International Journal of Pancreatology, 5 (1989) 117-121 $02.00 Copyright �9 1989 by The Humana Press Inc. All rights of any nature whatsoever reserved.

Splenic Vein Thrombosis in Patients with Acute Pancreatitis

Christopher Rogers t and Edward C. Klatt*.2

l'~Los Angeles County-University of Southern California Medical Center, Los Angeles, CA; 1Resident in Pathology, LAC-USC Medical Center and Cliniciat Instructor, University

of Southern California School of Medicine, 1200 N. State St., Los Angeles, CA 90033; and 2Chief of Autopsy, LAC-USC Medical Center and Assistant Professor of Pathology,

University of Southern California School of Medicine

Received June 7, 1988; Revised September 27, 1988; Accepted November 3, 1988

Summary

We performed a retrospective autopsy case-control study to identify clinical characteristics of acute pancreatitis associated with splenic vein thrombo- sis. Age, sex, spleen weight, presence or absence of gastrointestinal hemor- rhage, and pancreatic pseudocyst were not associated with splenic vein thrombosis. Patients with peak serum amylase over 10,000 U/L were at high risk for splenic vein thrombosis. We conclude that, of the factors examined, only the peak serum amylase may be of value in diagnosing splenic vein thrombosis in patients with acute pancreatitis.

Key Words: Autopsy; inflammation; pancreas.

I N T R O D U C T I O N

Splenic vein thrombosis can be an underdiagnosed complication of acute pancreatitis. In a large autopsy series, splenic vein thrombosis was present in 13.1 ~ o f patients in whom acute pancreatitis was a primary or precipitating cause o f death (1). However, splenic vein thrombosis is reportedly recognized in only 43~ of symptomatic patients (2) and very few asymptomatic patients with pancreatitis (3). Splenic vein thrombosis may be associated with portal hypertension and variceal bleeding, which may originate from stomach, esophagus, duodenum, or colon (2,4-6). This form of portal hypertension is successfully treated by splenectomy in most cases (2, 4, 7, 8). Moreover, portal system angiography could be performed in the subgroup of patients with acute pancreatitis at high risk for splenic vein thrombosis. Previous studies

*Author to whom all correspondence and reprint requests should be addressed.

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118 Rogers and.Klatt

have reported signs of splenic vein thrombosis in acute pancreatitis that in- clude esophageal or gastric varices in the absence of liver disease (2,4, 7,8), splenomegaly (2,8), and pancreatic pseudocyst (2). However, no controlled study of the significance of these factors has been performed.

We conducted a retrospective autopsy case-control study with clinico- pathologic correlation of patients who died from acute pancreatitis, to iden- tify the clinical characteristics of these patients that were associated with the presence of splenic vein thrombosis.

MATERIAL AND METHODS

Cases autopsied between January 1958 and December 1987 were selected from the files of the autopsy departments of Los Angeles County-University of Southern California Medical Center and The Hospital of the Good Samari- tan. A total of 42,524 autopsies were performed during this period. Cases were included for study if acute pancreatitis was the immediate or contributing cause of death and the portal venous system (both splenic and portal veins) was examined completely at autopsy. Patients were excluded from study if there had been a splenectomy or if chronic pancreatitis was present micro- scopically. A total of 72 cases met the study criteria. The autopsy gross patho- logic findings and clinical summaries of these individuals were reviewed to determine presence of a thrombus in the splenic vein, the patient's age and sex, spleen weight at autopsy, presence or absence of gastrointestionat hem- orrhage during the final hospitalization (gross hemorrhage or positive stool occult blood test), peak serum amylase (reported in U/L), and presence or absence of a pancreatic pseudocyst during the final hospitalization or at au- topsy. We did not look for reported gastric or esophageal varices because these conditions are difficult to correlate at autopsy with clinical findings. Significance of the differences between variables was evaluated using either the Chi-square test with Yates' correction for continuity, or Student 's two- tailed t test for unpaired data. A p value of less than 0.05 was necessary to re- ject the null hypothesis.

RESULTS

Of the 72 patients studied, 11 (15~ had splenic vein thrombosis at autopsy. This figure is similar to that of Renner et al. (1), who surveyed a similar au- topsy series and found that 13.1% of patients had splenic vein thrombosis. Both figures may be overestimates, because acute pancreatitis either caused or contributed to death in both studies, so patients at autopsy probably had more severe disease than the average living patient.

Table 1 compares individuals with and without splenic vein thrombosis. Only peak serum amylase level was significantly associated with thrombosis; patients with splenic vein thrombosis had higher peak serum amylase. Figure 1 illustrates the distribution of peak serum amylase levels in patients with and without splenic vein thrombosis.

Splenic vein thrombosis was not significantly associated with either spleen weight or pancreatic pseudocysc In addition, we found no association be-

International Journal o f Pancreatology Volume 5, 1989

Table 1 Comparison of Patients With and Without Splenic Vein Thrombosis

Cases with Cases with thrombus present thrombus absent p

Number 11 Mean age 54 Number of males 6 (55%) Mean spleen wt, gm 180 Gastrointestinal hemorrhage 3 (27%) Mean peak serum amylase, U / L 6613 Pancreatic pseudocyst 1 (9%)

61 48 NS a 46 (75~ NS

199 NS 24 (39%) NS

2469 < 0.02 2 (3070) NS

~Abbreviation: NS = not significant (p > 0.05).

20

A

o 16 O O

X

- J

" - " 12 LU GO < .._1 >..

:E

8 :E

n" LU GO v < uJ 4

0

O O

O

8 o

0

co

THROMBUS ABSENT

0

O

0 0

0 0

THROMBUS PRESENT

Fig. 1. Peak serum amylase in patients with and without splenic vein thrombosis. Extremely high amylase was associated with increased risk of thrombosis.

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120 Rogers and Klatt

tween gastrointestinal hemorrhage and splenic vein thrombosis. In fact, the patients without thrombosis had a higher prevalence of gastrointestinal hem- orrhage than those with thrombosis (although the difference did not reach statistical significance).

DISCUSSION

We did not identify any clinical criteria that absolutely distinguish patients who have splenic vein thrombosis from those who do not. Nevertheless, splenic vein thrombosis was associated with high peak serum amylase levels. Figure 1 shows that extreme elevations of serum amylase (over 10,000 U/L) were associated with an increased probability of splenic vein thrombosis. Of individuals with serum amylase over t0,000 U/L, 3 of 4 (75%) had splenic vein thrombosis; of those with lower serum amylase, 7 of 53 (13%) had splenic vein thrombosis (p < 0.02).

We did not find any association between splenic vein thrombosis and gastro- intestinal hemorrhage. Splenectomy may, however, result in resolution of gastrointestinal bleeding in many cases (2,4, 7,8). It is likely that many of the patients in our series bled from sources other than varices. We emphasize the need for a careful search for nonvariceal sources of bleeding before subject- ing patients with acute pancreatitis to splenectomy.

Moossa and Gadd (8) suggest that splenic vein thrombosis be suspected in patients with pancreatitis and gastroesophageal varices, splenomegaly with- out portal hypertension, cirrhosis or hematologic disorders, gastric varices on gastroscopy or barium study, collateral vessels in the left upper quadrant during intravenous pyelography, or in any patient undergoing an elective operation for a complication of acute pancreatitis. We would add patients with extremely high serum amylase to this list. Such patients comprised 4 of 72 (6%) of those with acute pancreatitis in this study.

ACKNOWLEDGMENT

The authors are grateful to William Kern for his assistance in the prepara- tion of this report.

REFERENCES

1 Renner IG, Savage WT, Pantoja JL, et al. Death due to acute pancreatitis: A retrospec- tive analysis of 405 autopsy cases. Dig. Dig. Sci. 1985; 30: 1005-1018.

2 Madsen MS, Petersen TH, Sommer H. Segmental portal hypertension. Ann. Surg. 1986; 204: 72-77.

3 Itzchak Y, Glickman MG. Splenic vein thrombosis in patients with a normal size spleen. Invest. Radiol. 1977; 12: 158-163.

4 Little AG, Moossa AR. Gastrointestinal hemorrhage from left-sided portal hypertension: An unappreciated complication of pancreatitis. Am. J. Surg. 1981; 141: 153-158.

5 Amin R, Alexis R, Korzis J. Fatal ruptured duodenal varix: A case report and review of literature. Am. J. Gastroenterol. 1985; 80: 13-18.

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Vein Thrombosis in Acute Pancreatitis 121

6 Burbige ER, Tarder G, Carson S, et al. Colonic varices: A complication of pancreatitis with splenic vein thrombosis. Am. J. Digest. Dis. 1978; 23: 752-755.

7 Haf t RC, Page CP, Andrassy R J, et al. Splenectomy: Its place in operations for inflam- matory disease of the pancreas. Am. J. Surg. 1977; 134: 555-557.

8 Moossa AR, Gadd MA. Isolated splenic vein thrombosis. World J. Surg. 1985; 9: 384- 390.

International Journal o f Pancreatotogy Volume 5, 1989