Acute fatty liver in pregnancy presenting in the second trimester: A systematic literature review

Abstract

Objective

We present clinical features and outcomes of second-trimester acute fatty liver of pregnancy (AFLP), a serious but rare condition.

Results

Fourteen pregnant women with AFLP or compatible biopsy were identified in the literature. Diagnosis occurred between 20 and 27 + 6 weeks of gestational age. In total, 50% were primigravid. Thirteen cases met the Swansea criteria while the other case had a compatible liver biopsy. In total, 10 out of 11 cases had microvesicular steatosis on their liver biopsy. Common maternal complications included acute renal failure, hypoglycaemia, liver failure, encephalopathy, intensive care unit admission and need for blood transfusions. Seven deliveries were on the day of diagnosis, five within four weeks, and two within three months. One maternal death, seven fetal deaths and three neonatal deaths occurred.

Conclusion

AFLP diagnosed in the second trimester is a rare condition. Neonatal mortality and maternal morbidity are high. Most cases had nonspecific symptoms and clinical findings, but a majority had compatible biopsies.

Keywords

Acute fatty liver of pregnancy

Introduction

Acute fatty liver in pregnancy (AFLP) is a pathology related to fatty acid metabolism during pregnancy.^1,2 Higher levels of free fatty acids from an altered metabolism in pregnancy, particularly in the third trimester, allow for fetal and placental growth and development, however, free acids can accumulate and cause hepatotoxicity.^1,2 The incidence of AFLP is around 5 cases per 10,000 pregnancies.^3,4 It is a rare pathology, with high maternal morbidity and mortality, and high neonatal mortality.^3,5

Twin pregnancy, body mass index (BMI) less than 20 kg/m², previous AFLP, and long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency are risk factors for AFLP.^1,3 Clinical presentation is heterogeneous in severity and can include nonspecific symptoms, such as nausea, vomiting, and abdominal pain, to severe, life-threatening liver or renal failure.^6–8 The diagnosis of AFLP is based on clinical presentation and clinical findings, and can be confirmed with the Swansea criteria.^4,8,9 To limit maternal liver damage, management usually includes immediate delivery without regard to the gestational age or severity of presentation.^1,4,10

Diagnosis of AFLP is usually around 36 weeks' gestation and the disease is often only considered in the third trimester.³ Few data are available on the presentation and evolution of AFLP cases diagnosed in the second trimester, but a few cases are reported in the literature.^11–16 Our systematic review presents the clinical features, evolution, and outcomes of 14 cases of AFLP presenting in the second trimester.

Methods

Literature review

We performed a systematic search of publications from 1946 to August 2021. The following electronic databases were searched: MEDLINE (Ovid), CINAHL Complete (EBSCOhost), Embase (Ovid), EBM Reviews—Cochrane Database of Systematic Reviews (Ovid), EBM Reviews—ACP Journal Club (Ovid), EBM Reviews—Database of Abstracts of Reviews of Effects (Ovid), EBM Reviews—Cochrane Clinical Answers (Ovid), EBM Reviews—Cochrane Central Register of Controlled Trials (Ovid), EBM Reviews—Cochrane Methodology Register (Ovid), EBM Reviews—Health Technology Assessment (Ovid) and EBM Reviews—NHS Economic Evaluation Database (Ovid). We searched several clinical trial registries, including ClinicalTrial.gov, International Clinical Trials Registry Platform and ISRCTN. Google Scholar was searched, and the first 20 results were screened, which resulted in additional results.

Search strategies were designed by a librarian at the Bibliothèque du Centre hospitalier de l’Université de Montréal.

The search included articles in all languages, but only articles with an English or French abstract available were included.

We searched the reference list and primary articles for relevant articles not already identified. Two separate and independent evaluators used covidence to screen and evaluate all articles.

Inclusion criteria included having women 18 years and older, diagnosis of AFLP made between 13 and 27 + 6 weeks, and diagnosis made by a clinician or having a compatible liver biopsy that showed centrilobular microvesicular steatosis. Exclusion criteria included having women with another hepatic disease related to pregnancy or another concomitant hepatic disease. Articles without sufficient data on the cases to establish the diagnosis, evolution, and outcome were also excluded from the study. Articles presenting multiple cases of AFLP but without clinical characteristics, for specific women of interest were excluded.

Data collection

Each article was reviewed to collect information on maternal characteristics, including age, parity, BMI pre-conception, weight at the first visit, gestational age at diagnosis, and personal medical history (hypertension, chronic kidney disease, pre-eclampsia, caesarean section, AFLP, haemolysis elevated liver enzymes and low platelets (HELLP) syndrome, intrauterine growth restriction (IUGR) and LCHAD status.¹⁷ Clinical presentation was also documented following the Swansea criteria, which includes vomiting, abdominal pain, polyuria and polydipsia, encephalopathy, elevated bilirubin, hypoglycaemia, elevated uric acid, leucocytosis, elevated liver enzymes, hyperammonaemia, renal failure, coagulopathy, ascites or hyperechogenic liver at ultrasounds, and biopsy with centrilobular microvesicular steatosis. Diagnosis was confirmed if 6 or more Swansea criteria were present. Maternal outcomes were also extracted from articles which included method of delivery, obstetric complications and disease complications. Fetal characteristics, birthweight, sex, gestational age at delivery and outcomes were collected. We also verified if fetal LCHAD screening was done.

Method of delivery was documented as vaginal (spontaneous or induced) or caesarean section. Indication for induction, if needed, was reported. Caesarean section indications, such as elective, fetal malpresentation, placental insertion anomaly, clinician decision related to maternal comorbidities or in labour with abnormal fetal tracing or labour dystocia (failed induction, stopped progression, altered descent) were documented.

Obstetric complications were documented, including pre-eclampsia, gestational diabetes, postpartum haemorrhage, need for transfusion of blood products or plasmapheresis. Pre-eclampsia was defined by gestational hypertension (systolic blood pressure (BP) > 140 mmHg or diastolic BP >90 mmHg, beginning at >20 weeks) with either aggravating or de novo proteinuria (urinary protein: creatinine ratio ≥ 30 mg/mmol), or at least one adverse condition or severe complication, as defined by the Society of Obstetricians and Gynaecologists of Canada (SOGC).¹⁸ Postpartum haemorrhage was defined by loss of more than 500 ml of blood after vaginal delivery or 1000 ml after caesarean section.

Maternal complications were documented as renal failure, severe renal failure, liver failure, disseminated intravascular coagulation (DIC), hypoglycaemia with need of treatment, ascites, hepatic encephalopathy defined as altered level of consciousness or asterixis, intensive care unit admission, liver transplant and haemodialysis.¹⁹ Renal failure was defined by elevation of serum creatinine by 26.5 μmol/L in 48 h. Severe renal failure was defined by serum creatinine more than 150 μmol/L. DIC was defined with the International Society on Thrombosis and Haemostasis criteria (international normalized ratio (INR) > 1.5, and platelets < 100 × 10⁹/L).²⁰

Fetal outcomes were defined by: prematurity, neonatal respiratory distress syndrome (NRDS), neonatal intensive care unit (NICU) admission and perinatal mortality.^21,22 Prematurity was defined as delivery before 37 weeks with a subgroup before 34 weeks. Perinatal mortality was defined by fetal mortality after 22 weeks or neonatal mortality within 7 days of delivery.²³

Risk of bias

Case reports are considered low in the hierarchy of evidence, since they present individuals or a small number of women, typically without a control group, which could introduce various forms of bias and limit the generalizability of findings. To decrease bias, we included only well-documented case reports.

Statistics

Summary statistics were calculated to describe patient characteristics and their outcomes. Dichotomous variables are reported as percentages and continuous variables are reported by mean with standard deviation or median with interquartile range. Any pregnancies from the same woman were analyzed as two different events. Sample sizes and denominators vary due to missing data.

Results

We retrieved 8,855 articles of which 2268 were duplicates, and 5987 were excluded after screening with covidence due to irrelevance. We excluded 470 articles for language other than English or French, other hepatic pathology, AFLP diagnosis unproven, age under 18 years, or insufficient data. Cases were extracted from eleven case reports, two case series and one retrospective cohort study for a total of 14 women diagnosed with second-trimester AFLP (Figure 1).

Figure 1.

PRISMA 2020 flow diagram for systematic review.

Maternal characteristics

Maternal characteristics are described in Table 1. Diagnosis occurred between 20 and 27 + 6 weeks of gestation age. Mean maternal age was 29 years, 50% were primigravid and all were singleton pregnancies, except for one pregnancy. BMI before conception or during the first trimester was available for three pregnancies. No woman had BMI less than 20 kg/m². One out of ten cases reported had pregestational hypertension. None had pre-eclampsia, CKD, HELLP or previous AFLP. Two had previous caesarean sections. Only three women had LCHAD deficiency screening, and all were negative.

Table 1.

Maternal characteristics and clinical presentation.

	N	Mean (range)
Age (y)	14	29 (19–41)
Gestational age at diagnosis (y)	14	24.3 (20–27.7)
	P/N	%
Nulliparity	6/13	46.2
Twin pregnancy	1/14	7.1
BMI < 20 kg/m²	0/3	0
Swansea criteria	P/N	%
Vomiting	13/14	92.8
Abdominal pain	10/14	71.4
Polydipsia and/or polyuria	0/9	0
Encephalopathy	7/13	53.8
Bilirubin > 14 μmol/L	12/13	92.3
Hypoglycaemia <4 mmol/L	9/12	75.0
Uric acid >340 μmol/L	4/6	66.6
Leucocytosis > 11 × 10⁶/L	8/12	66.6
Ascites or hyperechogenic liver on ultrasound	5/13	38.4
Transaminase elevation >42 U/L	14/14	100.0
Ammonia > 47 mmol/L	5/7	71.4
Kidney failure (serum creatinine >150 µmol/L)	6/13	46.1
Coagulopathy (INR > 1.5 s or PTT > 34 s)	11/11	100
Compatible liver biopsy	10/11	90.9
6 or more Swansea criteria	13/14	92.9

N: available sample size; P: number of cases; INR: international normalized ratio; PTT: partial thromboplastin time; BMI: body mass index.

Table 1 describes maternal clinical presentation. Thirteen women had more than six Swansea criteria at diagnosis. One case had insufficient information to collect all Swansea criteria but had a liver biopsy that suggested AFLP. The most frequent symptoms were vomiting (93%) and abdominal pain (71%). Hypoglycaemia (75%), elevated bilirubin (92%), abnormal liver enzymes (100%), and coagulopathy (100%) were the most frequent paraclinical findings. Ten cases had had a liver biopsy showing microvesicular steatosis. One of the biopsies was obtained during the autopsy.

Maternal outcomes

Table 2 describes maternal and obstetric complications. Acute renal failure (75%), hypoglycaemia (80%), encephalopathy (43%) and liver failure (45%) were the most common maternal complications. In total, 9 out of 11 women were admitted to an intensive care unit. Three women had haemodialysis and one woman needed liver transplant. Two women were treated with plasmapheresis. Blood product transfusions were needed in seven of the eight cases that reported that information. One maternal death occurred in a woman whose autopsy revealed acute pancreatitis, acute fatty liver, pulmonary oedema, and cerebral haemorrhage.²⁴

Table 2.

Maternal and obstetric complications.

Maternal complications	P/N	%
Acute renal failure	9/12	75.0
Severe renal failure	6/12	50.0
Haemodialysis	3/13	23.0
DIC	2/7	28.5
Hypoglycaemia	8/10	80.0
Ascites	3/12	25.0
Encephalopathy	6/14	42.8
Liver failure	5/11	45.4
Liver transplant	1/13	7.6
ICU admission	9/11	81.1
Death	1/14	7.1
Obstetric complications	P/N	%
Pre-eclampsia	1/14	7.1
Gestational diabetes	1/14	7.1
Post-partum haemorrhage	3/12	25.0
Transfusion blood products	7/8	87.5
Plasmapheresis	2/13	15.3

N: available sample size; P: number of cases; DIC: disseminated intravascular coagulation.

Few obstetric complications were observed: one case each of pre-eclampsia and gestational diabetes and three postpartum haemorrhages. There were four spontaneous vaginal deliveries and four caesarean deliveries for fetal distress or labour dystocia. Four caesareans were associated with intrauterine fetal demise. There were two induced vaginal deliveries, including one for pregnancy termination. Seven deliveries were on the day of diagnosis, five within the following four weeks, and two within three months.

Fetal outcomes

Data on fetal birthweight was available for five cases and four of these were under 800 g at birth. All were born prematurely and 12 of them before 34 weeks. Only three fetuses out of 12 cases reported had NICU admissions. Of those three, only one had NRDS. Five cases provided the fetus’ sex and only one was female. There were seven fetal deaths, and three neonatal deaths reported. Screening for LCHAD deficiency was not mentioned for any case (Table 3).

Table 3.

Obstetric and fetal outcomes.

	Gestational age at diagnosis^a	Gestational age at delivery^a	Delivery method	Reason for caesarean or induction	Fetal sex/weight (gm)	Fetal outcome
Wong et al. 2020¹¹	20	20	CS	IUFD	M/NA	FD
Ramadan et al. 2021¹²	20	20	IOL	Pregnancy termination	M/325	ND
Onwuagbu et al. 2018²⁵	21	25 + 3	IOL	NA	F/720	ND
Yassin et al. 2011¹⁵	23	36	SVD	–	NA/2900	A
Fujimura et al. 1998²⁶	23	23 + 2	CS	Fetal distress/labour dystocia	M/NA	FD
Hoare et la. 1994²⁷	24	34	SVD	–	NA/NA	A
Ringers et al. 2016²⁸	25	25	SVD	–	NA/NA	ND
Hartwell, et al 2014²⁹	26	26	CS	IUFD	NA/NA	FD
Jwayyed et al. 1999³⁰	26	26	CS	IUFD	NA/NA	FD
Modir et al. 2008³¹	27	27	CS	Fetal distress/labour dystocia	NA/NA	A
Cruciat et al. 1982²⁴	27 + 5	27 + 6	CS	IUFD	NA/800	FD
Suzuki et al. 2001³²	23 + 6	24 + 1	SVD	–	M/650	FD
Oliveira et al. 2014³³	27 + 6	27 + 6	CS	Fetal distress/labour dystocia	NA/NA	A
Bernuau et al. 1983³⁴	27 + 7	28 + 5	CS	Fetal distress/labour dystocia	NA/NA	FD

CS: caesarean section; IOL: induction of labour; SVD: spontaneous vaginal delivery; IUFD: intrauterine fetal dismise; M: male sex; F: female sex; FD: fetal death; ND: neonatal death; A: alive; NA: not available.

^aGestational age at diagnosis and at delivery reported in weeks + days.

Discussion

Acute fatty liver in pregnancy remains a rare but critically significant obstetric emergency with severe maternal and fetal implications. This systematic review of 14 cases diagnosed in the second trimester sheds light on the clinical nuances of this condition, challenging the conventional belief that AFLP occurs only in the third trimester. AFLP in the second trimester is a rare but recognized condition. The findings highlight several critical aspects of second-trimester AFLP. Maternal presentations were marked by diverse symptoms, with vomiting and abdominal pain being the most common. The Swansea criteria proved valuable in confirming diagnoses even in the second trimester, emphasizing the need for clinicians to keep AFLP in mind regardless of the trimester of presentation.^8,35 In cases with atypical evolution, liver biopsy remains an important diagnostic tool to confirm diagnosis. Although a transjuglar route is an alternative for a percutaneous route in presence of coagulopathy, the decision to undergo a liver biopsy should be done by a multidisciplinary team in an experimented centre.³⁶ Unlike the typical presentation of AFLP, a minority of the cases in this review had an unusual delay between diagnosis and delivery. In these cases, we question whether there was a subacute presentation of AFLP and whether close inpatient monitoring should be considered in stable patient instead of immediate delivery. Although this brings up the question of how to discriminate that subset of patient. Reporting of these atypical cases in the literature is important to help identify common characteristics in this subset of women. The maternal complications, including acute renal failure, hypoglycaemia, encephalopathy and liver failure, underscore the gravity of AFLP, necessitating intensive care, haemodialysis, and, in some cases, liver transplants. Obstetrically, second-trimester AFLP poses challenges—close monitoring, such as regular capillary blood glucose monitoring, is essential because of high maternal morbidity and often leads to preterm delivery and interventions like induction and caesarean section due to fetal distress.³⁷ Despite the severe morbidity, only one maternal death was observed from this review. Fetal outcomes were unfortunately grim, with a high incidence of prematurity, neonatal death, and significant NICU admissions. Interestingly, the lack of reported cases screened for LCHAD deficiency raises questions about the potential underlying genetic predispositions in AFLP cases during the second trimester.

Strengths of the study include an extensive literature review, with more than 6000 articles screened and validated by two independent reviewers to limit introductory bias. Clear inclusion criteria for AFLP diagnosis during second trimester allowed for identification of cases. Limitations to only English or French articles might have introduced study bias. We used the Swansea criteria or a positive liver biopsy as inclusion criteria. The Swansea criteria of presence ≥6 abnormal variables have a positive predicted value of 85% for AFLP.³⁸ We may not have captured all AFLP in our review.

We excluded 277 articles for insufficient data and may have missed real cases (attribution bias). We mainly found case reports, so we may have missed less severe cases (selective and publication reporting).

Clinicians should be aware of AFLP in the second trimester, although it is rare. Therefore, it is important to have a precise diagnosis, and clinicians should quickly consider a hepatic biopsy if doubts remain on the diagnosis. Better understanding of the subclinical presenting is important as there is a subset of women who may not require immediate delivery. These cases need appropriate multidisciplinary management to reduce maternal morbidity and prevent maternal mortality. The absence of LCHAD deficiency or other genetic anomaly screening in the fetuses of reported cases suggests a potential area of improvement. Exploring genetic predispositions and antenatal screening could help mitigate the impact of AFLP on both maternal and fetal outcomes. We are retrospectively analyzing data from hospitals in Québec for the presence of AFLP in the second trimester and will report in the future. We hope that with additional cases of typical and atypical evolution, we will better understand if there is a subacute presentation to this disease and if so, how it could be differentiated to provide better fetal and maternal outcomes.

Footnotes

Acknowledgments

John Davison provided editorial assistance to the authors during preparation of this manuscript.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

No ethical approval for this study was needed.

Informed consent

Informed consent was not sought for the present study. The study design did not involve any direct patient contact.

Guarantor

MM.

Contributorship

LB designed the study, collected the data, contributed to data analysis, and drafted the manuscript. MM overviewed the conduct of the study, contributed to study design, collected the data, interpreted results and reviewed the manuscript. All authors read and approved the final manuscript.

ORCID iD

Michèle Mahone

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