Question 1a

College Answer

Principles of management include resuscitation (of someone who may well have lost >25% of blood volume), establishing a diagnosis, and definitive treatment while avoiding therapies that might worsen his underlying condition.

Resuscitation includes assessment of airway protection and breathing adequacy, which combined with neurological impairment indicates need for emergency intubation.

Circulatory support requires adequate intravenous access, but may not need to be too aggressive (as excessive resuscitation may worsen portal hypertension), and could be guided by factors including usual blood pressure (? accept MAP of 60 mmHg), urine output, and other signs of circulatory compromise.

Temporary use of a Sengstaken Blakemore tube (or equivalent eg Minnesota) may be considered if blood loss is uncontrollable. Invasive monitoring may be useful, but is not necessary in the early phase of resuscitation.

Establishing  a  diagnosis  for  the  cause  of  bleeding  includes  immediate  examination  (signs suggesting non-GI haemorrhage, chronic liver disease), history (from family/observers) of immediate event and possible precipitants (drugs, retching etc). Differential diagnosis of causes for jaundice should be considered (including hepatitic and toxins). More detailed history and examination will need to be completed later.

Immediate commencement of therapy (eg. intravenous vasoconstrictor such as somatostatin or vasopressin) should be considered while organising urgent endoscopy (which will usually result in banding or sclerotherapy for varices, and injection for some other pathologies). Initial investigations should include cross match, coagulation tests, full blood count, urea & electrolytes, liver function tests, blood glucose and paracetamol level. An ascitic tap should be undertaken early for microscopy and culture (as infection may well be present). Some rationale should have been given for the investigations listed.

Candidates should be aware of therapies that may be specifically required (correction of coagulopathy [FFP &/or platelets], prophylactic antibiotics, laxatives eg. lactulose; beta-blockers once stable, proton pump inhibitors) or contraindicated (sedatives worsening hepatic encephalopathy).

Discussion

I have attempted to force the coherent college answer into a familiar system.

(a)       Outline the principles of, and rationale for, the initial management of this patient.

• Attention to the ABCS, with management of life-threatening problems simultanous with a rapid focused examination and a brief history. History will focus on determining whether the source of the bleeding was indeed the gut (rather than a tracheal or bronchial source) and whether the vomiting preceded the hematemesis (which would be suspicious for a Mallory-Weiss tear or Boerhaave's syndrome)

• Airway:
  • This patient is likely to have hematemesis again; the airway needs to be protected
• Breathing/ventilation
  • Once he is intubated, ventilation settings will depend on the specifics of gas exchange and lung compliance
• Circulatory support
  • The inital stages of resuscitation will consist of replacement of blood and blood products
• Supportive management
  • Sedation should consist of anaesthetic agens with a short half-life and no long-lasting metabolites, such as propofol and remifentanyl
• Specific investigations
  • CXR to confirm ETT position and rule out GI perforation
  • FBC, G&H, coags, fibrinogen, EUC and CMP
  • Ultrasound of the abdomen to investigate the severity of portal hypertension
• Specific management
  • This patient requires urgent gastroscopy and banding or sclerotherapy of the varices
  • If a gastroscopy cannot be performed urgently, he will need to have a CT angiogram, with a view to proceed to angioembolisation of the bleeding vessels.
  • If blood loss is uncontrollable and gastroscopy/angioembolisation is delayed, a Sengstaken-Blakemore tube can be advanced and an attempt to tamponade the bleeding can be made.
  • Lactulose should be used to decrease the likelihood of hepatic encephalopathy