Clin J Gastroenterol (2011) 4:147–150 DOI 10.1007/s12328-011-0214-0
CASE REPORT
Portal vein thrombosis associated with ischemic colitis Akitoshi Kobayashi • Hideaki Mizumoto Takeshi Ando • Shoichi Matsutani
•
Received: 1 October 2010 / Accepted: 7 February 2011 / Published online: 26 March 2011 Ó Springer 2011
Abstract We report the case of a 52-year-old male who was admitted for sudden abdominal pain and hematochezia. Colonoscopy showed erosion and edema in the mucosa of the descending colon, leading to a diagnosis of ischemic colitis. Blood tests revealed hepatic dysfunctions. Using abdominal ultrasonography (US), thrombus was observed in the left branch of the portal vein and a part of the right branch. Although the Doppler method detected blood flow in the right branch, no blood flow signal was observed in the left branch. Since coagulation examinations were almost normal, and there was no past history of liver cirrhosis or malignancy, it was diagnosed to be portal vein thrombosis (PVT) associated with ischemic colitis. Anticoagulation therapy was initiated for PVT. According to the results of the US and abdominal computed tomography performed 3 months after starting the treatment, thrombus in the right branch had diminished but remained in the umbilical region of the left branch. Due to atrophy of the lateral segment of the liver, we terminated the treatment. Ischemic colitis is not a rare disease; however, when accompanying hepatic dysfunction, it is necessary to take the complications associated with PVT into consideration. Keywords Portal vein thrombosis Ischemic colitis Anticoagulation therapy
A. Kobayashi (&) H. Mizumoto T. Ando Department of Gastroenterology, Funabashi Municipal Medical Center, 1-21-1 Kanasugi, Funabashi, Chiba 274-8588, Japan e-mail: [email protected] S. Matsutani Department of Nursing, Chiba College of Health Science, Chiba, Japan
Introduction Portal vein thrombosis (PVT) is a comparatively rare disease comprising 5-15% of all mesenteric ischemic disorders [1]. It is caused by various morbidities, such as cirrhosis, malignant disease, abdominal infection, and anomaly in coagulation ability, etc. [2–6]. Among gastrointestinal diseases, cases of PVT associated with ulcerative colitis and Crohn’s disease have been reported [7–9]; however, no reports exist on PVT associated with ischemic colitis. In this report, we describe a rare case of PVT associated with ischemic colitis.
Case report A 52-year-old male complained of sudden lower abdominal pain and hematochezia, and was urgently admitted to our hospital in December 2008. He had been healthy without any underlying diseases, and had no symptoms before hospitalization. He was proper habitus, and his nutritional status was good. On admission, his body temperature was 37.0°C, blood pressure and heart rate values were 122/60 mmHg and 84 beats/min, respectively. Physically, he had mild abdominal tenderness, without rebound. The laboratory findings on admission revealed a mild elevation of the aspartate animotransaminase, alanine aminotransaminase, white blood cell count and the C-reactive protein (Table 1). In order to examine hematochezia, colonoscopy was performed on the same day of admission. Erosion and edema were observed in the mucosa of the descending colon (Fig. 1). According to histopathological examinations, no specific findings were observed, even though severe edema and inflammation were found in the submucosa. The result of stool culture was negative, and
123
148 Table 1 Laboratory data on admission
Clin J Gastroenterol (2011) 4:147–150
Hematology
Serology
White blood cell
13,800/ll
Red blood cell
5.69 9 106/mm3
Hemoglobin Hematocrit
16.8 g/dl 50.8%
Prothrombin time Activated partial thromboplastin time
12.8 s 33.1 s
Platelet
24.3 9 104/mm3
Fibrinogen
377 mg/dl
Antithrombin III
106%
Chemistry
0.57 mg/dl
Total protein
7.8 g/dl
Fibrin/fibrinogen degradation products
2.9 lg/ml
Albumin
5.1 g/dl
D-dimer
1.55 lg/ml
Blood urea nitrogen
13 mg/dl
Protein C
98%
Creatinine
0.82 mg/dl
Protein S
97%
Aspartate aminotransferase
81 IU/l
Alanine aminotransferase
81 IU/l
HBs Ag
(-)
c-Glutamyl transpeptidase
86 IU/l
HCV Ab
(-)
Alkaline phosphatase
261 IU/l
Total bilirubin
0.9 mg/dl
Lactate dehydrogenase
236 IU/l
Blood glucose
116 mg/dl
there was no history of antibiotic medication. We therefore diagnosed the patient to have ischemic colitis [10]. Using abdominal ultrasonography (US) to examine the presence of hepatic dysfunction on the 4th day of hospitalization, thrombus was observed in the entire umbilical region of the left branch of the portal vein and a part of the right branch. By the Doppler method, blood flow signals were detected in the right branch of the portal vein, while no signals were observed in the left branch (Fig. 2a, b). Using abdominal computed tomography (CT), thrombus was observed in the umbilical region of the left branch of the portal vein without contrast effects (Fig. 3). In the blood test of the coagulation system, other than the D-dimer showing a mild increase, no abnormalities were observed including antithrombin III, protein S and protein C. From these results, we diagnosed the presence of PVT associated with ischemic colitis. On the 7th day of hospitalization, after confirming that hematochezia had disappeared, intravenous administration of heparin (10,000 units/day) was initiated as anticoagulation therapy. Thereafter, it was changed to warfarin (3 mg/day) as oral medication, and the patient was discharged from hospital without any symptoms. Although the patient’s liver function transiently worsened, he demonstrated a good response during hospitalization. US performed 3 months after starting the anticoagulation therapy, showed that thrombus in the right branch of the portal vein had disappeared. The umbilical region of the left branch was occupied by a high-echo image, and the Doppler method detected no blood flow signals. In addition, according to the CT findings, a cord-like structure without contrast effects was observed in the umbilical region of the left branch, and the lateral segment of the
123
C-reactive protein Coagulation system
Hepatic virus marker
Stool Stool culture
Negative
liver was severely atrophied. We decided at this point that the anticoagulation therapy no longer had any effect and discontinued the medication. Although 2 years has passed since the discontinuation of the treatment, no hepatic dysfunctions or symptoms have been observed, and no changes have been observed in the blood flow signals of the portal vein on US.
Discussion Several causes of PVT in adults have been reported including abdominal inflammatory lesions such as chronic pancreatitis and cholecystitis, cirrhosis, malignant disease, splenectomy, abdominal trauma, myeloproliferative disorders, prothrombotic coagulation disorder, and after endoscopic injection sclerotherapy for esophageal varices [2–6], etc. Cirrhosis is the most frequency etiology accounting for 24–32% of cases [2, 4]. Among gastrointestinal diseases, there are reports on PVT being associated with ulcerative colitis, Crohn’s disease [7–9], diverticulitis, and appendicititis. For inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn’s disease, 1.3% of these patients had thrombosis as a complication, and it has been reported that 0.1% of these patients developed thrombosis in the portal vein and the superior mesenteric vein (SMV) [11]. We thought that ischemic colitis and PVT had occurred simultaneously in our case for the following reasons. Until hospitalization, the patient did not have any symptoms, such as abdominal pain or fever. There was no past history of liver cirrhosis, malignancy, abdominal infection, etc., which cause PVT. No cause for PVT was identified based
Clin J Gastroenterol (2011) 4:147–150
149
Fig. 1 Colonoscopy showed erosive and inflamed mucosa of the descending colon
Fig. 3 CT showed the portal vein thrombus in the umbilical region of a left branch without contrast effects (black arrow)
Fig. 2 US showed the portal vein thrombus in a part of the right branch (a) (white arrow) and the entire umbilical region of the left branch of the portal vein (b) (white arrow). By the Doppler method, blood flow signals were not detected in the umbilical region of a left branch
on examination of the patient’s coagulation system. The laboratory data, including a liver function test, 3 weeks before hospitalization, were normal. Furthermore, since the
patient’s liver function at the time of hospitalization transiently worsened and thereafter gradually improved, it is thought that the liver dysfunction had thus been caused by PVT which occurred simultaneously with ischemic colitis. Because severe edema and inflammation were seen in the colonic submucosa, which was thought to be the cause of PVT in our patient, portal bacteremia might have been associated. Capron et al. [9] reported that bacteria could readily gain access to the portal blood through the eroded and inflamed mucosal surface of the colon in cases of ulcerative colitis. Furthermore, Dhillon et al. [12] reported that microvascular thrombosis has been frequently documented in ischemic conditions of the gastrointestinal mucosa. Abdominal pain, nausea and vomiting, and fever are symptoms of PVT, and when thrombus reaches the SMV in a short period of time, bowel ischemia is caused, which may lead to gastrointestinal bleeding [4, 13]. In addition, when thrombus occupies a part of the portal vein so that sufficient blood flow to the liver is maintained, only mild hepatic dysfunctions are caused [7] as was observed in our patient. The diagnosis of PVT is mainly based on radiological findings, such as US, CT, magnetic resonance imaging (MRI), and angiography. In these modalities, US is a noninvasive and repeatable method for diagnosis of PVT [14, 15]. In addition, by using the Doppler mode, it is possible to confirm the presence of blood flow signals. It is a useful method that should be first conducted when PVT
123
150
is suspected. CT shows thrombus as a structure without contrast effects, and should be conducted when bowel ischemia is suspected because it enables evaluation of the intestinal wall [16]. It is also possible to differentiate hepatoma based on the difference in contrast effects. MRI makes is possible to confirm characteristics of thrombus by utilizing the fact that the signal intensity varies with time [17]. Angiography detects thrombus as a deficient image in the portal vein. In recent years, due to the development of diagnostic imaging such as multi-detector CT and MR angiography, there has been a decline in the need to perform angiography only for the purpose of diagnosis. Treatment for PVT is divided into non-surgical therapy and surgical therapy. Non-surgical therapy includes thrombolysis and anticoagulation [8, 13, 18, 19]. For thrombolysis, urokinase and tissue plasminogen activator are used in many cases, including intravenous administration and administration from the superior mesenteric artery. For anticoagulation therapy, heparin, wafarin, and antithrombin III are used. When thrombus acutely advances from the portal vein to SMV, intestinal infarction may be caused. In that case, it requires surgical therapy such as thrombectomy and bowel resection [20]. In the present case, PVT was confirmed by US on the 4th day of hospitalization. However, we hesitated to initiate anticoagulation therapy due to gastrointestinal bleeding. This delay in treatment may have led to the inadequate results in the above case. Since the progression of PVT to SMV can be fatal, treatment should be started as soon as possible if thrombus is suspected. Although few studies on the appropriate timing of heparin administration for the treatment of PVT accompanied by gastrointestinal bleeding have been reported to date, if it is possible to control the bleeding, then the immediate initiation of such treatment is strongly recommended. Due to improvements in diagnostic ability along with advances in medical equipment, the number of reports of PVT will increase. It is expected that a treatment for the management of PVT will be established in the future particularly when it is associated with gastrointestinal bleeding. In conclusion, we reported a rare case of PVT associated with ischemic colitis. When it is diagnosed as ischemic colitis and accompanied by hepatic dysfunction, it is necessary to take the complications associated with PVT into consideration.
References 1. Grendell JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology. 1982;82:358–72.
123
Clin J Gastroenterol (2011) 4:147–150 2. Okuda K, Ohnishi K, Kimura K, Matsutani S, Sumida M, Goto N, et al. Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients. Gastroenterology. 1985;89: 279–86. 3. Valla DC, Condat B. Portal vein thrombosis in adults: pathophysiology, pathogenesis and management. J Hepatol. 2000;32: 865–71. 4. Witte CL, Brewer ML, Witte MH, Pond GB. Protean manifestations of pylethrombosis. A review of thirty-four patients. Ann Surg. 1985;202:191–202. 5. Tateishi A, Mitsui H, Oki T, Morishita J, Maekawa H, Yahagi N, et al. Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation. J Gastroenterol Hepatol. 2001;16:1429–33. 6. Shudo R, Yazaki Y, Honda M, Sugawara K. A case in which danaparoid sodium was effective for portal venous thrombosis developed after endoscopic injection sclerotherapy for esophageal varices. Clin J Gastroenterol. 2008;1:110–5. 7. Hagimoto T, Seo M, Okada M, Shirotani T, Tanaka K, Tomita A, et al. Portal vein thrombosis successfully treated with a colectomy in active ulcerative colitis. Dis Colon Rectum. 2001;44: 587–90. 8. Tsujikawa T, Ihara T, Sasaki M, Inoue H, Fujiyama Y, Bamba T. Effectiveness of combined anticoagulant therapy for extending portal vein thrombosis in Crohn’s disease. Report of a case. Dis Colon Rectum. 1996;39:823–5. 9. Capron JP, Remond A, Lebrec D, Delamarre J, Dupas JL, Lorriaux A. Gastrointestinal bleeding due to chronic portal vein thrombosis in ulcerative colitis. Dig Dis Sci. 1979;24:232–5. 10. Williams LF, Wittenberg J. Ischemic colitis: a useful clinical diagnosis, but is it ischemic? Ann Surg. 1975;182:439–48. 11. Talbot RW, Heppell J, Dozois PR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc. 1986;61:140–5. 12. Dhillon AP, Anthony A, Sim R, Wakefield AJ, Sankey EA, Hudson M, et al. Mucosal capillary thrombi in rectal biopsies. Histopathology. 1992;21:127–33. 13. Condat B, Pessione F, Hillaire S, Denninger MH, Guillin MC, Poliquin M, et al. Current outcome of portal vein thrombosis in adults: risk and benefit of anticoagulant therapy. Gastroenterology. 2001;120:490–7. 14. Subramanyam BR, Balthazar EJ, Lefleur RS, Horii SC, Hulnick DH. Portal venous thrombosis: correlative analysis of sonography, CT, and angiography. Am J Gastroenterol. 1984;79:773–6. 15. Van Gansbeke D, Avni EF, Delcour C, Engelholm L, Struyven J. Sonographic features of portal vein thrombosis. Am J Roentgenol. 1985;144:749–52. 16. Mathieu D, Vasile N, Grenier P. Portal thrombosis: dynamic CT features and course. Radiology. 1985;154:737–41. 17. Zirinsky K, Markisz JA, Rubenstein WA, Cahill PT, Knowles RJR, Auh YH, et al. MR imaging of portal venous thrombosis: correlation with CT and sonography. AJR. 1988;150:283–8. 18. Suzuki S, Nakamura S, Baba S, Sakaguchi S, Ohnuki Y, Yokoi Y, et al. Portal vein thrombosis after splenectomy successfully treated by an enormous dosage of fibrinolytic agent in a short period: report of two cases. Surg Today. 1992;22:464–9. 19. Condat B, Pessione F, Denninger MH, Hillaire S, Valla D. Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy. Hepatology. 2000;32:466–70. 20. Boley SJ, Kaleya RN, Brandt LJ. Mesenteric venous thrombosis. Surg Clin North Am. 1992;72:183–201.
CASE REPORT
Portal vein thrombosis associated with ischemic colitis Akitoshi Kobayashi • Hideaki Mizumoto Takeshi Ando • Shoichi Matsutani
•
Received: 1 October 2010 / Accepted: 7 February 2011 / Published online: 26 March 2011 Ó Springer 2011
Abstract We report the case of a 52-year-old male who was admitted for sudden abdominal pain and hematochezia. Colonoscopy showed erosion and edema in the mucosa of the descending colon, leading to a diagnosis of ischemic colitis. Blood tests revealed hepatic dysfunctions. Using abdominal ultrasonography (US), thrombus was observed in the left branch of the portal vein and a part of the right branch. Although the Doppler method detected blood flow in the right branch, no blood flow signal was observed in the left branch. Since coagulation examinations were almost normal, and there was no past history of liver cirrhosis or malignancy, it was diagnosed to be portal vein thrombosis (PVT) associated with ischemic colitis. Anticoagulation therapy was initiated for PVT. According to the results of the US and abdominal computed tomography performed 3 months after starting the treatment, thrombus in the right branch had diminished but remained in the umbilical region of the left branch. Due to atrophy of the lateral segment of the liver, we terminated the treatment. Ischemic colitis is not a rare disease; however, when accompanying hepatic dysfunction, it is necessary to take the complications associated with PVT into consideration. Keywords Portal vein thrombosis Ischemic colitis Anticoagulation therapy
A. Kobayashi (&) H. Mizumoto T. Ando Department of Gastroenterology, Funabashi Municipal Medical Center, 1-21-1 Kanasugi, Funabashi, Chiba 274-8588, Japan e-mail: [email protected] S. Matsutani Department of Nursing, Chiba College of Health Science, Chiba, Japan
Introduction Portal vein thrombosis (PVT) is a comparatively rare disease comprising 5-15% of all mesenteric ischemic disorders [1]. It is caused by various morbidities, such as cirrhosis, malignant disease, abdominal infection, and anomaly in coagulation ability, etc. [2–6]. Among gastrointestinal diseases, cases of PVT associated with ulcerative colitis and Crohn’s disease have been reported [7–9]; however, no reports exist on PVT associated with ischemic colitis. In this report, we describe a rare case of PVT associated with ischemic colitis.
Case report A 52-year-old male complained of sudden lower abdominal pain and hematochezia, and was urgently admitted to our hospital in December 2008. He had been healthy without any underlying diseases, and had no symptoms before hospitalization. He was proper habitus, and his nutritional status was good. On admission, his body temperature was 37.0°C, blood pressure and heart rate values were 122/60 mmHg and 84 beats/min, respectively. Physically, he had mild abdominal tenderness, without rebound. The laboratory findings on admission revealed a mild elevation of the aspartate animotransaminase, alanine aminotransaminase, white blood cell count and the C-reactive protein (Table 1). In order to examine hematochezia, colonoscopy was performed on the same day of admission. Erosion and edema were observed in the mucosa of the descending colon (Fig. 1). According to histopathological examinations, no specific findings were observed, even though severe edema and inflammation were found in the submucosa. The result of stool culture was negative, and
123
148 Table 1 Laboratory data on admission
Clin J Gastroenterol (2011) 4:147–150
Hematology
Serology
White blood cell
13,800/ll
Red blood cell
5.69 9 106/mm3
Hemoglobin Hematocrit
16.8 g/dl 50.8%
Prothrombin time Activated partial thromboplastin time
12.8 s 33.1 s
Platelet
24.3 9 104/mm3
Fibrinogen
377 mg/dl
Antithrombin III
106%
Chemistry
0.57 mg/dl
Total protein
7.8 g/dl
Fibrin/fibrinogen degradation products
2.9 lg/ml
Albumin
5.1 g/dl
D-dimer
1.55 lg/ml
Blood urea nitrogen
13 mg/dl
Protein C
98%
Creatinine
0.82 mg/dl
Protein S
97%
Aspartate aminotransferase
81 IU/l
Alanine aminotransferase
81 IU/l
HBs Ag
(-)
c-Glutamyl transpeptidase
86 IU/l
HCV Ab
(-)
Alkaline phosphatase
261 IU/l
Total bilirubin
0.9 mg/dl
Lactate dehydrogenase
236 IU/l
Blood glucose
116 mg/dl
there was no history of antibiotic medication. We therefore diagnosed the patient to have ischemic colitis [10]. Using abdominal ultrasonography (US) to examine the presence of hepatic dysfunction on the 4th day of hospitalization, thrombus was observed in the entire umbilical region of the left branch of the portal vein and a part of the right branch. By the Doppler method, blood flow signals were detected in the right branch of the portal vein, while no signals were observed in the left branch (Fig. 2a, b). Using abdominal computed tomography (CT), thrombus was observed in the umbilical region of the left branch of the portal vein without contrast effects (Fig. 3). In the blood test of the coagulation system, other than the D-dimer showing a mild increase, no abnormalities were observed including antithrombin III, protein S and protein C. From these results, we diagnosed the presence of PVT associated with ischemic colitis. On the 7th day of hospitalization, after confirming that hematochezia had disappeared, intravenous administration of heparin (10,000 units/day) was initiated as anticoagulation therapy. Thereafter, it was changed to warfarin (3 mg/day) as oral medication, and the patient was discharged from hospital without any symptoms. Although the patient’s liver function transiently worsened, he demonstrated a good response during hospitalization. US performed 3 months after starting the anticoagulation therapy, showed that thrombus in the right branch of the portal vein had disappeared. The umbilical region of the left branch was occupied by a high-echo image, and the Doppler method detected no blood flow signals. In addition, according to the CT findings, a cord-like structure without contrast effects was observed in the umbilical region of the left branch, and the lateral segment of the
123
C-reactive protein Coagulation system
Hepatic virus marker
Stool Stool culture
Negative
liver was severely atrophied. We decided at this point that the anticoagulation therapy no longer had any effect and discontinued the medication. Although 2 years has passed since the discontinuation of the treatment, no hepatic dysfunctions or symptoms have been observed, and no changes have been observed in the blood flow signals of the portal vein on US.
Discussion Several causes of PVT in adults have been reported including abdominal inflammatory lesions such as chronic pancreatitis and cholecystitis, cirrhosis, malignant disease, splenectomy, abdominal trauma, myeloproliferative disorders, prothrombotic coagulation disorder, and after endoscopic injection sclerotherapy for esophageal varices [2–6], etc. Cirrhosis is the most frequency etiology accounting for 24–32% of cases [2, 4]. Among gastrointestinal diseases, there are reports on PVT being associated with ulcerative colitis, Crohn’s disease [7–9], diverticulitis, and appendicititis. For inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn’s disease, 1.3% of these patients had thrombosis as a complication, and it has been reported that 0.1% of these patients developed thrombosis in the portal vein and the superior mesenteric vein (SMV) [11]. We thought that ischemic colitis and PVT had occurred simultaneously in our case for the following reasons. Until hospitalization, the patient did not have any symptoms, such as abdominal pain or fever. There was no past history of liver cirrhosis, malignancy, abdominal infection, etc., which cause PVT. No cause for PVT was identified based
Clin J Gastroenterol (2011) 4:147–150
149
Fig. 1 Colonoscopy showed erosive and inflamed mucosa of the descending colon
Fig. 3 CT showed the portal vein thrombus in the umbilical region of a left branch without contrast effects (black arrow)
Fig. 2 US showed the portal vein thrombus in a part of the right branch (a) (white arrow) and the entire umbilical region of the left branch of the portal vein (b) (white arrow). By the Doppler method, blood flow signals were not detected in the umbilical region of a left branch
on examination of the patient’s coagulation system. The laboratory data, including a liver function test, 3 weeks before hospitalization, were normal. Furthermore, since the
patient’s liver function at the time of hospitalization transiently worsened and thereafter gradually improved, it is thought that the liver dysfunction had thus been caused by PVT which occurred simultaneously with ischemic colitis. Because severe edema and inflammation were seen in the colonic submucosa, which was thought to be the cause of PVT in our patient, portal bacteremia might have been associated. Capron et al. [9] reported that bacteria could readily gain access to the portal blood through the eroded and inflamed mucosal surface of the colon in cases of ulcerative colitis. Furthermore, Dhillon et al. [12] reported that microvascular thrombosis has been frequently documented in ischemic conditions of the gastrointestinal mucosa. Abdominal pain, nausea and vomiting, and fever are symptoms of PVT, and when thrombus reaches the SMV in a short period of time, bowel ischemia is caused, which may lead to gastrointestinal bleeding [4, 13]. In addition, when thrombus occupies a part of the portal vein so that sufficient blood flow to the liver is maintained, only mild hepatic dysfunctions are caused [7] as was observed in our patient. The diagnosis of PVT is mainly based on radiological findings, such as US, CT, magnetic resonance imaging (MRI), and angiography. In these modalities, US is a noninvasive and repeatable method for diagnosis of PVT [14, 15]. In addition, by using the Doppler mode, it is possible to confirm the presence of blood flow signals. It is a useful method that should be first conducted when PVT
123
150
is suspected. CT shows thrombus as a structure without contrast effects, and should be conducted when bowel ischemia is suspected because it enables evaluation of the intestinal wall [16]. It is also possible to differentiate hepatoma based on the difference in contrast effects. MRI makes is possible to confirm characteristics of thrombus by utilizing the fact that the signal intensity varies with time [17]. Angiography detects thrombus as a deficient image in the portal vein. In recent years, due to the development of diagnostic imaging such as multi-detector CT and MR angiography, there has been a decline in the need to perform angiography only for the purpose of diagnosis. Treatment for PVT is divided into non-surgical therapy and surgical therapy. Non-surgical therapy includes thrombolysis and anticoagulation [8, 13, 18, 19]. For thrombolysis, urokinase and tissue plasminogen activator are used in many cases, including intravenous administration and administration from the superior mesenteric artery. For anticoagulation therapy, heparin, wafarin, and antithrombin III are used. When thrombus acutely advances from the portal vein to SMV, intestinal infarction may be caused. In that case, it requires surgical therapy such as thrombectomy and bowel resection [20]. In the present case, PVT was confirmed by US on the 4th day of hospitalization. However, we hesitated to initiate anticoagulation therapy due to gastrointestinal bleeding. This delay in treatment may have led to the inadequate results in the above case. Since the progression of PVT to SMV can be fatal, treatment should be started as soon as possible if thrombus is suspected. Although few studies on the appropriate timing of heparin administration for the treatment of PVT accompanied by gastrointestinal bleeding have been reported to date, if it is possible to control the bleeding, then the immediate initiation of such treatment is strongly recommended. Due to improvements in diagnostic ability along with advances in medical equipment, the number of reports of PVT will increase. It is expected that a treatment for the management of PVT will be established in the future particularly when it is associated with gastrointestinal bleeding. In conclusion, we reported a rare case of PVT associated with ischemic colitis. When it is diagnosed as ischemic colitis and accompanied by hepatic dysfunction, it is necessary to take the complications associated with PVT into consideration.
References 1. Grendell JH, Ockner RK. Mesenteric venous thrombosis. Gastroenterology. 1982;82:358–72.
123
Clin J Gastroenterol (2011) 4:147–150 2. Okuda K, Ohnishi K, Kimura K, Matsutani S, Sumida M, Goto N, et al. Incidence of portal vein thrombosis in liver cirrhosis. An angiographic study in 708 patients. Gastroenterology. 1985;89: 279–86. 3. Valla DC, Condat B. Portal vein thrombosis in adults: pathophysiology, pathogenesis and management. J Hepatol. 2000;32: 865–71. 4. Witte CL, Brewer ML, Witte MH, Pond GB. Protean manifestations of pylethrombosis. A review of thirty-four patients. Ann Surg. 1985;202:191–202. 5. Tateishi A, Mitsui H, Oki T, Morishita J, Maekawa H, Yahagi N, et al. Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation. J Gastroenterol Hepatol. 2001;16:1429–33. 6. Shudo R, Yazaki Y, Honda M, Sugawara K. A case in which danaparoid sodium was effective for portal venous thrombosis developed after endoscopic injection sclerotherapy for esophageal varices. Clin J Gastroenterol. 2008;1:110–5. 7. Hagimoto T, Seo M, Okada M, Shirotani T, Tanaka K, Tomita A, et al. Portal vein thrombosis successfully treated with a colectomy in active ulcerative colitis. Dis Colon Rectum. 2001;44: 587–90. 8. Tsujikawa T, Ihara T, Sasaki M, Inoue H, Fujiyama Y, Bamba T. Effectiveness of combined anticoagulant therapy for extending portal vein thrombosis in Crohn’s disease. Report of a case. Dis Colon Rectum. 1996;39:823–5. 9. Capron JP, Remond A, Lebrec D, Delamarre J, Dupas JL, Lorriaux A. Gastrointestinal bleeding due to chronic portal vein thrombosis in ulcerative colitis. Dig Dis Sci. 1979;24:232–5. 10. Williams LF, Wittenberg J. Ischemic colitis: a useful clinical diagnosis, but is it ischemic? Ann Surg. 1975;182:439–48. 11. Talbot RW, Heppell J, Dozois PR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc. 1986;61:140–5. 12. Dhillon AP, Anthony A, Sim R, Wakefield AJ, Sankey EA, Hudson M, et al. Mucosal capillary thrombi in rectal biopsies. Histopathology. 1992;21:127–33. 13. Condat B, Pessione F, Hillaire S, Denninger MH, Guillin MC, Poliquin M, et al. Current outcome of portal vein thrombosis in adults: risk and benefit of anticoagulant therapy. Gastroenterology. 2001;120:490–7. 14. Subramanyam BR, Balthazar EJ, Lefleur RS, Horii SC, Hulnick DH. Portal venous thrombosis: correlative analysis of sonography, CT, and angiography. Am J Gastroenterol. 1984;79:773–6. 15. Van Gansbeke D, Avni EF, Delcour C, Engelholm L, Struyven J. Sonographic features of portal vein thrombosis. Am J Roentgenol. 1985;144:749–52. 16. Mathieu D, Vasile N, Grenier P. Portal thrombosis: dynamic CT features and course. Radiology. 1985;154:737–41. 17. Zirinsky K, Markisz JA, Rubenstein WA, Cahill PT, Knowles RJR, Auh YH, et al. MR imaging of portal venous thrombosis: correlation with CT and sonography. AJR. 1988;150:283–8. 18. Suzuki S, Nakamura S, Baba S, Sakaguchi S, Ohnuki Y, Yokoi Y, et al. Portal vein thrombosis after splenectomy successfully treated by an enormous dosage of fibrinolytic agent in a short period: report of two cases. Surg Today. 1992;22:464–9. 19. Condat B, Pessione F, Denninger MH, Hillaire S, Valla D. Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy. Hepatology. 2000;32:466–70. 20. Boley SJ, Kaleya RN, Brandt LJ. Mesenteric venous thrombosis. Surg Clin North Am. 1992;72:183–201.
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