One reasonable cause of unexplained and unexpected fetal death is occlusion of umbilical cord blood flow. Not all potential causes of umbilical cord occlusion would necessarily be evident at delivery. I submitted a study to NIH that aimed to discover the incidence in fetal death of two such “invisible” anatomic configurations. The two configurations are occult cord prolapse and functional short cord segment due to cord wrapping.
The first is familiar from cases of fetal compromise in livebirths. The cord prolapse puts a loop of cord at two risks for occlusion: First is direct pressure between the presenting part and the uterine wall. The second is the risk of kinking if the loop becomes a “V”. The anatomy and physiology of this kinking is analogous to bending a straw or making a “V” in a soft hose to stop water flow.
The second configuration is less familiar but may account for the increased incidence of stillbirth with multiple cord wrappings. A medical student and I investigated this mechanism in vitro. Based on our in vitro study, we found that the shorter the cord segment being twisted, the fewer degrees of twist (rotation) are needed to stop umbilical vein flow. A functional short segment occurs if a cord wrapping around the fetus begins close to the placental insertion. At least in vitro the cord wrapping around a pipe is sufficient to anchor the cord and prevent propagation of the twist along the wrapped portion, creating a functional short cord segment. Then that cord segment extending past the wrap is the critical length that determines the degree of torsion needed to stop flow in vitro. A rotation of as little as 180 degrees applied to a few centimeters of free cord will stop flow. In vivo, the rotation would be applied by the turning of the fetus.
Both a functional short segment and an occult cord prolapse might not be evident after the delivery. Multiple cord wrappings or tight nuchal cord may be indirect indicators of a risk of short fetal to placental segment. Placental evidence of obstructed fetal blood flow (fetal vascular malperfusion lesions) likewise may be indirect evidence of obstructed umbilical blood flow.
The NIH reviewers of the grant did not have significant criticism of the hypothesis, per se, but rather to the fact that I had no preliminary data. The radiologist on the study confirmed that the equipment we had would be able to image the whole cord and its relationships. However, the at-risk cord configurations had not been demonstrated in an actual case. A further valid criticism was that I had been unable to find a collaborator in fetal maternal medicine. I did obtain IRB approval for the study. The study also had a questionnaire that would provide a more systematic clinical history of immediate postmortem events. The catch 22 is that to get preliminary data requires funding, but funding requires preliminary data. One possible strategy would be to order an MRI before delivery as an extension of the autopsy with minimal risk to the mother. I have no idea if medical insurance would cover the cost of the MRI.
I have retired and will not be pursuing this project. I want to offer this protocol to anyone who will pursue it. I think the PI on the study should be an obstetrician, not a pathologist. A careful clinical history and pathological study of the placenta and fetal autopsy are important, but not necessary components to gather the preliminary MRI data. A secondary benefit of the study is that the MRI would also provide a virtual postmortem exam of the fetus, which may show important quantifiable information about the redistribution of organ blood volumes, and heart dilatation.
Note: references supporting this blog are in the NIH study protocol. The protocol is identified as SUMT (Stillbirth Umbilical cord MRI Tipping point study) in the list of pages on this site. (I can no longer add titles into the side boxes with my free version of WordPress)
obstetrical pathology 
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