708 SECTION III Anesthetic Management
The prevalence of liver disease is increasing in the Clot breakdown may be enhanced by an imbalance
United States. Cirrhosis, the terminal pathology in of the fibrinolytic system.
the majority of liver diseases, has a general popu- Chronic liver disease is characterized by the
lation incidence as high as 5% in some autopsy impaired synthesis of coagulation factors, resulting
series. It is a major cause of death in men in their in prolongation of the prothrombin time (PT) and
fourth and fifth decades of life, and mortality rates international normalized ratio (INR) (Table 33–1).
are increasing. Ten percent of the patients with liver However, the anticoagulant factors (protein C, anti-
disease undergo operative procedures during the thrombin, and tissue factor pathway inhibitor) are also
final 2 years of their lives. The liver has remarkable reduced and may balance out any effect of a prolonged
functional reserve, and thus overt clinical manifesta- PT. This may be confirmed by assessing thrombin
tions of hepatic disease are often absent until exten- generation in the presence of endothelial-produced
sive damage has occurred. When patients with little thrombomodulin. Adequate thrombin production
hepatic reserve come to the operating room, effects requires an adequate number of functioning platelets.
from anesthesia and the surgical procedure can pre- If the platelet count is >60,000/µL, coagulation may
cipitate further hepatic decompensation, leading to well be normal in a patient with severe cirrhosis.
frank hepatic failure. The patient with cirrhosis will typically have
hyperfibrinolysis. However, there is a delicate bal-
ance between the activators and inactivators that
COAGULATION regulate the conversion of plasminogen to plasmin,
IN LIVER DISEASE and, therefore, individual laboratory tests may not
In stable chronic liver disease, the causes of exces- give a true picture of the state of fibrinolysis. The
sive bleeding primarily involve severe thrombocyto- thromboelastography (TEG®), rotational thrombo-
penia, endothelial dysfunction, portal hypertension, elastometry (ROTEM®), and Sonoclot® technolo-
renal failure, and sepsis (see Chapters 32 and 51). gies are the optimal methods of demonstrating the
However, the hemostatic changes that occur with global state of the coagulation system at a specific
liver disease may cause hypercoagulation and moment in time in any patient with liver disease (see
thrombosis, as well as an increased risk of bleeding. Chapter 51).
TABLE 331 Coagulation test abnormalities.1
PT PTT TT Fibrinogen
Advanced liver disease ↑ ↑ N or ↑ N or ↓
DIC ↑ ↑ ↑ ↓
Vitamin K deficiency ↑↑ ↑ N N
Warfarin therapy ↑↑ ↑ N N
Heparin therapy ↑ ↑↑ ↑ N
Hemophilia
Factor VIII deficiency N ↑ N N
Factor IX deficiency N ↑ N N
Factor VII deficiency ↑ N N N
Factor XIII deficiency N N N N
1
PT, prothrombin time; PTT, partial thromboplastin time; TT, thrombin time; N, normal; DIC, disseminated
intravascular coagulation.
