At the beginning, the hepatocytes present small fat vacuoles (liposomes) around the nucleus (microvesicular fatty change). In this stage, liver cells are filled with multiple fat droplets that do not displace the centrally located nucleus. In the late stages, the size of the vacuoles increases, pushing the nucleus to the periphery of the cell, giving characteristic signet ring appearance (macrovesicular fatty change). These vesicles are well-delineated and optically "empty" because fats dissolve during tissue processing. Large vacuoles may coalesce and produce fatty cysts, which are irreversible lesions. Macrovesicular steatosis is the most common form and is typically associated with alcohol, diabetes, obesity, and corticosteroids. Acute fatty liver of pregnancy and Reyes syndrome are examples of severe liver disease caused by microvesicular fatty change. The diagnosis of steatosis is made when fat in the liver exceeds 5–10% by weight. Defects in fatty acid metabolism are responsible for pathogenesis of FLD, which may be due to imbalance in energy consumption and  its combustion,  resulting in lipid storage, or can be a consequence of peripheral resistance to insulin, whereby the transport of fatty acids from adipose tissue to the liver is increased. Impairment or inhibition of receptor molecules (PPAR-α, PPAR-γ and SREBP1) that control the enzymes responsible for the oxidation and synthesis of fatty acids appears to contribute to fat accumulation. In addition, alcohol use disorder is known to damage mitochondria and other cellular structures, further impairing cellular energy mechanism. On the other hand, non-alcoholic FLD may begin as excess of unmetabolised energy in liver cells.
A maternal age of 35 years or older is associated with AFE. Diagnosis
AFE is diagnosed when all other causes have been excluded. The presence of fetal squamous cells or other fetal tissues, including meconium, have been found in the maternal circulation after the event. Diagnosis is also based upon the signs and symptoms observed during the birth or procedures. Treatment
A case report on Amniotic Fluid Embolism published in the A & A Practice Journal in 2020 has revealed that when milrinone is administered as an aerosol, selective pulmonary vasodilation occurs without significant changes in mean arterial pressure or systemic vascular resistance; and if used immediately after Amniotic Fluid Embolism, inhaled milrinone may mitigate the pulmonary vasoconstriction.However, since the circumstances that lead to this complication are difficult to influence, treatment to resolve the symptoms and deteriorating vascular conditions can improve outcomes. Epidemiology
Amniotic fluid embolism is very uncommon and the rate at which it occurs is 1 instance per 20,000 births. Though rare, it comprises 10% of all maternal deaths. History
This rare complication has been recorded seventeen times prior to 1950. The complication was originally described in 1926 by J. R. Meyer at the University of Sao Paulo. A 1941 case study of eight autopsies of pregnant women who died suddenly during childbirth by Clarence Lushbaugh and Paul Steiner enabled widespread recognition of the diagnosis within the medical community, and was eventually republished as a landmark paper in the Journal of the American Medical Association. References


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