What are the three stages of sepsis


from Greek: σήψη ("sipsi") - putrefaction
Synonym: blood poisoning (lay term)
English: sepsis

1 definition

The sepsis is a life-threatening multiple organ failure, which is a misdirected systemicUnderlying immune response triggered by infection with pathogens. These are mostly bacteria, but viruses, fungi or parasites can also be the cause.

2 background

The definition of sepsis is inconsistent and the subject of ongoing discussion. Older definitions of sepsis are mainly based on the detection of pathogens in the blood ("bacteremia"). According to the recommendations of a consensus conference of the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) in 1991, sepsis is present if there is a systemic inflammatory response syndrome (SIRS) and clinical or microbiological infection can be proven.

Schuster and Werdan (2005) define sepsis as follows: "Sepsis is the totality of life-threatening clinical symptoms and pathophysiological changes in response to the action of pathogenic germs and their products, which enter the bloodstream from a focus of infection, activate the large biological cascade systems and special cell systems and trigger the formation and release of humoral and cellular mediators ".[1]

The 2016 Sepsis 3 consensus suggested that sepsis is a life-threatening (multi) organ failure triggered by a misdirected host's immune response to infection. The definition moves away from the originally dominant SIRS criteria and is instead based on the SOFA score. By definition, sepsis must have increased the SOFA score by 2 or more points.[2][3]

3 classification

A basic distinction is made between:

A distinction can also be made according to the origin and type of sepsis:

4 pathophysiology

Sepsis occurs when pathogenic agents or their toxins enter the bloodstream. The body's immune system is normally able to prevent this life-threatening disorder, so that a certain constellation of favorable factors must usually first be present. They include, for example:

  • impaired immune defense
  • massive infection with a high number of pathogens
  • increased pathogenicity of the pathogen
  • Infection of poorly delimited body regions (e.g. abdomen)

In the initial phase of sepsis, there is an untreated one hypodynames Initial stage before ("cold shock"). Typical signs are hypotension, low cardiac output and increased systemic vascular resistance.

Inflammatory mediators then lead to vasodilation with a reduction in systemic resistance. This hyperdyname The shock stage leads to a relative intravascular volume depletion. In some cases, there is increased vascular permeability, which is associated with an additional absolute lack of volume. A compensatory increase in cardiac output is typical for this phase. However, the increased catecholamine level, the disturbed myocardial microcirculation and a reduced sensitivity of the cardiac β-receptors lead to a relative heart failure (acute septic cardiomyopathy).

In some of the patients, decompensation occurs in one of the sepsis hypodyne Shock phase: the cardiac output decreases, the vascular resistance increases again.

If left untreated, tissue hypoxia leads to (multi) organ failure, especially of the lungs, kidneys and liver, as a result of the microcirculation disorder.

5 pathogens

Sepsis can be triggered by a variety of different pathogens. The main bacteria responsible for sepsis are - sorted by frequency:

In immunosuppressed patients, the spectrum of pathogens in question is significantly larger, since microorganisms can also become pathogenic here, which do not play a role in immunocompetent people.

6 key symptoms

see also: SIRS, septic shock, bacteremia

7 Diagnosis

In addition to clinical and organ-specific examinations, diagnostics primarily include focus search and microbiology:

  • Blood cultures
  • Blood count, fibrinogen, Quick, PTT, creatinine, electrolytes, lactate, CK, GOT, amylase, lipase
  • Blood gas analysis

8 diagnostic criteria

Severe sepsis is when all of the following three criteria are met:[4]

8.1 Evidence of an infectious origin of the inflammation

It must at least one the following criteria must be met:

8.2 Detection of a systemic inflammatory host reaction (SIRS)

To have to at least two the following criteria must be met:

8.3 Infection-related organ dysfunction

It must at least one of the following criteria must be met

  • Acute encephalopathy (reduced vigilance, restlessness, disorientation, delirium without the influence of psychotropic drugs)
  • Thrombocytopenia (platelets <100,000 / µl or platelet drop> 30% in 24 hours without blood loss as the cause)
  • Arterial hypoxemia (paO2 <10 kPa (75 mmHg) in ambient air, paO2 / FiO2 <33 kPa (250 mmHg) without manifest pulmonary or cardiac disease as the cause)
  • Arterial hypotension (systolic arterial blood pressure <90 mmHg or mean arterial blood pressure <70 mmHg for at least 1 hour despite adequate volume supply in the absence of other causes of shock)
  • Renal dysfunction (urine excretion <0.5 ml / kg / hour for at least one hour despite sufficient volume substitution and / or increase in serum creatinine> 2x above the reference range of the respective laboratory
  • Metabolic acidosis (base deficit> 5.0 mEq / l or a plasma lactate concentration> 1.5x above the reference range of the respective laboratory)

9 course parameters

Important parameters in the course of sepsis include

10 therapy

Sepsis patients should be treated and monitored in intensive care. The so-called "sepsis bundles" summarize the most important measures:[5]

10.1 Initial circulatory stabilization

Electrolyte solutions are infused within the first three hours (at least 30 ml / kg body weight). The further volume application depends on the hemodynamics. A goal-oriented administration (early-goal directed therapy, EGDT) of the 2012 guidelines (including ZVD 8 - 12 mmHg) is no longer required, as more recent studies have not been able to confirm the importance of EGDT.

10.2 Antimicrobial Therapy

Antimicrobial therapy should be started within the first hour after diagnosis of septic shock or severe sepsis. The test material for blood cultures (at least 1 blood culture from peripheral veins and one from each lumen of each vascular access older than 48 hours) and, if necessary, other cultures (e.g. urine, wound secretion, bronchial secretion) must before be won. Empirically, a broad-spectrum antibiotic is administered intravenously and / or antimycotics or antivirals. A therapy duration of 7 to 10 days is usually sufficient. Procalcitonin levels are helpful in identifying the possible end point of antimicrobial therapy.

10.3 Focus Control

Prompt diagnosis and elimination of the septic focus is critical. If intravascular catheters are a potential source of sepsis, they must be removed.

10.4 volume therapy

In the case of severe sepsis or septic shock, electrolyte solutions are recommended. HAES or gelatin are no longer used. If necessary, human albumin can also be given. The volume is given until the hemodynamics improve. Dynamic methods are suitable for assessment (e.g. stroke volume variation).

10.5 Vasopressors and inotropes

The goal is a mean arterial blood pressure of over 65 mmHg. Norepinephrine is used as the vasopressor of choice. If not enough, vasopressin can also be used. As a last resort, adrenaline is used. Dopamine is no longer recommended. If hypoperfusion persists despite volume and vasopressor administration, dobutamine can be considered.

10.6 Glucocorticoids

Low-dose hydrocortisone (200 mg / d IV) is only used for catecholamine-refractory septic shock. It has an anti-inflammatory effect and reduces the need for vasopressors. There is no recommendation for dexamethasone and high-dose glucocorticoids.

10.7 blood products

If the hemoglobin concentration is below 7.0 g / dl, red cell concentrates should be given (target Hb 7.0 - 9.0). Erythropoietin or antithrombin III are not recommended. Fresh Frozen Plasma is only suitable for bleeding or invasive procedures. Platelet concentrates come with a platelet count below 10,000 / mm3 or under 20,000 if there is a high risk of bleeding. In the case of active bleeding, surgery or invasive intervention, a platelet count of over 50,000 is required.

10.8 Other aspects

11 sources

  1. ^ Schuster HP, Müller-Werdan U: Definition and diagnosis of sepsis and multiple organ failure in Sepsis and MODS, Springer Verlag Berlin Heidelberg (2005)
  2. ^ Mervyn S et al .: The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA. 2016; 315 (8): 801-810. doi: 10.1001 / jama.2016.0287
  3. ↑ Epidemiological Bulletin, RKI, 9/2017
  4. ↑ Sepsis Working Group of the European Society of Intensive Care Medicine: Catalog of criteria for the diagnosis of sepsis at the German Sepsis Society e.V.
  5. ↑ Surviving Sepsis Campaign (SSC) International Guidelines for Management of Sepsis and Septic Shock 2016, accessed on July 9, 2019