Question 23

A 59-year-old patient was involved in a motor vehicle accident (MVA). Injuries included chest trauma, multiple long bone fractures and a decreased level of consciousness.

On arrival to the Emergency Department observations were:

  • Blood Pressure  75/60 mmHg
  • Heart Rate 120 beats/min
  • Respiratory Rate 30 breaths/min
  • Temperature 35.1°C

Initial investigations reveal:


Patient Value

Adult Normal Range


95 g/L*

120 – 160

Mean Cell Volume

82 fl

80 – 94

White Cell Count

15 x 109/L*

4.0 – 11.0

Platelet count

188 x 109/L

150 – 350


Patient Value

Adult Normal Range

Prothrombin Time

20.0 secs

12.0 – 16.5

International Normalised Ratio


0.9 – 1.3

Activated Partial Thromboplastin Time

52.0 secs

27.0 – 38.5


0.8 g/L

2.0 – 4.0


Patient Value

Adult Normal Range





7.35 – 7.45


150 mmHg (20 kPa)


33.0 mmHg (4.4 kPa)*

35.0 – 45.0 (4.7 – 6.0)




14.0 mmol/L*

22.0 – 26.0

Base Excess

-6.0 mmol/L*

-2.0 to +2.0


5.0 mmol/L*

0.5 – 1.3


139 mmol/L

135 – 145


3.8 mmol/L

3.5 – 5.0


105 mmol/L

95 – 105


5.8 mmol/L

3.5 – 6.0

Ionised Calcium

0.7 mmol/L*

1.0 – 1.1

a) Explain the abnormalities in the above investigations. (30% marks)

b) Outline your fluid and haemostatic resuscitation for this patient. Include your rationale in your answer. (70% marks)

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College answer

Not available.



So let's go through those abnormalities and list their explanations. This list is probably longer than what the examiners would have expected, as this 3-mark question could not possibly have expected all the problems to be listed. One can assume that for a full mark perhaps only six or so important points would have to have been raised from the investigations, and these are identified at the very end.

  • The patient is anaemic, because trauma.
  • The MCV is on the lower side of normal, which makes you wonder whether some of the anaemia is chronic
  • The white cell count is elevated, which is likely a  neutrophilia due to the acute stress
  • The INR is elevated, as is the APTT, and the fibrinogen is low, suggesting that the coagulopathy is due to factor depletion. Two possible (and not mutually exclusive) reasons could be consumption in clotting, and dilution by prehospital crystalloid resuscitation

Now, the gas:

  • The A-a gradient is increased. (713 × 0.5) - (33 / 0.8) - 150 = 165 mmHg.
    However, the patient is not hypoxemic. This A-a gradient can be explained by the chest injuries, and could represent pneumothorax, lung contusion, aspiration, fat embolism, or simply the poor V/Q matching of the severely empty patient.
  • The patient is mildly acidaemic
  • There is a mild metabolic acidosis (SBE is -6.0)
  • The CO2 is appropriately low;  it should be 34 mmHg if you calculate it by subtracting the SBE from 40. If you are calculating it using Winter's formula, it is  (14  × 1.5) + 8 = 29, in which case you'd think there is a mild respiratory acidosis. It is impossible to know which of these approaches the college wanted us to use, but - looking at the stem - the narrative that fits best is the one with the decreased respiratory drive, as the patient is said to be obtunded.
  • The anion gap is (139 - 105 - 14) = 20, i.e. it is elevated.
  • The lactate is raised, which is surely contributing to the anion gap elevation. The lactate elevation can be explained by haemorrhagic shock.
  • If one accepts 12 as the ideal normal AG, the delta ratio is therefore (20-12)/(24-14) = 0.8, which suggests that this metabolic acidosis is mixed, a combination of a HAGMA and NAGMA (but trending towards a pure HAGMA). This extra little contribution from non-anion-gap causes can be explained by a couple of litres of pre-hospital saline, which fits the "dilutional coagulopathy" narrative.
  • Lastly, the ionised calcium is low, mainly because calcium is an essential cofactor in clotting, and will be depleted by massive blood loss. Given that we are made to believe that these results were taken "on arrival to the Emergency Department", the alternative explanation in trauma (citrate due to massive transfusion) is less likely

Thus, the most important abnormalities to note are:

  • Anaemia, due to haemorrhage
  • Coagulopathy, which is dilutional and consumptive (likely due to haemorrhage and normal saline resuscitation)
  • Metabolic acidosis, which is due to a combination of
    • hyperlactataemia, due to haemorrhagic shock
    • excess chloride, due to normal saline resuscitation
  • Inadequate respiratory compensation for acidosis, due to decreased level of consciousness
  • Hypocalcemia, due to consumption in coagulation


"Fluid and haemostatic resuscitation" implies that the college expected the trainees to give this coagulopathic patient more crystalloid, which is perhaps the opposite of the term "haemostatic". Reading between the lines, it feels like the college wanted to explain the rationale for haemostatic resuscitation, and then to discuss the place of fluid choice within that rationale, meaning not necessarily "fluid" in the conventional watery sense, but more as volume. What follows is an attempt to construct an answer that would achieve this imaginary goal:

Haemostatic resuscitation for this patient:

  • Correct hypothermia by rewarming
    • Rationale: hypothermia impairs the activity of clotting factors and the cardiovascular effects of catecholamines
    • Rewarm with external warming device, eg. air circulation blanket
    • Warm all fluids and blood products with a warmer
    • Minimise heat loss by exposing only parts of the patient being worked on or examined
  • Correct acidosis with volume resuscitation
    • Rationale: acidosis is a negative influence on clotting function, cardiac output,  and propensity to arrhythmias
    • Most of the acidosis here is due to the lactate, which is being generated partly by the sympathetic response to hypovolemia, and partly by the tissue hypoperfusion
    • Volume resuscitation should correct this 
    • Any crystalloid being given should be a "balanced" crystalloid to prevent any contribution from hyperchloraemia
  • Correct hypocalcemia by replacing calcium
    • Ionised calcium is an essential co-factor in the clotting cascade
  • Correct coagulopathy by using mainly blood products for resuscitation
    • Use  "balanced" blood product transfusion (1:1:1) of platelets, plasma and PRBCs
    • Rationale: coagulopathy will develop if packed red cells are the sole resuscitation fluid; clotting factors also need to be replaced, in a proportion that resembles whole blood
  • Aim for a MAP closer to 70 to defend CPP until TBI is ruled out
    • One cannot set haemostatic endpoints lower than normal ("permissive hypotension") because the patient has a decreased level of consciousness and could have a traumatic brain injury,
    • Once a CT is performed to exclude the possibility of CNS trauma, one may change to a lower blood pressure target to prevent blood loss and reduce the need for aggressive volume resuscitation
  • Correct hyperfibrinolysis with tranexamic acid
    • Hyperfibrinolysis is a consequence of severe trauma; tranexamic acid is a safe and arguably effective method of protecting patients from this complication