What are the clinical consequences of superficial and deep venous obstructions?

Phlebotomy Essentials
6th Edition
ISBN:9781451194524
Author:Ruth McCall, Cathee M. Tankersley MT(ASCP)
Publisher:Ruth McCall, Cathee M. Tankersley MT(ASCP)
Chapter1: Phlebotomy: Past And Present And The Healthcare Setting
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What are the clinical consequences of superficial and deep venous obstructions?

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Step 1

Arteries and veins have three distinct layers; however, the primary tissue of arterioles is smooth muscle, whereas veins have primarily connective tissue.

The smooth muscle of arterioles is reflective of their capacity to withstand high pressures and to respond to changes in the body by relaxing or contracting.

The smooth muscle that is innervated by adrenergic fibres from the sympathetic nervous system can be found in all blood vessels except tiny venules and capillaries.

Step 2

Thrombi, emboli, vasospasm, external pressures, and structural changes cause arterial and venous blockages.

*Reflux (reverse flow) or restriction of venous blood flow cause chronic venous insufficiency pathophysiology. Prolonged valvular incompetence of superficial veins, deep veins, or the perforating veins that join them can result in chronic venous insufficiency. Venous hypertension of the lower extremities is the end result in every case.

*The most common causes of superficial incompetence include weaker or irregularly shaped valves, as well as a wider venous diameter, which inhibits normal valve congruence. In most situations, the leaking valve can be found near the point where the large saphenous vein meets the common femoral vein. Valve dysfunction can be inherited in certain cases, but it can also be caused by trauma, lengthy periods of standing, hormone imbalances, or thrombosis.

*The most common cause of deep vein dysfunction is a prior DVT, which causes inflammation, valve scarring and adhesion, and luminal narrowing. Valvular failure in a perforating vein permits more pressure to reach the superficial venous system. The resulting dilatation inhibits the valve cusps in the superficial veins from closing properly. The illness will affect the superficial veins in the majority of patients. The outflow blockage, capillary inflow, valve function, and muscle pump function all contribute to the resting venous pressure.

*Lower extremities discomfort, oedema, and venous microangiopathy may arise from persistently high venous hydrostatic pressure, regardless of the source. As red blood cells extravasate into the surrounding tissue, some patients develop permanent skin darkening as a result of hemosiderin deposition. Lipodermatosclerosis, or skin thickening caused by subcutaneous fat fibrosis, affects many of these patients. Ulcers can occur as the disease progresses due to disrupted microcirculation and skin weakness.

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