SEPSIS & SEPTIC SHOCK

 

Clinical Presentation: Sepsis is a clinical syndrome characterized by a dysregulated inflammatory response to infection. Rates of sepsis continue to rise secondary to medical advances such as the widespread use of indwelling intravascular catheters, increased implantation of prosthetic material such as, cardiac valves and artificial joints, and administration of immunosuppressive drugs and chemotherapeutic agents. These interventions serve to increase the risk of infection and subsequent sepsis. Sepsis is a continuum of conditions, from infection and bacteremia to sepsis and septic shock.  Shock

The septic condition:  Patients with early sepsis have infection and bacteremia and are at risk for progressing to sepsis and septic shock. Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated immune response to infection.  We have previously discussed the body's response to incoming infectious agents under specific immunity, which you can read about in the link below. 

Specific immunity

Etiology: Although evidence of infection is a diagnostic criterion for sepsis, only 28% of patients with sepsis have bacteremia, and slightly more than 10% will have primary bacteremia, defined as positive blood cultures without an obvious source of bacterial seeding. Common sites of infection among patients with sepsis syndrome include the respiratory tract, the genitourinary tract, abdominal sources such as, gall bladder, colon, and wound or soft tissue infections.  Respiratory tract infections

Bacteremia and sepsis:  Gram-negative bacteria including but not limited to; Enterobacteriaceae and Pseudomonas, previously the most common cause of sepsis, have been supplanted by gram-positive organisms, which now cause more than 50% of cases. Staphylococci are the most common bacteria cultured from the bloodstream, presumably because of an increase in the prevalence of chronic indwelling venous access devices and implanted prosthetic material. 

The incidence of fungal sepsis has risen dramatically owing to an increase in immunosuppressed and neutropenic patients.  Sepsis associated with P. aeruginosa, Candida, or mixed (polymicrobial) organisms is an independent predictor of mortality.

Pathogenesis. The normal host response to infection is recognition via pathogen recognition receptors and immune cell migration, primarily by neutrophils, to the site of infection, where they release inflammatory mediators. The process is highly regulated, with anti-inflammatory cytokines such as IL-10 suppressing release of inflammatory cytokines (eg, TNF-α). 

Pathophysiology:  Sepsis occurs when the inflammatory response overwhelms the local environment and becomes systemic. The cause of the systemic reaction is likely multifactorial and may include the effect of the microorganism, the release of large quantities of proinflammatory mediators, and even the genetic susceptibility of the individual. The different stages of sepsis (early sepsis to septic shock) represent a continuum, with patients often progressing from one stage to the next within days or even hours after admission.

Sepsis generally starts with a localized infection. Bacteria may then invade the bloodstream directly or may proliferate locally and release toxins into the bloodstream. These toxins can arise from a structural component of the bacteria such as endotoxin or may be exotoxins, which are proteins synthesized and released by the bacteria. 

RELATED;

1.  HAEMATOLOGICAL CONDITIONS

2.  STROKE

3.  ALTERED LEVEL OF CONSCIOUSNESS

4.  THE INTRAVENOUS DRUG ADMINISTRATION

5.  ENTEROBACTERIACEAE

6.  PSEUDOMONAS

7.  STAPHYLOCOCCUS