In die laaste tyd was daar heelwat berigte of gerugte oor outopsies of nadoodse ondersoeke wat op Covic 19 pasiënte gedoen was – daar was heelwat gedoen gedurende 2020 – in Italië, Amerika, China en in ander lande. En daar is ook sekere hart en long spesialiste, dokters wat uitbrei oor bloedklonte wat ontwikkel tydens die virusbesmetting, in die hart, longe en ander organe. Sommige pasiënte ervaar min tekens van die virus, terwyl ander, wat wel verwante siektes het soos hartsiektes, bloed of diabetes. Hier is ‘n paar artikels met skakels, om na te lees rakende outopsies wat gedoen is en of dit voldoende gaan wees, sal die toekoms leer. Sien ‘n video hieronder .
From China …
Although COVID-19 has a fairly broad range of effects, one of the more peculiar has been blood clots.
Researchers at the Michigan Medicine – University of Michigan identified a mechanism of how this happens. They appear to be caused in about half of patients having blood clots by an autoimmune antibody found in the blood that attacks cells and triggers blood clots. In COVID-19, these minuscule clots may also restrict blood flow in the lungs, which impairs oxygen exchange. In patients without COVID-19, these antibodies are typically seen in the autoimmune disease antiphospholipid syndrome.
The research was published in the journal Science Translational Medicine.
“Dipyridamole is an old drug that is safe, inexpensive, and scalable,” Kanthi said. “The FDA approved it 20 years ago to prevent clotting, but we only recently discovered its potential to block this specific type of inflammation that occurs in COVID.”
Researchers at Helmholtz Zentrum München, the German Research Center for Environmental Health, analyzed blood samples of almost 12,000 children in Bavaria between the ages of 1 to 18 between January 2020 and July 2020. They tested for SARS-CoV-2 dual-antibody positivity. They identified an average antibody frequency of 0.87% from April to July, which was six times higher than the incidence of virus-positive cases reported by the Bavarian Health and Food Safety Authority in the same period. They found that 47% of the children who tested antibody-positive were asymptomatic.
6 June 2020
Preliminary findings of autopsy pathology revealed SARS-CoV-2 viral particles in multiple organs of several cases, suggesting a variety of viral-transmission routes such as the digestive tract, skin and various body fluids (saliva, urine, semen, sweat and milk, etc.). These issues merit further investigation.
As of 22 April 2020, the COVID-19 Pathology Team has performed systematic autopsies on 37 COVID-19 cases. The team of the TMMU (Army Medical University), together with colleagues from Shanghai Jiao Tong University Medical School and Ruijin Hospital, the First Affiliated Hospital of the USTC and the Central Theater General Hospital, completed 27 cases from Wuhan Jin-yintan Hospital, Wuhan Huoshenshan Hospital, Tongji Zhongfaxincheng Hospital and Taikang Tongji Hospital.
The team of Huazhong University of Science and Technology Tongji Medical School completed 10 cases from Wuhan Jinyintan Hospital and Wuhan Central Hospital. In addition, percutaneous multiple-organ biopsy (‘minimally invasive autopsy’) was carried out in 54 cases. Among them, the team of Wuhan Union Hospital completed 30 cases from Wuhan Union Hospital West District and the team of TMMU completed 13 cases from Chongqing Three Gorges Central Hospital, Wuhan Tongji Hospital Zhongfaxincheng Hospital and Wuhan Huoshenshan Hospital. The team from Wuhan Tongji Hospital completed 9 cases from Wuhan Tongji Hospital Zhongfaxincheng Hospital and the team of the Fifth Clinical Medical Center of the PLA General Hospital completed two cases. Altogether, a total of 91 COVID-19 patients were pathologically inspected and diagnosed, which may represent the largest number of autopsy cases with the most comprehensive examination in the world thus far.
Furthermore, our systematic autopsy has established a basis for collaboration among a number of pathological institutions during the COVID-19 pandemic in China. During the process, anatomic pathologists and technicians also collaborated with engineers to establish the biosafety platforms for the autopsy of COVID-19 patients. Governmental laws and regulations played an important role in mobilizing a rapid response to this major public-health emergency.
It was discovered that SARS-CoV-2 infection causes injuries in multiple organs and tissues with prominent and extensive pulmonary lesions. The pathological characteristics of pulmonary lesions caused by SARS-CoV-2 infection were similar to those from SARS infection but differences have been noticed. Intensive spatial and temporal heterogeneity of pulmonary lesions was observed in individual patients.
Pathological changes in the respiratory system were most significant. Trachea and bronchus manifested mucosa congestion, increased secretion and focal epithelial exfoliation. Changes in pulmonary parenchyma presented with differences in extent and distribution. Under light microscopy, the parenchymal areas contained diffuse alveolar damage and exudative inflammation. Serous and fibrin exudate filled alveolar spaces, and hyaline membrane formation could be seen. The infiltrating leukocytes in the alveoli were mainly monocytes and macrophages.
Type II pneumocyte hyperplasia and focal pneumocyte exfoliation were clearly observed. Some areas of bronchial mucosa manifested epithelial exfoliation, mucin accumulation and mucin-plug formation. A few alveoli showed excessive inflation, septal rupture or cystic cavity formation. Focal pulmonary hemorrhage and consequential hemorrhagic infarction or necrosis were observed. Pulmonary vessels showed vasculitis, thrombosis (mixed thrombi and hyaline thrombi) and thromboembolism. Exudate organization (also termed pulmonary carnification) and pulmonary interstitial fibrosis were observed in cases with long disease duration (see pulmonary complications in Box 1). Under electron microscopy, coronavirus particles were observed in the cytoplasm of tracheal and bronchial mucosa epithelia and alveolar type II pneumocytes. Immunohistochemical staining demonstrated that some tracheal and bronchial mucosa epithelia and type II alveolar epithelial cells and the infiltrating macrophages, which express angiotensin converting enzyme 2 (ACE2), were positive for SARS-CoV-2 protein.
The trachea and pulmonary tissues (except some lung lobes) were positive for SARS-CoV-2 nuclear acid. Functionally, alveolar damage, exudation, interstitial inflammation and extensive thrombosis constituted a cause for ventilatory disorder. Airway epithelial hyperplasia, exfoliation and mucus congestion increased ventilation obstruction, especially in the small airway. Altogether, these changes were considered as a pathological basis for lethal respiratory failure.
Was noticed that the cadavers, especially the elders, had primary health conditions such as (i) respiratory diseases: chronic bronchitis, bronchiectasis, pulmonary fibrosis, emphysema and pulmonary bullae and other conditions; (ii) cardiovascular diseases: atherosclerosis in large and medium arteries, aneurysm rupture, cardiac hypertrophy, aged myocardial infarction, arteriolosclerosis and other conditions; (iii) digestive diseases: viral hepatitis and liver cirrhosis, chronic gastritis, calculous cholecystitis and other conditions; (iv) urinary diseases: chronic glomerulonephritis, renal cysts, chronic cystitis, benign hyperplasia of the prostate and other conditions; (v) hematologic abnormalities: bone-marrow steatosis and fibrosis and other conditions; (vi) brain lesions: aged cerebral infarction, lipofuscin accumulation and amyloid deposition. These existing conditions combined with the acute damage caused by SARS-CoV-2 constituted the pathological basis for multiple organ dysfunction syndrome, with more serious consequences from lesions in the lungs, heart, kidneys and liver.
The major cause of death shown by the autopsy cases with COVID-19 appeared to be multiple organ dysfunction syndrome, especially acute respiratory distress syndrome. Some autopsy cases died from complications including severe pulmonary infections (bacteria, fungi or multiple infection), pulmonary embolism or hemorrhagic shock
The first human cases of coronavirus disease-2019 (COVID-19), caused by the novel zoonotic pathogen severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), were reported at the end of December 2019 in Wuhan, China. On 12 March 2020, the World Health Organization (WHO) declared COVID-19 a global pandemic as it rapidly spread worldwide . In Italy, the first confirmed cases of COVID-19, reported on 31 January 2020, were 2 tourists from Wuhan, China. As of 19 August 2020, globally there have been 21 300 000 COVID-19 cases with 760 000 deaths reported to the WHO, of which Italy has reported 250 000 COVID-19 cases with 35 000 deaths .
Autopsies were performed at the National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS Hospital, Rome, Italy. The study was approved by the local ethics committee (approval number 9/2020).
11 September 2020 – Italy
To further define the pathology caused by SARS-CoV-2 across all body organs, we performed autopsies on 22 patients with COVID-19 (18 with comorbidities and 4 without comorbidities) who died at the National Institute for Infectious Diseases Lazzaro Spallanzani-IRCCS Hospital, Rome, Italy. Tissues from the lung, heart, liver, kidney, spleen, and bone marrow (but not the brain) were examined. Only lung tissues were subject to transmission electron microscopy.
COVID-19 caused multisystem pathology. Pulmonary and cardiovascular involvement were dominant pathological features. Extrapulmonary manifestations included hepatic, kidney, splenic, and bone marrow involvement, and microvascular injury and thrombosis were also detected. These findings were similar in patients with or without preexisting medical comorbidities.
SARS-CoV-2 infection causes multisystem disease and significant pathology in most organs in patients with and without comorbidities.
Clinical and epidemiological studies have established that COVID-19 presents as a spectrum of clinical manifestations from asymptomatic, to mild illness (up to 80% of patients), moderate (15% of patients), to severe illness (5% of patients). Increased mortality rates have been observed in older people (>70 years of age) and those with comorbidities [2, 3].
Reports from individual or small autopsy case studies [4–6] or limited postmortem studies [7–9] show that SARS-CoV-2, like SARS-CoV-1 in 2003, is a multisystem disease that predominantly affects the respiratory and cardiovascular system. SARS-CoV-2 has been detected in a range of clinical samples, such as bronchoalveolar lavage fluid, sputum, feces, and blood, indicating widespread dissemination .
Performing whole-body autopsies in patients who die of COVID-19 remains challenging due to infection control regulations and other logistical reasons [11, 12]. There is a need for more detailed and larger autopsy case series to further define the pathological manifestations of COVID-19  and determine the full extent of organ involvement. Here, we reported the whole-body postmortem examinations of 22 Italian patients who died of COVID-19, 4 of whom had no comorbidities.
Tokyo – 26 July 2020
Autopsies are an essential tool for understanding new diseases. Against this background, it is incomprehensible why there is great reluctance worldwide to perform autopsies on COVID-19 deceased patients. The article provides an overview of the status of the autopsy series published worldwide and shows the path taken by the city of Hamburg in Germany, where autopsies are ordered by the health authorities in the interests of disease control. The risk of infection posed by SARS-CoV-2-positive deceased persons may be overestimated. The scientific benefit that can be drawn from experience with autopsies and further examination of tissue samples is immeasurable.
As soon as the pandemic reached the various countries, many of them began a wide range of scientific activities, focusing on the development of vaccines, the characterization of virus properties and clinical aspects of COVID-19. Initially, clinical and radiological data on the lungs of COVID-19 patients were available, but patho-morphological investigations were rarely undertaken. Naturally, the first publications on this subject came from China in February and March 2020, including results of lung biopsies of both living patients ,  and deceased patients  being examined. The first published full autopsy with macroscopic photographs in a COVID-19 patient was provided in a medico-legal journal from China in February 2020 . Systematic examinations of autopsies were missing until then.
It is not quite clear why there has been a certain reluctance to perform autopsies of patients who died of COVID-19 until today. It is true that in Germany the Robert Koch Institute (a German health monitoring institution) – at least in the initial phase of the pandemic – had advised against performing autopsies. However, the author is not aware of such clear votes against autopsies by other large health organizations such as the WHO, the Royal College of Pathologists (UK) or the CDC (USA). (Fulfillable) guidelines regarding minimum requirements for safe autopsies, e.g. concerning personal protection and room exhaustion, do exist, however , , .
Apparently autopsies are carried out here and there in the USA, which is particularly affected by COVID-19. Davis and Williamson published a letter in early June 2020, which deals with the risk of infection during COVID-19 autopsies . A survey of 200 participating autopsy institutions has shown that at the time of writing there have been at least 225 autopsies in 14 states of the USA. For whatever reason, no major case series seem to have been investigated so far.
If publications on COVID-19 autopsy series are seen as an indicator for the autopsy frequency in the respective country, Germany, Italy, the USA, Switzerland, Austria and Great Britain seem to be countries where autopsies are performed at all – at least in individual centers. The studies used as a basis for this conclusion were PubMed-listed studies (search terms were COVID-19, SARS-CoV-2, autop* and post mort* in various combinations) whose case numbers go beyond mere case reports (which are of course also important) (n > 2; see Table 1 ). Postmortem study results also come from Brazil, China and France, but the tissue examined was obtained using different biopsy techniques (“minimally invasive autopsy”).
If an Autopsy has been done, people will be sure, is the person dead because of any other disease (like cancer), heart problems or the virus.
Despite the increasing number of published studies on COVID-19, in all the examined studies the lack of a well-defined pathophysiology of death among patients who died following COVID-19 infection is evident. Autopsy should be considered mandatory to define the exact cause of death, thus providing useful clinical and epidemiologic information as well as pathophysiological insights to further provide therapeutic tools.
A total of 50 articles met the inclusion criteria. However, only 7 of these studies reported autopsy-based data. Discussion: The analysis of the main data from the selected studies concerns the complete analysis of 12,954 patients, of whom 2269 died (with a mortality rate of 17.52%). Laboratory confirmation of COVID-19 infection was obtained in all cases and comorbidities were fully reported in 46 studies.
The most common comorbidities were: cardiovascular diseases (hypertension and coronary artery disease), metabolic disorders (diabetes, overweight, or obesity), respiratory disorders (chronic obstructive pulmonary disease), and cancer.
The most common reported complications were: acute respiratory distress syndrome (ARDS), acute kidney injury, cardiac injury, liver insufficiency, and septic shock. Only 7 papers reported histological investigations.
Nevertheless, only two complete autopsies are described and the cause of death was listed as COVID-19 in only one of them. The lack of postmortem investigation did not allow a definition of the exact cause of death to determine the pathways of this infection. Based on the few histopathological findings reported in the analyzed studies, it seems to be a clear alteration of the coagulation system: frequently prothrombotic activity with consequent thromboembolism was described in COVID-19 patients. As a scientific community, we are called on to face this global threat, and to defeat it with all the available tools necessary.
Done by: S. Karger AG, Base
Several cases of pneumonia reported in Wuhan, China in late 2019 led to identification of a novel coronavirus, later designated as SARS coronavirus-2 (SARS-CoV-2), the etiologic agent of COVID-19 [3, 4]. Since that time, SARS-CoV-2 has spread rapidly across the world causing more than ten million infections and more than half a million deaths by early summer 2020.
We report the clinicopathologic findings from 32 autopsy studies conducted on patients who died of COVID-19 including routine gross and microscopic examination with applicable special and immuno histochemical staining techniques.
Twenty-seven (84%) of patients had macroscopic and/or microscopic thrombi at autopsy and Twenty-two (69%) had elevated D-dimers. Thrombi were most frequently in respiratory (n = 25, 78%) and cardiovascular (n = 8, 25%) systems.
Results: SARS-CoV-2 infection was confirmed by nasopharyngeal RT-PCR in 31 cases (97%) and by immuno histochemical staining for SARS-CoV-2 spike-protein in the lung in the remaining 1 case (3%). The ethnically diverse cohort consisted of 22 males and 10 females with a mean age of 68 years (range: 30–100).
Patients most commonly presented with cough (17 [55%]), shortness of breath (26 [81%]), and a low-grade fever (17 [55%]). Thirty-one (97%) of the patients had at least 1 comorbidity (mean = 4). Twenty-eight patients (88%) had widespread thromboembolic disease, as well as diffuse alveolar damage (30 [94%]), diabetic nephropathy (17 [57%]) and acute tubular injury. Patterns of liver injury were heterogeneous, featuring 10 (36%) with frequent large basophilic structures in sinusoidal endothelium, and increased immunoblast-like cells in lymph nodes.
Conclusion: This series of autopsies from patients with COVID-19 confirms the observation that the majority of severely affected patients have significant pulmonary pathology. However, many patients also have widespread microscopic thromboses, as well as characteristic findings in the liver and lymph nodes.
Washington – 1 July 2020
Among the most important findings, consistent across several studies, is confirmation the virus appears to attack the lungs the most ferociously. They also found the pathogen in parts of the brain, kidneys, liver, gastrointestinal tract and spleen and in the endothelial cells that line blood vessels, as some had previously suspected. Researchers also found widespread clotting in many organs.
Another unexpected finding, pathologists said, is that oxygen deprivation of the brain and the formation of blood clots may start early in the disease process. That could have major implications for how people with covid-19 are treated at home, even if they never need to be hospitalized.
At their best, autopsies can reconstruct the natural course of the disease, but the process for a new and highly infectious disease is tedious and requires meticulous work. To protect pathologists and avoid sending virus into the air, they must use special tools to harvest organs and then dunk them in a disinfecting solution for several weeks before they are studied. They must then section each organ and collect small bits of tissue for study under different types of microscopes.
One of the first American investigations to be made public, on April 10, was out of New Orleans. The patient was a 44-year-old man who had been treated at LSU Health. Richard Vander Heide remembers cutting the lung and discovering what were probably hundreds or thousands of microclots.
“I will never forget the day,” recalled Vander Heide, who has been performing autopsies since 1994. “I said to the resident, ‘This is very unusual.’ I had never seen something like this.”
But as he moved onto the next patient and the next, Vander Heide saw the same pattern. He was so alarmed, he said, that he shared the paper online before submitting it to a journal so the information could be used immediately by doctors. The findings caused a stir at many hospitals and influenced some doctors to start giving blood thinners to all covid-19 patients. It is now common practice. The final, peer-reviewed version involving 10 patients was subsequently published in the Lancet in May.
Other lung autopsies — including those described in papers from Italy of 38 patients, a Mount Sinai Health study on 25 patients, and a collaboration between Harvard Medical School and German researchers on seven — have reported similar findings of clotting.
Most recently, a study out last month in the Lancet’s eClinicalMedicine, found abnormal clotting in the heart, kidney and liver, as well as the lungs of seven patients, leading the authors to suggest this may be a major cause of the multiple-organ failure in covid-19 patients.
The next organ studied up close was the heart. One of the most frightening early reports about the coronavirus from China was that a significant percentage of hospitalized patients — up to 20 to 30 percent — appeared to have myocarditis that could lead to sudden death. The condition involves the thickening of the muscle of the heart so that it can no longer pump efficiently.
Classic myocarditis is typically easy to identify in autopsies, pathologists say. It occurs when the body perceives the tissue to be foreign and attacks it. In that situation, there would be large dead zones in the heart, and the muscle cells known as myocytes would be surrounded by infection-fighting cells known as lymphocytes. But in the autopsy samples taken so far, the dead myocytes were not surrounded by lymphocytes — leaving researchers scratching their heads. It was said a couple of patients he performed autopsies on had gone into cardiac arrest in the hospital, but when he examined them, the primary damage was in the lungs — not the heart.
Of all the coronavirus’s manifestations, its impact on the brain has been among the most vexing. Patients have reported a host of neurological impairments, including reduced ability to smell or taste, altered mental status, stroke, seizures — even delirium.
An early study from China, published in the BMJ’s Journal of Neurology, Neurosurgery & Psychiatry, in March, found 22 percent of the 113 patients had experienced neurological issues ranging from excessive sleepiness to coma — conditions typically grouped together as disorders of consciousness. In June, researchers in France reported that 84 percent of patients in intensive care had neurological problems, and a third were confused or disoriented at discharge. Also this month, those in the United Kingdom found that 57 of 125 coronavirus patients with a new neurological or psychiatric diagnosis had experienced a stroke due to a blood clot in the brain, and 39 had an altered mental state.
Based on such data and anecdotal reports, Isaac Solomon, a neuropathologist at Brigham and Women’s Hospital in Boston, set out to systematically investigate where the virus might be embedding itself in the brain. He conducted autopsies of 18 consecutive deaths, taking slices of key areas: the cerebral cortex (the gray matter responsible for information processing), thalamus (modulates sensory inputs), basal ganglia (responsible for motor control) and others. Each was divided into a three-dimensional grid. Ten sections were taken from each and studied.
He found snippets of virus in only some areas, and it was unclear whether they were dead remnants or active virus when the patient died. There were only small pockets of inflammation. But there were large swaths of damage due to oxygen deprivation. Whether the deceased were longtime intensive care patients or people who died suddenly, Solomon said, the pattern was eerily similar. When the brain does not get enough oxygen, individual neurons die, and that death is permanent. To a certain extent, people’s brains can compensate, but at some point, the damage is so extensive that different functions start to degrade.
Rapkiewicz said it is too early to know whether the newest batch of autopsy findings can be translated into treatment changes, but the information has opened new avenues to explore. One of her first calls after noticing the unusual platelet-producing cells was to Jeffrey Berger, a cardiac specialist at NYU who runs a National Institutes of Health-funded lab that focuses on platelets.
Berger said the autopsies suggest anti-platelet medications, in addition to blood thinners, may be helpful to stem the effects of covid-19. He has pivoted a major clinical trial looking at optimal doses of blood thinners to examine that question as well.
Indien dit dan so lewensgevaarlik is dat die hele wêreld “lockdowns” moet kry, hoekom het hulle dan nie alle vorige hartsiektes of ander verwante siektes, waar soveel sterftes is en bloedklonte veroorsaak, al die lande onder “lockdown” geplaas nie.
Waarom word daar onderskeid gemaak en alle ernstig verwante siektes word as deel van die virus getel. Nog nooit was daar soveel lande gedwing tot algehele “lockdown” nie, want indien dit net bloedklonte is wat vorm, hoef dit mos nie te sluit daarvoor nie. Volgens die video’s is daar ander simptome ook, nie net die bloedvat probleem nie, wat moontlik die grootste oorsaak is vir sterftes.
Met al hierdie “lockdowns” is daar al miljoene besighede wat hul deure moes sluit omdat hulle nie die voorwaardes kan nakom nie. Hoeveel mense gaan agterna sterf van honger omdat besighede hul deure moet sluit. Klein besighede word ingesluk deur groot besighede. In Suid-Afrika is dit swart bemagtiging besighede wat seëvier.
Wat is die aksie uit die reaksies van aantasting?
Aanvullings van Son (Vitamine D) en Sinc, asook ander vitamines en minerale. Dis ons mense wat beter en gesonder moet lewe, ons moet versigtig wees wat ons eet, ons moet kyk na vetsug en bloeddruk probleme. Genoeg ontspanning wat die oorsake (swakplek wat virus aanval) reeds veroorsaak het.
Nog ‘n sondebok, wat ook in Dr Hansen se video genoem word, is sweet, wat afloop in enige gesig, gaan in neus, oë of mond in. As iemand nies, kan dit ook in jou oë beland, nie noodwendig in jou mond of neus (lug) nie. Dis nie reg dat jy jouself moet blootstel aan ‘n masker wat besmet is en dan nog sweet wat in plekke inloop waar jy besmet kan raak nie. Dis ander mense wat hulself eerder beter moet beskerm en gesonder lewensstyl leef.
DR HANSEN (ITALY)
12 Coronavirus Autopsy Cases Reveal the TRUTH How COVID 19 Patients Dying
COVID 19: What Doctors Are Learning From Autopsy Findings of COVID 19
Patients Once the Coronavirus is deeply embedded in the body, it begins to cause more severe disease. This is where the direct attack on other organs with ACE2 receptors can occur, including heart muscle, kidneys, blood vessels, liver, and the brain. Early findings, including those from multiple autopsies and biopsy reports, show that viral particles can be found only in the nasal passages and throat and in tears, stool, kidneys, liver, pancreas, and heart. One case report found evidence of viral particles in the CSF, meaning the fluid around the brain. That patient had meningitis.
So the coronavirus is sometimes going to all these different organs through attaching to the ACE2 receptors that are there, but that’s not even the whole story. ⏩ Timestamps, click to skip ahead! 00:00 – Common Symptoms of COVID 19 01:40 – What we know about COVID 02:25 – Early findings of Multiple Autopsy and Biopsy Reports of COVID 19 03:02 – Microscope Picture of the Coronavirus and Kidney Cells 03:20 – COVID Autopsy Findings Because in some COVID 19 cases, by the time the body’s immune system figures out the body are being invaded, it’s like unleashing the military to stomp out the virus, and in that process, there’s a ton of collateral damage.
This is what we refer to as the cytokine storm. When the COVID gets into the alveolar cells, meaning the tiny little air sacs within the lungs, it makes a ton of copies of itself and goes onto invading more cells. The alveoli’s next-door neighbor is guessed who, yeah, the tiniest blood vessels in our body, capillaries. And the lining of those capillaries is called the endothelium, which also has ACE2 receptors. And once the coronavirus invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. Early autopsy results are also showing widely scattered clots in multiple organs.
In one study from the Netherlands, 1/3rd of hospitalized with COVID 19 got clots despite already being on prophylactic doses of blood thinners. So not only are you getting the inflammation with the cytokine storm, but you’re also forming blood clots that can travel to other parts of the body, and cause major blockages, effectively damaging those organs.
So it can cause organ damage by 1) Directly attacking organs by their ACE2 receptor – Yes! 2) Indirectly attacking organs by way of collateral damage from the cytokine storm – Yes! 3) Indirectly cause damage to organs through blood clots – Yes! 4) Indirectly cause damage due to low oxygen levels, improper ventilator settings, drug treatments themselves, and/or all of these things combined – Yes! Endothelial cells are more vulnerable to dying in people with preexisting endothelial dysfunction, which is more often associated with being a male, being a smoker, having high blood pressure, diabetes, and obesity. Blood clots can form and/or travel to other parts of the body. Blood clots travel to the toes and cause blockages in blood flow there, meaning ischemia or infarction can cause gangrene. And lots of times, patients with gangrene require amputation and “COVID toes.” So is antiphospholipid antibody syndrome the cause of all these blood clots in patients with severe COVID? Maybe. Some patients with APS have catastrophic APS, where these patients can have strokes, seizures, heart attacks, kidney failure, ARDS, skin changes like the ones I mentioned. Viral infectious diseases, particularly those of the respiratory tract, have been reported as CAPS the triggers for CAPS. Various factors increase the risk of developing arterial thrombosis. Classically, the cardiovascular-dependent risk factors implicated in clotting have been hypertension, meaning high blood pressure, high cholesterol levels, smoking, diabetes, age, chemotherapy, and infection degree. All of these contribute toward developing arterial thrombosis. A lot of patients with severe COVID 19 have certain labs that resemble DIC, such as increased PT/INR, increased PTT, decreased levels of platelets. But the reason why these Coronavirus patients who developed clots in the study I mentioned earlier, the reason they don’t have DIC, is actually 2 reasons, one, they didn’t have extensive bleeding, and two, they did not have low fibrinogen levels. And if it’s truly DIC, you would have both of those things. Anyway, you can probably glean from this video why it’s so hard for doctors to figure out what is going on with this virus. The variable ways of this disease can present in different patients, and how organs can suffer damage, yes, this is really complicated. Are BLOOD CLOTS the reason why COVID 19 patients are dying?
Video Link – https://youtu.be/qoJ4VDaGSfY Doctor Mike Hansen, MD Internal Medicine | Pulmonary Disease | Critical Care Medicine Website: https://doctormikehansen.com/ IG Account: http://instagram.com/doctor.hansen/
The earliest signs of hypoxia are: Confusion. Restlessness. Shortness of breath
2 August 2018 (before the Corona virus)
Louisiana State University Health Sciences Center
Researchers have found how hypoxia (a low concentration of oxygen) decreases Protein S, a natural anticoagulant, resulting in an increased risk for the development of potentially life-threatening blood clots (thrombosis). Although hypoxia has been associated with an increased risk for thrombosis, this research showed for the first time a molecular cause.
“Hypoxia is common in many diseases including cancer, alcoholism, sickle cell anemia, nonalcoholic fatty liver disease and more,” notes Dr. Majumder. “Human Protein S (PS) is a natural blood anticoagulant. Although discovered 40 years ago, the exact mechanism of PS’s anticoagulant action was deduced only in the last few years. Our earlier work found that PS inhibits a key clotting protein, Factor IXa. We knew that PS deficiency could occur in hypoxia but not why. With this study, our group identified the gene regulatory mechanism by which oxygen concentration controls PS production.”
Hypoxia is a condition in which there is decreased oxygenation in the body tissues. It can be generalized, affecting the entire body, or local, affecting a specific part of the body. Hypoxia can cause damage to multiple organs and lead to fatal complications.
Hypoxemia is decreased oxygen in the blood. Hypoxemia can lead to hypoxia.