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Variceal bleeding due to segmental portal hypertension caused by chronic pancreatitis
676
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 13, Number 6 • November 1995
patients with acute and severe renal failure due to multiple myeloma. Clin Nephrol 1990;34:247-254 10. Dean D, Busmanis I, Hussein S: Four cases of IgD multiple myeloma. Pathology 1991 ;23:339-343
VARICEALBLEEDINGDUE TO SEGMENTALPORTAL HYPERTENSIONCAUSEDBY CHRONICPANCREATITIS To the Editor:--Upper gastrointestinal bleeding from gastroesophageal varices secondary to splenic vein thrombosis caused by pancreatitis is being recognized with increasing frequency. The leftsided portal hypertension may lead to bleeding gastric and esophageal varices. 1-6 Usually these patients have alcoholic pancreatitis, but this complication may also result from suppurative, traumatic, or hereditary pancreatitis. 7 The diagnosis should be suspected in every patient who presents with variceal bleeding in the absence of signs of liver disease. Treatment of choice is splenectomy if the obstruction is confined to the splenic vein. Because surgery may not be feasible in patients with liver cirrhosis, distinction between this surgically curable disease and other causes of portal hypertension is important. We report a patient with chronic pancreatitis who had symptomatic splenic vein thrombosis as its complication. A 37-year-old nonalcoholic woman was sent to our emergency department (ED) because of massive hematemesis. She had had diabetes mellitus for 9 years and was being treated with insulin. She was found to have type IV hyperlipidemia four years earlier. Serum triglyceride was approximately 3,000 mg/dL. Five attacks of acute pancreatitis had been noted during follow-up. Physical examination found marked splenomegaly without ascites. Her conjunctiva was pale but sclera was not icteric. Laboratory studies showed that hemoglobin was 6 g/dL, platelet count 45,000/IxL, and blood sugar 240 mg/dL. Serum amylase, lipase, bilirubin, SGOT, SGPT, and calcium levels, as well as prothrombin time, were normal. Endoscopy showed prominent gastric varices over fundus (Figure 1). The esophagus was free of varices. After histoacryl injection, bleeding stopped temporarily. After her condition was stabilized, several studies were performed. Abdominal ultrasonography showed marked splenomegaly with thrombi detected in the splenic vein at the splenic hilum (Figure 2). There was no evidence of liver cirrhosis. Computed tomography
FIGURE 1. Endoscopy shows prominent varices (V) at the gastric fundus.
FIGURE 2. Abdominal ultrasound shows markedly enlarged spleen (sp) with thrombus (arrowheads) in the main splenic vein (sv) at the hilum.
of the abdomen showed pseudocyst formation in the pancreatic tail and numerous collaterals in the retroperitoneal region (Figure 3). Celiac angiography showed no filling of the splenic vein, indicating splenic vein thrombosis near the splenic hilum and tortuous short gastric veins (Figure 4); however, the portal vein and the superior mesenteric vein were normal. Three days after the first attack, another episode of massive bleeding combined with hypotension occurred. Gastric variceal bleeding caused by segmental portal hypertension induced by chronic pancreatitis was suspected, and laparotomy was performed. Operative findings included marked splenomegaly with extensive collateral vessels at the hilum, prominent varicose veins over posterior wall of gastric fundus, pancreas, and retroperitoneum, severe inflammatory adhesions in the upper abdomen, and a pseudocyst with pus in the pancreatic tail. Liver was normal. Splenectomy and distal pancreatectomy were performed. Pathology showed fibrosis in pancreas tissue and pseudocyst formation. The postoperative course was smooth. No rebleeding was noted during follow-up.
FIGURE 3. Contrast-enhanced abdominal computed tomography shows splenomegaly (SP) with prominent collaterals (arrow). There is a pancreatic pseudocyst abutting the splenic hilum (arrowhead).
CORRESPONDENCE
677
the pancreas should be actively sought because this complication is one of the rare instances when the problem of portal hypertension can be treated satisfactorily by splenectomy. YEONG-L[ANa LXN, MD PEI-MING YANG, MD GUAN-TARN HUANG, MD TZONG-HsI LEE, MD SEH-HUANG CHAU, MD YvK-MIN6 TSANG, MD SHIH-MING WANG, MD National Taiwan University Hospital Taipei, Taiwan, ROC
References
FIGURE 4. Venous phase of celiac angiogram shows collaterals at the esophagogastric junction and greater omentum. The splenic vein is not opacified. The opaque plaque at the esophagogastric junction is caused by previous sclerotherapy (arrow). Occlusion of the splenic vein as a consequence of chronic pancreatitis has been recognized with increasing frequency. 1-1oIts prevalence was either 2.2% or 24% in two surgical series, depending on whether splenic vein obstruction had been systematically searched for with splenoportography. 11'12 Extrahepatic portal hypertension should be considered in any patient with chronic pancreatitis who has splenomegaly and gastrointestinal bleeding. Diagnosis can be made with abdominal ultrasonography, computed tomography, and angiography. Sonographic features of splenic vein thrombosis may be an echogenic thrombus within the lumen of the vein, demonstration of splenic vein collateral circulation, and enlargement of the thrombosed segment of the vein. 13 On computed tomography, hypodense thrombi will be found in the splenic vein while the portal vein is normal.i4 Angiography is the key to diagnosis and usually shows esophagogastric varices, an obliterated splenic vein, and splenomegaly. The frequency of variceal bleeding in patients with splenic vein thrombosis secondary to chronic pancreatitis is not high. 3'6'8'15 The most common location of varices is the fundus of the stomach, and gastric varices are easily missed endoscopically unless they have been suspected. Treatment for patients with splenic vein thrombosis and gastroesophageal varices depends on the presence or absence of bleeding and the magnitude of bleeding. In the past, surgery was quickly performed on patients with active bleeding unresponsive to medical management. At present, sclerotherapy seems applicable. Since gastric varices caused by segmental portal hypertension are largely located at the fundus, sclerotherapy for active bleeding usually has had poor results. 16 Although bleeding can be stopped temporarily, rebleeding soon occurs. Therefore, it has been postulated that diagnosed splenic vein thrombosis caused by chronic pancreatitis with massive bleeding should be treated with splenectomy, If the obstruction is confined to the splenic vein, splenectomy is the treatment of choice, a7 If a pancreatic pseudocyst is also found, cystojejunostomy or resection of pseudocyst is favored. 8 As a result of severe adhesions, splenectomy may be difficult and the risk of brisk bleeding during operation is high, as occurred in this case. To reduce perioperative bleeding, ligation of the splenic artery is recommended before mobilizing the spleen with a great number of collaterals in the ligaments. In conclusion, in patients with variceal bleeding and chronic pancreatitis, splenic vein thrombosis caused by inflammatory disease of
1. Rignault D, Mine J, Moire D: Splenoportographic changes in chronic pancreatitis. Surgery 1968;63:571-575 2. McDermott WV Jr: Portal hypertension secondary to pancreatic disease. Ann Surg 1960;152:147-150 3. Little AG, Moossa AR: Gastrointestinal hemorrhage from left-sided portal hypertension: An unappreciated complication of pancreatitis. Am J Surg 1981;141:153-158 4. Harnar T, Johansen K, Haskey R, et al: Left-sided portal hypertension from pancreatic pseudotumor. Am J Gastroenterol 1982 ;77:639-641 5. Stone RT, Wilson SE, Passaro E: Gastric portal hypertension. Am J Surg 1978;136:73-79 6. Warshaw AL, Jin G, Ottinger LW: Recognition and clinical implications of mesenteric and portal vein obstruction in chronic pancreatitis. Arch Surg 1987;122:410-417 7. McEIroy R, Christiansen PA: Hereditary pancreatitis in a kinship associated with portal vein thrombosis. Am J Med 1972; 52:228-241 8. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: A diagnosable and curable form of portal hypertension. Surgery 1973;74:961-972 9. Mossa AR, Gadd MA: Isolated splenic vein thrombosis. World J Surg 1985;9:384-390 10. Madsen MS, Petersen TH, Sommer H: Segmental portal hypertension. Ann Surg 1986;204:72-77 11. Bradley EL II1: The natural history of splenic vein thrombosis due to chronic pancreatitis: Indications for surgery. Int J Pancreatol 1987;2:87-92 12. Leger L, Lenriot JP, Lemaigre G: L'hypertension at la stase portales segmentaires dans les pancreatites chroniques. A propos de 126 cas examines par splenoportographie et splenomanometrie. J Chir 1968;95:599-608 13. Van Gansbeke D, Avni EF, Delcour C, et al: Sonographic features of portal vein thrombosis. AJR Am J Roentgenol 1985; 144:749-752 14. Vogelzang RL, Gore RM, Anschuetz SL, et al: Thrombosis of the splanchnic veins: CT diagnosis. AJR Am J Roentgenol 1988;150:93-96 15. Bernades P, Baetz A, Levy P, et al: Splenic and portal venous obstruction in chronic pancreatitis. A prospective longitudinal study of a medical-surgical series of 266 patients. Dig Dis Sci 1992;37:340-346 16. Gimson AES, Westaby D, Williams R: Endoscopic sclerotherapy and management of gastric variceal haemorrhage. Gut 1989;30:A1497 (abstr) 17. Longstreth GF, Newcomer AD, Green PA: Extrahepatic portal hypertension caused by chronic pancreatitis. Ann Intern Med 1971 ;75:903-908
NEBULIZED FENOTEROLVERSUS IV AMINOPHYLLINE TREATMENT OF ACUTE SEVEREASTHMA To the Editor.'--From July 1991 to June 1993, 30 patients visited the emergency department (ED) at National Taiwan University Hospital, where acute severe asthmatic attacks were investigated. Informed consent was obtained from all patients included in this clinical trial. All of these patients had forced expiratory volume in one second (FEV1) <30% of predicted value and peak expiratory
AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 13, Number 6 • November 1995
patients with acute and severe renal failure due to multiple myeloma. Clin Nephrol 1990;34:247-254 10. Dean D, Busmanis I, Hussein S: Four cases of IgD multiple myeloma. Pathology 1991 ;23:339-343
VARICEALBLEEDINGDUE TO SEGMENTALPORTAL HYPERTENSIONCAUSEDBY CHRONICPANCREATITIS To the Editor:--Upper gastrointestinal bleeding from gastroesophageal varices secondary to splenic vein thrombosis caused by pancreatitis is being recognized with increasing frequency. The leftsided portal hypertension may lead to bleeding gastric and esophageal varices. 1-6 Usually these patients have alcoholic pancreatitis, but this complication may also result from suppurative, traumatic, or hereditary pancreatitis. 7 The diagnosis should be suspected in every patient who presents with variceal bleeding in the absence of signs of liver disease. Treatment of choice is splenectomy if the obstruction is confined to the splenic vein. Because surgery may not be feasible in patients with liver cirrhosis, distinction between this surgically curable disease and other causes of portal hypertension is important. We report a patient with chronic pancreatitis who had symptomatic splenic vein thrombosis as its complication. A 37-year-old nonalcoholic woman was sent to our emergency department (ED) because of massive hematemesis. She had had diabetes mellitus for 9 years and was being treated with insulin. She was found to have type IV hyperlipidemia four years earlier. Serum triglyceride was approximately 3,000 mg/dL. Five attacks of acute pancreatitis had been noted during follow-up. Physical examination found marked splenomegaly without ascites. Her conjunctiva was pale but sclera was not icteric. Laboratory studies showed that hemoglobin was 6 g/dL, platelet count 45,000/IxL, and blood sugar 240 mg/dL. Serum amylase, lipase, bilirubin, SGOT, SGPT, and calcium levels, as well as prothrombin time, were normal. Endoscopy showed prominent gastric varices over fundus (Figure 1). The esophagus was free of varices. After histoacryl injection, bleeding stopped temporarily. After her condition was stabilized, several studies were performed. Abdominal ultrasonography showed marked splenomegaly with thrombi detected in the splenic vein at the splenic hilum (Figure 2). There was no evidence of liver cirrhosis. Computed tomography
FIGURE 1. Endoscopy shows prominent varices (V) at the gastric fundus.
FIGURE 2. Abdominal ultrasound shows markedly enlarged spleen (sp) with thrombus (arrowheads) in the main splenic vein (sv) at the hilum.
of the abdomen showed pseudocyst formation in the pancreatic tail and numerous collaterals in the retroperitoneal region (Figure 3). Celiac angiography showed no filling of the splenic vein, indicating splenic vein thrombosis near the splenic hilum and tortuous short gastric veins (Figure 4); however, the portal vein and the superior mesenteric vein were normal. Three days after the first attack, another episode of massive bleeding combined with hypotension occurred. Gastric variceal bleeding caused by segmental portal hypertension induced by chronic pancreatitis was suspected, and laparotomy was performed. Operative findings included marked splenomegaly with extensive collateral vessels at the hilum, prominent varicose veins over posterior wall of gastric fundus, pancreas, and retroperitoneum, severe inflammatory adhesions in the upper abdomen, and a pseudocyst with pus in the pancreatic tail. Liver was normal. Splenectomy and distal pancreatectomy were performed. Pathology showed fibrosis in pancreas tissue and pseudocyst formation. The postoperative course was smooth. No rebleeding was noted during follow-up.
FIGURE 3. Contrast-enhanced abdominal computed tomography shows splenomegaly (SP) with prominent collaterals (arrow). There is a pancreatic pseudocyst abutting the splenic hilum (arrowhead).
CORRESPONDENCE
677
the pancreas should be actively sought because this complication is one of the rare instances when the problem of portal hypertension can be treated satisfactorily by splenectomy. YEONG-L[ANa LXN, MD PEI-MING YANG, MD GUAN-TARN HUANG, MD TZONG-HsI LEE, MD SEH-HUANG CHAU, MD YvK-MIN6 TSANG, MD SHIH-MING WANG, MD National Taiwan University Hospital Taipei, Taiwan, ROC
References
FIGURE 4. Venous phase of celiac angiogram shows collaterals at the esophagogastric junction and greater omentum. The splenic vein is not opacified. The opaque plaque at the esophagogastric junction is caused by previous sclerotherapy (arrow). Occlusion of the splenic vein as a consequence of chronic pancreatitis has been recognized with increasing frequency. 1-1oIts prevalence was either 2.2% or 24% in two surgical series, depending on whether splenic vein obstruction had been systematically searched for with splenoportography. 11'12 Extrahepatic portal hypertension should be considered in any patient with chronic pancreatitis who has splenomegaly and gastrointestinal bleeding. Diagnosis can be made with abdominal ultrasonography, computed tomography, and angiography. Sonographic features of splenic vein thrombosis may be an echogenic thrombus within the lumen of the vein, demonstration of splenic vein collateral circulation, and enlargement of the thrombosed segment of the vein. 13 On computed tomography, hypodense thrombi will be found in the splenic vein while the portal vein is normal.i4 Angiography is the key to diagnosis and usually shows esophagogastric varices, an obliterated splenic vein, and splenomegaly. The frequency of variceal bleeding in patients with splenic vein thrombosis secondary to chronic pancreatitis is not high. 3'6'8'15 The most common location of varices is the fundus of the stomach, and gastric varices are easily missed endoscopically unless they have been suspected. Treatment for patients with splenic vein thrombosis and gastroesophageal varices depends on the presence or absence of bleeding and the magnitude of bleeding. In the past, surgery was quickly performed on patients with active bleeding unresponsive to medical management. At present, sclerotherapy seems applicable. Since gastric varices caused by segmental portal hypertension are largely located at the fundus, sclerotherapy for active bleeding usually has had poor results. 16 Although bleeding can be stopped temporarily, rebleeding soon occurs. Therefore, it has been postulated that diagnosed splenic vein thrombosis caused by chronic pancreatitis with massive bleeding should be treated with splenectomy, If the obstruction is confined to the splenic vein, splenectomy is the treatment of choice, a7 If a pancreatic pseudocyst is also found, cystojejunostomy or resection of pseudocyst is favored. 8 As a result of severe adhesions, splenectomy may be difficult and the risk of brisk bleeding during operation is high, as occurred in this case. To reduce perioperative bleeding, ligation of the splenic artery is recommended before mobilizing the spleen with a great number of collaterals in the ligaments. In conclusion, in patients with variceal bleeding and chronic pancreatitis, splenic vein thrombosis caused by inflammatory disease of
1. Rignault D, Mine J, Moire D: Splenoportographic changes in chronic pancreatitis. Surgery 1968;63:571-575 2. McDermott WV Jr: Portal hypertension secondary to pancreatic disease. Ann Surg 1960;152:147-150 3. Little AG, Moossa AR: Gastrointestinal hemorrhage from left-sided portal hypertension: An unappreciated complication of pancreatitis. Am J Surg 1981;141:153-158 4. Harnar T, Johansen K, Haskey R, et al: Left-sided portal hypertension from pancreatic pseudotumor. Am J Gastroenterol 1982 ;77:639-641 5. Stone RT, Wilson SE, Passaro E: Gastric portal hypertension. Am J Surg 1978;136:73-79 6. Warshaw AL, Jin G, Ottinger LW: Recognition and clinical implications of mesenteric and portal vein obstruction in chronic pancreatitis. Arch Surg 1987;122:410-417 7. McEIroy R, Christiansen PA: Hereditary pancreatitis in a kinship associated with portal vein thrombosis. Am J Med 1972; 52:228-241 8. Salam AA, Warren WD, Tyras DH: Splenic vein thrombosis: A diagnosable and curable form of portal hypertension. Surgery 1973;74:961-972 9. Mossa AR, Gadd MA: Isolated splenic vein thrombosis. World J Surg 1985;9:384-390 10. Madsen MS, Petersen TH, Sommer H: Segmental portal hypertension. Ann Surg 1986;204:72-77 11. Bradley EL II1: The natural history of splenic vein thrombosis due to chronic pancreatitis: Indications for surgery. Int J Pancreatol 1987;2:87-92 12. Leger L, Lenriot JP, Lemaigre G: L'hypertension at la stase portales segmentaires dans les pancreatites chroniques. A propos de 126 cas examines par splenoportographie et splenomanometrie. J Chir 1968;95:599-608 13. Van Gansbeke D, Avni EF, Delcour C, et al: Sonographic features of portal vein thrombosis. AJR Am J Roentgenol 1985; 144:749-752 14. Vogelzang RL, Gore RM, Anschuetz SL, et al: Thrombosis of the splanchnic veins: CT diagnosis. AJR Am J Roentgenol 1988;150:93-96 15. Bernades P, Baetz A, Levy P, et al: Splenic and portal venous obstruction in chronic pancreatitis. A prospective longitudinal study of a medical-surgical series of 266 patients. Dig Dis Sci 1992;37:340-346 16. Gimson AES, Westaby D, Williams R: Endoscopic sclerotherapy and management of gastric variceal haemorrhage. Gut 1989;30:A1497 (abstr) 17. Longstreth GF, Newcomer AD, Green PA: Extrahepatic portal hypertension caused by chronic pancreatitis. Ann Intern Med 1971 ;75:903-908
NEBULIZED FENOTEROLVERSUS IV AMINOPHYLLINE TREATMENT OF ACUTE SEVEREASTHMA To the Editor.'--From July 1991 to June 1993, 30 patients visited the emergency department (ED) at National Taiwan University Hospital, where acute severe asthmatic attacks were investigated. Informed consent was obtained from all patients included in this clinical trial. All of these patients had forced expiratory volume in one second (FEV1) <30% of predicted value and peak expiratory