Pathogenesis and hemodynamic disorders
Normally, the body responds to infection locally: T cells, macrophages, leukocytes, and platelets are activated. Only a small amount of cytokines enters the bloodstream, maintaining a balance between pro-inflammatory and anti-inflammatory mediators. Adaptive mechanisms are triggered: the bone marrow increases leukocyte production, the liver synthesizes acute-phase proteins, and body temperature rises.
If anti-inflammatory mechanisms are insufficient, the process takes a pathological course. There is a massive release of pro-inflammatory cytokines into the systemic circulation. They have a destructive effect on the vascular endothelium, leading to the release of a huge amount of nitric oxide, a most potent vasodilator. As a result, the permeability of the vascular wall is impaired, microcirculation suffers, and DIC (disseminated intravascular coagulation) is triggered.
Development of shock and target organ damage
Bacterial toxins exacerbate the hemodynamic catastrophe. Selective venular spasm occurs, which, along with progressive DIC, leads to blood sequestration in the microvasculature.
Due to high vascular permeability, the liquid portion of the blood, and subsequently formed elements, transudate into the interstitial space. Circulating blood volume (CBV) drops precipitously. Hypovolemia develops, and blood return to the heart decreases. Despite compensatory tachycardia, cardiac output drops, which manifests as a persistent decrease in blood pressure.
Impaired tissue perfusion causes acute hypoxia and profound tissue acidosis. Pathogen toxins and oxygen starvation disrupt organ function up to necrosis. Severe morphofunctional changes in vital organs develop: shock lung, shock kidney, and shock uterus.
Modern diagnostic criteria
Modern diagnostic approaches have been revised. Systemic inflammatory response syndrome (SIRS) and the presence of bacteria in the blood (bacteremia) are not mandatory signs of sepsis.
Establishing the diagnosis requires two mandatory criteria:
- Presence of a focus of infection.
- Signs of multiple organ dysfunction (SOFA score $\ge$ 2 points) or the presence of distant ischemic foci.
The SOFA score evaluates the function of key body systems using a number of parameters:
- Respiration: oxygenation index (p<sub>a</sub>O<sub>2</sub>/FiO<sub>2</sub>).
- Coagulation: platelet count.
- Liver: bilirubin concentration.
- Cardiovascular system: blood pressure levels and the need for vasopressors (dopamine, adrenaline, noradrenaline).
- CNS: level of consciousness on the Glasgow Coma Scale.
- Kidneys: creatinine level and daily diuresis.
Clinical presentation and laboratory markers
The clinical picture consists of symptoms of infection and organ dysfunction. The patient may present with fever (above 38.3 °C) with chills or, conversely, hypothermia (below 36 °C). Tachycardia, dyspnea, moist cough, intestinal paresis, and altered mental status are characteristic. An important sign is arterial hypotension (a drop in systolic BP below 90 mmHg, mean arterial pressure below 70 mmHg, or a drop in systolic pressure by 40 mmHg), which in the initial stages can be temporarily corrected by crystalloid infusion. Acute oliguria (diuresis less than 0.5 ml/kg/h for 2 hours) unresponsive to adequate fluid resuscitation is also noted.
Laboratory criteria include:
- Changes in the complete blood count (leukocyte formula): leukocytosis (over 12,000/L), leukopenia (less than 4,000/L), or a shift to the left (more than 10% immature forms).
- A twofold increase in C-reactive protein (CRP) and procalcitonin.
- Hyperglycemia (glucose greater than 7.7 mmol/L).
- Signs of renal and hepatic impairment: elevated creatinine (over 44.2 µmol/L) and bilirubin (over 70 µmol/L).
- Hyperlactatemia (lactate over 4 mmol/L).
- Markers of DIC: thrombocytopenia, prolonged aPTT (over 60 s), and increased INR (over 1.5).
For quick memorization of the mandatory criteria for sepsis, use the rule "OF": Focus of infection + Organ Failure (SOFA ≥ 2).
Class and exam questions
Is the presence of bacteria in the blood mandatory for diagnosing sepsis?
No, bacteremia is not a mandatory criterion. Its detection only confirms the diagnosis and helps the physician choose appropriate antibacterial therapy.
Why does blood pressure persistently drop in sepsis?
Due to a massive release of nitric oxide, sharp vasodilation occurs. Fluid moves into the interstitium, circulating blood volume drops, and cardiac output decreases even against the background of pronounced tachycardia.
Which organs are primarily affected in septic shock?
Due to acute hypoxia, tissue acidosis, and the action of bacterial toxins, necrotic changes develop. The so-called shock lung, shock kidney, and shock uterus are formed.
What else to study on this topic
- A detailed analysis of parameters and scoring according to the SOFA scale.
- Mechanisms of DIC development against the background of endothelial dysfunction.
- Pathophysiology of tissue acidosis and hypoxia in septic shock.
- Differential diagnosis of systemic inflammatory response syndrome (SIRS) and sepsis.
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