ABSTRACT
BACKGROUND: The association between autonomic dysfunction and long-COVID syndrome is established. However, the prevalence and patterns of symptoms of dysautonomia in long-COVID syndrome in a large population are lacking. OBJECTIVE: To evaluate the prevalence and patterns of symptoms of dysautonomia in patients with long-COVID syndrome. METHODS: We administered the Composite Autonomic Symptom Score 31 (COMPASS-31) questionnaire to a sample of post-COVID-19 patients who were referred to post-COVID clinic in Assiut University Hospitals, Egypt for symptoms concerning for long-COVID syndrome. Participants were asked to complete the COMPASS-31 questionnaire referring to the period of more than 4 weeks after acute COVID-19. RESULTS: We included 320 patients (35.92 ± 11.92 years, 73% females). The median COMPASS-31 score was 26.29 (0-76.73). The most affected domains of dysautonomia were gastrointestinal, secretomotor, and orthostatic intolerance with 91.6%, 76.4%, and 73.6%, respectively. There was a positive correlation between COMPASS-31 score and long-COVID duration (p < 0.001) and a positive correlation between orthostatic intolerance domain score and post-COVID duration (p < 0.001). There was a positive correlation between orthostatic intolerance domain score and age of participants (p = 0.004). Two hundred forty-seven patients (76.7%) had a high score of COMPASS-31 >16.4. Patients with COMPASS-31 >16.4 had a longer duration of long-COVID syndrome than those with score <16.4 (46.2 vs. 26.8 weeks, p < 0.001). CONCLUSIONS: Symptoms of dysautonomia are common in long-COVID syndrome. The most common COMPASS-31 affected domains of dysautonomia are gastrointestinal, secretomotor, and orthostatic intolerance. There is a positive correlation between orthostatic intolerance domain score and patients' age.
Subject(s)
COVID-19 , Orthostatic Intolerance , Primary Dysautonomias , COVID-19/complications , COVID-19/epidemiology , Cross-Sectional Studies , Female , Humans , Male , Prevalence , Primary Dysautonomias/epidemiology , Primary Dysautonomias/etiology , Syndrome , Post-Acute COVID-19 SyndromeABSTRACT
BACKGROUND: The emergence of dysautonomia as a consequence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; or COVID-19) is becoming more prevalent. We have seen evidence in several post-COVID patients and in the literature of varying degrees of autonomic dysfunction. Symptoms, among others, include inappropriate tachycardia, sweating, anxiety, insomnia and blood pressure variability from the effects of excessive catecholamine, as well as cognitive impairment, fatigue, headaches and orthostatic intolerance from decreased brain perfusion. CASE PRESENTATION: We present a case of severe dysautonomia in a previously healthy 27-year-old runner. About five weeks after her initial mild COVID-19 infection, the patient began to develop weakness, which progressed into severe post-exertional fatigue, slowed cognition, headaches, blurred vision and generalized body aches. She also endorsed palpitations, especially when getting up from a seated or lying position as well as with mild exertion. She became reliant on her husband for help with her activities of daily living. Exam was significant for orthostasis; laboratory workup unremarkable. Over the following months, the patient's symptoms have improved slowly with fluid and sodium intake, compression stockings and participating in a graduated exercise program. CONCLUSIONS: Dysautonomia as a consequence of infection with COVID-19 is becoming increasingly discussed, especially as more patients recover from COVID-19. This is a case of a non-hospitalized patient with a mild initial presentation and significant, debilitating dysautonomia symptoms. More research on its pathophysiology, especially in relation to a precedent viral insult, as well as its treatment, is needed.
Subject(s)
COVID-19 , Primary Dysautonomias , Activities of Daily Living , Adult , COVID-19/complications , Exercise , Female , Humans , Primary Dysautonomias/diagnosis , Primary Dysautonomias/etiology , SARS-CoV-2Subject(s)
COVID-19 , Primary Dysautonomias , Small Fiber Neuropathy , COVID-19/complications , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Humans , Primary Dysautonomias/etiology , SARS-CoV-2 , Small Fiber Neuropathy/etiology , Syndrome , Vaccination/adverse effects , Post-Acute COVID-19 SyndromeABSTRACT
The clinical characteristics of Guillain-Barré syndrome (GBS) after coronavirus disease 2019 (COVID-19) remain unclear due to the small number of cases. We herein report a case of a Japanese patient with post-COVID-19 GBS who presented with facial and limb muscle weakness, sensory deficits, and autonomic dysfunction. Nerve conduction studies revealed demyelination. Head magnetic resonance imaging showed contrast enhancement in the bilateral facial nerves. Systemic management, including intubation, intravenous immunoglobulin therapy, and rehabilitation, improved the patient's condition. This was the first Japanese case of acute inflammatory demyelinating polyneuropathy after COVID-19 and was characterized by autonomic dysfunction and facial nerve enhancement.
Subject(s)
COVID-19 , Guillain-Barre Syndrome , Primary Dysautonomias , Facial Nerve , Guillain-Barre Syndrome/complications , Guillain-Barre Syndrome/diagnosis , Humans , Primary Dysautonomias/etiology , SARS-CoV-2ABSTRACT
BACKGROUND: Individuals who contract coronavirus disease 2019 (COVID-19) can suffer with persistent and debilitating symptoms long after the initial acute illness. Heart rate (HR) profiles determined during cardiopulmonary exercise testing (CPET) and delivered as part of a post-COVID recovery service may provide insight into the presence and impact of dysautonomia on functional ability. OBJECTIVE: Using an active, working-age, post-COVID-19 population, the purpose of this study was to (1) determine and characterize any association between subjective symptoms and dysautonomia; and (2) identify objective exercise capacity differences between patients classified "with" and those "without" dysautonomia. METHODS: Patients referred to a post-COVID-19 service underwent comprehensive clinical assessment, including self-reported symptoms, CPET, and secondary care investigations when indicated. Resting HR >75 bpm, HR increase with exercise <89 bpm, and HR recovery <25 bpm 1 minute after exercise were used to define dysautonomia. Anonymized data were analyzed and associations with symptoms, and CPET outcomes were determined. RESULTS: Fifty-one of the 205 patients (25%) reviewed as part of this service evaluation had dysautonomia. There were no associations between symptoms or perceived functional limitation and dysautonomia (P >.05). Patients with dysautonomia demonstrated objective functional limitations with significantly reduced work rate (219 ± 37 W vs 253 ± 52 W; P <.001) and peak oxygen consumption (VÌo2: 30.6 ± 5.5 mL/kg/min vs 35.8 ± 7.6 mL/kg/min; P <.001); and a steeper (less efficient) VÌe/VÌco2 slope (29.9 ± 4.9 vs 27.7 ± 4.7; P = .005). CONCLUSION: Dysautonomia is associated with objective functional limitations but is not associated with subjective symptoms or limitation.
Subject(s)
COVID-19 , Heart Failure , Primary Dysautonomias , COVID-19/complications , COVID-19/diagnosis , Exercise , Exercise Test , Humans , Oxygen Consumption/physiology , Primary Dysautonomias/diagnosis , Primary Dysautonomias/etiologyABSTRACT
Guillain-Barré syndrome (GBS) is a peripheral nervous system disease caused by an immune-mediated inflammatory mechanism, usually triggered by a previous infectious process or vaccine; its typical presentation is a rapid and progressive bilateral limb hyposthenia, associated with sensory deficits and reduction or absence of osteotendinous reflexes. However, also autonomic nervous system can be involved with heart rate fluctuations, blood pressure instability, pupillary dysfunction, and urinary retention. Since the beginning of COVID-19 pandemic, GBS has been reported among neurological complications of SARS-CoV-2 infection, although etiopathological mechanisms still have to be clearly defined. We report the case of a 79-year-old man with multiple comorbidities, including diabetes, who was affected by SARS-CoV-2 interstitial pneumonia and developed dysautonomic symptoms after 10 days of hospitalization. A neurological evaluation was performed, and GBS was considered as a possible cause of the clinical manifestations. This hypothesis was confirmed by electrophysiological study and further supported, ex-juvantibus, by the satisfactory response to immunoglobulin treatment. In our opinion, this case of pure dysautonomic presentation of GBS in a SARS-CoV-2 positive patient is relevant because it suggests to consider GBS upon SARS-CoV-2 infection even if the symptoms have uncommon characteristics (e.g., pure vegetative manifestations) and if there are confounding factors which could lead to a misdiagnosis (e.g., old age, SARS-CoV-2 infection consequences and diabetes).
Subject(s)
COVID-19/complications , Guillain-Barre Syndrome/diagnosis , Guillain-Barre Syndrome/virology , Primary Dysautonomias/virology , Aged , Guillain-Barre Syndrome/complications , Humans , Male , Primary Dysautonomias/etiology , SARS-CoV-2ABSTRACT
The emergence of the novel SARS coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in an unprecedented pandemic that has been accompanied by a global health crisis. Although the lungs are the main organs involved in COVID-19, systemic disease with a wide range of clinical manifestations also develops in patients infected with SARS-CoV-2. One of the major systems affected by this virus is the cardiovascular system. The presence of preexisting cardiovascular disease increases mortality in patients with COVID-19, and cardiovascular injuries, including myocarditis, cardiac rhythm abnormalities, endothelial cell injury, thrombotic events, and myocardial interstitial fibrosis, are observed in some patients with COVID-19. The underlying pathophysiology of COVID-19-associated cardiovascular complications is not fully understood, although direct viral infection of myocardium and cytokine storm have been suggested as possible mechanisms of myocarditis. In this Review, we summarize available data on SARS-CoV-2-related cardiac damage and discuss potential mechanisms of cardiovascular implications of this rapidly spreading virus.
Subject(s)
COVID-19/complications , Cardiovascular Diseases/etiology , Arrhythmias, Cardiac/diagnosis , Arrhythmias, Cardiac/etiology , Cardiovascular Diseases/diagnosis , Fibrosis/diagnosis , Fibrosis/etiology , Humans , Myocarditis/diagnosis , Myocarditis/etiology , Primary Dysautonomias/diagnosis , Primary Dysautonomias/etiology , Thrombosis/diagnosis , Thrombosis/etiology , Vasculitis/diagnosis , Vasculitis/etiology , COVID-19 Drug TreatmentABSTRACT
INTRODUCTION: Many patients with mild or severe COVID-19 do not make a full recovery and have a wide range of chronic symptoms for weeks or months after infection, often of a neurological, cognitive or psychiatric nature. The epidemiological evidence, diagnostic criteria and pathogenesis of post-COVID-19 syndrome are reviewed. DEVELOPMENT: Post-COVID-19 syndrome is defined by persistent clinical signs and symptoms that appear while or after suffering COVID-19, persist for more than 12 weeks and cannot be explained by an alternative diagnosis. The symptoms can fluctuate or cause relapses. It is a heterogeneous condition that includes post-viral chronic fatigue syndrome, sequelae in multiple organs and the effects of severe hospitalisation/post-intensive care syndrome. It has been reported in patients with mild or severe COVID-19 and irrespective of the severity of the symptoms in the acute phase. Between 10% and 65% of survivors who had mild/moderate COVID-19 present symptoms of post-COVID-19 syndrome for 12 weeks or more. At six months, subjects report an average of 14 persistent symptoms. The most common symptoms are fatigue, dyspnoea, anxiety, depression, and impaired attention, concentration, memory and sleep. The underlying biological mechanisms are unknown, although an abnormal or excessive autoimmune and inflammatory response may play an important role. CONCLUSIONS: Clinical manifestations are diverse, fluctuating and variable, although fatigue and neurocognitive complaints predominate. There is no defined consensus on post-COVID-19 syndrome and its diagnostic criteria have not been subjected to adequate psychometric evaluation.
TITLE: Síndrome post-COVID-19: epidemiología, criterios diagnósticos y mecanismos patogénicos implicados.Introducción. Numerosos pacientes con COVID-19 leve o grave no tienen una recuperación completa y presentan una gran variedad de síntomas crónicos durante semanas o meses tras la infección, con frecuencia de carácter neurológico, cognitivo o psiquiátrico. Se revisan las evidencias epidemiológicas, los criterios diagnósticos y la patogenia del síndrome post-COVID-19. Desarrollo. El síndrome post-COVID-19 se define por la persistencia de signos y síntomas clínicos que surgen durante o después de padecer la COVID-19, permanecen más de 12 semanas y no se explican por un diagnóstico alternativo. Los síntomas pueden fluctuar o causar brotes. Es una entidad heterogénea que incluye el síndrome de fatiga crónica posvírica, la secuela de múltiples órganos y los efectos de la hospitalización grave/síndrome poscuidados intensivos. Se ha descrito en pacientes con COVID-19 leve o grave y con independencia de la gravedad de los síntomas en la fase aguda. Un 10-65% de los supervivientes que padeció COVID-19 leve/moderada presenta síntomas de síndrome post-COVID-19 durante 12 semanas o más. A los seis meses, los sujetos relatan un promedio de 14 síntomas persistentes. Los síntomas más frecuentes son fatiga, disnea, alteración de la atención, de la concentración, de la memoria y del sueño, ansiedad y depresión. Se desconocen los mecanismos biológicos que subyacen, aunque una respuesta autoinmunitaria e inflamatoria anómala o excesiva puede tener un papel importante. Conclusiones. Las manifestaciones clínicas son diversas, fluctuantes y variables, aunque predominan la fatiga y las quejas neurocognitivas. No existe un consenso definido sobre el síndrome post-COVID-19 y sus criterios diagnósticos no se han sometido a una evaluación psicométrica adecuada.
Subject(s)
COVID-19/complications , SARS-CoV-2 , Autoimmunity , Brain/metabolism , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/physiopathology , Cardiovascular Diseases/etiology , Cognition Disorders/etiology , Cognition Disorders/physiopathology , Coronavirus Infections/complications , Dyspnea/etiology , Fatigue Syndrome, Chronic/etiology , Gastrointestinal Diseases/etiology , Hospitalization , Host-Pathogen Interactions , Humans , Inflammation , Mental Disorders/etiology , Nervous System Diseases/etiology , Organ Specificity , Pandemics , Primary Dysautonomias/etiology , Risk Factors , Severe Acute Respiratory Syndrome/complications , Post-Acute COVID-19 SyndromeABSTRACT
"I am now eight-and-a-half months into my journey with long COVID My symptoms include diagnosed post-COVID tachycardia and acute fatigue. I also have chest tightness and breathlessness from time to time; anxiety; muscle aches and pains, especially in the evening; memory loss; and insomnia."-38-year-old female from the U.K.