Shock Syndromes II

Patients with chronic liver disease often have episodes of clinically meaningful bleeding events

confounded by decreased concentrations of most endogenous procoagulant factors, except for factor

VIII and von Willebrand factor.

risk of bleeding, despite their poor correlation with onset and duration of bleeding after liver biopsy or

predicting the occurrence of GI hemorrhage.

This is likely explained by the parallel reduction in endogenous anticoagulants (e.g., antithrombin,

protein C) in chronic liver disease, leading to a “balanced state of coagulation.”

Randomized controlled trials evaluating recombinant activated factor VII (rFVIIa) to reverse the

coagulopathy of chronic liver disease showed dramatically improved PT, but rFVIIa failed to alter

bleeding complications during liver transplantation or control bleeding in variceal hemorrhage.

The American Association for the Study of Liver Diseases (AASLD) 2017 updated guideline for managing

portal hypertensive bleeding in cirrhosis recommends against the use of fresh frozen plasma or rFVIIa

to correct an INR because INR is not a reliable indicator of coagulation in cirrhosis, and evidence is

lacking that this improves outcomes. In addition, the American Gastroenterological Association (AGA)

2021 guidelines on coagulation in cirrhosis state that the balanced nature of alterations in hemostasis

associated with end-stage liver disease is complex and that an elevated INR is not necessarily predictive

of bleeding outcomes in patients with cirrhosis. For patients with stable cirrhosis (with known baseline

abnormal coagulation parameters) undergoing common GI procedures, the AGA suggests against the

use of extensive preprocedural testing (including repeated measurements of PT/INR or Plt) and against

the routine use of blood products (e.g., fresh frozen plasma and Plt) for bleeding prophylaxis.

Global clotting tests (e.g., the thrombin generation test or TEG) have the potential to characterize

coagulopathy in chronic liver disease but may not be routinely available, and optimal transfusion

thresholds remain undefined.

Rapid identification and correction of the source of bleeding is the definitive treatment (e.g., surgical

exploration, angiographic embolization, stabilization of the pelvic ring, damage control surgery).

Indications: Diminished mental status or absent radial pulse (SBP less than 90 mm Hg)

Benefits: Fluids restore intravascular volume, reverse tissue hypoperfusion, and correct oxygen

deficit.

Risks: Fluids do not increase oxygen-carrying capacity, can precipitate dilutional coagulopathy,

and lead to interstitial fluid accumulation, including the development of pulmonary edema and

worsening acute respiratory distress syndrome.

lead to hyperchloremic metabolic acidosis. This has been linked to adverse renal effects, including

an increased risk of acute kidney injury in some studies. However, not all studies have shown

a definitive causal relationship between saline use and acute kidney injury. The strength of this

association may depend on the context (eg, volume administered, patient population). Evidence of

their effect on mortality and morbidity is still emerging.

Colloids: Confer no incremental benefit over crystalloids, were associated with increased mortality

in a subgroup analysis of patients with severe brain injury in the SAFE trial, likely secondary to

hypo-osmolarity. Synthetic colloids (e.g., hydroxyethyl starches) contribute to coagulopathy and

the risk of acute kidney injury and should therefore be avoided.