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jeopardized.
It was not until the work of Cole, Lathe, and Billing in 19545 that
any clear idea of the reason for this began to emerge. They showed
The 25th Simpson Smith Lecture, West London Hospital
254
SURGICAL JAUNDICE
that it was possible by chromatography to separate direct-reacting bilirubin into two distinct moieties, which they designated pigment I and
pigment II. In 1955 Billing6' 7 found that both pigments accumulated
in the serum in obstructive jaundice and in 1956 Billing and Lathe8
showed that pigment II constituted most of the bilirubin in fresh
human bile.
It then only remained for Bollman and Hoffman in 1957 to demonstrate that after hepatectomy direct-reacting pigment I accumulated in
the serum, and the mystery was cleared up. Obviously a direct-reacting
Hours
Fig. 1. Bilirubin concentrations in blood and lymph before and after obstruction of the common bile duct following cholecystectomy.
pigment could be made in the body which had not traversed the liver
and been excreted in the bile. Thus at last the 'van den Bergh hypothesis' was laid to rest and we could move on.
In the meantime, however, a further obstacle was encountered. It was
in 1930 that Rich9 had published his celebrated paper on 'The Pathogenesis of the Forms of Jaundice'. In this he reviewed the available
evidence and attempted a classification of jaundice on the basis of
whether or not the pigment responsible for the icterus had been excreted into the biliary tree. Of the van den Bergh test he wrote, 'I shall
not enter into a description of this now well-known test other than to
mention that when it is applied to bilirubin which has not yet passed
255
Ho D. RITCHIE
too,t
ISO
160
150
140
130
t120
*111100
90-
a Sio
60
'j40
30
20
Algter
to0
30 hours
obstruction (3)
1.5
2.5 3.0 3.5 4.0 4.5 5.0
2.0
Bile output otter releose in mi.
Fig. 2. Secretion of bromsulphalein into the bile during obstruction of the
0 0.
1.0
bile into the biliary tree continues unchecked. Secondly that it is then
regurgitated or 'vomited back' into the lymph or blood. He went on to
elaborate his subdivision of jaundice into two main types, calling that
variety which results from a primary failure of the liver cells to secrete
bilirubin into the ducts 'retention' jaundice and that which he believed
to be due to passage of formed bile from the biliary tree back into the
256
SURGICAL JAUNDICE
lymph and blood 'regurgitation' jaundice. He did not himself offer any
experimental evidence for these views.
Thirty years later, however, studies during bile duct obstruction
showed a different situation10. It can be seen from Figure 1 that after
24 hours of obstruction all evidence of 'regurgitation', into the fymph at
least, has disappeared. But what of secretion into the biliary tree during
this latter period? Serial analysis of pent-up bile where biliary obstruction had been present for several days gave the required information.
When bromsulphalein, which is handled by the liver in much the same
way as bilirubin, is used as a tracer none of it can be found in bile
from the biliary tree once obstruction has been present for a day or
two (Fig. 2).
And so we now know that during biliary obstruction a short phase
of 'regurgitation' lasting 24 hours ensues, but only in the absence of a
functioning gallbladder. Thereafter and throughout the period of obstruction secretion of bile into the biliary tree does not apparently
occur. Thus in its turn the 'regurgitation' hypothesis of Rich was found
to be suspect and we had to return to the drawing board as it were,
to re-think how we should now subdivide jaundice.
Classifications of jaundice abound in the literature. Some have served
a useful purpose, others have not. Table I shows four of the best known
of these. The pathological classification of McNee in the top left-hand
corner is still widely used and serves to remind particularly the
undergraduate of the main causes. It is, however, in difficulty when, for
example, the cholestatic variety of viral hepatitis is being considered.
TABLE I
TYPES OF JAUNDICE
Rich
McNee
"Retention"
Haemolytic
"Regurgitation"
Toxic or infective
Obstructive
Prehepatic
Hepatic
Posthepatic
N. American
Medical
Surgical
IL D. RITCHIE
(1961-1965)
NIL
(1950-1961)
0.14%
0.17%
SURGICAL JAUNDICE
259
IL D. RITCHIE
We must bear in mind, however, that while these tests may help
us to avoid laparotomy in medical jaundice they do not solve all our
problems in the diagnosis of obstructive jaundice. They will not demonstrate stones in the common bile duct or high bile duct neoplasms, but
here the need for early operation is perhaps less.
This then would appear to be a safe method of expediting the diagnosis of certain types of jaundice. But many problems remain. So often
in jaundice due to panpreatic carcinoma, for example, the surgeon finds
the lesion too far advanced to be able to do more than a palliative
operation.
In reviewing the whole field, however, we may be reassured by the
knowledge that once more we are moving forward, and in the words
of Horace: 'Quad optanti divom promittere nemo auderet volvenda
dies en attulit ultro'-'What no one of the Gods would dare to promise
in answer to our prayers-lo, time itself as it rolls its course, has accomplished for us' !
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11.
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REFERENCES
EHRLICH, P. (1883) Quoted by van den Bergh (ref. 3).
PROSCHER, -. (1900) Quoted by van den Bergh (ref. 3).
VAN DEN BERGH, H. A. (1918). Die Gallenfarbstoff im Blute. Leiden, van Doesburgh.
BARRON, E. S. G., and BUMSTEAD, J. H. (1928) J. exp. Med., 47,999.
COLE, P. G., LATHE, G. H., and BILLING, B. H. (1954) Biochem. J., 57, 514.
BILLING, B. H. (1955) J. clin. Path. 8, 126.
BILLING, B. H. (1955) J. clin. Path.. 8, 130.
BILLING, B. H., and LATHE, G. H. (1956) Biochem. J., 63, vi.
RICH, A. R. (1930) Johns Hopk. Hosp. Bull., 47, 338.
RITCHIE, H. D. (1959). Ch.M. Thesis University of Edinburgh.
SHALDON, S., and SHERLOCK, S. (1957) Brit. med. J., 2, 734.
DATTA, D. V., SHERLOCK, S., and SCHEUER, P. J. (1963) Gut, 4, 223.
TURNER, M. D., and SHERLOCK, S. (1964). In Surgery of the Gall Bladder and Bile Ducts, ed. R. Smith
and S. Sherlock. London, Butterworths.
HARVILLE, D. D., and SUMMERSKILL, W. H. J. (1963) J. Amer. med. Ass., 194,257.
ZAMCHEK, M., and KLAUSENSTOCK, 0. (1953). New Engl. J. Med., 249, 1062.
GEORGE, P., YOUNG, W. B., WALKER J. G., and SHERLOCK, S. (1965) Brit. J. Surg., 52, 779.
GEORGE, P. (1966). In Postgraduate Gastroenterology, ed. T. J. Thompson and I. E. Gillespie. London,
Bailli6re.
THORBJARNARSON, B. (1967) Surgery, 61, 347.
GLENN, F., EVANS, J. A., MUJAHED, Z., and THORBJARNARSON, B. (1962) Ann. Surg., 156, 451.
THORBJARNARSON, B., MUJAHED, Z., and GLENN, F. (1967) Ann. Surg., 165, 33.
BOURKE, J. B., SWANN, J. C., BROWN, C. L., and RITCHIE, H. D. (1972) Lancet, 1, 605.
260