[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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