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

Acute Purulent Infection
Purulent Skin and Subcutaneous Infections

The most common forms of purulent Skin infections and subcutaneous tissue can be outlined According to the following scheme.

A boil (furuncle) is an acute purulent-necrotic inflammation of a Hair follicle and its associated sebaceous gland. It typically develops in areas with hair growth and a high concentration of Sebaceous Glands, such as the face and back. The primary causative agents are Staphylococcus aureus and Staphylococcus epidermidis.

The Development of a furuncle is promoted by A number of predisposing factors: poor skin hygiene, minor skin trauma (abrasions, scratches, picking or squeezing), Metabolic Disorders (Diabetes Mellitus, malnutrition, vitamin deficiency), general exhaustion, nervous and mental fatigue, etc.

The disease begins with the appearance of a painful skin lesion centered around a hair follicle, where the surrounding skin becomes noticeably hyperemic. Soon, a painful infiltrate with a necrotic core develops. The area of necrosis eventually breaks down, forming a small abscess.

In most cases, a furuncle causes only mild systemic symptoms (general malaise, low-grade fever, headache, loss of appetite). Marked signs of intoxication occur only when the inflammatory process spreads to adjacent Tissues, Lymphatic vessels, or Blood Vessels.

Laboratory findings typically show mild leukocytosis and a left shift in the differential leukocyte count.

By the 7th to 10th day, the purulent core sloughs off, pus discharges, and the patient's condition gradually improves. The resulting crater progressively cleanses and fills with granulation tissue.

The size of a furuncle varies from 0.5 to 2.5 cm in diameter. The complete cycle of its development and resolution lasts on average 8–14 days.

Furuncles located on the face require special attention due to their severe clinical course and high risk of dangerous complications. Infection from the primary focus can spread via V.facialis, v.angularis, v.ophthalmica, plexus pterygoideus into the cavernous sinus, potentially causing Purulent meningitis or encephalitis. Surgical literature describes cases of upper lip furuncles where death occurred within days of the onset of inflammation.

In the absence of complications (and excluding facial localization), patients with furuncles are treated on an outpatient basis. Depending on the stage of the disease, local Treatment may be conservative or surgical.

The skin surrounding the furuncle is treated with 1% salicylic alcohol or hibitane, and a dressing with an antibiotic-containing emulsion (from the penicillin group or synthomycin) is applied. Some surgeons recommend dusting the furuncle with crystalline sodium salicylate or salicylic acid.

Warm compresses should be avoided during the treatment of a furuncle, as they soften the skin and create favorable conditions for the spread of infection. Ointment-based dressings should also be avoided (with the exception of Water-soluble ointments containing antiseptic agents, such as dioxidine or iodopyrin).

In the early stages, physical therapy such as quartz lamp irradiation and UHF therapy is applied.

Squeezing a furuncle is strictly prohibited, as this can lead to the spread of infection. Such manipulations are particularly hazardous on the face.

During the stage of purulent breakdown, the skin around the furuncle is wiped with 70% alcohol or a 3% iodine solution, and the necrotic core is removed using forceps. Subsequently, the furuncle is managed in the same manner as a standard infected wound.

If There is a systemic bodily reaction, patients are administered Antibiotics intramuscularly or intravenously, along with oral sulfonamides and multivitamins, particularly ascorbic acid. In cases of intoxication, detoxification therapy is performed.

Special attention must be given to the treatment of facial furuncles (Fig. 67), particularly in the nasal and upper lip regions. This treatment must be carried out in a hospital Setting. Conservative management is indicated, including high doses of antibiotics, quartz irradiation, UHF therapy, and strict rest. If facial edema, lymphangitis, lymphadenitis, headache, or malaise develops, some surgeons recommend wide surgical incision, as well as ligation of the v.angularis running along the nasolabial fold toward the palpebral fissure.

In individuals who neglect personal hygiene, suffer from vitamin deficiencies, or have debilitating systemic conditions, multiple furuncles may appear across various PARTS OF THE body. This condition is known as furunculosis. Individual furuncles typically present in various Selection/3.html">Stages of development simultaneously (some are just beginning, others are forming a necrotic core, while others are healing).

When treating furunculosis, primary focus should be placed on general systemic measures. First and foremost, the underlying cause of the condition must be identified. Patients are prescribed a high-calorie diet, brewer's Yeast, Vitamins, antibiotics, and guidance on personal hygiene. For the treatment of furunculosis, some authors recommend autohemotherapy sessions, wherein 3–5 ml of venous blood is withdrawn and injected into the gluteal Muscles every 1–2 days. The application of staphylococcal toxoid, anti-staphylococcal plasma, and anti-staphylococcal gamma globulin is also effective. Antibiotics are selected based on microbial sensitivity testing. Occasionally, transfusions of fresh preserved blood and general quartz irradiation are administered. Treatment should be conducted under the supervision of a general practitioner.

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Fig. 67. Abscessing facial furuncle

A carbuncle (carbunculus) is an acute purulent-necrotic inflammation of multiple adjacent hair follicles, sebaceous glands, and surrounding soft tissues, accompanied by Necrosis of the skin and subcutaneous layer. It is caused by Staphylococcus aureus. A key characteristic of a carbuncle is its rapid progression, with the inflammatory process extending deep into the tissues and accompanied by extensive thrombosis of small blood vessels, leading to tissue necrosis. A carbuncle presents as an infiltrate of varying sizes that rises above the skin surface, displaying a purplish-blue discoloration. After some time, The surface of the carbuncle becomes covered with numerous small necrotic foci from which pus discharges. The surrounding soft tissues are heavily infiltrated, dense, and extremely painful.

Fig. 68. Carbuncle of the upper lip

The patient's general condition is severely impaired: there are marked signs of intoxication, body Temperature rises to 39–40 °C, the pulse is rapid (100–120 bpm), and the Tongue is dry and coated. Delirium may occur. Blood tests reveal changes characteristic of an acute inflammatory process.

Carbuncles are typically solitary. Their sizes vary, ranging from 5 to 10 cm in diameter. They most commonly develop in areas prone to chronic skin irritation (such as the lower back and the back of the neck).

Carbuncles located on the face (Fig. 68) follow a particularly severe clinical course, especially in patients with diabetes mellitus.

Carbuncles are primarily treated surgically, as general and local antibiotic therapy, alongside penicillin-novocaine blockades, are usually ineffective. The condition progresses with deep purulent tissue melting, while skin necrosis develops at the center of the carbuncle. The necrotic masses (cores) discharge through the resulting opening. Such patients require surgical intervention. Under general anesthesia, a deep cruciate incision is made. Necrotic tissues are excised, and the wound is washed with an antiseptic and packed.

Subsequent management follows the standard principles of purulent surgery.

Phlegmon (phlegmon) is a diffuse purulent inflammation of the subcutaneous tissue characterized by a tendency to spread. Phlegmons can be located subcutaneously, intermuscularly, retroperitoneally, or in the lesser pelvis. They are categorized into superficial and deep forms. Depending on their anatomical Location, they have specific designations: inflammation of the pararenal tissue is termed paranephritis; of the perirectal tissue, paraproctitis; of the mediastinal tissues, mediastinitis; and around the Lymph Nodes, adenophlegmone.

Microorganisms penetrate tissues via hematogenous and lymphogenous routes, or from a contiguous purulent focus. Frequently, phlegmon is triggered by an external infection, such as trauma or injections administered without proper adherence to asepsis rules. Phlegmon tends to spread both horizontally and deep into tissues through fascial clefts that transmit blood Vessels and nerves, transforming a superficial phlegmon into a deep one.

The development of phlegmon goes through several stages.

During the first 2 days, vascular dilation is observed, accompanied by the exudation of the liquid portion of the blood into the interstitial tissue and the accumulation of leukocytes (serous phlegmon). Timely treatment can lead to the complete reversal of these pathological changes.

Between days 3 and 4, multiple small purulent foci form without coalescing. When tissues are incised during this period, free pus is not detected; instead, the tissues appear edematous and sometimes exhibit a yellow-green discoloration (purulent phlegmon). Tissue incision at this stage can halt the progression of the disease.

Over days 5 and 6, the previously formed microabscesses merge, infiltrating the tissue and involving progressively larger areas. When a phlegmon is opened at this stage, green liquid pus is discharged. Thrombosis of small vessels occurs within the inflammation zone, which can lead to tissue necrosis (necrotic phlegmon).

Phlegmons can be caused by aerobic, anaerobic, and putrefactive infections, as well as by the subcutaneous injection of chemical agents—frequently inflicted intentionally (artificial phlegmon).

Phlegmons may be situated supra- and subfascially.

The Diagnosis of superficial phlegmons is straightforward. Patients complain of pain and Swelling in the affected area, general weakness, and decreased working capacity. The lesion exhibits progressive edema, tissue induration, poorly demarcated skin erythema, local hyperthermia, and impaired function. Over time, due to purulent melting and tissue necrosis, the dense infiltrate softens, and the fluctuation sign appears, indicating abscess formation.

Parallel to local manifestations, the patient's general condition deteriorates. Tachycardia develops, and body temperature rises to 38–39 °C. Headaches and chills appear, and the patient loses their appetite. Blood tests reveal changes characteristic of an inflammatory process.

Diagnosing deep phlegmons is more challenging because surface skin changes are absent. In such cases, deep Palpation revealing a dense, painful mass is often helpful. Combined with high BODY TEMPERATURE AND other signs of inflammation, this assists in establishing the diagnosis. The body temperature in phlegmons typically remains persistently elevated.

Phlegmons are frequently complicated by lymphangitis, lymphadenitis, thrombophlebitis, erysipelas, and Sepsis. Depending on the clinical course, Three types of phlegmons are distinguished: circumscribed, which lacks a tendency to spread; progressive, which rapidly involves new tissues and is caused by streptococci or anaerobic microorganisms; and woody, caused by low-virulence microbes. The latter runs a chronic course characterized by excessive Connective Tissue proliferation and minimal pus formation. Upon palpation, the affected tissues feel hard, board-like, and painless.

The treatment of phlegmons is performed in an inpatient setting. In the Cytology/cytology/16.html">Early stages of the disease (characterized by a small, mildly painful infiltrate with minimal temperature response and blood abnormalities), Conservative Methods may be applied: bed rest, immobilization of the affected area (limb), intramuscular antibiotic administration, regional novocaine blockades, and physical therapy (UHF therapy, quartz lamp). If the condition progresses, surgery must not be delayed. Under general anesthesia, the phlegmon is widely opened through one or more incisions, all fascial septa are divided, purulent pockets are connected, and necrotic tissues are excised. The wound is loosely packed and drained. Depending on the body's systemic response, supportive medical therapy of varying intensity is administered.

After excising all non-viable tissues and rinsing the wound, some authors insert 2–3 polyvinyl chloride tubes into its cavity and apply primary sutures. In the postoperative period, the wound is irrigated with an antiseptic solution through these tubes.

Following the drainage of a phlegmon, the patient's condition gradually improves, body temperature decreases, pain subsides, and edema resolves. Subsequently, the wound cleanses and pink granulation tissue appears, making it possible in some cases (with large wounds) to apply secondary sutures.

An abscess (abscessus) is a localized inflammation characterized by the accumulation of pus within various tissues and Organs, surrounded by a pyogenic capsule. The accumulation of pus within natural Body Cavities (such as the pleural cavity, Gallbladder, Appendix, or joint) is referred to as empyema.

Abscesses can be located in soft tissues and organs. They are classified into superficial and deep abscesses. Superficial (typically subcutaneous) abscesses are easy to diagnose, although the Clinical presentation largely depends on the virulence of the infection and the patient's reactivity.

Abscesses, much like phlegmons, are caused by exogenous or endogenous infections. Additionally, abscesses may develop secondary to hematoma suppuration or the administration of concentrated medicinal solutions into tissues (such as analgin, magnesium sulfate, or cordiamine).

The pyogenic membrane forms during the Evolution of the abscess and consists of connective tissue lined on its inner surface by granulation tissue.

Local and systemic clinical manifestations of superficial abscesses resemble those of phlegmon: local swelling, tenderness, skin erythema, fever, chills, tachycardia, and hematological alterations. On palpation, the affected area feels soft and demonstrates the fluctuation sign. This sign is elicited using the following technique: fingers of both hands are placed on opposite sides of the swelling, applying even pressure. While holding the fingers of the left hand stationary, gentle tapping motions are executed with the right hand.

When fluid (pus) is present within the tissue, these impacts are perceived by the fingers of the left hand due to the Displacement of the fluid.

It is somewhat more difficult to diagnose deeply located abscesses. In such cases, alongside general clinical signs and pain upon deep palpation, specialized supplementary diagnostic methods can be helpful: radiography (lung abscess), ultrasound, or computed tomography (Liver abscess). Occasionally, punctures aid in the diagnosis (for subphrenic and pelvic abscesses).

The outcomes of an abscess can vary. A small abscess, given prompt and comprehensive therapy, may resolve. A larger or untimely treated abscess will rupture onto the skin surface (if located superficially) or into adjacent tissues, hollow organs, or body cavities (a liver abscess may rupture into the peritoneal cavity, and a lung abscess into the pleural cavity). In certain cases, abscesses become encapsulated: a thick capsule forms around them, and the pus becomes denser.

The treatment of an abscess is surgical. Under local anesthesia or various types of inhalation and non-inhalation anesthesia, the abscesses are opened. If they are superficially located, this Procedure is straightforward. Deep abscesses can sometimes be difficult to incise due to their anatomical location, proximity to vital organs and large vessels, and so on. For better pus drainage, it is advisable to open the abscess near its base. After opening the abscess and evacuating the pus, the septa are broken down digitally, and any potential purulent pockets are opened. Pus is sampled for Bacteriological examination and to determine microbial sensitivity to antibiotics. The abscess cavity is rinsed with an antiseptic solution and drained using rubber strips and polyvinyl chloride tubes. If complete evacuation through the main incision fails, the abscess is drained through one or two additional counter-incisions. Following the incision, the abscess is managed as a purulent wound. An abscess must be opened carefully to avoid damaging the pyogenic capsule.

Acute purulent abscesses should be differentiated from so-called cold abscesses, which occur in bone or joint tuberculosis. The pus formed in these cases melts adjacent tissues, tracks down through interfascial spaces, and accumulates in lower areas, forming an abscess (for instance, in spinal tuberculosis, pus may descend to the anterior surface of the thigh). Such abscesses are termed cold abscesses because they are not accompanied by pain, local or general fever, or skin hyperemia. They are characterized by a prolonged, latent, and chronic course. These abscesses should not be incised, as secondary infection may ensue; instead, they are aspirated via puncture.

In certain cases of superficially located abscesses, the approach can be similar to that used for phlegmon: after excising the abscess along with its capsule and all altered tissues, it is drained with polyvinyl chloride tubes, and primary sutures are applied. This accelerates wound healing.

ERYSIPELAS

Erysipelas is an acute, progressive inflammation of the dermis or mucous membranes involving the lymphatic vessels. It is most commonly caused by Group A streptococci, which penetrate The Lymphatic system of the skin through damaged skin or mucous membranes (wounds, abrasions, cracks) and multiply there. Erysipelas most frequently occurs on the lower extremities and face, though it can affect other parts of the body. It is classified as a contagious disease. The onset of infection is promoted by increased microbial virulence and decreased bodily reactivity.

Erysipelas may complicate the course of other purulent processes, such as purulent wounds, phlegmon, and abscesses.

The penetration of microbes into the skin causes dilation of Blood and Lymphatic vessels, initiating serous-hemorrhagic inflammation. The resulting exudate detaches the epidermis, leading to The formation of blisters. When microbes invade the subcutaneous tissue, inflammation of that tissue (phlegmon) develops. Compression of dermal vessels by the exudate or their thrombosis leads to skin necrosis.

Depending on the aforementioned pathomorphological changes, several Clinical forms of erysipelas are distinguished: erythematous, bullous, phlegmonous, and gangrenous.

The mildest form is erythematous erysipelas (erysipelas erythematosa). It is characterized by a sudden onset, presenting as localized, bright red patches on the skin or mucous membranes with irregular, well-defined borders (resembling a geographic map). Local temperature is elevated, and the skin is slightly edematous. Body temperature ranges from 38–39 °C. The pulse is rapid, 100–120 bpm. Symptoms include headache, dizziness, general weakness, occasional nausea, vomiting, and chills. In the area of redness, the patient experiences warmth, burning, tightness, and a stinging pain.

As the pathological process progresses, the erythematous form transitions into bullous erysipelas (erysipelas bullosa), which is characterized by the appearance of blisters filled with serous fluid. Subsequently, these blisters rupture, leaving behind yellow, crusty scabs. The patient's general condition worsens.

In phlegmonous erysipelas (erysipelas phlegmonosa), serous-purulent inflammation and marked tissue edema develop in the subcutaneous tissue. The patient's general condition is very severe, accompanied by signs of intoxication (high fever, tachycardia, dry tongue, nausea, vomiting, altered mental state, and delirium).

In the gangrenous form (erysipelas gangrenosa), the affected area of skin undergoes necrosis, turning dark brown or even black. Phlegmonous and gangrenous forms of erysipelas rarely affect the facial skin.

Depending on the spread and clinical course, distinctions are made: creeping erysipelas, where the process progressively encompasses new areas; migratory erysipelas, which affects various parts of the body; and recurrent erysipelas, which frequently repeats. An allergic factor plays an important role in erysipelas recurrences, rooted in the sensitization of the Organism.

Frequent recurrences of erysipelas in the same area lead to the obliteration of lymphatic vessel walls, resulting in impaired lymph drainage, thickening of the subcutaneous tissue, and the development of elephantiasis. Recurrences are also attributed to the fact that erysipelas does not confer Immunity.

Complications of erysipelas depend on the LOCATION OF THE pathological process. Localization on the face and scalp can lead to secondary meningitis. Erysipelatous inflammation of the extremities is complicated by phlebitis and thrombophlebitis. Furthermore, erysipelas can cause metastatic lesions of mucous bursae, tendon sheaths, joints, and muscles.

Treatment of patients with erysipelas is carried out in hospital settings (preferably in isolated wards). Topically, osmotically active water-soluble ointment dressings are applied to reduce pain. Good results are achieved by ultraviolet (quartz) irradiation of the affected areas in erythematous or suberythrematous doses. To prevent the spread of infection, rest is prescribed (restriction of speech and a liquid diet for facial localization), along with a general tonic, high-calorie, vitamin-rich diet. Antibiotics (penicillin group drugs) and sulfonamides (sulfadimezin, sulfadimethoxine) are administered. In cases of recurrent erysipelas, non-specific immunity is stimulated (transfusions of leukocyte mass and blood, administration of levamisole, tactividin, etc.), and direct endolymphatic therapy is performed, which makes it possible to achieve high antibiotic concentrations not only in the lymphatic system but also in the purulent focus and adjacent tissues.

In bullous erysipelas, the blisters are opened, followed by the application of ointment dressings (synthomycin emulsion, streptocide suspension, tetracycline ointment).

Both phlegmonous and gangrenous forms of erysipelas require Surgical treatment (opening of abscesses, drainage, excision of necrotic tissues). Following erysipelas, the body becomes sensitive (sensitized) to infection, which explains why the condition frequently recurs. The cause of reinfection in sensitized patients is the presence of a chronic streptococcal infection focus in the body (dental caries, chronic tonsillitis, etc.).

A variant of erysipelas is erysipeloid (erysipeloides). This disease typically affects the skin of the hand, particularly the fingers, and less frequently localizes on the Nose, Cheeks, or neck. It results from the penetration of the swine erysipelas bacillus into the body. Those at risk include people who handle raw meat (butchers, cooks, housewives, veterinarians). The incubation period is 3–7 days.

Erysipeloid presents with serous inflammation of all skin layers, accompanied by pronounced edema, dilation of lymphatic vessels, and lymphostasis.

Clinical presentation: itching and burning in the affected area (most commonly a single finger), mild edema, and redness. Occasionally, adjacent joints become swollen and painful. The General condition of patients changes very little. The duration of the acute period is 10–20 days, after which the disease assumes a chronic course. There is a tendency toward recurrence.

The treatment of erysipeloid and erysipelas is similar. Additionally, novocain blockades, radiotherapy, administration of specific antitoxic serum, and oil-balsamic dressings are employed.

HYDRADENITIS

Hydradenitis is an inflammation of the apocrine Sweat Glands, predominantly in the axillary regions, caused by Staphylococcus aureus. The development of hydradenitis is promoted by poor hygiene and excessive sweating.

In its local manifestations, it resembles furunculosis. A localized, painful, and firm swelling appears in the affected area. It differs from a furuncle in that it lacks a central necrotic core with a hair follicle. Sometimes several such swellings appear nearby and eventually merge. The skin over them becomes red or bluish-purple.

Neighboring lymph nodes are frequently involved in the process. The general condition in hydradenitis is rarely affected, and body temperature is typically low-grade (subfebrile).

The dense nodules formed in the sweat gland areas subsequently soften, and pus discharges from the resulting fistulae. Due to the presence of hair in the axilla, excessive sweating, and chronic skin irritation during movement, the process tends to spread to other sweat glands. They suppurate and form a series of abscesses. Colloquially, this condition is known as "bitch's teat" (hidradenitis suppurativa).

The course of hydradenitis is protracted, characterized by alternating periods of exacerbation and remission.

Treatment of hydradenitis is both local and general. Local treatment begins with hygiene care of the affected area (most commonly the axilla): hair is clipped, and the skin is wiped with a 2–3% formalin solution (to reduce sweating). Dry heat and physiotherapy Procedures (UHF therapy, Sollux lamp, quartz lamp) are then prescribed. Infiltration of the lesions with a penicillin-novocain solution is recommended.

General treatment involves antibacterial therapy (antibiotics, sulfanilamide drugs), autohemotherapy, and specific immunotherapy (staphylococcal toxoid, antistaphylococcal y-globulin). In cases of frequent recurrences, radiotherapy is prescribed. The aforementioned measures are combined with general supportive therapy (a dairy- and plant-based diet, vitamins) and hygienic measures (treating the affected skin with a 2% boric or camphor alcohol solution).

Surgical intervention is used in cases of suppuration (abscesses are incised and drained). For recurrent axillary hydradenitis, complete excision of the hair-bearing skin with local plastic defect reconstruction is sometimes performed.