COVID: Know Thine Enemy——-A Multisystem Disease
Effects of the novel Coronavirus on multiple systems
Based on the experience of SARS, COVID was expected by most people to be a respiratory illness. However, it quickly became apparent that, as well as spreading much more readily than the SARS virus, SARS-CoV-2 was producing a much more complicated illness that affected multiple bodily systems.
More than half of the people hospitalised because of Covid-19 have blood or protein in their urine, indicating kidney damage. Acute kidney failure (aka acute kidney injury) is common. According to a preliminary study from Wuhan, 20 per cent of patients suffer this complication. People with acute kidney injury may be five times as likely to die from Covid-19 as patients without it are.
The mechanisms of COVID-related renal injury are complex, often multifactorial, and are still being investigated. It is possible that the virus affects the kidneys directly: the enzyme ACE2, to which the virus attaches, is present in the kidneys, as I have noted. Renal damage may be related to clotting affecting renal blood vessels. Finally, these patients are often very unwell, with low blood pressure and fluid depletion, both of which can cause acute renal failure. Factors that make acute kidney injury more likely include: chronic kidney disease, heart failure, diabetes, and age over 65 years. A detailed discussion of COVID-related renal damage can be found here.
Abnormalities of taste or smell seem to be common in COVID. New loss of taste and/or smell is now one of the criteria we are being told to look out for. The mechanism of this is unclear, but it is difficult to study as it tends to be transient.
Other neurological effects include stroke (due to haemorrhage or arterial blockage), headache, altered mental state, and severe complications such as Guillain-Barré syndrome and acute necrotising encephalopathy. Further discussion of the neurological effects of COVID can be found here.
Gastrointestinal symptoms have been reported in 2-40% of COVID patients. Diarrhoea may be the presenting symptom of the disease. It is unclear whether SARS-CoV-2 infects the gut. It may produce its effects via neurological involvement, or through production of cytokines (see “Cytokine Storms” below). Viral RNA has been found in stool samples, sometimes at high levels. This raises the possibility of faeco-oral spread of infection.
Cardiovascular events associated with COVID-19 include myocardial damage, especially in those with severe infections. Inflammation of heart muscle, and of the pericardium (the membrane that covers the heart) has been described. Heart rhythm abnormalities have been noted, and impaired cardiac function or heart failure. Heart disease was found to be the most common pre-existing health condition in people who died from Covid-19 during March in England and Wales, according to data from the Office of National Statistics. COVID can be accompanied by a hypercoagulable state (with increased blood clotting in arteries and veins). People with ischaemic heart disease have a higher mortality rate when they get COVID-19, and it is possible that part of the explanation may be that they develop small clots in the coronary arteries, causing myocardial damage, or death.
As mentioned before, clots may also develop in the pulmonary circulation (pulmonary thromboembolism). Chest pain in COVID patients could be related to this, or to myocardial disease.
Increased redness and swelling of the conjunctivae, with increased secretions is commonly associated with COVID (up to 32% in a Chinese case series). SARS-CoV-2 RNA could be detected in tears, which could represent another means of the virus spreading (see “Gastrointestinal Effects”).
Cytokines are small proteins that have a wide variety of bodily functions, including immune regulation. When a pathogen like SARS-CoV-2 enters the body, cytokines stimulate cells involved in the immune response to attack and destroy the invading organism. This is a normal reaction, but in some patients it develops excessively, and the body, in addition to attacking the virus, begins to damage itself. This situation is termed a Cytokine Storm, and it is often associated with a high mortality.
SARS-CoV-2 is not the only virus that can provoke this sort of reaction. Cytokine Storms may have been responsible for many of the deaths in the 1918 Influenza Pandemic, as well as some the deaths due to SARS and MERS. The H5N1 Influenza virus is also know to cause Cytokine Storms. The reason why some viruses commonly trigger this abnormal response is not understood, and it is the subject of current research.
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