Question 5

College comments

Syllabus topic/section: 2.1.11 Haematological and Oncological Intensive Care 2.1.13 Trauma Intensive Care

Discussion: 

A structured approach was necessary here and answers that were poorly structured did not score as well. Candidates who did well noted the need for explanation of the key abnormalities, not simply an outline as directed in the stem. Similarly, part (b) called for a discussion of the additional investigations rather than simply providing a list.

Candidates are reminded to read the question carefully and with particular reference to the glossary terms to ensure they have the best opportunity to include the relevant information in their answers. The rubric is provided to aid the candidate's future study.
 

Rubric

Interpretation

"Outline" and "explain" is a strange mixture of exam vocabulary terms, as surely "explain" alone would have been enough. And which abnormalities are "key", versus those which are non-key? The rubric offers some answers.

Without too much effort, we can see the patient is clearly haemolysing.

• There is anaemia. Hb is 64
• The MCV is at the borders of elevated; these cells are satisfyingly plump. But you would be forced to describe them as normocytic and normochromic.
• The CRP, fibrinogen, platelets and WCC are elevated (neutrophilia is the dominant feature), suggesting some kind of proinflammatory state
• The presence of metamyelocytes (immature neutrophils) suggests bone marrow stress, with these white cells rushed to production
• Nucleated RBCs and reticulocytes similarly suggests a pressure to produce cells, suggesting there is a state of accelerated erythropoiesis
• The electrolytes are trivially deranged; only calcium is marginally low, which suggests that it may have been consumed in clot production (but there are numerous other possibilities)
• Urea and creatinine are elevated, with a disproportionally higher urea, suggestive of either  accelerated protein catabolism or a volume-depleted state (urea:creatinine ratio in mmol:µmol is 0.13, where anything over 0.1 is considered to be consistent with pre-renal causes)
• The serum proteins are depressed, which is totally on brand for anybody with critical illness, and is probably a "non-key abnormality"
• The conjugated bilirubin is lower than the total bilirubin, which suggests a significant proportion of the bilirubin is unconjugated, meaning that cholestasis is not responsible for this hyperbilirubinaemia
• The LFTs are deranged in a pattern that is not entirely consistent with cholestasis, and noteably the LDH is raised, which supports the idea that haemolysis is occurring. 

Judging by the rubric, this was all unnecessary, and the most important elements were:

• Normocytic normochromic anaemia
• Haemolysis, suggested by raised LDH, conjugated/unconjugated bilirubin ratio, presence of reticulocytes and nucleated RBCs
• Inflammation or infection, suggested by raised CRP, fibrinogen, leukocytosis
• Bone marrow stress (left shift of neutrophils)
• AST: ALT ratio > 2:1 and raised GGT, consistent with alcohol-related liver disease 
• Pre-renal AKI (urea:creat >0.1)
• Hypoalbuminaemia consistent with critical illness
• Normal phosphate, suggesting that rhabdomyolysis is not the source for LHD AST and renal dysfunction

This 69-word answer would have fit within the 4-mark timeframe and would have hopefully satisfied the pickiest of examiners.  Contrary to the rubric, it would have been impossible for the candidates to discriminate between intravascular and extravascular haemolysis here, as this would require further investigations. 

b) 

"Discuss" here suggests that advantages, disadvantages and controversies were sought, which would have been hard to do in three minutes. In any case, the investigations for anaemia are largely uncontroversial. "Discuss" here probably meant "include your rationale for the investigations", which should probably have looked something like this:

• Haemoglobin production
  • Iron studies, B12, folate
  • Not likely to yield the cause of the anaemia, but will be useful to guide therapy to correct it
• Blood loss
  • examination (eg. drains), CT of the injured areas, endoscopy, angiography
  • They told us the patient was haemodynamically stable, but that does not exclude a slow ooze from abrasions or oesophageal varices
• Haemolysis
  • DAT, blood film, haptoglobin, RBC antigen chimaerism (eg. following a transfusion of uncrossmatched or incorrectly matched blood)
  • A specific review of the post-trauma transfusion history, looking for massive transfusion and/or a history of rushed matching or uncrossmatched O-negative transfusion
  • Rapid fluorescent spot test and methaemoglobin level for G6PD

c)

The management of this anaemia would have been dependent on the kind of anaemia you convinced yourself this was, on the basis of investigations in b). Some sort of broad answer to cover all possibilites would have had to look like this:

• Assure that haemostasis is achieved
• Exclude transfusion complications and assure correct matching, and then transfuse red cells to achieve a haemoglobin of >70g/L
• Exclude anaemia of chronic inflammation and infection, and then replace haematinics to reinforce erythropoiesis (iron infusion, B12 and folate replacement)
• If an autoimmune cause of the anaemia is revealed, the management would differ depending on the cause, and could consist of:
  • Corticosteroids and/or splenectomy for warm haemolysis
  • Rituximab for cold haemolysis
  • Plaspmapheresis for acute fulminant antibody-mediated haemolysis
  • Eculizumab for atypical HUS