Antibiotics (Properties, Application, Interaction) - M.P. Cherenko 1999

Acute Purulent Infection
Purulent Diseases of the Lymphatic and Blood Vessels

Lymphangitis is the inflammation of the Lymphatic vessels and typically occurs as a secondary process. If a primary focus of inflammation (such as a furuncle, carbuncle, Phlegmon, abscess, erysipelas, or hidradenitis) remains uncontained, the infection can spread into the lymphatic vessels and cause inflammation of their walls. In addition to acute infectious processes, lymphangitis can be triggered by various injuries, including cut, puncture, and animal bite wounds, abrasions, scratches, and Burns.

Lymphangitis is most commonly caused by staphylococci.

Depending on the clinical course, lymphangitis is classified as acute, subacute, or chronic. Based on the severity of inflammation, it is divided into simple (serous) and purulent lymphangitis; According to the type of vessel involvement, it is classified as capillary, reticular (lymphangitis reticularis), or truncal (lymphangitis truncularis).

When lymphangitis is localized in the subcutaneous tissue, it is readily diagnosed. Patients experience a burning sensation, itching, and mild tenderness in the Skin over the affected lymphatic vessels. Red streaks become visible on the skin, extending from the site of infection toward the regional Lymph Nodes (typically from the periphery to the center). Palpation along their path reveals firm, tender subcutaneous cords. Local and, occasionally, systemic body Temperature rises. As with any other infection, the patient's general condition deteriorates (manifesting as tachycardia, chills, headache, increased sweating, and changes in Blood counts).

In reticular lymphangitis, skin hyperemia is observed without clear boundaries, which distinguishes this condition from erysipelas.

Acute lymphangitis can sometimes be complicated by thrombolymphangitis. In such cases, the lumen of the lymphatic vessel—which may dilate up to 0.5–0.7 cm in diameter—becomes occluded by a thrombus composed of fibrin, leukocytes, endothelium, and Bacteria.

Severe forms of lymphangitis can be complicated by an abscess, phlegmon, or thrombophlebitis.

Treatment of lymphangitis should begin with the eradication of the primary focus. First and foremost, the affected area must be immobilized. If a lower limb is affected, it should be immobilized in an elevated position. Local heat (compresses or heating pads) and ointment dressings are applied to the affected area; Antibiotics and sulfonamides are prescribed. Massage and rubbing are strictly contraindicated. Physiotherapy Procedures (such as quartz therapy and UHF therapy) are recommended.

Lymphadenitis is an acute or chronic inflammation of the lymph nodes. Acute lymphadenitis is caused by the invasion of nonspecific, common microflora (such as streptococci and staphylococci) into the lymph nodes via the lymphatic pathways. Chronic lymphadenitis can develop due to both nonspecific and specific microflora (most commonly tuberculosis).

The entry of microbes into the lymphatic pathways does not necessarily lead to an inflammatory process. Lymph possesses bactericidal properties, causing invading microbes to lose their virulence or even perish. An additional portion of microbes is destroyed within the lymph node through phagocytosis.

Acute lymphadenitis, much like lymphangitis, is a complication of an underlying inflammatory process. The focus may be localized in various lymph groups, most frequently affecting the axillary, inguinal, and cervical lymph nodes. Based on the character of the exudate, serous, hemorrhagic, fibrinous, and purulent lymphadenitis are distinguished. In purulent lymphadenitis, the lymph node undergoes purulent melting, transforming into an abscess.

The inflammatory process can spread from the lymph nodes to surrounding Tissues, resulting in adenophlegmon.

Clinically, superficial lymphadenitis presents beneath the skin as one or more enlarged, matted, and highly tender lymph nodes. The overlying skin is hyperemic. Upon palpation, the lymph nodes are painful and adherent to the skin. Organ function in the area affected by the inflammatory process is impaired. Local temperature is elevated. If suppuration of the lymph node occurs, fluctuation can be observed. Initially, lymph nodes are mobile upon palpation, becoming fixed only after the process spreads to adjacent tissues.

Systemic manifestations include fever, headache, malaise, tachycardia, and blood count alterations.

Streptococcal lymphadenitis has a more severe clinical course than staphylococcal lymphadenitis. This is because Staphylococcal infections rapidly block the lymphatic vessels and result in less

absorption of tissue breakdown products and toxins.

Chronic nonspecific lymphadenitis is caused by low-virulence infections. The process typically localizes in the skin, with the source of infection originating from inflammatory conditions in the Oral Cavity (such as carious Teeth or tonsillitis). The lymph nodes enlarge slowly and are soft and mildly tender. The patient's general condition remains unaffected, and suppuration of the lymph nodes is rare.

Chronic specific lymphadenitis is typically caused by pathogens of actinomycosis, Syphilis, tuberculosis, tularemia, or plague. Cervical tuberculous lymphadenitis is the most common presentation and manifests as a manifestation of a systemic disease. The affected lymph nodes are fused into a conglomerate and are slightly tender. Caseous necrosis eventually develops. The skin over the lymph nodes thinned out, and the contents may rupture externally, forming chronic fistulae.

Treatment of acute lymphadenitis, much like lymphangitis, must begin with the elimination of the primary focus. Conservative therapy is administered in the early stages according to the General Principles of purulent surgery (heat and physical therapy Applications, infiltration of the inflammatory focus with a penicillin-novocain solution, and immobilization). In cases of abscess formation, surgical intervention is indicated alongside systemic therapy.

Treatment of chronic nonspecific lymphadenitis should be aimed at resolving the underlying condition. In some cases, Connective Tissue may develop within the lymph nodes (indurative chronic lymphadenitis). The lymph nodes then become firm, mildly tender, and unresponsive to conservative treatment, necessitating surgical removal.

Treatment of chronic tuberculous lymphadenitis involves the administration of specific antituberculosis therapy and quartz lamp irradiation of the lymph nodes.

Arteritis (arteriitis) is the inflammation of Arteries. It may occur As a result of the spread of inflammation from adjacent tissues or due to inflammation of the tunica intima caused by microbes circulating in the bloodstream. In the first scenario, the disease begins in the adventitia (perivascularitis) and extends toward the media of the vessel wall; In the second, it originates in the tunica intima (endovasculitis) and progresses toward the adventitia. Arteritis can also develop when microbes infiltrate the vessel wall via other pathways. Regardless of the route of infection, thrombus formation (thromboangiitis) subsequently occurs within the artery. The inflammatory process may be localized or extend along the length of the artery.

Arteritis can be serous or purulent. The Clinical presentation of arteritis includes sharp pain at the site of inflammation; a diminished peripheral pulse distal to the affected artery; trophic disorders in the distal extremities; fever; and changes in blood composition.

A formidable complication of purulent arteritis is ulceration or Necrosis of the vessel wall, which can lead to severe secondary hemorrhages. Arterial thrombosis, particularly in the extremities, can lead to gangrene. Softened, infected thrombi may detach, enter the bloodstream, and seed infections in other tissues and Organs.

Treatment for arteritis should primarily focus on eradicating the primary source of infection. If located in the extremities, immobilization is required. Systemic antibacterial therapy is indicated. Some authors recommend administering penicillin-group drugs with novocain directly into the arterial lumen proximal to the lesion site (10 ml of a 1% solution or 50–60 ml of a 0.25% novocain solution combined with 200,000–300,000 IU of penicillin).

Phlebitis and thrombophlebitis. Phlebitis refers to the inflammation of a vein wall, whereas thrombophlebitis is the inflammation of a vein wall accompanied by the simultaneous formation of a blood clot (thrombus) within it. The presence of a thrombus in the lumen of a vein without inflammation of its wall is termed phlebothrombosis.

Since the wall of a vein is thinner than that of an artery, inflammatory processes occur in it more frequently.

Inflammation of a vein can originate either in its outer layer (periphlebitis) or inner layer (endophlebitis). In both cases, the entire vessel wall is rapidly involved in the process. Initially, the venous wall becomes infiltrated with serous and, over time, purulent exudate. A blood clot forms within the lumen of the vein. The Development of phlebitis is promoted by a decrease in the body's reactivity, trauma to the venous wall (frequently during puncture), slowing of blood flow within the vein, and increased Blood Coagulation properties.

This condition most commonly affects the Vessels of the lower extremities.

Based on their localization, phlebitis is classified into superficial and deep forms (depending on which Veins are affected). Superficial veins—the great and small saphenous veins (v. saphena magna and parva)—are located in the subcutaneous tissue, whereas deep veins—the anterior and posterior tibial, popliteal, and femoral veins (v. tibiales anteriores and posteriores, v. poplitea, v. femoralis)—lie beneath the fascia, within Muscles, and so forth. Both systems communicate with each other through anastomoses.

Acute phlebitis can be simple (serous) or purulent. In the case of the first form, the vein wall sustains minor damage, thrombi do not form, and its lumen remains patent. Such a process typically resolves with full recovery. Purulent phlebitis is characterized by The formation of suppurating thrombi within the lumen of the vein.

In superficial phlebitis, red streaks appear on the skin along the PROJECTION OF THE affected veins. Palpation reveals longitudinal, dense cords. The patient may experience elevated body temperature, tachycardia, headache, chills, general weakness, and altered blood composition.

The treatment of superficial phlebitis is similar to that of lymphangitis: immobilization, bed rest, elevation of the limb, compresses with dimexide solution, heparin ointment, venoruton gel, and antibacterial drugs.

Damage to the intima leads to the formation of a thrombus in the vein lumen, which, combined with the inflammation of the vessel wall, contributes to the development of thrombophlebitis. Its danger lies in the fact that thrombi obstruct the vein lumen, thereby disrupting Blood Circulation. Furthermore, infected thrombi can be disseminated throughout the body via the Circulatory system, resulting in new foci of inflammation in distant organs and tissues. When entering the bloodstream, thrombi may also migrate to the pulmonary artery, causing Pulmonary Embolism and death.

Thromboembolism can be superficial or deep. It most frequently affects the superficial VEINS OF THE lower extremities, pelvic veins, and rectal veins, and less commonly the veins of the upper extremities. This is facilitated by varicose veins, which are more prevalent in women and caused by venous stasis (Pregnancy, prolonged standing, traumatic injury to the vein, etc.). Slowed BLOOD FLOW IN the veins and alterations in blood composition also play a significant role in the onset of thrombophlebitis.

A distinct form is migratory thrombophlebitis, which affects superficial veins and can shift to various anatomical sites. It is frequently accompanied by concurrent arterial involvement (Buerger's disease).

Both phlebitis and thrombophlebitis can occur in simple and purulent forms.

According to their clinical course, thrombophlebitis is subdivided into acute, subacute, and chronic forms. Downward and upward forms (spreading either from top to bottom or bottom to top) are also distinguished.

In ascending thrombophlebitis, as the process spreads upward and involves progressively new segments of the vein, There is a risk of it extending to the common iliac vein. Such patients require immediate surgical intervention—ligation of the great saphenous vein at its junction with the femoral vein (the Troyanov–Trendelenburg operation).

Thrombophlebitis of the superficial veins of the lower extremities manifests as serpiginously bulging veins beneath the skin in the area of the great or small saphenous vein. The overlying skin is hyperemic with a cyanotic hue. A characteristic doughy consistency (pasty edema) of the limb is present. Palpation along the course of the veins reveals dense, highly tender cords. To the Touch, the affected limb feels cooler than the healthy one. In simple thrombophlebitis, the patient's general condition is hardly disturbed, whereas in purulent thrombophlebitis, body temperature rises to 38–39 °C, chills occur, and Sepsis sometimes develops. If the thrombus suppurates, the lesion loses its density, and a fluctuation sign may appear.

Purulent inflammation of veins is observed more frequently than purulent inflammation of arteries, which is explained by the greater structural strength of arterial walls.

In deep vein thrombophlebitis, the limb is edematous, the skin is tense, pale with a cyanotic tint, and local temperature is elevated. Induration and tenderness of the muscles (particularly the calf muscles) are observed.

Thrombophlebitis of the lower extremities associated with purulent inflammation of the pelvic cellular tissue surrounding the Uterus and thrombophlebitis of the visceral pelvic veins, sometimes observed postpartum, follow a peculiar clinical course. This condition is known as white or blue phlegmasia (phlegmasia alba dolens and phlegmasia caerulea dolens).

White phlegmasia is characterized by persistent limb Swelling, pain, pallor of the skin, and a decrease in its temperature.

Blue phlegmasia is characterized by pronounced edema of the entire limb extending to the Perineum and buttocks, skin cyanosis, the sudden onset of severe pain in the limb, and absent arterial pulses; venous Gangrene of the limb occasionally develops.

The treatment of acute superficial thrombophlebitis of the lower extremities primarily involves resting the affected limb. Bed rest (with the limb elevated) is prescribed until acute symptoms subside (to prevent the spread of infection and potential thromboembolism). For subacute and chronic thrombophlebitis, thermal procedures (dry heat, warming compresses), dressings with heparin ointment, and troxevasin gel are indicated. Physiotherapy procedures (infrared radiation) are effective. Good outcomes are achieved with paranephric novocaine blockades.

In acute deep vein thrombophlebitis of the leg or leg and pelvis, alongside conservative measures (bed rest with an elevated and immobilized limb, anticoagulant and antibiotic therapy, etc.), surgical intervention is frequently employed—the placement of filters in the INFERIOR VENA CAVA to prevent pulmonary embolism.

Leeches are utilized in the treatment of thrombophlebitis, particularly of deep veins. They are applied to the skin of the affected area where they attach, and the hirudin released into the bloodstream helps dissolve the thrombus.

Modern Methods for the Prevention and treatment of thrombophlebitis include Direct and Indirect anticoagulants, thrombolytic agents, and drugs that improve microcirculation and reduce the aggregation of blood formed elements.

Direct anticoagulants include heparin (5000 IU 4 times a day) and low-molecular-weight heparins, whereas indirect anticoagulants include pelentan (0.1–0.15 g twice a day), neodicumarol (0.05–0.1 g twice a day), and phenindione (0.01 g twice a day). Anticoagulants should be prescribed only under the control of a coagulogram or, at the very least, the prothrombin index. The index should not drop by more than 40–50% (with a normal range of 75–100%).

Among thrombolytic agents, Trypsin and Chymotrypsin are used (0.07 mg/kg of body weight, intravenously twice a day).

An effective standard preparation is thrombolytin (a mixture of trypsin and heparin in a 6:1 ratio). It exhibits anticoagulant and thrombolytic effects (0.1 mg 3 times a day intravenously or intramuscularly).

Fibrinolytic drugs include fibrinolysin (20,000–40,000 IU combined with heparin, intravenously).

To improve microcirculation, low-molecular-weight dextrans (rheopolyglucin) are infused intravenously.

In cases of suppuration of a thrombophlebitic node, incision and drainage of the abscess are indicated.

After acute symptoms subside, the patient is initially allowed to move in bed; after 2–3 days, the leg is lowered, and subsequently, the patient is permitted to walk with the limb firmly bandaged.

For chronic thrombophlebitis, especially when accompanied by varicose veins, radical surgery to remove the thrombosed nodes is required.

Prevention of thrombophlebitis consists in the timely Treatment of the underlying pathological conditions. In the presence of varicose veins, timely surgery should be performed. If surgery is contraindicated (e.g., in elderly patients), the limb is firmly bandaged in an elevated position or elastic stockings are recommended. To prevent thrombophlebitis in the postoperative period, Therapeutic Exercises and early ambulation are indicated. If there are purulent foci on the limbs, they must be eliminated.

Among the complications of thrombophlebitis, post-thrombotic syndrome stands out. When a thrombus dissolves or undergoes canalization, venous patency is restored, creating conditions for normal Blood Circulation in the limb. However, if the thrombus is replaced by connective tissue, significant impairments of venous outflow occur in the limb. It becomes swollen and painful, its trophic function is disrupted—leading to ulcer development—and the patient's working capacity sharply declines.

A highly dangerous complication of thrombophlebitis is embolism, particularly of the pulmonary artery, which can lead to pulmonary infarction and even death.