Inferior Vena Caval Thrombosis
ICDCM Index Terms Starting With 'F' Thrombophlebitis an IBC 10
Inferior vena caval IVC thrombosis is an essential diagnosis while evaluating any neoplastic lesion, or portal hypertension. It is also important to differentiate bland thrombus from tumour thrombus. Bland thrombus can be an isolated thrombus. However, it is commonly arising from deep vein thrombosis of lower extremities.
While any neoplastic lesion can cause IVC thrombosis, renal cell carcinoma is the most common malignancy to extend into IVC 1. Other tumours that have a tendency for IVC thrombosis are hepatocellular carcinoma Thrombophlebitis an IBC 10, adrenocortical cancer and Krampfadern sind häufiger krank tumourprimary leiomyoma or leiomyosarcoma of the IVC.
Also, subclassification into infrahepatic, hepatic and suprahepatic extension can further help the surgeon. On all imaging, they appear as persistent filling-defect within IVC. Chronic thrombosis can lead to peri-caval and peri-aortic collateral formation 1. You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Unable to process the form. Check for errors and try again. Thank you for updating your details. Log in Sign up. Articles Cases Courses Quiz.
Inferior vena caval thrombosis Dr Praveen Jha et al. Cases and figures Imaging differential diagnosis, Thrombophlebitis an IBC 10. Sheth S, Fishman EK. Imaging of the inferior vena cava with MDCT.
Krampfadern Werbung article Share article View revision history. Synonyms or Alternate Spellings: Case 2 Case 2, Thrombophlebitis an IBC 10. Case 4 Case 4. Case 5 Case 5. Case 7 Case 7. Paracaval lipoma Paracaval lipoma. Loading Stack - 0 images remaining.
Thrombophlebitis an IBC 10 IBC Medical Policies
Aug 01, Author: The general concepts of deep venous thrombosis DVT and thrombophlebitis are discussed in detail in Deep Venous Thrombosis. 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 the image below.
As appreciation of the impact of these factors on the patient has improved, therapy has become more directed. The clinical presentation of IVCT varies, depending on extent and location of the thrombus, Thrombophlebitis an IBC 10.
Because of the variability in signs and symptoms, using a classification system to describe the clinical features may aid in the diagnosis of this condition. Thrombophilic screening and evaluation of the clotting and fibrinolytic systems may aid in the diagnosis of IVCT.
Contrast venography remains the criterion standard as the optimal diagnostic study for this condition. Medical management of vena caval thrombosis focuses on anticoagulation and thrombolytic therapy. Surgical management of this condition consists of caval interruption, thrombectomy, or Thrombophlebitis an IBC 10 interventions.
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, whereas 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 tendinous portion of the diaphragm and terminates at its junction with the right atrium. The symptomatology related to IVCT follows directly from the anatomic location of the thrombus and the degree of the lumen occupied by the thrombus.
However, Thrombophlebitis an IBC 10, 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. Numerous malignancies have been associated with IVCT. The intravascular tumor extends from the renal vein and can propagate as far as the heart.
It can partially or completely occlude the IVC. Not all intravascular Thrombophlebitis an IBC 10 of the kidney represent tumor thrombus. In one case report, a patient who underwent radical nephrectomy for presumed RCC was subsequently found to have only renal vein thrombosis. Numerous other less common tumors reportedly involve the IVC. Intuitively, it is reasonable that any structure anatomically related to the IVC can generate either direct compression or vascular invasion.
Retroperitoneal leiomyosarcoma, [ 5 ] adrenal cortical carcinoma, [ 6 ] and renal angiomyolipoma [ 7 ] have all presented in association with IVCT. Even hepatic hemangioma has caused IVCT from extrinsic 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 a thrombus, Thrombophlebitis an IBC 10.
An activity as innocuous as bicycle riding has reportedly caused IVCT. Although this clinical situation is 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 tissue-plane configurations.
One reported case described incorporation of the IVC into the aneurysm [ 10 ] ; the wall of the IVC was actually part of the wall of the aneurysm. Hepatic abscesses, Thrombophlebitis an IBC 10, either from amebae or echinococci, Thrombophlebitis an IBC 10, 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 Thrombophlebitis an IBC 10 reportedly been clinically associated with 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.
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 Thrombophlebitis an IBC 10. Direct trauma to the IVC may be the result of either penetrating or blunt trauma. Other mechanisms observed secondary to trauma include extension of hepatic venous thrombosis and thrombus formation after perihepatic packing.
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, Thrombophlebitis an IBC 10. Patients with a recent history of medical care may present Thrombophlebitis an IBC 10 iatrogenic IVCT.
The expansion of endovascular technology has led to increased recognition of iatrogenic IVCT. Awareness of the association of these procedures with Thrombophlebitis an IBC 10 allows clinicians to make educated decisions. Thrombophlebitis an IBC 10 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.
Anomalies of the IVC have been described more frequently 0. Various abnormalities of the IVC have been described, including complete absence, Thrombophlebitis an IBC 10, partial absence, or presence of bilateral IVC. 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. A case report has described an absent IVC and left renal hypoplasia and a right hypertrophic kidney.
The association of an absent or hypoplastic kidney is related or may contribute to an absent IVC to perinatal renal vein thrombosis, Thrombophlebitis an IBC 10. 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 mentioned above; however, they are noted 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. 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 US estimates can be generated:. These numbers are estimates generated from various population-based studies.
The outcome of patients with IVCT is often determined by the underlying condition that initially caused the thrombosis, Thrombophlebitis an IBC 10. However, some general statements can be made.
The impact and outcome of IVCT are as variable as the clinical presentation. In one study, only one third of patients had a correct diagnosis before venography.
Adult patients with ligation of their vena cava reportedly have either no symptoms or mild edema after ligation. Symptoms of chronic limb pain and chronic abdominal pain were observed. Another series of pediatric patients with IVCT secondary to central venous access identified no sequelae unless concurrent superior vena cava thrombosis was present. If the cava is occluded, pulmonary embolization does not present a significant risk.
However, if a caval lumen remains, embolization may occur. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism.
The epidemiology of venous thromboembolism. Thrombosis of the inferior vena cava and malignant disease. Renal vein thrombosis misdiagnosed as a renal cell carcinoma with a tumor thrombus in the inferior vena cava. From Hamburg kaufen Varikosette archives of the AFIP. Leiomyosarcoma of the retroperitoneum and inferior vena cava: Adrenal cortical carcinoma associated with venous tumour thrombus extension, Thrombophlebitis an IBC 10.
Renal angiomyolipoma associated with inferior vena caval tumour thrombus. Pulmonary Thrombophlebitis an IBC 10 due to compression of the inferior vena cava by a hepatic hemangioma. Tex Heart Inst J. Inferior vena cava thrombosis following a cycle ride.
J R Soc Med. Flynn P, Zammit-Maempel I. Compression of the inferior vena cava by right renal cysts:
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Inferior vena caval (IVC) thrombosis is an essential diagnosis while evaluating any neoplastic lesion, or portal hypertension. It is also important to differentiate.
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