuse our patient, typically 4 units of red cells and 2 units of fresh frozen plasma coming first.
On top of that of course, let’s call our registrar or anaesthetics for some more experienced hands.
And we need to transfuse because resuscitation is the name of the game here. The main goal is supporting circulation, so getting two wide bore venous cannulae in is very important - to illustrate the difference this can make, pushing a litre of fluid through a blue cannula, that is a 22G cannula takes 22 minutes. If instead we put a grey cannula in that reduces to 6 minutes, and you can push 1L through an orange, a 14G cannula in just 3½ minutes.
An urgent set of blood markers need to be taken so we know what we need to give - including a full blood count, group and save, coagulation screen and so on. Cross matched and group appropriate blood is the best thing we can give, but obviously O-negative blood is available in emergencies.
So now let’s think about management - what are we going to do about the bleeding site? The answer is usually going to lie with an endoscopy. This is going to mean calling the on-call endoscopist, which may be a gastroenterologist or a surgeon, and they may ask for the Glasgow-Blatchford score.
This is a risk stratification tool for people with an upper GI bleed and helps to decide whether or not they are likely to need intervention. It’s worth noting that use of this score is somewhat controversial for inpatients, but I have been asked for it before.
We’re doing the endoscopy ultimately to decide whether or not the bleeding is variceal, that is coming from ruptured varices. Once they have had endoscopy, you may then decide to calculate the Rockall score, which estimates the risk of a rebleed as well as the mortality risk for that patient.
If we assumed the bleeding was non-variceal, and was perhaps coming from a pseudoaneurysm or ulcer, the bulk of treatments are done during the endoscopy. The endoscopist may decide to thermally coagulate the site using heat, use surgical clips or inject medicines like adrenaline to cause vasoconstriction and stop the bloodflow. Once the bleeding has been quelled, the patient should be given a proton pump inihibitor such as omeprazole to protect the lining of the stomach and promote recovery.
But in our patient the endoscopist finds that the cause of the bleeding is ruptured oesophageal varices, which have likely developed secondary to our patient’s cirrhosis.
Before we even get to this stage however, if you suspect your patient has bleeding oesophageal varices, NICE recommends giving terlipressin immediately to constrict the smooth muscle in the vessels and reduce bloodflow, alongside prophylactic antibiotics as per your trust guidelines. Oesophageal varices are usually managed via band ligation, in which a rubber band is placed around the bleeding vessel which cuts off the bloodflow and stops the bleeding. If this does not work, then TIPS (a transjugular intrahepatic portosystemic shunt). As you might be able to decipher from the name, this procedure involves diverting (shunting) bloodflow from the portal vein to the hepatic vein, which allows blood to bypass the liver and therefore reduces pressure in the portal system and thus the bloodflow to the varices.
The only other (somewhat rogue) option is a balloon tamponade, sometimes known as a Sengstaken-Blakemore tube. This is essentially a tube inserted through the mouth or nose that contains a balloon, which is passed through to the stomach - one balloon inflates inside the stomach, and another inside the oesophagus, putting pressure on the gastrooesophageal junction and stopping bloodflow to the varices. I’ve never seen it used in practice, but they are there in case of emergency.
After all of this review NSAIDS, anticoagulants, antiplatelets, come up with a safety netting plan and refer to appropriate specialists for aftercare and further planning.