The most common cause of death in COVID-19 patients is Viral pneumonia leading to ARDS and acute respiratory failure.
However, as most of such patients need ventilatory support, secondary bacterial infections (Ventilator Associated Pneumonia - VAP, and other types are common). As most of patients needing ICU admissions are >65 years (50%) with comorbidities, many of such patients may die due to underlying comorbidities, rather than COVID-19.
There are reports that patients recovered from COVID-19 infection as evidenced by 2 negative SARS-CoV-2 tests (although this is rarely being tested) by RT-PCR, but later on succumbed to complications induced by Coronavirus, or due to the comorbdities.
This has been one of the problem of high reported case fatality rate in Italy (It was later on found that only 10% of such patients in North Italy directly died of COVID-19).
Ultimately the cause of death is always cardiac arrest.
An important factor to consider when trying to interpret variation in causes of death between countries is differences in cultural interpretation of quality of life. This impacts the social and medical ethics and the delivery, limitation and withdrawal of life sustaining therapies.
In many Western cultures quality of life is valued far more than quantity of life. In those settings limitation and even withdrawal of life sustaining therapies resulting in cardiac arrest are a common mode of death.
In many Eastern cultures quantity of life is valued more than quality of life. In these settings treatment limitations and withdrawals of therapy are rare. Admission to intensive therapy units and prolonged organ support are common.
Mode of death is often failure of resuscitation after cardiac arrest.
These differences are magnified when there are limited resources particularly in Western countries. The social and medical acceptance of treatment limitations is increased; this may significantly increase case fatality rates.
Covid-19 is generally a mild, self-limiting illness.
In a small percentage of cases it is severe (i.e. causes respiratory failure) or critical (i.e. causes multi-organ failure).
The availability of healthcare in general and specifically critical care will affect the case fatality rate of these patients. In China and Italy where large numbers of healthcare professionals were infected the capacity to deliver healthcare was substantially reduced. So excess deaths occurred.
The cause of respiratory failure has not, at present, been fully elucidated. There are several theories currently under investigation. However a systemic inflammatory response results in the progression to multi-organ failure.
The patients who are dying are generally those with impaired immunity. These patients are dying because of the damage the virus is causing to their bodies. However, some apparently normal patients are dying. I suspect that these patients are dying from an exaggerated immune response (i.e. cytokine storm and other pathological immune responses).
This is a very dynamic situation and the answers to this question may be completely different tomorrow.
The mechanism of death is increased inflammatory response of the host with cytokine storm. This phenomenon is behind pulmonary, kidney and heart lesions. The final event is a multi organic failure.
The viral pneumonitis may cause the respiratory failure in some cases. However, it is frequently through cytokine lung damage that things happen.
The median time from SARS-CoV-2 symptom onset to the development of pneumonia is approximately 5 days, and the median time from symptom onset to severe hypoxaemia and ICU admission is approximately 7 - 12 days. The acute hypoxaemic respiratory failure - sometimes with severe hypercapnia - from acute respiratory distress syndrome (ARDS) is the most common complication (in 60-70% of patients admitted to the ICU), while hypoxaemia, without respiratory distress, is developed in few elderly patients. This means that the respiratory problem is the evolution most common that conditions the elevated number of deaths. Data from Intensive Care National Audit and Research Centre (ICNARC), based on a sample of 3883 coronavirus patients, reported that death rate on 2249 patients admitted to intensive care with coronavirus now stands at more than 51% (51.6%), of which 871 patients have died, 818 patients have been discharged alive from critical care and 2194 patients were last reported as still receiving critical care. Of the 871 people who died, 53.6% were male, while 46.3% women. Unfortunately, mechanical ventilation (MV) may amplify the lung-specific inflammatory response in preinjured lungs by elevating cytokine release and augmenting damage to the alveolar integrity, and preinjured lungs are more sensitive to MV at later phases of sepsis, and this situation may be a result of differing immune status. The ventilator-associated lung injury (VALI) are the deleterious effects of high positive pressure ventilation, determined by three mechanisms identified as biotrauma, barotrauma/volutrauma and atelectrauma. In particularly, biotrauma, is the mechanical stimulus that involves the application of positive pressure during mechanical ventilation triggers, through a process of mechanotransduction, a biological response characterized by the secretion of proinflammatory cytokines and the emergence of a neutrophilic infiltrate. As a result, there is a release of inflammatory mediators from the ventilated lung that can lead to a systemic dissemination, contributing to the development of the multiple organ dysfunction syndrome. The biotrauma contributes to the persistence of the inflammatory process and it is associated with worse prognosis in patients with ARDS. In barotrauma/volutrauma, the subjects submitted to high ventilatory pressures showed alveolar damage by over-stretching, consisting in perivascular and alveolar oedema, and that use of high volumes can cause breakage of the alveolar walls. The pulmonary over-stretching is increased due to the coexistence of healthy alveoli and non-aerated collapsed areas. This regional heterogeneity can aggravate the lung damage in previously healthy aerated alveoli and in the interface aerated/non-aerated areas, even when low volumes are used for ventilation. In stelectrauma, the mechanical ventilation may result in cyclic variations of alveoli aeration, that lead to epithelium damage due to the emergence of shear forces at the interfaces between air and fluid in the injured lung, and the generation of open-collapse alveoli phenomena. Therefore, about fifty percentage of patients treated with invasive mechanical ventilation died, and that 53% of deaths were related to respiratory failure.
For to don't be late and avoid, as much as possible mechanical ventilation, is necessary proceed, especially for people ≥60 years, to check, twice day, oxygen saturation and temperature, even if without symptoms and when respiratory rate ≥30 breaths per min, oxygen saturation ≤93%, and temperature ≥37.5 °C, immediately calls service of emergency.
To the excellent explanation by Dr. Zagami we may add that Disseminated Intravascular Clotting plays an important role in the final events.
Up till now I faced many cases of Covid-19 intubated and non intubated
No fertility happed to our patient
Most of our treatment are supportive
Severe Covid 19 patients develop ARDS/ thromboembolism and progress to sepsis and septic shock
This causes MODS and death
I agree with Muhammad. Moreover acute hypoxia caused by viral pneumonia usually results in the appearance of asystole.
The prognosis for CA in patients with COVISD-19 is much lower than for cardiac arrest due to other causes
Divya R. I think there is not an one cause but many causes affect collectively for death of COVID-19 patients.
https://link.springer.com/article/10.1007/s00134-020-05991-x?fbclid=IwAR1EbkrPza14Iwx-dNFQDrlYG2HRomm-8Lb7NEvWZIqP1Gff8EBDaLmL7lg
Dear Praneeth Silva
I agree with you, but from data analysis showed in above article, emphasize that "among the 68 fatal cases, 36 patients (53%) died of respiratory failure, five patients (7%) with myocardial damage died of circulatory failure, 22 patients (33%) died of both, and five remaining died of an unknown cause." In my remark the data are superimposable with those come out by article by you cited. This one uniquely to certify the greater issue of mechanical ventilation.
ARDS/ thromboembolism ,sepsis and hypoxia may be the cause of death in COVID-19
Please see the link below.
https://www.thelancet.com/action/showPdf?pii=S2213-2600%2820%2930165-X
In SARS-CoV-2 infection, at least five stages of the disease process are identified: pre-exposure prophylaxis, post-exposure prophylaxis, outpatient treatment, hospital admission, and late-stage critical care (admission to an intensive care unit). Each stages represent a different pathogenetic evolution. So, not is possible to merge the various phases in one's. Clinical trials to evaluate possible drug treatments are widely concentrated (61.6%) on the patients who have been admitted to hospital. In randomised clinical trials using lopinavir-ritonavir, and hydroxychloroquine, administrated in hospital patients, has been proved the ineffectiveness of these drugs in COVID-19 disease. Nevertheless, it doesn't need to forget how such convincing evidence is reported for hospitalized patients, that are the two last stage of the process. “RECOVERY trial”, traslate this partial result at whole stages of the disease, incurring in the Will Rogers phenomenon. This misinterpretation of disease states exists among both the public and the scientific communities, and today the only profit is that to assemble us to find a suitable treatment, avoiding “compassionate” term, to attack all the pre-hospitalization phases of the infection, to prevent hospital admission.
During the different early SARS-CoV-2 stages (pre-hospitalization) must be put in field more appropriate therapeutic strategies searchable by multiple criteria to prevent further disease progression.
I consider that Dr. Zagami's answers are very clear and forceful. Additionally, I would like to remind you that the complications of some patients are associated with other conditions such as the presence of prolonged silent hypoxia, for which reason they go to hospitals late; and on the other hand, to patients with coinfections, and it is this coinfection that causes death.
To further the debate on the possibility of coinfection, I share the following manuscript.
Article Are we now observing an increasing number of coinfections be...
Dear dr. Jorge Andrés Sánchez-Duque, I agree with you, and your article is true to life, especially when affirm "The identification of clinical and epidemiological risk factors of each patient that could suggest a coinfection by a virus, bacteria, and fungi, even three pathogens.... ". I thinks "when the bank doors give way, whoever passes, there enters to raid !". In the SARS-CoV-2 early phase, the pathogenetic sequence are represented by neutrophils activation (NETs) with extracellular release of lysosomial enzymatic set, ROS generation that determine endothelial damage, and subsequent immunothrombus process, what it brings to decrease of the gases exchange, evolving in local and after systemic hypoxia. If such are the mechanisms, consequential therapy is!