What are the general diagnostic criteria for septic shock?

Septic shock is a clinical emergency that affects more than 230,000 patients each year in the United States. So what are the general diagnostic criteria for septic shock?

Hemodynamic monitoring for diagnosis of septic shock

Hemodynamic monitoring devices can identify the main physiological manifestations of septic shock. The clinical role of these monitoring devices lies in the devices themselves, the algorithms associated with the devices, and the static/dynamic targets derived from the algorithms. Likewise, there is a lack of consensus and considerable debate regarding the clinical role of these devices.

Invasive hemodynamic monitoring

Decades ago, standard care for patients in shock included invasive monitoring devices such as a pulmonary artery catheter (PAC) or a continuous central venous oxygen saturation (ScvO2) catheter. PAC can estimate cardiac output and measure mixed venous oxygen saturation, which, combined with other parameters, can help to identify the cause of shock and potentially affect patient outcomes. A 2013 Cochrane review of 2923 general ICU patients (the proportion of patients with shock was not reported) found no difference in mortality between patients who received a PAC and those who did not. A secondary analysis of the Fluid and Catheter Treatment Trial, which enrolled 774 patients with acute respiratory distress syndrome (ARDS), demonstrated that PAC increased hospital costs in 40% of patients with shock but did not result in a change in mortality. Continuous ScvO2 monitoring catheters can be an alternative to PACs, but in a recent RCT validating resuscitation in septic shock, they did not show an advantage over lactate clearance (Table 2). There is a consensus recommendation that PAC placement is not routinely used in the treatment of patients with shock and is recommended only in a few cases with combined right ventricular dysfunction or severe ARDS. The use of PACs in the United States has declined significantly over the past 15 years.

Non-invasive hemodynamic monitoring

The use of minimally invasive or noninvasive techniques, such as arterial pulse contour analysis or goal-directed cardiac ultrasound, can further elucidate the physiology of shock. Calibrated pulse contour analysis devices provide continuous measurement of cardiac output, beat-to-beat stroke volume, pulse pressure variability, and other parameters. In one study, 388 hemodynamically unstable patients from 31 ICUs were randomized to either 24-hour minimally invasive hemodynamic monitoring or conventional monitoring. There was no treatment plan related to the monitoring device, and there was no difference between the intervention group and the control group in the reversal rate of hemodynamic instability within 6 hours or the mortality rate. Two small randomized trials also found that pulse contour analysis-guided treatment strategies did not improve 28-day mortality or time to shock resolution compared with other strategies. Existing studies are verifying the effectiveness of noninvasive stroke rate variability monitoring to guide fluid resuscitation in septic shock. A recent systematic review did find benefit from pulse contour analysis to optimize hemodynamics in patients undergoing high-risk surgery. The use of pulse contour analysis in patients in shock outside the operating room is somewhat limited because it requires controlled ventilation, a satisfactory arterial pressure waveform, and the absence of arrhythmias.

Targeted ultrasound can help clarify the central hemodynamic status and the etiology of shock in unclassified patients. It reveals right and left heart chamber size and contractility, pericardial effusion, and the diameter and collapsibility of the inferior vena cava, which indicates hypovolemia, among other features. At the time of publication, our search found no powered RCTs showing that targeted ultrasound changes patient-related outcomes in patients with septic shock. However, recent guidelines and consensus opinions recommend that targeted ultrasound is the best clinical tool for the initial evaluation of hemodynamically unstable patients with septic shock (Table 2).

Tissue damage markers

Systemic markers of local tissue damage include blood lactate levels, alkali excess, tissue oxygen saturation measured by near-infrared spectroscopy, or various microcirculatory changes, which can indicate the presence of shock in the body. These examinations can not only refine the clinical diagnosis of shock, but also serve as observation indicators for the optimization and stabilization stages of shock (Table 2). Currently, lactate was not included in the 2001 ESICM/SCCM (Society of Critical Care Medicine) consensus on the definition of septic shock, but was proposed in the 2014 ESICM expert consensus on circulatory shock. Although continuous blood lactate measurement has become widely used in practice, its specific threshold for diagnosing shock and its role in monitoring remain unclear. In an open-label randomized clinical trial conducted in 4 ICUs, a regimen that aimed to reduce lactate levels by 20% every 2 hours in addition to guideline-based resuscitation was tested; only the secondary outcome (ICU length of stay) was significantly reduced, but too few patients with shock were included (19%). At the time of our review, no clinical trials that included patient-centered outcome measures were conducted to evaluate the use of near-infrared spectroscopy or tissue oxygen saturation in the diagnosis or management of septic shock.

Uncertain areas

From a biological perspective, there is no perfect definition or cutoff for shock, and guidelines, quality improvement, and trial registries should have a unified definition that balances sensitivity and specificity (Box). Not all patients with shock have typical clinical presentations, but atypical presentations may be just as important. For example, a patient with normal blood pressure and elevated blood lactate may have a prognosis similar to that of a typical shock patient, but hyperlactatemia may be caused by hypoxia-induced microcirculatory insufficiency, inflammatory response-induced accelerated glucose catabolism, or impaired lactate clearance. The host response to shock is also complex, including both pro-inflammatory and anti-inflammatory responses at the local and systemic levels. Although these are not widely accepted, they can be further clarified through biological phenotypes. Some candidate approaches include immunophenotyping, genome-wide expression mosaics, or clinical-metabolomics approaches. Third, a consensus on the definition of shock is that it needs to be applied across different phases of care (eg, from prehospital to emergency department to ICU). Uncertainty regarding optimal treatment has arisen because of differences in lactate and shock criteria used by various institutions in major trials.