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

Chronic non-specific infection

Chronic non-specific infection, much like acute infection, is defined by its Clinical presentation rather than a specific nosological category. There is no sharp boundary separating acute (purulent or putrid) and chronic non-specific infections. The primary criteria distinguishing them are the milder inflammatory manifestations and the more protracted course of a chronic infectious disease or injury-related infectious complication (such as a wound or fracture) compared with acute forms of surgical non-specific infection.

Chronic forms of infection are generally defined as those lasting longer than 2–3 months from onset to recovery.

Most cases of chronic non-specific infection result from the chronicity of an acute infection characterized by a slow and prolonged course. Only a small fraction of cases begin with an insidious, chronic trajectory. The latter are referred to as primary chronic infections, whereas the former represent complications of acute infections (secondary chronic infections). The causative agents of chronic non-specific infection are identical to those of acute infections. They are predominantly staphylococci (primarily Staphylococcus aureus), streptococci, pneumococci, Escherichia coli, Pseudomonas aeruginosa, Fungi, and bacteroides.

Most commonly, chronic infection develops in burn and purulent wounds, especially following the drainage of purulent foci (phlegmonous-necrotic forms of erysipelas, carbuncles). Secondary forms include hematogenous, traumatic, and—rarely—contact osteomyelitis, as well as its primary chronic variants (Brodie's abscess, Garre's sclerosing osteomyelitis, albuminous osteomyelitis), chronic Purulent diseases of the rectum and pararectal tissue (chronic paraproctitis with fistula formation), tenosynovial and bone infections, chronic thrombophlebitis, Arthritis and perichondritis, Chronic lung abscess or Pleurisy, chronic salpingitis and salpingo-oophoritis, chronic hidradenitis, chronic periodontitis, and others.

The causes driving the transition from an acute infection to a chronic one are numerous. They can be categorized into local and general factors, as well as objective and iatrogenic ones.

Among local factors, poor tissue vascularization in the area of the infection focus is paramount. This may stem from prior pathological tissue Changes in the affected area—such as post-traumatic or post-burn scarring—or from the Anatomical and physiological Features of the region (e.g., the distal lower extremities). Other local factors playing a significant role in chronic infection include a high concentration of dead or necrobiotic Cells within the focus, the presence of sequestered tissue deep within the purulent cavity (either bone or soft tissue, such as necrotic pancreatic fragments in purulent pancreatitis), or foreign bodies (metal, wood, stone, fabric, including polymers like surgical sutures, xenografts, etc.), inadequate drainage of local infection foci, and poor pathways for the outflow of exudate and necrotic debris. Additionally, the chronic course is fueled by the continuous Introduction of new microbial flora from endogenous sources—such as the rectum into the pararectal tissue in chronic paraproctitis, or from the Bronchi via fistulae into the Lungs or Pleura—or from exogenous sources (airborne contamination or non-sterile dressings).

The chronic course of osteomyelitis—usually following acute hematogenous or, less frequently, traumatic osteomyelitis—is driven by the spread of infection throughout the bone, The formation of numerous sequestra, and the systemic exhaustion of the patient due to intoxication. In such patients, fistulae are invariably visible on the Skin overlying the affected bone, continuously or intermittently discharging pus and small fragments of necrotic bone (sequestra). When these fistulae close for a few days, the infection flares up, manifesting as fever and acute soft tissue inflammation around the closed tract. This triggers a recurrence, causing the fistula to reopen with a discharge of pus or pus mixed with a sequestrum. These forms of osteomyelitis are most frequently localized in the long or spongy BONES OF THE lower extremities.

Among systemic factors, the most critical are advanced age—with its inherent dystrophic-sclerotic tissue changes and diminished resistance to pathogenic microorganisms—along with anemia, hypoproteinemia, hypovitaminosis, and certain underlying conditions such as Diabetes Mellitus, hypo- or hypercorticism, malignant tumors, cardiac and respiratory diseases, radiation sickness, Central Nervous system trauma (particularly Spinal Cord injuries), AIDS, and other immunodeficiency states.

Not least among the factors driving primary or secondary chronic infection are the intrinsic Properties of the pathogens themselves, including their virulence and resistance to antimicrobial agents, particularly Antibiotics.

Many instances of acute infection transitioning into chronic states are caused by improper, non-radical, or untimely Treatment—in other words, iatrogenic factors.

Shortcomings in the surgical and conservative Management of acute infections frequently stem from delayed surgical intervention, inadequate opening of the infection focus (insufficient incision of the skin and underlying Tissues), failure to break down internal septa, leaving non-drained pockets, incomplete debridement of necrotic tissue, sequestra, and foreign bodies (such as non-absorbable suture material). Other surgical missteps promoting chronicity include neglecting adjunctive conservative treatments (physiotherapy, general supportive care, etc.) and practices that foster microbial resistance to antiseptics. Examples include prescribing antibiotics without performing an antibiogram, violating dosing schedules, or using topical antibiotics restricted to systemic use (such as Penicillins and Cephalosporins). Iatrogenic factors also encompass insufficient attention to the patient's general condition, including anemia, hypovitaminosis, hypoproteinemia, impaired Carbohydrate METABOLISM, and depressed immunological resistance.

Clinical manifestations of chronic infection are primarily characterized by a significantly lower intensity of the inflammatory process—especially its exudative and proliferative components—and reduced intoxication compared to acute infections (subfebrile or even normal body Temperature, mild pain syndrome), alongside moderate anemia (barring chronic Sepsis) and pronounced functional alterations in major body systems and Internal Organs.

While this Overview of chronic infection does not capture every possible clinical trajectory, it outlines its general direction and hallmark features.

The morphological hallmarks of chronic infection include the suppression—sometimes to the point of complete arrest—of reparative and regenerative processes. This is clinically and pathologically manifested by sluggish granulation tissue development and its abnormal quality (typically sparse, pale gray, or cyanotic; occasionally exuberant yet fragile, purulent-infiltrated, dull, and bleeding). Tissue sclerosis is frequently observed surrounding the infection foci. Exudative responses are also typically weak. Necrotic-dystrophic changes occasionally dominate within chronic foci. Various degrees of mostly moderate anemia are observed (except in chronic sepsis, where anemia is severe), along with an elevated ERYTHROCYTE SEDIMENTATION RATE (ESR) and a mild leukocytosis with a slight shift to the left. Urine analysis frequently reveals proteinuria, leukocytes, and hyaline casts, indicating dystrophic and inflammatory renal changes. Amyloidosis of the Kidneys and other organs may occasionally develop.

Thrombophlebitis and lymphangitis develop around the infection focus. In the bones (when infected), features of bone necrosis appear with sequestra formation enclosed within a well-formed capsule surrounded by osteosclerosis, while adjacent soft tissues and bones display Osteoporosis.

The Diagnosis of chronic non-specific surgical infection relies on the same Methods used for acute infections. Identifying the underlying drivers that promote the chronic course assumes particular importance.

The cornerstone diagnostic tools for chronic infection include a comprehensive clinical examination, microbiological, biochemical, radiological, and ultrasound investigations.

Management of patients with chronic purulent infection must likewise be multimodal, combining local and systemic measures. Both the local and systemic factors sustaining the chronic infection must be systematically eradicated.

Surgical intervention remains the primary treatment modality for chronic infection. The timing, nature, and extent of surgery depend on the patient's general condition, the localization and type of the infection focus, and the response to conservative therapy. Surgery involves opening the purulent or putrid focus, excising necrotic tissue, and removing foreign bodies. In some cases, resection of part or even an entire organ (a segment, lobe, or whole lung) is necessary. Crucially, the infection focus must be isolated from ongoing contamination by microbial flora originating from the bowel or other hollow viscera.

Superficial infection foci require surgical exploration: verifying whether they are adequately opened, effectively drained, and thoroughly cleared of purulent extensions, necrotic debris, sequestra, and foreign bodies. Microbial culture of the focus and susceptibility testing against antiseptics and antibiotics are mandatory.

For deep-seated infection foci, dynamic monitoring of organ function is performed to determine their exact Location and nature (assessing for pus, sequestra, and adhesions to adjacent structures). These foci must be surgically drained or completely excised.

Complete excision of superficial purulent foci (localized abscesses) is not always feasible due to poorly developed capsule formation. More commonly, these abscesses are simply opened and drained. Abscesses located within visceral organs are treated via resection or removal of the affected organ whenever physiologically permissible (e.g., treating a chronic lung abscess via lobectomy, a splenic abscess via splenectomy, or a renal carbuncle via nephrectomy). Superficial chronic infection foci that fail to close spontaneously due to large skin defects must be surgically closed with a skin graft as soon as the wound bed is thoroughly cleansed. This must be preceded by correcting or significantly mitigating Metabolic Disorders, such as anemia, hypoproteinemia, dehydration, and glycemic imbalances.

Therapy for infected patients requires active topical antiseptics targeted against the specific pathogens, and in many instances, systemic antibiotics. Prior to prescribing antibiotics or antiseptics, identifying the causative microorganisms and testing their antibiotic susceptibility is strictly required. Alongside antiseptics (applied to purulent wounds, cavity irrigations, and soaks), local Management of chronic purulent infection incorporates Proteolytic Enzymes, sorbents, moist dressings with hydrophilic bases, ultraviolet and laser irradiation, as well as aerotherapeutic chambers and units.

For chronic sepsis, ultraviolet Blood irradiation (UVBI), transfusions of whole blood and packed red Blood Cells are utilized. Prostaglandin inhibitors, antihistamines, hemoperfusion, and lymphosorption are also employed.

Systemic medical therapy (In addition to standard systemic antimicrobial regimens) for chronic infection includes infusions of detoxifying agents (such as rheopolyglucukin), protein and carbohydrate solutions, and—less frequently—lipid emulsions, along with immunostimulants and immunomodulators.