Three main sources of intoxication
Three pathways for the entry of toxic substances into the bloodstream play a key role in the development of surgical endogenous intoxication.
1. Primary source (focus of inflammation) It is within the zone of inflammation that microorganisms multiply and die, which is accompanied by a massive release of bacterial endo- and exotoxins. Simultaneously, tissue breakdown develops, releasing toxic mediators into the bloodstream: cytokines, interleukins, and prostaglandins. Against the background of inflammation, local metabolism is disrupted—anaerobic processes begin to prevail over aerobic ones, which inevitably leads to a critical accumulation of under-oxidized products (primarily lactic and pyruvic acids). The main consequence of this cascade is toxic damage to vital organs: the brain, heart, liver, and kidneys.
2. Second source (impairment of detoxification systems) This stage is associated with progressive liver and kidney dysfunction. The organs lose their ability to fully bind and excrete toxins. As a result, the body retains not only poisons from the primary purulent focus, but also accumulates normal nitrogen metabolism metabolites, such as urea and creatinine.
3. Third source (absorption from the gastrointestinal tract) This mechanism is particularly characteristic of patients with peritonitis and intestinal paresis. Digestive products, bile, and enzymes accumulate, stagnate, and decompose within the lumen of the gastrointestinal tract. Their massive absorption through the damaged intestinal wall back into the bloodstream catastrophically increases general toxemia.
Characteristics and components of toxemia
Clinically, endogenous intoxication manifests as pronounced toxemia. The severity of the patient's condition is always proportional to the scale of the purulent-inflammatory process and the volume of necrotic tissues.
A whole spectrum of pathological components circulates in the blood:
- Directly bacteria (bacteremia) and bacterial toxemia.
- Products of deep tissue breakdown, including necrotic bodies and various polypeptides.
- Circulating immune complexes (CIC), the concentration of which steadily increases.
- High concentrations of urea.
- Proteolytic enzymes (e.g., aggressive lysosomal proteases released from disintegrated leukocytes).
- Various pathological metabolites, such as acetone and ethanol.
Local manifestations of the purulent process
The local clinical picture largely depends on the stage of the disease, the nature of the pathological process, and its anatomical localization.
If the purulent focus is located superficially (in the skin, subcutaneous adipose tissue, muscles, or breast tissue), it will be characterized by five classical signs of inflammation:
- Redness (rubor) — occurs due to pronounced local hyperemia.
- Edema and swelling (tumor) — the result of inflammatory exudation.
- Pain (dolor) — due to compression and irritation of nerve endings.
- Increased local temperature (calor) — tissues over the focus feel hotter than healthy areas.
- Impairment of function (functio laesa) — limitation of mobility or failure of the organ to perform its task.
When inflammation is localized in internal organs, specific local signs inherent to a particular nosology come to the fore (e.g., characteristic symptoms in acute peritonitis or purulent pleurisy).
Differential diagnosis: General reaction or Sepsis?
A clear distinction between a severe systemic reaction to a local purulent process and true sepsis is absolutely key to establishing the correct diagnosis, choosing treatment tactics, and assessing the further prognosis.
| Sign | General reaction to the purulent process | Sepsis |
|---|---|---|
| Response to treatment | Intoxication symptoms sharply weaken or completely disappear shortly after surgical opening and drainage of the focus. | Symptoms remain almost unchanged, and toxemia persists even after adequate surgical intervention. |
| Bacteremia | Present, but may be exclusively transient in nature. | Stable detection of bacteria in the blood in the complete absence of clinical improvement after sanitation of the purulent focus. |
Laboratory diagnostics of intoxication
Laboratory tests are used to confirm toxemia and assess its severity. An increase in serum levels of urea, circulating immune complexes (CIC), polypeptides, necrotic bodies, as well as an increase in serum proteolytic activity, objectively indicates the progression of intoxication.
The following shifts in laboratory tests directly indicate severe intoxication:
- Progressive anemia.
- Pronounced leukocytosis with a sharp left shift of the leukocyte formula.
- Appearance of toxic granulation of neutrophils (an important morphological marker).
- Hypoproteinemia and dysproteinemia (decrease in total protein and disruption of the ratio of its fractions).
To finally clarify the diagnosis of purulent-inflammatory diseases, surgeons actively use special research methods: puncture of suspicious formations, radiological and endoscopic methods, as well as detailed clinical and biochemical laboratory studies of the obtained exudate.
The classical signs of superficial inflammation are easy to remember in the form of the Latin rhyme: Rubor, tumor, calor, dolor et functio laesa (Redness, swelling, heat, pain, and loss of function).
Class and exam questions
What role does the gastrointestinal tract play in the development of toxemia?
In peritonitis and intestinal paresis, the gastrointestinal tract becomes the third source of intoxication. Digestive juices, bile, and enzymes stagnate, decompose, and are massively absorbed into the blood, increasing toxemia.
How to distinguish a normal reaction to an abscess from sepsis based on treatment outcomes?
In a usual reaction, intoxication symptoms sharply decline after opening and draining the focus. In sepsis, severe symptoms persist even after adequate surgical sanitation.
What else to study on this topic
- Mechanisms of vital organ damage (brain, heart, liver) by bacterial toxins.
- The role of cytokines, interleukins, and prostaglandins in the pathogenesis of tissue breakdown.
- Transient bacteremia: causes and control methods.
- Biochemical analysis of purulent exudate: interpretation of results.
- Features of dysproteinemia development in severe surgical infections.
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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