Massive blood product transfusion

The contents and properties of packed red blood cells, the physiology of acute haemorrhage and the physiological responses to a moderate-volume blood transfusion are detailed in other chapters. CICM have asked about this only in Question 1 from the first paper of 2005.

Definition of a "massive transfusion"

A "massive transfusion" is defined by the volume of blood lost. Most people are happy to call the replacement of one's entire blood volume a massive transfusion. That would be about 7% of a person's body weight, or about 10 units of PRBCs in a normal-looking adult. Others use time-defined criteria (the replacement of half of one's blood volume over 4 hours) or bleeding-defined criteria (rate of blood loss in excess of 150ml/min).

A brief word on the management of massive haemorrhage

Apart from the recommendations strictly related to the use of blood products, the NBA guidelines statement on massive transfusion also offers its 2 cents worth to the management of severe trauma.

• Use permissive hypotension (SBP 80-100)
• Correct acidosis
• Correct hypothermia
• Correct hypocalcemia

This- in brief summary - is the essence of haemostatic resuscitation, the new dogma of managing traumatic haemorrhage, which is well explored in another chapter from the Trauma section.

Ratio of blood prodcts in massive transfusion

One specific feature of the NBA document is that no recommendation is made for any specific ratio of PRBCs to other blood products. However, a massive transfusion protocol template is offered, which can be downloaded and printed; it suggests that the senior clinicial officer order packages of 2 units of FFP and 4 units PRBCs, and continue doing so until the bleeding is controlled. Platelets and cryoprecipitate are also recommended, and though a "ratio" is not specified, doses are suggested.

Thus, a single "massive transfusion resuscitation volume" would include:

• 4units of PRBCs
• 2 units of FFP (15ml/kg)
• 1 adult dose of platelets
• 3-4g of fibrinogen (in cryoprecipitate).

The evidence behing various transfusion ratios is explored more thoroughly in the chapter on haemostatic resuscitation.

Management of massive transfusion-associated complications

We are grateful to the deep dive performed by a reader (thank you Tejas Jade)  that revealed several baffling statements in the literature regarding the behaviour of potassium and chloride in the patient recovering from massive transfusion. From a direct reading of the chapter for the 3rd ed. of Critical Care Medicine by Luce (2008, p. 1655-1675) and the paper by Sihler & Napolitano (2010), one might think that metabolic alkalosis and hypokalemia are the inevitable consequences of massive transfusion. But both are dated works (2008 is so 1990s), and what's worse, they both refer to even more dated works for support. An outrageous example of this is the part where Judith Luce references a 1962 paper by Schweiser and Howland which describes "thirty-five patients ... who received acid-citrate-dextrose preserved blood in volumes ranging from none to 21 pints".

Without clicking the link or examining the reference list, a modern day reader might come to accept this as fact, but in fact the intensivist practicing in the 21st century will never encounter such phenomena because the packed red cells we infuse these days will never contain this much citrate, no matter how many pints one ends up transfusing. In the 1960s, banked whole blood was primarily preserved using Acid-Citrate-Dextrose (ACD) solution, which came in two standard formulas (Solution A and Solution B) containing roughly 2.2g to 2.45g/L of trisodium citrate (or 8-9 mmol/L, three times more than what we routinely use for citrate dialysis). Australian red cell storage practices involve washing the cells and storing them in SAG-M solution, which means the citrate content is minimal.

The 1960s explanations of the underlying causes of the observed hypokalemia are now also better informed. More than hypokalemia, these days hyperkalemia is the more frequently observed phenomenon, with the hypokalemia described in older papers ascribed to several phenomena:

• Citrate-induced alkalosis and  catecholamine release (Carmichael et al, 1984) - presumably, these patients were overdosed with citrate and remained underresuscitated, with a resulting potassium shift which effectively concealed the added potassium of the red cells.
• Recovery of donor red cell Na⁺/K⁺-ATPase activity, according to Sihler & Napolitano (though admittedly this contribution cannot be massive considering how few cells are transfused and how metabolically inert we expect them to be after a month of cold storage)
• Co-infusion of potassium-poor fluids and blood components (given that red cells are not the largest contributor to the total transfused volume) adds to the hypokalemia; but concomitant acidosis subtracts from it (or.. adds to hyperkalemia?)