A list of all serious symptoms
Covid-19, caused by the novel coronavirus SARS-CoV-2, is generally a respiratory infection and some of its key symptoms are coughing, and shortness of breath.
Some people have, however, reported other symptoms, including loss of smell, heart trouble, and diarrhea. Here’s a list of all non-respiratory symptoms reported in patients.
GI symptoms can contribute significantly to morbidity in infected patients with regard to the gastrointestinal system. Some symptoms include nausea, vomiting, diarrhea, and/or abdominal discomfort. Other gastrointestinal symptoms included epigastric pain, belching, and anorexia.
Gastrointestinal manifestations can be overlooked. Though GI symptoms are not prominent in most cases and are not life-threatening, doctors should identify these symptoms in order to prevent the potential spread of Covid-19.
Some studies have shown that GI symptoms can present before the onset of typical respiratory symptoms. Studies have shown that infected patients can shed viral particles in their stool. The virus also has been detected in biopsies of the esophagus, stomach, duodenum, and rectum.
Reports suggest that COVID-19 can infect the cardiac tissue by binding to
the angiotensin-converting enzyme (ACE) receptors (antennas
located in heart tissues), which can result in myocardial inflammation and
damage .Among the reported cardiac manifestations of COVID-19 are;
Myocardial injury is defined as an elevation in biomarkers such as cardiac
troponin. The increased prevalence of cardiac injury among patients with
COVID-19 could be explained by the significantly higher levels of cardiac
troponin I in severely ill patients.
A wide variety of arrhythmias have been observed in patients with Covid-19. A study shows that patients suffered from cardiac arrests, atrial fibrillation events, decreased/increased heartbeat. Irregular heartbeats contribute to severity of disease.
Heart failure and acute cardiac injury were more common in deceased
patients, regardless of their cardiovascular history. Specifically, a study
reported heart failure in 24% of deceased patients, nearly half of whom did not have any history of cardiovascular disease or hypertension.
Right heart failure can also occur in patients with severe lung injury and ARDS (acute respiratory syndrome).
Reports suggest that COVID-19 can infect the cardiac tissue by binding to the angiotensin-converting enzyme (ACE) receptors (antennas located in heart tissues), which can result in myocardial inflammation and damage.
The patients infected with COVID-19 showed similar laboratory abnormalities, including decreased total lymphocyte count (a component of white blood cells in body), prolonged prothrombin time, elevated d-dimer levels and increased lactate dehydrogenase.
A recent study showed laboratory derangements in Covid-19 patients were of lymphopenia (a decrease in lymphocytes count) (35–75% of cases), increased LDH (27–92% of cases), elevated and d-dimer (36–43% of cases).
Hypercoagulability signals worsen the prognosis in patients infected with Covid-19 compared to a healthy control, d-dimer, FDP, and fibrinogen levels increase in patients with the virus, while their antithrombin (AT) levels are significantly reduced.
The data suggests that deregulated thrombin generation and abnormal
activation of the coagulation cascade can lead to the development of
disseminated intravascular coagulation or clotting, and is
associated with worsening pneumonia and mortality.
DIC was a significantly more common in non-survivors (71.4%) versus
survivors (0.6%) . Early monitoring of these parameters can help guide medical management such as the use of VTE (venous thromboembolism)
prophylaxis and prompt cure.
AKI is of particular interest as it is associated with poorer outcomes in
general population and Covid-19. Patients with AKI were more likely to have severe symptoms with prolonged hospitalisation.
They were more likely to have lower lymphocyte counts, higher C-reactive
protein, lactate dehydrogenase levels, and higher abnormal chest radiography.
The pathophysiology of AKI patients with AKI is not completely understood
but is likely to be multifactorial.
Microemboli and thrombi as a result of a hypercoagulable state has been
proposed as a possible cause of AKI .However, the relationship between severe COVID-19 and AKI is likely to be bidirectional.