Sunday, August 30, 2020

200 CMAAO CORONA FACTS and MYTH COVID: Non COVID phase

 

200 CMAAO CORONA FACTS and MYTH COVID:  Non COVID phase

 

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

 

1071:  Minutes of Virtual Meeting of CMAAO NMAs on “Covid-19 Update”

 

29th August, 2020, Saturday

 

9.30am-10.30am

 

Participants

 

Member NMAs

 

Dr KK Aggarwal, President CMAAO

Dr Marthanda Pillai, Member World Medical Council

Dr Alvin Yee-Shing Chan, Hong Kong

Dr Prakash Budhathoky, Nepal

 

Invitees

 

Dr Russell D’Souza, UNESCO Chair in Bioethics, Australia

Dr S Sharma, Editor IJCP Group

 

Key points from the discussion

 

  • Three acute phase reactants– CRP, ESR and IL-6. In a resource-limited country, of the three, choose CRP. It is indicator of intensity of inflammation. CRP cannot rise without increase in IL-6. Raised CRP, presume that the d-dimer is high.
  • We do not know how China which has a higher population density than India has managed to control the disease. Mortality is 3 per million; new cases are 9.
  • Antigens of various diseases such as typhoid, malaria, chikungunya, and dengue are false positive in Covid-19.
  • All overseas players and support staff underwent two COVID-19 RT-PCR tests before flying in to the UAE and could fly only if the tests are negative. If not, then the same 14-day quarantine period and two negative tests to be able to fly to the UAE. The players and support staff will be tested on Day 1, Day 3 and Day 6 of their quarantine in the UAE and after clearing that, they will be tested every fifth day during the 53-day event.” Instead of three tests, pooled testing of the teams can be done daily.
  • Giving oxygen without anticoagulation has no significance. You have to give aspirin/anticoagulation. For cases under home care, rivoraxaban (10 mg prophylaxis) can be given in place of LMWH; it is cheaper, can be taken by the patient, onset of action is 10 hours.
  • According to TOI report, 87,000 healthcare workers in India are infected with Covid; there have been 573 deaths; 74% cases and over 86% deaths are from six states: Maharashtra, Tamil Nadu, Delhi, West Bengal, Gujarat and Karnataka. The number projected seems to be very high and needs to be checked.
  • Doctors have high viral load so have higher chances of developing hypercoagulable state. Should prophylactic anticoagulation be started on right on Day 1 of the illness for doctors/HCWs?
  • There are three phases of the illness: Covid (1-9 days, infectious phase), post-Covid (after 9 days, non-infectious, persistent inflammation) and non-Covid (after 3 months). After 3 months, the patient should be treated as non-Covid, instead of post-Covid. This has medicolegal issues
  • In Hong Kong, the third wave is partly controlled. There have been less than 20 cases per day for the last week or more. One-third of confirmed cases have no known source of origin; so the chain of spread of infection is not known. Universal community testing scheme will start from 1st September to find out silent carriers. The Hong Kong government has agreed to expand to high risk group tracing and testing even with universal testing. With opening up of economy, better monitoring of industries so that there will not be a fourth wave. The third wave began with 9 cases with mutated virus strain (d614g). At that time, sailors coming to Hong Kong had been exempted from testing and quarantine; also restrictions of social distancing were relaxed. This created the third wave.
  • Reinfection: A person from Spain positive in March and became negative reached Hong Kong and tested positive again in July. This raises a question whether this virus can re-infect. It was a mutated virus with 24 gene differences. It formed antibodies quickly, caused no symptoms and not serious and disappeared early. We need to be vigilant about this. People in post-Covid phase getting recurrent corona-like illness may be getting re-infection with a different strain.
  • Another case of re-infection reported in the US; a young person who had severe symptoms and required oxygen and assisted breathing in the second infection.
  • A study from Mumbai has reconfirmed the US study that antibodies do not last for more than 3 months.

 

 

 

 

 

 

 

 

Wednesday, August 26, 2020

196 CMAAO CORONA FACTS and MYTH COVID : Dentistry

 

196 CMAAO CORONA FACTS and MYTH COVID : Dentistry

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

 

1068: Study finds anaemia associated with severe COVID-19 illness

DG alerts excerpts: Research published in the Journal of Medical Virology point to anaemia being an independent risk factor tied to severe coronavirus disease 2019 (COVID‐19) said with Zheying Tao, Department of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China, and colleagues.

The odds ratio (OR) of anaemia related to severe manifestations of COVID‐19 in the study was 3.47and 3.77 after adjusting for baseline data and laboratory indices, respectively.

The retrospective, observational study involved a total of 222 patients with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) admitted to Wuhan Ninth Hospital from December 1, 2019, to March 20, 2020. Among these, 202 were non-severe COVID-19 cases and 20 had severe disease. In addition, 79 (35.6%) of the 222 patients had anaemia, defined as haemoglobin level <120 g/L in women and <130 g/L in men, while the other 143 patients did not.

The authors reported that in severe COVID-19 patients, haemoglobin levels showed a significant decline when compared to non-severe patients (128 g/L vs 111.5 g/L, P=0.002). Further, significantly more patients in the severe group met the diagnostic criteria for anaemia (32.2% vs 70.0%, P=0.001).

The prevalence of severe illness in the anaemic group was significantly higher than that in the non-anaemic group (8.1% vs 17.7%, P=0.001). Compared to patients without anaemia, those with anaemia were older and more likely to have chronic kidney disease (0.0% vs 3.8%), cardiovascular disease (CVD) (3.5% vs 15.2%), and chronic obstructive pulmonary disease (COPD) (0.0% vs 10.1%) (all P<0.05).

COVID-19 patients with anaemia were predisposed to more severe inflammatory responses, coagulation disorders, and organ injuries. Specifically, more patients had elevated levels of C-reactive protein (CRP) (8.5% vs 24.7%) and procalcitonin (PCT) (1.3% vs 15.6%) in the anaemic group (all P<0.05). Patients with anaemia also showed significantly higher levels of erythrocyte sedimentation rate (ESR), D-dimer, myoglobin, T‐pro brain natriuretic peptide (T‐pro‐BNP) and urea nitrogen (BUN) (all P<0.05).

Forty-six patients were classified as having mild anaemia, whereas 29 and 4 patients were classified as having moderate and severe anaemia.

There was no significant difference in the proportion of severe patients or in mortality between the anaemia subtypes. However, severity of anaemia was "positively and strongly" associated with inflammatory responses and also positively associated with coagulation disorders, while no significant relationship with organ injuries was observed.

In univariate analysis, baseline data including age ≥60 years, anaemia, any comorbidities, hypertension, CVD, COPD, and laboratory indices containing CRP ≥10 mg/L, lactate dehydrogenase (LDH) ≥250 U/L, D-dimer ≥0.5 mg/L and creatinine ≥133 ╬╝mol/L were significantly associated with greater disease severity in patients with COVID-19.

Anaemia remained significant as an independent risk factor for patients with severe COVID-19 in the multivariable analysis, even after adjusting for baseline data and laboratory indexes.

Three patients died in the severe COVID-19 group (15%) compared to none in the non-severe group.

The prevalence of anaemia in hospitalised COVID-19 patients was up to 35.5%, which was "much higher" than a previous report that had found the frequency of anaemia in COVID-19 patients to be 15%.

As anaemia and low haemoglobin could decrease oxygen delivery, it is possible that COVID-19 patients are more susceptible to severe illness due to worse pulmonary function and poor tissue oxygenation.

Those with moderate-to-severe anaemia were more likely to present with dyspnea symptoms and lower levels of PaO2 and SaO2 than patients with mild anaemia.

Myocardial injury and renal dysfunction were more remarkable in patients with anaemia, possibly due to a progressive reduction in blood oxygen content and limited tissue oxygen delivery.

Thus, it is difficult to verify whether SARS-CoV-2 has a direct role in anaemia, as well as if patients have anemia of chronic disease."

 

Tuesday, August 25, 2020

195 CMAAO CORONA FACTS and MYTH COVID : Dentistry

 

195 CMAAO CORONA FACTS and MYTH COVID : Dentistry

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

 

1067: Update on Covid-19

 

IMA-CMAAO Webinar on “COVID-19 and Dentistry”

 

22nd August, 2020

4-5pm

 

Participants

 

Dr KK Aggarwal, President CMAAO

Dr Ramesh K Datta, Hony Finance Secretary IMA

Dr Jayakrishnan Alapet

Dr S Sharma

 

Faculty

 

Prof Dr Mahesh Verma

Prosthodontist

Vice Chancellor, Guru Gobind Singh Indraprastha University

Former, Director and Principal of Maulana Azad Institute of Dental Sciences

 

Key points from the discussion

 

  • Dentistry has progressed in the past few decades and it is now a huge group of Dental Sciences.
  • Nine specialties where MDS is offered: Oral medicine & Radiology, Prosthodontics, Conservative Dentistry & Endodontics, Orthodontics, Pediatric Dentistry and Preventive Dentistry, Periodontology, Oral & Maxillofacial surgery, Oral Pathology and Public Health Dentistry.
  • The dental profession has been very aware and proactive in strategising how to tackle the infection.
  • Initially only emergent and urgent cases such as pain, infection, bleeding, trauma, were attended to and elective procedures were delayed or postponed.
  • Guidelines for dental professionals were the first guidelines issued by the health ministry.
  • Every patient is a potential source of infection, whether Covid-19 or not.
  • All specialties other than oral medicine, oral pathology and a little bit of orthodontics generate aerosols as dentists work with a hand high speed instrument. Air and water produces a splatter of droplets with microbes.
  • The risk of infection in the dental profession is because of close proximity to the patient, micro-organisms in the mouth (remain viable and suspended in the air for long time as droplets) and droplets adhere to the surfaces (fomites).
  • Safety not only of the patient/doctor, but also the staff in the immediate vicinity and other staff is important.
  • For aerosol procedures, gown (impervious), mask (N95and triple layer), face shield, goggles, shoe cover, gloves are required.
  • Clinic is cleaned and sterilized before and after every patient. This is time-consuming so fewer patients are attended to now. One chamber works at a time, more ventilation, exhaust, windows open, extra-oral suction system, HEPA filters, UV lights, more air changes in AC (8-12/hour)
  • Infection and biomedical waste protocols are strictly followed now as increased risk of cross infection.
  • Earlier dentistry as a speciality was studied after completing MBBS (UK Royal Colleges), including in India (Annamalai University). As there are lot of biomechanical procedures involved, dentistry soon grew as a separate speciality.
  • Dentists work together with many medical specialities like ENT, plastic surgery, oncosurgery.
  • Often oral manifestations of a disease appear first and so are first incidentally diagnosed by dentists.
  • Oral cavity has lot of ACE2 receptors. So, the coronavirus can cause gingivitis, periodontitis. It does not involve tooth. But, if periodontium is affected, it can loosen the tooth.
  • Oral hygiene is very important as the oral cavity has millions of different pathogens. It is important to reduce the viral load before any procedure so fewer aerosols are formed. Ask the patient to do pre-treatment or pre-procedural rinse with hydrogen peroxide, povidone iodine.
  • Three basics for dental health: Brushing, flossing and swish (with water).

 

 

 

Monday, August 24, 2020

193 CMAAO CORONA FACTS and MYTH COVID : Formula of six

 

193 CMAAO CORONA FACTS and MYTH COVID : Formula of six

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

1065: Minutes of Virtual Meeting of CMAAO NMAs on “Asian countries update – Formula of Six”

 

22nd August, 2020, Saturday

 

9.30am-10.30am

 

Participants

 

Member NMAs

 

Dr KK Aggarwal, President CMAAO

Dr Yeh Woei Chong, Singapore Chair CMAAO

Dr Marthanda Pillai, Member World Medical Council

Dr Alvin Yee-Shing Chan, Hong Kong

Dr Marie Uzawa Urabe, Japan

Dr Md Jamaluddin Chowdhury, Bangladesh

Dr Prakash Budhathoky, Nepal

Dr Subramaniam Muniandy, Malaysia

 

Invitees

 

Dr Russell D’Souza, UNESCO Chair in Bioethics, Australia

Dr S Sharma, Editor IJCP Group

 

Key points from the discussion

 

Six things to remember in COVID-19

 

If you do not have Covid-19, ask yourself

 

  • “Am I at risk?”Age, sex (males more at risk), am I vaccinated (flu, pneumonia, MMR, BCG), do I have any comorbid condition, am I immunocompromised, is my profession high risk e.g. healthcare worker dealing with microdroplets.
  • “Is my environment at risk?”My room, my office, travel, kitchen, drawing and dining table, toilet – are they well ventilated or not.
  • “Am I prepared” Who will be my treating doctor, which hospital if I need admission, do I have stand-by oxygen, first aid box, notification (who should I notify), which lab for home test
  • “What do I do if I get it?” Do I need to isolate/quarantine/inform contacts, interpretation of rapid antigen test or RTPCR; start observing for symptoms; start treatment for Day 1
  • Observation days: 1-6 days (watch for hypoxia complications), Day 9 (allowed to meet family), Day 14 (no quarantine), Day 28 (consider plasma donation), Day 40, Day 90
  • 0-9 days: Nutrition, 6MWT, cohort isolation, blood tests, teleconsult, treatment
  • 9-90 days: Observe (for post-Covid symptoms), appeal, plasma donation, antibodies, antigen Ct value, nutrition

 

Six things to do to tackle Covid-19

 

  • During first 6 days (6am, 6pm) 6MWT, 6 parameters, 6 feet distance (ideal)
  • 6 parameters: Shortness of breath, cough or difficulty talking, SpO2, increase in temperature, distance and heart rate
  • 6 tests on Day 1: CBC with ESR, CRP, LDH, ferritin, d-dimer, IL-6
  • Six instruments at home: SpO2 monitor, PEFR, BP, thermometer, glucometer, smell and taste
  • Six gene targets: E, N, S, RdRp, ORF 1a, ORF 1b; gene targets may remain in the body for about 120 days
  • Reception (whosoever visits my home): Jaggery (taste), rose (smell), wash feet/hands, namaste (greet), ask to sit a higher place (no face to face meeting)
  • Decontaminate: 6 g bleaching powder in 900 ml water to make 0.1% solution
  • 6 Treatment options: Oxygen, plasma, steroids, heparin, antibiotics, antiviral

 

Six things for prevention

 

  • Contact time in last 48 hours, contact distance (was it less than 6 feet [ideal]), was the area cross ventilated, was the person wearing a mask and was the person coughing/sneezing
  • Appeals (ask for): Prevent, test, home (quarantine), cohort (two covid-positive persons can stay in isolation together), day 9, day 14 (stop quarantine, shift to monitoring)
  • 6 ways to clean and sanitize: Soap, sanitizer, disinfectant, UV, ozone, air purifier
  • 6 tastes: Astringent, bitter, pungent, sweet, sour, salt. In Covid-19, salt and bitter tastes are retained, while the rest are lost.
  • Mistakes: Missing first case in your family, first cluster in your colony, first spread, misinterpreting antigen / antibody test, missing Days 1-3 (pneumonia develops on Day 3)
  • 6 supplements: Vitamin C, D, B12, iron, zinc, thymosin alpha

 

Six things about the virus

 

  • Six different behaviors: Viral, bacterial, HIV-like, it causes immunoinflammation (antigen triggered), thromboinflammation and cytokine storm
  • Six strains: L strain (original strain in Wuhan), strains S, V, G, GR, and GH.

 

 

  • New definition: Acute manageable thrombo immunoinflammatory disease with post-viral state
  • The CDC has recommended maintaining a distance of 2 m (6 feet), while WHO has recommended maintaining a distance of 1 m (3 feet) as 2 m distancing may be difficult in developing countries.
  • The third wave in Hong Kong is coming down from 114 new cases in a day in July to 18 cases per day now. Hong Kong will launch en masse population screening program to identify silent carriers; screening will be voluntary. Should the rules about social gatherings be relaxed is a dilemma because of apprehension of another wave of the infection, which might exhaust the resources.
  • The first sero survey (done between June 27 and July 10) in Delhi showed 22.8% seroprevalence; the second sero survey (done in the first week of August) shows a seroprevalence of 28.3% (males 28.3%, females 32.2%, <18 years 35%, 18-49 years 29%, >50 years 31%).
  • Seroprevalence is 51.5% in Pune; in Mumbai, it is 57% in slums and 16% in residential societies
  • A study in Bangladesh conducted by the Institute of Epidemiology, Disease Control and Research and the International Centre for Diarrhoeal Disease Research, Bangladesh in Dhaka (RTPCR) has shown 9% of population in Dhaka has the infection.
  • Nepal is testing for Covid-19 with Gene Xpert test for emergency cases; it has 100% specificity, but sensitivity is around 50%. RT PCR is the gold standard.
  • Singapore is reaching the tail end of the outbreak in dormitories; community cases in the last week have been 0-2 in a day. Challenge is the next wave of infection, opening up of economy. Singapore is looking to open up travel to selected destinations.
  • Malaysia has detected D614g strain of the virus (mutation of SARS-CoV-2 virus) in a cluster of cases, which has been termed as the “Sivaganga cluster”. The index case belongs to Sivaganga in Tamil Nadu.
  • In Australia, all travel within the country has been stopped. Cases are coming under control in Victoria.

 

 

 

 

194 CMAAO CORONA FACTS and MYTH COVID : Post-Covid 19 inflammation

 

194 CMAAO CORONA FACTS and MYTH COVID : “Post-Covid 19 inflammation”

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

 

1066: Round Table Expert Zoom Meeting on “Post-Covid 19 inflammation”

 

22nd August, 2020

11am-12pm

 

Participants

 

Dr KK Aggarwal

Dr AK Agarwal

Dr Ashok Gupta

Dr JA Jayalal

Dr Atul Pandya

Dr Jayakrishnan Alapet

Dr Shantanu Tripathi

Prof Bejon Misra

Dr (Major) Prachi Garg

Ms Ira Gupta

Dr S Sharma

 

Key points from the discussion

 

  • Delhi has seroprevalence of 28%, but asymptomatic persons with no increase in CRP/ESR do not develop antibodies. We have been able to tackle the disease in Delhi, Mumbai and Pune.
  • In countries where 6 feet (2 m) social distancing is not possible, reduce the distance to 3 feet (1 m).
  • The need of the hour is one vaccine, one movement. Polio has been almost eradicated because of global effort for one polio vaccine, but this is not the case with Covid-19.
  • The government may revise its testing strategy to testing on demand.
  • We should come out with a consensus statement regarding international travel stating under what conditions the 7-day quarantine could be exempted.
  • Covid-19 disease has two phases: Viral phase and post-viral phase.
  • Viral phase can be divided into aggressive phase and non-aggressive phase. About 33% of patients in non-aggressive phase go into post-viral phase manifested as persistence of gene target positive for 120 days, fever, recurrent diarrhea, episodes of costochondritis, abdominal pain/nausea/vomiting, calf pain, rash, cystitis, lower abdominal pain, loss of smell/taste etc.
  • Pyrexia vs thermia: pyrexia is because of the organism (first 9 days); thermia is not due to the virus (after 9 days), it is caused by thermodysregulation in the hypothalamus. The fever is low grade, appears after exertion, all inflammatory marker are normal.
  • Phytoestrogens reduce IL-6; hence, soya, rich source of phytoestrogens can help.
  • Some patients have post-Covid persistent inflammatory state – rising inflammatory markers or reducing but not rapidly.
  • Do CRP as follow up test. If normal, then IL-6 is normal; if high, then IL-6 is high. This means that the person can still go into delayed cytokine storm.
  • After 9 days, even if no fever but raised CRP/ESR with/without increased IL-6: Curcumin (TNF like activity), soya protein (reduces IL-6), NSAIDs (nimesulide, mefenamic acid, naproxen, indomethacin), hydroxychloroquine (discarded but remerging in post-covid illness).
  • If the patient develops symptoms again e.g. diarrhea with raised ESR/CRP, is it re-infection? We do not know.
  • If first diagnosed as post-Covid illness after having missed earlier diagnosis, the prognosis may be unfavorable.
  • In high prevalence area, both antigen and antibody tests should be done together.
  • According to the CDC, the virus particle may be detected in the body for up to 120 days. This is persistent inflammation or the persistent virus particle, which is causing the inflammation.
  • Do baseline CBC with ESR, CRP, IL-6, LDH, ferritin, d-dimer. A rapid rise in any of these is important.
  • If CT scan is positive on Day 3 (pneumonitis) with more than 2-fold rise in CRP/ESR or rapid rise (>2-fold) in IL-6, this is the time to give remdesivir. If available give it on Day 1, but definitely on Day 3 along with LMWH (to reduce thrombosis) and steroid (to reduce IL-6). Give heparin for 9 days, then shift to dabigatran/rivoraxaban x 40 days or even more, depending on the hypercoagulable state of the patient.
  • Patients with GI symptoms (diarrhea) may have more severe disease and higher mortality.
  • Off-label use is anecdotal evidence. Off-label use does not require trial; it is a shared decision made by the patient and all legal heirs and the doctor after informed consent. Consent may be routed through Ethics Committee if it is a hospital policy.
  • If post-Covid patient needs oxygen, this means either resolving pneumonia or that the patient has developed lung fibrosis.

 

 

 

Saturday, August 22, 2020

192 CMAAO CORONA FACTS and MYTH COVID : Autopsy reports of COVID 19 patients

 

192 CMAAO CORONA FACTS and MYTH COVID : Autopsy reports of COVID 19 patients

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

1064: Medscape excerpts

 

1.           Every organ in the body is pretty much affected.

2.           Conducting COVID autopsies has been like going to a police line up where one might not be able to definitively pick out the perpetrator but unlikely suspects can be eliminated

3.           We've learned through autopsy that there's no direct tissue pathology to account for the acute symptoms that are seen" in the heart, the kidney, and the brain

4.           Pathologists have postulated a handful of hypotheses about the causes of extensive organ damage in COVID-19, including that hypoxia resulting from compromised lung function may be causing secondary injuries

5.           obesity pre-disposes the infected to worse morbidity and mortality. Obesity in and of itself is a pathologic state, that it leads to atherosclerosis, increased clotting, fatty liver disease, and often, enlarged hearts.

6.           SARS-CoV-2 is exhibiting a selectivity for the lungs. In one decedent, bone marrow response was observed with many myeloid precursors in the peripheral blood vessels typical in an overwhelming infection.

7.           The cells that SARS-CoV-2 may be targeting are the type II pneumocytes

8.           Those lung surface cells secrete a fatty substance to keep the lobes pliable. And that, precipitates the diffuse alveolar damage and acute respiratory failure that we are observin

9.           Immunohistochemistry testing and electron microscopy "confirmed viral tropism for pulmonary II pneumocytes.

10.         Viral antigen in lung tissue was higher than with SARS or MERS.

11.         Extensive detection in epithelial cells of the upper respiratory tract is unique among these highly pathogenic coronaviruses

12.         COVID-19 autopsies have confirmed clinicians' reports of increased clotting. The virus may very well be infiltrating the endothelium and causing injury to the blood vessel.

13.         Myocarditis is typical of viral diseases, but it has been frustratingly inconsistent in COVID-19 autopsies. Most have reported very little inflammation of the heart muscle. At least one death has been directly attributed to COVID-19–induced lymphohistiocytic and eosinophilic myocarditis.  And German researchers report in JAMA Cardiology that 60 of 100 patients who had recovered from COVID-19 had ongoing myocardial inflammation, as measured by cardiovascular magnetic resonance imaging (MRI). Many collegiate football programs, reporting evidence of myocarditis in athletes who have recovered from COVID-19, said they would postpone their seasons.

14.         But, looks like, what they are seeing by [MRI] is not true myocarditis but something else as per Richard S. Vander Heide, MD, PhD, MBA, a professor of pathology at Louisiana State University Health Sciences Center in New Orleans

15.         So far, autopsy studies have found no typical myocarditis in nearly every case.

16.         Vander Heide and colleagues published cardiopulmonary findings from 10 autopsies conducted on African Americans who died from COVID-19 in The Lancet in May and updated it with an additional 12 cases in Circulation in July. Six of the 22 had a history of heart disease. All had diffuse alveolar damage — a histopathologic marker of Acute Respiratory Distress Syndrome (ARDS) — in addition to pulmonary thrombi and microangiopathy. In all the cases, the virus was not found in the heart muscle cells and there was no evidence of what the authors called "typical lymphocytic myocarditis. In the newer study, Vander Heide and colleagues used electron microscopy to find what appeared to be viral particles in the vascular cells in the heart, lungs, and kidneys. Vander Heide, whose primary research interest is myocardial cell injury and adaptation, believes the infection of these endothelial cells is leading to clotting abnormalities in the heart's small vessels, causing inflammation. The heart cells are dying, but not from myocarditis. Instead, he thinks it's likely that the clotting is causing cell death from ischemia.

17.         Some pathologists are looking at vascular changes, which are "among the distinctive features of COVID-19," write Maximilian Ackermann, MD, and colleagues in an article published in May in the New England Journal of Medicine.

18.         They compared lungs of seven patients who died from COVID-19 with seven who died from ARDS secondary to influenza, as well as those from 10 age-matched, uninfected patients. The COVID-19 lungs exhibited severe endothelial injury, which appeared to be associated with intracellular SARS-CoV-2 virus.

19.         There also was widespread vascular thrombosis with microangiopathy and occlusion of alveolar capillaries and significant new vessel growth from an unusual form of angiogenesis called intussusceptive angiogenesis — a reactive formation of new vessels where one splits into two, said co-author William W. Li, MD, president and medical director of the Angiogenesis Foundation.

20.         Venous thromboembolism has also been observed in patients, including in a study at the University Medical Center Hamburg-Eppendorf in Germany that was published in May in the Annals of Internal Medicine.

21.         Coronavirus infections may be a trigger for venous thromboembolism

22.         Several potential mechanisms include endothelial dysfunction, systemic inflammation, and a pro-coagulatory state.

23.         Researchers at Hospital Graz II in Graz, Austria, also homed in on thrombosis, with evidence of it in all 11 autopsies they conducted, according to an article published in Annals of Internal Medicine.

24.         Pathologists were initially reluctant to take on COVID-19 autopsies, especially any that would involve aerosol-generating procedures. The College of American Pathologists attempted to allay fears with guidelines that recommend techniques that minimize those procedures, including using hand shears or other alternatives to an oscillating bone saw (also recommended by the CDC) or using a vacuum shroud with the bone saw.

25.         Williamson pointed out that there have been no reported cases of SARS-CoV-2 transmission from a corpse to any pathologist, morgue technician, or assistant. Still, his informal survey in March of pathologists on a LISTSERV he manages found that only six out of 50 respondents were conducting autopsies. A month later, that number had risen to 30.

26.         The CDC recommends autopsies be done in a negative pressure suite, which are more common at academic centers.

 

 

Friday, August 21, 2020

191 CMAAO CORONA FACTS and MYTH COVID CDC Immunity Three Months

 

191 CMAAO CORONA FACTS and MYTH COVID CDC Immunity Three Months

 

Dr K Aggarwal

President CMAAO

With input from Dr Monica Vasudev

1063:  ERS: Study of nose and throat reveals why people with COVID-19 may lose their sense of smell

Researchers studying tissue removed from patients noses during surgery believe they may have discovered the reason why so many people with COVID-19 lose their sense of smell, even when they have no other symptoms.

 

They found extremely high levels of angiotensin converting enzyme II (ACE-2) only in the area of the nose responsible for smelling. This Enzyme is thought to be the 'entry point' that allows coronavirus to get into the cells of the body and cause an infection.

 

Findings, published in the European Respiratory Journal, offer clues as to why COVID-19 is so infectious and suggest that targeting this part of the body could potentially offer more effective treatments.

 

While other respiratory viruses generally cause loss of the sense of smell through obstruction of airflow due to swelling of the nasal passages, this virus sometimes causes loss of smell in the absence of other nasal symptoms.

 

The team used tissue samples from the back of the nose of 23 patients, removed during endoscopic surgical procedures for conditions such as tumours or chronic rhinosinusitis, an inflammatory disease of the nose and sinus. They also studied biopsies from the trachea (windpipe) of seven patients. None of the patients had been diagnosed with coronavirus.

 

In the lab, the researchers used fluorescent dyes on the tissue samples to detect and visualise the presence of ACE2 under a microscope and compare levels of ACE2 in different cell types and parts of the nose and upper airway.

 

They found by far the most ACE2 on the lining cells of the olfactory epithelium, the area at the back of the nose where the body detects smells.

 

The levels of ACE2 in these cells was between 200 and 700 times higher than other tissue in the nose and trachea, and they found similarly high levels in all the samples of olfactory epithelium, regardless of whether the patient had been treated for chronic rhinosinusitis or another condition. ACE2 was not detected on olfactory neurons, the nerve cells that pass information about smells to the brain.

 

The levels of ACE2 - the COVID-19 'entry point' protein were highest in the part of the nose that enables us to smell. These results suggest that this area of the nose could be where the coronavirus is gaining entry to the body.

 

The olfactory epithelium is quite an easy part of the body for a virus to reach, it's not buried away deep in our body, and the very high levels of ACE2 there might explain why it's so easy to catch COVID-19.

 

[Professor Andrew P. Lane, director of the division of rhinology and skull base surgery, and Dr Mengfei Chen, research associate, and colleagues from Johns Hopkins University School of Medicine, Baltimore, USA.]