Introduction Donation after circulatory death (DCD) has emerged as an important strategy to expand the donor pool in liver transplantation. However, compared to brain-dead donors, DCD grafts are more vulnerable to hypoxic injury due to unavoidable periods of warm ischemia.
Introduction
Donation after circulatory death (DCD) has emerged as an important strategy to expand the donor pool in liver transplantation. However, compared to brain-dead donors, DCD grafts are more vulnerable to hypoxic injury due to unavoidable periods of warm ischemia. A key concept is donor warm ischemic time (dWIT), particularly the functional dWIT, during which hepatic oxygen delivery becomes critically compromised. The liver has remarkable autoregulatory mechanisms—primarily the hepatic arterial buffer response and high oxygen extraction capacity—but these mechanisms fail beyond certain thresholds of hypoperfusion and hypoxia. This results in ischemia-reperfusion injury (IRI), the central driver of graft dysfunction and complications after transplantation.
Problem Statement
Despite increasing use of DCD grafts, there is poor understanding of the exact physiological thresholds of hepatic hypoxia and the lack of standardized definitions of functional warm ischemia time, leading to variability in graft selection, discard rates, and clinical outcomes.
Summary
This review provides a mechanistic framework linking hepatic physiology to DCD outcomes. The liver receives dual blood supply—75% from the portal vein and 25% from the hepatic artery—with intrinsic autoregulation maintaining oxygenation even with reduced flow. However, during DCD, progressive hypotension and hypoxemia eventually overwhelm these compensatory mechanisms. Functional dWIT—when oxygen delivery falls below critical thresholds—is the most relevant determinant of graft injury, yet remains inconsistently defined across centers.
Hepatic injury primarily occurs during reperfusion rather than ischemia itself. During ischemia, the liver becomes metabolically primed, accumulating inflammatory mediators. Upon reperfusion, a cascade of sterile inflammation occurs involving neutrophils, Kupffer cells, cytokines, and endothelial dysfunction, leading to hepatocyte necrosis and microcirculatory failure.
Clinical correlates from hypoxic hepatitis and congestive hepatopathy suggest that both hypoxia and congestion contribute to injury. Additional factors such as donor hemodynamic trajectory, oxygen saturation, cardiac function, and underlying liver quality (steatosis/fibrosis) further influence outcomes.
Future directions include better physiological definition of functional dWIT, real-time monitoring of hepatic oxygenation, and use of emerging technologies such as machine perfusion to mitigate ischemia-reperfusion injury. This integrated physiological approach may reduce graft discard and improve outcomes in DCD liver transplantation.
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