SIRS/Sepsis/MODS

Question 1

According to Zahar et al. (2011), how do pathogen species and infection site influence mortality in severe sepsis and septic shock?

Answer 1

Neither pathogen species nor infection site significantly predicted mortality; host factors like age, severity scores, organ dysfunction, and comorbidities were stronger predictors.

Question 2

According to Zahar et al. (2011), what clinical implications arise from the finding that pathogen type does not predict mortality?

Answer 2

Emphasize early recognition, resuscitation, and organ support rather than focusing solely on the infecting pathogen; antimicrobial therapy remains important for bacterial clearance but prognosis depends largely on host response.

Question 3

What limitations did Zahar et al. (2011) acknowledge in their study on sepsis outcomes?

Answer 3

Observational design, potential unmeasured confounders, and heterogeneous patient population.

Question 4

According to Baron et al. (2013), what are best practices for blood culture collection in suspected sepsis?

Answer 4

Obtain at least two to three sets from separate venipuncture sites before antibiotics, ensure adequate volume, use proper labeling, and optimize transport and handling to maximize yield and minimize contamination.

Question 5

According to Baron et al. (2013), which organisms commonly represent skin contaminants in blood cultures?

Answer 5

Coagulase-negative staphylococci, Corynebacterium spp., Bacillus spp.; growth in only one culture set may suggest contamination rather than true bacteremia.

Question 6

What is the importance of the “pre-analytical phase” in microbiologic testing, according to Baron et al. (2013)?

Answer 6

It includes test selection, specimen collection, handling, and transport; this phase is the most error-prone and crucial for diagnostic accuracy.

Question 7

According to Drewry et al. (2017), what is the impact of fever and antipyretic therapy on mortality in septic patients?

Answer 7

Fever is associated with improved survival; routine antipyretic therapy showed no mortality benefit and may trend toward harm, so fever suppression should be individualized.

Question 8

According to Henning et al. (2017), what clinical outcome is associated with absence of fever in emergency department patients with suspected septic shock?

Answer 8

Afebrile patients had significantly higher in-hospital mortality and received delayed antibiotics and fluids, suggesting fever absence is a poor prognostic marker.

Question 9

What are the 5 components of the 1-hour Surviving Sepsis Campaign (SSC) bundle as updated by Levy et al. (2018)?

Answer 9

1) Measure lactate, 2) Obtain blood cultures before antibiotics, 3) Administer broad-spectrum antibiotics, 4) Administer 30 mL/kg crystalloid for hypotension or lactate ≥4 mmol/L, 5) Apply vasopressors if hypotensive after fluids to maintain MAP ≥65 mmHg.

Question 10

According to Singer et al. (2016) (Sepsis-3), how is sepsis defined?

Answer 10

Life-threatening organ dysfunction caused by a dysregulated host response to infection.

Question 11

What are the two main types of lactic acidosis seen in sepsis, as described by Suetrong and Walley (2016)?

Answer 11

Type A (due to tissue hypoxia and anaerobic metabolism) and Type B (due to impaired lactate clearance or increased aerobic glycolysis).

Question 12

According to Koenig & Verlander (2015), how does peritoneal fluid glucose measurement aid in diagnosing septic peritonitis in dogs?

Answer 12

A blood-to-peritoneal fluid glucose difference >20 mg/dL is highly sensitive and specific for septic peritonitis, reflecting bacterial consumption of glucose.

Question 13

What is the physiological basis for using vasopressors after fluids in sepsis, as discussed in these studies?

Answer 13

Vasopressors restore vascular tone lost due to nitric oxide and inflammatory mediator–induced vasodilation, maintaining systemic vascular resistance and organ perfusion pressure.

Question 14

According to Neiman et al. (2020), how does serum total thyroxine (tT4) at ICU admission predict outcomes in critically ill dogs?

Answer 14

Lower tT4 concentrations are significantly associated with increased mortality, reflecting non-thyroidal illness syndrome and impaired metabolic regulation.

Question 15

According to Khanna et al. (2017) (ATHOS-3 trial), what effect did angiotensin II have in vasodilatory shock patients?

Answer 15

Angiotensin II significantly increased MAP in catecholamine-refractory vasodilatory shock, with a higher proportion of patients achieving target blood pressure compared to placebo.

Question 16

What are common risks of aggressive fluid resuscitation in sepsis, highlighted across multiple sources?

Answer 16

Fluid overload, pulmonary edema, abdominal compartment syndrome, and worsened oxygen diffusion leading to organ dysfunction.

Question 17

According to Marik et al. (2017), what was the reported effect of combination therapy with hydrocortisone, vitamin C, and thiamine in septic shock?

Answer 17

The retrospective before-after study suggested a large mortality reduction, though randomized trials are needed for confirmation.

Question 18

What pathophysiologic mechanisms explain sepsis-related organ dysfunction?

Answer 18

Cytokine storm, endothelial injury, microvascular thrombosis, mitochondrial dysfunction, immune dysregulation, and impaired oxygen utilization.

Question 19

Why is lactate clearance a better prognostic marker than initial lactate level in sepsis?

Answer 19

Clearance reflects recovery of tissue perfusion and metabolism, correlating better with survival and response to therapy.

Question 20

How does the absence of fever in sepsis patients relate to immune function and prognosis?

Answer 20

Afebrile patients may have blunted cytokine production, immune exhaustion, or hypothalamic dysfunction, associated with worse outcomes and delayed treatment.

Question 21

What are the clinical benefits of early recognition and intervention in sepsis, as supported by these studies?

Answer 21

Reduces bacterial load, limits immune-mediated injury, improves organ perfusion, and decreases mortality.

Question 22

According to Levy et al. (2018), what are the criticisms of the rigid 1-hour SSC bundle for sepsis?

Answer 22

Concerns include possible overtreatment of patients without true sepsis, potential iatrogenic harm, and strain on emergency department resources.

Question 23

According to Seymour et al. (2017), how does time to antibiotic administration affect mortality in mandated emergency sepsis care?

Answer 23

Each hour delay in antibiotics is associated with a significant increase in in-hospital mortality, emphasizing the need for rapid treatment.

Question 24

What monitoring strategies optimize fluid therapy and vasopressor titration in septic small animals?

Answer 24

Dynamic assessments like pulse pressure variation (PPV), stroke volume variation (SVV), echocardiography, lactate clearance, and clinical perfusion parameters guide individualized therapy.

Question 25

How does endothelial glycocalyx damage contribute to sepsis pathophysiology?

Answer 25

Glycocalyx degradation increases capillary permeability, promoting interstitial edema, leukocyte adhesion, microthrombosis, and worsening organ dysfunction.

Question 26

According to Klainbart et al. (2017), what coagulation abnormalities are common in septic cats?

Answer 26

Disseminated intravascular coagulation (DIC) signs including thrombocytopenia, prolonged PT/PTT, and decreased antithrombin activity.

Question 27

What is the physiological rationale behind using balanced crystalloids rather than normal saline in septic patients?

Answer 27

Balanced crystalloids reduce the risk of hyperchloremic metabolic acidosis and renal vasoconstriction, which are associated with saline use.

Question 28

How does mitochondrial dysfunction contribute to lactic acidosis in sepsis?

Answer 28

Impaired oxidative phosphorylation leads to reliance on anaerobic glycolysis, increasing lactate production despite adequate oxygen availability.

Question 29

According to Suetrong and Walley (2016), why should lactate be interpreted cautiously in sepsis?

Answer 29

Lactate elevation may result from increased production and/or decreased clearance; not all elevated lactate reflects tissue hypoxia.

Question 30

What role does the hypothalamic-pituitary-adrenal (HPA) axis play in sepsis?

Answer 30

It mediates stress response via cortisol release, modulating inflammation, vascular tone, and metabolism to maintain homeostasis during critical illness.

Question 31

According to Silverstein & Santoro Beer (2015), what are the controversies around vasopressor choice in veterinary septic shock?

Answer 31

Debate exists regarding the optimal vasopressor considering efficacy, side effects, species differences, and individual patient factors.

Question 32

How do fever and elevated temperature physiologically enhance immune defense in sepsis?

Answer 32

Fever promotes leukocyte function, enhances cytokine production, inhibits pathogen replication, and improves antigen presentation.

Question 33

What is non-thyroidal illness syndrome (NTIS) and how does it affect septic patients, according to Neiman et al. (2020)?

Answer 33

NTIS is characterized by low thyroid hormone levels without primary thyroid disease, impairing metabolism and correlating with worse outcomes.

Question 34

What is the significance of polymicrobial infections in sepsis outcomes, per Zahar et al. (2011)?

Answer 34

Polymicrobial infections do not significantly alter mortality compared to monomicrobial infections, underscoring host response importance.

Question 35

How do vasopressors help in catecholamine-resistant septic shock?

Answer 35

Agents like angiotensin II (per Khanna et al. (2017)) act via non-adrenergic pathways to restore vascular tone and blood pressure when catecholamines fail.

Question 36

According to Marik et al. (2017), what is the rationale for using vitamin C, hydrocortisone, and thiamine in sepsis?

Answer 36

To reduce oxidative stress, restore endothelial function, enhance catecholamine synthesis, and improve mitochondrial metabolism.

Question 37

Why is early goal-directed therapy (EGDT) no longer considered superior to usual care?

Answer 37

Trials (ProCESS, ARISE, ProMISe) showed no mortality benefit of EGDT; contemporary usual care includes early recognition and treatment protocols.

Question 38

What are the physiological consequences of fluid overload in septic patients?

Answer 38

Edema formation, impaired oxygen diffusion, pulmonary compromise, and increased mortality risk.

Question 39

According to Koenig & Verlander (2015), why is rapid point-of-care glucose measurement useful in septic peritonitis diagnosis?

Answer 39

Allows early differentiation of septic versus non-septic effusions by detecting glucose consumption in infected peritoneal fluid.

Question 40

What are the clinical signs and prognosis associated with absence of fever in septic patients?

Answer 40

Absence of fever is linked to immune dysfunction, delayed recognition, reduced treatment intensity, and increased mortality.

Question 41

How do antimicrobial stewardship principles integrate with sepsis management in veterinary medicine?

Answer 41

Appropriate drug selection, dose, duration, and culture-guided therapy minimize resistance and optimize patient outcomes.

Question 42

According to Baron et al. (2013), why is timing of blood culture collection critical in sepsis diagnosis?

Answer 42

Cultures should be collected before antimicrobial administration to maximize sensitivity and guide targeted therapy.

Question 43

How does Baron et al. (2013) define the “input sensor” in the microbiologic diagnostic system?

Answer 43

The clinician’s suspicion of infection prompting specimen collection based on clinical signs and context.

Question 44

What is the “controller algorithm” in microbiologic diagnostics according to Baron et al. (2013)?

Answer 44

The laboratory processes and decision trees (e.g., media selection, incubation conditions) that govern pathogen detection and identification.

Question 45

According to Baron et al. (2013), what is the “actuator” in the diagnostic feedback loop?

Answer 45

The clinician who uses lab results to adjust antimicrobial therapy and patient management.

Question 46

What are the main mechanisms by which bacteria develop antimicrobial resistance?

Answer 46

Enzymatic drug inactivation (e.g., β-lactamases), target site modification, efflux pumps, reduced permeability, and biofilm formation.

Question 47

How does Drewry et al. (2017) explain the immune consequences of fever suppression in sepsis?

Answer 47

Antipyretics may blunt cytokine signaling and impair host immune defense, potentially worsening outcomes.

Question 48

According to Henning et al. (2017), how does fever influence clinician behavior in sepsis management?

Answer 48

Fever acts as a salient clinical sign that prompts faster initiation of antibiotics and fluids.

Question 49

What are the physiological effects of fever on metabolic rate and oxygen consumption?

Answer 49

Fever increases basal metabolic rate, oxygen demand, and CO₂ production, which can stress cardiovascular and respiratory systems.

Question 50

How does Khanna et al. (2017) describe angiotensin II’s action in vasodilatory shock?

Answer 50

It acts on AT1 receptors causing vasoconstriction, increased systemic vascular resistance, and aldosterone-mediated volume retention.

Question 51

According to Levy et al. (2018), when should vasopressors be initiated in septic shock management?

Answer 51

Vasopressors should be started if MAP remains <65 mmHg after adequate fluid resuscitation to restore perfusion pressure.

Question 52

What is the role of lactate measurement in sepsis, as emphasized by Suetrong and Walley (2016)?

Answer 52

Lactate levels assess tissue hypoperfusion and metabolic dysfunction; serial measurements guide resuscitation efficacy.

Question 53

What are the key elements of the 3-hour and 6-hour SSC bundles prior to the 2018 update?

Answer 53

3-hour: lactate measurement, blood cultures, antibiotics, fluids; 6-hour: vasopressors, volume and perfusion reassessment, repeat lactate.

Question 54

What is the significance of mitochondrial dysfunction in sepsis-related organ failure?

Answer 54

Impaired mitochondrial oxidative phosphorylation leads to decreased ATP production, forcing reliance on anaerobic metabolism and contributing to organ dysfunction.

Question 55

According to Marik et al. (2017), what were the proposed benefits of hydrocortisone, vitamin C, and thiamine in septic shock?

Answer 55

Antioxidant effects, improved endothelial integrity, enhanced vasopressor responsiveness, and correction of metabolic derangements.

Question 56

How does immune dysregulation contribute to the “dysregulated host response” in sepsis?

Answer 56

An imbalance of pro- and anti-inflammatory cytokines leads to excessive inflammation, tissue injury, and later immunosuppression increasing infection risk.

Question 57

What are the physiological bases for choosing norepinephrine as the first-line vasopressor in septic shock?

Answer 57

Potent α1-mediated vasoconstriction with minimal β1-mediated tachyarrhythmias and proven mortality benefit in humans.

Question 58

According to Seymour et al. (2017), what is the relationship between treatment timing and mortality in sepsis?

Answer 58

Earlier administration of antibiotics and fluids is associated with improved survival, underscoring urgency in care delivery.

Question 59

According to Koenig & Verlander (2015), how is the diagnostic utility of peritoneal fluid glucose described for septic peritonitis?

Answer 59

A significant glucose gradient between blood and peritoneal fluid is a sensitive and specific indicator, allowing rapid bedside differentiation.

Question 60

What are the hemodynamic goals in sepsis management reflected in the SSC guidelines?

Answer 60

Restore MAP ≥65 mmHg, optimize cardiac output and tissue oxygen delivery, and correct volume deficits through fluids and vasopressors.

Question 61

What pathophysiological changes in sepsis cause vasodilation and hypotension?

Answer 61

Excess nitric oxide, inflammatory cytokines, endothelial dysfunction, and vascular smooth muscle hyporesponsiveness.

Question 62

What is the clinical significance of the afebrile septic patient phenotype?

Answer 62

These patients often have impaired immune responses, delayed recognition, reduced treatment intensity, and increased mortality.

Question 63

According to Neiman et al. (2020), how might thyroid hormone monitoring inform prognosis in critical illness?

Answer 63

Low total thyroxine is associated with higher mortality and may identify patients at higher risk requiring intensive support.

Question 64

What are the potential risks of excessive fluid resuscitation in septic veterinary patients?

Answer 64

Pulmonary edema, tissue edema impairing oxygen diffusion, abdominal hypertension, and organ dysfunction.

Question 65

What antimicrobial stewardship principles are emphasized in managing sepsis in veterinary medicine?

Answer 65

Use culture and sensitivity to guide therapy, limit broad-spectrum use, optimize dosing and duration, and avoid unnecessary antimicrobials.

Question 66

How do vasopressors like vasopressin complement catecholamines in septic shock?

Answer 66

Vasopressin acts on V1 receptors causing vasoconstriction via non-adrenergic pathways, useful in catecholamine-resistant vasoplegia.

Question 67

What are common coagulation abnormalities seen in septic cats, per Klainbart et al. (2017)?

Answer 67

Disseminated intravascular coagulation (DIC) markers including thrombocytopenia, prolonged clotting times, and reduced anticoagulant factors.

Question 68

How does the loss of endothelial glycocalyx worsen sepsis outcomes?

Answer 68

Increases vascular permeability and leukocyte adhesion, promoting edema, microthrombosis, and organ injury.

Question 69

What is the rationale for individualized fluid and vasopressor therapy in septic patients?

Answer 69

Patient comorbidities, volume status, and response vary; dynamic monitoring allows tailored resuscitation minimizing complications.

Question 70

What role do pattern recognition receptors (PRRs) play in sepsis pathophysiology?

Answer 70

PRRs detect pathogen-associated molecular patterns (PAMPs), triggering innate immune activation and systemic inflammation.

Question 71

What are the benefits and limitations of qSOFA as a sepsis screening tool, per Singer et al. (2016)?

Answer 71

Simple and quick for early risk stratification but lacks sensitivity and should prompt further evaluation, not replace clinical judgment.

Question 72

According to Marik et al. (2017), what further research is needed for combination metabolic resuscitation in sepsis?

Answer 72

Large, randomized controlled trials to confirm mortality benefit, optimal dosing, safety, and patient selection.

Question 73

According to Baron et al. (2013), what is the recommended blood volume per culture bottle to optimize sensitivity?

Answer 73

At least 8–10 mL per aerobic and anaerobic bottle is recommended; underfilling reduces sensitivity, especially in low-level bacteremia.

Question 74

What receptor does norepinephrine primarily act upon in septic shock?

Answer 74

α1-adrenergic receptors causing potent vasoconstriction, with some β1 activity increasing heart rate and contractility.

Question 75

What receptor subtype does phenylephrine selectively stimulate?

Answer 75

Pure α1-adrenergic receptor agonist; causes vasoconstriction without β-adrenergic cardiac effects.

Question 76

What receptor mediates vasopressin’s vasoconstrictive effects in septic shock?

Answer 76

V1 receptors on vascular smooth muscle, activating phosphatidylinositol signaling to cause vasoconstriction.

Question 77

What receptor does angiotensin II primarily bind to exert its vasoconstrictive action?

Answer 77

Angiotensin II type 1 (AT1) receptor, causing arteriolar vasoconstriction and aldosterone release.

Question 78

What was the approximate percentage of patients achieving target MAP in the angiotensin II group in ATHOS-3?

Answer 78

Approximately 69.9% achieved MAP ≥75 mmHg or ≥10 mmHg increase within 3 hours vs. 23.4% in placebo (p < 0.001).

Question 79

What was the typical starting dose of angiotensin II in the ATHOS-3 trial?

Answer 79

20 ng/kg/min, titrated up to a maximum of 80 ng/kg/min in the first 3 hours.

Question 80

What is the recommended initial fluid bolus volume for septic patients in the 2018 SSC bundle?

Answer 80

30 mL/kg intravenous crystalloid fluid administered rapidly within the first hour.

Question 81

What sensitivity and specificity cutoff did Koenig & Verlander (2015) report for peritoneal fluid glucose difference in septic peritonitis?

Answer 81

Sensitivity 94%, specificity 100% for blood-to-peritoneal glucose difference >20 mg/dL (1.1 mmol/L).

Question 82

What dosing schedule did Marik et al. (2017) use for hydrocortisone, vitamin C, and thiamine?

Answer 82

Hydrocortisone 50 mg IV every 6 hours, vitamin C 1.5 g IV every 6 hours, thiamine 200 mg IV every 12 hours.

Question 83

What is the target mean arterial pressure (MAP) recommended for septic shock resuscitation?

Answer 83

Maintain MAP ≥65 mmHg to ensure adequate organ perfusion.

Question 84

According to Seymour et al. (2017), by how much does mortality increase per hour of antibiotic delay?

Answer 84

Each hour delay in antibiotics increases in-hospital mortality risk by approximately 4–7%.

Question 85

What are the typical heart rate and stroke volume effects of β1-adrenergic receptor stimulation?

Answer 85

β1 stimulation increases heart rate (chronotropy), contractility (inotropy), and conduction velocity (dromotropy), increasing cardiac output.

Question 86

What is the physiologic role of the α1-adrenergic receptor in septic shock?

Answer 86

Causes vasoconstriction of arterioles and veins, increasing systemic vascular resistance and venous return.

Question 87

What are the two main types of lactic acidosis in sepsis and their causes?

Answer 87

Type A: tissue hypoxia leading to anaerobic metabolism; Type B: non-hypoxic causes such as mitochondrial dysfunction, β-adrenergic stimulation, and impaired clearance.

Question 88

What lactate cutoff defines septic shock in the Sepsis-3 criteria?

Answer 88

Serum lactate >2 mmol/L in the presence of persistent hypotension requiring vasopressors despite adequate fluids.

Question 89

What dosing range is typical for norepinephrine in veterinary septic shock?

Answer 89

Usually 0.05–1.0 μg/kg/min IV infusion, titrated to effect while monitoring for tachyarrhythmias.

Question 90

What are the typical effects of hydrocortisone in septic shock management?

Answer 90

Reduces systemic inflammation, restores vascular responsiveness to catecholamines, stabilizes endothelial barrier, and modulates immune response.

Question 91

How does thiamine deficiency contribute to lactic acidosis?

Answer 91

Thiamine is a cofactor for pyruvate dehydrogenase; deficiency impairs aerobic metabolism leading to pyruvate shunting to lactate.

Question 92

What are the common adverse effects noted in the angiotensin II group in ATHOS-3?

Answer 92

Increased risk of thromboembolic events including deep vein thrombosis and arterial thrombosis.

Question 93

What is the significance of central venous oxygen saturation (ScvO₂) monitoring in sepsis?

Answer 93

Reflects balance between oxygen delivery and consumption; low ScvO₂ indicates inadequate oxygen delivery or increased extraction.

Question 94

What are typical dosing ranges for dopamine as a vasopressor in veterinary medicine?

Answer 94

Low dose (1–5 μg/kg/min) primarily dopaminergic; moderate dose (5–10 μg/kg/min) β1 effects; higher doses (>10 μg/kg/min) α1 vasoconstriction.

Question 95

What is the recommended number of blood culture sets to maximize detection sensitivity in sepsis?

Answer 95

At least two to three sets from different venipuncture sites before antibiotics.

Question 96

What is the typical time frame for preliminary blood culture identification?

Answer 96

Preliminary identification within 24–48 hours; final ID and susceptibilities within 48–72 hours.

Question 97

What is the pathophysiologic role of V2 vasopressin receptors?

Answer 97

Mediate antidiuretic hormone effects in the kidney, promoting water reabsorption; excessive stimulation can cause hyponatremia.

Question 98

What are the physiological effects of fever on leukocyte function?

Answer 98

Enhances neutrophil chemotaxis, phagocytosis, T and B cell proliferation, and reactive oxygen species production.

Question 99

What percentage of patients had mortality reduced from 40.4% to 8.5% in the hydrocortisone, vitamin C, and thiamine study by Marik et al. (2017)?

Answer 99

Reported mortality dropped to 8.5% from 40.4% in the treatment group, although data are from a retrospective study requiring further validation.

Question 100

What is pulse pressure variation (PPV) and why is it relevant?

Answer 100

PPV is the variation in pulse pressure during mechanical ventilation, used to predict fluid responsiveness in critically ill patients.

Question 101

What is the definition of compensatory anti-inflammatory response syndrome (CARS)?

Answer 101

A late-stage immunosuppressive state in sepsis characterized by T-cell exhaustion and increased IL-10, leading to impaired pathogen clearance.

Question 102

What is the typical MAP goal for vasopressor therapy in septic shock?

Answer 102

Maintain MAP ≥65 mmHg to ensure adequate tissue perfusion.

Question 103

How does norepinephrine influence lactate levels?

Answer 103

Has minimal effect on increasing lactate compared to epinephrine, which can increase lactate through β2 stimulation.

Question 104

What are the typical doses for hydrocortisone in septic shock in veterinary medicine?

Answer 104

Common doses are 1–2 mg/kg/day IV divided q6-8h, but protocols vary by institution and patient.

Question 105

What is the COX-2 enzyme’s role in fever generation?

Answer 105

Upregulated by pyrogenic cytokines; catalyzes synthesis of prostaglandin E2 (PGE2), which resets hypothalamic thermoregulatory setpoint.

Question 106

What is the half-life of vitamin C in critically ill patients and typical dosing?

Answer 106

Vitamin C half-life is short (~2 hours); dosing ranges from 1.5 g IV q6h to higher experimental doses in clinical trials.

Question 107

What is the role of the Warburg effect in sepsis-related lactate production?

Answer 107

Cells shift toward aerobic glycolysis even with adequate oxygen, increasing lactate production driven by β-adrenergic stimulation and inflammation.

Question 108

What are the proposed mechanisms of mitochondrial dysfunction in sepsis?

Answer 108

Oxidative stress, nitric oxide-mediated damage, calcium overload, and impaired electron transport chain activity reduce ATP production.

Question 109

What is the impact of volume overload on oxygen delivery?

Answer 109

Interstitial edema impairs oxygen diffusion to tissues despite adequate blood flow, worsening hypoxia.

Question 110

What are the reported sensitivity and specificity values for qSOFA in sepsis screening?

Answer 110

Sensitivity ~50–60%, specificity ~75–85%; used as a rapid bedside screening tool, not definitive diagnostic.