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PANCREATIC TAIL ADENOCARCINOMA PRESENTING AS EARLY SINISTRAL
PORTAL HYPERTENSION
AVINASH KUMAR*, SHALU GUPTA**, ASHOK KUMAR MATHUR***
*Senior Registrar; **Assistant Professor; ***Associate Professor
and Unit Head, Department of Gen. Surgery, SMS Medical College
and Hospital, Jaipur.
http://www.bhj.org/journal/2002_4403_jul/case_453.htm
The patient had sinistral portal hypertension, a clinical
syndrome consisting of splenic vein thrombosis caused by
pancreatic adenocarcinoma of tail manifested as isolated gastric
varices with patent portal vein and normal hepatic function. By
presenting this case, I want to draw attention to a rare
syndrome, sinistral (left-sided) portal hypertension secondary
to pancreatic adenocarcinoma of the tail.
CASE REPORT
The patient, a 45-year-old woman who weighed over 52 kg, was in
her usual state of health until three months prior to admission
when she started experiencing weakness, fatigue, constipation
causing abdominal discomfort relieved after bowel movement. She
denied dietary changes, weight changes, and any trauma. She also
denied any history of alcohol abuse, diabetes, peptic ulcer
disease, GI bleeding, anaemia, nausea, vomiting, abdominal pain,
aspirin, or NSAID use.
Her physical exam was unremarkable. Her following laboratory
studies were normal; serum chemistries, complete blood count,
liver function test, prothrombin time, and partial
thromboplastin time.
Preoperative endoscopy was normal. USG and Computed tomography
of the abdomen with contrast was performed, the splenic vein as
well as the portal vein and superior mesenteric vein were not
visualized. However, a five-centimeter mass involving the
pancreatic tail and splenic hilum was seen. The spleen itself
was enlarged.
At laparotomy, we found a large indurated mass involving the
pancreatic tail, spleen and transverse mesocolon and there was
splenic vein thrombosis. Left-sided segment of the portal venous
system, namely, the splenic side was dilated and tortuous. Liver
and peritoneal cavity was free of metastasis.
We performed En bloc distal pancreatectomy, splenectomy and
segmental transverse colon resection and anastomosis. Patient
had uneventful postoperative recovery. Prophylactically
non-selective cardiac beta-blocker was prescribed to prevent
first variceal bleeding.
Biopsy proved to be pancreatic adenocarcinoma,
moderately-to-poorly differentiated, infiltrating into the
peripancreatic soft tissue, spleen and transverse mesocolon.
TNM classification of T4N1M1 and pathologic stage IVB, grade 2-3
(AJCC 1997) was given.
DISCUSSION
Pancreatic cancer is notorious for presenting with vague and
non-specific symptoms including weight loss, abdominal pain, and
anorexia with or without jaundice. However, physicians should be
aware that in the presence of splenic vein thrombosis, this
finding alone puts pancreatic cancer high on the differential
diagnosis.
An uncommon form of upper gastrointestinal bleeding with an
incidence of less than 1%, sinistral portal hypertension (SPH)
is a clinical syndrome should splenic vein thrombosis (SVT)
manifest itself with bleeding gastric varices in a patient with
a patent portal vein and normal hepatic function.[1,2] The
phrase sinistral (segmental or left-sided) portal hypertension
is used because the portal hypertension is confined to the
left-sided segment of the portal venous system, namely, the
splenic side. Although bleeding is the most common manifestation
in this syndrome, SPH can occur without bleeding as in our case
and SVT can occur without evidence of SPH.[2,6]
SVT is a well known complication of pancrepancreatic cancer.
This condition is not surprising as the splenic vein runs in
close association with the pancreas for its entire length. Thus,
any inflammation let alone malignancy may involve the splenic
vein. Inflammation may induce spasm resulting in stasis and
subsequent intimal damage thereby predisposing to thrombosis.[3]
Pancreatic carcinoma may cause SVT by direct invasion, extrinsic
compression via mass effect, or hypercoagulable state.[2,3]
Splenic vein thrombosis (SVT) classically presents with the
triad of isolated gastric varices, splenomegaly, and normal
hepatic function.[1] The most common aetiologies of SVT are
pancreatic neoplasm chronic pancreatitis, and pancreatic
pseudocyst although other causes include trauma, tuberculosis,
retroperitoneal fibrosis, peptic ulcer disease, or a
hypercoagulable state.[1,3-5]
SVT usually presents with isolated gastric varices resulting
from decompression through the left gastric vein via the short
gastric veins or epiploic venous system. However, SVT may
present in the absence of gastric varices or the presence of
oesophageal varices, and therefore, a high index of suspicion is
required for the correct diagnosis in some cases. The reason for
this variable presentation is due to variable drainage of the
left gastric vein. In 17% of the population, the left gastric
vein drains into the splenic vein preventing decompression via
this route and instead, ultimately results in increased venous
flow to the azygous venous system via oesophageal veins
producing oesophageal, but not gastric varices.[3,7] Regardless
of the location of the varices, liver function is normal.
In any circumstance, the diagnosis of SVT is made most
accurately by selective intra-arterial digital splenic
angiogram.[5] CT scan as well as ultrasound may also demonstrate
a splenic vein thrombus with the additional bonus of
demonstrating any other abnormal abdominal, especially
pancreatic, pathology.[1,2] Splenectomy remains the most
effective procedure in treating bleeding gastric varices.[1,2]
CONCLUSION
Pancreatic cancer should be suspected in-patients with splenic
vein thrombosis. It is a rare condition that unfortunately does
not help the physician in diagnosing pancreatic cancer
any earlier.
REFERENCES
1.Han D, Feliciano D. The American Surgeon 1998; 64 : 558-62.
2.Evans G, Yellin A, Weaver F, Stain S. The American of Surgery
1970; 56 : 758-63.
3.Little A, Moossa A. The American J Surgery1981; 141 : 153-58.
4.Williams N, Gerrand C, London N. Postgraduate Medical Journal
1992; 68 : 928-29.
5.Illig K, Spitzer R, Oates T. The American Surgeon 1997; 63 :
1005-6.
6.Glyn M. Archives of Surgery 1986; 121 : 723-25.
7.Stone R, Wilson S, Passaro E. The American J Surgery 1978; 136
: 73-8.
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