Although COVID-19 is known to cause acute respiratory disease, it can alsolead to
Blood clots, thrombosis, inflammation, and an overwhelmed immune system
Scientists believe that complications caused byincreased blood clotting can be caused by a virus attacking the cells that line the blood vessels. When the virus infects the cells of the blood vessels, the inflammation intensifies and the blood begins to form clots, large and small. These blood clots can spread throughout the body and damage organs, creating a vicious cycle of blood clots.
In order to combat clotting and itsColombian experts, many of whom are co-authors of the review, are conducting a randomized clinical trial to investigate the optimal dose and timing of anticoagulant drugs in critically ill COVID-19 patients.
Unobstructed inflammation can alsooverstimulate the immune system. Dysregulation of the immune response and cytokine release syndrome are symptoms of severe COVID-19. Such a reaction of the body is due to the excessive activation of innate immunity in conditions of lymphodepletion of T cells.
In previous preclinical and humanStudies with pathogenic coronaviruses have suggested rapid viral replication, antagonism of interferon signaling, and activation of neutrophils and monocyte macrophages as mediators of hyperinflammation.
Increased serum inflammatory markers -C-reactive protein, ferritin, ESR, D-dimers, fibrinogen and lactate dehydrogenase are a signal that the disease has entered a critical phase of the disease and the likelihood of death in patients with COVID-19 is high.
And although doctors initially avoided usingsteroids for global suppression of the immune system, a recent clinical study showed that at least one steroid, dexamethasone, reduced mortality in ventilated patients by a third. Randomized clinical trials are currently underway to target specific components of inflammation and the immune system.
Heart problems: ischemia, cardiomeopathy, and other disorders
SARS-CoV-2 can cause both direct andindirect cardiovascular complications: myocardial damage, acute coronary syndromes (ACS), cardiomyopathy, arrhythmias and cardiogenic shock, as well as the aforementioned thrombotic complications.
Thrombus formation and blood clots can causeheart attacks, but the virus infects the heart in other ways. The mechanism of heart damage itself is currently unclear, since the virus is not often released from cardiac tissue at autopsy.
The heart muscle can be damaged by systemicinflammation and the accompanying release of cytokines - a flood of immune cells that normally cleanse infected cells but can spiral out of control in severe cases of COVID-19.
Patients with viral infections are generally at risk of ischemia, which is increased in patients with COVID-19, given reports of disproportionately increased hypercoagulability.This can lead to a possible increase in thrombotic-mediated coronary artery disease.
Other potential etiologies of damagenon-COVID-19 specific myocardial infarctions include severe ischemia or MI in patients with preexisting coronary artery disease, stress-mediated myocardial dysfunction, tachycardia-induced cardiomyopathy, and myocardial stunning after resuscitation or prolonged hypotension.
Acute renal failure and the need for dialysis
Another surprising finding was the high proportion ofpatients with COVID-19 in the intensive care unit with acute kidney damage. Acute kidney injury has been found to be a common complication of COVID-19 and has been associated with mortality.
The ACE2 receptor used by the virus tocell penetration, is found in high concentrations in the kidney and is likely to cause kidney damage. Studies in China have reported renal complications, but in New York, clinicians have observed renal failure in 50% of patients in the intensive care unit.
In a study conducted in the United States, out of about 5500of patients admitted with COVID-19 to the New York hospital system, acute kidney damage occurred in 37%, with 14% of patients requiring dialysis. This is a very high number.
Other effects associated with renal manifestations include:
- electrolyte disturbances (such as hyperkalemia, hyponatremia, and hypernatremia),
- metabolic acidosis,
- Hematuria
- proteinuria.
Data on long-term kidney damage are not currently available, but a significant proportion of patients are likely to require continuous dialysis.
Future research after patients who have experienced complications during hospitalization for COVID-19 will be critical, the scientists said.
Neurological disorders: from headache to delirium and hallucinations
Neurological symptoms, including headache, dizziness, fatigue, and loss of smell, can occur in about a third of patients.
Nonspecific mild neurological symptoms reported in hospitalized COVID-19 patients also include myalgia, fatigue, and anorexia.
Thrombus-induced strokes occur in 6% of cases. Stroke, confusion, or impaired consciousness have also occurred in severe COVID-19.
Patients with COVID-19 can be intubated for two to three weeks; a quarter need a ventilator for 30 days or more.These are very long intubation periods, and patients require a lot of sedatives.Delirium, delirium was a well-known disease even before the advent of COVID.Hallucinations may not be so much the effect of the virus as the effect of a long-term sedative effect.
Case reports also describemeningoencephalitis, hemorrhagic syndrome of posterior reversible encephalopathy and acute necrotizing encephalopathy. Some patients had acute inflammatory demyelinating polyneuropathy (Guillain-Barré syndrome).
It is also noted that patients with COVID-19 also experienced ocular manifestations such as a single conjunctival hyperemia, conjunctivitis and retinal changes.
Dermatological manifestations
For the first time, the dermatological manifestations of COVID-19 appeared in a single-center observational study in Italy, with a frequency of 20% in hospitalized patients.
Approximately 44% of patients had cutaneousmanifestations at the onset of the disease, while in other patients they developed later. In this small study, there was no correlation with disease severity. Cutaneous manifestations included erythematous rash, urticaria, and chickenpox-like chickenpox. Other cutaneous signs included maculopapular rash, vesicular lesions and living body lesions, and / or necrotic lesions.
Gastrointestinal manifestations and liver failure
The review authors state that the incidence of gastrointestinal manifestations ranges from 12% to 61% in patients with COVID-19.
They cite a recent meta-analysis of 29 studies, most of which were conducted in China, that report the combined prevalence of individual symptoms and include:
- anorexia – 21% of cases
- nausea and/or vomiting – 7% of cases
- diarrhea – 9% of cases
- abdominal pain – 3% of cases.
A cumulative prevalence of abnormal liver function is also reported to be 19%.
Meanwhile, laboratory markers associated with infection include elevated hepatic transaminases, elevated bilirubin, and low serum albumin.
Gastrointestinal symptoms may be associated with a longer duration of illness, but not associated with increased mortality, the researchers said.
Endocrine manifestations of the disease: complications in diabetics and the risk of ketoacidosis
The review authors note that a number of endocrine manifestations are observed in patients without preexisting endocrine disease.
In addition, patients with diabetes and / or obesity are known to be at risk of developing more severe COVID-19.
At the same time, in patients hospitalized withthe use of COVID-19, a number of disorders of glucose metabolism are observed, including: worsening hyperglycemia, euglycemic ketosis, classic diabetic ketoacidosis.
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