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© Borgis - New Medicine 1/2017, s. 31-36 | DOI: 10.5604/01.3001.0009.7846
*Jacek Wadełek
Diagnosis and treatment of patients in septic shock
Department of Anaesthesia and Intensive Care, St. Anne’s Hospital of Traumatic Surgery, Mazovian Rehabilitation Centre “STOCER” GmbH in Warsaw, Poland
Head of the Department: Elżbieta Kurmin-Gryz, MD
Sepsis and septic shock are a clinical emergency. Sepsis is defined as a life-threatening organ dysfunction due to a dysregulated host response to infection, and organ dysfunction is defined as an acute change in Sequential Organ Failure Assessment (SOFA) score greater than 2 points secondary to an infectious cause. Septic shock is defined as sepsis with persisting hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mm Hg or higher, and blood lactate level greater than 2 mmol/l (18 mg/dl) despite adequate volume resuscitation. The diagnosis of septic shock begins with medical history and physical examination focused on the signs and symptoms of infection, with the aim of recognizing complex physiologic manifestations of shock. Clinicians should understand the importance of prompt administration of antibiotics, vasopressors and intravenous fluids aimed at restoring adequate circulation. They should also be aware of the limitations of the protocol-based therapy.

Shock is a life-threatening circulatory failure that leads to inadequate tissue perfusion. The most typical signs of shock is hypotension (systolic blood pressure below 90 mm Hg or mean arterial pressure below 65 mm Hg), accompanied by clinical signs of organ hypoperfusion (1-3). Historically, the signs and symptoms of shock were attributed to the response of the nervous system to trauma associated with vasomotoric changes and hypovolemia. In the mid-twentieth century, Blalock and Weil divided shock into following groups: cardiogenic, obstructive, hypovolemic, and angiogenic (4, 5). While this simplified division is valuable from the point of view of the professional training, diagnosing shock is much more complex. Currently, septic shock is the most common form of the non-cardiogenic shock, and it also includes some patophysiological characteristics described by Blalock and Weil. In February 2016, a new definitions of sepsis and septic shock were created. According to the definition, septic shock is a form of sepsis in which severe circulatory problems lead to the disruption of normal cellular metabolism (6). Septic shock also has a higher risk of death compared to other forms of sepsis (6). Septic shock is characterized by the need of administering vasopressors in order to maintain mean arterial blood pressure above 65 mm Hg in spite of adequate fluid therapy, and blood lactate level above 2 mmol/l. The prevalence of sepsis and septic shock is steadily growing globally. Septic shock occurs in more than 230,000 patients in the United States each year, and is a cause of 40,000 deaths annually (7). Primary risk factors for septic shock are the fifth reason of premature mortality in people of working age. Up to this day, sepsis was diagnosed when an infection resulted in the occurrence of at least two criteria for systemic inflammatory response (SIRS) (tab. 1) (8-10). Due to the fact that diagnosing sepsis based on two SIRS signs does not have sufficient sensitivity and diagnostic significance, the need for a new definition and diagnostic criteria was determined. In 2016, a new working group was appointed. The working group suggested to replace the concept of severe sepsis with the term sepsis, and to base the severity of organ failure on the Sequential Organ Failure Assessment (SOFA) score (9, 11) and its simplified version – quick SOFA (qSOFA) score (tab. 2) (10, 11). The existing definition of severe sepsis is included in table 3. (8, 10).
Tab. 1. Definitions and criteria of sepsis and septic shock (8-10)
TermsExisting (1991, 2001)Newly developed (2016)
SepsisSystemic inflammatory response syndrome (SIRS) due to infection
Life-threatening organ dysfunction caused by a dysregulated host response to infection. The response causes tissue and organ dysfunction (corresponds to the previous definition of severe sepsis)
Severe sepsisSepsis leading to organ failure or severe organ dysfunction (corresponds to the new definition of sepsis)Term no longer used
Organ dysfunction criteria
Used for the diagnosis of severe sepsis, presented in table 3.
Used for the diagnosis of sepsis, an acute change in total Sequential Organ Failure Assessment (SOFA) score equal to or greater than 2 points in case of suspected or diagnosed infection (tab. 2.)
Septic shockA type of severe sepsis with acute circulatory failure characterized by persistent hypotension despite adequate fluid therapy, requiring the use of vasopressors (systolic blood pressure < 90 mm Hg, mean arterial pressure < 65 mm Hg or a decrease in systolic blood pressure > 40 mm Hg
Sepsis in which circulatory, metabolic, and cellular disorders are so severe that they significantly increase mortality. Hypotension with elevated blood lactate level, persistent despite adequate fluid therapy and requiring the use of vasopressors in order to raise mean arterial pressure above 60 mm Hg (blood lactate concentration > 2 mmol/l = 18 mg/dl)
Scale recommended for the early identification of patients at higher risk of death
Imprecise: SIRS criteria, organ dysfunction and extended criteria for sepsis are all in useqSOFA score, two or more of the following signs:2. systolic arterial pressure ≤ 100 mm Hg
3. respiratory rate ≥ 22/min
Determination of the severity of the inflammatory responseSIRS, two or more of the following signs:
1. body temperature > 38 °C or < 36 °C
2. heart rate > 90/min
3. respiratory rate > 20/min or paCO2 < 32 mm Hg
4. white blood cells > 12,000/μl or < 4,000/μl or > 10% immature neutrophiles
Not specified. It has been concluded that inflammatory response was only one elements of the response to the infection and it is not the most important aspect of this response. It has been underlined that organ dysfunction significantly increases the risk of death
Tab. 2. Sequential Organ Failure Assessment (SOFA) score (10, 11)
Organ or systemScore
Respiratory system
PaO2/FiO2 [mm Hg (kPa)]≥ 400 (53.3)< 400 (53.3)< 300 (40)< 200 (26.7)< 100 (13.3)
platelets [× 103/μl]≥ 150< 150< 100< 50< 20
bilirubin [μmol/l (mg/dl)]< 20 (1.2)20-32 (1.2-1.9)33-101 (2.0-5.9)102-204 (6.0-11.9)> 204 (12)
Circulatory system
Mean arterial pressure OR administration of vasopressors [μg/kg/min] requiredMAP ≥ 70 mm HgMAP < 70 mm Hgdobutamine (any dose) or dopamine < 5norepinephrine ≤ 0.1 or epinephrine ≤ 0.1 or dopamine 5.1-15norepinephrine > 0.1 or epinephrine > 0.1 or dopamine > 15
Central nervous system
Glasgow coma scale1513-1410-126-9< 6
Serum creatinine [μmol/l (mg/dl)]< 110 (1.2)110-170 (1.2-1-9)171-299 (2.0-3.4)300-440 (3.5-4.9)> 440 (5.0)
Diuresis [ml/day]< 500< 200
Tab. 3. The classic diagnostic criteria of sepsis-related organ dysfunction (8, 10)
1) tissue hypoperfusion associated with sepsis or
2) organ(s) dysfunction caused by infection, i.e. ≥ 1 of the following:
a) hypotension caused by sepsis
b) blood lactate above the upper limit
c) diuresis < 0.5 ml/kg/h for > 2 h despite adequate fluid therapy
d) PaO2/FiO2 < 250 mm Hg, if lungs are not the source of the infection, and < 200 mm Hg, if the lungs are the source of the infection
e) serum creatinine > 176.8 μmol/l (2 mg/dl)
f) serum billirubin > 34.2 μmol/l (2 mg/dl)
g) platelets < 100 000/μl
h) International Normalized Ratio > 1.5)
Advances in diagnostic process of septic shock
The diagnosis of septic shock is multifactorial and includes: an initial assessment of the etiology and clinical signs and symptoms, of the hemodynamic parameters, of the cellular changes, and of the grade of tissue dysfunction.
Initial assessment

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1. Vincent JL, De Backer D: Circulatory shock. N Engl J Med 2013; 369: 1726-1734.
2. Antonelli M, Levy M, Andrews PJ et al.: Hemodynamic monitoring in shock and implications for management. International Consensus Conference. Intens Care Med 2007; 33: 575-590.
3. Dellinger RP, Levy MM, Rhodes A et al.: Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock, 2012. Intens Care Med 2013; 39: 165-228.
4. Millham FH: A brief history of shock. Surgery 2010; 148: 1026-1037.
5. Weil MH, Shubin H: Proposed reclassification of shock states with special reference to distributive defects. Adv Exp Med Biol 1971; 23: 13-23.
6. Seymour CW, Rosengart MR: Septic Shock: Advances in Diagnosis and Treatment. JAMA 2015; 314: 708-17.
7. Murray CJ, Atkinson C, Bhalla K et al.: US Burden of Disease Collaborators. The state of US health, 1990-2010: burden of diseases, injuries, and risk factors. JAMA 2013; 310: 591-608.
8. Levy MM, Fink MP, Marshall JC et al..: International Sepsis Definitions Conference. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intens Care Med 2003; 29: 530-538.
9. Singer M, Deutschman CS, Seymour CW et al.: The third international consensus definitions for sepsis and septic shock (Sepsis-3). JAMA 2016; 315: 801-810.
10. Vincent JL, Moreno R, Takala J et al.: Working Group on Sepsis-Related Problems of the European Society of Intensive Care Medicine. The SOFA (Sepsis-related Organ Failure Assessment) score to describe organ dysfunction/failure. Intens Care Med 1996; 22: 707-710.
11. Angus DC, Seymour CW, Coopersmith CM et al.: A Framework for the Development and Interpretation of Different Sepsis Definitions and Clinical Criteria. Crit Care Med 2016; 44: 113-121.
12. Shankar-Hari M, Deutschman CS, Singer M: Do we need a new definition of sepsis? Intens Care Med 2015; 41: 909-911.
13. Dellinger RP, Carlet JM, Masur H et al.: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004; 32: 858-873.
14. Caironi P, Tognoni G, Masson S et al.: Albumin replecement in patients with severe sepsis or septic shock. N Engl J Med 2014; 370: 1412-1421.
15. Annane D, Siami S, Jaber S et al.: Effects of fluid resuscitation with colloids vs crystalloids on mortality in critically ill patients presenting with hypovolemic shock: the CRISTAL randomized trial. JAMA 2013; 310: 1809-1817.
16. Perner A, Haase N, Guttormsen AB et al.: Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 2012; 367: 124-134.
17. Myburgh JA, Finger S, Bellomo R et al.: Hydroxyethyl Starch or Saline for Fluid Resuscitation in Intensive Care. N Engl J Med 2012; 367: 1901-1911.
18. Oba Y, Lone NA: Mortality benefit of vasopressor and inotropic agents in septic shock: a Bayesian network meta-analysis of randomized controlled trials. J Crit Care 2014; 29: 706-710.
19. The ProCESS Investigators: A Randomized Trial of Protocol-Based Care for Early Septic Shock. N Engl J Med 2014; 370: 1683-1693.
20. The ARISE Investigators and the ANZICS Clinical Trials Group: Goal-Directed Resuscitation for Patients with Early Septic Shock. N Engl J Med 2014; 371: 1496-1506.
21. The ProMISe Trial Investigators: Trial of Early, Goal-Directed Resuscitation for Septic Shock. N Engl J Med 2015; 372: 1301-1311.
22. The SEPSISPAM Investigators: High versus Low Blood-Pressure Target in Patients with Septic Shock. N Engl J Med 2014; 370: 1583-1593.
23. The TRISS Trial Group and the Scandinavian Critical Care Trials Group: Lower versus Higher Hemoglobin Threshold for Transfusion in Septic Shock. N Engl J Med 2014; 371: 1381-1391.
otrzymano: 2017-01-19
zaakceptowano do druku: 2017-02-09

Adres do korespondencji:
*Jacek Wadełek
Department of Anaesthesia and Intensive Care, St. Anne’s Hospital of Traumatic Surgery, Mazovian Rehabilitation Centre “STOCER” GmbH,
Warsaw, Poland
16/20 Barska Str., 02-315 Warsaw, Poland
tel. +48 22 579 52 58
e-mail: WAD_jack@poczta.fm

New Medicine 1/2017
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