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Chapter 33 (page 171)
Extent of Duodenal Spread as Determined Microscopically
In the majority of 38 cases culled from the literature, Castleman (l936) found that the
extent of duodenal invasion was not more than 1.0 to 2.0 cm; in isolated cases it could be
5.0 cm. In 6 of his autopsy specimens the extent of duodenal spread varied from 4.0 mm
to 2.3 cm.
In 8 of 9 cases Zinninger and Collins (l949) found the extent of duodenal invasion to vary
from 3.0 mm to 2.0 cm; in an unusual case it was 6.0cm. In 14 cases Eker and Efskind
(l952) found the distance of duodenal infiltration beyond Brunner's glands to be short; 6
of these were adenocarcinomas and in these cases the invasion stopped at Brunner's
In 92 percent of 151 cases Majima et al. (l964) found duodenal spread to be 1.0 cm or
less; in a further 6 percent it was 2.0 cm or less. Paramanandhan (l967) examined 29
cases. In more than half no tumor tissue was detected beyond the first 3.0 cm of the
duodenum; in one it extended for 22.6 cm. Koehler et al. (l977) concluded than in as
many as half the cases the tumor extended no more than 1.0 cm beyond the pylorus.
In 3 of our 7 cases duodenal extension was 2.0 cm or less; in 3 it appeared to extend as
far as the commencement of Brunner's glands, and in one it was 5.0 cm.
According to Castleman (l936) pyloric adenocarcinoma usually spreads along the
submucosa into the duodenum, and rarely along the mucosa; spread often occurs in
lymphatics. In 14 cases Coller et al. (l941) found that direct spread along the walls
occurred in some cases, and in others spread was via submucosal and intermuscular
Zinninger and Collins (l949) stated that duodenal spread occurred mostly through direct
infiltration of the muscular layers or through subserosal lymphatics; in 3 of 9 cases it
also occurred in the submucosa. Spread may also take place via lymphatics to isolated
lymph nodes beyond the pylorus, without the duodenal walls being involved.
In 6 cases of gastric adenocarcinoma Eker and Efskind (l952) noted duodenal spread
along all layers of the walls, but in the mucous membrane it stopped at the
commencement of Brunner's glands. In 4 of 6 cases of mucinous scirrhus carcinoma the
duodenal mucosa was spared; in the remaining 2 cases the duodenal mucosa was
involved for distances of 2.0 mm and 7.0 mm (all the other layers were also involved). In
2 cases of gastric colloid carcinoma the greatest spread occurred in the submucosa.
In 151 cases Majima et al. (l964) found serosal spread to the duodenum in 115; in a few
cases there was direct spread in the submucosa. In none could continuous extension in
the mucosa be demonstrated; in 5 cases of duodenal mucosal invasion, spread had
occurred via lymphatic channels. In 29 necropsy specimens Paramanandhan (l967) found
invasion of the duodenal submucosa the most frequent route of spread, followed by the
serosa and other layers of the walls; the duodenal surface epithelium appeared to remain
intact. Spread also commonly occurred to the subpyloric and other lymph nodes.
Ming (l973) stated that in most cases duodenal invasion occurred subserosally and that
the duodenal mucosa was not involved; the reason for this phenomenon was not known.
In 20 cases Koehler et al. (l977) found tumor cells predominantly in the duodenal
muscular and submucous layers; mucosal invasion was noted occasionally.
Three of our 7 cases were well differentiated adenocarcinomas. In 2 spread had taken
place along the submucosa and to a lesser extent in the mucosa; in one spread occurred
along the serosa and muscular layers. Three cases were poorly differentiated
adenocarcinomas; in one spread was seen in the muscular layer and small blood vessels,
in one in the submucosa but not in the superficial mucosa, and in one in the mucosa. One
case was a mucinous adenocarcinoma; in this case spread occurred in all layers of the
Linitis plastica was a type of carcinoma in which tubal spread occurred, and it had to be
considered separately (Fernet et al. l965; Hawley et al l970; Öman et al. l972).
Does a Duodenal Barrier Exist?
From the foregoing it appears that in the majority of cases duodenal spread of pyloric
adenocarcinoma is limited to the proximal 2.0 to 3.0 cm of its first part; this is seen even
in the presence of widespread extension in the stomach itself, contiguous spread to other
organs, e.g. the pancreas and widespread haematogenous and lymphatic metastases.
The question arises whether a barrier exists in the first part of the duodenum (as opposed
to a barrier at the pylorus), preventing further downward spread. It is assumed that a
possible barrier will have to be of an anatomical or a biochemical nature.
Paramanandhan (l967), while commenting on the infrequency with which pyloric
adenocarcinoma invades the duodenal mucosa (it has less respect for the deeper
components of the duodenal wall), stated that the following factors had to be taken into
account in explaining the phenomenon: (1) scarcity of lymphatic connections between
the stomach and duodenum; (2) normal upward flow of lymph from duodenum to
stomach; (3) alkalinity of duodenum; (4) spasmodic contraction of the pyloric
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