CASE REPORT – OPEN ACCESS International Journal of Surgery Case Reports 4 (2013) 432–434
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Isolated superior mesenteric venous thrombophlebitis with acute appendicitis Mohsen Mohamed Karam a,∗ , Mohaed Fahmy Abdalla b , Said Bedair b a b
Hamad Medical Corporation, G Surgery, 46 Teba Garden, Doha, Qatar Alkhor Hospital, Qatar
a r t i c l e
i n f o
Article history: Received 22 October 2011 Accepted 24 October 2011 Available online 2 December 2011 Keywords: Thrombophlebitis Thrombophlebosis Portapyemia Appendicitis
a b s t r a c t INTRODUCTION: Isolated superior mesentericveinous thrmbophlebitis is a rarely recognised condition associated with a high morbidity. It usually develops secondary to infection in the drainage area of the portal venous system, like appendix. PRESENTATION OF CASE: We report a case of neglected perforated acute appendicitis complicated by superior mesenteric venous pyelephlebitis patiant represented with a vague pain to right of umlicus, which is atypical this why cat scan was done and showed obstructed superiormesentric vein, portal vein was free with acute appendicitis. Appendicectomy and treatment with broad-spectrum antibiotics, anticoagulation, and platelets led to a full recovery. Follow-up imaging after one month revealed complete canalization of superior mesentric vein. DISCUSSION: Abdominal pain if atypical like our case report need imaging diagnosis. Modern diagnostic imaging techniques help the early diagnosis of acute phase pylephlebitis. CT can detect primary source of infection, extent of pylephlebitis, CT scan is the most reliable initially. Ultrasound scan with color flow Doppler is also a sensitive test for confirming partial patency of the portal vein and portal vein thrombosis accidentally discovered complete obliteration of superior mesenteric vein with thrombosis which remained not propagated by serial Doppler ultrasound of liver. Appropriate treatment should be initiated as soon as possible. To avoid extension to portal vein. The principal treatment for pylephlebitis is to remove the source of infection as appendicectomy. Anticoagulants must be used. Regarding the treatment of portal thrombosis, post operative use of heparin has been advocated. CONCLUSION: Cat scan play an important role in case of atypical abdominal pain. © 2013 Published by Elsevier Ltd on behalf of Surgical Associates Ltd.
1. Introduction Superior mesenteric venous thrombophlebitis is uncommon. It is usually secondary to infection in the drainage area of the portal venous system. Hepatic abscess formation may occur if the thrombus extends through the portal vein. Clinical diagnosis is almost impossible but preoperative diagnostic imaging may increase recognition. 2. Case report A 28-year-old Indian male presented with a 10 day history of vague, dull aching abdominal pain, mainly periumbilical. He complained of nausea but no vomiting or anorexia. His bowel habit was unremarkable and he had no urinary symptoms. On admission his temperature was 38 degrees, heart rate 90 beats per minute, and blood pressure 116/60 mmHg. His abdomen was lax, only tender to the right of umbilicus near the midline. Investigations revealed an elevated white cell count (17.8 × 103 /L). His liver function tests
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[email protected] (M.M. Karam).
were deranged, with mildly elevated AST (65 U/L), ALT (60 U/L) and bilirubin (30 mol/L). His alkaline phosphatase levels were raised (316 U/L). An abdominal computed tomography scan with contrast demonstrated extensive superior mesenteric venous (SMV) thrombosis with acute appendicitis. Duplex ultrasound examination suggested complete SMV occlusion. A gangrenous appendix was removed the next day. No bowel ischaemia was detected. Postoperatively, he was heparinized and subsequently warfarinized. The warfarin was discontinued after one month. Follow-up duplex ultrasound demonstrated recanalization of the SMV.
3. Discussion Pylephlebitis is defined as serious septic thrombophlebitis of the portal vein or one of its tributaries, e.g. superior mesenteric vein. It usually develops secondary to infection in the drainage area of the portal venous system,1 typically appendicitis or diverticulitis. SMV thrombosis is an uncommon cause of bowel ischemia in adults.2 It was first recognized more than 100 years ago by Eliot3 who described intestinal gangrene resulting from mesenteric venous occlusion. The exact incidence of SMV thrombophlebitis is unknown. It may not be recognized at laparotomy and may be
2210-2612/$ – see front matter © 2013 Published by Elsevier Ltd on behalf of Surgical Associates Ltd. doi:10.1016/j.ijscr.2011.10.019
CASE REPORT – OPEN ACCESS M.M. Karam et al. / International Journal of Surgery Case Reports 4 (2013) 432–434
missed at autopsy.4 Greater use of diagnostic radiological imaging may lead to increased recognition. Before the advent of antibiotics, mesenteric portal vein thrombosis and liver abscess formation complicated up to 50% of cases of appendicitis, diverticulitis, and other inflammatory bowel conditions.5 Since the routine administration of antibiotics and early surgical intervention, the incidence of ascending infectious portal thrombophlebitis has dropped to 0.05% for acute appendicitis and 3% for a ruptured appendix.6 Clinically, pylephlebitis or at least portal bacteremia should be suspected in any patient with suspected appendicitis who has rigors.7 Pylephlebitis secondary to infections (e.g. appendicitis) has been distinguished from thrombosis alone (without infection) due to other causes by its typically non-occlusive nature and absence of portal hypertension. In appendicitis, spread occurs via the ileocolic vasculature to the superior mesenteric vein and eventually to the portal vein.8 Pylephlebitis can also give rise to septic emboli within the liver, leading to intrahepatic abscess formation.9 Deranged liver enzymes were evident in our case and could have been indicative of early hepatic involvement. In our patient, pylephlebitis was detected at the level of superior mesenteric vein and not propagated to confluent of splenoportal vein and early recognition led to early management. The clinical features of pylephlebitis are non-specific. High fever, chills, malaise, right quadrant pain, and tenderness are the initial clinical manifestations. Gollapudi10 reported that only 30% of patients with pylephlebitis present with localizing clinical signs of a primary source of sepsis. Laboratory findings, such as leucocytosis and mild abnormalities of liver function tests, are usually non-specific, but jaundice is rare except in case of multiple liver abscesses.11,12 Cultures revealed no microorganisms in our case. Baril et al.11 reported that bacteremia is present in less than one-half of patients, whereas, Balthazar and Gollapudi13 reported that up to 80% of patients have positive blood cultures and Escherichia coli, Bacteroides fragilis, Proteus mirabilis, Klebsiella pneumoniae, and Enterobacter spp. are the most common microorganisms isolated.12,13 Modern diagnostic imaging techniques help the early diagnosis of acute phase pylephlebitis. The sensitivity and specificity of CT scans for pylephlebitis are not known. However, CT scans could simultaneously detect the primary source of infection, extent of pylephlebitis, and intrahepatic abnormalities, such as liver abscess. Thus, CT scan is the most reliable initial diagnostic choice.13,14 Air bubbles or thrombi of the portal venous system are the critical CT findings of pylephlebitis13 . Ultrasound scan with color flow Doppler is also a sensitive test for confirming partial patency of the portal vein and portal vein thrombosis.15 The principal treatment for pylephlebitis is to remove the source of infection and eradicate the toxic microorganisms using appropriate antibiotics. Immediate surgical intervention is necessary in most cases, but Stitzenberg et al.16 reported that interval laparoscopic appendectomy can be performed 3 months after treatment with antibiotics and anticoagulants. Regarding the treatment of portal thrombosis, post operative use of heparin has been advocated1 but a benefit of adjunctive heparin therapy has not been clearly demonstrated. Harch et al. recommended anticoagulation on the presumption that the process might extend and lead to enteric ischaemia.17 Proponents of anticoagulation identified several factors such as documented progression of thrombus while on antibiotics, fever unresponsive to treatment, and the presence of hypercoagulable state to justify therapy.18 Anticoagulation may also reduce septic embolization to the liver from infected portal thrombi and prevent liver abscess. The optimum duration of anticoagulation is unclear in the literature. If thrombosis is associated with sepsis and not complicated by infarction or embolization and
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no underlying thrombophilic factors are identified, then a short duration of therapy seems a reasonable approach, however. Open thrombectomy and venous ligation19 appear to have been largely abandoned as therapy for pylephlebitis. Operative or radiological interventions in the form of thrombectomy and thrombolysis with direct intravascular infusion of thrombolytics have been advocated20 for mesenteric and portal vein non-suppurative thrombosis with bowel compromise. Nishimori et al.14 reported a patient with septic thrombophlebitis and liver abscess who had appendicectomy and thrombus removal from the SMV using a Fogarty catheter. The mortality rate reported of up to 32% in cases with SMV thrombosis will in part be due to the severity of the associated condition14 rather than the thrombosis itself but it has been suggested that the complications of untreated portal or SMV thrombosis could be catastrophic.21 The reported high mortality rate without anticoagulation and a decreased recurrence rate reported after anticoagulation15 support our decision to use it in our patient. 4. Conclusion Superior mesenteric venous thrombophlebitis is a rare but potentially fatal complication of acute intra-abdominal suppuration such as appendicitis. A high index of suspicion is required to allow prompt recognition and treatment. Conflict of interest statement The authors have no conflict of interests to declare. Funding None. Ethical approval Consent from patient available. Author contributions All authors read, reviewed and wrote the paper. References 1. Plemmons RM, Dooley DP, Longfield RN. Septic thrombophlebitis of the portal vein (pylephlebitis): diagnosis and management in the modern era. Clin Infect Dis 1995;21:111. 2. Grendell JH, Ochner PK. Mesenteric vein thrombosis. Gastroenterology 1982;82:358–72. 3. Eliot JW. The operative relief of gangrene of the intestine due to occlusion of the mesenteric vessels. Ann Surg 1895;21:9–23. 4. Klinefelter Jr HF, Grose WE, Crawford HJ. Pyelephlebitis. Bull Johns Hopkins Hosp 1960;106:65–73. 5. Slovis TL, Haller JO, Cohen HL, Berdon WE, Watts Jr FB. Complicated appendiceal inflammatory disease in children pylephlebitis and liver abscess. Radiology 1989;171:823–5. 6. Scwartz SI, Shives GT, Spencer FC, Storer EH, editors. Principles of surgery. 4th ed. New York: McGraw-Hill; 1984. p. 1245–55. 7. Ruff ME, Friedland IR, Hickey SM. Escherichia coli septicemia in nonperforated appendicitis. Arch Pediatr Adolesc Med 1994;148:853. 8. Mchardy G. The appendix, chapter 144. In: Berk JE, editor. Bockus gastroenterology, vol. 4. 4th ed. Philadephia: WB Saunders; 1985. p. 2609–24. 9. Daly JM, Adams JT, Fantini GA, Fischer JE. Abdominal wall, omentum, mesentery, and retroperitoneum, chapter 13. In: Schwartz SI, et al., editors. Principles of surgery, vol. 2, 7th ed. New York: McGraw-Hill; 1999. p. 157. 10. Giuliano CT, Zerykier A, Haller JO, Wood BP. Radiological case of the month. Pylephlebitis secondary to unsuspected appendiceal rupture. Am J Dis Child 1989;143:1099–100. 11. Baril N, Wren S, Radin R, Ralls P, Stain S. The role of anticoagulation in pylephlebitis. Am J Surg 1996;172:449–52. 12. Lim HE, Cheong HJ, Woo HJ, Kim WJ, Kim MJ, Lee CH, et al. Pylephlebitis associated with appendicitis. Korean J Intern Med 1999;14:73–6.
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