Familial Icterus of New-Born Infants

Abstract

Pfannenstiel1 gave the first detailed description of familial icterus of newborn children. He described two fatal cases and collected the scattered reports in the literature. The cause of familial icterus of newborn children is unknown. The disease has nothing in common with Buhl's or Winckel's disease. There is no evidence to prove that familial icterus is due to septic processes. It is not present at birth, but appears during the first days of life. In none of the cases is there a history of birth injury, nor does it seem to be due to toxemia of pregnancy. Most of these children are strong, robust and mature at birth. One might say that the children are in a sense physically defective and very soon become incapacitated to carry on extra-uterine existence. It is possible that the liver failed in the performance of its extra-uterine function.

Congenital Defect of the Scalp: An Infant with a Bullous Lesion at Birth

“…They have been variously attributed to trauma, amniotic adhesions, or developmental defect. The usual appearance at birth varies from a punched out, granulating ulcer to a thin cicatrix with no skin appendages (Abt, 1917). The appearance seen in the present case has not so far been recorded in an infant at birth although Ingalls in 1933 described five embryos of from 15 to 187 mm.…”

Congenital Skin Defect of the Newborn

“…On the scalp they are 191 192 ARCHIVES OF DISEASE IN CHILDHOOD usually small and situated in the mid line of the vertex. On the trunk, lsions descibed by Hochstetter (1894) and Sutton (1935) are almost identical; whilst on the limbs the defects of the skin of the knees in the cases of Braun (1894) and Abt (1917) are similar. Our second case was similar to the one described by Rogatz and Davidson (1943).…”

Localized Congenital Defects of the Scalp

“…In this circular type of defect, the lesion is usually confined to the skin (Abt, 1917;Anderson and Novy, 1942;Calloway et al, in this case) and may penetrate to the dura (Kehrer, 1910 1930). In a case described by Terruhn, the defect was symmetrical and extended through the skin, periosteum and bone to the cerebral membranes and allowed the convolutions of the brain to be clearly seen.…”