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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
Summary
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.
Introduction
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
01234
Respiratory system
PaO2/FiO2 [mm Hg (kPa)]≥ 400 (53.3)< 400 (53.3)< 300 (40)< 200 (26.7)< 100 (13.3)
Coagulation
platelets [× 103/μl]≥ 150< 150< 100< 50< 20
Liver
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
Kidneys
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
At the bedside, a clinician initiates the diagnostic process with the question: “is the patient in shock?”. The guidelines for the diagnosis of the septic shock define the basic elements of diagnosis, i.e. suspected or documen-ted infection with accompanying arterial hypotension and organ hypoperfusion (e.g. oliguria, impaired consciousness, impaired peripheral circulation, and an increase in blood lactate concentration). However, some parameters of the definition of shock have not been clearly defined, e.g. adequate fluid resuscitation, no vasopressors, and threshold blood pressure. The recently published consensus of the European Society of Intensive Care Medicine (ESICM) suggest the possibility of a shock in the absence of arterial hypotension. Currently, there is no reference, bedside standard for diagnosing shock. The results of observational studies report a high mortality rate (from 29% to 46%) due to the imprecise diagnosis of shock (12). If the diagnosis of septic shock is made, the clinician must ask himself a question: “what is the reason for the patient’s current state?”. The identification of risk factors forces to take immediate action. Multiple biomarkers and molecular diagnostic tests are performed in parallel with blood culture in order to differentiate sterile inflammatory process from a similar pathophysiological process related to infection. Patients in septic shock present with impaired myocardial contractility in about 30% of cases. A quick evaluation of the underlying mechanism of shock is of paramount importance, as the delay in adequate treatment worsens patient’s condition. Hemodynamic monitoring may help explain the patophysiological phenomena that are characteristic for septic shock. Clinical application of specialized monitoring equipment may depend on the hardware, built-in algorithms of the device, and static/dynamic target of the parameter. There is ongoing discussion concerning the usefulness of the devices in the diagnosis and treatment of septic shock.
Invasive hemodynamic monitoring

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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
Strona internetowa czasopisma New Medicine