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eMedicine Specialties > General Surgery > Abdomen

Inferior Vena Caval Thrombosis

Author: Luis G Fernandez, MD, KHS, FACS, FASAS, FCCP, FCCM, FICS, Assistant
Clinical Professor of Surgery and Family Practice, University of Texas Health Science Center;
Adjunct Clinical Professor of Medicine and Nursing, University of Texas, Arlington; Chairman,
Division of Trauma Surgery and Surgical Critical Care, Chief of Trauma Surgical Critical Care
Unit, Trinity Mother Francis Health System; Brigadier General, Texas Medical Rangers,
TXSG/MB
Coauthor(s): Douglas M Geehan, MD, Associate Professor, Department of Surgery, University
of Missouri at Kansas City
Contributor Information and Disclosures

Updated: Dec 29, 2008

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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 image below).

Virchow's triad/venous thromboembolism (VTE) risk factors.

[ CLOSE WINDOW ]
Virchow's triad/venous thromboembolism (VTE) risk factors.

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 image below.

Photo showing dilated superficial abdominal veins (upper quadrant), with bruising and
thrombosed large abdominal veins (lower quadrant).

[ CLOSE WINDOW ]
Photo showing dilated superficial abdominal veins (upper quadrant), with bruising and
thrombosed large abdominal veins (lower quadrant).

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 images below.

Photo showing dilated superficial abdominal veins (upper quadrant), with bruising and
thrombosed large abdominal veins (lower quadrant).

[ CLOSE WINDOW ]

Photo showing dilated superficial abdominal veins (upper quadrant), with bruising and
thrombosed large abdominal veins (lower quadrant).
Abdominal CT scan shows absent inferior vena cava with thrombosis of the very
prominent collateral veins in the abdominal wall, corresponding to the right side of the
abdomen as seen in the image above.

[ CLOSE WINDOW ]

Abdominal CT scan shows absent inferior vena cava with thrombosis of the very
prominent collateral veins in the abdominal wall, corresponding to the right side of the
abdomen as seen in the image above.

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 image below.
Veins of the abdomen and the thorax; superior vena cava, inferior vena cava,
brachiocephalic veins, and azygous veins. This lithograph plate is from Gray's Anatomy.
Unless stated otherwise, it is from the online edition of the 20th US edition of Gray's
Anatomy of the Human Body, originally published in 1918.

[ CLOSE WINDOW ]
Veins of the abdomen and the thorax; superior vena cava, inferior vena cava,
brachiocephalic veins, and azygous veins. This lithograph plate is from Gray's Anatomy.
Unless stated otherwise, it is from the online edition of the 20th US edition of Gray's
Anatomy of the Human Body, originally published in 1918.

More on Inferior Vena Caval Thrombosis

Overview: Inferior Vena Caval Thrombosis
Workup: Inferior Vena Caval Thrombosis
Treatment: Inferior Vena Caval Thrombosis
Follow-up: Inferior Vena Caval Thrombosis
Multimedia: Inferior Vena Caval Thrombosis
References
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[ CLOSE WINDOW ]

Further Reading
[ CLOSE WINDOW ]

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

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Luis G Fernandez, MD, KHS, FACS, FASAS, FCCP, FCCM, FICS, Assistant Clinical
Professor of Surgery and Family Practice, University of Texas Health Science Center; Adjunct
Clinical Professor of Medicine and Nursing, University of Texas, Arlington; Chairman, Division
of Trauma Surgery and Surgical Critical Care, Chief of Trauma Surgical Critical Care Unit,
Trinity Mother Francis Health System; Brigadier General, Texas Medical Rangers, TXSG/MB
Luis G Fernandez, MD, KHS, FACS, FASAS, FCCP, FCCM, FICS is a member of the
following medical societies: American Association for the Surgery of Trauma, American College
of Chest Physicians, American College of Legal Medicine, American College of Surgeons,
American Society of Abdominal Surgeons, American Society of General Surgeons, American
Society of General Surgeons, American Society of Law, Medicine & Ethics, American Trauma
Society, Association for Surgical Education, Association of Military Surgeons of the US,
Chicago Medical Society, Illinois State Medical Society, International College of Surgeons, New
York Academy of Sciences, Pan American Trauma Society, Society of Critical Care Medicine,
Society of Laparoendoscopic Surgeons, Southeastern Surgical Congress, Texas Medical
Association, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Douglas M Geehan, MD, Associate Professor, Department of Surgery, University of Missouri

at Kansas City
Douglas M Geehan, MD is a member of the following medical societies: American College of
Surgeons, American Institute of Ultrasound in Medicine, American Medical Association,
Association for Academic Surgery, Phi Beta Kappa, Society of American Gastrointestinal and
Endoscopic Surgeons, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Managing Editor

Michael A Grosso, MD, Consulting Staff, Department of Cardiothoracic Surgery, St Francis

Hospital
Michael A Grosso, MD is a member of the following medical societies: American College of
Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular
Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum
and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of
Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale
University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-
New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American
Gastroenterological Association, American Physiological Society, American Society of
Nephrology, Association for Academic Surgery, International Society of Nephrology, New York
Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

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