Chapter 1: What are the initial symptoms of acute fatty liver disease of pregnancy?
Imagine a 29-year-old previously healthy patient who presents to the hospital with a one-week history of feeling increasingly unwell with asthenia, polyuria, and polydipsia. What diagnoses come to mind? What if she is a primogravid at 33 weeks of gestation and also presenting with jaundice? Does this change her differential diagnosis and subsequent management?
First coined as acute yellow atrophy of the liver in 1903, this rare pregnancy-specific complication occurs in approximately 1 in 10,000 deliveries. It causes hepatic microfascicular steatosis due to an impairment in fatty acid beta-oxidation.
It is an obstetric emergency generally occurring in the third trimester, in which multi-organ fatty infiltration can quickly lead to liver failure and potentially catastrophic maternal and fetal consequences, including death. Today, our patient has acute fatty liver of pregnancy, AFLP, and you are the doctor.
Welcome to The Internet Work, a podcast written by medical residents and students meant to serve you better on the wards and on call. Today's episode is titled D-Liver. It's Crucial. This podcast is all about keeping it real. Residency is hard physically, mentally, emotionally.
Chapter 2: How does gestational age affect the differential diagnosis for liver disease?
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So, if you're in the market, which, let's be real, we kind of always are, head to wearfigs.com and use code FIGSCA at checkout for 20% off your first order. Again, that's wearfigs.com, code FIGSCA. Time for a minute physiology. While the exact pathophysiology of AFLP remains unclear, current theories are based on fetal placental and maternal impairments in fatty acid oxidation.
AFLP typically presents in the third trimester and more rarely in the second trimester. This timing likely reflects physiologic changes which peak in late pregnancy, such as the progressive shift in maternal metabolism towards a greater reliance on fatty acids for energy and increased fatty acid production to support fetal and placental growth.
Therefore, more fatty acids are being transferred to the fetal-placental unit, which would normally be oxidized by the placenta and the fetus to a lesser extent. However, if there are fetal placental defects and fatty acid oxidation, damaging free radicals can accumulate and enter the maternal circulation, overwhelming her own capacity for oxidation.
As a result, these toxic compounds lead to multi-organ microfascicular fatty deposition and eventual injury, primarily manifested by liver failure. Interestingly, impaired fetoplacental beta-oxidation from a deficiency in long-chain hydroxy-axyl-CoA dehydrogenase has widely been identified as a risk factor for developing AFLP, as 20% of cases are linked to this fetal enzyme deficiency.
Other risk factors include nulliparity, male fetus, maternal BMI of less than 20, prior history of AFLP, multifetal pregnancies, and the co-occurrence of hypertensive disorders of pregnancy. When approaching pregnancy cases, it's important to remember that there are two patients to assess and manage, the pregnant mother and the fetus.
For AFLP, you first want to ensure that both the mother and the fetus are stable, since this disease has a historically high mortality rate, with maternal and fetal mortality rates previously estimated at 10-15% and 20-25% respectively.
However, as we will discuss, the estimated maternal and fetal mortality rates have decreased to 2-12% and 10-15% recently through early detection and management of liver failure and fetal distress. Another challenge in approaching pregnant patients is the inclusion of both pregnancy-related and non-pregnancy-related pathologies in the differential diagnosis.
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