Coagulación en daño hepático crónico / Coagulation in chronic liver disease

Cirrhotic patients frequently exhibit abnormal coagulation tests such as prothrombin time (PT) and activated partial thromboplastin time (APTT) due to impairment in hepatic synthesis of coagulation factors. Due to these abnormalities and also to the numerous bleeding episodes that characterize advanced or decompensated liver cirrhosis, these patients were traditionally considered as “anticoagulated”. More recently, this paradigm has been challenged due to the increased occurrence of thrombotic complications among this population. This can only be understood when analyzed under the prism of the cellular theory of coagulation, which describes the complex interactions between endothelial, platelets and inflammatory cells that determine the status of coagulation, anticoagulation and fibrinolysis. The liver participates actively in this process contributing to the maintenance of a dynamic equilibrium in healthy patients. During liver failure there is evidence of impairment of synthesis of factors involved in the coagulation process, but also in anticoagulation and fibrinolysis. However, stable cirrhotic patients tend to maintain a delicate dynamic equilibrium. This equilibrium can be altered in acute decompensations leading to hemorrhagic or thrombotic complications.

Los pacientes con cirrosis presentan disminución en la producción de factores de coagulación de síntesis hepática, esto determina alteración del tiempo de protrombina (TP) y tiempo de tromboplastina parcial activada (TTPa). Esta característica, junto con los episodios de sangrado, que se presentan frecuentemente en pacientes descompensados y en etapa avanzada de la enfermedad, significó que por muchos años se considerara a los pacientes con daño hepático crónico como “anticoagulados”. En los últimos años este paradigma ha sido desafiado por estudios que muestran una mayor frecuencia de trombosis en esta población. Este fenómeno se comprende mejor con la teoría celular de la coagulación que integra a la ecuación las membranas celulares, especialmente de endotelio, plaquetas y células inflamatorias, y que permite visualizar las complejas interacciones entre factores coagulantes, anticoagulantes y fibrinolisis. El hígado participa en forma activa en este proceso que determina un amplio equilibrio dinámico en individuos sanos. El daño hepático claramente altera la coagulación, sin embargo, la evidencia actual demuestra que en la mayoría de los pacientes se produce un delicado rebalance hemostático, que determina una coagulación efectiva. Si este frágil equilibrio se altera, se produce un desbalance que puede generar un estado hemorrágico o trombótico.

Anesthetic management of a patient with polycythemia vera undergoing emergency repair of a type-A aortic dissection and concomitant coronary artery bypass grafting: a case report / 대한마취과학회지

Polycythemia vera is a chronic progressive myeloproliferative disease characterized by increased circulating red blood cells, and the hyperviscosity of the blood can lead to an increased risk of arterial thrombosis. In a previous survey regarding postoperative outcomes in polycythemia vera patients, an increased risk of both vascular occlusive and hemorrhagic complications have been reported. Aortic surgery involving cardiopulmonary bypass may be associated with the development of a coagulopathy, and as a result, the occurrence of thrombotic complications should be avoided after coronary anastomosis. Thus, optimizing the hemostatic balance is an important concern for anesthesiologists. However, only a few cases of anesthetic management in polycythemia vera patients undergoing concomitant aorta and coronary arterial bypass surgery have ever been reported. Here, we experience a polycythemia vera patient who underwent an emergency repair of a type-A aortic dissection and concomitant coronary artery bypass grafting, and report this case with a review of the relevant literature.