CBL 3: A PATIENT WITH HAEMATEMESIS

Question 1

Q1. What are the differential diagnoses for a history of vomiting blood?

Answer 1

• Peptic Ulcer disease (PUD) accounts for 40% to 50% of the cases.
• Of those, the majority is secondary to duodenal ulcers (30%).
• Aside from PUD, erosive esophagitis accounts for 11%,
• duodenitis for 10%,
• Varices 5% to 30% (depending if the population studied have a chronic liver disease),
• Mallory-Weiss tear 5% to 15%
• vascular malformations for 5%.

Question 2

How do you calculate alcohol consumption in units? [1]

Answer 2

Multiplying the total volume of a drink (in ml) by its ABV (measured as a percentage) and dividing the result by 1,000.

E.g.
So to find the number of units in a pint of 4% ABV beer, calculate:

4 (ABV%) x 568 (ml) ÷ 1,000 = 2.3 units

Question 3

What is his alcohol consumption in units?

He has been drinking approximately 10 cans of strong
lager a day

Answer 3

4 (ABV%) x 5680 (ml) ÷ 1,000 = 23 units

Question 4

What are likely health risks
associated with his alcohol consumption and intravenous drug use?

Answer 4

Alcohol:
- Cirrhosis
- Stroke
- Pancreatic cancer
- Stomach cancer
- Mouth, oesophageal and throat cancers
- Alcohol withdrawal

IV drug use:
- Hep B
- Hep C
- HIV

Question 5

Injecting bacteria from used or dirty needles or failing to clean the skin before an injection can cause several types of infections.

Name 3 diseases [3]

Answer 5

Cellulitis
- Group A streptococcal bacteria causes most cases of cellulitis in the general population. However, people who inject IV drugs are also at risk of cellulitis from other bacteria and even fungi.

Necrotizing Fasciitis

Endocarditis

Question 6

What were the abnormal findings you identified on general physical
examination and abdominal examination?

Answer 6

• jaundiced
• hypotensive (from bleeding)
• tachycardic to compensate for the bleeding
• shifting dullness: ascites
• tremor:
  
  • correlates with liver disease

Question 7

Why does a patient with decompensated liver often present with jaundice?

Answer 7

In liver cirrhosis, portal blood flow is distorted accompanied by a decrease in hepatic clearance of bilirubin.

In addition, portosystemic shunting as well as splenomegaly results in an increase in hemolysis and production of bilirubin.

These together result in an increase in the concentration of unconjugated bilirubin in serum.

In advanced cirrhosis, glucuronyl conjugation of bilirubin and biliary excretion of conjugated bilirubin are markedly impaired and jaundice appears

Question 8

What blood results signifiy an upper GI bleed? [1]

Answer 8

Raised blood urea nitrogen (BUN): urea:creatitine raised

The higher the ratio, the more likely is from upper GI bleed

A BUN/Cr ratio of greater than or equal to 36 suggests upper gastrointestinal bleeding, whereas a ratio of less than 36 is not helpful in locating the source of bleeding.

Question 9

Why does an raised urea:creatitine ratio suggest an upper GI bleed but not a lower one? [1]

Answer 9

Bleeding from colon; Hb doesn’t get digested to urea there

Question 10

What would a differential diagnosis of raised urea:creatitine? [5]

Answer 10

INCREASED UREA:CREATININE RATIO – (Drivers Can use GPS)

• dehydration/prerenal failure
• corticosteroids
• GI haemorrhage
• protein-rich diet
• severe catabolic state

Question 11

Which pathologies indicate that a liver is decompensated? [5]

Answer 11

Characterised by:

• jaundice
• ascites
• hepatic encephalopathy
• hepatorenal syndrome
• variceal haemorrhage

Question 12

When is giving platelets indicated? [2]

Answer 12

Platelets are given in active bleeding plus thrombocytopenia (platelet count less than 50)

Question 13

Q8. What will be the key goals of immediate management of this patient?

Answer 13

The initial management can be remembered with theABATED mnemonic:

• A–ABCDE approach to immediate resuscitation
• B–Bloods
• A–Access (ideally 2 x large bore cannula)
• T–Transfusions are required
• E–Endoscopy (within 24 hours)
• D–Drugs (stopanticoagulantsandNSAIDs)

Question 14

How do you acute treat oesophageal bleeding? [6]

Answer 14

blood transfusion

PLUS –
terlipressin or somatostatin analogue

PLUS –
prophylactic antibiotics

PLUS –
endoscopy + endoscopic variceal band ligation

CONSIDER –
balloon tamponade or Danis stent

CONSIDER –
transjugular intrahepatic portosystemic shunt

Terlipressin: Treat
Propanolol: Prevent

Question 15

When is giving fresh frozen plasma indicated in a patient? [2]

Answer 15

Give fresh frozen plasma (FFP) to patients who are actively bleeding and have a prothrombin time (or international normalised ratio) or activated partial thromboplastin time >1.5 times normal

Question 16

What additional investigations will you request to assess this patient’s
underlying disease? [2]

Answer 16

OGD: Oesophago-Gastro-Duodenoscopy

Question 17

What time frame do you conduct OGD in variceal bleeding? [1]

Answer 17

If the patient is unstable with severe acute upper GI bleeding, do this urgently, immediately after resuscitation.[35][39]

For all other patients with upper GI bleeding, do this within 24 hours of admission

Question 18

Q11. Explain the likely reasons for this patient being drowsy?

Answer 18

Hepatic encephalopathy

Under normal conditions, ammonia is produced by bacteria in the gastrointestinal tract (e.g., breakdown product of amines, amino acids, purines, and urea) followed by metabolism and clearance by the liver. In the case of cirrhosis or advanced liver dysfunction, however, there is either a decrease in the number of functioning hepatocytes, portosystemic shunting, or both, resulting in decreased ammonia clearance and hyperammonemia.

Once ammonia crosses the blood-brain barrier, it has multiple neurotoxic effects. These include alterations in molecular transport (e.g., amino acids, electrolytes, water) in astrocytes and neurons, increased synthesis of glutamine from glutamate by astrocytes, inhibition of excitatory and inhibitory postsynaptic potential generation, impaired amino acid metabolism, and impaired energy utilization as a result of increased GABA activity.

Question 19

What is the first, second and third line treatment of HE? [3]

Answer 19

1ST LINE –
* supportive care + reversal of precipitating factors + investigation of alternative causes of altered mental status

PLUS –
lactulose

2ND LINE –
* supportive care + reversal of precipitating factors + investigation of alternative causes of altered mental status

PLUS –
rifaximin ± lactulose

3RD LINE –
supportive care + reversal of precipitating factors + investigation of alternative causes of altered mental status

PLUS –
L-ornithine-L-aspartate or branched-chain amino acids

CONSIDER –
rifaximin ± lactulose

Question 20

Describe the MoA for the treatment of HE with the following

• rifaximin
• lactulose
• L-ornithine-L-aspartate

Answer 20

• rifaximin: antibiotic; Cirrhotic patients have altered gut microbiota that could affect their cognitive capacity.19 The administration of antibiotics in HE is based on altering the bacterial flora and reducing endotoxaemia by decreasing the production and absorption of gut-derived neurotoxins.
• lactulose: reduce the intestinal production/absorption of ammonia
• L-ornithine-L-aspartate: optimizing liver ammonia removal by residual hepatocytes and stimulates ammonia removal by muscle.

Question 21

What is the difference in presentation of Hep B and Hep C? [2]

Answer 21

Hep B is more insidious - causes long term scarring of the liver until decompensated

Hep C is more acute