Abstract
Desensitisation with therapeutic plasma exchange (TPE) is essential for ABO-incompatible (ABO-I) liver transplants (LTs). However, excessive citrate load and coagulation disturbances after TPE have been poorly studied, in particular in cirrhotic patients with hypocapnic alkalosis, metabolic compensation and electrolyte imbalances. We retrospectively evaluated 1123 consecutive LT recipients (923 ABO-compatible [ABO-C], 200 ABO-I) from November 2008 to May 2015. TPE was generally performed a day before LT and blood sampling was performed before anaesthesia induction. We performed propensity score matching (PSM) and inverse probability treatment weighting (IPTW) analyses. In 199 PSM pairs, metabolic alkalosis was prevalent in ABO-I LT recipients (expectedly due to citrate conversion) with higher pH ≥ 7.50 (IPTW-adjusted odds ratio [aOR] = 2.23) than in ABO-C LT recipients. With increasing cirrhosis severity, the arterial pH and bicarbonate levels showed dose-dependent relationships, whereas mild hypoxaemia was more prevalent in ABO-I LT recipients. ABO-I LT recipients exhibited worsened hypokalaemia ≤3.0 mmol/l (17.6%, aOR = 1.44), hypomagnesaemia ≤1.7 mg/dl (27.6%, aOR = 3.43) and thrombocytopenia <30,000/µl (19.1%, aOR = 2.26) confirmed by lower maximal clot firmness (P = 0.001) in rotational thromboelastometry (EXTEM), which necessitated platelet transfusions. Preoperative identification of these change may prevent worsening of severe electrolyte disturbances and thrombocytopenia for optimal LT anaesthesia.
Highlights
Liver cirrhosis (LC) has deleterious effects on many organ systems and is accompanied by metabolic and acid-base disturbances such as hyperventilatory hypocapnic alkalosis with metabolic compensation and electrolyte imbalances[1,2,3]
The first primary finding of this study is that the pre-transplant therapeutic plasma exchange (TPE), typically performed until the day before the liver transplants (LTs) surgery, regional citrate anticoagulation (RCA) and fresh frozen plasma (FFP) altered acid-base status in LC patients, shifting it from respiratory alkalosis to the metabolic alkalosis
The pre-existing electrolyte disturbances were worsened, and the risk of severe hypokalaemia and hypomagnesaemia were significantly higher in ABO-I Living-donor LT (LDLT) recipients
Summary
Liver cirrhosis (LC) has deleterious effects on many organ systems and is accompanied by metabolic and acid-base disturbances such as hyperventilatory hypocapnic alkalosis with metabolic compensation and electrolyte imbalances[1,2,3]. It may cause hypocalcaemia and hypomagnesaemia, inducing cardiac arrhythmias[16], and cause pronounced acid-base imbalances, even after the cessation of TPE. Few studies have demonstrated the feasibility of citrate anticoagulation in patients with cirrhosis[16]; a systematic assessment of complications and outcomes in this special cohort who undergo LT usually a day after TPE has been poorly studied. Given its reported decreased citrate metabolism in LT recipients, we set up to evaluate the hypotheses that pre-transplant TPE with citrate alters the expected pattern of the acid-base status, worsens respiration dysfunction, provokes electrolyte imbalances and aggravates the coagulation dysfunction. We assessed whether the aggravated coagulation status has an impact on the need for intraoperative transfusions
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