Obstructive Jaundice as a Complication
of Pancreatitis
BERNARD R. WEINSTEIN, M.D., ROY J.
HYMAN J. ZIMMERMAN,
Chicago, Illinois
P ERSISTENT obstructive jaundice pro-
duced by pancreatitis is a well-docu-
mented phenomenon (1-10). In patients
without demonstrable extrahepatic biliary
tract disease, often alcoholics, the jaundice
has been shown to be the result of obstruc-
tion of the intrapancreatic portion of the
common bile duct by the inflammatory
lesion, or its sequelae (8-10).
Transient obstructive jaundice produced
by pancreatitis, however, has received
much less attention than its more per-
sistent form. Rapidly subsiding jaundice
in alcoholic patients is frequently at-
tributed to intrahepatic cholestasis sec-
ondary to parenchymal hepatic disease
(fatty metamorphosis (11, 12), "alcoholic
hepatitis" (IS, 14), or cirrhosis), despite
the frequent association of pancreatitis
with alcoholism (15-21). Absence of a read-
ily recognizable etiology for extrahepatic
obstruction permits this formulation.
The present account of 24 patients with
obstructive jaundice, proved or presumed
to be caused by pancreatitis, is presented
to indicate the frequency of this phe-
nomenon and the variability of the as-
Received June 15, 1962; accepted for publication
July 19, 1962.
From the Departments of Medicine, Veterans
Administration West Side Hospital and Mount
Sinai Hospital, the Chicago Medical School, and
the University of Illinois College of Medicine, Chi-
cago, Illinois.
Supported in part by grant MTG-5225 from the
United States Public Health Service.
Requests for reprints should be addressed to H.
J. Zimmerman, M.D., Chicago Medical School, 710
Wolcott Street, Chicago 12, Illinois.
245
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
KORN, M.D., F.A.C.P., and
M.D., F.A.C.P.
sociated clinical features. In 10 patients,
obstruction of the common bile duct was
proved at surgical exploration or autopsy.
In 14 patients with a clinical diagnosis
of pancreatitis, transient jaundice, sugges-
tive of extrahepatic obstruction, was pre-
sumed to have been produced by the
pancreatitis.
MATERIALS AND METHODS
All patients in this report were male chronic
alcoholics, admitted to the Veterans Administra-
tion West Side Hospital during the years
1957-1961. The average age was 42 years, with
the youngest patient 27 years and the oldest
78 years.
Two groups of patients are presented (Table
1). Group 1 comprises the 10 patients with
persistent obstructive jaundice demonstrated at
laparotomy, autopsy, or both, to be secondary
to pancreatitis. Group 2 includes 14 patients
with a clinical diagnosis of pancreatitis who
were observed during an episode strongly sug-
gestive of obstructive jaundice.
The following studies were performed in
these patients: serum bilirubin level (total and
partition) by the method of Malloy and Evelyn
(22); alkaline phosphatase by the method of
Bodansky (23); thymol turbidity by the pro-
cedure of Maclagen (24), as modified by Shank
and Hoagland (25); serum glutamic-oxalacetic
transaminase activity (GOT) and serum glu-
tamic-pyruvic transaminase (GPT) utilizing the
Reitman and Frankel procedure (26); cephalin
flocculation by the Neefe modification of the
Hanger method (27); and serum protein analy-
sis by the Weichselbaum modification (28) of
the Kingsley biuret method (29).
Amylase levels in the serum or urine were
determined by the modified Somogyi method
(30). We have accepted as the upper limit of
normal 200 units/100 ml of serum, 4000 units/
 WEINSTEIN, KORN, AND ZIMMERMAN
246
TABLE 1. Clinical Material
Group Age Evidence
Patients
yr
1 33-78 Anatomical:
(Proved) Autopsy
Laparotomy
Laparotomy and
autopsy
Total
2 jaundice was slight, had G O T and GPT
(Presumptive) 27-48 Clinical
24-hr urine, and 280 units/1 hr urine specimen
(31).
Cholecystography revealed no evidence of
gall bladder disease in the 14 patients in group
2. Liver biopsy (Vim-Silverman needle, inter-
costal approach) was performed in 11 of the
14 patients with a presumptive diagnosis of
obstructive jaundice due to pancreatitis. These
were obtained at varying intervals after re-
covery from the acute episodes. Specimens of
liver and pancreas were obtained at surgical
exploration or autopsy in the 10 patients of
group 1.
RESULTS
GROUP 1
Data on the patients with the proven
diagnosis of common duct obstruction sec-
ondary to pancreatitis are shown in Table
2. All of the patients had clinical jaundice.
In one, patient 8, the bilirubin level was
only 2.5 mg per 100 ml on the day after
admission to the hospital. In the re-
mainder, it varied from mild elevations
(bilirubin level, 5 to 10 mg per 100 ml)
to deep jaundice (bilirubin level, 15 to 38
mg per 100 ml). The duration of jaundice
prior to admission, in 9 of the 10 patients,
ranged from 2 to 14 days. One patient, no.
9, stated that he had had "yellow eyes"
for 6 months. Serum alkaline phosphatase
levels were in a range suggestive of ob-
structive jaundice (17 to 28 Bodansky
units) in 5 patients (patients 2, 3, 6, 7, and
9). Two patients, nos. 1 and 4, had only
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
Annals of
Internal Medicine
moderately elevated levels of alkaline
phosphatase but had bilirubin levels above
No. of 30 mg per 100 ml. These 2 patients had
cirrhosis as well as pancreatitis. In the re-
maining 3, (patients 5, 8, and 10), the
bilirubin and alkaline phosphatase levels
3 were only slightly or moderately elevated.
5 Levels of serum GOT were elevated in 7
2
of 8 patients. In 6, the degree of elevation
was slight, ranging from 46 to 152 units.
The serum G P T values, which were lower,
10
are shown in Table 2. Patient 8, whose
14 levels of 490 and 530 units, respectively.
Serum amylase levels were determined
on admission in only 3 of the 10 patients.
Two of these, patients 2 and 10, had ele-
vated values. Amylase levels in patients 1,
7, and 9 were obtained several days after
entry to the hospital and were normal.
In the remaining patients, the diagnosis of
pancreatitis was not considered until later
in the hospital course. Only 3 of these 10
patients had abdominal pain of moder-
ately severe or severe intensity (patients
4, 8, and 10). Nausea and vomiting were
present only in patients 8 and 10.
The clinical features of 5 of these 10
alcoholic patients led to an initial diag-
nosis of cirrhosis. Three of the 5 had
hepatomegaly, spider nevi, and evidence of
portal hypertension. In these 3, patients
1, 2, and 3, the jaundice was persistent,
and appeared to be obstructive rather than
hepatocellular in type. Another patient
(no. 4), with moderately severe abdominal
pain on admission, died in hepatic failure
with ascites, fector hepaticus, and termi-
nal coma. Deep jaundice with a bilirubin
level of 33 mg per 100 ml was attributed
to "steatonecrosis" during his 13-day hos-
pital course. The fifth patient with cir-
rhosis (no. 5) died 2 hours after admission
to the hospital in profound shock. No
history could be obtained. In this patient,
cirrhosis was suspected on physical exami-
nation and confirmed at autopsy.
In 3 of these cirrhotic patients (nos. 1,
 February 1963
Volume 58, No. 2

TABLE 2. Pertinent Clinical and Laboratory Data of the 10 Patients of Group 2

(Proven Obstructive Jaundice due to Pancreatitis)

Patient Age Bilirubin Serum Serum Cephalin Thymol Serum Serum Serum Serum Abdominal Pathologic Findings
(mg/100 ml) Alkaline Amylase Floccu- Turbidity Albumin Globulin GOT GPT Pain*
Phos- (Somogyi lation (units) (g/100 (g/100 (Karmen (Karmen Cause of Cirrhosis
Total Direct phatase units) (48 hr) ml) ml) units) units) Common of Liver
(Bodansky Duct
units) Obstruc-
tion!

1G. H. 41 38.0 23.0 10.7 123J neg. 1.0 3.8 4.6 60 22 + PC +

2C. 0.§ 42 7.0 4.6 34.6 233 neg. 0.8 4.0 2.2 46 41 0 F +
3 J. W.§ 58 16.6 11.3 28.2 — 3+ 8.7 2.6 3.1 101 58 0 PC +
4R. R. 78 33.0 19.0 8.8 — 4+ 10.0 2.3 4.5 — — ++ P +
5H. L. 44 6.1 3.4 6.0 — 4+ 3.6 2.0 3.5 65 5 - PC +
6 A.M. 43 7.9 5.4 17.1 — neg. 1.4 3.6 2.8 32 — -f F 0
OBSTRUCTIVE JAUNDICE

7G. C. 33 14.4 8.7 17.0 31J 1+ lipemia 4.0 3.0 152 18 + F 0

8 J. K. 61 2.5 1.1 6.5 184 4+ 2.0 3.8 2.3 490 530 +++ F 0

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

9 J. M. 37 5.6 3.7 38.6 87J 1+ 3.4 3.9 3.5 9 0 — 0 PC 0
10 F. C. 39 6.8 3.0 4.0 571 — — — — — — +++ P 0

* Pain graded: mild (+), moderately severe (++), severe (+++).

t PC=pseudocyst of pancreas; F=pancreaticfibrosis;P=pancreatic "phlegmon."
t Amylase value obtained late in hospital course.
S Clinical diabetes and Dancreatic calcification on X rav also present.
247
 Annals of
248 WEINSTEIN, KORN, AND ZIMMERMAN
Internal Medicine

TABLE 3. Pertinent Clinical and Laboratory

(Presumptive Obstructive Jaundice

Patient Age Hospital Bilirubin Serum Amylase* Thymol Cephalin Serum

Day (mg/100 ml) Alkaline (Somogyi units) Turbidity Floccu- Albumin
Phos- (units) lation (g/100
Total Direct phatase (48 hr) ml)
(Bodansky
units)

11 J. 0 . 32 1 7.0 3.0 15.8 671 1.8 4+ 4.1

3 2.8 1.1 4.9
12 F. E. 47 1 19.7 12.6 36.6 312 1.6 neg. 3.9
20 3.0 1.5 12.0
13 M. D. 35 1 4.9 4.1 9.4 204 16.3 4+ 3.9
8 1.3 0.9 2.6 830/hr.
(urine)
14 A. J. 27 1 7.0 4.3 12.0 835 ~~ ~~*
4 0.9 0.3
6 0.7 0.4 5.6 "

15 S. M. 39 1 icteric 11.2 171* 3.6 neg. 4.1

4 9.2 5.2 9.5
17 1.8 1.1 4.6
16 W. F. 47 1 4.3 2.3 27.0 152 1.4 3+ 4.2
6 1.2 0.5 9.3
17 R. H. 45 1 15.7 11.6 10.0 71 lipemia 1+ 3.5
3 16.6 11.0 — 1.6
6 6.1 4.4 10.0
18 J. R. 40 1 15.3 10.7 7.0 82 21.0 neg. 3.3
3 3.9 2.5 — 2.8
7 1.4 0.6 3.0
19 A. F. 35 1 5.5 3.9 10.5 480/hr. 14.8 neg. 4.2
3 0.9 0.5 — (urine)
7 — — 4.0 3.4
20 J. M. 33 1 3.0 2.0 24.4 249 1.0 neg. 3.6
6 0.5 0.3
14 6.6
21 W. G. 35 1 icteric — 5300/24 hr. 4.0 1+ —
6 1.8 0.9 7.0 (urine)
10 0.9 0.3 12.7
22 0.4 0.2 4.0
22 B. H. 34 1 11.9 7.4 16.5 279 2.8 neg. 3.0
10 2.3 1.8 24.0
35 1.2 0.4 4.0
23 R. R. 48 1 4.8 2.5 21.5 105J 2.8 1+ 4.0
13 1.8 0.9 7.6
24 J. F. 47 1 14.0 9.5 29.7 32J 5.3 2+ 3.7
10 5.8 3.7 12.0
24 3.4 2.6 5.6

* Serum levels unless otherwise specified.

t Pain graded: mild (+)> moderately severe ( + + ) , or severe ( + + + ) .
t Obtained late in hospital course.
§ Cholestasis graded: mild ( + ) , moderate ( + + ) , or marked ( + + + ) .
II Pancreatitis clinically (patient 15) or surgically (patients 12 and 17) diagnosed on previous admission.

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 Volume 58, No. 2 OBSTRUCTIVE JAUNDICE
February 1963 249
Data of the 14 Patients of Group 2
Due to Pancreatitis)

Serum Serum Serum Abdominal Painf Nausea Liver Biopsy Remarks

Globulin GOT GPT and
(g/100 (Karmen (Karmen Past Current Vomiting Cir- Choles-
ml) units) units) History rhosis tasis§

2.7 96 59 ++ +++ + + +++ Epigastric mass

2.8 12 107 +++11 ++ 0 — — Epigastric mass

Transient hyperglycemia

2.7 92 104 + + + + 0 +

— 146 — — +++ + — — No stigmata of cirrhosis

2.2 32 57 +++" ++ + 0 + + + Hemolytic anemia

Diabetes mellitus

2.6 110 22 ++ + ++ + + +++ Transient hyperglycemia

2.6 206 84 ++" ++ + 0 ++ Diabetic glucose tolerance

test
2.7 36 27 + +++ + — — Transient hypercholestero-
lemia
No stigmata of cirrhosis

2.1 50 37 0 + + 0 + Hemolytic anemia

2.5 107 48 0 0 0 0 +

— 145 54 +++ + + 0 ++ Diabetes mellitus

3.5 253 140 + + 0 0 +++ Hemolytic anemia

3.0 50 39 ++ + + 0 ++ Diabetes mellitus

2.2 510 68 + + + 0 0 + ++ Diabetes mellitus

Hemolytic anemia; transi-
ent hyperchoesterolemia

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 WEINSTEIN, KORN, AND ZIMMERMAN Annals of
250 Internal Medicine

choledocholithiasis. One patient (no. 9)

with prolonged painless jaundice was
categorized as having obstructive jaundice
of obscure origin, prior to laparotomy.
Only in patient 10 was the clinical diag-
nosis of severe pancreatitis with jaundice
made preoperatively. Exploratory laparot-
omy was performed in patients 6, 7, and
9 after more than 30 days of hospital ob-
servation. The persistent jaundice was
found to be due to common duct obstruc-
tion by chronic pancreatitis in patients 6
and 7, and by a pancreatic pseudocyst in
patient 9. One patient (no. 8) returned to
the hospital for an elective, interval chole-
cystectomy 2 months after an observed
episode of obstructive jaundice. This epi-
sode had been accompanied by right upper
quadrant pain and fever and chills, pre-
sumed to represent ascending cholangitis
with choledocholithiasis. Obstruction of the
common bile duct was found to be caused
FIGURE 1. Graphic summary of the clinical and by an indurated, chronically inflammed
laboratory data of patient 11.
pancreas. The gall bladder was distended
and the common bile duct was dilated, but
2, and 3), obstruction of the common bile
duct within the pancreas was shown at
exploratory laparotomy, and the obstruc-
tion was relieved by a "shunting" pro-
cedure. Gross and microscopic examination
of the pancreas in these 3 patients showed
evidence of acute and chronic pancreatitis.
Each of them had pseudocyst formation
within the head of the pancreas. In 2 of
the 3 (patients 1 and 3), compression of
the common duct appeared to be caused
by the pseudocyst. Of the 2 cirrhotic pa-
tients who died, one (no. 4) had obstruc-
tion of the common duct caused by a large
edematous inflammatory mass ("phleg-
mon") involving the head of the pancreas,
and the other (no. 5) had compression of
the duct by a pseudocyst associated with
necrotizing pancreatitis.
The early diagnosis in the remaining 5
patients (without cirrhosis) of group 1 was
obstructive jaundice. In patients 6, 7, and
8, who were admitted with right upper FIGURE 2. Graphic summary of the clinical and
quadrant pain, the tentative diagnosis was laboratory data of patient 16.

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 Volume 58. No. 2 OBSTRUCTIVE JAUNDICE
February 1963 251
no stones were found. This patient died
10 days postoperatively of an acute myo-
cardial infarction. Autopsy revealed no ad-
ditional cause for the jaundice.
Patient 10, who was recognized to have
pancreatitis, died 4 days after admission.
Autopsy confirmed the diagnosis of pan-
creatitis and revealed that the edematous,
boggy pancreas was compressing and oc-
cluding the common bile duct.
Autopsy examination in patients 3, 4, 5,
8, and 10 revealed no evidence of biliary
tract stones or of an obstructing neoplasm.
Of the remaining 5 patients in this group,
4 (patients 1, 2, 7, and 9) have been fol-
lowed for 2 to 4 years since laparotomy.
Patient 6 had a recurrence of abdominal
pain and obstructive jaundice one year
postoperatively. He was re-explored and,
again, no evidence of stones or carcinoma
was found. A second biliary shunt was per-
formed, and he has remained asymptomatic FIGURE 3. Graphic summary of the clinical and
for 2 years more. laboratory data of patient 17.

admission to the hospital and subsided

GROUP 2
Data on the 14 patients with the clinical
diagnosis of pancreatitis and transient
jaundice, which was presumed to be ob-
structive, are shown in Table 3. Graphic
summaries of the clinical and laboratory
data of 3 of these patients are illustrated
in Figures 1, 2, and 3. None of the pa-
tients in this group had a history of ex-
posure to drugs capable of producing
intrahepatic cholestasis. Following sub-
sidence of jaundice in these 14 patients,
cholecystography revealed no evidence of
gall bladder disease or calculi.
All of these patients had jaundice on
admission to the hospital. In 2 patients
(nos. 15 and 21), initial serum bilirubin
levels were not determined. In 7 of the
remaining 12, the serum bilirubin levels
were mildly elevated (3 to 7 mg per 100
ml). Five patients had deep jaundice
(bilirubin levels of 11.9 to 19.7 mg per 100
ml). In these 14 patients, jaundice had
been present for one to 30 days prior to
within 3 to 25 days after entry. The total
duration of jaundice varied from 6 to 42
days.
Serum alkaline phosphatase levels were
suggestive of obstructive jaundice (15.8 to
36.6 Bodansky units) in 7 patients (nos. 11,
12, 16, 20, 22, 23, and 24). Two of the
remaining 7 patients (nos. 17 and 18) had
moderately elevated values (10 and 7 Bo-
dansky units) associated with serum bili-
rubin levels of approximately 16 mg per
100 ml. The other 5 patients had some-
what elevated bilirubin levels with alkaline
phosphatase values of 7 to 12.7 Bodansky
units.
Serum GOT levels were slightly elevated
(50 to 253 units) in 10 of these 14 patients.
Simultaneous GPT values were normal or
only slightly elevated (48 to 140 units).
Patient 24, who was deeply jaundiced, had
GOT and GPT levels of 510 and 68 units,
respectively. Other laboratory data are
summarized in Table 4.
The clinical features of these 14 jaun-

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 252 WEINSTEIN, KORN, AND ZIMMERMAN Annals of
Internal Medicine

diced alcoholic patients led to the follow-
ing initial diagnoses: cirrhosis in one pa-
tient (no. 24); cirrhosis and pancreatitis in
2 patients (nos. 11 and 16); pancreatitis in
5 patients (no. 12, 13, 14, 17, and 18); and
cholestatic jaundice of unknown etiology
in 6 patients (nos. 15, 19, 20, 21, 22, and
23).
After a period of observation, the diag-
nosis of pancreatitis in these 14 patients
was inferred from an analysis (Table 4)
of the history, physical findings, and sup-
porting laboratory data (amylase levels,
transient hyperglycemia, transient hyper-
lipemia).
Eight of the 14 patients had abdominal
pain of sufficient severity at the time of
admission to support the diagnosis of pan-
creatitis. Four of these, patients 11, 12, 13,
and 14, had elevated amylase levels. Pa-
tient 12 had transient hyperglycemia. Two
patients (nos. 11 and 12) * had had previ-
ous episodes of abdominal pain and pre-
sented with palpable epigastric masses
* Patients 11 and 12 were readmitted to the hos-
pital with severe abdominal pain, one and 2 years,
respectively, after the observations of the present
study. Both were again jaundiced. Obstruction of
the common bile duct due to chronic pancreatitis
was demonstrated at autopsy in patient 11, and
at laparotomy in patient 12.
which subsided during hospitalization.
These masses were considered to be pan-
creatic pseudocysts. Laparotomy had been
performed on patient 12 three years previ-
ously during an episode of acute abdominal
pain. Review of the records of that hos-
pitalization revealed that pancreatitis with-
out evidence of biliary tract disease had
been demonstrated at laparotomy.
The remaining 4 patients (nos. 15, 16,
17, and 18) with moderately severe or se-
vere abdominal pain had normal serum
amylase values. The normal serum amy-
lase level in patient 15 was obtained late
in his hospital course; elevated amylase
values had been obtained during previous
hospital admissions for abdominal pain.
A past history of severe or moderately
severe recurrent abdominal pain was ob-
tained in 3* of these patients (nos. 15, 16,
and 17). Lactescence of the serum was
noted in patient 17 during the first 2
days of hospitalization. This patient had
had pancreatitis diagnosed at exploratory
laparotomy during an episode of acute ab-
dominal pain several years previously. Pa-
tient 18 had transient, marked elevation of
the thymol turbidity value that was con-
sidered to represent hyperlipemia. Transi-
ent hyperglycemia was detected in patient

TABLE 4. Supportive Evidence for the Diagnosis of Pancreatitis in the 14 Patients of Group 2

Patients Previous Hyper- Transient Diabetes Abdominal Previous

Pain* lipemiaf Hyper- Mellitus Mass SurgeryJ
Episodes glycemia

Severe* abdominal pain

Elevated amylase level 4 2 — 1 — 2 1
Normal amylase level 4 3§ 2 1 2 — 1

No severe* abdominal pain

Elevated amylase level 4 1 1 — 1 — —
Normal amylase level! I 2 2 1 — 2 — —

Total 14 8 4 2 5 2 2

* Pain of sufficient severity to suggest diagnosis of pancreatitis.

f Transient lactescence of serum, transient hypercholesterolemia or transiently elevated thymol turbidity,
t Laparatomy during previous admission that revealed pancreatitis on gross examination.
§ One patient had had previous admissions with abdominal pain and elevated amylase levels, but without
jaundice.
II Both normal levels were obtained late in the hospital course.

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 Volume 58, No. 2 OBSTRUCTIVE JAUNDICE
February 1963
16, while patients 15 and 17 had mild
diabetes mellitus.
The remaining 6 patients (nos. 19-24)
in this group had, on admission, only mild
or negligible abdominal complaints. Four
of these (patients 19, 20, 21, and 22) had
elevated amylase values. Patient 19 had
an initially elevated thymol turbidity
which returned to normal within 6 days.
Patient 21 had mild diabetes mellitus and
a past history of episodes of recurrent se-
vere abdominal pain. The 2 remaining pa-
tients (nos. 23 and 24), with no significant
abdominal distress on admission, had nor-
mal amylase levels obtained late in their
hospital courses. Both had mild diabetes
mellitus and past histories of recurrent
episodes of moderately severe or severe ab-
dominal pain. Patient 24 had, on admis-
sion, a serum cholesterol level of 605 mg
per 100 ml, which, 3 days later, had de-
creased to 300 mg per 100 ml.
The histological diagnosis of Laennec's
cirrhosis could be made in 3 (specimens
11, 16, and 23) of the 11 needle biopsy
specimens. Moderate to marked cholestasis
(Figure 4) was seen in these specimens, and
in 5 other patients whose livers did not
show cirrhosis (patients 15, 17, 21, 22, and
23). Varying degrees of fatty metamorphosis
and periportal inflammation and fibrosis
were present in all of the biopsy speci-
mens, but there was minimal necrobiosis
or necrosis.
Four of these patients were considered
to have a transient hemolytic anemia. In
3 patients, 15, 22, and 24, the anemia
developed rapidly during the first week in
the hospital. These anemias were associ-
ated with a reticulocytosis of 10 to 15 per
cent. The fourth patient (no. 19) had a
hemoglobin value of 9.8 g per 100 ml
with reticulocytosis, nucleated red blood
cells, spherocytes, and marked polychro-
masia seen on the peripheral smear. There
was no evidence of blood loss in these
patients.
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
253
FIGURE 4. (Patient 17) Photomicrograph of the
liver biopsy specimen from patient 17, obtained
on the twenty-third hospital day, revealing numer-
ous bile thrombi and minimal parenchymal cellu-
lar abnormality. Hematoxylin and eosin stain,
X200.
DISCUSSION
Jaundice, usually mild and transient, oc-
curs in 15 to 25 per cent of the patients
with pancreatitis (32-38). Although its spe-
cific etiology in many cases is obscure,
it has generally been ascribed to mechani-
cal compression of the intrapancreatic por-
tion of the distal common bile duct by the
inflammatory lesion, "toxic" injury to the
liver, or concomitant choledocholithiasis
(35, 39, 40). Persistent obstructive jaundice
resulting from pancreatitis, in alcoholic
patients without demonstrable biliary tract
disease, has been reported not infrequently
(1-9). The first 10 patients (group 1) of
the report illustrate this phenomenon. Ob-
struction of the terminal common bile
duct in these patients was proved at lapa-
rotomy or autopsy.
The anatomical basis for obstruction of
the common bile duct in pancreatitis has
been clearly demonstrated. The terminal
portion of the common duct is completely
enclosed in the posterior portion of the
head of the pancreas in 60 to 80 per cent
of all individuals. In the remainder, it
lies within a groove on the posterior sur-
face of the head of the pancreas (41, 42).
Distortion, narrowing ("stenosis"), and
 WEINSTEIN, KORN, AND ZIMMERMAN Annals of
254 Internal Medicine

kinking of the intrapancreatic segment of scant reference to this phenomenon may

the common bile duct (pars pancreatica)
may be produced by progressive fibrosis of
the pancreatic tissue (8-10). Compression
of the common duct may also be produced
by edema (42) or by a pseudocyst (7) of
the pancreatitis. Cholangiography, per-
formed usually at the time of operation,
has revealed the possible series of changes
that produce displacement and compres-
sion of the common bile duct in pan-
creatitis (Figure 5).
Despite the frequent association of
transient jaundice with pancreatitis and
alcoholism, relatively few authors have
considered the jaundice to be primarily a
consequence of common bile duct obstruc-
tion due to the pancreatitis (32-34). The
be explained by the difficulty of establish-
ing the diagnosis of pancreatitis, the in-
ability to demonstrate the obstruction of
the common duct by pancreatitis, and its
occurrence in alcoholic patients. In the
alcoholic, transient jaundice of apparent
obstructive type is usually ascribed to intra-
hepatic cholestasis associated with paren-
chymal hepatic disease (11-14).
In the 14 patients of group 2, the diag-
nosis of transient obstructive jaundice was
based on clinical analysis without anatomi-
cal confirmation and, accordingly, was con-
sidered to be a presumptive one. The
jaundice was considered to be obstructive
because of the disproportionately high
levels of serum alkaline phosphatase, the

FIGURE 5. Anatomical sketches illustrating possible progressive changes of the common duct
in pancreatitis. (A) normal common duct; (B), (C), (D) progressive displacement and compres-
sion of the common duct. (From SACHS, M., PARTINGTON, P.: Cholangiographic diagnosis of
pancreatitis. Amer. J. Roentgenol. 76: 32, 1956. Courtesy of the authors and Charles C Thomas,
publisher.)

Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016

 Volume 58. No. 2 OBSTRUCTIVE JAUNDICE
February 1963
rapid decline of the levels of serum bili-
rubin and alkaline phosphatase or both of
these. Seven of the 14 patients had serum
alkaline phosphatase values greater than
15 Bodansky units. Levels above this are
much more characteristic of cholestatic
than of hepatocellular jaundice (43). In the
7 other patients with values below 15
Bodansky units, the prompt subsidence of
the elevated serum alkaline phosphatase
levels or jaundice, or a subsidence of both,
was considered to be more consistent with
reversible extrahepatic obstruction than
with hepatocellular or intrahepatic chole-
static jaundice. The transient obstructive
jaundice in these 14 patients could not be
attributed to choledocholithiasis, since
cholecystography performed after recovery
revealed normal gall bladder function
without evidence of calculi. Similarly, there
was no history of ingestion of drugs that
are known to produce jaundice.
In the 3 patients with cirrhosis in group
2, the possibility that the jaundice resulted
from parenchymal cell failure had to be
considered. It is well known, however, that
the patient in the jaundiced phase of cir-
rhosis ["steatonecrosis" (44), "florid cir-
rhosis'' (45)] is usually severely ill with
evidence of impending hepatic coma. Re-
covery, when it occurs, is usually slow. The
rapid improvement of these patients would
not support such a diagnosis. The histo-
logic features of the jaundiced phase of
cirrhosis are characteristic. Mallory bodies
and other necrobiotic changes with vary-
ing degrees of fatty metamorphosis (and
cirrhosis) are regularly seen (44). In the
11 patients studied by liver biopsy, these
parenchymal abnormalities were either
minimal or absent. Eight had fatty meta-
morphosis with slight portal fibrosis, and
3, cited above, had fatty cirrhosis. Chole-
stasis of varying degrees was seen. In 8
patients with only slight parenchymal
changes, the cholestasis was marked (Fig-
ure 4). Several authors have attributed
jaundice in patients with fatty meta-
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
255
morphosis of the liver to intrahepatic
cholestasis (11-12). In our experience (46),
jaundice, with bilirubin values above 5
mg per 100 ml, is rare in patients with
fatty metamorphosis (or "fatty cirrhosis"),
unless there is either extensive paren-
chymal necrosis or extrahepatic obstruc-
tion. The reports ascribing cholestasis to
uncomplicated fatty metamorphosis have
made insufficient reference to the possibil-
ity of pancreatitis as a cause of the jaun-
dice.
The difficulty of establishing the diag-
nosis of pancreatitis led to the exclusion
from this report of other instances of jaun-
dice suspected to be caused by this
condition. Fourteen patients with a pre-
sumptive diagnosis of jaundice caused by
pancreatitis (group 2) were selected for
presentation. Amylase levels were deter-
mined early in the acute illness in only 10
of these patients; 8 had elevated values.
The 6 patients with normal amylase levels
had histories of abdominal pain and lab-
oratory findings suggestive of pancreatitis.
Pain was absent or minimal in 4 of the 8
patients with elevated amylase levels. Eight
of these 14 patients described previous
episodes of abdominal pain strongly sug-
gestive of recurrent pancreatitis, and in 2
of these, pancreatitis had been diagnosed
previously at exploratory laparotomy.*
The diagnosis of pancreatitis is usually
based on an elevated serum amylase level
and the characteristically severe abdominal
pain. The insensitivity of these criteria
for establishing the diagnosis of pancreati-
tis has been commented on by numerous
investigators. All gradations in the severity
of pancreatic pain have been reported (7,
34, 35). Indeed, the entity of "painless
pancreatitis" is being more frequently
noted and reported (2, 47-50). Similarly,
hyperamylasemia is not an invariable find-
* Readmission of 2 of these patients subsequent
to this study confirmed the diagnosis of chronic
pancreatitis by laparotomy in one and autopsy
examination in the other.
 256 WEINSTEIN, KORN, AND ZIMMERMAN
ing in pancreatitis. Elevated values can be
obtained on admission in only approxi-
mately 50 per cent of cases (51-55). The
demonstration of elevated amylase levels
is dependent on the number of determina-
tions, the elapsed time interval after the
onset of symptoms, the amount of residual
functioning pancreatic tissue, and numer-
ous other factors.
The frequent occurrence of transient
hyperglycemia (35) and hyperlipemia (20,
55-57) in pancreatitis is well established.
Transient hyperglycemia has been reported
in up to 80 per cent of the episodes of
pancreatitis. Transient disturbances in fat
metabolism can be manifested chemically
by elevated levels of total serum lipids and
cholesterol, or either, and grossly by lact-
escence of the serum. Hyperlipemia may
be inferred from rapidly changing thymol
turbidity values. Thymol turbidity is
known to be increased by elevated levels
of serum triglycerides and phospholipids,
and has been used as a measure of gastro-
intestinal lipid absorption (58). A rapid
decrease (within a few days) of an initially
high thymol turbidity would more likely
reflect transient hyperlipemia as the cause
of the initial elevation, rather than an
abnormality of the serum proteins result-
ing from hepatic or other disease states.
The syndrome of hemolytic anemia,
hyperlipemia, and jaundice in alcoholic
patients with fatty metamorphosis (or
"fatty cirrhosis") of the liver has been re-
ported by Zieve (59). Several patients with
this syndrome, whom we have observed,
have had abdominal pain with hyperamyla-
semia and have been given a clinical diag-
nosis of pancreatitis. Four patients in the
present series had evidence of hemolysis,
as well as an obstructive type of jaundice.
Two had hyperlipemia and therefore may
be considered to represent instances of the
"Zieve syndrome/'
Most patients with pancreatitis do not
have obstructive jaundice, and most in-
stances of jaundice in the alcoholic are the
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
Annals of
Internal Medicine
result of liver disease. However, the diag-
nosis of pancreatitis should be entertained
in the chronic alcoholic patient who pre-
sents with jaundice and abdominal pain.
SUMMARY
Twenty-four chronic alcoholic patients
presenting with obstructive jaundice
proved or presumed to be caused by pan-
creatitis are reported. In 10 patients, com-
mon bile duct obstruction by pancreatitis
was demonstrated at surgical exploration,
autopsy, or both. In 14 patients with the
clinical diagnosis of pancreatitis, transient
jaundice was presumed to have been due
to compression of the common duct by
the pancreatitis. It is suggested that the
phenomenon of common bile duct obstruc-
tion in pancreatitis is more frequent than
has previously been recognized.
S U M M A R I O IN INTERLINGUA
Es reportate le casos de 24 patientes alcoholic
con jalnessa obstructive que esseva causate—
demonstratemente o presumitemente—per le
presentia de pancreatitis. In 10 del casos, ob-
struction del commun ducto biliari per pan-
creatitis esseva demonstrate al exploration
chirurgic, al necropsia, o a ambes. In 14 del
casos, le diagnose de transiente jalnessa obstruc-
tive causate per pancreatitis esseva presump-
tive e basate in le analyse clinic sin confirma-
tion anatomic. Esseva opinate que le jalnessa
esseva le plus compatibile con un reversibile
obstruction extrahepatic a causa del dispro-
portion temente alte nivellos de phosphatase
alcalin del sero, a causa del rapide declino del
nivellos de bilirubina e de phosphatase alcalin
del sero, o a causa de ambes. Le transiente
jalnessa obstructive in iste 14 patientes non
poteva esser attribuite a choledocholithiasis,
proque le cholecystographia que esseva execu-
tate post le restablimento revelava un vesica
biliari a function normal sin ulle evidentia de
calculos. Esseva trovate nulle antecedente de in-
gestion de pharmacos que cognoscitemente
produce jalnessa. In 11 patientes studiate per
biopsia hepatic, minime grados de necrobiosis
o de necrosis esseva notate. Tres habeva cir-
rhosis grasse, e marcate grados de cholestatis
esseva observate in 8 specimens bioptic.
Le diagnose de pancreatitis in iste 14 pa-
tientes esseva acceptate a base de un analyse—
 Volume 58, No. 2 OBSTRUCTIVE JAUNDICE
February 1963
post prolongate observationes—del historia
clinic, del constatationes physic, e de datos
confirmatori de laboratorio (nivellos de
amylase, hyperglycemia transiente, hyperli-
pemia transiente). Quatro patientes in le
presente serie habeva evidentia de hemolyse si
ben como jalnessa de typo obstructive. D u o
habeva hyperlipemia e pote esser considerate,
per consequente, como exemplos del syndrome
de Zieve.
Es suggerite que le phenomeno del obstruc-
tion del commun ducto biliari como resultato
de pancreatitis es plus frequente que lo que
esseva supponite in le passato.
REFERENCES
I. FRASER, J.: The surgical treatment of obstruc-
tive jaundice in pancreatic disease. Brit. J.
Surg. 26: 393, 1938.
2. EDMONDSON, H. A., BULLOCK, W. K., MEHL,
J. W.: Chronic pancreatitis and lithiasis.
Amer. J. Path. 25: 1227, 1949.
3. SELESNICK, S.: Recurrent jaundice in chronic
relapsing pancreatitis. Gastroenterology 21:
230, 1952.
4. MAIMON, S. N., KIRSNER, J. B., PALMER, W. L.:
Chronic recurrent pancreatitis. Arch. Intern.
Med. 81: 56, 1948.
5. PETERSON, L. W., COLE, W. H.: Chronic scleros-
ing pancreatitis causing complete stenosis of
the common bile duct. Arch. Surg. 51: 15,
1945.
6. ROBSON, A. W. M.: The pathology and surgery
of certain diseases of the pancreas. Lancet
1: 733, 845, 911, 1904.
7. WAUGH, J. M., LYNN, T. E.: Clinical and surgi-
cal aspects of pancreatic pseudocyst. Arch.
Surg. 77: 47, 1958.
8. SACHS, M. D., PARTINGTON, P. F.: Cholangio-
graphy diagnosis of pancreatitis. Amer. J.
Roentgenol. 76: 32, 1956.
9. BISGARD, J. D.: Pancreatitis as a cause of com-
plete obstruction of the common duct. Ann.
Surg. 124: 1009, 1946.
10. POPPEL, M. H.: Roentgen Manifestations of
Pancreatic Disease, Charles C Thomas,
Springfield, Illinois, 1951, p. 327.
II. BALLARD, H., BERNSTEIN, M., FARRAR, J. T.:
Fatty liver presenting as obstructive jaundice.
Amer. J. Med. 31: 196, 1961.
12. GOLDBERG, M., THOMPSON, C. M.: Acute fatty
metamorphosis of the liver. Ann. Intern.
Med. 55: 416, 1961.
13. CATES, H. B.: Acute hepatitis of alcoholism:
a clinical and laboratory study. Ann. Intern.
Med. 15: 244, 1941.
14. BECKETT, A. G., LIVINGSTONE, A. V., HILL, K. R.:
Acute alcoholic hepatitis. Brit. Med. J. 2:
1113, 1961.
15. CLARKE, E.: Pancreatitis in acute and chronic
alcoholism. Amer. J. Dig. Dis. 9: 428, 1942.
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
257
16. DOMZALSKI, C. A., WEDGE, B. M.: Elevated
serum amylase in alcoholics. Amer. J. Clin.
Path. 18: 43, 1948.
17. WEINER, H. A., TENNANT, R.: A statistical study
of acute hemorrhagic pancreatitis (hemor-
rhagic necrosis of the pancreas). Amer. J.
Med. Sci. 196: 167, 1938.
18. HOWARD, J. M., ERHLICH, E. W.: The etiology
of pancreatitis. Ann. Surg. 152: 135, 1960.
19. SMALL, M., LONGARINI, A., ZAMCHECK, N.: Dis-
turbances in digestive physiology following
acute drinking episodes in "skid-row" alco-
holics. Amer. J. Med. 26: 575, 1959.
20. ALBRINK, M. J., KLATSKIN, G.: Lactescence of
serum following episodes of acute alcoholism
and its probable relationship to acute pan-
creatitis. Amer. J. Med. 22: 26, 1957.
21. BOCKUS, H. L., KALSER, M. H., ROTH, J. L. A.,
BOGOCH, A. L., STEIN, G.: Clinical features
of acute inflammation of the pancreas. Arch.
Intern. Med. 96: 308, 1955.
22. MALLOY, H. J., EVELYN, K. A.: The determina-
tion of bilirubin with the photoelectric
colorimeter. / . Biol. Chem. 119: 481, 1937.
23. BODANSKY, A.: Determination of plasma
phosphatase. Proc. Soc. Exp. Biol. Med.
28: 760, 1931.
24. MACLAGEN, N. F.: Thymol turbidity test: a
new indicator of liver dysfunction. Nature
(Lond.) 154: 670, 1944.
25. SHANK, R. E., HOAGLAND, C. L.: A modified
method for the quantitative determination
of the thymol turbidity reaction of serum.
/ . Biol. Chem. 162: 133, 1946.
26. REITMAN, S., FRANKEL, S.: Colorimeter method
for the determination of serum transami-
nase activity. Amer. J. Clin. Path. 28: 56,
1957.
27. NEEFE, J. R., REINHOLD, J. G.: Photosensitivity
as a cause of falsely positive cephalin-chole-
sterol flocculation tests. Science 100: 83, 1944.
28. WEICHSELBAUM, T. E.: Accurate and rapid
method for determination of proteins in
small amounts of blood serum and plasma.
Amer. J. Clin. Path. 10: 40, 1946.
29. KINGSLEY, C. R.: Direct biuret method for the
determination of serum proteins as applied
to photoelectric and visual colorimetry. / .
Lab. Clin. Med. 27: 840, 1942.
30. LEVINSON, S. A., MACFATE, R. P.: Clinical Lab-
oratory Diagnosis, 5th Ed., Lea and Febiger,
Philadelphia, 1956, p. 283.
31. SAXON, E. I., HINKLEY, W. C , VOGEL, W. C ,
ZIEVE, L.: Comparative value of serum and
urinary amylase in the diagnosis of acute
pancreatitis. Arch. Intern. Med. 99: 607,
1957.
32. PALMER, E.: Clinical Gastroenterology, Paul B.
Hoeber, Inc., Medical Division of Harper
& Brothers, New York, 1957, p. 580.
33. POLLOCK, A. V.: Acute pancreatitis. Brit. Med.
J. 1: 6, 1959.

258 WEINSTEIN, KORN, AND ZIMMERMAN
34. COMFORT, M. W., GAMBILL, E. E., BAGGENSTOSS,
A. H.: Chronic relapsing pancreatitis.
Gastroenterology 6: 239, 376, 1946.
35. RICHMAN, A.: Acute pancreatitis. Amer. J.
Med. 21: 246, 1956.
36. GROSS, J. B., COMFORT, M. W.: Chronic pan-
creatitis. Amer. J. Med. 21: 596, 1956.
37. FALLIS, L. S.: Acute pancreatitis. Amer. J. Surg.
46: 593, 1939.
38. KOSTER, H., KASMAN, L. P.: Acute pancreatitis.
Arch. Surg. 29: 1014, 1934.
39. POPPER, H., SCHAFFNER, F.: Liver: Structure and
Function, McGraw-Hill Book Company, New
York, 1957, p. 633.
40. CATTELL, R. B., WARREN, K. W.: Surgery of the
Pancreas, W. B. Saunders Company, Phila-
delphia, 1953, p. 69.
41. HOWARD, J. M., JORDAN, G. L.: Surgical Diseases
of the Pancreas, J. B. Lippincott Company
Philadelphia, 1960, p. 14.
42. LICHTMAN, S. S.: Diseases of the Liver, Gall-
bladder and Bile Ducts, Vol. II, 3d Ed., Lea
& Febiger, Philadelphia, 1953, p. 1269.
43. WEST, M., ZIMMERMAN, H. J.: Serum enzymes
in hepatic disease. Med. Clin. N. Amer. 43:
371, 1959.
44. ZIMMERMAN, H. J.: The evolution of alcoholic
cirrhosis. Med. Clin. N. Amer. 39: 241, 1955.
45. POPPER, H., SZANTO, P. B., PARTHASARATHY, M.:
Florid cirrhosis. Amer. J. Clin. Path. 25: 889,
1955.
46. BRADUS, S., KORN, R. J., CHOMET, B., ZIMMER-
MAN, H. J.: Unpublished data.
47. BARTHOLOMEW, L. G., COMFORT, M. W.: Chronic
pancreatitis without pain. Gastroenterology
31: 727, 1956.
48. GAMBILL, E. E., PUGH, D. G.: Pancreatic cal-
cification. Arch. Intern. Med. 81: 301, 1948.
Downloaded From: http://annals.org/ by a Duke Medical Library User on 12/21/2016
Annals of
Internal Medicine
49. SNELL, A. M., COMFORT, M. W.: Incidence and
diagnosis of pancreatic lithiasis; a review oi
18 cases. Amer. J. Dig. Dis. 8: 237, 1941.
50. DREILING, D. A., MAZURE, P. A., COHEN, N.,
MOSKOVITS, H., TODARO, R. T., PAULINO-
NETTO, A.: Newer horizons in the etiology
of pancreatitis: metabolic and endocrinologic
factors. Amer. J. Dig. Dis. 7: 112, 1962.
51. DEMETRIADES, A. D., POLAYES, S. H.: Acute pan-
creatic necrosis. Amer. J. Dig. Dis. 3: 427,
1958.
52. HEFFERNON, E. W., CASSIET, A. C : A survey oi
acute hemorrhagic pancreatitis. Gastroenter-
ology 35: 251, 1958.
53. PHILLIPS, A. M.: Chronic pancreatitis—patho-
genesis and clinical features. Arch. Intern.
Med. 93: 337, 1954.
54. O'BRIEN, J. J., THAYER, T. R.: Pancreatitis;
observations on 131 patients. New Engl. J,
Med. 253: 355, 1955.
55. WANG, C, ADLERSBERG, D., FELDMAN, E. B.:
Serum lipids in acute pancreatitis. Gastro-
enterology 36: 832, 1959.
56. WANG, C , STRAUSS, L., ADLERSBERG, D.: Experi-
mental pancreatitis and plasma lipids. Gastro-
enterology 35: 465, 1958.
57. ERHLICH, E. W., SPITZER, J., HOWARD, J. M.:
Pancreatitis with hyperlipemia. Surg, sorum
11: 373, 1960.
58. POPPER, H., STEIGMAN, F., DYNIEWICZ, H.,
DUBIN, A.: Use of thymol turbidity as a lipid
absorption test. / . Lab. Clin. Med. 34: 105,
1949.
59. ZIEVE, L.: Jaundice, hyperlipemia and hemo-
lytic anemia: a heretofore unrecognized syn-
drome associated with alcoholic fatty livei
and cirrhosis. Ann. Intern. Med. 48: 471,
1958.