INTRODUCTION: Hemodynamic instability is a common occurrence during liver transplantation (LT). Hypotension and hemodynamic instability during graft reperfusion are most commonly consequences of the postreperfusion syndrome (PRS). CASE OUTLINE: In this report, we present a case of severe cardiovascular collapse leading to cardiac arrest which occurred in the course of graft reperfusion during LT. Persistent hypotension, non-responsive to regular measures such as volume filling and the use of vasopressors, yielded the question of whether other mechanisms were involved in causing it. Diffuse redness of the face and body, swelling of the face, lips and tongue with tongue prolapse, accompanied with severe cardiovascular collapse indicated that it was an anaphylactic reaction. This caused a dilemma as to what instigated the reaction. The trigger may have been the pharmacological substance administered during the graft reperfusion, or the one administered immediately prior to the reperfusion.The substances in question would most likely be either the University of Wisconsin preservation solution (UW), which was administered during the reperfusion, or Hepatect, which the patient received immediately prior to reperfusion. CONCLUSION: The clinical syndrome resulting from degranulation of mast cells and basophils in anaphylaxis is very similar to the PRS in LT. Clinical features play the most important role in establishing a timely diagnosis and early treatment of anaphylaxis. Swift administration of epinephrine reduces the chances of a fatal outcome. Better information on both donor and recipient can improve the efficiency of therapy and prophylaxis for anaphylaxis.
INTRODUCTION: Hemodynamic instability is a common occurrence during liver transplantation (LT). Hypotension and hemodynamic instability during graft reperfusion are most commonly consequences of the postreperfusion syndrome (PRS). CASE OUTLINE: In this report, we present a case of severe cardiovascular collapse leading to cardiac arrest which occurred in the course of graft reperfusion during LT. Persistent hypotension, non-responsive to regular measures such as volume filling and the use of vasopressors, yielded the question of whether other mechanisms were involved in causing it. Diffuse redness of the face and body, swelling of the face, lips and tongue with tongue prolapse, accompanied with severe cardiovascular collapse indicated that it was an anaphylactic reaction. This caused a dilemma as to what instigated the reaction. The trigger may have been the pharmacological substance administered during the graft reperfusion, or the one administered immediately prior to the reperfusion.The substances in question would most likely be either the University of Wisconsin preservation solution (UW), which was administered during the reperfusion, or Hepatect, which the patient received immediately prior to reperfusion. CONCLUSION: The clinical syndrome resulting from degranulation of mast cells and basophils in anaphylaxis is very similar to the PRS in LT. Clinical features play the most important role in establishing a timely diagnosis and early treatment of anaphylaxis. Swift administration of epinephrine reduces the chances of a fatal outcome. Better information on both donor and recipient can improve the efficiency of therapy and prophylaxis for anaphylaxis.