Karl E. Mason aq^ 



Li — .Superficial congestion aioinul right shoulder and over both parietal regions 



L2 — Normal 



L3 — Superficial congestion in posterior auricular and left parietal regions 



L4 — Superficial congestion in right shoulder and o\er lumbar vertebrae 



Lr, — Extensive congested plexuses over dorsum of trunk and head. Multi]jlc petechiae 



overlying cervical and thoracic spinal cord, with distention of vertebral vessels on each 



side; other jjetechial spots over cerebrum and cerebellum 



The vascular changes described are unquestionably pathognomonic for 

 vitamin E deficiency. Their incidence, and that of late fetal death, have con- 

 sistently proved to be inversely proportional to the magnitude of borderline 

 levels of giaded dosage in bio-assays of the various natural and synthetic forms 

 of vitamin E. It has been conclusively demonstrated that the daily administra- 

 tion of relatively large amounts of ascorbic acid or vitamin K (2-methylnaptho- 

 quinone) during the first sixteen days of pregnancy does not influence eithci 

 the occurrence or the character of the vascular injury. Furthermore, vitamin 

 E-deficient fetuses have been found to contain a normal content of vitamin 

 C as measured by the silver nitrate technique, and rats suffering from pro- 

 longed deficiency of vitamin E have shown no alteration in blood-clotting 



time.* 



Discussion 



The ultimate cause of fetal death in the vitamin E-deficient fetus at the six- 

 teenth day of gestation is undoubtedly the same as that operative at earlier 

 stages of development, namely, diminiuion of the circulating blood to a level 

 inadequate for continued survival of fetal tissues. The question of paramount 

 importance is whether this ischemic state is brought about by a suppression 

 of hematopoiesis, as suggested by Evans and Burr^ in their study of younger 

 fetuses, or by a defect in the vascular wall leading to congestion, stasis, and 

 extravasation of blood into the tissues. Acceptance of the first explanation 

 implies that the vascular injury is the natural result of decreased blood vol- 

 ume. Acceptance of the second alternative implies that the evidence sugges- 

 tive of impaired hematopoiesis is really an artifact caused by vascular dilation 

 and congestion associated with hemorrhage into the soft tissues. It cannot be 

 denied, however, that both processes might be operative at diff^erent periods 

 of the development or even simultaneously. 



The observations presented here afford some evidence that the hemato- 

 poietic activity of the liver at the sixteenth day of development may not be 

 appreciably depressed in fetuses exhibiting early vascular lesions. However, 

 the variable picture encountered in different fetuses and the rapid telescop- 

 ing of the terminal events have so far made it impossible to state with cer- 

 tainty whether phenomena suggestive of hematopoietic dysfunction are the 

 cause of, or the result of, the vascular lesions. 



Little can be said at present concerning the exact cause or nature of the 



* I am indebted to Dr. C. P. Leblond for analysis of the fetal tissues by silver nitrate precipi- 

 tation, to Dr. Sarah Hooker and Mr. R. \. Bruce for determinations on the blood-clotting 

 time. 



