Sepsis: 10 things you need to know to save lives

Proper assessment, treatment, and transport of patients with sepsis saves lives

By Bob Sullivan

The following is paid content sponsored by Pulsara

Sepsis is the third leading cause of death in the United States [1], and survival depends on early recognition and treatment. Here are 10 things you need to know about sepsis to save lives: 

Image courtesty of invisioner
Image courtesty of invisioner

1. Sepsis is an overreaction to infection that can progress to shock.

Sepsis is a body-wide inflammatory response to infection that injures tissues and organs. Harm from this immune response is often worse than damage from the actual infection. Sepsis can be triggered by relatively minor infections, and can continue after the invading microbes are neutralized.

Sepsis causes blood clots to form in the microvasculature, which inhibits oxygen delivery and causes vital organs to fail. Severe sepsis also causes systemic vasodilation and increased capillary permeability, which causes hypotension and fluid leakage out of the vascular space. This causes septic shock, which further inhibits perfusion to vital organs. Forty percent of patients diagnosed with severe sepsis die.[1]

2. Trauma…STEMI…stroke…SEPSIS ALERT!

Like other conditions that prompt a team response in hospitals, management of sepsis requires multidisciplinary team members to deliver time-critical interventions. Several hospitals improved mortality from severe sepsis by over 50% since implementing sepsis teams and early goal-directed therapy. This includes door-to-treatment guidelines for lactate measurement to detect sepsis, administration of antibiotics to fight the infection, and fluid resuscitation for shock.[2]

Sepsis care teams work across the hospital and respond to the ED when a patient arrives. There is also a movement to direct severe sepsis patients to larger hospitals that offer comprehensive critical care services and care for a high volume of sepsis patients. EMS recognition of severe sepsis, initiation of treatment, transport to the most appropriate facility, and early notification of the hospital can help patients receive treatment goals faster.

3. Add a temperature to your vitals to find SIRS.

Early identification of sepsis begins with assessing patients for systemic inflammatory response syndrome (SIRS), which is defined as a patient having two or more of the following:

  • Pulse > 90
  • Respiratory rate > 20
  • Temperature > 38 C (100.4 F) or < 36 C (96.8 F)
  • Elevated white blood cell count (generally tested in hospital)

Identifying SIRS requires a temperature to be taken with vital signs; which is done on every patient in the hospital, but is less common in EMS. Either a fever or documented hypothermia (temp < 36 C) with other reported assessment findings may prompt a sepsis response that affects the patient’s entire hospital course.

4. Consider the many sources of sepsis.

A sepsis diagnosis is defined as a patient with SIRS criteria and a source of infection. Begin a search for one after assessing the patient’s temperature and vital signs. Medical causes of infection include pneumonia, urinary tract infections, meningitis, abdominal infections, ear infections (primarily in children), and recent surgery.

Sepsis can also be caused by skin abscesses, infected wounds - even from minor scrapes and cuts - and bedsores. Indwelling medical devices, such as dialysis shunts, urinary catheters, tracheostomies, central lines, and medication ports are also possible sources of infection. Another clue is a prescribed antibiotic; get familiar with what these medications are and inquire why the patient is taking it.

5. Lactate may be the new 12-lead.

Prehospital 12-lead ECG’s improve mortality for STEMI patients by identifying patients who need immediate reperfusion therapy and reducing the time to definitive care in the hospital. In severe sepsis, lactic acid is released into the bloodstream as hypoxic tissues use anaerobic metabolism for energy. This can be detected with a point-of-care lactate reading, which is above 4 mmoL in severe sepsis. Some EMS services have adopted lactate meters and protocols to activate a team in the hospital.

An elevated lactate is not specific for sepsis; any cause of shock will increase it, as well as seizures and endurance athletic training. A lactate level may even be normal in advanced stages of sepsis because the compensatory mechanisms producing it have failed. If available, incorporate a lactate reading into other assessment findings.

6. End-tidal CO2 may also help detect severe sepsis.

Tissue hypoxia in sepsis triggers an increased respiratory rate, but micro clots and hypotension impair blood flow back to the lungs to excrete waste products. Therefore, patients with severe sepsis may have an elevated respiratory rate with a low end-tidal CO2 reading. These waste products then accumulate in the blood, one of them being lactate. One study found that an end-tidal CO2 (ETCO2) reading < 25 mmHG with two or more signs of SIRS correlated with a lactate reading above 4 mmOL and suggests severe sepsis.[3]

There are other causes of a low ETCO2 reading besides severe sepsis, including hemorrhagic shock and respiratory alkalosis from hyperventilation syndrome (patients having a panic attack are likely to have an elevated pulse and respiratory rate as well). Consider ETCO2 findings along with other assessment findings for SIRS and a source of infection.

7. Septic patients can be sicker than they look.

Tissue hypoxia and organ failure in sepsis can begin before hypotension, and patients may look relatively well during that time. Known as “cryptic shock,” these patients are at greater risk of delayed treatment, and by the time they decompensate it is often too late. The key is identifying those patients and initiating aggressive treatment before they develop hypotension and begin to look sick.

8. Sepsis does not discriminate based on age or health status.

Sepsis is most common in the elderly and immunocompromised, such as those with HIV, hepatitis, organ transplants, on chemotherapy, or taking steroids.

However, it can affect healthy children and young adults from minor illnesses and injuries. Approximately 42,000 children in the United States develop severe sepsis each year, and 4,400 of them die.[1]

Young and previously healthy people are at a higher risk than elderly people for post-sepsis syndrome, which includes amputations, organ dysfunction, cognitive impairment, debilitating muscle and joint pain, fatigue, and PTSD.[1] Be on the lookout for signs of sepsis in younger patients, as well as provider complacency while assessing them.

9. Fill the tank and shrink the tank.

Administer IV fluids (in the absence of pulmonary edema) to patients with suspected sepsis, even if they are normotensive. Start with a 20 mL/kg bolus, and administer up to two liters of normal saline or lactated ringers. Systemic vasodilation may be lurking, and it is important to increase fluid volume before that occurs.

One of the characteristics of septic shock is hypotension that does not improve with IV fluid. A vasopressor is indicated to constrict peripheral blood vessels and reduce fluid leakage out of the vasculature. It is important to remember that vasopressors are a last resort. However, if they are needed, Norepinephrine (Levophed) is the preferred vasopressor for septic shock[2], but Dopamine is more commonly used by EMS. Anticipate the need and calculate an infusion rate for a vasopressor in any hypotensive septic patient.

10. Early antibiotics - in the field?

Early antibiotics are another time-sensitive treatment for sepsis, and the goal is to administer them within one hour of arrival at the hospital. Some critical care transport teams have added antibiotics to initiate during inter-facility transfers, and other services have investigated the feasibility and safety of implementing them on ground ambulances.[4] Early studies look promising, and antibiotics may soon be another tool for EMS to save lives of severe sepsis patients.


[1] Sepsis Alliance. What is Sepsis? Retrieved from:

[2] Dellinger RP. Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine. 2013;41(2):580–637.

[3] Hunter CL, Silvestri S, Dean M, et al. End-tidal carbon dioxide is associated with lactate levels and mortality in emergency department patients with suspected sepsis. American Journal of Emergency Medicine. 2013;31(1):64-71.

[4] Mayfield TR, Meyers M, Mackie J. Abstract: Incidence of Adverse Reactions to Initial Antibiotic Administration in Severe Sepsis Patients.

About the author:

Bob Sullivan, MS, NRP, is a paramedic instructor at Delaware Technical Community College. He has been in EMS since 1999, and has worked as a paramedic in private, fire-based, volunteer, and municipal EMS services. Contact Bob at his blog, The EMS Patient Perspective

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