Inflammation - local and systemic signs of inflammation, SIRS, CARS, MODS
Inflammation[edit | edit source]
Inflammation is a complex biological response of vascularized tissues to harmful stimuli such as pathogens, damaged cells, or irritants. The primary objectives of inflammation are to eliminate the initial cause of cell injury, remove necrotic cells and tissues, and initiate tissue repair. Inflammation may be localized or systemic depending on the extent of injury and the magnitude of mediator release.
Local Signs of Inflammation[edit | edit source]
The classical description of inflammation includes five cardinal local signs, originally described by Celsus and later expanded by Virchow. These signs result from vascular and cellular changes occurring at the site of injury.
- Redness (Rubor): Caused by vasodilation of arterioles and capillaries, leading to increased blood flow to the affected area.
- Heat (Calor): Results from increased blood flow and enhanced local metabolic activity.
- Swelling (Tumor): Occurs due to increased vascular permeability, allowing plasma proteins and fluid to leak into the interstitial space, forming an exudate.
- Pain (Dolor): Produced by the stimulation of sensory nerve endings by inflammatory mediators such as bradykinin and prostaglandins, as well as by pressure exerted by tissue edema.
- Loss of Function (Functio Laesa): Results from pain, swelling, and structural damage to tissues, leading to impaired normal function.
Systemic Signs of Inflammation[edit | edit source]
When inflammatory mediators gain access to the circulation, systemic manifestations develop. These features collectively constitute the acute phase response.
Systemic signs include fever, malaise, anorexia, tachycardia, and alterations in leukocyte count (leukocytosis or leukopenia). The liver plays a central role by producing acute-phase proteins such as C-reactive protein (CRP), fibrinogen, and serum amyloid A, while the synthesis of albumin is reduced. These changes serve both protective and diagnostic purposes.
Systemic Inflammatory Response Syndrome (SIRS)[1][edit | edit source]
Systemic Inflammatory Response Syndrome (SIRS) is a clinical syndrome characterized by a generalized inflammatory state affecting the entire body. It may occur in response to infectious or non-infectious insults.
SIRS is diagnosed when two or more of the following criteria are present:
- Abnormal body temperature (>38°C or <36°C)
- Tachycardia (heart rate >90 beats per minute)
- Tachypnea (respiratory rate >20 breaths per minute or arterial PaCO₂ <32 mmHg)
- Abnormal white blood cell count (>12,000/mm³, <4,000/mm³, or >10% immature neutrophils)
Common causes include severe infection (sepsis), trauma, burns, pancreatitis, and ischemia–reperfusion injury.
Compensatory Anti-Inflammatory Response Syndrome (CARS)[edit | edit source]
Compensatory Anti-Inflammatory Response Syndrome (CARS) represents a counter-regulatory immune response that follows or overlaps with SIRS. Its primary purpose is to limit excessive inflammation and prevent host tissue damage.
CARS is characterized by immunosuppression, decreased production of pro-inflammatory cytokines (such as TNF-α and IL-1), and increased levels of anti-inflammatory cytokines including IL-10 and transforming growth factor-β (TGF-β). Prolonged or excessive CARS may result in impaired host defense, leading to secondary infections, poor wound healing, and increased mortality.
Multiple Organ Dysfunction Syndrome (MODS)[edit | edit source]
Multiple Organ Dysfunction Syndrome (MODS) is defined as the progressive dysfunction of two or more organ systems such that homeostasis cannot be maintained without medical intervention. MODS commonly develops as a consequence of uncontrolled systemic inflammation, particularly in severe sepsis or trauma.
The pathogenesis involves widespread endothelial injury, microvascular thrombosis, impaired tissue perfusion, and mitochondrial dysfunction. Organs commonly affected include the lungs (acute respiratory distress syndrome), kidneys (acute kidney injury), liver (hepatic dysfunction), cardiovascular system (shock), central nervous system (encephalopathy), and the hematologic system (disseminated intravascular coagulation).
MODS is associated with a high mortality rate and represents the most severe end of the inflammatory response spectrum.
- ↑ Kumar V, Abbas AK, Aster JC. Robbins and Cotran Pathologic Basis of Disease. 10th ed. Philadelphia: Elsevier; 2021. Hall JE, Guyton AC. Guyton and Hall Textbook of Medical Physiology. 14th ed. Philadelphia: Elsevier; 2021.
