[Gambas-user] Holidays again - long term covid damage details

Richard Terry richard.h.terry at gmail.com
Mon Aug 31 00:14:28 CEST 2020


Hi List,

I enclose some detailed info about the long term damage from covid (I'm 
in general practice in australia - this content was from August). A bit 
of a summary at the top, detail down below

The global death rate from corona will be low, probably 0.7-1.5% max, 
flu is 0.1%, obviously taking out more of the top end of our society - 
being in that age group I'm not that enthralled.

This is not the issues sadly. This has turned out to be a  virus causing 
cardiovascular and multi-system damage. which gets entry via the lungs. 
One of our Aussie GP's quite young fitness guy now has scarred 
myocardium and lungs, can't do much in way of exercise.

Aside from the paralysis of the hospital system in the acute phase Long 
term complications are now appearing: neurological, cardiovascular, 
renal, diabetes, liver, even in persons who had either asymptomatic or 
mild disease


  * To date, the long-term sequelae from COVID-19 have been found to
    involve almost every organ system.
  * Lasting effects can occur after infection of any severity, including
    asymptomatic and mild cases.
  * Patients of all ages can be affected, including those with no prior
    comorbidities.
  * Respiratory complications are the best described, including fibrosis
    and reduced diffusing capacity, and restrictive ventilatory defects.
  * Neurological sequelae include acute ischaemic stroke, Guillain-Barré
    syndrome and transverse myelitis.
  * Myocardial inflammation and associated dyspnoea, fatigue, chest pain
    and palpitations may persist for months after infection onset.
  * Acute kidney injury associated with COVID-19 is typically severe and
    has resulted in end-stage kidney disease in a number of recovered
    patients with no pre-existing renal disease.
  * Rarely, children may develop a post-infectious inflammatory
    syndrome, similar to Kawasaki disease, including development of
    coronary artery aneurysms


      *General health*

One US study found that only two-thirds of COVID-19 outpatients had 
returned to overall baseline health at 14-21 days after first testing 
positive for SARS-CoV-2.

In contrast, a previous similar survey found almost all outpatients with 
influenza had returned to baseline health within 14 days of illness.^1

As expected, a greater proportion of patients hospitalised with COVID-19 
have ongoing symptoms.

In the US study, only one-third of inpatients had returned to baseline 
health at 14-21 days, while an Italian study found that almost 90% of 
inpatients had ongoing symptoms at a mean of 60 days after initial onset 
of symptoms.

Fatigue, dyspnoea and joint pain were the most common symptoms described 
in the latter study.^2

    *A proportion of hospitalised COVID-19 patients with ongoing
    symptoms post-discharge could fit under the umbrella of
    post-intensive care syndrome (PICS), defined as persistent
    cognitive, psychiatric or physical dysfunction after a critical
    illness.*


    While the incidence of PICS in COVID-19 patients is unknown, they
    are likely to be at greater risk as a result of prolonged critical
    illness and intubation.

    Similarly, the potential for COVID-19 to cause a chronic
    fatigue-like syndrome in non-critically ill patients is emerging.^3

    In addition to multisystem syndromes, COVID-19 can cause
    organ-specific long-term sequelae, including respiratory,
    neurological, psychiatric, vascular, cardiac, renal and immune
    effects, as summarised below.


          *Respiratory*

    Respiratory complications are the best-described sequelae of COVID-19.

    Serial CT-scan studies from China have shown persistent ground-glass
    opacities in almost all severe cases and one-third of non-severe
    cases at 30 days post-discharge, with lung fibrosis also developing
    in a significant proportion of severe cases.

    An isolated reduction in diffusing capacity was the most common
    abnormality found in these studies on pulmonary-function testing,
    followed by a restrictive ventilatory defect.^4,5

    Corona virus lung CT/A. Lung CT of a 44-year-old man in acute stage,
    with demonstrated bilateral peripheral ground-glass opacities (GGO).
    Lung total severity score (TSS) is 7.
    B. Follow-up CT of patient (from A) 30 days post-discharge showing
    that patchy GGO had obvious absorption. TSS is 3
    C. CT of a severe patient during acute stage showing diffuse GGO.
    Consolidation can also be seen in some areas. TSS is 13.
    D. CT of patient (from C) obtained 30 days post-discharge.
    Peripheral fibrosis consists of irregular linear opacities.
    Concomitant presence of GGO is also visible. TSS is 5./

    /Respir Res. 2020; 21: 163./

    ------------------------------------------------------------------------


          *Neurological*

    COVID-19 is associated with a range of neurological sequelae.

    Acute cerebrovascular events, primarily ischaemic stroke, have been
    described in around 5% of admitted patients.

    The aetiology of stroke in COVID-19 patients is likely
    multifactorial, with coagulopathy, cardiac arrhythmias and direct
    viral infection of CNS vascular tissue all postulated as potential
    causes.^6

    SARS-CoV-2 may directly infect CNS neural tissue. A small autopsy
    series in Germany found conspicuous pan-encephalitis and meningitis
    in all examined cases.^7

    Anosmia and dysgeusia are prominent symptoms of COVID-19.

    The pathophysiology of these is not yet fully explained.

    They may be a direct result of viral invasion of the olfactory
    epithelium via ACE2 receptors or secondary to associated local
    immune responses.^8

    Guillain-Barré syndrome and transverse myelitis are rare but
    well-described complications, with an average onset 5-10 days after
    onset of COVID-19 symptoms.^9,10


          *Psychiatric*

    Survivors of SARS-CoV-1 infection have high rates of psychiatric
    disorders at 3-5 years of follow-up, including PTSD (54%),
    depression (39%), pain disorder (36%), panic disorder (32%) and OCD
    (15%).^11

    While SARS-CoV-1 caused a consistently high severity of acute
    illness, unlike the variable nature of the severity of SARS-CoV-2,
    it is reasonable to expect that survivors of severe COVID-19 are at
    a similar risk of long-term psychiatric disease.

        *For COVID-19 survivors, this risk is compounded by the
        concurrent impact of lockdown measures on psychosocial wellbeing
        society wide.*


          *Vascular *

    COVID-19 is associated with a hypercoagulable state, which may
    account for a large proportion of the morbidity and mortality of the
    disease in the lungs and in other systems.

    Up to one-third of COVID-19 patients in ICU develop extensive DVT or
    pulmonary embolism, in many cases despite prophylactic anticoagulation.

    Direct viral invasion of endothelial cells via ACE2 receptors may be
    an important contributor to the pathogenesis of thrombosis in
    COVID-19.^6


          *Cardiac *

    Myocardial injury is common in acute COVID-19, occurring in up to
    20% of inpatients, while acute decompensated heart failure
    complicates up to 50% of severe cases.^12

    A recent German cohort study found 60% of COVID-19 patients had
    ongoing myocardial inflammation as assessed by cardiac MRI at two
    months post-onset of infection.

        *One-third had ongoing dyspnoea and exhaustion, usually with
        only mild exertion, while around 20% reported atypical chest
        pain or palpitations.*

    Importantly, only one-third of this cohort had severe acute COVID-19
    requiring hospitalisation, with 20% having asymptomatic infection
    and 50% mild to moderate symptoms.

    In addition, the severity and extent of myocardial involvement did
    not differ based on the acute severity of COVID-19.^13


          *Renal*

    COVID-19 is associated with acute kidney injury (AKI) in around 10%
    of admitted patients.

    AKI associated with COVID-19 is often severe, with around two-thirds
    of patients with COVID-associated AKI requiring renal replacement
    therapy.^14

    As with other complications of COVID-19, the pathogenesis of AKI is
    uncertain and likely to be multifactorial.

    Direct virus-mediated injury, cytokine storm, coagulopathy and
    microangiopathy are all possible pathways.^15

    Long-term follow-up of COVID-19 patients with AKI is ongoing, but
    there are already anecdotal reports of end-stage kidney disease and
    ongoing dialysis requirement for patients with no pre-existing
    chronic kidney disease.

        *Certainly, the high severity of AKI and requirement for renal
        replacement therapy associated with COVID-19 are strong risk
        factors for later development of chronic kidney disease.*

    In other settings, the adjusted relative risk of progressive chronic
    kidney disease in patients requiring renal replacement therapy for
    AKI is 25 times greater than baseline, with an overall risk at six
    years’ follow-up of more than 60%.^16


          *Immunological*

    Severe COVID-19 is associated with significant immunological
    derangements, which appear to be central to the pathogenesis of the
    disease.

    Lymphopenia of both CD4+ and CD8+ T cells and a marked inflammatory
    response similar to a cytokine storm are strongly associated with
    severe COVID-19.

    Post-acute immunological sequelae include paediatric inflammatory
    multisystem syndrome temporally associated with SARS-CoV-2 (PIMS-TS)
    and chilblain-like acral lesions termed ‘COVID toes’.

    In children, PIMS-TS is a rare post-infectious syndrome associated
    with COVID-19 and resembles Kawasaki disease.

    Corona virus cervical spine/Spine MRI. A. Short tau inversion
    recovery sequence on sagittal plane view. Extensive, ill-defined,
    patchy, hyperintense signal noted throughout the central aspect of
    the spinal cord. B. T2-weighted axial cut (arrow) indicating mild
    enlargement of the caliber of the spinal cord and hyperintense
    signal without pathologic contrast enhancement./

    /Brain Behav Immun Health. 2020 May; 5: 100091/

    ------------------------------------------------------------------------

    Like COVID-19 itself, PIMS-TS has a wide spectrum of severity,
    ranging from mild to severe, with some deaths reported.

    PIMS-TS, in turn, is likely to have its own long-term sequelae,
    including coronary artery abnormalities similar to those found in
    Kawasaki disease.

    ‘COVID toes’ usually develop after the resolution of acute symptoms
    of disease but, in fact, are most common after asymptomatic
    SARS-CoV-2 infection.

    At symptom onset of COVID toes, SARS-CoV-2 PCR is usually not
    detectable, while SARS-CoV-2 IgG and IgM are.

    Histopathology of the lesions show a vasculitis, which may be due to
    direct injury arising from endothelial infection by SARS-CoV-2 or,
    more likely, by a subsequent autoimmune reaction.^17

    Spontaneous resolution of COVID toes usually occurs over 2-8 weeks.

    ------------------------------------------------------------------------

    *Read more: */COVID-19 and cruises: A match made in hell
    <https://www.ausdoc.com.au/therapy-update/covid19-and-cruises-match-made-hell>/

    ------------------------------------------------------------------------


          *Conclusion*

    What we don’t know about COVID-19 could, and eventually will, fill a
    textbook. In the meantime, we are increasingly aware that COVID-19
    causes a large range of post-acute sequelae involving almost every
    organ system.

    Similar to the acute disease itself, the post-acute sequelae of
    COVID-19 range from mild to life-threatening.

    They affect patients of all ages and those with no prior comorbidities.

    This knowledge is further argument, if one was needed, that every
    possible measure should be taken by all individuals, and by society
    at large, to avoid infection with SARS-CoV-2.

    Regards

    Richard

On 31/8/20 6:12 am, Benoît Minisini wrote:
> Le 30/08/2020 à 21:20, Jussi Lahtinen a écrit :
>> The corona will constantly kill less probably for several reasons.
>> But we have learned how to deal better with the coronal patients 
>> (what drugs to use, etc). And because the hospitals are less crowded 
>> now,
>> and thus we can offer proper care for the patients.
>>
>> So far the corona has killed globally around 800 000 people. 
>> Influenza viruses kill on average 500 000 in a *whole* year.
>> Also corona seems to cause a lot more complications like lung damage 
>> and strokes.
>> So, really, be careful.
>>
>>
>> Jussi
>>
>
> 800 000? How could we know? The COVID19 deaths and the influenza 
> deaths are not counted the same way. Moreover, a lot of deaths were 
> first attributed to COVID19, and then attributed to something else a 
> few months later. At the end of the year, I guess we will see no 
> significative change on the global number of deaths.
>

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