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“The only thing necessary for these diseases to the triumph is for good people and governments to do nothing.”


     

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.