Obstetric cholestasis (OC) is associated with significant perinatal mortality and maternal morbidity. Fetal outcome may be improved with increased antenatal surveillance and timely intervention. Frequently attributed to the Scandinavian authors Alvar Svanborg and Leif Thorling, the first case report was by Ahlfeld in 1883 who elegantly described recurrent jaundice in a pregnant patient that remitted with delivery. During the 1950's various terminologies originated describing some of the characteristic features of the disease: icterus gravidarum, cholestatic hepatosis and recurrent jaundice during pregnancy, all synonymous with ‘obstetric cholestasis.’ Ahlfeld's original patient did not complain of itching but over the recent years pruritis has become the commonest manifestation. Obstetric cholestasis is the most common disorder of liver function unique to pregnancy and second only to acute viral hepatitis as a cause of jaundice in the third trimester.

For several decades, visual analysis of the antepartum fetal heart rate tracing has been a primary mode of fetal surveillance despite lack of proof from randomized trials that its use leads to a reduction in perinatal mortality in high risk pregnancies. A meta-analysis of these trials offered the same conclusion. The trials were performed in the early 1980's with fetal monitors with poor signal to noise ratios and poorer testing schemes in comparison to today. Therefore the results may no longer be pertinent, however, it is unlikely that these trials will be repeated because of present medico-legal constraints. Nonetheless, the use of non-stress testing alone is an accepted mode of fetal surveillance because of associated low fetal death rates within 1 week of a normal test; 1.9 to 3.2/1000 patients tested. The expense associated with this low fetal death rate is a low positive predictive value of 25% to 50%. Interrelated with this inefficiency, is the considerable inter- and intra-observer variation in the interpretation of antepartum fetal heart rate tracings. Variation in the interpretation of antepartum fetal heart rate tracings continues to exist despite the increase in experience and knowledge of fetal heart rate monitoring and improvement in fetal heart rate monitors. The end result is a form of fetal surveillance that is of questionable value and inefficient, requiring frequent back up testing to clarify fetal condition.

Attwood traces the earliest possible description of a case of amniotic fluid embolism (AFE) to 1825. The next case was described by Meyer some 101 years later. Not until 1941 was this obstetric catastrophe recognised as constituting a true syndrome with its own clinical and pathological characteristics. Any combination of sudden and profound shock, dyspnoea, cyanosis, apprehension, seizures, and the failure of rapid blood coagulation may herald the clinical onset of an AFE. Liban was the first to report the detection of squamous cells throughout the systemic circulation, an observation which was not explained at the time. Many have commented upon the ominous fetal heart pattern that almost invariably accompanies AFE if the fetus is in-utero at the time of the embolus.

The spectrum of abdominal wall defects includes exomphalos (omphalocoele), gastroschisis, and bladder and cloacal exstrophy. These congenital anomalies are readily recognised on a prenatal ultrasound scan. A raised maternal serum alpha-fetoprotein (MSAFP) should also prompt an ultrasound examination looking specifically for these anomalies, as well as neural tube defects. The influence of prenatal diagnosis on the peri- and postnatal management and outcome is still the subject of debate. Most published work relies on patient numbers too small to be of use statistically. Attempting to draw objective conclusions is made difficult because published series come from units with differing facilities and levels of expertise in the many professional groups involved in the management of these often complex anomalies.