The aim of CytoSorb therapy is to stem an excessive and uncontrolled immune response and thus regain control over the course of the disease.
Any stimulus to the human body and its tissues exceeding the physiological level can cause inflammation. This applies to pathogenic germs (bacteria, viruses, fungi, parasites), physical stimuli (friction, pressure, injury or foreign bodies), chemical stimuli (toxins, various proteins, metals, acids, alkalis), thermal stimuli (heat, cold), radiation (UV, infrared, ionizing radiation) or certain enzyme disorders, such as in acute pancreatitis.
The organism endeavors to limit the damage as locally as possible and to eliminate the cause. That is why there is a local inflammatory reaction. In severe or repeated damage or in addition to existing problems of the immune system, however, can detect a whole organism – systemic – inflammation. This can get excessively out of control, resulting in serious complications, even outside the area originally affected by the injury, including multiple organ failure and death.
If this occurs due to infection, it is called sepsis or septic shock, however, non-infectious triggers, such as e.g. a severe trauma, major surgery or shock conditions can lead to a similar overreaction of the body (systemic hyperinflammation) with almost identical consequences.
The clinical situation is characterized by various disorders of the organ functions:
- Hemodynamic failure with massive nitric oxide (NO)-mediated peripheral vasodilation
- Systemic capillary leak with edematous changes and tissue damage through immigration of activated immune cells
- Relative and absolute hypovolemia and hypotension
Coagulation and microcirculation disorders
- Consecutive organ dysfunction and organ failure
In sepsis, pathogen-associated ligands, so-called PAMPs (pathogen associated molecular patterns) promote activation of inflammatory cells. These include endo- and exotoxins, but also fragments of bacterial DNA and viral RNA. In non-infectious events such as trauma, burns or pancreatitis, this is done by the body’s own substances, which are released by the destruction of large cell areas – so-called DAMPs (damage associated molecular patterns).
Activation leads to an initial release of pro-inflammatory mediators, including TNF-α, IL-β, IL-6 and others. These affect blood clotting, the complement system and vascular permeability. The formation of anti-inflammatory cytokines (IL-4, IL-10, TGF-β) is said to dampen the inflammatory response and leads to the deactivation of immune cells after successful control of the inflammatory focus. However, these anti-inflammatory cytokines can also adversely affect the course of the disease by promoting an infection or its progression by weakening the defenses reaction.