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Review
. 2021 Jul;61 Suppl 1(Suppl 1):S301-S312.
doi: 10.1111/trf.16462. Epub 2021 May 31.

Plasma as a resuscitation fluid for volume-depleted shock: Potential benefits and risks

Daan P van den Brink  1   2 , Derek J B Kleinveld  1   2   3 , Pieter H Sloos  2   3 , Kimberly A Thomas  4 , Jakob Stensballe  5   6 , Pär I Johansson  6 , Shibani Pati  7 , Jason Sperry  8 , Philip C Spinella  4 , Nicole P Juffermans  2   9
Affiliations
Review

Plasma as a resuscitation fluid for volume-depleted shock: Potential benefits and risks

Daan P van den Brink et al. Transfusion. 2021 Jul.
No abstract available

Keywords: FFP transfusion; blood management; plasma derivatives.

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Conflict of interest statement

The author has disclosed no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Proposed mechanisms of albumin, S1P and adiponectin on endothelial barrier function. In shock, adiponectin, albumin and S1P levels are commonly low. Plasma transfusion can replenish these components. Moreover, albumin also stimulates red blood cells and platelets to release S1P. S1P binds to S1P1 receptors activating Rac1. Rac1 activation has widespread physiological functions in the endothelial cell. It upregulates both endothelial tight junctions and adherent junctions and induces actin cytoskeletal reorganization strengthening endothelial barrier function, reducing endothelial permeability. Also, RAC1 inhibits MMP function resulting in reduced glycocalyx breakdown further retaining endothelial function. By replenishing adiponectin, inflammation is reduced by adiponectin‐mediated inhibition of TNF‐α and reduction of inflammatory cell response. By binding of adiponectin to AdipoR2, NF‐κβ signaling is inhibited leading to reduced inflammation, endothelial permeability, and activation. AdipoR2, adiponectin receptor 2; MMP, matrix metalloproteinase; Rac1, Ras‐related C3 botulinum toxin substrate 1; RBC, red blood cell; S1P, Sphingosine‐1‐Phosphate; S1P1, sphingosine‐1‐Phosphate receptor 1; TNF‐α, tumor necrosis factor‐α
FIGURE 2
FIGURE 2
Proposed mechanisms of shock‐induced microthrombi formation. Shock results in inflammation‐mediated activation of the endothelial cells with release of VWF. High amounts of VWF will multimerize and form prothrombotic ULVWF multimers with high platelet‐binding affinity. In normal conditions, ULVWF multimers are cleaved by ADAMTS13 into smaller, less prothrombotic VWF monomers. However, as ADAMTS13 levels are decreased during shock, the ULVWF multimers will promote platelet aggregation, resulting in microthrombi formation. This process may result in obstruction of microcirculation, inflammation, increased endothelial permeability, edema which leads to organ damage. Furthermore, the thrombin burst in shock is not counterbalanced by antithrombin. Antithrombin levels and activity are low in shock, further fueling thrombin‐induced platelet aggregation and microthrombi formation. ADAMTS13, a desintegrin and metalloproteinase with thrombospondin type 1 motifs, member 13; AT, antithrombin; ULVWF, ultra‐large von Willebrand Factor multimers; VWF, von Willebrand Factor
FIGURE 3
FIGURE 3
(A) Proposed effects of crystalloids on shock‐induced microthrombi formation. (B) Proposed effects of crystalloids on shock‐induced microthrombi formation. The proposed effects of crystalloids (A) and plasma (B) on the formation of shock microthrombi formation are shown. Infusion of crystalloids leads to dilution of ADAMTS‐13 and AT, which promotes platelet aggregation and microthrombi formation aggravating endothelial permeability and organ injury. Furthermore, crystalloid infusion directly leads to glycocalyx breakdown which may be caused by a protein poor environment. Plasma transfusion is thought to replenish proteins such as ADAMTS‐13 and AT. By replenishing ADAMTS‐13, ULVWF multimer formation is hampered resulting in reduced platelet aggregation. By replenishing AT, thrombin‐mediated platelet aggregation is inhibited. Both processes lead to less microthrombi formation and thus less obstruction of the microcirculation and associated organ damage. Furthermore, plasma is thought to be directly beneficial to the glycocalyx by providing a protein‐rich environment. ADAMTS‐13, a desintegrin, and metalloproteinase with thrombospondin type 1 motifs, member 13; AT, antithrombin; ULVWF, ultra‐large von Willebrand factor multimers; VWF, von Willebrand factor
FIGURE 4
FIGURE 4
Effects of plasma relative to crystalloids for patients in intravascular volume‐dependent shock
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