Clinical Pathology · MU Sofia

134. Sepsis. Septicemia. Septicopyemia. Chroniosepsis. Organ damage characteristics.

Explains sepsis as a dysregulated host response to infection, covering its two stages of early hyperinflammation followed by immunosuppression, and the Sepsis-3 definitions of sepsis and septic shock. It distinguishes septicaemia from sepsis, then describes pyaemia and septicopyaemia with septic emboli and multiple abscesses in organs, with a museum kidney photograph and an endocarditis example. It closes with chroniosepsis, linked to a non-healing septic wound.

Inside: 1 section · 1 labelled picture · 16 flashcards · 3 min

Topic 134 of 138 in the MU Sofia syllabus for Clinical Pathology (Medicine, Year 4). The free AceMed note covers it in 1 section, about 551 words (3 min of reading), with 16 flashcards.

In this note

  1. Sepsis. Septicemia. Septicopyemia. Chroniosepsis. Organ damage characteristics

Sepsis. Septicemia. Septicopyemia. Chroniosepsis. Organ damage characteristics

First, Sepsis Sepsis is an emergency, immune related disease where the body’s response to infection causes damage to the self. Most commonly the infection is bacterial, but can be fungal, viral or protozoan as well, the primary infection can arise from anywhere in the body. Sepsis is a result of both microbial and host factors, and occurs in two stages, early on we have excessive inflammation, followed by a prolonged period of immunosuppression. Either stage can be fatal. Sepsis is more likely in those with a weakened immune system, as it relies on the bacteria getting away from the local, and into the systemic.

Remember: the current (Sepsis-3) definitions: sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection; septic shock is sepsis with hypotension needing vasopressors to keep mean arterial pressure at 65 mmHg or more, and lactate above 2 mmol/L despite adequate fluids.

In sepsis the bacterial pathogen is recognised by its pathogen associated molecular patterns (PAMPs), by the pattern recognition receptors (PRRs) of the innate immune system. This causes a series of signalling cascades, up regulating expression of pro inflammatory cytokines. This triggers an uncontrolled immune response, as leukocytes are not recruited to the specific site, but rather the entire body, effectively causing systemic inflammation. The body detects this and tries to compensate, by shifting the proinflammatory T helper cell 1 to TH2, known as ‘compensatory anti-inflammatory response syndrome’. The problem with this, is that apoptosis becomes worse in the immunosuppressive stage, and multiple organ failure ensues.

The consequences of sepsis can be:

  • End organ dysfunction (aka multiple organ dysfunction)
  • Acute respiratory distress syndrome (fluid accumulation in the lungs)
  • Encephalopathy
  • Liver disruption with disruption to clotting factor synthesis
  • Oliguria
  • Heart failure due to cytokines that depress myocardial function
  • Septic shock

Septicemia Sepsis and Septicemia are sometimes used interchangeably, but they are separate.

While sepsis is the extreme inflammatory response to infection, septicemia is the actual having bacteria/bacterial toxins in the bloodstream. Another way of thinking of it is that Septicemia causes sepsis.

These days, septicemia has been replaced by the more useful, bacteremia.

Septicopyemia Septicopyemia is Septicemia + Pyaemia. As we’ve covered septicemia above, here we’ll consider pyemia.

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