A parenchyma-wise technique for the ex vivo procurement of segment 4 (S4) grafts, based on the detailed architecture of the segment, is proposed. Eighteen normal, fresh livers from adult cadavers were injected differentially with colored latex; dissection casts were prepared; and the intricate architecture of S4 was studied. The portal vein elements of the sheath forming most of the inferior part of S4 (S4b) and the superficial major fraction of its superior part (S4a) arose constantly from the medial aspect of the umbilical part of the left portal vein branch. The arterial elements arose constantly from a branch, whose diameter ranged from 2.00 to 3.35 mm (mean = 2.61 ± 0.54 mm) and whose length ranged from 15.15 to 45.65 mm (mean = 27.98 ± 12.13 mm). The biliary elements coalesced as a single duct at the corner, which was formed from the umbilical and transverse parts of the left portal vein branch; the duct's diameter ranged from 2.90 to 6.85 mm (mean = 3.90 ± 1.34 mm). Theoretically, this parenchymal mass-S4b and the superficial fraction of S4a-could be procured for implantation in an infant, and the rest of the liver could be split for an adult and a child. The portal vein branches of the graft would be procured with a patch from the medial aspect of the donor's umbilical portion of the left portal vein branch. This umbilical portion would be reconstructed with a patch from the donor's round ligament. The recipient's portal vein would be reconstructed through the fashioning of a conduit anastomosed with the graft's venous patch.

The term "aberrant bile ducts" has been used to designate three heterogeneous groups of biliary structures: (1) bile ducts degenerating or disappearing (unknown etiology, diverse locations); (2) curious biliary structures in the transverse fissure; and (3) aberrant right bile ducts draining directly into the common hepatic duct. We report our observations on these three groups. Twenty-nine fresh human livers of stillborns and adults were injected differentially with colored latex and dissected. Adult livers showed portal venous and hepatic arterial branches, and bile ducts not associated with parenchyma, subjacent to and firmly adherent with the liver capsule: elements of ramifications of normal sheaths were present on the liver's surface. These ramifications, having lost parenchyma associated with them, then sequentially lost their portal branches, bile ducts and arterial branches. This process affected the ramifications of the sheaths in the left triangular ligament, adjacent to the inferior vena cava, in the gallbladder bed and anywhere else on the liver's surface and resulted in the presence of bile ducts accompanied by portal venous and/or hepatic arterial branches and not associated with parenchyma for a period of time. This first group represented normal bile ducts that do not meet the criteria of aberration and could be appropriately designated "remnant surface bile ducts." Such changes were not found in the transverse fissures and review of the literature revealed that the curious biliary structures are the microscopic peribiliary glands. The third group met the criteria of aberration and the anatomy of a representative duct is described.

The most frequent site at which the common fibular nerve is affected by compression, trauma, traction, masses, and surgery is within and around the fibular tunnel. The aim of this study was to determine whether there were protective mechanisms at this site that guard against compression of the nerve. Twenty-six lower limbs of 13 preserved adult cadavers (11 males and two females) were used. Proximal to the entrance of the tunnel, three anatomical configurations seemed to afford the required protection for the nerve: reinforcement of the deep fascia; tethering of the common fibular nerve to both the tendon of the biceps femoris and the reinforced fascia; and the particular arrangement of the deep fascia, fibular head, and soleus and gastrocnemius muscles. At the entrance of the tunnel, contraction of the first segment of fibularis longus muscle could afford the required protection. In the tunnel, contraction of the second and third segments of fibularis longus muscle could guard against compression of the nerve. The tough fascia on the surface of fibularis longus muscle and the fascial band within it, which have long been accused of compression of the nerve, may actually be elements of the protective mechanisms. We conclude that there are innate, anatomical protective mechanisms which should be taken into consideration when decompressing the common fibular nerve. To preserve these mechanisms whenever possible, the technique should be planned and varied according to the underlying etiology.