The present study found that the in-hospital mortality rate of liver failure in pregnancy was 27.4% and most of the deaths were recorded in the first 7 days after admission. Patients suffered in-hospital death had a significant lower gestational age, a higher incidence rate of hepatorenal syndrome and were more likely to receive hysterectomy but less likely to receive intrauterine balloon tamponade. The baseline aspartate aminotransferase, total bilirubin, indirect bilirubin and platelet levels were significantly higher, while cholinesterase, prothrombin activity and creatinine levels were significantly lower in patients who died in the hospital than that in patients discharged alive. The change tendencies of total bilirubin level and prothrombin activity were greatly different between patients died in the hospital and patients discharged alive. Moreover, patients with liver failure caused by hepatitis B had a higher in-hospital mortality rate compared with those caused by AFLP.
The incidence rate of liver failure in pregnancy is about 1–10 per million person-years but with a high mortality rate, and it is one of the main indirect factors leading to maternal death [12]. In this study, the in-hospital mortality rate of patients with liver failure was 27.4%, which was similar to that previously reported in China [13]. From the cumulative death curve, we found that the mortality rate of patients with liver failure increased rapidly within 7 days after admission, while it slowed down after 7 days. As delivery were carried out as soon as possible in patients with liver failure, the results indicated that delivery was an important factor leading to the rapid change of the condition in patients with liver failure. Liver failure in pregnancy might develop rapidly after delivery and the risk of death becomes highest in a short period of 7 days. Thus, in clinical practice, it is necessary to carefully and actively manage patients with liver failure in the early stage to reduce mortality. It was reported that patients with liver failure was mainly of late pregnancy (after 28 weeks), which was consistent with what was found in the present study. Besides, the gestational age of patients died in the hospital was significantly lower, suggesting that the early onset of liver failure in pregnancy might be related to poor prognosis. The results also found that the postpartum bleeding rate was numerically higher in those died during hospitalization, and the hysterectomy rate was significantly higher in patients died in the hospital. On the contrary, the utilization rate of intrauterine balloon tamponade was significantly higher in those survived. Patients with liver failure frequently suffered from coagulation dysfunction, leading to a higher risk of postpartum hemorrhage than normal pregnant women. Postpartum hemorrhage could further aggravate coagulation dysfunction and lead to a vicious circle. Vrachnis et al. reported that the success rate of hemostasis was 94.4% in postpartum hemorrhage patients treated with intrauterine balloon tamponade [14]. However, there has been no study in the application of intrauterine balloon tamponade in patients with liver failure. In this study, 32 patients were treated with intrauterine balloon tamponade and 27 of them survived, suggesting that active use of intrauterine balloon tamponade in patients with liver failure might alleviate postpartum hemorrhage and improve survival rate.
The change tendencies of important laboratory examinations in patients with liver failure illustrated that total bilirubin and prothrombin activity changed in totally different ways in patients died in the hospital or discharged alive, while changes in aspartate aminotransferase and cholinesterase changes were similar between the two groups. Of note, though having a similar change tendency, aspartate aminotransferase was significantly higher at baseline in patients suffered in-hospital death. Aspartate aminotransferase is an intracellular functional enzyme of the liver. After the damage and destruction of hepatocytes, aspartate aminotransferase will soon be released into the blood, therefore the level of aspartate aminotransferase can sensitively reflect the degree of necrosis of hepatocytes especially in the onset stage of the disease [15, 16]. However, when the disease progresses, the level of aspartate aminotransferase will tend to be stable or even decreased with a broad necrosis of hepatocytes, but the increase of total bilirubin will persist. When liver disease progresses to liver failure, considerable amounts of hepatocytes have been damaged, which is in line with the results of this study that the aspartate aminotransferase level reached the peak at admission. As the disease progressively deteriorated in patients who finally dead during hospitalization, the aspartate aminotransferase level of them decreased, while the total bilirubin level continuously increased, leading to the phenomenon "bilirubin-transaminase separation", which could indicate poor prognosis [13]. In survived patients, the levels of aspartate aminotransferase and total bilirubin decreased simultaneously, indicating that the injury of hepatocytes might have been slowed down or even stopped and the liver gradually recovered. It has been reported that cholinesterase level reflected the synthesis function of the liver and was related to the prognosis of patients with liver failure [17, 18]. In the present study, the level of cholinesterase reached the nadir at admission and increased after that. Within 7 days after admission, the cholinesterase level of in-hospital dead patients was lower than those survived, suggesting that the liver damage was more severe among in-hospital dead patients. However, the change tendencies didn’t differ significantly among discharge dead or alive patients, indicating that the baseline cholinesterase level might be more closely associated with prognosis. Most of the coagulation factors are synthesized in the liver, thus coagulation dysregulation is one of the parameters reflecting liver dysfunction. The important coagulation function marker, prothrombin activity, has been reported to be related tightly to prognosis in liver failure patients [19–21]. In the present study, prothrombin activity decreased apparently at baseline in patients with liver failure. But after admission, an increasing trend was observed in patients survived while no improvement was found in died patients. These results indicated that liver synthesis function was poor and coagulation dysfunction was difficult to be corrected in in-hospital dead patients with liver failure, and that the dynamic change of prothrombin activity level was associated with the prognosis of patients with liver failure and should be carefully tracked during hospitalization.
There are some limitations of this study. Firstly, due to the rarity of liver failure in pregnancy, the sample size of this study is still relatively small. Secondly, this is a single-center study, which may affect the generalizability of the results. Thirdly, as a retrospective analysis, bias caused by data collection and management amendment might exist.