A condition affecting the system of veins in legs with venous hypertension resulting in different pathologies that involve swelling, ulcerations, pain, skin changes, and edema is called chronic venous insufficiency (Eberhardt and Raffetto, 2005).
It is necessary to understand normal venous function and anatomy to analyze the venous insufficiencies pathology. The peripheral venous system serves as a conduit returns blood into the heart and as a reservoir where blood is stored. Appropriate operation of the peripheral venous system is dependent on a series of muscle pumps and valves (Eberhardt and Raffetto, 2005). Blood entering the venous system of lower extremities has to go against fluctuating thoracoabdominal pressures and against gravity so as to get back to the central circulation in a standing person.
Another type of the venous system – superficial – represents a variable and complicated network similar to a web of interconnected veins, most of them unnamed (Fronek, 2007). Some superficial veins that have a big size occupy rather a constant position, e.g. deep veins, which function as a conductor used to deliver blood centrally into the deep venous system. In the lower extremities, the main superficial veins are called the great saphenous vein (GSV), running from ankles to the growing and the small saphenous vein (SSV), running from ankles to the knees.
The GSV starts in the middle of the foot and goes anterior to the middle of malleolus, after which it passes through the medial tibia in a posterior manner, ascending across the knees. It continues anteromedially above the knee, which is superficial in relation to the deep fascia, passing over the foramen ovale and joining the femoral vein located at the groin crease that is placed in the saphenofemoral junction (SFJ).
The SSV starts in the lateral part of feet (Fronek, 2007). From there it goes posteriorly lateral right into the Achilles tendons located in the lower part of calves. In case of the most people SSV is lying superficial in relation to the deep fascia right in the middle, reaching the upper part of the calves, where it is going into the popliteal space located in the middle of two heads of the gastrocnemius muscle. In 2/3 of all the cases, SSV is going into the popliteal vein located above the knee joint and in the rest of the cases it is joining other veins (in the majority of cases it is the deep muscular veins in the thigh or GSV).
Blood delivered in SSV and GSV by multiple superficial veins is delivered directly into the deep system via the saphenopopliteal junction (SPJ) and the SFJ. Still, the SFJ and SPJ are not unique ways into the deep system from the superficial one (Fronek, 2007). Superficial veins are directly connected to many perforating veins that are passing through the deep fascia openings to get joined with the deep veins of calves or thighs. Perforating veins involve venous valves preventing blood reflux into the superficial system from the deep veins.
The deep venous system eventually receives all the venous blood when it goes to the right atrium of the heart. In the majority of cases, the deep venous system involves 5 main elements: two above and three below the knees. Popliteal vein (PV) is the main deep venous trunk in legs that is going from the knees until it reaches anteriorly and upward via the abductor canal in the distal thigh, in which its name is the femoral vein (FV) that continues for the rest of the course in the thighs.
Three pairs of deep veins are located in the lower leg, namely: the posterior tibial vein (PSV), which drains the foot medial aspect; the anterior tibial vein (ATV), which drains the foot dorsum; and the peroneal vein, which is draining the foot lateral aspect (Fronek, 2007). ATV from the ankle passes anterolateral into the interosseous membrane, PSV goes up posteromedially under the medial tibia edge, and the peroneal vein goes up posteriorly via the calves. Sinusoids of veins in the calf muscles are joined so that they form gastrocnemius and soleal intramuscular venous plexi, joining the peroneal vein in mid-calves. In the majority of situations, each of them represents veins pair flanking an artery having the same name; in this way, there are 6 deep veins under knees of a patient in a typical situation. Right under the knee, two peroneal veins join with the four posterior and anterior tibial veins to form the single large PV.
The PV goes about in the back of the knee, then passing anteromedially right in the distal thigh via the abductor canal, from where on it is named the FV. The FV and the PV are essentially the same ones, forming the longest and largest deep vein of the legs (Fronek, 2007). The deep femoral vein (DFV) is a stubby, short vein, which generally originates in the terminal muscle tributaries in the deep lateral thigh muscles, but may be in communication with the PV in about 10% of patients. The DFV and the FV are joined together in the proximal thigh, forming the common femoral vein (CFV) that goes above the groin crease to turn into the iliac vein.
A bicuspid valves series are positioned along the superficial and deep veins ensuring that blood is moving in the cephalic direction, which allows for preventing the blood return to the feet when a person is standing. One of the valves of lower extremities is located in the common FV or less frequently in the external iliac vein. Venous valves frequency rises from proximal to distal leg to stop pressure increase in the distal veins that results from the gravity effects (Eberhardt and Raffetto, 2005). Perforating veins involve one-way valves preventing blood reflux into the superficial system from the deep veins.
The valves work together with venous muscle pumps that allows for returning blood to the heart against gravity. Muscle pumps contraction takes place primarily in calves, but also in thighs and feet, which delivers blood from the venous plexi up the deep venous system, due to raised pressure in the fascia compartments. Owing to the valve system, blood is not forced distally through the perforator system or within the deep venous system to the superficial system. Right after ambulation, pressure in the lower extremity veins is low by the norm (15 to 30 mm Hg) as the venous system is freed by the muscle pump work. Muscle pump relaxation in this case lets blood return via arterial inflow in the superficial and the distal deep venous systems to the deep venous system. Venous pathology can develop in case pressure in veins increases and blood return gets impaired because of several mechanisms. The possible reasons are: venous obstruction, perforator valve incompetence, valvular incompetence of the axial superficial or deep veins, or a combination of the components. The factors are sharpened by dysfunction of muscle pump in legs (Eberhardt and Raffetto, 2005). The mechanisms work to form hypertension of veins in particular with ambulation or standing. Venous hypertension left without attention can bring about subcutaneous tissue fibrosis, dermal changes with hyperpigmentation, and final ulceration.
Upon failure of the deep veins’ valves, normal volume of blood passes away from the leg, but refill takes place by both pathological retrograde venous flow and arterial inflow. The pressure in veins right after ambulation can be normal or a little bit elevated, but veins are rapidly refilled within development of high pressure in veins without contraction of muscles. Valves dysfunction in the deep venous system very often is a result of the previous deep vein thrombosis (DVT).
Incompetence or dysfunction of the superficial venous system valves allows for retrograde blood flow and increased pressures of hydrostatic character. Failure of valve can be primarily the consequence of some pre-existing weakness in the valve leaflets or vessel wall, or can be secondary to superficial phlebitis, direct injury, or excessive venous distention that results from high pressure or hormonal effects (Eberhardt and Raffetto, 2005). Valves failure that are positioned at the junctions of the superficial and deep systems, most notably at the saphenopopliteal and saphenofemoral junctions, let high pressure to get into the superficial veins. Thus, varicose veins and venous dilatation are created and propagated down the extremity from the proximal junction place.
Deep veins obstruction can limit the blood outflow, which can cause raised pressure in veins with secondary muscle pump dysfunction and muscle contraction. This state can develop due to intrinsic process in veins, such as DVT in the past with venous stenosis or insufficient recanalization.
Muscle pumps dysfunction can lead to the situation when venous blood is not efficiently emptied from the distal extremity. Dysfunction of muscle pumps seems to be the main mechanism in the formation of incompetence of superficial venous and venous ulcers and other its complications. In case of long standing, veins are gradually filled and get distended, which allows the valves to open and raise pressure, which is directly connected to the blood column height (Eberhardt and Raffetto, 2005). Muscle pump contraction will reduce venous pressure by freeing the veins again.
The CVI main clinical characteristics are the following: dilated edema, veins, cutaneous changes, and leg pain. Varicose veins represent superficial veins that are dilated and are getting larger and more and more tortuous. They tend to develop superficial thrombophlebitis bouts. Edema starts in the gaiter (or perimalleolar) area and get up the lower extremity with dependent accumulation of fluid. The leg discomfort or pain can be described as aching or heaviness after long standing; the state gets better when legs are elevated. Edema causes pain by increasing subcutaneous and intracompartmental pressure and volume. There is also observed from venous distention special tenderness in the area of varicose veins. Deep venous system obstruction can lead to claudication of veins, or severe leg cramping with ambulation (Eberhardt and Raffetto, 2005). Cutaneous changes involve hyperpigmentation of skin from eczematous dermatitis and hemosiderin deposition. Fibrosis can form in the subcutaneous tissue and dermis (lipodermatosclerosis). There is an elevated risk of leg ulceration, cellulitis, and delayed wound healing. Many of these clinical disease manifestations/complications were present in pt. 380.
As demonstrated in pt. 380 patients suffering from poor circulation and/or high blood pressure are at great risk of stasis dermatitis development, which is an illness causing excessive fluid to be accumulated under the skin, making it difficult to feed cells for blood and dispose of its waste products. The result of this state is often swelling of ankles, legs and feet, which is often manifested in older adults (Flugman, 2012). Accumulation of fluid due to a combination of venous insufficiency and high blood pressure, is a state in which flow of blood through veins is deferred. Molecules, similar to fibrinogen, which is a protein present in blood plasma, go into tissue, and these molecules create a barrier around skin blood vessels. It stops oxygen from going to tissue cells that can result in damage of cell. Stasis dermatitis may also result in leg ulcers, bone and skin infections, as well as permanent scarring (Berman, 2012).
Stasis dermatitis may raise the likelihood of skin infection, the same as with any state that results in chronic skin disruption, such as eczema. In result of open wounds a person can be left vulnerable to bacteria that can enter skin, as may intravenous use of drugs, as it permanently ruptures the skin. The cellulitis pathophysiology can be made worse by immune system that got weak due to states such as HIV or diabetes. Cellulitis is a widespread infection of the soft tissues underneath the skin and itself skin. It takes place when bacteria invade normal or broken skin and begin spreading into the soft tissues and under the skin (Cellulitis, 2011). This brings about inflammation and infection. Inflammation represents a process in which the body reacts to the bacteria. The cellulitis pathophysiology of is usually treated before it gets to life-threatening and severe stage. The most widespread treatment of cellulitis is antibiotics, which are usually taken within two weeks. In case oral antibiotics turn out to be not effective, a patients can be given intravenous antibiotics and hospitalized.
Osteomyelitis is a chronic or acute bone infection. Osteo means bone and myelo means the marrow cavity; both of them are parts of the disease. The infection may be a result of direct contamination or penetration of the open wound or fracture (exogenous origin); extension from a contiguous place; seeding via the bloodstream (hematogenous spread); or infections of skin in people with vascular insufficiency state. All organisms types, involving parasites, viruses, bacteria, and fungi, can cause osteomyelitis, but those infections that are developing in result of certain pyogenic bacteria in mycobacteria are the most widespread (Porth, 2009).
Hematogenous osteomyelitis starts with organisms that are infectious reaching the bone via the bloodstream. Acute hematogenous osteomyelitis happens mostly in kids. In the case of adults, it is observed most widely in patients who are debilitated and in those who have a history of chronic urinary tract infections, chronic infections of skin, intravenous drug users, as well as those people who are suppressed immunologically.
The most common osteomyelitis cause in the United States is extension or direct penetration of bacteria from an outside source (Porth, 2009). Bacteria can get directly into bones through open fracture, a penetrating wound, or surgery. Foreign material introduction into the wound, inadequate debridement or irrigation, and extensive injury of tissue raise the susceptibility of bones to infection.
Chronic osteomyelitis is mostly observed in adults. Most often this type of infections develop secondary to an open wound to the bone or tissue that surrounds it. Chronic osteomyelitis has been recognized as an illness for a long time. Still, the cases of illness development has reduced in the previous century due to surgical techniques, improvements and the introduction of broad-spectrum antibiotic therapy. The state of chronic osteomyelitis involves all bone inflammatory processes, with the exclusion of rheumatic illnesses, which develop due to microorganisms. It may be the result of inadequate or delayed treatment of acute to much of osteomyelitis or genius osteomyelitis that developed as a result of direct bone contamination by exogenous organisms. Osteomyelitis may continue for years, starting spontaneously, after minor trauma, or in events when resistance gets lower.
The main characteristic of chronic osteomyelitis is infected dead bone presence, called sequestrum, which is separated from the living bone. Involucrum, a new bone sheet, is formed around the bone that is dead. Radiologic techniques like bone scans, x-ray films, Sino grants are applied to distinguish the infected place (Porth, 2009). Infection around a total joint prosthesis or chronic osteomyelitis may be hard to diagnose due to the classic indicators of infection that are not obvious and the blood glucose site counts can be not increased. Such subclinical infection may be present for many years. For the definitive diagnosis bone scans are used along with bone biopsy.
The chronic bone infections treatment starts with one copters to define the microorganism along with its antibiotic therapy sensitivity. The aim in choosing osteomyelitis antimicrobial treatment is using the kind of drug that has the highest bactericidal activity while having the least toxicity, and at the lowest possible price. Intravenous therapy usually continues for about six weeks, and after initial antibiotic therapy surgery is done to get rid of sequestra or the foreign bodies’ and then long-term antibiotic therapy. It is usually required to immobilize the affected part with limitation of weight-bearing on legs. Sometimes external fixation devices are used.
In case of people suffering from vascular insufficiency, osteomyelitis can form as a result of skin lesion, which is demonstrated in pt. 380. Most often it is related to ischemic or chronic foot ulcers in people with long-standing diabetes (Porth, 2009). Deferred arterial circulation, neuropathic reasons in a loss of protection reflexes, and repetitive trauma are the main contributors to skin figure. People suffering from vascular insufficiency osteomyelitis usually present with problems that seem at first unrelated to the disease, such as cellulitis, ingrown toenails, or perforating footballs, which is making diagnosis harder. Moreover, pain is often released by peripheral neuropathic. Osteomyelitis can be defined in case of bone exposure in the author bed or after debridement radiological evidence.
Disease treatment depends on the oxygenation tension of the tissues involved in the disease. Antibiotic therapy and debridement can benefit people who love good oxygenation tension in the site that is infected. Hyperbaric oxygen therapy can be applied as adjunctive treatment. When oxygen tension is inadequate, amputation can be indicated.
Works Cited
Berman, K. (2012). Stasis dermatitis and ulcers. Retrieved from http://www.nlm.nih.gov/medlineplus/ency/article/000834.htm.
Cellulitis. (2011). Retrieved from http://www.webmd.com/skin-problems-and-treatments/tc/cellulitis-topic-overview
Eberhardt, Robert T. & Raffetto, Joseph D. (2005). Contemporary Reviews in Cardiovascular Medicine: Chronic Venous Insufficiency. Circulation, 111, 2398-2409.
Flugman, Scott L. (2012). Stasis Dermatitis Medication. Retrieved from http://emedicine.medscape.com/article/1084813.
Fronek, Helane S. (2007). The Fundamentals of Phlebology: Venous Disease for Clinicians. New Jersey: RSM Press.
Porth Pathophysiology: Concepts of Altered Health States. (2009). New York: Lippincott Williams & Wilkins.
