Symptoms of COVID-19
The symptoms of COVID-19 are variable depending on the type of variant contracted, ranging from mild symptoms to a potentially fatal illness.[1][2] Common symptoms include coughing, fever, loss of smell (anosmia) and taste (ageusia), with less common ones including headaches, nasal congestion and runny nose, muscle pain, sore throat, diarrhea, eye irritation,[3] and toes swelling or turning purple,[4] and in moderate to severe cases, breathing difficulties.[5] People with the COVID-19 infection may have different symptoms, and their symptoms may change over time. Three common clusters of symptoms have been identified: one respiratory symptom cluster with cough, sputum, shortness of breath, and fever; a musculoskeletal symptom cluster with muscle and joint pain, headache, and fatigue; and a cluster of digestive symptoms with abdominal pain, vomiting, and diarrhea.[5] In people without prior ear, nose, or throat disorders, loss of taste combined with loss of smell is associated with COVID-19 and is reported in as many as 88% of symptomatic cases.[6][7][8]
Published data on the neuropathological changes related with COVID-19 have been limited and contentious, with neuropathological descriptions ranging from moderate to severe hemorrhagic and hypoxia phenotypes, thrombotic consequences, changes in acute disseminated encephalomyelitis (ADEM-type), encephalitis and meningitis. Many COVID-19 patients with co-morbidities have hypoxia and have been in intensive care for varying lengths of time, confounding interpretation of the data.[9]
Of people who show symptoms, 81% develop only mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) that require hospitalization, and 5% of patients develop critical symptoms (respiratory failure, septic shock, or multiorgan dysfunction) requiring ICU admission.[10]
At least a third of the people who are infected with the virus do not develop noticeable symptoms at any point in time.[11][12][13] These asymptomatic carriers tend not to get tested and can still spread the disease.[13][14][15][16] Other infected people will develop symptoms later (called "pre-symptomatic") or have very mild symptoms and can also spread the virus.[16]
As is common with infections, there is a delay between the moment a person first becomes infected and the appearance of the first symptoms. The median delay for COVID-19 is four to five days[17] possibly being infectious on 1-4 of those days.[18] Most symptomatic people experience symptoms within two to seven days after exposure, and almost all will experience at least one symptom within 12 days.[17][19]
Most people recover from the acute phase of the disease. However, some people continue to experience a range of effects, such as fatigue, for months, even after recovery.[20] This is the result of a condition called long COVID, which can be described as a range of persistent symptoms that continue for weeks or months at a time.[21] Long-term damage to organs has also been observed after the onset of COVID-19. Multi-year studies are underway to further investigate the potential long-term effects of the disease.[22]
The Omicron variant became dominant in the U.S. in December 2021. Symptoms with the Omicron variant are less severe than they are with other variants.[23]
Cardiovascular[edit]
Coagulopathy is established to be associated with COVID-19 in those patients in critical state.[43] Thromboembolic events, such as blood clots show with high risk in COVID-19 patients in some studies.[44] Other
cardiovascular complications may include heart failure, arrhythmias, and heart inflammation.[45][46][47][48][49] They are common traits in severe COVID-19 patients due to the relation with the respiratory system.[50]
Hypertension seems to be the most prevalent risk factor for myocardial injury in COVID-19 disease. It was reported in 58% of individuals with cardiac injury in a recent meta-analysis.[51]
Several cases of acute myocarditis associated with COVID-19 have been described around the globe and are diagnosed in multiple ways. Taking into consideration serology, leukocytosis with neutrophilia and lymphopenia was found in many patients. Cardiac biomarkers troponin and N-terminal (NT)-prohormone BNP (NT-proBNP) were seen elevated. Similarly, the level of inflammation-related markers such as C-reactive protein (CRP), D-dimer, IL-6, procalcitonin was significantly increased, indicating an inflammatory process in the body. Electrocardiogram findings were variable and ranged from sinus tachycardia, ST-segment elevation, T-wave inversion and ST-depression.[52] In one case, viral particles were seen in the interstitial cell, and another case reported SARS-CoV-2 RT–PCR positivity in the cardiac tissue suggestive of direct viral injury to the myocardium.[53][54] Endomyocardial biopsy [EMB] remains the gold standard invasive technique in diagnosing myocarditis; however, due to the increased risk of infection, it is not done in COVID-19 patients.
The binding of the SARS-CoV-2 virus through ACE2 receptors present in heart tissue may be responsible for direct viral injury leading to myocarditis.[52] In a study done during the SARS outbreak, SARS virus RNA was ascertained in the autopsy of heart specimens in 35% of the patients who died due to SARS.[55] It was also observed that an already diseased heart has increased expression of ACE2 receptor contrasted to healthy individuals.[56] Hyperactive immune responses in COVID-19 Patients may lead to the initiation of the cytokine storm. This excess release of cytokines may lead to myocardial injury.[52]
Blood clots and bleeding[edit]
Patients are at increased risk of a range of different blood clots, some potentially fatal, for months following COVID infection. The Guardian wrote, "Overall, they [a Swedish medical team] identified a 33-fold increase in the risk of pulmonary embolism, a fivefold increase in the risk of DVT (deep vein thrombosis) and an almost twofold increase in the risk of bleeding in the 30 days after infection. People remained at increased risk of pulmonary embolism for six months after becoming infected, and for two and three months for bleeding and DVT. Although the risks were highest in patients with more severe illness, even those with mild Covid had a threefold increased risk of DVT and a sevenfold increased risk of pulmonary embolism. No increased risk of bleeding was found in those who experienced mild infections." Anne-Marie Fors Connolly at Umeå University said, "If you suddenly find yourself short of breath, and it doesn't pass, [and] you've been infected with the coronavirus, then it might be an idea to seek help, because we find this increased risk for up to six months."[68]
Stages of COVID-19 infection[edit]
There are three stages, according to the way COVID-19 infection can be tackled by pharmacological agents, in which the disease can be classified.[75] Stage I is the early infection phase during which the domination of upper respiratory tract symptoms is present. Stage II is the pulmonary phase in which the patient develops pneumonia with all its associated symptoms; this stage is split with Stage IIa is without hypoxia and Stage IIb having hypoxia. Stage III is the hyperinflammation phase, the most severe phase, in which the patient develops acute respiratory distress syndrome (ARDS), sepsis and multi-organ failure.[75]
A similar stereotyped course was postulated to be: the first phase of an incubation period, a second phase corresponding to the viral phase, a third phase corresponding to the state of inflammatory pneumonia, a fourth phase corresponding to the brutal clinical aggravation reflected by acute respiratory distress syndrome (ARDS), and finally, in survivors, a fifth phase potentially including lung fibrosis, and persisting in the form of "post-covid" symptoms.[76]