The mortality from acute fatty liver of pregnancy has been reduced significantly to 18%, and is now related primarily to complications, particularly DIC (Disseminated Intravascular Coagulation) and infections. After delivery, most mothers do well, as the stimulus for fatty acid overload is removed. The disease can recur in future pregnancies, with a calculated genetic chance of 25%; the actual rate is lower, however. Mortality of the foetus has also diminished significantly, but still remains 23%, and may be related to the need for premature delivery. History
The disease was first described in 1940 by H. L. Sheehan as an "acute yellow atrophy" of the liver, then thought to be related to delayed chloroform poisoning. See also
Fatty liver

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Cardiogenic
Congestive heart failure which is due to the hearts inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in pulmonary wedge pressure and edema – this usually is due to left ventricular failure, but may also be from arrhythmias, or fluid overload, (e.g. from kidney failure or intravenous therapy). Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow in blood vessels and causes the elevation in wedge pressure and subsequent pulmonary edema. Non-cardiogenic
Negative pressure pulmonary edema in which a significant negative (internal) pressure in the chest (such as from an inhalation against an upper airway obstruction) ruptures capillaries and floods the alveoli with blood. Negative pressure pulmonary edema has an incidence in the range of 0.05-0.1% in cases of general anesthesia. The negative pressure causes a significant increase in preload, thereby increasing pulmonary blood volume. There is also a significant increase in left ventricular afterload, which causes a decreased cardiac output. The increase in pulmonary blood volume and pressure along with a decrease in cardiac output to the lungs will increase the pulmonary transudative pressures and the risk of pulmonary edema. With all this occurring, pulmonary vascular resistance increases causing a shift of the intraventricular septum. The ventricular septal shift to the left causes a left ventricular diastolic dysfunction, which further increases pulmonary hydrostatic pressures and the risk. Neurogenic causes  (seizures, head trauma, strangulation, electrocution).