Case e Report Dupllication of Inferior Vena V Cava a with Pulm monary Th hromboem mbolism – A Rare e case repo ort Hem mant Gupta a,1 Ayaz Ahmed,2 Maya Len nde,3 Balra am Yadav v,4 Tanvee er 5 6 Halg gale, Samk kit Mutha. 1 2 Hon. Associate Professor, 2,3 Assistant Professor, 4 Chief Reside ent, 5,6Senio or Resident Grant Medical Co ollege and Sir S J.J. Group of Hospita als, Mumbaii, India E-ma ail: drtanve [email protected] . Inter rnational Journal J of Clinical Ca ases and I Investigatio ons. Volum me 6 (Issu ue st 2), 24:30, 2 1 January J 2015. Absttract Klippel Feil syndrome (SKF)) is a rare co ongenital dissease. It is characterized mainly b by the in ncorrect union or fusion of two cervical verte brae or more. This ma alformation is respo onsible for limitation of o movemen nt of the he ead and a ssignificant rrisk of spina al cord injury. Othe er variables anomalies may be asssociated with h increased morbidity . We report the e case of a child who consulted for short stature with abnorma al and palmed Neck sexua al differenc ciation. The e existence of short k associate ed with congenital strabismu us oriented diagnosiis and ha as linked a abnormalitie es prese ent to Klippel Feil syndrome Keyw words: Dup plication of inferior ve ena cava, D Deep vein thrombosis s, pulmonarry throm mboembolism Intro oduction: Veno ous thrombo oembolism (VTE), is one o of the leading ca auses of ca ardiovascula ar mortality. VTE typically orriginates as s deep ven ous thromb bosis (DVT)) in a lowe er 1 1 extre emity. The incidence off DVT is estimated at 1 in 1,000 in ndividuals/ye ear. nferior vena a cava (IVC C) is a rare e finding in radiologic studies. Th he Dupliication of in w incide ence is abou ut 0.2-3%. Its symptom matic presen ntation is ev ven rarer. T There are few reporrted cases with IVC duplication and throm mbosis of lower extremities witth assoc ciated pulmonary throm mboembolism m.2,3,4,5,6,7 erential dia agnosis is lymphade nopathy, a aortic aneurysm, an nd Its main diffe retroperitoneal cysts. c The significance e of duplica ation of the e IVC is tha at it may b be 24 associated with the recurrence of pulmonary thromboembolism if the anatomical variation goes undiagnosed.2 Case Report: Our patient was a 35 year old male a chronic alcoholic since 8 years, admitted with pain in abdomen and distension of abdomen with swelling and pain in the left lower limb extending upto the left inguinal region. He also had pitting edema of left leg and significant size difference between circumferences of his two legs. He had no history of DVT, clotting disorders, peripheral vascular disease, non-healing ulcerations on the extremities, cerebrovascular accidents. All his other physical examination was within normal limits. Almost all routine blood investigations of this patient were within normal limits Colour duplex sonology of the left lower limb revealed deep vein thrombosis with complete lumen occluding thrombus of the common femoral, superficial femoral and deep femoral veins. In view of his pain in abdomen and distension of abdomen a CT abdomen (plain + contrast) was done. Findings were suggestive of Duplication of the inferior vena cava with complete lumen occluding thrombus in the left deep femoral vein superficial femoral vein common femoral vein, external iliac, internal iliac, common iliac and left inferior vena cava upto its confluence with the right suprarenal IVC. Also incidentally noted was pulmonary embolism involving right main pulmonary artery (saddle thrombus) and lobar pulmonary artery supplying the left lower lobe. A 2D ECHO of the patient was done which was normal and then the patient was started on heparin. The patient developed intra-abdominal hematoma after 3 days of size 11*14 *7cm.A triple vessel angiogram and renal angiogram was done which was normal. The patient’s heparin was stopped and he was given Fresh frozen plasma infusion. He was kept under observation for 12 days. The patient was monitored with repeated Ultrasonography of the abdomen which revealed decrease in the size of the hematoma. The patient was restarted on heparin with careful monitoring for any bleeding. After full anticoagulation with heparin for 5 days and starting warfarin international normalized ratio (INR) range was between 2 and 3, he was discharged from hospital. We plan to continue anticoagulation for 6 months Discussion: Anatomical variation of the inferior vena cava occurs in 0.4-4% of the population (MAYO, GRAY, LOUIS et al., 1983). The most common variant is duplication of the inferior vena cava (ARTICO, LORENZINI, MANCINI et al., 2004). Their identification is important in the clinical realm because it may reduce misdiagnoses. The formation of the IVC is a complex event. It is formed between the 6th weeks and 8th weeks of embryonic development via a series of anastomoses and regressions of the primitive trunk including: Posterior cardinal veins, subcardinal veins, and supracardinal veins.4 During the normal embryogenesis, the left subcardinal and left supracardinal veins regress. Failure of normal regression of any of the paired venous structures leads to abnormal persistence, duplication, or both.5 The literature strongly suggests that the non-regression of the left supracardinal vein during embryonic development leads to the occurrence of a second abdominal vessel, which is generally positioned to the left 25 of the aorta in adults. As shown by Natsis, Apostolidis, Noussios et al. (2010), however, the configuration of this supernumerary vessel and thus its embryonic origin is quite variable. These authors have proposed that duplications of the inferior vena cava be classified as complete or incomplete. Where complete, the most likely etiological cause is the persistence of the left supra-subcardinal anastomosis, of the post-subcardinal anastomosis, and probably of the intersubcardinal anastomosis, which in turn results in the persistence of the left supracardinal vein. Such a case may also be associated with an absence of iliac anastomosis (posterior distal intercardinal anastomosis). In cases of incomplete duplication, in which the supernumerary vena cava to the left is smaller and sometimes irregular, the likely cause is inadequate regression of the supracardinal vein. Phlebography is indicated as the gold standard for diagnosing duplication of the IVC.[5] but due to invasiveness, other authors have recommended that the combination of CT and ultrasound are satisfactory for an adequate diagnosis. In our case report of IVC duplication, there is a normal IVC along the right side of the spine.2 Few studies consider double IVC to be the cause of DVT, perhaps due to retrograde stasis.6,7 .Venous return difficulty causes stasis and thereby increases the probability of thrombosis.4 DVT might be associated with other routine pre-existing illnesses, such as lower limb fractures, cancer, the use of hormonal contraceptives, prior abdominal surgeries in elderly patients, genetic predisposition to thrombosis. Treatment choices include observation for asymptomatic duplication, anticoagulation therapy, placing an IVC filter below the renal veins in both the main right IVC and the duplicated left IVC segment. We started the patient on anticoagulation for 6 months Conclusion: This case demonstrates the importance of IVC duplication in the presence of DVT, the challenge of diagnosis, and the various therapeutic options available for a symptom-causing IVC duplication as some previous studies make a point of it.2,3,4,5,6 References 1. Morris TA. Natural history of venous thromboembolism. Crit Care Clin. 2011;27:869–84. [PubMed] 2. Milani C, Constantinou M, Berz D, Butera JN, Colvin GA. Left sided inferior vena cava duplication and venous thromboembolism: Case report and review of literature. J Hematol Oncol. 2008;1:24–28. [PMC free article][PubMed] 3. Ng WT, Ng SS. Double inferior vena cava: A report of three cases. Singapore Med J. 2009;50:e211–3.[PubMed] 4. Saad KR, Saad PF, Amorim CA, Armstrong D, Soares BL, Neves PC, et al. Duplication of the inferior vena cava: Case report and a literature review of anatomical variation. J Morphol Sci. 2012;29:60–4. 26 5. Anne N, Pallapothu R, Holmes R, Johnson MD. Inferior vena cava duplication and deep venous thrombosis: Case report and review of literature. Ann Vasc Surg. 2005;19:740–3. [PubMed] 6. Gayer G, Luboshitz J, Hertz M, Zissin R, Thaler M, Lubetsky A, et al. Congenital anomalies of the inferior vena cava revealed on CT in patients with deep vein thrombosis. AJR Am J Roentgenol. 2003;180:729–32. [PubMed] 7. Chee YL, Culligan DJ, Watson HG. Inferior vena cava malformation as a risk factor for deep venous thrombosis in the young. Br J Haematol. 2001;114:878–80. [PubMed] 27 Figures Figurre 1 28 Figurre 2 29 Figurre 3 30
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