June 2, 2025

Perhaps no topic in medical literature has received as much attention in the past few years as sepsis and septic shock, which are the topics for this month’s continuing education presentation. Over the past 10 years, Critical Care and Infectious Disease experts have offered several revisions and modifications with regard to:

• The definition of sepsis: “Life-threatening organ dysfunction due to dysregulated host response to infection.” 

• Removing “severe sepsis” as an actual category of the sepsis continuum. 

• The nature, origin, and production of lactate in sepsis: Lactate is now believed to be generated as a byproduct of pyruvate overproduction due to endogenous epinephrine stimulation. This refutes the theory that lactate is produced during “anaerobic metabolism.” However, most texts still adhere to the production of lactate as a result of anaerobic metabolism.  

• The cause of acidosis in sepsis (current theories suggest that acidosis in sepsis is not due to “lactic acid” but rather due to chloride and hydrogen ion accumulation and loss of bicarbonate). 

• Recommendations regarding whether invasive monitoring of central venous pressure (CVP) is necessary or beneficial. 

Despite all the flurry of activity and revisions in the sepsis arena, many of the fundamental aspects remain the same. Early identification, immediate resuscitation, and antibiotic administration are paramount, key to patient survival. To this end, the EMS provider must be able to suspect sepsis based on history, including the all-important septic risk factors, physical examination, and ancillary testing. Be aware of the risk factors for sepsis, which include diabetes, chronic renal failure, cancer, post-op patients, those with indwelling devices, and those patients on immunosuppressant medications. Sepsis can be diagnosed at the bedside by an astute EMS provider, nurse, nurse practitioner, PA, or physician. No complicated testing is required for sepsis identification, but early identification is essential to a good outcome. Prompt resuscitative and definitive treatment translates to decreased mortality. Remember: Systemic Inflammatory Response Syndrome (SIRS) + Suspected Infection = Sepsis 

We are all familiar with SIRS criteria as an indicator for the presence of sepsis—any two of these criteria make the patient “SIRS-positive.” Although there are several potential causes of SIRS, such as pancreatitis, burns, overdose, trauma, pulmonary embolism, etc., sepsis should always remain a high-level consideration in the differential diagnosis of a SIRS-positive patient. 

If a patient is SIRS-positive, the clinician must “look for the infection” which may or may not be obvious. Common sources of sepsis include: 

• The urinary tract, especially in patients who have undergone surgery or instrumentation of the urinary tract and those with a Foley catheter. Clues for urinary tract infection include dysuria, hematuria, fever, chills, flank pain, and cloudy urine noted in the Foley collection bag.  

• The respiratory tract, where patients with pneumonia may have fever, chills, productive cough, shortness of breath, and pleuritic chest pain. Physical findings could include increased respiratory rate, low pulse oximetry, accessory muscle use, crackles, or wheezes noted on lung auscultation. 

• The skin and joints, where the EMS provider should examine the skin for signs of erythema, warmth, and tenderness to palpation. Wounds can become secondarily infected, including non-traumatic wounds (infected foot wounds on diabetics, decubiti on debilitated patients), post-surgical wounds, and post-traumatic wounds, such as lacerations and punctures. Signs of septic arthritis (joint infections) include joint swelling, redness, tenderness, and decreased range of motion.  

• The GI tract, where the provider should inquire about vomiting, diarrhea, and abdominal pain. Patients with appendicitis, diverticulitis, ascending cholangitis, acute pancreatitis, mesenteric ischemia and bowel obstruction and perforation are all examples of gut-related sepsis. The physical findings could include diminished bowel sounds, abdominal distention, tenderness to palpation, and guarding. Rebound tenderness indicates peritonitis, which is a serious complication often noted in the patient with abdominal sepsis.  

Early recognition and treatment are key to survival. Treatment includes crystalloid fluids, vasopressors as needed, and early antibiotic administration. More to come next week.  

Stay well,

Andrew Garlisi, MD EMS Medical Director

University Hospitals EMS Training & Disaster Preparedness Institute

June 9, 2025

Sepsis diagnosis can often be challenging. Since signs and symptoms may be subtle at first, emergency providers might miss these clues, which could delay definitive treatment. It is not uncommon for sepsis victims to complain of general weakness and fatigue, which are very nonspecific symptoms. Elderly patients often experience changes in mental status or difficulty ambulating. Sepsis should remain high on the list in the differential diagnosis of nonspecific symptoms, especially in high-risk patients.  

Risk factors are a crucial component of a comprehensive history and can contribute to a more robust differential diagnosis. Risk factor assessment is important in patients with possible acute coronary syndrome, thoracic aortic dissection, cardiac tamponade, or pulmonary embolism. The same is true for sepsis. Patients with diabetes, chronic renal failure on dialysis, cancer, autoimmune diseases (Crohn’s, rheumatoid arthritis, psoriasis, lupus, etc.), indwelling devices, frequent hospitalizations, recent invasive procedures, and chronic exposure to healthcare facilities are among the high-risk patients.  

Since sepsis can affect anyone of all ages and has a multitude of presentations, the diagnosis can be difficult. A high index of suspicion, coupled with a concise history and physical examination, goes a long way in pointing to the diagnosis.  

Ancillary testing can be a valuable adjunct in the diagnosis of sepsis, which results in organ dysfunction. The brain is often the target organ that reveals early signs of sepsis. A urinary tract infection in the susceptible chronic nursing home patient frequently manifests as “acute mental status change.” Glucose testing should be obtained in all patients with encephalopathy. Patients could experience hypoglycemia, especially if they are chronically malnourished or if they have had frequent vomiting and reduced food intake. The other extreme, hyperglycemia, can also be a consequence. Patients under the stress of sepsis have increased adrenal cortisol production, which increases blood glucose. Furthermore, endogenous epinephrine production (a consequence of the septic process) breaks down glycogen into glucose.  

The 12 lead EKG may reveal tachyarrhythmias and signs of ischemia in patients with underlying heart disease. Lung dysfunction, as a result of sepsis, could manifest by impairment in oxygen exchange, resulting in a decrease in oxygen saturation on pulse oximetry.  

As systemic perfusion decreases during the septic process, cells are impaired in their ability to produce ATP and carbon dioxide. CO2 reduction is detected by waveform capnography. As ATP energy diminishes, the cells and tissues break down and eventually die. Organ dysfunction is the consequence. Capnography remains a vital indicator of perfusion at the cellular level. Some squads have utilized pre-hospital point-of-care lactate testing. The cause of lactate excess in sepsis is still being debated by experts. Recently, many researchers have postulated that lactate (not lactic acid) is produced by the release of endogenous epinephrine, which breaks down glycogen into glucose. In the past, lactate was believed to be the product of anaerobic metabolism (without oxygen), but in fact, most patients with sepsis have adequate oxygen supplies and still produce lactate. Normally, glucose would be utilized in the metabolic pathway known as glycolysis to make pyruvate, which enters the Krebs cycle. When excess pyruvate is produced, the Krebs cycle pathway is overwhelmed. Some of the glucose excess is therefore converted into lactate. These scientists contend that lactate, not lactic acid, is the actual chemical (the difference is one hydrogen ion in lactic acid, which lactate lacks).  

Regardless of how or why lactate accumulates, it remains an important indicator of sepsis severity, and serial lactate measurements provide insight into patient response to treatment. Thank you to all my EMS and ED colleagues!  

Stay well,

Andrew Garlisi, MD

EMS Medical Director

University Hospitals EMS Training & Disaster Preparedness Institute