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POST-COVID CONDITIONS

For many people, being exposed to COVID-19 results in illness characterized by mild symptoms that resolve in a matter of days or weeks. However, some patients experience severe, debilitating symptoms that last for several months and may not improve over time. Other patients recover from COVID-19 but are vulnerable to many types of associated health conditions as a result of the initial viral infection, known as “Post-COVID Conditions.” These conditions affect nearly every organ in the body and range from benign to life-threatening.

There appears to be a reciprocal relationship between COVID-19 and Post-COVID Conditions: Post-COVID Conditions represent underlying health factors that place patients at higher risk of severe illness from COVID-19 while patients who experience severe illness from COVID-19 have a greater risk of developing these Post-COVID Conditions. However, even a patient who recovers from an asymptomatic or mild case of COVID-19 is at risk of developing one or more Post-COVID Conditions. Patients who already live with a Post-COVID condition prior to being exposed to COVID-19 may find that the underlying condition suddenly worsens as a result of the COVID-19 infection.

This page contains a description of the health conditions that patients have a heightened risk of developing after recovering from COVID-19.

NOTE: Our understanding of the association between COVID-19 and the risk of developing these conditions continues to evolve. This page will be updated as new information becomes available.

This page was last updated on 4/11/2022.

People who recover from COVID-19 “exhibit significant cognitive deficits.” These cognitive deficits include “brain fog . . . low energy, difficulty concentrating, disorientation and difficulty finding the right words.” Patients who were hospitalized and who received medical assistance for respiratory symptoms of COVID-19 developed greater cognitive deficits than patients who recovered at home. Cognitive deficits were greatest for patients who were put onto a ventilator but even patients with mild illness can experience cognitive deficits. One study found that fatigue and neurocognitive impairment are the two post-acute symptoms of COVID-19 that have the greatest impact on general health and working capacity for six to twelve months after recovering from acute COVID-19.

People who recover from COVID-19 experience a “reduction in grey matter thickness and tissue-contrast in the orbitofrontal cortex and parahippocampal gyrus . . . tissue damage in regions functionally-connected to the primary olfactory cortex and . . . reduction in global brain size.” These effects were observed in both hospitalized and non-hospitalized patients and were associated with cognitive decline. Additional study is needed to determine whether these effects can be reversed over time.

Detailed data regarding the association between COVID-19 infection and sleep disorders is currently lacking. However, one study found that 26 percent of COVID-19 patients who were followed up after being discharged from the hospital reported sleep difficulties. Another study found that insomnia and sleep disturbances were commonly reported by patients recovering from COVID-19.

COVID-19 infection can cause the sudden worsening of a previous headache disorder, potentially making the headache disorder chronic. This is common with patients with migraine disorders. Some people without a history of migraine disorder have reported acquiring a migraine disorder as a result of a COVID-19 infection. Notably, some patients who did not experience headache during acute COVID-19 infection have developed persistent headaches following recovery from COVID-19. Symptoms of headache and migraine following recovery from COVID-19 are often closely associated with other symptoms of COVID-19, including insomnia, memory loss, dizziness, and fatigue, among others.

COVID-19 infection that reaches the brain can cause diverse neurological and dysexecutive syndromes, including aphasia, which is a language expression and comprehension disorder. Some patients experiencing acute COVID-19 infection have exhibited symptoms of aphasia, but the symptoms typically resolve within a few weeks to a few months following recovery from COVID-19. The incidence of aphasia in some patients can also be attributed to a stroke or blood clot caused by the acute COVID-19 infection.

One study found that, among patients diagnosed with COVID-19, 33 percent developed a neuropsychiatric disorder during the first six months of recovery. In the same period of time, nearly 13 percent of patients recovering from COVID-19 developed a neuropsychiatric disorder without having any prior history of such disorders. The risk for developing a neuropsychiatric disorder is greatest for patients who experienced severe COVID-19. The neuropsychiatric disorders studied include intracranial hemorrhage, ischemic stroke, Parkinsonism, Guillain-Barre syndrome, encephalitis, dementia, mood disorders, anxiety disorders, psychotic disorders, and substance use disorders, among others.

One study found that people who recover from COVID-19 have an estimated 40 percent heightened risk of developing diabetes for up to a year following the initial infection. This risk exists even for people who had only mild symptoms of COVID-19 and the condition predominantly manifests as Type 2 Diabetes. Patients who were hospitalized or admitted to intensive care during their acute COVID-19 infection have roughly triple the risk of developing diabetes compared to people who did not have COVID-19. Another study found a significantly higher rate of new-onset diabetes in patients with COVID-19, which is associated with higher mortality rates and adverse events.

COVID-19 increases the risk of developing chronic kidney disease and acute kidney injury. Types of kidney damage include “inflammation, kidney fibrosis, and abnormal kidney gene expression.” Patients who experienced severe COVID-19 are at the highest risk of developing these conditions. This risk endures for at least thirty days following a diagnosis with COVID-19. One study found that 35 percent of patients had reduced kidney function six months after recovering from COVID-19. Some patients may recover from kidney damage caused by COVID-19, but some damage to the kidneys caused by COVID-19 may be permanent. The long-term effects of COVID-19 on the kidneys are largely unknown.

People who recover from COVID-19 often experience persistent symptoms of lung damage, including pulmonary fibrosis. Pulmonary fibrosis is characterized by scarred lung tissue, decreased lung function, cough, and frailty. One study found that 20 percent of non-ventilated patients with COVID-19 displayed “fibrotic-like radiographic abnormalities” four months after hospitalization. The risk of pulmonary fibrosis is higher for patients with severe COVID-19 and those who received ventilator support during hospitalization. The damage to lung tissue caused by COVID-19 may be permanent.

Patients with asymptomatic or mild COVID-19 symptoms can develop lung abnormalities while patients who develop severe COVID-19, characterized by viral pneumonia and respiratory failure, have a higher risk of developing persistent lung abnormalities. Symptoms of these abnormalities, including impaired lung function, persistent fatigue, decreased functional capacity and decreased quality of life, have been reported up to six months after hospital discharge.

COVID-19 can cause damage to the eyes, including hemorrhages, cotton wool spots, retinal vein occlusions, arterial occlusions, localized retinal infarcts, and ocular inflammation. This damage can manifest between one and six weeks after the initial onset of COVID-19 symptoms.

One study found that COVID-19 can cause small nerve fibre damage in the cornea between four and twelve weeks after acute COVID-19 infection. This study found that the extent of corneal nerve damage is likely associated with the severity of COVID-19 infection.

Some people who have recovered from COVID-19 have reported sudden onset sensorineural hearing loss and tinnitus. One study found that patients with COVID-19 had “significantly worse high frequency pure tone audiometer thresholds and [transient evoked otoacoustic emissions] amplitudes,” which suggests a potential relationship between COVID-19 infection and cochlear damage.

COVID-19 directly and indirectly acts on the nervous system, which can cause neuropathic pain. During acute COVID-19 infection, neuropathic pain manifests as “headache, dizziness, muscle pain, ataxia, and olfactory/taste disorders.” One study found that neuropathic pain was reported by up to 2.3 percent of hospitalized COVID-19 patients, but suggested that the prevalence of neuropathic pain is underestimated because chronic neuropathic pain can arise months after injury to the nervous system. Neuropathic pain associated with COVID-19 can also be caused by acute ischemic stroke, acute transverse myelitis, and Guillain-Barre syndrome.

Depending on the severity of a person’s COVID-19 illness, they may develop one or more skin conditions. Asymptomatic disease can result in a Chilblain-like acral pattern, which typically affects the feet and hands and is associated with pain, burning, and itching. Mild COVID-19 can cause urticarial rash, which predominantly affects the trunk and limbs, with associated swelling. Mild COVID-19 can also cause confluent erythematous, maculopapular, or morbilliform rash, which are symmetrical lesions that start on the trunk and can cause itchiness from secondary lesions or skin eruptions. Papulovesicular exanthem is also associated with mild COVID-19, which is characterized either by small, widespread papules, vesicles, and pustules of varying sizes or a localized pattern of lesions on the chest, upper abdomen, or the back. COVID-19 can cause two ring-shaped lesions: mild COVID-19 can result in livedo reticularis-like lesions, which are transient, symmetrical, and dusky patches that form around a pale center; severe COVID-19 illness can result in livedo racemosa-like lesions, which are large, irregular, violet, and asymmetrical rings. Severe COVID-19 can also cause purpuric vasculitic pattern lesions, which affect peripheral body parts and regions where two skin areas meet or rub together. These lesions can evolve into hemorrhagic blisters and, ultimately, necrotic-ulcerative lesions. Fortunately, many of these skin conditions can be treated with topical corticosteroids and antihistamines.

Patients who recover from COVID-19 are at heightened risk of developing several cardiovascular conditions, including “abnormal heart rhythms, heart muscle inflammation, blood clots, strokes, myocardial infarction, and heart failure.” Patients who experienced asymptomatic or mild COVID-19 illness are at risk of developing cardiovascular conditions as a consequence of the viral infection, but patients who were hospitalized had the highest risk of developing these conditions. One study found that these risks remained for twelve months following the initial COVID-19 infection.

Patients who recover from COVID-19 are at significantly higher risk for developing deep vein thrombosis, pulmonary embolism, and bleeding following the initial infection. The risk is highest for patients with severe illness caused by COVID-19 and one study observed a higher risk among patients who were exposed to COVID-19 during the first wave of the pandemic. The heightened risk of pulmonary embolism extended for up to six months after recovery from COVID-19, while the heightened risk for deep vein thrombosis extended for up to three months after recovery.

Up to six months after recovery from COVID-19, chest pain, heart palpitations, and heartbeat irregularities are common symptoms experienced by patients. Patients with both mild and severe COVID-19 have a heightened risk of myocardial damage and myocarditis. One study found that the vascular system endures persistent inflammation following recovery from COVID-19, along with “significantly lower systemic vascular function and higher arterial stiffness.” These patients were found to continue experiencing reduced cerebral vascular function and higher central arterial stiffness even if their other symptoms of COVID-19 had resolved. Additional research is needed to determine which cardiovascular complications will result in chronic illness.

A diagnosis with COVID-19 has a significant correlation with newly-onset erectile dysfunction in men. The cause for this relationship is not fully understood, but may be related to the location of ACE2 receptors in the testes, endothelial damage to erectile tissue, testicular damage, and psychological factors.

The coronavirus gains access to the human body through ACE2 receptors, which are found in several endocrine glands, including the pancreas, thyroid, ovaries, and testes. This makes the endocrine system vulnerable to destruction and alteration from COVID-19. Symptoms of damage to the endocrine system following COVID-19 infection include thyroid dysfunction, adrenal insufficiency, hypogonadism, changes to menstrual cycles, hyperglycemia, and ketoacidosis. Some of these symptoms can resolve on their own, but more research is needed to understand the long-term impacts that COVID-19 has on the endocrine system.

The gastrointestinal system is vulnerable to damage from COVID-19 because it contains ACE2 receptors that the virus uses to access the body. Damage from COVID-19 can result in significant systemic disease involving the gastrointestinal tract, liver, biliary tract, and pancreas. Symptoms of damage to the gastrointestinal system include acute pancreatitis, anorexia, nausea, vomiting, diarrhea, gastrointestinal bleeding, lesions in the upper gastrointestinal tract, and ischemic lesions in the colon. One study found that COVID-19 patients sustained acute mucosal injuries to the gastrointestinal system and many had features of ischemic colitis, which is inflammation of the large intestine or colon.

COVID-19 has widespread impacts on the musculoskeletal system, causing damage to the muscles, joints, nerves, soft tissues, and bone. Many patients report experiencing myalgia, which presents as muscle aches and pain, and myositis, which is muscle inflammation. Myositis can lead to rhabdomyolysis, which is a life-threatening condition associated with kidney failure, compartment syndrome, and intravascular coagulation. After recovering from COVID-19, patients may experience long-term symptoms of muscle damage, including sarcopenia (muscle loss) and cachexia (muscle wasting). Peripheral neuropathy, or nerve damage, is a common manifestation of COVID-19 illness. Peripheral neuropathy commonly manifests as pain, numbness, weakness, and tingling sensations. Guillain-Barre syndrome has also been reported, with symptoms beginning within three to four weeks after the initial onset of COVID-19 symptoms. This condition occurs as a result of nerve damage and causes muscle weakness and paralysis. COVID-19 has the ability to trigger rheumatological diseases, including “systemic lupus erythematosus, dermatomyositis, Graves’ disease, rheumatoid arthritis, and psoriatic spondyloarthritis.” The damage that COVID-19 causes to soft tissues can result in disseminated intravascular coagulation, gangrene, and bleeding complications.

One study examined how COVID-19 affected the skeletal system of mice and found that the virus caused significant decreases in bone volume and an increase in osteoclasts, which are cells that can lead to bone loss. Bone loss was observed even in mice who had asymptomatic COVID-19 infection. This study suggests that COVID-19 patients may be at a higher risk of developing osteoporosis and bone fractures, with the damage to the musculoskeletal system possibly being permanent.

Some long-term symptoms of COVID-19 suggest that the virus damages the peripheral nervous system, which is responsible for signaling between the central nervous system and other parts of the body. Damage to this nervous system can manifest as difficulty coordinating muscle movements, muscle weakness and cramps, loss of senses, including taste, smell, touch, sight, and hearing, and interruption of regulatory functions, including breathing, digestion, heart, and gland functions. Symptoms of regulatory functions being interrupted include excessive or limited sweating, heat intolerance, blood pressure and heart rate irregularities, lightheadedness, and difficulty concentrating.

Fatigue is one of the most common symptoms that people experience after recovering from COVID-19. Researchers have observed many similarities between people who have recovered from COVID-19 and those who have myalgic encephalopathy and chronic fatigue syndrome. Symptoms of chronic fatigue can be linked to permanent damage that the virus causes to the heart, lungs, and the kidneys. Fatigue can also manifest as post-exertional malaise, which is the sudden onset of long-lasting extreme fatigue following ordinary activities. Many people overcome symptoms of chronic fatigue following recovery from COVID-19, but many others experience debilitating fatigue that does not improve.

“Cognitive deficits in people who have recovered from COVID-19,” The Lancet, July 22, 2021, https://doi.org/10.1016/j.eclinm.2021.101044.

Prevalence, determinants, and impact on general health and working capacity of post-acute sequelae of COVID-19 six to 12 months after infection: a population-based retrospective cohort study from southern Germany,” MedRxiv, March 15, 2022, https://doi.org/10.1101/2022.03.14.22272316.

“SARS-CoV-2 is associated with changes in brain structure in UK Biobank,” Nature, August 19, 2021, https://doi.org/10.1038/s41586-022-04569-5.

“Sleep disorders and COVID-19,” Sleep Medicine, July 18, 2021, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8286239/.

“Sleep in post-COVID-19 recovery period and its impact on different domains of quality of life,” The Egyptian Journal of Neurology, Psychiatry, and Neurosurgery, December 14, 2021, https://doi.org/10.1186/s41983-021-00429-7.

“Toward a better understanding of persistent headache after mild COVID-19: Three migraine-like yet distinct scenarios,” The Journal of Head and Face Pain, August 7, 2021, https://doi.org/10.1111/head.14197.

“COVID-19 and Aphasia,” Current Neurology and Neuroscience Reports, October 21, 2021, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8529864/.

“6-month neurological and psychiatric outcomes in 236 379 survivors of COVID-19: a retrospective cohort study using electronic health records,” The Lancet, April 6, 2021, https://doi.org/10.1016/S2215-0366(21)00084-5.

“Risks and burdens of incident diabetes in long COVID: a cohort study,” The Lancet, March 21, 2022, https://doi.org/10.1016/S2213-8587(22)00044-4.

“New-onset diabetes in COVID-19 and clinical outcomes: A systematic review and meta-analysis,” World Journal of Virology, September 25, 2021, https://doi.org/10.5501/wjv.v10.i5.275.

“Long COVID and kidney disease,” Nature Reviews Nephrology, September 9, 2021, https://doi.org/10.1038/s41581-021-00487-3.

“Pulmonary fibrosis 4 months after COVID-19 is associated with severity of illness and blood leucocyte telomere length,” Thorax, http://dx.doi.org/10.1136/thoraxjnl-2021-217031.

“Long-Term Impact of COVID-19: A Systematic Review of the Literature and Meta-Analysis,” Biomedicines, July 27, 2021, https://doi.org/10.3390/biomedicines9080900.

“Retinal manifestations in patients with SARS-CoV-2 infection and pathogenetic implications: a systematic review,” International Ophthalmology, July 30, 2021, https://doi.org/10.1007/s10792-021-01996-7.

“Corneal confocal microscopy identifies corneal nerve fibre loss and increased dendritic cells in patients with long COVID,” British Journal of Ophthalmology, July 26, 2021, http://dx.doi.org/10.1136/bjophthalmol-2021-319450.

“Sudden irreversible hearing loss post COVID-19,” BMJ Case Reports, October 13, 2020, http://dx.doi.org/10.1136/bcr-2020-238419.

“Potential for increased prevalence of neuropathic pain after the COVID-19 pandemic,” Pain Reports, January 27, 2021, https://doi.org/10.1097/PR9.0000000000000884.

“Skin Manifestations Associated with COVID-19: Current Knowledge and Future Perspectives,” Dermatology, January 2021, https://doi.org/10.1159/000512932.

“Impact of COVID-19 on the Endocrine System: A Mini-review,” Endocrinology, September 20, 2021, https://doi.org/10.1210/endocr/bqab203.

“Gastrointestinal mucosal damage in patients with COVID-19 undergoing endoscopy: an international multicentre study,” BMJ Open Gastroenterology, February 24, 2021, http://dx.doi.org/10.1136/bmjgast-2020-000578.

“COVID-19 and Gastrointestinal Disease: Implications for the Gastroenterologist,” Digestive Diseases, March 2021, https://doi.org/10.1159/000512152.

“Musculoskeletal involvement of COVID-19: review of imaging,” Skeletal Radiology, February 18, 2021, http://dx.doi.org/10.1007/s00256-021-03734-7.

“Osteoclast-mediated bone loss observed in a COVID-19 mouse model,” Bone, January 2022, https://doi.org/10.1016/j.bone.2021.116227.

“Coronavirus and the Nervous System,” National Institute of Neurological Diseases and Stroke, Updated on February 25, 2022, https://www.ninds.nih.gov/Current-Research/Coronavirus-and-NINDS/nervous-system.

“Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome,” Proceedings of the National Academies of Sciences, August 16, 2032, https://doi.org/10.1073/pnas.2024358118.

“The COVID Heart—One Year After SARS-CoV-2 Infection, Patients Have an Array of Increased Cardiovascular Risks,” JAMA, https://doi.org/10.1001/jama.2022.2411.

“Risks of deep vein thrombosis, pulmonary embolism, and bleeding after covid-19: nationwide self-controlled cases series and matched cohort study,” BMJ, April 6, 2022, https://doi.org/10.1136/bmj-2021-069590.

“COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences,” Frontiers in Cell and Developmental Biology, February 15, 2022, https://doi.org/10.3389/fcell.2022.824851.

“COVID-19 Infection Is Associated With New Onset Erectile Dysfunction: Insights From a National Registry,” The Journal of Sexual Medicine, December 15, 2021, https://doi.org/10.1016/j.esxm.2021.100478.

“Tip of the iceberg: erectile dysfunction and COVID-19,” International Journal of Impotence Research, February 12, 2022, https://doi.org/10.1038/s41443-022-00540-0.

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