Septicemia

Septicemia is acute systemic infection from pathogenic bacteria invading the bloodstream and multiplying, with chills, high fever, rash, arthralgia, and hepatosplenomegaly; some patients develop irritability, cold extremities/cyanosis, thready rapid pulse, tachypnea, and hypotension. Mortality is 30-50%, especially in the elderly, children, the chronically ill, and immunocompromised; delayed treatment and complications worsen prognosis.

Common Symptoms

Station doctor; fever; persistent remittent fever; ascites; septicemia; liver failure; wet lower-limb gangrene; purulent discharge; meningitis

Causes and Pathogenesis

Any pathogenic or opportunistic bacterium may cause septicemia. Before 1950, hemolytic streptococci and pneumococci predominated (>50%), staphylococci ~20%, Gram-negative bacilli ~12%. After broad-spectrum antibiotics/corticosteroids/immunosuppressants, the spectrum shifted: Gram-negative bacilli dominated after the 1960s; staphylococci remain important due to resistance; Gram-positive cocci rose to 55% (CDC, 1986-89). Chinese data show Gram-negative bacilli 63-68%. Besides E. coli, Klebsiella, Pseudomonas, Aerobacter, Proteus are common; fungi include Candida albicans, Aspergillus, Cryptococcus. Anaerobes account for 8-26% (Bacteroides fragilis, Peptostreptococcus). Polymicrobial septicemia (~10%) is common in severe immunodeficiency. Toxin mechanisms: (1) staphylococcal TSST-1 stimulates monocyte IL-1/TNF release; (2) TSST-1 plus streptococcal erythrogenic toxin forms superantigens binding MHC-II and T-cell Vβ; (3) toxins generate arachidonic acid metabolites via lipoxygenase/cyclooxygenase; (4) staphylococcal α-toxin releases platelet PF4/PF5 activating the intrinsic cascade and DIC; (5) toxins damage endothelium forming pores causing ion/fluid leaks. Gram-positive wall peptidoglycan/lipoteichoic acid activates complement. Pathology varies with pathogen/duration/comorbidities: early inflammatory changes with cloudy swelling/focal necrosis/fatty change; mononuclear-phagocyte hyperplasia causes hepatosplenomegaly; capillary damage causes petechiae/rashes; multi-organ edema, joint effusion, purulent meningitis, pleurisy may occur. Pathogens enter via broken skin/mucosa or from latent foci via lymphatics/veins. Transient bacteremia occurs with intact immunity; severe host conditions, high pathogen load, and virulence lead to SIRS and multi-organ failure.

Treatment

Drug therapy, supportive therapy

Preventive Measures

Closely monitor high-risk patients; investigate and treat promptly at the first sign. Do not squeeze furuncles/carbuncles. Remove infected indwelling catheters promptly. Strict isolation for burn units and chemotherapy/BMT patients. Strengthen disinfection in wards previously housing septicemia patients to prevent spread of resistant S. aureus, Pseudomonas, and fungi.

Department to Visit

It is recommended to visit the Infectious Diseases department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.