359 new deaths. At least it appears not to have “jumped” today. Today’s “The Times” brings a deep depression on me. It appears that the Francis Crick Institute is now researching what tests might be done on people to predict whether they will develop severe Covid-19. I first identified two tests in my blog on May 1st, and another a couple of weeks later. Fine, you might say, great minds are thinking alike here but if there is clear evidence that some abnormal tests are a marker, as was quite apparent at the end of April, why has it taken a month not to introduce them but to research them?
This adds even more weight to my contention that a serious error has been made in excluding front-line physicians from SAGE. It is quite clear that there will be a second wave, whether or not we have a Track and Trace system. Why? Because there are large numbers of asymptomatic SARS-CoV-2 carriers who will not be picked up in a timely fashion. Also because social distancing, especially among the young, has been abandoned (come to Rye or Camber Sands and you will see proof). We cannot keep locking and unlocking the nation piecemeal; people will rebel. So let’s just abandon the whole exercise as a waste of time and money, and concentrate on what matters:
How do you stop SARS-CoV-2 from developing into Covid-19?
1. Identify who has it through testing (though this is not reliable)
2. Check those with symptoms:
a. Pulse oximetry showing an oxygen saturation of less than 91-93%
b. Elevated serum ferritin
c. Elevated D-dimer
3. Treat aggressively in the event of abnormalities – because these suggest the development of a cytokine storm and coagulation defect leading to thrombosis, using
a. High dose steroid
b. Cytokine antagonist (anakinra, tocilizumab, known as biologics)
c. Low molecular weight heparin (LMWH)
All of these treatments are in use (for other things), safe (when used and monitored properly) and theoretically effective. There is already anecdotal evidence from centres that use such a regime, as well as ancillary evidence suggesting people on these, especially the biologics, for other conditions have a reduced incidence of Covid-19.
The fuss over ethnicity persists. In the British Medical Journal this week there’s an editorial suggesting we need a public inquiry now, “before a second wave develops”; BMJ 2020; 369 doi: https://doi.org/10.1136/bmj.m2052. As we are continuing to learn more and more about how the virus causes damage, how it spreads, how it may not produce symptoms, for me an inquiry now is a complete waste of time, but the authors suggest that the ethnic issue requires “representation from the communities affected”.
I am bemused by this. It’s not a scientific justification but a politically correct one. Consider as an analogy sickle-cell anaemia. This affects black people. It has nothing to do with deprivation or discrimination because it is a genetically determined condition. Another condition, beta-thalassaemia, affects people of Middle-Eastern and Eastern European origin. Again, no mystery here – it’s genetic. So, given that there is evidence of predisposition for BAME people (or at least, some of them) on a genetic basis, what contribution can community representatives make to a scientific and clinical investigation. Socio-political correctness trumps science? I think not.
The text of my BMJ response is reproduced below.
Dear Editor,
There should be an inquiry into the response to Covid-19, but not now. There are still too many unknowns, both epidemiological and clinical, for an inquiry to be able to draw any sensible conclusions. In response to the five points suggested for scrutiny I suggest:
1. A major exclusion from discussions has been that of clinicians at the sharp end. The problem with Covid-19 is that it may kill people; local government leaders are unlikely to be able to contribute anything sensible to the clinical discussion of how to stop it killing people.
2. Any review of procurement must be set in context with the similar problems faced by other countries. Furthermore, as it becomes increasingly clear that mechanical ventilation is unhelpful in many cases (because it will not restore blood oxygen levels if the alveolar epithelium is significantly damaged) the whole purpose of setting up ventilator-equipped Nightingale hospitals must be reviewed.
3. I don’t think that structural disconnect between health and social services altered the spread. What mattered was the SARS-CoV-2 was far more infectious than believed. The care home “epidemic” may well have been caused by the central directive to empty hospitals without testing patients before discharge; the only benefit of involving more agencies would have been to increase the pool of those whose working principle, when confronted with a plan, is to work out what could possibly go wrong with it.
4. It is apparent that any ethnic predisposition to Covid-19 may have a genetic basis, and attempts to present the subject in sociological terms is unscientific and runs the risk of serious predisposing factors being overlooked. What purpose is served by bringing in representatives from “the communities involved” other than to pay lip service to political correctness? Unless the proposed representatives have a firm grasp of statistics, epidemiology, genetics and risk factor correlation their presence would be a hindrance.
5. Brexit is irrelevant.
What is actually required is not some multi-function set of panels looking at peripheral issues, which will end up, as with all inquiries, stuffed with the wrong people, but an immediate development of treatment to stop Covid-19 from being a serious clinical problem. There is growing evidence (and the fact that it is growing so rapidly underlines my contention that an inquiry now is a waste of time, because the Science is constantly changing) that the serious multisystem disease seen is a function of (1) deep viral exposure and (2) a subsequent cytokine storm. The first has been partly addressed by PPE; the second has hardly been addressed at all.
There are two stages for this second part.
First, the development of risk-indicating tests. The required tests are already available; oxygen saturation measurement (as Dr Rammya Mathew suggested in a previous column (1), and as I have been arguing for weeks, availability of pulse oximeters enables this), and tests in deteriorating patients that point to cytokine overactivity and thrombotic risk such as serum ferritin and D-dimer.
Second, the development of cytokine storm management. In those who have abnormal tests showing they are developing a cytokine storm, the use of cytokine blockers, low molecular weight heparin in treatment not prophylactic doses, and steroids (in high dose, given early) must be instituted. Early. Current thinking that one should reserve these for late cases is analogous to treating cancer only when it gets to stage 4; it then does not work. Neither does dribbling in too little. Likewise treating with antiviral agents may reduce the ongoing storm but will do nothing to mitigate a storm that is already present. Which is the more important – the storm or the virus? My money is on the storm.
These are the measures that need to be in place before a second peak. Then patients may get SARS-CoV-2 but not die from Covid-19. A second wave is unstoppable if, as in Singapore, it transpires that large numbers of infected people are asymptomatic. That is why what matters is treating the severely ill with things that work. Deciding that is a matter for clinicians, not epidemiologists, public health doctors, social service or community groups or a public inquiry.
In conclusion Stephen Glover points out that in the 1968 influenza epidemic (which killed twice as many people as Covid-19 has yet done) there was no panic. He asks why (2). That might be an interesting subject for an inquiry.
It is now six weeks since I first wrote about the likelihood of severe Covid-19 being due to a cytokine storm. Clinicians with experience of dealing with this have not been consulted, as far as I am aware. I have had no response to my repeated attempts to highlight this with the powers that be – not even acknowledgement of receipt of my communications. If I am proved correct (and I concede that The Science may yet come up with alternative mechanisms for severe illness), I wonder how many lives would not have been lost.
References:
1. Mathew R. Innovation during the pandemic. BMJ, 12th May 2020. https://doi.org/10.1136/bmj.m1855
2. Glover S. News spreads faster than the virus. The Oldie, June 2020, 63
I am currently writing an open letter to Matt Hancock, with a draft protocol for where to go from here. As it appears that he doesn’t answer emails I shall send it the old way, on paper in an envelope, first class. I have an appropriate stamp of HMS Warspite firing a full broadside on D-Day 1944. Copies to… many!
The Wry Observer 