COVID19 and Healthcare
These past few weeks have been crazy to say the least. But we wanted to gather the data we have been able to track thus far as it relates to the novel coronavirus and healthcare.
First things first, please stop wearing gloves in public, this is unnecessary. I’ve seen people outside, in stores wearing gloves to protect themselves, after touching a doorknob, then touching their car keys, cell phones, their face. This is counterproductive. In terms of wearing masks outdoors, this is recommended for those who are older, immune-compromised and so on. But when you wear your mask, be sure to (remove your gloves if you are incompetent enough to wear them in public) and wash your hands, because once you remove your mask your mask can be infected with what ever is on your hands. The best way to prevent the spread is to social distance, keep from small, close-quartered areas, wash your hands for 20+ seconds, avoid touching your eyes, nose and mouth.
Coronavirus (SARS-Cov-2) is an interesting virus, it utilizes "crowned" spikes on glycoprotein-envelopes that are critical for RNA replication. Anti-S2 compounds may be something to investigate. This is just fancy terms for: this virus is hard to infiltrate, defensively. It is effectively "inactivated" by lipid-solvents including 62-75% ethanol, chlorine-containing disinfectants, 0.5% hydrogen peroxide and 0.1% sodium hypochlorite (aka bleach) within one-minute (Ko, Rolain & Lee, 2020). Please don't attempt to mix, match or create your own disinfectant solutions, it is dangerous, and you will more likely do more harm.
Transmission: Respiratory-droplets (i.e. coughing, sneezing, suctioning, intubating), aerosolized transmission while in close-quarters (i.e. military barracks, college dorms, nursing homes, prisons, etc.), for infection close proximity is necessary. Usually the spread occurs in family members, healthcare workers and other close-contacts.
Studies have also shown that SARS-CoV-2 when aerosolized (coughed, sneezed, sprayed via secretions) can remain airborne and virally-effective for more than 3+ hours post-aerosolization, so in hospitals negative pressure rooms are key. If not available, cover the patients mouth with a surgical mask, use viral-filters on masks and decrease your exposures by wearing N95 or higher-grade respirators (Ko et al., 2020). The virus can remain active on:
· Plastics from up-to (approx.) 72-96 hours,
· Steel surfaces (including surgical stainless steel) for up-to 72-96 hours
· Copper surfaces or pennies for up-to 24-96 hours
· Cardboard for 24-96 hours if surfaces remain uncleaned by above products
Incubation periods have differed in various sources, some recommendations state 3-7 days and up to 2-weeks with documented cases having the “longest” time from infection-to-symptoms of 12.5 days with SARS-CoV-2 doubling on average every 7-days with an average infected-to-infection rate of 2.2 people (1:2.2)(Holshue, DeBolt & Lindquist, 2020).
This viral infection is capable in producing an excessive immune reaction in the host creating a “Cytokine Storm” with Interleukin-6 (IL-6) being the host protagonist. IL-6 is produced by activating leukocytes and promoting differentiation of B-lymphocytes, in turn stimulates production of acute-phase proteins (which plays important roll in thermoregulation, bone maintenance and CNS function). The cytokine storm or “cytokine release syndrome” is an acute systemic inflammation syndrome characterized by fever and MODs (multiple organ dysfunction)(Johnson & Gottlieb, 2020). The large increase of acute-proteins causes edema and proteinaceous exudates (large protein globules) and vascular congestion occurs due to combined inflammatory clusters of fibrinoid materials, multi-nucleated giant cells and hyperplasia of pneumocytes in the lungs (Xu et al., 2020).
Thus far, numbers of “mild disease” as it relates to COVID-19 is approximately 81% in both non-pneumonia and pneumonia. “Severe disease” accounts for 16-18% resulting in ARDS, dyspnea (SP02% >93%) and respiratory frequency of 30+ per minute.
Over 31 articles were reviewed with 46,959 patients from the United States and China, below are the percentages and average rates of the COVID-19 clinical presentation (Xi, Jing & Zhang, 2020):
Initial presentation includes:
· Fever (100.4+) – 87.7%
· Dry, hacking cough – 58.1%
· Dyspnea – 38.3%
· Muscle soreness/fatigue – 35.5%
· Chest distress/pain – 31.2%
· Conjunctivitis – 0.8%
The fever is often elevated, waxes and wanes and is hard to control and break. The cough is non-productive in early stages. Some cases also included mild nausea, some vomiting and GI upset. Interestingly, if the patient is complaining of dyspnea and hypoxia, ARDS usually follows within (on average) 2.5 days post-onset (Xi, Jing & Zhang, 2020)
Of this review, the average age of those clinically reviewed was a mean age of 46.62 years, with 55.6% of male gender. Thirty-six percent had co-morbidities to include hypertension (18.3%), cardiovascular disease (11.2%), diabetes (10.3%) and COPD (3.9%).
The outcomes of those patients included 29.3% needed ICU-level of care, 28.8% were diagnosed with ARDS, 8.5% had MODs and 6.8% had died from COVID-19 complications.
Aside subjective symptomology, some clinical presentations that have been noted include imaging and serum-based labs.
o Bilateral pneumonia in lower lobes (45.7%)
o Ground glass opacification (69.9%)
o Bilateral pneumonia (75.5%)
o Unilateral pneumonia (20.4%)
o Ground glass opacification (69.6%)
o Irregular HALO (54.4%)
o White Blood Cells (normal or decreased in late stage progression)
o Lymphocyte # (decreased in early stages)
o AST/ALT (increased)
o LDH (increased)
o Inflammatory markers:
§ ESR (elevated)
§ CRP (elevated)
§ Ferritin (elevated)
§ Troponin (possibly elevated, severe condition)
§ Dimer (late stage, severe condition, blood clot?)
o Neutrophil #: (increased in late stage, hemolysis risk, PE*)
o Procalcitonin (elevated if severe infection, poor prognosis)
In the review of literature, white blood cells were either within normal limits or decreased, unless the pneumonia had turned bacterial or patient was/is septic their WBC counts are normal. Statistics also show that mechanically ventilated patients are more likely to get HAI-PNA (approx. 12% currently) than bacterial infections from the viral pneumonia itself. Complications from COVID-19 include multiorgan failure (evidenced by AST/ALT, CRP etc.), congestive heart failure, shock, renal injury, sepsis, striated muscle lysis and diffuse intravascular coagulation rate (leading to pulmonary emboli in some).
Hypercapnia is rare in COVID-19 infections, acute hypoxemic respiratory failure is dominant. Cardiac injury in these positive patients (33% in United States) is a late complication (cardiomyopathy, pericarditis, congestive heart failure) therefore excessive fluids and re-hydration (despite increased lactic acid, hypotension and tachycardia) is not recommended. If patients are extremely hypotensive, we’ve been using vasopressors (Norepinephrine drips at 0.1-0.3) to assist with cardiac dysfunction and mechanical ventilation.
Procalcitonin is increased (usually) in the profoundly critical patients. Procalcitonin is usually used to differentiate viral and bacterial pneumonia and determine necessary antibiotics. In the absence of systemic infection, procalcitonin is restricted to the neuroendocrine (thyroid) cells and remains there until matured into calcitonin. When systemic inflammation does occur (by bacterial infection), procalcitonin is synthesized in a majority of tissues (often causing acute/chronic kidney disease) and is released into the bloodstream. In these situations, IL-6 will also be elevated. Rarely does viral infections cause an increase in procalcitonin, but due to the “cytokine storm” caused by COVID-19, the procalcitonin is evident. After this occurs and the prognosis worsens, the patient becomes more ill, within 2-4 hours of inflammatory stimulus these levels rise and peak at 24-48 hours (.
Once procalcitonin is notably elevated, monitor the declining lymphocyte count, the rise in D-dimer, Ferritin and IL-6. Usually these are indicative of non-survivors and death progression.
While managing patients, we’ve been aiming for a target SP02% of 90-96% (85-92% for chronic lung disease) and avoiding hyperoxygenation (unless pre-intubation). Our target is maintained by (preferred) low-flow nasal cannula at 6L/min. to minimize aerosol exposure. This is recommended over venturi/NRB R 10-20L/min which increases exposures ten-fold. Also using the ICU-based “SOFA scale” (Sequential Organ Failure Assessment) to focus on organ dysfunction and morbidity.
Be advised, in our experiences we’ve noted that intubated COVID-19+ patients require an increased dosage of RSI-related drugs and because of this and their pre-septic conditions their blood pressures are unstable and often require vasopressors to adequately profuse while allowing for oxygenation.
If you have any questions or would like clarification please feel free to email us at email@example.com
Holshue, M., DeBolt, C. & Lindquist, S. (2020). First Case of 2019-Novel Coronavirus in the United States. N Engl J Med 2020, Vol 382(4)929-936.
Johnson, S. & Gottlieb, D. (2020) What is Working for COVID-19 Patients. Emerg News Journal: Breaking News. Lippincott, Williams and Williams, Current 04/07/2020
Ko, W., Rolain, J. & Lee, N. (2020) Arguments in favor of Remdesivir for treating SARS-CoV-2 Infections. Int J Antimicrob Agents 2020:105933.
Wang, M., Cao, R. & Zhang, L. (2020) Remdesivir and Chloroquine Effectively inhibits the recently emerged novel Coronavirus (2019-nCoV) in vitro. Cell Res 2020, Vol 30(2) 269-271.
Xi, Y., Jing, Q. & Zhang, J. (2020) Imaging and Clinical Features of Patients with 2019 Novel Virus: COVID-SAR-2. Eu J of Nuc Med and Med Imaging. May 2020, Vol. 47(5):1275-1280.
Xu, Z., Shi, L., Wang, Y., Zheng, J, Huang, L. & Zhang, C. (2020). Pathological Findings of COVID-19 Associated with Acute Respiratory Distress Syndrome: Case Report. The Lancet Journal. Vol 8(4): 420-422. Doi: 10.1016/S2213-2600(20)20076-x/