What is septicemia

SIRS and sepsis

This article takes into account the guidelines that can be viewed on the AWMF. You can consult the version of the guideline available at the time this article was published.

Table of Contents

Image: “Sepsis Steps” by Hadroncastle. License: CC BY-SA 4.0


Activation of the cell systems and release of cellular mediators in sepsis

Sepsis is the term used to describe all life-threatening clinical symptoms that arise as a reaction to pathogenic germs and their products that penetrate the bloodstream from the focus of infection. They activate cascade systems and special cell systems and trigger the formation and release of cellular mediators.

In order to create a basis for clinical and epidemiological studies, the clinical pictures SIRS, sepsis, severe sepsis and septic shock are uniformly defined.

Systematic Inflammatory Response Syndrome

As systemic inflammatory response syndrome, short SIRS, is the name given to the first stage, which is independent of the triggering agent. For the diagnosis of SIRS, at least 2 of the following criteria must be present:

  • Fever> 38 ° C or hypothermia <36 ° C in the rectal or invasive measurement
  • Tachycardia with a heart rate> 90 / min
  • Tachypnea with a frequency> 20 / min or hyperventilation with a PCO2 <33 mmHg
  • Leukocytosis with> 12,000 / mm³ or leukopenia <4,000 / mm³ or> 10% immature neutrophils in the blood

For diagnosis sepsis must also have one infectious genesis are present. This means that an infection must be present via microbiological evidence or based on clinical criteria.

Note:As soon as SIRS is triggered by an infection, it is a question of sepsis. It is sufficient that an infection can be assumed to be the trigger.

Acute organ dysfunction in severe sepsis

As severe sepsis applies to every sepsis with at least one acute organ dysfunction consists. Acute organ dysfunctions include:

  • Acute encephalopathy with reduced vigilance, restlessness and disorientation
  • Arterial hypotension with systolic blood pressure> 90 mmHg or MAP <70 mmHg for at least 1 hour despite adequate fluid intake and exclusion of other causes of shock
  • Relative or absolute thrombocytopenia, i.e. a drop in platelets by more than 30% within 24 hours or a platelet drop <100,000 / mm³ (thrombocytopenia due to bleeding must be excluded)
  • Arterial hypoxemia with PaO2 <75 mmHg in ambient air or a PaO2 / FiO2 ratio of <250 mmHg with oxygen therapy (heart and lung diseases must be excluded as the cause of the hypoxemia.)
  • Renal dysfunction with a diuresis rate of <0.5 ml / kg / h for at least 2 hours in spite of sufficient volume administration or an increase in serum creatinine twice over the local creatinine limit range
  • Metabolic acidosis with a base excess <-5 mmol / l or a lactate concentration> 1.5 times above the local reference range

The septic shock

The septic shock is defined as sepsis with a for Systolic blood pressure of <90 mm Hg or MAP <70 mm Hg sustained for at least 2 hours or vasopressin replacement to raise blood pressure above these levels. The hypotension persists despite volume administration and cannot be explained by any other form of shock.

The PIRO concept

The PIRO concept is the attempt to further develop the above consensus criteria for sepsis. In analogy to the TNM classification of malignant tumors, a classification of sepsis has been proposed.

P stands for predisposition, I. For infection, R. For inflammatory response and O For Organ dysfunction. This classification can be used to stratify the risk of sepsis.

Other important terms are:

  • Bacteremiais the presence of facultative pathogenic bacteria in the bloodstream without circulatory involvement and other signs of intoxication.
  • Endotoxinemia is defined as the presence of endotoxins in the blood even without simultaneous bacteremia. Lipopolysaccharides from the membrane of gram-negative bacteria act as endotoxins.
  • Septicemia is the intoxication of the whole organism by microorganisms, endotoxins, toxins and pyrogens.
  • With acute decrease in O2-Supply of vital organs with functional and structural changes, one speaks of septic-toxic shock. It can lead to multiple organ failure within a very short time.


Increasing incidence of sepsis

The incidence of sepsis is on average in the European area 5 illnesses per 1,000 hospital patients indicated and increasing steadily. The reasons for the increasing incidence are more invasive examination techniques, which represent a gateway for pathogenic germs, as well as the increase in the survival rate of patients with chronic diseases such as malignancies, liver diseases and HIV.

The treatment costs of a patient with sepsis are around € 23,000 and account for almost 40% of the total costs of intensive care medicine in Germany.


Cause of sepsis syndrome

The sepsis syndrome arises on the basis of a predisposing immune deficiency in diseases such as general infection, trauma and extensive operations, intoxication, chemotherapy, after splenectomy (OPSI = overwhelming postsplenectomy infection) and amicrobial inflammation.

Before antibiotics were used, streptococci were the most important pathogen in septic processes. Today one finds more gram negative bacteriaand staphylococciwhich is due to the years of use of antibiotics effective against gram-negative bacteria in intensive care medicine and the resulting development of resistance.

With 25% is Escherichia coli today the bacterium most frequently isolated from blood cultures of septic patients. Staphylococcus aureus with 20%, Staphylococcus epidermidis (8%), enterococci, Klebsiella and pseudomonads are also common. The most common sources of infection are the Peritonitis, pneumonia, meningitis and Operating areas. In intensive care patients, bacteria can also enter the body through other ports such as intravenous and intra-arterial catheters, peritoneal dialysis and ventilation tubes.


Hypodynamic stage of sepsis

This is in the outer membrane of gram-negative bacteria Lipopolysaccharide, short LPS, embedded. After bactericidal antibiosis or when the bacteria multiply on a massive scale, the LPS and thus proinflammatory potential is released into the circulation.

In the untreated early phase of sepsis there is often one hypodynamic stage in front. This phase is defined by Hypotension, low cardiac output, and increased systemic resistance and will too cold shock called. In this phase, adequate volume substitution is most important, as circulatory shock is responsible for around 40% of deaths from sepsis.

Note:The untreated early phase of sepsis (hypodynamic form) should not actually occur, since adequate volume substitution must always take place.

Hypodynamic initial stage of sepsis

Arterial and venous vasodilation is then triggered by mediators, which leads to system arterial hypotension with relative intravascular volume deficiency due to reduced systemic vascular resistance and venous pooling. One speaks of hyper dynamic initial stage.

If a capillary leak syndrome with increased vascular permeability occurs, it is an absolute volume deficiency. Typical for this phase is a increased cardiac output, whereby the hypovolemia can be temporarily compensated. As a result of this hypocirculation, the blood is only slightly depleted of O2 and the mixed venous O2 saturation is high (SvO2> 80%).

Even at this stage, there is also a reduced myocardial contactility, recognizable from the fact that the measured increase in cardiac output does not correspond to the extent of the reduced systemic vascular resistance. This is due to various mediators such as TNF-α and endotoxins. The permanently increased plasma catecholamine levels as well as the disturbed myocardial microcirculation also ensure a reduced sensitivity of the cardiac β-receptors. The relative heart failure in septic syndrome is also called acute septic cardiomyopathy designated.

Hypodynamic shock phase of sepsis

In some of the patients, hypercirculation at a later point in time suggests a decompensation of the body's own mechanisms that regulate homeostasis hypodynamic shock phase around. The cardiac output decreases again, the resistance increases again. With sufficient volume substitution, however, the hyper-dynamic circulatory constellation is maintained in most patients, often even into the final phase.

Even in the hyperdynamic phase, however, functional restrictions of vital organs can lead to organ failure. The blood is drawn into the organs by failure of the arteriolar vasomotion, that is, the rhythmic contraction and dilatation of the arterioles. As a result, arteriovenous shunts open, which are then increasingly perfused. This in turn leads to Tissue hypoxia and nutritional disorders.

Clinical studies have shown that systemic oxygen consumption is reduced, while the oxygen supply is generally increased as a result of septic hypermetabolism. But even with low avDO2 values, adequate cellular oxygenation should not be assumed, because in septic syndrome there is an oxygen utilization disorder at the mitochondrial level. The affinity of hemoglobin for oxygen is also increased, so that it is more difficult for the oxygen to be delivered to the tissue.

The The core problem of sepsis syndrome isthus the microcirculation disorderwhich persists despite the counter-regulation of the circulatory system. If left untreated, tissue hypoxia leads to single or multiple organ failure, which is associated with a mortality of 50 - 80%. In the Timing of the MOF (Multi Organ Failure) here stands the lung first of all, followed by kidney and liver.


Clinical parameters and markers of sepsis

The picture of sepsis is initially characterized by a germ invasion. It comes to acute deterioration in general condition With fever and in around a third of patients with chills. There is one in the blood count Leukocytosis, whereby leukopenia is primarily possible. The differentiation from the SIRS is only possible through the detection of a sepsis lesion or a source of infection.

Germ invasionFever, chills, bacteremia, red, warm, dry skin or pale, cold, clammy skin, petechial bleeding
HemodynamicsTachycardia, drop in blood pressure (especially diastolic value)
CoagulationPlatelet fall, coagulation factors drop
Organ dysfunctionTachypnea (PO2 and PCO2 decrease), restlessness, confusion, renal / hepatic insufficiency, encephalopathy, respiratory insufficiency, myocardial insufficiency


The usual clinical parameters such as body temperature, leukocyte and platelet count and parameters of the coagulation system (Quick, PTT) are usually unable to correctly depict the extent of the complexity of the inflammatory process. For this reason, further laboratory parameters must be determined. Count among them IL-6 and IL-8 as pro-inflammatory mediators.

That too Lipopolysaccharin binding protein (LBP) and C-reactive protein (CRP) can be used for assessment. In which Procalcitonin Mostly preferred to CRP because it only becomes highly positive with bacterial infection, while CRP also increases with other causes of SIRS, such as pancreatitis, burns, and major trauma. In addition, procalcitonin allows a more significant prediction of the severity of the infection.

Also the neurohumoral markers ANP (atrial natriuretic peptide) and the BNP / NT per BNB (brain natriuretic peptide) can be increased in patients with septic shock, whereby the BNB increase is an expression of cardiac dysfunction.

The Lactic acidosis is a sign of tissue hypoxia.

Note:The standard parameters such as Quick, PTT, white blood cell count and platelet count should not be underestimated in daily clinical work, as they have an indicator function.

Microbiological diagnostics

Although Blood cultures are positive in only around 12-20% of bacteremia, they are essential for the detection of germs in suspected sepsis. If the fever rises (usually if the temperature is above 38.5 ° C), they should be removed under sterile conditions before the start of antibiotic treatment.

The minimum is to fill one aerobic and one anaerobic culture bottle with about 10 ml of blood, whereby usually 3 pairs of blood culture bottles are taken from different veins (or for example from a CVC or port and peripheral veins). In the case of unfavorable vascular conditions or centralization, the femoral vein or artery can also be punctured. If the patient is already on antibiotic therapy, cultures should be taken during the therapeutic trough level. For this purpose there are also extra blood culture bottles, which contain exchange resins that bind the antibiotics and thus render them ineffective.

Image: “Blood culture tubes: orange label for anarobes, blue label for aerobes, and yellow label for pediatrics” by James Heilman. License: CC BY-SA 3.0

Depending on the clinical picture, more should of course also be used Samples such as urine, liquor or bronchial secretions obtained and examined microbiologically.

Note:The more and more frequently samples are taken, the greater the chance of detecting pathogens.

The focus search always includes the physical examination, anamnesis and imaging diagnostics.

Clinical FindingsPossible cause of sepsis
Vitium-typical sound during cardiac auscultationEndocarditis
Pulmonary rattling noises / weakened auscultation findings on pulmonary examinationPneumonia, pleural empyema
Abdominal tenderness / flank painPancreatitis, cholecystitis, pyelonephritis
Abdominal defense tensionPeritonitis, pancreatitis
MeningismMeningitis, encephalitis
Redness, overheating, pain in the skinPhlegmon, abscess


Basic monitoring and extended monitoring are recommended for monitoring septic patients in the intensive care unit, especially for patients who are hemodynamically difficult to control. The extended hemodynamic monitoring includes transthoracic or transesophageal echocardiography for recording the left ventricular pump function.

Also a Pulmonary artery catheter should be used to determine cardiac output and systemic vascular resistance. Above all, they are also suitable PiCCO systems. They enable the measurement of cardiac output, extravascular lung water, intrathoracic blood volume and systemic vascular resistance by using a combination of arterial pulse contour analysis and transpulmonary indicator dilution methods. The sepsis guidelines by Dellinger et al. 2008 according to (Survival Sepsis Campaign) mainly owns the Oxygen saturation a high priority as a monitoring parameter.


Detection and removal of the sepsis

The basis of successful sepsis therapy is the detection of the sepsis and its removal. Abscesses have to be drained and infected foreign bodies removed. If it is assumed that a central venous catheter or port is colonized and is the focus, the Time to positivity used. If the blood culture from the central catheter is positive well before the culture from a peripheral vein, it can be assumed that the CVC is infected. If endoprostheses are infected, they must be removed in a new operation and, if necessary, replaced with spacers containing antibiotics.

The antibiotic therapy must be adapted to the focus and the expected range of germs. In the case of unknown sepsis, the antibiosis must cover all gram-negative and positive germs, including anaerobes. Often one happens Combination of broad-spectrum penicillins such as piperacillin or 3rd generation cephalosporins (such as cefotaxime with an aminoglycoside such as gentamycin). Therapy should start with intravenous antibiotics within the first hour after detection of severe sepsis and continue for 7-10 days.

If the septic course of the disease persists with the administration of antibiotics, a secondary infection, an infected foreign body, an infected thrombosis and abscesses must be excluded. It can also be a so-called drug fever act under medication.

In addition to the causal therapeutic measures, the rapid initiation of cardiovascular and organ-supporting supportive therapy is a decisive prognostic factor. In the early goal directed therapy he follows if sepsis is suspected, immediate volume therapy. In one study, mortality could be reduced by 16% compared to conventional intensive therapy.

Be used to replenish the intravascular volume Colloids or crystalloids used. Volume administration can result in a steady-state phase with hypercirculatory warm shock. In addition, a Catecholamine therapy with norepinephrine respectively.

Note:The sepsis guideline requires reaching the hemodynamic target corridors within the first 6 hours after diagnosis.

If circulatory failure is therapy-resistant despite high doses of noradrenaline, vasopressors such as Terlipressin can be used. The administration of dobutamine is indicated in patients with myocardial dysfunction.

Endotracheal intubation and ventilation may be necessary in support of respiratory insufficiency. As in up to 40% of patients with severe sepsis one acute respiratory distress syndrome (ARDS) ventilation should occur Lung protection with low tidal volumes occur, hypercapnia can be tolerated. A minimum of positive end-expiratory pressure (PEEP) should be used to prevent lung collapse. To avoid ventilator-induced pneumonia, patients should be positioned with the head of the bed raised at 45 °.

Due to the tissue hypoxia are Erythrocyte preparations to be transfused at hemoglobin levels below 7 g / dl. Correction of the coagulation factors is also advisable in the event of a deficiency.

The intensive insulin therapy to achieve normoglycemia in the sense of a Sepsis prophylaxis delivers surprisingly favorable results in postoperatively ventilated intensive care patients. In patients who are already septic, the benefit is controversial.

The general administration of immunoglobulins is not recommended, as there are no reliable prospective studies on this. Even the administration of high-dose glucocorticoids does not improve the survival rate in patients with sepsis. On the other hand, low-dose hydrocortisone in combination with catecholamines can buffer a disturbance of the hypothalamus-pituitary-adrenal cortex axis, which often occurs in the context of sepsis.

Note: Only norepinephrine is able to effectively raise systemic blood pressure. The guideline of the German Sepsis Society recommends avoiding dopamine as a vasopressor.


The time interval between the onset of the disease and the time of initiation of therapy or acute treatment within the first 24 hours have a decisive influence on the course and prognosis of sepsis. One speaks of the so-called golden hours. Similar to other emergency medical clinical pictures, e.g. myocardial infarction or apoplexy, only the immediate diagnosis and subsequent initiation of therapy can prevent the often fatal course of sepsis.

One of the main reasons for the unchanged high mortality rate of severe sepsis and septic shock, both in hospitalized patients and in patients admitted to the emergency room, is the late diagnosis and the resulting delay in treatment.

The MEDS score (Mortality-in-Emergency-Department-Sepsis-Score) is designed for use in the emergency room with suspected systemic infection. He aims Predictors of Increased Mortality to be identified in the initial phase of hospital treatment. It is also important, for example, to select patients who are clinically largely normal, but show a creeping septic course with global tissue hypoxia.

MEDS score based on Shapiro et al. 2003:

1.Terminal-stage disease (life expectancy <30 days)6 points
2.Respiratory failure (tachypnea, low oxygen saturation, high oxygen demand3 points
3.Septic shock (persistent hypotension with system RR <90 mmHg after the initial fluid challenge of 20-30 ml / kg body weight3 points
4.Platelets <150,000 / mm³3 points
5.Age> 65 years3 points
6.Infection of the lower respiratory tract2 points
7.Home residents2 points
8.reduced mental status2 points


While the mortality at 5 - 7 points is 3.3%, it is 10 times higher at 31.6% for 13 and more points.

In addition to the lethality predictors of the MEDS score, there are increased serum lactate concentration and a increased mixed venous oxygen saturation as an expression of a lack of tissue extraction, groundbreaking parameters of an early disturbed tissue oxygenation.

The Lethality the sepsis is total around 28%. It mainly depends on the age of the patient and is around 10% in children and 38% in those over 85 years of age.

Popular exam questions about sepsis

The solutions can be found below the references.

1. What does not belong to the diagnostic criteria of the SIRS?

  1. Fever> 38.5 ° C or hypothermia <36 ° C
  2. Heart rate> 90 / min
  3. Tachypnea> 20 / min
  4. Leukocytosis> 12,000 / mm³ or leukopenia <4,000 / mm³ or> 10% immature neutrophils in the blood
  5. Proven infection as the cause

2. A 66-year-old patient received a total hip replacement 5 days ago due to coxarthrosis on the left. Now the patient is feverish with temperatures of up to 39.2 ° C and becomes circulatory unstable. The surgical wound is very red and overheated. You suspect an infection and take several aerobic and anaerobic blood cultures and wound swabs. What then is decisive for a successful therapy of sepsis?

  1. Circulatory stabilization with the help of volume replacement therapy and norepinephrine
  2. Antibiosis with broad-spectrum antibiotics such as piperacillin in combination with gentamycin
  3. Surgical rehabilitation with wound debridement, jet lavage and removal of the populated endoprosthesis
  4. Intensified insulin therapy
  5. Administration of immunoglobulins, activated protein C and hydrocortisone

3. In the MEDS score, what is not one of the predictors associated with increased sepsis mortality?

  1. Age> 65 years
  2. Platelets <150,000 / mm³
  3. Home residents
  4. Age <5 years
  5. Respiratory failure
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J. Schulte am Esch et al .: MLP Duale Series - Anesthesia, Georg Thieme Verlag, 2007

C. Madler, K.-W. Jauch, K. Werdan: Acute Medicine - The First 24 Hours, Urban & Fischer, 2009

K. Reinhard: S2 guideline diagnosis and therapy of sepsis, Thieme, 2007

R. Beale, J. M. Janes et al .: Global utilization of low-dose corticosteroids in severe sepsis and septic shock: a report from the PROGRESS registry. In: Critical care (London, England). Volume 14, Number 3, 2010, p. R102, ISSN 1466-609X. doi: 10.1186 / cc9044. PMID 20525247. PMC 2911744

Prevention, diagnosis, therapy and aftercare of sepsis: 1. Revision of the S-2k guidelines of the Deutsche Sepsis-Gesellschaft e. V. (DSG) and the German Interdisciplinary Association for Intensive and Emergency Medicine (DIVI) In: Ger Med Sci. Volume 8, 2010, Doc14

E. Rivers, B. Nguyen, S. Havstad, J. Ressler, A. Muzzin, B. Knoblich, E. Peterson, M. Tomlanovich: Early goal-directed therapy in the treatment of severe sepsis and septic shock. In: The New England journal of medicine. Volume 345, Number 19, November 2001, pp. 1368-1377, ISSN 0028-4793. doi: 10.1056 / NEJMoa010307. PMID 11794169.

AWMF guideline sepsis

Solutions to the questions: 1E, 2C, 3D

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