Intoxication syndrome
The development of sepsis most commonly occurs acutely. In some patients, the onset is preceded by pre-sepsis — an alternation of febrile waves and periods of normal temperature (apyrexia).
The leading clinical feature is intoxication syndrome, which includes:
- Acutely developing fever (most commonly hectic or intermittent, less frequently continuous).
- "Shaking" chills upon temperature elevation and feelings of heat during its decline.
- Profuse sweating.
- Marked weakness (myasthenia), forcing the patient to remain bedridden even during periods of temperature normalization.
- Joint, muscle, and bone pain.
- Headache, insomnia, lethargy, or delirium.
In addition, a characteristic clinical sign is hepatosplenomegaly (enlargement of the liver and spleen). The patient's general condition deteriorates extremely rapidly.
Involvement of the skin and mucous membranes
Due to systemic microcirculatory disturbances, the skin acquires a pale-grey ("earthy") hue. In individuals with dark skin or mild jaundice, the color resembles "café au lait". Facial features become sharp, and the eyes and cheeks appear sunken.
Various rashes and trophic changes are typical:
- Hemorrhagic syndrome: ranging from small petechiae (including in the conjunctiva) to large ecchymoses. Caused by systemic vasculitis with fibrinoid necrosis.
- Pustular rash: pustular elements are painless, lack infiltration, and are surrounded by a thin rim of hyperemia.
- Trophic disorders: in the acute course, pressure ulcers, bullae, and foci of dry necrosis rapidly form.
In the area of the entry portal (primary focus), sluggish healing is observed: granulations become pale and bleed, the discharge becomes turbid and foul-smelling, and the base is covered with a necrotic coating.
Organ pathology: respiratory system and central nervous system
The respiratory system reacts to microcirculatory disturbances among the first. Increased permeability of the air-blood barrier leads to fluid transudation into the interstitium and alveoli.
Acute respiratory distress syndrome ("shock lung") develops. Clinically, this manifests as tachypnea (shortness of breath), nasal flaring, and cyanosis. Septic multisegmental pneumonia with early tissue destruction is possible, while physical and radiological findings often lag behind the clinical picture.
Central nervous system involvement presents as toxic encephalopathy (neurotoxicosis), arising from thromboembolism and hemorrhages in brain tissue. Patients may be agitated or lethargic, with altered consciousness, infectious psychoses, or coma. In severe cases, septic meningoencephalitis with focal neurological signs develops.
Cardiovascular disorders
Hemodynamic disturbances manifest as arterial hypotension, tachycardia, muffled heart sounds, and weakened pulse. Toxic endomyocarditis, arteritis, and thrombophlebitis frequently develop.
With the development of septic (bacterial) endocarditis, the infection affects the valvular apparatus. In this case, loud murmurs are auscultated, the intensity and timbre of which may change throughout the day. Myocarditis leads to cardiac enlargement and displacement of the apex beat to the left. An important pathognomonic sign of subacute and protracted endocarditis is Osler's nodes — the result of microembolism of the vessels in the palms.
Briefly: answers to topical questions
What clinical and laboratory criteria are included in the SOFA score for diagnosing sepsis?
To assess organ dysfunction using the SOFA score, 6 organ systems are evaluated. The criteria of the score include:
- Respiratory system — PaO2/FiO2.
- Coagulation system — platelet count.
- Liver — bilirubin level.
- Cardiovascular system — mean arterial pressure and/or need for vasopressors.
- Central nervous system — Glasgow Coma Scale score.
- Kidneys — creatinine and/or urine output.
Which microorganisms are most commonly the causative agents of sepsis?
Sources indicate that causative agents of sepsis can be gram-positive and gram-negative microorganisms. It is also noted that particularly dangerous infections — plague, anthrax, glanders — frequently present in the form of sepsis.
For bacterial (septic) endocarditis as a form of sepsis, the most commonly indicated pathogens are:
- white and golden staphylococci;
- alpha-hemolytic streptococcus (Streptococcus viridans);
- Escherichia coli;
- Pseudomonas aeruginosa;
- Proteus;
- Klebsiella.
In the clinical case of surgical sepsis, Staphylococcus aureus (Staphylococcus aureus) is highlighted.
Which laboratory markers (biomarkers) are used to confirm sepsis?
For the laboratory assessment of inflammatory changes and suspected sepsis, the sources indicate the following parameters:
- C-reactive protein (CRP) — exceeds the upper limit of normal by more than 2 standard deviations.
- Plasma procalcitonin — exceeds the upper limit of normal by more than 2 standard deviations.
- Presepsin — indicated as a marker of sepsis.
- Lactate — a level > 2 mmol/L indicates impaired tissue perfusion.
At the same time, sources explicitly state that no single biomarker has sufficient accuracy for diagnosing sepsis.
The tetrad of lesions in bacterial septic endocarditis is Vascular-Valve-Kidney-Spleen (KVPS): Valves, vAsculitis, Kidneys, Spleen.
Class and exam questions
Why are there no purulent metastases in septicemia?
It is believed that purulent metastases do not have time to develop due to the rapid course of the process, or the body completely loses the ability to mount a leukocytic reaction. In essence, septicemia proceeds like infectious-toxic shock.
What kind of spleen is characteristic of sepsis?
A "large septic spleen" is formed — it is flabby, hyperplastic, with pronounced leukocytosis and yields a profuse pulp scraping.
What are Janeway lesions and Lukin-Libman spots?
These are manifestations of hemorrhagic syndrome in septic endocarditis. Janeway lesions are petechiae on the skin and subcutaneous tissue, while Roth spots / Lukin-Liebmann spots are petechial hemorrhages in the conjunctiva.
What else to study on this topic
- Pathogenesis of hematogenous and lymphogenous metastasis
- Clinical and morphological features of septicopyemia
- Classification of sepsis by primary focus localization
- Morphological presentation of septic endocarditis
- Criteria for systemic inflammatory response syndrome (SIRS)
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