eMedicine Specialties > General Surgery > Abdomen
Inferior Vena Caval Thrombosis
Updated: Dec 29, 2008
Introduction
Thrombosis of the inferior vena cava (IVC) is an underrecognized entity with a variety of clinical presentations. The general concepts of deep venous thrombosis (DVT) and thrombophlebitis are discussed in detail in Deep Venous Thrombosis and Thrombophlebitis. However, the implications and complexity of inferior vena caval thrombosis (IVCT) merit specific attention.
From a global standpoint, IVCT represents a subset of DVT. Virchow recognized and described the factors predisposing a patient to venous thrombosis. The triad of stasis, vessel injury, and hypercoagulability formulated by Virchow remain the foundation for our understanding of the pathophysiology of DVT in general and for IVCT in particular (see Media file 1).
As appreciation of the impact of these factors on the patient has improved, therapy has become more directed.
Problem
Understanding the anatomy of the IVC and its tributaries is essential to understanding the variability in the clinical presentations of patients with IVCT. The IVC is formed by the confluence of the left and right common iliac veins. Numerous paired segmental lumbar veins drain into the IVC throughout its length. The right gonadal vein empties directly into the cava, while the left gonadal vein generally empties into the left renal vein. The azygous system has connections with the IVC or the renal veins at the level of the renal veins. The next major veins encountered are the renal veins, followed by the hepatic veins. No valves are within the IVC. The cava enters the thoracic cavity through the tendonous portion of the diaphragm and terminates at its junction with the right atrium.
Several congenital anomalies of venous anatomy can involve the IVC, and their presence can increase the likelihood of IVCT. The symptomatology related to IVCT follows directly from the anatomic location of the thrombus and the degree of the lumen occupied by the thrombus.
Frequency
The exact number of patients who have IVCT remains elusive because of the clinical variability in presentation. By compiling information from several epidemiologic studies that investigated DVT prevalence, the following estimates can be generated:
- The DVT rate in the United States is 60-180 cases per 100,000 population per year.
- The frequency of IVCT in patients with DVT is 4-15%.
- In the United States, 165,000-493,000 cases of DVT occur each year.
- In the United States, 6600-74,000 cases of IVCT occur each year.
These numbers are estimates generated from various population-based studies. Various groups within the general population have a greater propensity for IVCT, as discussed in Etiology.
Etiology
To a large degree, the etiology of IVCT mirrors that of DVT in general. However, specific situations relate to the IVC only, but the wide variety of these situations all relate in one or more ways to Virchow's classic description.
Tumors
Numerous malignancies have been associated with IVCT. Perhaps the most familiar is renal cell carcinoma. The intravascular tumor extends from the renal vein and can propagate as far as the heart. The tumor can partially or completely occlude the IVC. Not all intravascular irregularities of the kidney represent tumor thrombus. One case has been reported of a patient who underwent radical nephrectomy for presumed renal cell carcinoma and was subsequently found to have only renal vein thrombosis. Other genitourinary tumors that reportedly cause IVCT include seminomas and teratomas.
Numerous other less common tumors reportedly involve the IVC. Intuitively, any structure that is anatomically related to the IVC can generate either direct compression or vascular invasion. Retroperitoneal leiomyosarcoma, adrenal cortical carcinoma, and renal angiomyolipoma have all been reported as presenting in association with IVCT. Even hepatic hemangioma has caused IVCT from extrinsic compression. Additionally, malignancy itself is a risk factor for DVT and thus represents a risk factor for the extension of DVT into the IVC.
Compression
Extrinsic compression may also result from nontumoral sources and increase the likelihood of IVCT. The distortion of the normal caval anatomy generates both venous stasis and turbulent flow. This situation facilitates the formation of thrombus. An activity as innocuous as bicycle riding has reportedly caused IVCT. The spectrum of medical diagnoses that can cause compression of the IVC is determined by those structures anatomically adjacent to the IVC.
Aneurysms of the abdominal aorta can compress the vena cava and cause thrombosis. Although this clinical situation is somewhat uncommon, the implications for surgical repair of the aneurysm are significant. The surgeon must be prepared for enlarged venous collaterals and the possibility of unusual configurations of the tissue planes. One reported case described incorporation of the IVC into the aneurysm. In this particular case, the wall of the IVC was actually part of the wall of the aneurysm. Knowing that abdominal aortic aneurysm is a risk factor for IVCT should heighten clinical suspicion in appropriate cases.
Hepatic abscesses, either from amebae or echinococci, can also generate thrombosis of the IVC from compression. Because of the propensity of these processes to evolve over time, patients may present without symptoms suggestive of IVC occlusion. They may only demonstrate evidence of the primary process or of collateral venous hypertrophy. The initial presenting symptom may even be pulmonary embolization.
Other retroperitoneal organ systems that have been shown to cause IVCT include the pancreas and the kidneys. Polycystic disease of the right kidney has reportedly been clinically associated with thrombosis of the IVC. Pancreatic pseudocysts have been observed to cause thrombosis of the IVC. Acute pancreatitis has also been found to generate thrombosis of the IVC. The pathophysiology of the evolution of the thrombosis may reflect either the local impact of inflammation of the pancreatic head or the impact of a hypercoagulable state on the IVC. Although IVCT in the setting of pancreatitis is uncommon, this clinical entity may account for an unexplained deterioration in the status of a patient with acute pancreatitis.
Hematoma/trauma
Other aspects of compression can be attributed to the presence of a hematoma adjacent to the cava or the iliac systems. Psoas hematomas and other hematomas of the retroperitoneum have been identified as causing IVCT. In one case, the hematoma was the result of a common iliac artery injury. Because the venous system was not involved, the presumed mechanism of compression of the cava by clot seems credible.
Unique among causes, trauma combines the limbs of the Virchow triad. Stasis, vessel injury, and hypercoagulability may all exist in the same clinical situation. Direct trauma to the IVC may be the result of either penetrating or blunt trauma. In the absence of venous laceration, blunt endothelial damage has been postulated to cause IVCT. Other mechanisms observed secondary to trauma include extension of hepatic venous thrombosis and thrombus formation after perihepatic packing.
Dysfunctional coagulation system
By necessity and function, the balance between the coagulation system and the fibrinolytic system is delicate and dynamic. Disorders that disrupt this balance can cause a situation in which IVC thrombus formation may occur. The nephrotic syndrome is a classic example. Patients with this syndrome have urinary protein losses. Both renal vein thrombosis and IVCT have been described. The exact mechanism of the hypercoagulability of patients with the nephrotic syndrome has not been fully delineated. However, these patients have massive urinary protein loss, and diminished levels of antithrombin III have been observed.
Iatrogenic
Patients with a recent history of medical care may present with iatrogenic IVCT. The expansion of endovascular technology has led to increased recognition of iatrogenic IVCT. Interventions that reportedly have identifiable rates of IVCT include (1) hepatic transplantation, (2) dialysis access, (3) femoral venous catheters, (4) pacemaker wires, and (5) vena caval filters.
Awareness of the association of these procedures with IVCT allows clinicians to make educated decisions. Recognizing the association allows an accurate risk-benefit assessment for a given procedure. Additionally, recognizing these factors may aid in determining a prompt diagnosis in patients who have postprocedural clinical changes.
Other
Numerous other clinical situations have been associated with IVCT. They may meet some classification criteria to be listed in one or more of the categories listed above; however, they are listed here for clarity and can include (1) developmental anomalies of the IVC, (2) retroperitoneal fibrosis, (3) pregnancy, and (4) oral contraceptives.
Although not all-inclusive, the foregoing information provides a review of many of the known clinical situations in which IVCT may be evident. Knowledge of the potential for thrombosis of the IVC increases physicians' level of clinical awareness in patients who present with the identified primary processes.
Congenital absence of inferior vena cava
Iqbal and Nagaraju reported their experience with a case of congenitally absent inferior vena cava (IVC).1 This is an extremely rare anomaly that is associated with idiopathic deep vein thrombosis (DVT), particularly in the young.
Symptoms associated with severe venous hypertension (eg, bilateral lower extremity edema, varicose veins, nonhealing venous ulcers, caput medusae, other manifestations of collateral venous system hypertension/dilatation) may be varied in their manifestation and, in some cases, may not be apparent until later in life.
Retrospectively, as Iqbal and Nagaraju have discussed in this case, there can be clues indicating the presence of such an anomaly from a young age. The issue of whether early recognition of this condition would affect the prognosis and the treatment in many of these patients still remains in doubt.
Case presentation
A 54-year-old man was admitted with 3 weeks of abdominal pain and localized swelling over the right flank. Examination revealed palpable “snake-like” tortuous, tender lumps on the abdominal wall with overlying bruising. He was noted to have bilateral lower limb varicose veins.
See Media file 2.
He was a nonsmoker, and there was no significant family history of disease. He had no upper or lower gastrointestinal symptoms. There was no change in weight or appetite. There was no history of cardiorespiratory disease, and his exercise tolerance was not limited.
He was not able to volunteer any further information in regard to his past medical history other than that he was under annual review by nephrologists for mild chronic renal impairment due to an atrophic left kidney. This was diagnosed by ultrasound of the renal tract. There was no evidence of any other imaging modalities or radiologic investigations undertaken to investigate the cause of his atrophic kidney.
His past history revealed chronic nonhealing venous leg ulcers, as well as varicose veins necessitating varicose vein ligation at a very young age. The ulcers eventually needed skin grafting.
During this current admission he was investigated and diagnosed with DVT.
A CT scan, performed to search for intra-abdominal cancer, revealed the absence of the IVC with extensive thrombosed collaterals of the superficial abdominal and azygous veins and a congenitally atrophic left kidney.
See Media file 3.
On further review of his medical history, it was revealed that he had been diagnosed as a child with bilateral Perthes disease, in addition to nonhealing venous ulcers on the medial aspect of his right ankle.
At the age of 21 years, he underwent skin grafting of a nonhealing ulcer. One year later, he was readmitted with recurrence of ulcers in the same region and was then noted to have dilated varicose veins and thrombophlebitis that was treated with crepe bandaging for 2 years. Treponemal serology then was negative. In 1977, he had ligation of the varicose vein that was "feeding the ulcerated part of the leg." In 1979, he was discharged from follow-up with complete healing of the leg ulcers.
He was commenced on low molecular weight heparin and warfarin. Low molecular weight heparin was stopped when the international normalized ratio (INR) was greater than 2.
Discussion
Absent IVC is uncommon. Anomalies of the IVC have been described more frequently (0.6-2%) in those with other cardiovascular defects2 and less so in otherwise healthy individuals. Various abnormalities of the IVC have been described, including complete absence, partial absence, or presence of bilateral IVC.3
Controversy exists as to whether an absent IVC has a true embryonic etiology or whether it is the result of perinatal IVC thrombosis causing regression and disappearance of the once present IVC.4
There has been one previous report in the literature of an absent IVC and left renal hypoplasia and a right hypertrophic kidney.5 A more common association recognized is right renal aplasia, as suggested in a review by Gayer et al, where all 9 patients with complete absence of the IVC had an absent or very small right kidney.6
The association of an absent or hypoplastic kidney is related (or may contribute to an absent IVC) due to perinatal renal vein thrombosis.7 Veen and colleagues have proposed to name this condition KILT (Kidney and IVC abnormalities with Leg Thromboses) syndrome (when associated with DVT).5
It is estimated that DVT occurs 1 case per 1000 patient-years.8 In up to 80% of patients who are affected, a risk factor can be identified. Ruggeri et al presented 4 cases of absent IVC over a 5-year period presenting with idiopathic DVT in patients younger than 30 years.9 This was estimated to represent 5% of cases of idiopathic DVT in young people.
Chee et al similarly noted that up to 5% of 20- to 40-year-old patients presenting with DVT had an IVC anomaly (4 in total; of which 3 had a complete absence of IVC).10 This was much higher than the expected 0.5%.
The ideal imaging modality to help diagnose an IVC anomaly must have high diagnostic accuracy and also be safe and reproducible. It is difficult to establish a diagnosis of any IVC anomaly by ultrasound. Various clues are recognized on radiologic imaging that could help diagnose an absent IVC or anomaly. One of the more common and helpful clues is well developed and possibly dilated intrathoracic hemiazygous and/or azygous continuations. These collateral circulations as well as other retroperitoneal venous pathways are usually well developed before symptoms present.11
The most reliable, noninvasive methods to establish a diagnosis of IVC anomalies are CT with intravenous contrast or magnetic resonance scan. CT scan, unlike ultrasound, is a good imaging modality of the retroperitoneal space.12 Another accurate, but more invasive, imaging modality is venography, which is particularly useful if any surgery is planned.
It is hypothesized that blood return with an absent IVC is inadequate, despite adequate collaterals, resulting in chronic venous hypertension in the lower extremities and causing venous stasis that precipitates thrombosis.
Gayer et al recommended that all patients with an IVC anomaly be screened for a thrombophilic disorder.13 In their series, 7 of 9 patients with an IVC anomaly and DVT had a positive thrombophilic screen.6
There have been 3 case reports in the English language medical literature of thromboembolism due to an IVC anomaly (absence of the infrarenal portion of the IVC, infrarenal IVC hypoplasia). In all of these cases, the thrombophilic screen was negative.14,15,16 It was hypothesized that multiple emboli from DVT in the common and superficial femoral veins migrate through the well-developed hemiazygous and/or azygous system to the pulmonary circulation.
There is very little evidence available on the surgical correction or the treatment of this uncommon anomaly. A case report of a complete absence of the IVC but patent iliac veins and nonhealing pretibial ulceration described successful treatment with a prosthetic graft from the iliac vein to the intrathoracic azygous vein.7 Success was defined as complete healing of the ulcer up to 30 months after surgery.
Conclusion
In conclusion, this patient had an extensive past medical history of idiopathic varicose ulceration with evidence of chronic venous hypertension from a young age. He was managed with difficulty but achieved eventual healing of his ulcers as a young adult. In later life, he developed extensive DVT with worsening of his lower limb and abdominal varicosities.
The very limited data from the literature suggest that, in cases of an absent IVC in young people (some data, in patients younger than 30 years; other data, in patients aged 20–40 years), an abdominal CT scan should be performed.
In this case, with a relevant and extensive past history, a review of the limited literature would support further radiologic investigations to exclude an intra-abdominal deep venous anomaly.
The authors concluded that it is unlikely that surgical correction of the IVC was warranted in the management of this particular patient.1 They also concluded that, based on their review of the available literature, surgical options in this patient population are limited.1
Their review revealed no consensus regarding the duration of anticoagulation; however, it would be reasonable for this particular patient to remain on lifelong anticoagulation given the ongoing risk of further DVT and pulmonary embolism, even if the thrombophilic screen is negative.1
Knowledge of the association of other anomalies in patients with an absent IVC, such as renal atrophy or agenesis, can highlight underlying vascular anomalies, which are in and of themselves of significant clinical importance.
The clinician must have a profound awareness of the associated elements that make up the clinical complex of congenital vena caval thrombosis in order to avoid diagnostic and treatment pitfalls.
Presentation
Patients with IVCT may present with a spectrum of signs and symptoms. This variability is a significant part of the challenge of diagnosis. Using a classification system may help the clinician make the correct diagnosis. Patients may present with symptoms that are predominantly thrombotic in origin or predominantly embolic in nature. Additionally, the thrombotic findings are dependent on the degree of occlusion of the cava and on the location between the iliac confluence and the right atrium.
The classic presentation of IVCT includes bilateral lower extremity edema with dilated, visible superficial abdominal veins. Intuitively, this constellation makes sense, although it is not universally found. In one study, almost 60% of patients did not have bilateral leg edema. In addition, if the thrombus is confined to the cava and does not involve the iliac or femoral system, the collateral pathways form along the posterior abdominal wall. This scenario may have significant impact on surgical procedures involving this anatomic region.
Thrombosis occurring at the level of the renal veins raises the possibility of renal cell carcinoma. However, more commonly, thrombosis at this level suggests a nephrotic syndrome. Occlusive thrombus of the IVC at the juxtarenal level can affect renal function by altering renal perfusion.
Budd-Chiari syndrome merits specific attention. A discussion of the entire syndrome is beyond the scope of this article, but the essentials as they relate to IVCT are important. Patients typically have significant ascites, portal hypertension, hepatomegaly, collateral vein enlargement, and hepatic fibrosis. The pathophysiology of this syndrome centers on either IVC or hepatic venous thrombosis. If at the hepatic venous level, 2-3 of the major hepatic veins must be occluded before the syndrome can develop. Both hypercoagulable states and membranous venous webs have been postulated as the etiologic agents of Budd-Chiari syndrome.
Finally, patients who have IVCT may present only after having a pulmonary embolism. The lack of uniform symptoms and the significant number of asymptomatic patients contribute to this feature of IVCT. In one retrospective review of all patients who had cavography to document IVC thrombus, 20% had angiographically proven pulmonary embolism with no symptoms of DVT. Thus, pulmonary embolism may be the first sign of IVCT.
Relevant Anatomy
See Media file 4.
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Further Reading
Keywords
inferior vena caval thrombosis, IVC thrombosis, IVCT, deep venous thrombosis, DVT, thrombophlebitis, renal cell carcinoma, renal vein thrombosis, RVT, hepatic venous thrombosis, HVT, Virchow triad, Virchow's triad, Budd-Chiari syndrome
