Controversies in the management of COVID-19

Professor Dr. Md. Toufiqur Rahman
MBBS, FCPS, MD
Professor, Cardiology
CMMC, Manikganj
Controversies in the
management of Covid-19

Controversies in the management of Covid-19
 Origin of virus??
 Transmission of virus??
 First case in Wuhan?
 Aerosol transmission? Fomites? Re- infection/
reactivation
 Vaccine/ safety & efficacy/ antibody test/
community transmission?
 Case definition?
 Pathophysiology/ pathology
 Cardiovascular manifestations/ risk?
 ACS
 Role of aspirin
 Low platelet in covid-19
 Anti-coagulants
 ACEI/ARB/ARNI
 Diuretics
 Clinical features
 High risk groups
 Antibiotics
 HCQ& Lopinavir, Ritonavir
 Anti viral drugs- remdisivir/ favipiravir
 Biological therapy- tocilizumab
 Convalescent plasma therapy
 Systemic steroids
 Ivermectin
 NSAIDs
 Respiratory failure
 Other management in covid 19- fluid/ nebulization
 Chemoprophylaxis
 Bronchial asthma
 Anti diabetics

COVID- 19 epidemic – A coronavirus disease
• SARS-CoV-2 is an RNA virus
• Relates to SARS-CoV and MERS-CoV
• Primary host ? bats
• Intermediate host ? pangolins
• Full genome published in GenBank
• Several strains?????.
Shereen MA et al. J Adv Res. 2020 Mar 16;24:91-98.
Controveries in the management of Covid-19

Updated Status
■ First appear in Wuhan, china in 31st December 2019???.
■WHO defined global health emergency on 30th
January 2020.
■WHO Declared Pandemic on 11th march 2020.
■So far more then 1Crore 56 lac people affected &
more then 6.37 lac patient died(24.7.2020)
■In Bangladesh first case detected on 8th march now
more then 2 lac 18 thousand confirmed cases &
about 2836 death(24.7.2020)

Transmission
• Man to man transmission??
• Mostly, droplet infection, also airborne????? Aerosol?
• Direct contact, e.g., touching, shaking hands??
• Fomites, e.g., touching contaminated object??
• ? Faecal-oral transmission
• Re-infection????
• Re-activation????
• Severity of disease is dose dependent? Viral load? Mask?

• Using sequential samples from SARS-CoV-2 infected individuals collected up to
94 days , we demonstrate declining nAb titres in the majority of individuals.
• For those with a low nAb response, titres can return to base line over a relatively
short period
• We demonstrate that the magnitude of the nAb response is dependent upon the
disease severity
• A similar decline in nAb titres was also observed in a cohort of seropositive
healthcare workers from Guy’s and St Thomas’ Hospitals.
• this transient nAb response is a feature shared by both a SARS-CoV-2 infection
that causes low disease severity and the circulating seasonal coronaviruses that
are associated with common colds.
• This study has important implications when considering widespread serological
testing, Ab protection against re-infection with SARS-CoV-2 and the durability of
vaccine protection.
Re-infection
Longitudinal evaluation and decline of antibody responses in 1 SARS-CoV-2 infection
https://doi.org/10.1101/2020.07.09.20148429.this version posted July 11, 2020.
Department of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.

Vaccine
 More than 102 now
 Spike protein/RNA?
 Degree and duration of protection in doubt??
 T cell immunity???? Asymptomatic? Re-infection??
 CanSino Biologics Inc. viral vector vaccine, China (Phase 3)
 University of Oxford’s viral vector vaccine, UK (Phase 3)-
short term efficacy/safety published in LANCET
 Biontech’s mRNA vaccine, Germany (Phase 1/ Phase 2)
 Moderna’s mrna vaccine, USA (Phase 1)
The Global Alliance for Vaccines and Immunisation. https://www.gavi.org/vaccineswork/covid-19-vaccine-race, accessed 10
May.
Dr. Elisa Granato, the first human to
receive hAdOx1 nCoV-19 vaccine from
Oxford Vaccine Group.
Antibody test??? Herd immunity???
Community transmission high

Any case with fever/ feverish/any other
symptoms of Covid-19 or patient with any new
symptoms/ abnormal symptoms should be
suspected, investigated and treated as Covid-19
until other diagnosis is confirmed during
Pandemic and large scale community
transmission.
Feverish/cough/sore throat/
itching/myalgia/headache/ vertigo/severe
weakness/ SOB/ Chest
tightness/Rhinorrhoea/Flatulence/ Diarrhoea/

Late cytokine storm??
Late Auto-immune ??
Happy Hypoxia??
Iron- RBC theory/ HCQs??
Coagulopathy???

How COVID-19 Virus damage organs
• Direct attacking organ mediated through ACE 2 receptor.
• Indirectly attacking organ by the way of collateral damage
from cytokine storm.
• Indirectly cause damage by means of micro or macro vascular
clot as a part of systemic coagulopathy triggered by
endothelial injury & cytokine storm.
• Indirectly cause damage by low oxygen, inappropriate
ventilator setup, drug side effects all individually or in
combination.

Autopsy finding of COVID-19 patient
• Diffuse alveolar damage with micro vascular
thromboembolism.
• Alveoli are filled with fluid, protein WBC and debris.
thus increase gas exchange barrier.
• Viral particle were found in nose, throat, tear, stool,
kidney, liver, pancreas heart and CSF.
• Feature of coagulopathy as evident by DVT, PE, Stroke,
acute limb ischemia.

Viral infection & Effect on CVS
Direct
myocardial
invasion may
be related
with ACE 2
Salt a&
water
retention
Sympathetic
activation
Cytokine
release
Vasculitis/Hyper
-coagulopathy
Pneumonia/ARDS/
Systemic infection
Myocarditis
Heart Failure Arrhythmia Myocardial Ischemia
Plaque instability

Cardiovascular manifestations in COVID-19
• Arrhythmias
• Myocardial injury
• Acute MI
• Myocarditis
• Pericarditis
• Pericardial effusion ±
tamponade
• Pulmonary embolismChapman AR et al. Circulation. 2020 Apr 6. doi:
10.1161/CIRCULATIONAHA.120.047008.

Asymptomatic biomarker elevation.
Acute Coronary Syndrome including AMI.
Cardiomyopathy/ Stress cardiomyopathy/Takasubo???.
Arrhythmia.
Heart Failure.
Myocarditis, Pericarditis and myopericarditis.
Fulminant myocarditis and cardiogenic shock.
Spectrum Of Cardiovascular Involvement in COVID -19

In one study patient with severe symptom with COVID-
19, 58% had HTN, 25% had heart disease & 44% had
arrhythmia
Mortality data of NHC china 35% had HTN, 17% had CAD
Thus Patient with under lying CVD can aggravate &
increase the severity of symptom & might act as a
precipitating factor to worsen the condition lead to
death.
Relation of COVID-19 with pre-existing CVD

Overall mortality 0.2-3%
More the age higher the
mortality,(>85yrs60%).
Among ICU patient
mortality is 80%.
MORTALITY DUE TO COVID-19 INFECTION

COVID-19 is a
respiratory
disease????,
but many patients also
have CVD, HTN, acute
cardiac injury and
myocarditis
How many days we have
to be cautious???
Death before discharge?
Death after discharge
staying in home?
Death during competitive
sports? কর োনো জয়ী??

COVID- 19 and ACS
• Should be diagnosed on the basis of clinical presentation, ECG features,
and raised biomarkers – Type1/Type 2 MI- STEMI?- No obstruction- CAG
normal/ Endothelitis? Vasculitis? Role of Thrombolytics?
• Elevated troponin in isolation, may indicate myocardial injury, not AMI
• Thrombolytic therapy ??? may be the practical reperfusion strategy?
• Primary PCI ??? should only be done if dedicated cath lab and adequate
protection can be ensured
• Standard pharmacological therapy is advocated.

Is there any role of aspirin in COVID-19 ??
Early use of aspirin in covid-19 patients, which has the effects of inhibiting:
 Virus replication.
 Anti-platelet aggregation.
 Anti-inflammatory and anti-lung injury.
 Is expected to reduce the incidence of severe and critical
patients.
 Shorten the length of hospital duration and reduce the
incidence of cardiovascular complications.
Aspirin 100mg daily is on phase 2, phase 3 Trial.
 DAPT+ LMWH/UFH/DOAC-NOAC ??????/ Post PCI/ CABG/ PVD/Post MI

Thromboprophylaxis in COVID- 19 illness
• Indicated in all hospitalized patients without active bleeding
• Held if platelet count <25 x 109/L, or fibrinogen <0.5 g/L
• Abnormal PT or aPTT is not a contraindication
• LMW heparin is favoured, ? Intermediate intensity
• Rivaroxaban 10 mg daily for ?3 months for post-discharge prophylaxis
• Aspirin may be for low-risk patients post-discharge.
American Society of Hematology on COVID- 19. Available at:
https://www.hematology.org/covid-19/covid-19-and-vte-anticoagulation

Anticoagulant
Anti-inflammatory
Endothelial protection
Antiviral?
Potential impact of
Heparin
In COVID
HEPARIN & COVID-19
LMWH/ UFH Vs DOAC ?????

Anticoagulation
Strongly recommended each individual should be on DVT Prophylaxis
(LMWH 40 mg SC daily or Heparin 5000 units SC BD) until there is any
contraindication.
COVID-19 can lead to hypercoagulable state due to systemic
hyperinflammation and direct viral endothelial injury.
D-dimers and DIC screening (INR, APTT, Fibrinogen) should be routinely
checked.
Should be vigilant for venous thromboembolism (DVT/PE) and
consider for therapeutic anticoagulation if there is evident clinical or
biochemical (High level of D-dimer >1,000-2,000 ng/ml) suspicion.
There is post discharge 4-6 weeks of oral anticoagulation (Rivaroxaban
10 mg daily) or prophylactic LMWH also suggested in high risk cohort.

AnticoagulationControversies in the management of Covid-19

British Thoracic Society guidance on VTE in COVID-19
VTE risk Anticoagulation regimen
Standard risk
(D-Dimer <1,000mcg/L)
Standard prophylactic dose LMWH:
Enoxaparin 40 mg once daily
High risk
(D-Dimer <1,000-3,000mcg/L)
Intermediate dose LMWH:
Enoxaparin 40 mg twice daily
Acute VTE, proven or suspected
(D-Dimer <3,000mcg/L)
Therapeutic dose LMWH
Anticoagulation for 3 months.
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&cad=rja&uact=8&ved=2ahUKEwjD9av_75fpA
hUTxzgGHaDDAWQQFjABegQIAxAB&url=https%3A%2F%2Fwww.brit-thoracic.org.uk%2Fdocument-
library%2Fquality-improvement%2Fcovid-19%2Fbts-guidance-on-venous-thromboembolic-disease-in-patients-with-
covid-19%2F&usg=AOvVaw1wijaI_6yIc_iYAM2V6TfV

5/12/18

COVID- 19 and heart failure
• Should be diagnosed and treated as per current
guidelines
• ACE inhibitors and ARBs should be continued
• ARNI should be used as per current guidelines

• Angiotensin-converting–enzyme (ACE) inhibitors and angiotensin-receptor blockers
(ARBs) have physiologic effects that could be either beneficial or harmful in patients
with COVID-19 (NEJM JW Cardiol May 2020 and N Engl J Med 2020; 382:1653). In
three retrospective studies, researchers have addressed this issue.
• In a single-center Chinese study that involved 362 hospitalized COVID-19 patients
with histories of hypertension, 32% were taking ACE inhibitors or ARBs on admission;
the drugs were continued if possible. Researchers found no difference in severity of
COVID-19 or mortality in users of ACE inhibitors or ARBs compared with nonusers.
Statistical adjustment for potentially confounding factors was not conducted.
Covid-19 and ACEI/ARB

In a multicenter Chinese study of 1128 hospitalized COVID-19 patients with histories of hypertension,
17% were taking ACE inhibitors or ARBs; the drugs were continued during hospitalization in two thirds
of these patients. Mortality was significantly lower in ACE inhibitor or ARB users than in nonusers (3.7%
vs. 9.8%). In a propensity-score matched analysis to adjust for potential confounders, mortality
remained significantly lower in ACE inhibitor or ARB users (adjusted hazard ratio, 0.37).
• Finally, U.K. researchers have posted a “preprint” report of 205 COVID-19 patients, 37 of whom who
took ACE inhibitors within 7 days before symptom onset or during hospitalization. The proportion
of patients who died or required critical care support was lower in ACE inhibitor recipients
than in other patients (14% vs. 29%); the difference was significant after adjustment for multiple
confounding variables (adjusted odds ratio, 0.29). Because only 9 patients were taking ARBs,
outcomes with ARBs were not examined.

• Mehra et al.conducted a database study involving patients who had been hospitalized in 11
countries on three continents. The study included 8910 patients who had received a
diagnosis of Covid-19, who had been admitted to the hospital between December 20, 2019,
and March 15, 2020, and who had either died in the hospital or survived to hospital
discharge. In multivariate logistic-regression analysis, an age greater than 65 years, coronary
artery disease, congestive heart failure, history of cardiac arrhythmia, chronic obstructive
pulmonary disease, and current smoking were associated with an increased risk of in-
hospital death. Female sex was associated with a decreased risk. Neither ACE inhibitors nor
ARBs were associated with an increased risk of in-hospital death. A secondary analysis that
was restricted to patients with hypertension (those for whom an ACE inhibitor or ARB
would be indicated) also did not show harm.

Mancia et al. conducted a case–control study involving patients with confirmed Covid-
19 in the Lombardy region of Italy, which has been severely affected by the pandemic.
In this analysis, 6272 people with confirmed SARS-CoV-2 infection that had been
diagnosed between February 21 and March 11, 2020, were compared with 30,759
controls who were matched according to age, sex, and municipality of residence. In a
conditional logistic-regression multivariate analysis, neither ACE inhibitors nor ARBs
were associated with the likelihood of SARS-CoV-2 infection. An additional analysis
comparing patients with severe or fatal infections with matched controls also did not
show an association between these drugs and severe Covid-19.
33

• Reynolds et al. conducted a study based on data from the electronic health records of
12,594 patients in the New York University (NYU) Langone Health system who were
tested for Covid-19 between March 1 and April 15, 2020. A total of 5894 patients had a
positive test, among whom 1002 had severe illness (defined as admission to the
intensive care unit, mechanical ventilation, or death). Propensity-score matching was
performed among all tested patients and among patients with hypertension (to assess
whether the likelihood of a positive test result was associated with each of several
antihypertensive drug classes), as well as among Covid-19–positive patients and all such
patients with hypertension (to assess whether the likelihood of severe illness among
those with a positive test was associated with the same drug classes). The investigators’
Bayesian analysis showed no positive association for any of the analyzed drug classes,
including ACE inhibitors and ARBs, for either a positive test result or severe illness.

Mehra et al. found that use of either ACE inhibitors or statins may be
associated with a lower risk of in-hospital death than nonuse, but
neither of the other two studies estimated a lower risk of Covid-19 or
the likelihood of a positive test among patients treated with these
agents. The unexpected result in the study by Mehra et al. may be due
to unmeasured confounding and, in the absence of a randomized trial,
should not be regarded as evidence to prescribe these drugs in patients
with Covid-19.
35

• Use of diuretics in HTN/ HF during Covid-19
positive patients??

Clinical features
Fever or chills
Cough
Shortness of breath or difficulty breathing
Fatigue
Muscle or body aches
Headache
New loss of taste or smell
Sore throat
Congestion or runny nose??
Nausea or vomiting
Diarrhea??
Symptoms may appear 2-14 days after
exposure to the virus.
CDC, May 13, 2020
Controversies in the management
of Covid-19

People at Increased Risk for Severe Illness
• 1. Older adults Age>65 years
• 2, Medical conditions ??? Anti-coagulants???
Level of evidence
Strongest and Most
Consistent Evidence
Conditions
1. Serious heart conditions, such as
heart failure, coronary artery
disease, or cardiomyopathies
2. Chronic Kidney disease
3. COPD?
4. Obesity (BMI> 30)???
5. Sickle cell disease
6. Solid organ Transplantation????
7. Type 2 Diabetes mellitus
Level of Evidence
Mixed Evidence
Conditions
1. Asthma?
2. Cerebrovascular disease
3. Hypertension?
4. Pregnancy?
5. Smoking
6. Use of corticosteroids or other
immunosuppressive
medications ?? SLE/RA?
Limited Evidence: Bone Marrow transplantation, HIV, Immune deficiencies, Inherited
Metabolic disorders, Other chronic lung diseases, neurological conditions, liver disease, Type 1
diabetes mellitus, Thalassemia
CDC, June 25, 2020

Real-time RT-PCR test for SARS-CoV-2
 All suspects should have RT-PCR
 Gold standard
 High specificity, low sensitivity (65-95%)???
 Specimen:
– Upper airway specimens: Nasopharyngeal swab (first
choice), oropharyngeal swab
– Lower airway specimens: Bronchoalveolar lavage,
tracheal aspirate, pleural fluid, lung biopsy, sputum

Serological tests for SARS-CoV-2
• Low sensitivity, good specificity
• Still not recommended by WHO
• important for sero-surveillance
• Vaccine???
• Convalescent plasma therapy?? Neutralizing antibody titre?
• Passport to fly? Passport to work?

Current status of COVID- 19 tests
Test Specimen POC use Interpretation Use
NAAT
(RT-PCR)
NP swab, BAL,
sputum, blood, faeces
No Confirms current
infection
Individual
testing
Ab-based
immunoassay
Serum Yes Ig M 3-5 days of onset;
Ig G past infection
Community
surveillance
Ag-based
immunoassay
NP swab, BAL,
sputum, blood, faeces
Yes Confirms current
infection
Individual
testing
Clinical tests CT chest Yes Infection possible Triage
ESC Guidance for the Diagnosis and Management of CV Disease during the COVID-19 Pandemic. Available at:
https://www.escardio.org/Education/COVID-19-and-Cardiology/ESC-COVID-19-Guidance

CXR vs. CT scan of chest
Ground glass opacities in right lower lobe on CT (red arrows) are not visible on chest radiograph,
which was taken 1 hour prior to CT-study.
https://radiologyassistant.nl/chest/lk-jg-1
High sensitivity (94%) but low specificity (37%)
Less sensitive than CT scan of chest

Even before RT-PCR is available…..
• Ancillary tests can help!
• Normal or low WBC count, lymphopenia, high CRP,
low procalcitonin If associated with bilateral
pneumonia in CXR or ground-glass opacity in CT
chest diagnosis is COVID 19 during ongoing pandemic.
• Serological test specially antigen-based test can be
alternative test.

Supportive therapy
• Hydration, antipyretics (Paracetamol),
• close monitoring of vitals including Oxygen
saturation.

• Broad spectrum antibiotics should be considered for all
cases with Lung infiltrates
• According to the institute’s antimicrobial guideline. The
following is a suggestion:
• -IV Ceftriaxone 2 gm daily or IV Meropenem 1 gm TDS
plus oral Azithromycin or Doxycycline.
• Plus, IV Colistin and IV Vancomycin (If risk of MRSA
infection) if on mechanical ventilation.

Hydroxychloroquine (HQ) and Lopinavir/Ritonavir
• Hydroxychloroquine (HQ) and Lopinavir/Ritonavir
(Anti-HIV drug) are not recommended.
• There is increased cardiotoxicity associated with
HQ and increased mortality has been observed
(HQ + Azithromycin) in recent observational
studies.
• HQ alone or HQ + Azith / Lopinavir + Ritonavir are
not recommended except for trial

Anti-Viral drugs
A. Remdesivir 100 mg IV daily (200 mg on first day, then 100 mg daily) for 10 days
for severe cases.
Remdesivir 100 mg IV daily (200 mg on first day, then 100 mg daily) for total 5 days
can be considered for less severe cases.
Nil mortality benefit but reduces time to recovery.
Inclusion criteria:
???Saturation less than 94% or requiring supplemental oxygen or on mechanical
ventilation.
Exclusion criteria: Evidence of multi-organ failure, Ionotrops requirement to
maintain blood pressure, ALT > 5xULN, creatinine clearance < 30 ml/min, on ECMO.
Adverse effects: No available data. Deranged LFT, infusion-related reactions- low BP,
nausea, vomiting, sweating, and shivering.
B. Favipiravir 1600 mg PO BD on Day 1 then 600 mg BD for total 10 days.
This can be considered as a cost-effective alternative.

Biological Therapy
• Tocilizumab (Anti-IL-6) 8mg/kg (Max dose 800 mg; infusion over an hour) .
• Repeat dose after 8-12 hours if deteriorating or no clinical improvement.
Indication:
• Bilateral lung infiltrates
• Needs supplemental oxygen to maintain saturation above 92% or PaO2 /FiO2 <300 mmHg, RR >
30/min
• Features suggestive of cytokine storm(hyperinflammation) including ferritin ≥ 500, CRP>50,
LDH>250, Lymphocyte count <0.6, D-dimer >1000 ng/ml (at least 2 criteria fulfilled)
• Patient requires baseline QuantiFERON gold, Hepatitis B serology (including cAb), Hepatitis C
serology, baseline D-dimer, Troponin, CK
• Adverse effects: Mild neutropenia, deranged LFTs.
Exclusion:
• Active diverticulitis or oesophageal perforation
• LFT 5x times of the reference range
• Current TB, bacterial or fungal infection not being treated
Tocilizumab is advised to use even
at early stage! If features of
cytokine storm (at least 2 of these
criteria- CRP>50, Ferritin> 500,
LDH>250, Lymphocyte<600, D-
Dimer>1000)

Convalescent Plasma therapy
This has shown some efficacy in COVID cases on mechanical ventilation or
ECMO in observational data.
Controversies in the management of
Covid-19

Convalescent Plasma therapy
Covid-19

Systemic steroids???
• Systemic steroids should be avoided in early viremic phase
and in mild COVID cases given potential harm.
• Steroids can be considered in severe/critical COVID cases
requiring oxygen or ventilatory support ( RECOVERY Trial) ,
refractory septic shock, severe ARDS and evident cytokine
storm ( in addition to Tocilizumab).
• Methylprednisone 1-2 mg/kg BD or oral Dexamethasone 10
mg BD for 5-7 days.
Controversies in the management of Covid-
19

Ivermectin
• A single dose of Ivermectin (anti-parasitic drug) showed viral
clearance in 48 hours in laboratory setting.
• There is some weak human study
• Not recommended at this stage.
Covid-19

Different Drugs interaction in covid-19 patients
• Lopinavir/ritonavir – Reduction in effective dosage of clopidogrel increase effects of
ticagrelor & DOAC.
• In the absence of contraindications, is to use prasugrel.
• No co-administration of rivaroxaban, edoxaban.
• Reduced dosage of apixaban, warfarin.
• No dose adjustment of dabigatran.
• Rivaroxaban has no drug interaction with hydrxychloroquine or azithromycin.
• If patients have been taking antithrombotic agents for prior known thrombotic
disease, they should continue their antithrombotic agents as recommended.
• Remdesivir and immunomodulatory drugs show no significant interactions.

NSAIDs and Covid-19
• There are reports of NSAID use preceding clinical
deterioration in some patients with severe COVID-19 disease.
• recommended to avoid prescribing NSAIDs while patients
are admitted.
Myalgia/ arthalgia???/ RA/ SLE/AS/MCTD/Arthritis

Respiratory Failure
Supplemental oxygen with nasal prongs / full face
mask/ NRB mask to maintain saturation 92-96% (88-
92% in COPD).
• We recommend intermittent awake prone positioning
to improve VQ mismatching.
• HFNC and CPAP therapy in a safe clinical environment
should be considered prior to mechanical ventilation.
Oxygen/ Ventilator/NIV/ Prophylactic anticoagulant??
? ARDS/ PE/Pneumonia-bacterial/viral/coagulopathy-GGO

Fluid management: A conservative fluid management strategy is
recommended until evident tissue hypoperfusion. Where possible
avoid ‘maintenance' intravenous fluids, high volume enteral nutrition,
and fluid bolus for hypotension.
Suctioning: Closed inline suction catheters are recommended. Any
disconnection of the patient from the ventilator should be avoided to
prevent lung decruitment and aerosolization. If necessary, the
endotracheal tube should be clamped and the ventilator disabled (to
prevent aerosolization).
Nebulisation: Use of nebulisers is not recommended and use of
metered dose inhalers are preferred where possible.

• Bronchoscopy: Diagnostic bronchoscopy is not recommended. It is not
necessary for the diagnosis of viral pneumonia and should be avoided to
minimise risk of aerosolization. Tracheal aspirate samples for diagnosis of
COVD-19 are sufficient and Bronchio-alveolar lavage (BAL) is not usually
necessary.
• Extubation from mechanical ventilation: Standard weaning protocols
should be followed. HFNO and/or NIV (well fitted facemask with separate
inspiratory and expiratory limbs) can be considered as bridging therapy
post-extubation but must be provided with strict airborne PPE.
• Tracheostomy: This represents an aerosolizing procedure and must be
considered in clinical decision making. Optimal PPE should be utilized at all
times.

Chemoprophylaxis
• HQCs is not recommended now as chemoprophylaxis for health care
workers

COVID- 19 and bronchial asthma
• Standard guideline should be followed
• Inhalers with spacers should be
continued as usual
• Steroid as inhalers and rescue therapy
are not contraindicated

COVID- 19 and DM
 Insulin: Should not be stopped
 DPP4 inhibitors e.g., linagliptin, sitagliptin: Well tolerated
 Metformin: Should be stopped; dehydration and lactic acidosis???
 SGLT2 inhibitors e.g., empagliflozin: Should be stopped, risk
of dehydration and DKA ???
 GLP-1 receptor agonists, e.g., liraglutide: Dehydration likely?
Bornstein SR et al. Lancet Diabetes Endocrinol. 2020 Apr 23.
pii: S2213-8587(20)30152-2. doi: 10.1016/S2213-8587(20)30152-2.

Hospital discharge criteria
 Resolution of fever without antipyretics AND
 Significant improvement of respiratory symptoms AND
 Two negative RT-PCR test (only NP swab) 24 hours apart.
 If, 2 negative RT-PCR test could not be done:
 Must be met criteria 1 and 2 for consecutive 3 days.
 After discharge, home (or, institutional) isolation for 2 weeks.
Discharge criteria for COVID- 19 patients. Directorate General of Health, Government of
the People's Republic of Bangladesh, 5 May, 2020

Post-discharge care
• Home isolation for 2 weeks
• Avoid contact with infants, elderly
• Wearing masks and frequent hand washing by
patient and family members
• Monitoring of patient's condition.

Return to work criteria for HCW
 Symptomatic, confirmed or suspected HCW: 2 strategies:
 Test-based strategy (preferable)
 Non-test-based strategy
 Test-based strategy. Exclude from work until
 Resolution of fever and
 Improvement in respiratory symptoms (e.g., cough, SOB), and
 Negative RT-PCR from at least 2 consecutive specimens ≥24 hours apart.
https://www.cdc.gov/coronavirus/2019-ncov/hcp/return-to-
work.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-
ncov%2Fhealthcare-facilities%2Fhcp-return-work.html.

 Non-test-based strategy. Exclude from work until
 At least 3 days have passed since recovery defined as resolution of fever and
improvement in respiratory symptoms (e.g., cough, SOB); and,
 At least 7 days have passed since symptoms first appeared.
 Asymptomatic, ‘confirmed’ COVID- 19 HCW:
 10 days from first positive test.
Return to work criteria for HCW

Return to work practices
 Wearing facemask till complete resolution of all symptoms or 14
days after illness onset, whichever is longer.
 Avoidance of contact with severely immunocompromised
patients (e.g., transplant, haematology-oncology) for 14 days
after illness onset
 Self-monitor and re-evaluation if respiratory symptoms recur or
worsen.

Controversies in the management of COVID-19

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