A 51-year-old male with a history of cirrhosis secondary to Hepatitis C is admitted for the first time with haematemesis. His gastroscopy is complicated by aspiration. He is admitted to ICU ventilated.

The following results were obtained:


Patient Value

Adult Normal Range





7.35 – 7.45


109 mmHg (14.1 kPa)


29.0 mmHg (3.87 kPa)*

35.0 – 45.0 (4.60 – 6.00)




10.0 mmol/L*

22.0 – 26.0

Base Excess

-17.0 mmol/L*

-2.0 – +2.0


4.5 mmol/L*

0.5 – 1.6


144 mmol/L

135 – 145


4.4 mmol/L

3.5 – 5.0


114 mmol/L*

95 – 105


11.0 mmol/L*

3.5 – 6.0


Patient Value

Adult Normal Range


17.0 mmol/L*

3.0 – 8.0


110 µmol/L*

45 – 90


23 g/L*

35 – 50


41 g/L*

60 – 80

Total bilirubin

56 µmol/L*

< 26

Aspartate transferase

67 U/L*

< 35

Alanine transferase

101 U/L*

< 35

Alkaline phosphatase

78 U/L*

30 – 110

g-Glutamyl transferase

36 U/L

< 40

Calcium (total)

2.13 mmol/L

2.12 – 2.62

Interpret these results, giving likely reasons for the abnormalities. (40% marks)

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College answer

UEs: low HCO3 indicates metabolic acidosis, elevated Urea to Cr ratio likely related to GIT bleed (other causes are dehydration, excessive diuretics, high protein diet, steroids), elevated Cr likely due to kidney injury (likely pre-renal, renal causes possible (including hepatorenal syndrome), post-renal causes less likely).

ABG: There is an increased anion gap metabolic acidosis (20).
The delta ratio is 0.57 indicating a mixed high and a normal anion gap metabolic acidosis. High anion gap component likely secondary to shock from hypovolaemia, possibly sepsis from aspiration. Normal anion gap component may reflect saline resuscitation, renal impairment. There is partial respiratory compensation (expect the CO2 to be 23=1.5xHCO3 + 8), which is likely due to mechanical ventilation. There is an increased Aa gradient, presumably because of the aspiration. The elevated lactate may represent shock, liver impairment or treatment with catecholamines. Mildly elevated glucose presumably a stress response.

LFTS: Low albumin could indicate chronic synthetic liver disease or be due to acute sepsis/SIRS or related to volume expansion with non-albumin fluids. Elevated ALT related to hepatocellular injury most likely Hep C plus/minus hypoperfusion related to the haematemesis. Elevated bilirubin likely related to chronic cirrhosis (pre-hepatic causes are possible (including transfusion), and biliary obstruction is less likely as GGT/ALP not elevated).


This college answer is by far the best biochemistry answer CICM examiners have ever written, and should represent some kind of standard for all future examiners' answers. They will all be measured against it. 

Let's start with the gas:

  • The A-a gradient is increased. (713 × 0.4) - (29 / 0.8) - 109 = 139.9 mmHg.
    However, the patient is not hypoxamic.
  • The patient is acidaemic
  • There is a severe metabolic acidosis (SBE is -17.0)
  • The CO2 is appropriately low, but not quite low enough; it should be 23 mmHg, irrespective of whether your compensation calculation involves subtracting the SBE from 40 or calculating (HCO3-  × 1.5) + 8. Ergo, there is also a mild respiratory acidosis. Because the patient is mechanically ventilated, this technically is the fault of the intensivist. 
  • The anion gap is (144 - 114 - 10) = 20, i.e. it is elevated.
  • If one accepts 12 as the ideal normal AG, the delta ratio is therefore (20-12)/(24-10) = 0.57, which suggests that this metabolic acidosis is mixed, a combination of a HAGMA and NAGMA. 
  • The lactate is raised, which is surely contributing to the anion gap elevation.

Thus, this is an ABG of a patient who is

  • Hypoxic due to aspiration
  • Acidaemic due to underventilation and due to poor lactate clearance by a chronically diseased liver
  • Hyperlactataemic due to a combination of poor hepatic clearance and haemorrhagic shock
  • Hyperchloraemic most likely due to normal saline resuscitation

As for the biochemistry:

  • The urea is raised, more so than the creatinine, which suggests that this patient is digesting some of their own blood.
  • Creatinine is raised, which suggests there is some mild degree of renal impairment
  • Albumin is low, which is appropriate in the setting of cirrhosis
  • Total protein is also low, which again is not unexpected and may reflect a poor underlying nutritional state
  • The bilirubin is raised, which suggests a failure of hepatic synthetic function
  • The LFTs are otherwise only trivially abnormal, suggesting that there has been no acute kidney injury
  • The calcium is borderline, suggesting some of it has been depleted in the clotting cascade.