PCT and CRP are both proteins produced in response to infection and/or inflammation. They are probably the two most widely used clinical tests to diagnose and manage patients with sepsis, with the exception of lactate.
A procalcitonin test can help your health care provider diagnose if you have sepsis from a bacterial infection or if you have a high risk of developing sepsis.
Peripheral blood cultures are useful for investigating the infectious etiology of sepsis and for managing appropriate antimicrobial treatment. Other tests, including CBC and chemistries, provide a baseline to assess therapeutic response.
Some of these tests are used to identify the germ that caused the infection that led to sepsis. This testing might include blood cultures looking for bacterial infections, or tests for viral infections, like COVID-19 or influenza.
These results indicate that leukopenia (WBC <4,000) in severe sepsis patients leads to more severe outcome and hypercytokinemia than leukocytosis (WBC >12,000) in severe sepsis patients.
Severe breathlessness or sleepiness. It feels like you're going to die or pass out. Skin mottled or discoloured. An extremely high or a very low temperature; repeated vomiting; seizures; and a rash which doesn't fade when you press a glass against it are also possible 'red flags'.
Sepsis is considered present if infection is highly suspected or proven and two or more of the following systemic inflammatory response syndrome (SIRS) criteria are met: Hypotension. Heart rate > 90 beats per minute. Temperature < 36 (96.8 °F) or > 38 °C (100.4 °F)
Sepsis causes an inflammatory response in your body. Severe sepsis occurs when one or more of your body's organs is damaged from this inflammatory response. Any organ can be affected, your heart, brain, kidneys, lungs, and/or liver.
Systemic inflammatory response syndrome (SIRS) – body temperature >38°C or <36°C, heart rate >90 beats/min, respiratory rate >20 breaths/min, and white blood cell count >12,000/nm3 or >10% immature neutrophils – has been used as part of the definition of sepsis for decades.
Clinical indicators of septic shock were hypotension, mechanical ventilation, lactate levels between 2.0-3.9 or >4, hypothermia <36°C, radiotherapy-associated chemotherapy, Sequential Organ Failure Assessment score >3 and admittance through the emergency unit.
Thus, a serum lactate level >2 mmol/L may be a new emerging vital sign of septic shock.
Most sepsis is caused by bacterial infections, but it can also be caused by viral infections, such as COVID-19 or influenza; fungal infections; or noninfectious insults, such as traumatic injury.
As severe sepsis usually involves infection of the bloodstream, the heart is one of the first affected organs.
Ideally, these clinical criteria should identify all the elements of sepsis (infection, host response, and organ dysfunction), be simple to obtain, and be available promptly and at a reasonable cost or burden.
Serum concentration of calcitonin precursor, CRP, IL-6 and lactate were elevated according to the severity of illness. Based on receiver operating characteristic (ROC) curve analysis, they concluded that PCT is the most reliable marker for the diagnosis of sepsis, with 89% of sensitivity and 94% of specificity [29].
In laboratory tests, sepsis often coincides with high white blood cell counts. But in the highly acute phase, and especially in immunocompromised patients, there may also be a decrease in white blood cell counts.
These conditions include: pulmonary embolism (PE), adrenal insufficiency, diabetic ketoacidosis (DKA), pancreatitis, anaphylaxis, bowel obstruction, hypovolemia, colitis, vasculitis, toxin ingestion/overdose/withdrawal, and medication effect.
High heart rate or weak pulse. Fever, shivering, or feeling very cold. Confusion or disorientation. Shortness of breath.
In addition, a lower platelet count was observed in septic patients. This situation was due to production of many cytokines, endothelial damage, and bone marrow suppression in septic patients.
Background: In a patient with severe sepsis, we sometimes observe immediate decrease of the counts of white blood cells (WBCs) and neutrophils, which is known as an indicator for poor prognosis.
Lactate elevation in sepsis seems to be due to endogenous epinephrine stimulating beta-2 receptors (figure below). Particularly in skeletal muscle cells, this stimulation up-regulates glycolysis, generating more pyruvate than can be used by the cell's mitochondria via the TCA cycle.
Even though lactate produced in the presence of sepsis may not necessarily be the result of widespread hypoperfusion, lactate can be an indicator that anaerobic metabolism is taking place. Therefore, lactate is sensitive to sepsis, but not specific to sepsis.