A clinical coagulopathy score concurrent with viscoelastic testing defines opportunities to improve hemostatic resuscitation and enhance blood product utilization during liver transplantation.

BACKGROUND: An NIH clinical coagulopathy score has been devised for trauma patients, but no such clinical score exists in transplantation surgery. We hypothesize that that this coagulopathy score can effectively identify laboratory defined coagulopathy during liver transplantation and correlates to blood product utilization. METHODS: TEGs were performed and coagulopathy scores (1, normal bleeding - 5, diffuse coagulopathic bleeding) were assigned by the surgeons at 5 intra-operative time points. Blood products used during the case were recorded between time points. Statistical analyses were performed to identify correlations between coagulopathy scores, TEG-detected abnormalities, and blood product utilization. RESULT: Transfusions rarely correlated with the appropriate TEG measurements of coagulation dysfunction. Coagulopathy score had significant correlation to various transfusions and TEG-detected coagulopathies at multiple points during the case. High aggregate coagulopathy scores identified patients receiving more transfusions, re-operations, and longer hospital stays CONCLUSION: The combination of viscoelastic testing and a standardized clinical coagulopathy score has the potential to optimize transfusions if used in tandem as well as standardize communication between surgery and anesthesia teams about clinically evident coagulopathy.

Hepatopulmonary syndrome and portopulmonary hypertension.

The incidence of pulmonary vascular disorders is significantly increased in patients with liver disease. Intrapulmonary shunting with hypoxemia in patients with liver disease is diagnosed as hepatopulmonary syndrome (HPS), whereas precapillary pulmonary vessel obliteration is identified as portopulmonary hypertension (PPHTN). Because the symptoms of liver disease can mimic those of pulmonary vascular disease, all patients with hepatic failure should be screened for these two diseases. Pulse oximetry effectively screens for hypoxemia associated with HPS, whereas an elevated right ventricular systolic pressure estimated by echocardiography identifies patients at risk of having PPHTN. Liver transplantation is the only effective medical therapy for HPS. However, those who have a resting arterial oxygenation less than 50 mm Hg or a shunt measured by scintigraphic perfusion greater than 20% have an unacceptably high mortality rate following surgery. Compared with HPS, there are more therapeutic options that can bridge patients with PPHTN to transplantation. Drugs used to manage idiopathic pulmonary hypertension have shown promise in the treatment of PPHTN. Prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors have improved transplant survival. Despite treatment, however, perioperative mortality for patients with PPHTN remains high. Even with successful transplantation, HPS and PPHTN can persist or develop de novo. Long-term follow-up and surveillance of liver transplant recipients is thus indicated to identify HPS and PPHTN following surgery.