Etiology and main pathogens
Purulent-inflammatory diseases are exclusively infectious in nature. Transmission occurs via exogenous (from the external environment) or endogenous (from internal foci) pathways. The infection can be caused by a single pathogen (monoinfection) or a combination of them, which significantly worsens the process.
Key characteristics of common pathogens:
- Escherichia coli (Escherichia coli): Facultative anaerobe causing peritonitis and appendicitis. Causes extensive putrefactive tissue breakdown and severe intoxication, especially in association with staphylococci. Highly resistant to antibiotics.
- Proteus (Proteus): Gram-negative saprophytes causing putrefactive breakdown in wounds. A dangerous nosocomial pathogen resistant to antiseptics.
- Pneumococci (Streptococcus pneumoniae): Do not produce toxins. Most commonly cause pneumonia, and primary peritonitis in children.
- Gonococci (Neisseria gonorrhoeae): Capable of spreading via ascending (salpingo-oophoritis, pelvioperitonitis) or hematogenous (suppurative arthritis) routes.
- Anaerobic spore-forming flora: Clostridia (Cl. perfringens, etc.) cause gas gangrene, while the tetanus bacillus releases potent exotoxins (tetanospasmin, tetanolysin).
Local reaction and protective barriers
Microbial proliferation in the wound is facilitated by the presence of a nutritive medium (hemorrhages, necrosis) and synergy in polyinfection. In response, the body initiates a local neuro-reflex vascular reaction: arterial hyperemia is replaced by venous stasis and edema. Neutrophils accumulate in the focus, causing pain, local heat, and impaired function.
To wall off the process, the body builds a tiered defense:
- Leukocyte wall — forms first in response to invasion.
- Lymph nodes — act as a tissue filter.
- Granulation wall — created by connective tissue cells for reliable isolation.
- Pyogenic membrane — a dense capsule into which the granulation wall transforms during a prolonged course (typical of an abscess).
Types of clinical course
The severity and rate of symptom development depend on the body's reactivity:
- Hyperergic reaction: Fulminant course with rapid spread of infection, extensive edema, thrombosis, and lymphangitis. Accompanied by severe systemic intoxication. Prognosis is serious, with a high risk of mortality.
- Normergic reaction: Moderate volume of damage, subfebrile temperature, minor shifts in blood tests. The infection responds well to timely treatment.
- Hypoergic reaction: Inflammation is clearly localized. General symptoms are absent, and edema around the focus is practically non-existent. Spontaneous resolution of the process is possible.
General reaction and systemic shifts
If the barrier is weak or the flora is highly virulent, the infection breaks through via lymphogenous or hematogenous routes, causing generalization of the process. The absorption of bacterial toxins and necrosis products leads to intoxication syndrome.
Severe homeostatic disorders develop at the macroorganism level:
- Decreased BCC: Oligocythemic hypovolemia develops. In severe cases, the blood volume drops by 15–25%, and plasma volume by 7–10%.
- Dysproteinemia: Decrease in the albumin fraction with a compensatory increase in globulins (without a change in total protein).
- Water-electrolyte disturbances: Extracellular dehydration occurs against the background of intracellular edema (hydration). During the tissue breakdown phase, potassium is lost with purulent discharge (hypokalemia), and returns to the bloodstream during the regeneration phase. In the inflammation focus itself, potassium concentration drops, while sodium and chloride ions accumulate.
Time is tissue. Microbes have 5–6 hours of "incubation" in the wound before they start multiplying. This is the surgical window for primary surgical debridement.
Class and exam questions
Why do accidental wounds need to be treated within the first few hours?
Microbes that enter a wound require 5–6 hours to adapt to the new environment. If surgical debridement and excision of necrotic tissue are performed during this window, the development of a purulent process can be prevented.
What happens to electrolyte levels during extensive suppuration?
During the active inflammation and necrosis phase, potassium is heavily lost with the exudate, leading to hypokalemia. Meanwhile, sodium and chloride accumulate in the focus itself. During healing, potassium returns to the blood.
What is the danger of a hyperergic reaction to an infection?
It is accompanied by a lightning-fast spread of inflammation without the formation of reliable barriers. Thrombosis and severe general intoxication join rapidly, frequently leading to a fatal outcome.
What else to study on this topic
- Clinical features and treatment of anaerobic gas gangrene
- Specific surgical infection: pathogenesis of tetanus
- Nosocomial infection in a surgical hospital
- Diagnostic criteria and treatment principles for surgical sepsis
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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