Frequently Asked Questions(FAQ)

Those with functional lesions typically present with severe hypertension, with or without reduced excretory renal function, and few may present with flash pulmonary edema, cardiac failure, and Neurological features ranging from headache, visual disturbances to stroke. The severe increase in hydrostatic pressure drives fluid causing edema of the extremities and internal organs, including the brain. Acute hypertension can also damage the kidney, particularly in unilateral RAS, resulting in proteinuria and elevated creatinine concentration.

A substantial number of patients with chronic venous disease complain of disabling pain and swelling of the lower limbs without skin changes. It is possible that these symptoms are mainly attributable to obstruction and the iliac vein is the common outflow tract of the lower extremity, and chronic obstruction of this segment appears to result in more severe symptoms than does lower segmental blockage.

With the understanding that lower extremity deep venous thrombosis (DVT) can fragment and travel through the inferior vena cava (IVC) to the lung, the concept and functional goal of filters is to prevent Pulmonary Embolism by trapping venous thromboembolic in the vena cava, and not to prevent or treat venous clots.

Vena cava filter design categories includes Permanent filter, Temporary filter, Convertible filter, and Optional/retrievable filter. Duration of IVC Filter deployed in a patient with DVT depends on clinical presentation. For a patient with Recurrent DVT and high risk of bleeding with Anti coagulation Permanent filters is preferred with intention of providing life long protection. When protection from PE is no longer needed, in clinical conditions like Trauma, Major Surgery ,when the risk of bleeding has stopped then Temporary or Retrievable filters can be placed.

In aortic dissection, a tear occurs in the wall of the aorta. This causes bleeding into and along the aortic wall and, in some cases, completely outside the aorta (rupture).

The process of aortic dissection is dynamic and can occur anywhere along the course of the aorta, resulting in a wide spectrum of clinical manifestations. The presence of an “intimal flap,” representing the intimomedial septum between true and false Lumina, is the most characteristic pathology in acute aortic dissection. The origin of the intimal flap/tear is in the ascending aorta in 65%, the descending aorta in 25%, and in the arch and abdominal aorta in 10% of patients. The pathognomonic lesion is one of an intimal tear followed by blood surging either antegrade (typically) or retrograde (depending on the hemodynamic gradient between the true and false lumina) and cleaving the intima and media layers of the aortic wall longitudinally for a variable distance. Fenestrations (connections between the true and false lumina) occur within the intimal flap downstream, usually at branch vessel ostia, which are cleaved by the dissection process. These serve as sites of reentry of blood flow into the true lumen, thus maintaining false lumen patency.

Abdominal Aortic Aneurysm are defined as focal dilatations at least 50% larger than the expected normal arterial diameter. Abdominal Aorta can be termed as Aneurysmal when the diameter is 3.0cm’s but traditionally treatment has been recommended when the maximal cross-sectional diameter reaches 5.0 to 5.5 cm as the risk of Rupture and mortality increases beyond 5.0 cm diameter. The Infrarenal location is by far the most common for aortic aneurysms. Approximately 1.7% of women and 5% of men older than 65 years have an Infrarenal Aortic diameter greater than 3 cm.

Degenerative or Atherosclerosis is most common cause of AAA. Other causes can be Inflammatory, Connective Tissue disorders, Congenital Ana molies, Traumatic, Infectious, Arterial Dissections. Age, female sex, Smoking, Diabetes, Hypertension, Hypercholesterolemia, Family history of Aortic Anuerysm and Obesity are High risk Factors causing AAA

Most Abdominal Aortic Aneurysm (AAAs) are asymptomatic and discovered during abdominal imaging for an unrelated condition. AAAs can cause chronic back pain or abdominal pain that is vague and Occasionally, patients may feel a “pulse” in their abdomen or palpate a pulsatile mass. Rarely, large AAA’s cause symptoms from local compression, such as early satiety, nausea, or vomiting, urinary symptoms from ureteral compression; or venous thrombosis. Posterior erosion of AAAs into adjacent vertebrae can lead to back pain.

The first key point is to know that AAA have the potential to Rupture and only half of patients with AAA rupture survive to reach the hospital, many of whom do not have a known diagnosis of AAA before aneurysm rupture.

High risk of rupture if the diameter is more than 5 to 6 CMS with history of COPD, SMOKING, FEMALE GENDER,STATIN USE,DIAMETER EXPANSION OF MORE THAN 0.5 CMS/YEAR,UNCONTROLLED HYRERTENSION AND POSITIVE FAMILY HISTORY OF AAA. The mortality rate of surgery in Rupture AAA is approximately 50%, with 15% dying Intra operatively.