COVID 19 Webinar

RT PCR – gold standard, detects SARS COVID 2 RNA NAAT PCR

Lower respiratory sample – higher viral load

Tx: Supportive Care,

*currently there is no studies that COVID 19 shows superinfection bacterial -> no
empiric therapy but empiric therapy is reasonable if diagnosis is uncertain

Remdesivir – under investigation, inhibits viral RNA polymerases (RdRp)

Hydroxycholorquine/ chloroquine -> blocks COVID 19 thru entry of the virus by

increasing the endosomal pH because COVID 19 favors acidic pH
- no published clinical tril in the use of prevention of COVID 19

Lopinavir-Ritonavir – inhibits translation of RNA (proteolysis)

Tocilizumab – IL 6 inhibitors, inhibits inflammatory reactions

D3-7: activation of the innate immunity in the lungs maladaptive immune response

*still no facts when to give the immunomodulators and anti-viral therapy but
experts say we can give it as early correlating with the symptoms of the patient; if
there are signs of cytokine storm -> give immunomodulators

Zinc Sulfate – no current clinical evidence, 2010 study showed inhibition of the
repilaction of SARS – coronavirus

Vitamin C – no evidence available on the efficacy of IV Vit C

Tx Goals: to prevent further lung damage

When to intubate:
1. hemodynmically unstable
2. Sensorial deterioration
3. Severe respiratory distress despite initial oxygen sup
4. O2 sat < 90

High Flow Nasal Cannula – lesser aerosol dispersion

Rpt Testing: NPS after 14 days of 1st positive test or once patient is afebrile for 3
days, if positive repeat test for 14 days.

Discharged patients:
1. rest home for 2 weeks after discharged
2. monitor temperature

Alpha and Beta Coronavirus -> only kind to infect humans

Studies used for tx: previous studies on SARS and MeRs-COV

ACE 2 receptors – lungs, myocardium, GI tract, kidneys

RT PCR – 60-70% sensitive

Warning Lab tests:

Lymphopenia:
Lymphocytes -> expressed by ACE2 receptors, ACE2 receptors -> attaches COVID
19
Lymphocyte apoptosis
Acidosis: inhibitor of lymphocyte proliferation
Neutrophil lymphocyte ratio: >9 critical, 6-9 stressed level

Shifting to leukocytosis: secondary bacterial infection

CRP: inflammatory -> inc. macrophages -> generates IL-6 -> releases CRP
LDH: cell turnover! (inc. viral load -> inc. viral infection -> necrosis of cell
membrane -> inc. cell turn over)
ProCalcitonin: initially is low; lower-> due to interferon gamma (mediator for viral
replication) -> downregulates ProCalcitonin
*but in covid infections more of INTERFERON GENE (alpha gamma)
high -> bacterial superinfection

D-dimer: hypercoagulable state (vascular endothelial damage sec to COVID

infection)

30-50% asymptomatic patients may have pertinent findings in CXR and vice versa
with symptomatic patients
CXR: ground glass appearance, consolidation, usually peripheral infiltrates
Chest CT scan: low sensivity, ground glass appearance (increased attenuation in the
lung; diffused opacity) on the peripheral area and basal portions distribution
bilateral generally, interlobular septal thickening, marked consolidation

Homogenous consolidation -> ARDS