The prevalence and clinical spectrum of acute mesenteric venous thrombosis (AMVT) in Pakistan is largely unknown. The authors report two patients with acute mesenteric, portal and inferior vena cava venous thrombosis confirmed on CT imaging. The diagnoses were established within 24 hours of presentation and both patients were successfully treated with therapeutic heparin during hospital admission and continued on oral warfarin because of hypercoagulable state. The protocol that we currently use is evidence based and is leading to optimal outcome

Alvi, Abdul Rehman

Bibi, Shahida

Niazi, Sameullah Khan

ur Rehman, Zia

eCommons@AKU

eCommons@AKUSection of Cardiothoracic Surgery Department of SurgeryMay 2010Acute mesenteric, portal and inferior vena cava,venous thrombosis, anticoagulationAbdul Rehman AlviAga Khan UniversityShahida BibiAga Khan UniversityZia ur RehmanAga Khan UniversitySameullah Khan NiaziAga Khan UniversityFollow this and additional works at: http://ecommons.aku.edu/pakistan_fhs_mc_surg_cardiothoracicPart of the Surgery CommonsRecommended CitationAlvi, A., Bibi, S., ur Rehman, Z., Niazi, S. (2010). Acute mesenteric, portal and inferior vena cava, venous thrombosis, anticoagulation.Journal of the Pakistan Medical Association, 60(5), 397-9.Available at: http://ecommons.aku.edu/pakistan_fhs_mc_surg_cardiothoracic/18AbstractThe prevalence and clinical spectrum of acutemesenteric venous thrombosis (AMVT) in Pakistan is largelyunknown. The authors report two patients with acutemesenteric, portal and inferior vena cava venous thrombosisconfirmed on CT imaging. The diagnoses were establishedwithin 24 hours of presentation and both patients weresuccessfully treated with therapeutic heparin during hospitaladmission and continued on oral warfarin because ofhypercoagulable state. The protocol that we currently use isevidence based and is leading to optimal outcome.IntroductionAcute mesenteric Venous thrombosis (AMVT) is anuncommon but potentially life threatening type of acutemesenteric ischaemia but fortunately comprises 5-15% of allcauses.1,2 In 1895 Elliott first described the phenomenon ofacute mesenteric venous thrombosis and subsequently Abu etal identified 375 cases of AMVT in international literaturesince 1911-1984.2 In 22 years 72 cases were reported fromMayo clinic (1972-1993) and this comprises 6.2% of all casesof mesenteric ischaemia. The literature reported variousaspects of AMVT including probable etiology, presentation,diagnostic modalities and therapeutics.2,3 The diagnosis ofMVT remained a serious challenge to the clinicians and wasoften diagnosed on laparotomy with mortality of more than34%.4Advancement in radiological imaging like the CT scanhave enabled the early detection of the disease and openednew avenues in its management.3,4 Early diagnosis and betterunderstanding of the disease process have enabled theclinicians to avert the consequences of AMVT by appropriateanticoagulation and opened the door for non-operativemanagement.3Case ReportThe first case was of a 30 year old female who397 J Pak Med AssocCase ReportAcute mesenteric, Portal and Inferior Vena Cava (IVC) venous thrombosis:Optimal outcome achieved with anticoagulationAbdul Rehman Alvi, Shahida Bibi, Zia ur Rehman, Sameullah Khan NiaziDepartment of Surgery, Aga Khan University Hospital, Karachi.presented to the emergency room with complaints of centralabdominal pain, nausea and vomiting of 10 days duration.The past history was unremarkable and there was no historyof oral or injectable contraceptives. She looked dehydratedbut was stable haemodynamically with heart rate of100/minute, blood pressure of 120/80 mmHg and normalcore temperature. Abdomen was distended and tender ondeep palpation all over with increased tenderness in rightlower quadrant. However, no signs of peritonitis werepresent. The initial laboratory investigation showedhaemoglobin of 11.8 gm/dl (normal range: 11.1-14.5) withhaematocrit of 35% (normal range: 35.4-42 %), white cellcount of 9.4 (normal range: 4.0-10) x10E9/L with 74.6%neutrophils and platelet count of 426 (150-400) x10E9/L. Herserum amylase, electrolytes, liver function tests, arterialblood gas analysis and coagulation profiles were withinnormal limits. Plain abdominal X-rays and ultra-sonographywere normal. Double contrast CT scan abdomen was done toexplain the out of proportion severe abdominal pain. CT scanfindings were suggestive of small bowel ischaemia secondaryto extensive thrombosis involving the entire superiormesenteric vein, portal vein and partial thrombosis of inferiorvena cava was also demonstrated.After initial fluid resuscitation, she was started ontherapeutic intravenous heparin therapy, with an initialbolus of 10000 units followed by heparin infusion. Theheparin infusion was titrated to maintain the I.N.R in therange of 2.5 to 3 ratios. She was monitored closely in thehigh dependent unit and responded very well toanticoagulation therapy, with a decrease in the intensity ofabdominal pain and tenderness. Patient was started on oralanti coagulant (Tab.Warfarin) on third day of admissionwhen she was tolerating oral diet. She was discharged on8th day of admission on therapeutic oral anti coagulant andadvised to regularly monitor the Prothrombin Time (PT)and to keep INR in therapeutic range (2.5-3 ratio).The serum anticoagulant factors profile wasavailable and showed protein-C of 60% (72-106); protein- Sof 5% (65-110), antithrombin III of 94% (80-120) and factorV Leiden of 2.5% (1.75-2.80). On 6 months follow up sheremained asymptomatic, continued on oral warfarin, INRwas kept at 3 ratio. Patient was advised to continue life longanticoagulant therapy.The second patient was a 40 year old male who was inhis usual state of health until one week back when hedeveloped generalized abdominal pain, which graduallyincreased in intensity and was associated with anorexia andnausea. His past medical history was significant for deepvenous thrombosis of the left leg 18 months back and he wason oral warfarin for a period 6 months prior to the currentcondition. On clinical examination in the emergency room hewas found to be in severe abdominal pain but vital signs werewithin normal limits. His abdomen was distended and tenderall over on deep palpation, however, no signs of peritonitiswere present. The initial laboratory investigation showedhaemoglobin of 12.8 gm/dl (normal range: 13.7-16.3) withhaematocrit of 37.7% (41.9-48.7), white cell count of 8.1(normal range: 4.0-10) x10E9/L with neutrophils of 84%. Hisserum electrolytes, liver function tests, serum amylase, lipaseand arterial blood gas analysis were within normal limits.Abdominal ultrasonography and plain X-rays were normal.The double contrast CT scan of the abdomen revealedthrombosis of superior mesenteric vein, extensive thrombosisof portal vein, thrombus in Interior Vena Cava (IVC), mildascites and thickned oedematous colon.Patient was started on therapeutic intravenous heparininfusion and was monitored closely in high dependent unitwith serial APTT and INR to keep these parameters within thetherapeutic range. He responded very well on anti coagulanttherapy, with decreased abdominal pain and tenderness. Theserum anticoagulant factors results were available and showedprotein-S of 10% (normal range: 65-110), protein-C of 56%(normal range: 72-106), anti thrombin III 89% (normal range:80-120), factor V Leiden of 2.02 (normal range: 1.75-2.80),anticardiolipin IGG of 1.5, anticardiolipin IGM of 1.9 andserum homocystein of 15.71 H (normal range: 4.45-12.42).Patient was discharged on oral warfarin with theadvice to continue the drug life long. He remainedasymptomatic on 18 months follow up with no evidence ofrecurrent, portal hypertension or bowel stricture.DiscussionAcute mesenteric venous thrombosis is an uncommoncause of mesenteric ischaemia with mortality rate of 34-40%in early 1990.4 The high mortality was contributed to delay indiagnosis established on exploratory laparotomy. TheseVol. 60, No. 5, May 2010 398Figure: patients did not receive peri-operative anticoagulation therapy.Improved understanding of disease process and availability ofCT scan changed the management of AMVT with increasedemphasis on early anticoagulation therapy and the desiredresults were achieved in 15 patients with no mortality.5 Astudy from China reported 44 patients with AMVT whichwere divided into operative and non operative group. Theresults showed 39 % mortality in operated and 11% in nonoperated group. The authors proposed early anticoagulationtherapy to achieve the best outcome in AMVT.6A study fromIndia in 32 patients with AMVT further consolidated thepreference of early anticoagulation in all patients and surgicaltreatment in cases of peritonitis achieved low mortality.7 Aretrospective review of 57 patients showed optimal outcomewith early diagnosis on CT scan and prompt anticoagulationtherapy.8 The operative intervention was required only inclinical and radiological signs of bowel infarction and thestudy did not uphold the mandatory second look laparotomy.This case series and other reports10,11 show that thenumber of patients with primary AMVT continues to decreasewith increased facilities to recognize hypercoagulable state.An apparent increase of AMVT as we have experienced overthe past 7 years may be due to improved radiological imaginglike 64-sliced CT scan with high resolution angiographyfacilities and this is also experienced by other centers.6-8With high index of clinical suspicion in patients withabdominal pain and liberal use of CT scanning, enabled us toconfirm the diagnosis of AMVT. Reports suggest that earlyanticoagulant therapy improves outcome in both medical andsurgical treated patients.6-9 Both of the patients wereinvestigated for hypercoagulable state and were found to haveprotein C and S deficiencies. There are reports of 60-70%secondary AMVT and there is a suggestion to continuelifelong anticoagulation therapy and hence avoid recurrence ofthe disease.10,11Our case series shows that non-operative therapy is anoption when the diagnosis is confirmed on CT imaging andwhen the patient does not have peritonitis. Bowel ischaemiadue to AMVT is a reversible process with early anticoagulanttherapy.6-8 Prompt diagnosis has allowed us to manage thepatients non-operatively with optimal outcome, no mortalityand shorter hospital stay. With the protocol to continue oralanticoagulant (Tab.Warfarin) for lifelong in secondary AMVThas proven to be effective with no recurrence on follow up.ConclusionIn conclusion, acute mesenteric venous thrombosismust be kept in mind as a possible diagnosis with abdominalpain out of proportion to physical findings. Early CT imagingallows for immediate anticoagulation and seems to improveoutcome. Patients with AMVT should be screened forhypercoagulable state and patients with secondary AMVTshould be on life long anticoagulant treatment to preventrecurrence.References1. Rhee RY, Gloviczki P. Mesenteric venous thrombosis. Surg Clin North Am 1997;77: 327-37.2. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am1997; 77: 307-17.3. Kumar S, Sarr MG, Kamath PS. Mesenteric Venous Thrombosis. N Engl J Med2001; 345: 1683-8.4. Rhee RY, Gloviczki P, Mendonca CT, Petterson TM, Serry RD, Sarr MG, et al.Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg1994; 20: 688-97.5. Joh JH, Kim DI. Mesenteric and portal vein thrombosis: treated with earlyinitiation of anticoagulation. Eur J Vasc Endovasc Surg 2005; 29: 204-8.6. Zhang J, Duan ZQ, Sang Q, Luo YW, Xin SJ. Acute mesenteric venousthrombosis: A better outcome achieved through improved imaging and a changedpolicy of clinical management. Eur J Vasc Endoras Surg 2004; 28: 329-34. [ISSN1078-S884]7. Amarapurkar DN, Patel ND, Jatania J. Primary mesenteric venous thrombosis:astudy from western India. Indian J Gastro Enterol 2007; 26: 113-7.8. Salamah SMA, Mirza SM. Acute mesenteric venous thrombosis:Managementcontroversies. JK Practitioner 2004; 11: 242-7.9. Morasch MD, Ebaugh JL, Chiou AC, Matsumura JS, Pearce WH, Yao JS.Mesenteric venous thrombosis; a changing clinical entity. J Vas Surg 2001; 34:680-4.10. Hilaly MAA, Zidan FMA. Mesenteric vein thrombosis:Is it one diseases? Eur JVasc Endovasc Surg 1995; 9: 103-6.11. Agaoglu N, Turkyilmaz S, Ovali E, Ucar F, Agaoglu C et al. Prevelance ofprothobotic abnormalities in patients with acute mesenteric ischemia. World JSurg 2005; 29: 1135-8. [ISSN 0364-2313]399 J Pak Med Assoc

Acute mesenteric, portal and inferior vena cava, venous thrombosis, anticoagulation

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Acute mesenteric, portal and inferior vena cava, venous thrombosis, anticoagulation

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