By June 4 the total number of confirmed global COVID-19 cases exceeded 6.5 million. The United States has had more than 1.8 million, with more than 107,000 deaths.1
Around 80% of COVID-19 patients present with mild or no symptoms. Symptoms may include fever, cough, aches, pains, and weakness, all common to cold and flu. It is important to note the absence of fever does not exclude infection from COVID-19.
The overwhelming numbers of patients have made it necessary to manage patients with mild presentations at home. Others we can’t: Those presenting with more moderate signs and symptoms account for approximately 14% of the COVID-19 patients we encounter. They require hospitalization and will present with pneumonia or signs of sepsis. Cases of greatest severity account for 5% of COVID-19 patients; they will present as if they have severe ARDS or are in septic shock, and in worst-case scenarios will develop multiorgan system failure. They will require ICU admission, and if intubated, as reported from Bellevue Hospital in New York City, may have a mortality rate of up to 80%.
Patients with moderate to severe COVID-19 symptoms may present with what appears to be pneumonia, but instead of being localized to a single lung, it is more diffuse, found in all lobes of the lungs. They will develop leakage of fluid from the capillaries, akin to ARDS, causing fluid to leak into the alveolar sacs, leading to shunting and V/Q mismatch.
This is ARDS without being ARDS. Why? Because while the presentation is similar, COVID-19 does not respond to the typical therapies developed to treat ARDS. For example, steroids in COVID-19 are avoided for two reasons: They do not improve outcomes, and they increase the time frame over which patients shed the virus. CARDS (COVID acute respiratory distress syndrome) is a term proposed to describe this phenomenon in recent edition of JAMA.
Symptomatic patients exposed to SARS-CoV-2 will begin to develop symptoms in the 3–5-day time range. Severe signs and symptoms will begin to progress at the 10-day mark. Patients with severe presentations will have this simmering period beforehand. Patients do not appear tachypneic, but they are hypoxic. They have thick secretions that are difficult to mobilize. In the hospital they will receive oxygen, gradually increasing from 2–10 lpm. As their secretions build they need more O2 to maintain oxygenation. Nothing facilitates pulmonary hygiene, so the patient begins to spiral downward, since it is virtually impossible to for gas to exchange through the thick sputum. This is a hyperinflammatory phase, setting the patient up the cytokine storm that will ultimately force them to be intubated.
The EMS Picture
On the EMS side we see patients who have had mild symptoms and stayed home calling for help when their severity increases. The confounding issue here is that patients may take anywhere from hours to days to progress to extremis. Anyone who has an SpO2 below 92%–94% is getting ready to decompensate. The problem is these patients are sent home with instructions that when they become short of breath, they should come back, but tachypnea is a premorbid sign, and it may be too late for them. In reality they need be admitted and treated, not discharged home. The reason they are sent home is because many hospitals lack the capacity to manage the influx of patients.
If your patient still has mild symptoms, they may have clear lung sounds, but perform a thorough assessment—you may hear fine rales in the bases. This is hint of progression. For those mild patients whose disease has progressed rapidly, we are met with an awake, alert, oriented patient who most likely is not tachypneic, lulling us into a false sense of security. When we listen to their lungs, it is a horrible mix of course rales and diffuse rhonchi. We see pulse oximetry readings in the 80s, 70s, and, yes, even 60s, yet the patient has good mentation.
When we do see tachypnea, it is a critical clinical sign. Early tachypnea is significant because it may be a first sign of complete failure and a need for intubation, or it may be a preceding sign of a patient going into cardiac arrest. It is hypoxic decompensation, significant because of the growing dead space and shunting that’s gone on.
Patients who rapidly progress over the course of several hours have incredible amounts of infiltrates in their lungs, making them “stiff.” Gas exchange is impossible, and it is extremely difficult for them to breathe. In this situation we typically would transition from a nasal cannula to a nonrebreather mask, attempting to increase O2 to maintain saturation, and at a certain point we may be tempted to try CPAP/BiPAP. But Emory University has recommended its EMS providers not treat COVID-19 patients with CPAP/BiPAP because it delays intubation and CPAP makes the patient worse overall. The alveoli cannot tolerate the higher pressures, and the leakage of fluid we see during the clinical course of this disease is actually accelerated. The Emory experience has also demonstrated that prehospital CPAP/BiPAP patients have poor outcomes if they need to be intubated later. In the hospital we may see a short trial of CPAP/BiPAP, but they will terminate it very quickly if the patient doesn’t show signs of immediate improvement.
The secretions from that cytokine storm are so overwhelming, the patient continues to spiral downward. The mucus is thick and tenacious like mud. We end up performing a controlled intubation, transitioning from a nasal cannula or nonrebreather to higher levels of O2 to maintain oxygenation. The patient who is intubated, though, has an increased risk of death. Hospitals would prefer if we held off.
Hospitals have been using proning and high-flow nasal cannula (HFNC) to treat patients. HFNC isn’t turning up the liter flow to its highest setting; with a HFNC oxygen is humidified and warmed to a temperature of 37ºC. It delivers a range of FiO2 from 0.21–1. It is device-dependent and can deliver maximum flow rates between 50–60 lpm.
Why HFNC? That tenacious sputum and hyperinflammatory response all lead to an increase in airway resistance. The inability to facilitate pulmonary hygiene complicates matters further. Heated, humidified oxygen will help reduce some of that inflammation, and adding humidification will loosen some of the mucus, making it easier to expel. There are other benefits to HFNC, but they are not as clearly defined.
Hospitals are placing patients into prone positions. They can achieve the same effect, although not to the same extent, by placing patients on their sides. They will frequently do this early in the course of treatment, when a patient is on HFNC prior to intubation. Proning is not new; it has been done in the OR for years for patients who having brain and spinal surgeries and has been a staple in ARDS patients as well. You can even perform CPR in the prone position.2
Initiated early, proning has reduced the number of patients requiring intubation. Proning improves respiratory recruitment by taking advantage of the larger surface area of the posterior lungs. This improves V/Q matching and reduces atelectasis, resulting in improved pulmonary gas exchange.
In the hospital they have proning teams, which are crucial for patients who are intubated. In the prehospital care environment, with a few exceptions, no one is performing proning on intubated COVID-19 patients in the field.
Is there a role for proning prehospital? Yes, if it’s tolerated in the nonintubated patient, proning may improve pulmonary gas exchange. If a patient cannot tolerate being prone, see if they will bear transport in a lateral recumbent position. In the intubated patient being transported by EMS, proning may not be practical. It would be difficult to implement, since you need space and personnel to manage your patient, both of which are in short supply in the back of an ambulance.
Some services and emergency departments have reported the use of ipratropium has made symptoms worse in COVID-19. There is no concrete evidence one way or another. We are typically avoiding aerosol-generating procedures, but if we have extended transport times, this may be something to consider if we need to provide treatment. Overall prehospital medications and therapies for the COVID-19 patients are a moving target.
Prehospital patients are managed symptomatically. The clinical bundle for EMS would include airway and oxygenation—maintaining systemic oxygenation is paramount. The IV fluid of choice is crystalloids, but it is a conservative approach to improve the patient’s condition. Too much fluid too fast will exacerbate the leakage in the alveoli. If you must transition to vasopressors, norepinephrine is the vasopressor of choice. If it’s unavailable, epinephrine and vasopressin are acceptable alternatives. The Society of Critical Care Medicine strongly recommends against the use of dopamine.
Keep it simple—when we administer oxygen and/or IV fluids, we are looking for a:
Change in mental status;
Resolution of shortness of breath at rest;
Improvement in hypotension from baseline.
A quick way to determine the effectiveness of fluid resuscitation is to utilize dynamic parameters such as skin temperature and capillary refill time to determine the patient’s response.
With either a symptomatic or asymptomatic patient, viral load, proximity, and duration are all factors we know influence whether we will contract COVID-19. Age and comorbid factors play a role in determining the severity.
The only factors we can control are proximity and time. This is important because we lack adequate PPE. The University of Washington has noted that with adequate PPE, the infection rate for prehospital care providers is 1%. If you have adequate PPE for an entire shift, wear it for every call, every patient. You should also put a surgical mask on every patient until the pandemic is resolved. The insidious nature of the disease is staggering: Around 25% of COVID-19 patients are asymptomatic. You could be treating a patient for an unrelated issue who is shedding virus without your knowledge. Put a mask on everyone.
This may seem like an over-the-top approach. Leadership requires us to do what we need to do before the wheels come off the train, not after. We can minimize our exposure by avoiding aerosol-generating procedures such as nebulized medications, using supraglottic airways to perform airway management, and using HEPA filters on our BVMs.
The back of any EMS unit is an enclosed space that allows concentrations of virus to build up rapidly. Use air conditioning, exhaust ventilation, and open windows to create a flow of air through patient compartment away from you. There have been some videos posted online of homemade hoods to protect providers when aerosol-generating procedures cannot be avoided or simply in a mistaken belief that it affords a greater degree of protection. These makeshift hoods and tents end up concentrating virus. Without an enclosed venting system, we may end up inadvertently making a bad situation worse. Use good judgement no matter what choice you make—make the one that provides the safest solution to your crew.
The dynamics of COVID-19 seem ever-changing. It is simple tools and techniques that will see us through this pandemic. Use dynamic measures that that will tell you if your oxygen therapy and IV fluid treatment are working: skin temperature, capillary refill, improvement in mental status, resolution of shortness of breath at rest, and improvement of hypotension from baseline. Crystalloids are our fluid of choice. If you have a conscious patient, see if they will tolerate being transported in a prone or lateral recumbent position. When transporting patients turn on your exhaust fans and air conditioning and open the windows. Wear your PPE on every call for every patient and put a mask on every patient.
Daniel R. Gerard, MS, RN, NRP, is EMS coordinator for Alameda, Calif. He is a recognized expert in EMS system delivery and design, EMS/health-service integration, and service delivery models for out-of-hospital care.