EMS and the septic patient
Emerging technology helps us to improve detection and begin treatment early
By T. Ryan Mayfield
Webster’s defines septic as relating to purification, or the decomposition of organic matter. While decomposition is essential in the grand scheme of things, it is not entirely desirable in a living human. In recent years identification and treatment of septic patients has garnered much attention, but in many cases EMS education has not kept up.
So then, what is sepsis and how does it affect us as EMS providers? Currently there is no specific lab test to determine if a patient is septic. To make this diagnosis, the patient must meet a series of criteria.
Systemic Inflammatory Response Syndrome
The first step on the path to sepsis is the Systemic Inflammatory Response Syndrome, or SIRS, criteria. To meet the SIRS criteria your patient must have at least two of the following1:
- Pulse: > 90 bpm
- Respirations: > 20 or mechanically ventilated
- Temperature: >38 C (100.4 F) or <36 C (96.8 F)
- White blood cell count: >12,000 or < 4,000 or >10% immature
Newer revisions of the sepsis criteria have added additional items. None of these are diagnostic by themselves, but add more credence to the sepsis picture1.
- Decreased urine output
- Elevated blood lactate level
- Altered mental status
- Significant edema
Recognize that SIRS is not confined to sepsis alone. It is the body’s response to any major insult such as trauma, severe burns, pancreatitis, ischemia or infection. For this article, let's focus on the infection part. The most common infections seen are pneumonia, UTIs, and ear infections in children2.
If not stopped, SIRS can lead to severe sepsis, septic shock, and multiple organ dysfunction syndrome (MODS). Severe sepsis is defined as sepsis with the addition of hypoperfusion. This hypoperfusion is commonly defined as:
- Systolic blood pressure: < 90 mmHg; or
- Mean arterial pressure (MAP): <65; or
- Blood lactate: ≥ 4 mmol/l
Systolic blood pressure is a quick and easy measure that everyone understands. On the other hand, MAP and lactate requires a little more explanation.
Mean Arterial Pressure
If your initial training was like mine, you learned about the formula for MAP with the caveat from the instructor of, “you will never need to know that in the real world.” Because of this, immediately after the test it left your brain to make room for something else. Ten years after paramedic school, I finally read a great explanation of MAP and realized this is something that you do need to know in the real world. Fortunately, it's pretty straightforward.
For MAP to make sense, we need to have a few working definitions:
Systolic Pressure: Pressure in the arteries when the heart is contracting (systole)
Diastolic Pressure: Pressure in the arteries when the heart is at rest (diastole)
Simply put, when the heart contracts, it sends out gush of blood that temporarily increases the pressure in the arteries. In between the contractions, the pressure drops. In another words, if your patient’s pressure is 100/40, it means that when the heart is contracting (systole) there is enough pressure to perfuse the cells, but when the heart is at rest (diastole) the pressure is too low to adequately perfuse the cells.
Furthermore, diastole lasts about twice as long as systole, so two thirds of the time your patient’s cells do not have adequate perfusion.
There are a couple of ways to determine the MAP. Some prehospital monitors will show it next to the blood pressure reading. Otherwise, it can be estimated with the following formula:
Mean Arterial Pressure = (2 * Diastolic Pressure + Systolic Pressure) / 3
You can also download a "cheat card" here.
Lactate is a measure of tissue perfusion, and can tell you how well the cells are being oxygenated regardless of the blood pressure.
When the cells do not receive enough oxygen they convert to anaerobic metabolism. A byproduct of this anaerobic metabolism is equal parts lactate and hydrogen ions. If the anaerobic metabolism continues there will be a buildup of hydrogen leading to acidosis. Monitoring the lactate levels gives the caregiver an indicator of how well the cells themselves are being oxygenated.
Blood lactate monitoring is starting to make its breakthrough into EMS. There are a number of meters on the market that work like a glucometer and will give you the blood lactate from a finger stick. Most of these meters are developed for endurance athletes and have not been FDA approved, so make sure you know this before you purchase one for patient use.
The first and most important element in treating sepsis is to identify it. While there is still a lot about sepsis that we do not know, one thing that almost everyone can agree on is that early identification and early aggressive treatment leads to better patient outcomes3,4,5.
While not all SIRS criteria mentioned earlier are detectable in the EMS setting, most are. With the exception of the WBC, the other three SIRS criteria can be determined in the field. Since you only need two of the four criteria to say the patient has SIRS, a large number of them can be detected during your normal EMS patient assessment.
What would you look for to determine a documented or suspected infection? The easiest is if a doctor has prescribed them an antibiotic related to the presentation; that would be a documented infection. Suspected infection is a little less clear, but may include:
- New and/or worsening cough10.
- New onset of weakness or falls in the elderly10.
- Bed sores11
- Foul smelling or cloudy urine9.
- Warm or red areas around surgery sites8.
- Foul smelling or pus draining from the skin8.
- Small children pulling on their ears7.
Severe sepsis and septic shock
For patients to move from sepsis to severe sepsis and/or septic shock, they have to have the hypoperfusion component. EMS providers are trained to detect the signs and symptoms of shock. Detecting lactate levels with a meter will add additional key information to the suspicion of septic shock. Even without a lactate meter, a low systolic pressure, low MAP, and a new onset of altered mentation are great indicators.
Treatment of a sepsis patient depends on the severity. High flow oxygen is definitely a must for these patients, but if you have to assist ventilations, be careful. The patient’s lungs in this state can be susceptible to damage, so ventilations need to be slow and steady with just enough volume for the chest to rise6.
If the patient is in severe sepsis and/or septic shock, then they will fall under a medical shock protocol that most agencies already have in place. These patients need large volumes of fluids and the standard 20ml/kg or 2 liter initial bolus seen in most protocols is a good place to start. Fluid is the primary means of increasing perfusion, but vasopressors such as dopamine should also be considered if the fluid alone is not enough6.
If nothing else is learned from this summary remember this. They key to surviving sepsis is early identification and early aggressive treatment. If these patients can be identified by EMS and the hospital is given a heads up to prepare, the patient’s odds of survival will be greatly increased.
1. Levy MM, Fink MP, Marshall JC, et al. 2001 Society of Critical Care Medicine/European Society of Intensive Care Medicine/ American College of Chest Physicians/American Thoracic Society/ Surgical Infection Society: international sepsis definitions conference. Intensive Care Med 2003;29:530–8.
2. Angus DC, Linde-Zwirbe WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29:1303–9.
3. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Eng J Med 2001;345(19),1368-77.
4. Nguyen HB, Rivers EP, Abrahamian, FM et al. Severe sepsis and septic shock: review of the literature and emergency department guidelines. Ann Emerg Med 2006;48:28-54.
5. Jones AE, Focht A, Horton JM, et al. Prospective external validation of the clinical effectiveness of an emergency department-based early goal-directed therapy protocol for severe sepsis and septic shock. Chest 2007;132:425-32.
6. Dellinger RP, et al. Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012. Critical Care Medicine 2013;41(2), 580-637.
7. Ramakrishnan K, et al. Diagnosis and treatment of otitis media. American Family Physician. 2007;76:1650.
8. Frey R (2009). Incision care. In B Narins, ed., Gale Encyclopedia of Surgery and Medical Tests: A Guide for Patients and Caregivers, 2nd ed., vol. 4, pp. 835–838. Farmington Hills, MI: Gale.
9. Gupta K, Stamm WE (2008). Urinary tract infections. In DC Dale, DD Federman, eds., ACP Medicine, section 7, chap. 23. Hamilton, ON: BC Decker.
10. Niederman MS (2004). Pneumonia, including community-acquired and nosocomial pneumonia. In JD Crapo et al., eds., Baum's Textbook of Pulmonary Diseases, 7th ed., vol. 1, pp. 424–454. Philadelphia: Lippincott Williams and Wilkins.
11. Bluestein D, et al. Pressure ulcers: Prevention, evaluation, and management. American Family Physician. 2008;78:1186.
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