UGIB Q&A

 Q1. What is the anatomical level to ddx upper and lower GI bleed?

• at the duodenal-jejunal junction at the ligament of treitz
• UGIB are bleeding proximal to ligament of trietz
• LGIB can also cause from bleeding of small bowel, 
• those bleeding distal to the ligament of treitz can consider as lower GI bleed

Q2. What are your aims in assessment for a patient with UGIB?

• to assess if patient is stable
• if they are in active bleeding
• is it variceal or non variceal bleed

Q2. How to access the stability of the patient?

• vital signs
• mental status
• urine output. 

all these could help chart the grade of shock clinically - especially Heart Rate !

- if you notice from the table below. 

• the heart rate could already classify the type of shock into class I and class II and it also shows us "THERE is BLEEDING" 
• BP came 2nd as when we realise BP drop, shock is already grade 3. 
• and blood loss has already reached at least 1.5L
• if grade 2 systolic pressure is still normal and diastolic is low : 

Q3.  How do we access if they are still actively bleeding?

• colour of hemetemesis
• fresh blood
• coffee ground colour

• amount of hemetemesis
• large?

** anemic Sx is not enough to diagnose if they are still having active bleed. as acute bleed will cause collapse first even before they have the symptoms. 

Q3a. If patient has history of melena, is it usually active bleed or already stopped?

• Yes, usually it is active and has maroon colour, also called fresh melena 

• Blood is irritative to gut, they either comes out from the mouth or the anus. 
• opposite to fresh melena is old melena or stale melena
• Old melena: black is colour, and towards formed stool. 

Q4. Some of the black stool presentation still could be active bleed, what type of presentation we can see in this type of patient?

• large amount of black stool and watery
• also called watery melenic stool 
•  patient family/ Staff nurse can have complain of patient changing diapers multiple times however soaked. although it is not red, still considered active bleed. 
• can happen in both UGIB and LGIB

Rule out UGIB first as 80% of PR bleed is from upper GI, 20% from LGIB

•  Despite resuscitation, patient still has persistent tachycardia

Q5. How to access the source of bleeding, variceal vs non variceal?

• Patient's History
• variceal bleed: large amount of fresh hematemesis, has copious blood
• usually described as bowls of blood or cups of blood. 
• massive bleeding usually came from varices
• however it is usually PAINLESS
• causes:
• any history of liver disease: jaundice, stigmata of liver disease, portal hypertension secondary to chronic liver disease, hep B
• high risk behaviour
• non variceal bleed: cause is usually peptic ulcer disease (PUD)
• pain 
• have hx of epigastric pain
• cause: 
• long standing NSAIDS usage/ steroids usage
• hx of hyperuraemia (CKD)

Why do we need to differentiate variceal and non variceal bleed?

• variceal bleed: need urgent OGDS (no active bleed)
• non variceal still can wait and scope within 24 hours 

Q1: if patient is suspected with variceal bleed, he has active bleeding and continuously vomit blood. 
his vitals are not stable. Outline your acute management

• ABC
• A: If airway compromise to intubate , to secure airway
• insert 2 large bore IV cannula
• blood taking(FBC+coag) + GXM + safe O blood (preferably cross match blood)
• fluid resus with crystalloid then add colloid while waiting for blood and blood products
• can refer to the fluid and electrolyte QnA link here
• to arrest and stop the bleeding
• inserting sengstaken tube

• vital signs monitoring

THEN SEND pt to ICU once he is stable

since patient having active bleed, he is not fit for OGDS, as we couldnt view the source of bleeding clearly. the active bleed will obscure the lens of OGDS

** differences between UGIB 2 to PUD , pt who has variceal bleed, you will need urgent OGDS as long as they have no active bleed. those with UGIB 2 to PUD we still can wait and scope within 24 hours. 

Q1a: what do we do next once patient in ICU- medical therapy?

• start IVI octreotide
• on pt with and without active bleed. 
• replace blood loss and correct coagulopathy
•  FFP
• start antifibrinolytic agent eg: IV tranxenemic acid 500mg TDS
• transfused if needed
• start PPI infusion
• reduces mortality in variceal bleed
• due to reduce in acid in stomach, it also lower down incidence of rebleeding 
• start antibiotic
• as pt usually immunocompromised due to hepatic failure
• in various study shows abx may reduce mortality rate in bleeding pt
• 
  
• beta blocker
• usually given after patient recover
• as might cause low systemic blood pressure in acute setting

Q2: how does octreotide help with the bleeding?

• it inhibits release of glucagon 
• glucagon is splanchnic vasodilator
• when splanchnic circulation is reduced it will cause reduce in portal pressure

Q3: how long can we place the sengstaken tube?

• 48hours
• longest: 72 hours/3days
• as it is just a temporary solution to the problem. 
• however have to deflate the esophageal balloon intermittently every 2 hours
• important to reinfate to prevent hypoxia and necrosis of compressed tissue
• and esophageal perforation is fatal cause it is in the thoracic cavity if perforated. 

Q4: what is the PPI infusion that is given

• IVI pantoprazole 80mg stat then 8mg/hr
• GOLD STANDARD to give the regime stated above. 
• if no pantoprazole, omeprazole is also accepted

Q4b: why PPI is important and superior as medical treatment?

• proton pump inhibitor, blocks the H+/K+ ATPase
• inhibition is irreversible. 
• therefore causes profound and prolonged reduction of acid production

CPG malaysia for UGIB mx

do review back the summary done last time and come test yourself here!'https://yu4med.blogspot.com/2021/04/ugib.html