Updated: Sep 16
I have no doubt healthcare providers all over the world are conciously aware of every cough, scratchy throat, and body ache. Could this be it? Will I be laying prone in an ED bed texting with an SPO2 of 50%? As much as we try to follow the correct PPE procedures, social distance, and open doors with our elbows, the truth is, this virus is very contageous and our job puts us in front of the sickest people in our community.
I decided to write out my desired treatment plan if I catch this crap. This is a combination of "best data" and personal opinion. Please realize that at this point there is no vaccine or strong evidence for treatment.
When will I get tested?
The testing criteria is different depending on your region. There appears to be a lower threshold for testing healthcare providers because of their exposure to immunosupressed patients. While this makes sense, I will not get tested unless I meet two of the following:
- Develop a temperature (>100.4 oral)
- Dyspnea w/o exertion
- Multiple B lines on ultrasound per intercostal space (yes I have my own).
- Increased weakness
If I test positive:
I will self-isolate in my basement. I have a Lumify ultrasound and pulse oximeter I can use to monitor my daily disease progression. I will only go to the hospital if my shortness of breath becomes apparent upon rest or my SPO2 drops below 90% . This is purely because I do not have an oxygen source to supplement room air or power a CPAP device.
If I test negative:
I will self-isolate in my basement and unfortunately be unable to help take care of the baby in the middle of the night ????????♂️. If you hear the drums - it's just me trying to loosen up the secretions.
Most likely I will present to my local tertiary facility that has yet to experience many COVID19 patients. There will be an inherit desire to intubate me if my pulse ox follows the normal course we have seen in case reports. The "happy hypoxemic" with a saturation of 50% and speaking in full sentences without anxiety. I imagine I will present as what currently is classfied as a "Type L" patient. This patient has:
Low elastance (good compliance)
Low lung weight (less edema)
Low V/Q ratio ( shunt due to atelectasis)
Why I do not want to be intubated due to hypoxemia:
SARS-CoV-2 attacks type two pneumocytes. This particular pneumocyte is responsible for releasing surfactant. I am pretty sure everyone has heard of surfactant, but this junk is seriously important. Surfactant reduces the surface tension between air and water. Water has a higher surface tension because hydrogen loves to bond together tightly at the surface. If we infect our type 2 pneumocytes we decrease surfactant production and increase the risk of collapsing alveoli (atelectasis).
The longer the alveoli are collapsed, the harder it is to get them back... and keep them back. This will also depend on surfactant production within that region. It is reported that type L COVID19 patients respond very well to CPAP. Applying positive pressure to the alveoli will recruit lung units that have collapsed due to atelectasis. We recruit more lung by dropping our diaphragm with spontaneously generated negative pressure than we do with forced diaphragmatic displacement from positive pressure. This is precisely why I do not want to be intubated unless absolutely necessary. And when I say ABSOLUTELY NECESSARY, I mean mental status deterioration or signs of type two respiratory failure (failure to ventilate).
My hypoxemia should be treated with CPAP and positional optimization of alveolar blood flow (proning)
If I need to be intubated:
I think it is important that my respiratory goals are made clear:
1. Do not aim for an SPO2 of 100%. In fact, If you can keep me >85% I will be happy. Once we maximize a patient on 100% FIO2, the next normal progression is to increase PEEP. Type L COVID19 patients typically have good compliance and typically are not reported to need PEEP's above 10 cmH2O. Instead of increasing my PEEP, I would like you to increase my inspiratory time. It was once thought that PEEP should be set 2cmh2O above the lower inflection point of a pressure volume curve.
In reality, recruitment carries on past the lower inflection point and optimal lung recruitment takes longer than a second. For these reasons, I ask that once you get to a PEEP of 10 cmh2O - put me in APRV (airway pressure release ventilation). For an excellent breakdown of this mode check out Brian Kings blog here.
2. I believe there is a role for surfactant administration to maintain recruitment. Exogenous surfactant administration in adults is not well studied and not a routine practice. However, if you want to test it out on someone, I will volunteer and Sam Ireland will pay for it. Study looking at exogenous surf in adults here.
In the early viral stage of COVID-19 there does not appear to be an indication to administer steroids. If there was a role for antiviral therapy (i.g.hydroxy-chloroquine, chloroquine, remdesivir) it would be early. The use of steroids may have a role during the adaptive immune phase as illustrated below.
Illustration is orignally proposed by Hasan K. Siddiqi and recreated by FOAMfrat.
Like many infectious diesease progressions, it is rarely the initial viral response phase that is deadly - it's the body's immune response. Evidence interpretation for steroid use is lacking any statistical benefit, however the timing of when the steroid is administered is extremely salient. If given too early, immunosuppresion could increase viral replication. I am asking for steroids by day 5 - 10 of symptom onset if imaging and gases suggest worsening pulmonary condition and function. This is covered by Josh Farkas in a recent blog here.
There is well documented evidence of thrombotic events in COVID19 patients. There appears to be risk factors that potentiate the prevelance of either deep vein macro-vascular thrombosis or pulmonary micro-vascular thrombosis. If my D-Dimer increases >1500 ng/ml, please consider giving me low molecular weight heparin (lovenox) if my renal function is normal. If my renal function sucks.. just start heparin. What evidence we have for this D-Dimer cut off is found here.
Sedation & Paralysis:
If I am placed on APRV I request that you avoid paralysis if at all possible. Precedex is my desired sedation drug. Initially I may need some fentanyl as my body adjusts to intubation. The benefit of APRV is to allow me to breath on top of the P high. If my spontaenous effort is not communicating with the ventilator, I worry recruitment will remain sub-optimal.
It seems obvious, but get me off the ventilator as soon as possible. As mentioned above, recruitment is best performed by conscious diaphragmatic retraction. Place the ventilator into a CPAP mode while I am intubated and evaluate my spontaenous effort. I will admit that this area of care is beyond my expertise and I will have to trust that my care provider will keep me on the ventilator as minimal as possible.
In reality, my care will be in the hands of the pheneomenal providers who dedicate their life to caring for others. This blog was a unique way of laying out a care plan with what little literature we have on the current pandemic. Would you ask for something different? How would you want to be treated? I look forward to your response.
References are hyperlinked throughout the article.