Imaging Features of Acute Encephalopathy in Patients with COVID-19: A Case Series.
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ABSTRACT:
SUBMITTER: Kihira S
PROVIDER: S-EPMC7661067 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:RationaleAcute encephalopathy is a severe neurological complication of coronavirus disease 2019 (COVID-19). Most cases of acute encephalopathy associated with COVID-19 occur within several weeks of COVID-19 onset. We describe a case series of 6 patients who developed delayed encephalopathy (DE) after COVID-19.Patient concerns and diagnosesWe evaluated patients who recovered from COVID-19 and showed acute disturbance of consciousness or focal neurological deficits without recurrence of pneumonitis. Six patients, 2 females and 4 males, with ages ranging from 65 to 83 years were included. Durations of hospitalization due to COVID-19 were between 25 and 44 days. The severity of COVID-19 was moderate in 5 and severe in 1 patient. Patients were rehospitalized for acute disturbance of consciousness concomitant with postural tremor and, abnormal behavior, hemiplegia, aphasia, or apraxia between 34 and 67 days after the onset of COVID-19. Chest computed tomography showed no exacerbation of pneumonitis. Brain magnetic resonance imaging showed no specific findings except in 1 patient with an acute lacunar infarction. Electroencephalogram demonstrated diffuse slowing in all patients. Repeat electroencephalogram after recovery from encephalopathy demonstrated normal in all patients. One of the 6 patients had cerebrospinal fluid (CSF) pleocytosis. CSF protein levels were elevated in all patients, ranging from 51 to 115 mg/dL. CSF interleukin-6 levels ranged from 2.9 to 10.9 pg/mL. The immunoglobulin index was 0.39 to 0.44. Qlim(alb) < QAlb indicating dysfunction of the blood-brain barrier was observed in all patients. Severe acute respiratory syndrome coronavirus 2 reverse transcription polymerase chain reaction of CSF was negative in all patients. Neuronal autoantibodies were absent in serum and CSF.Interventions and outcomesImmunotherapy including steroid pulses was administered to 3 patients; however, symptoms of encephalopathy resolved within several days in all patients, regardless of treatment with immunotherapy, and their consciousness levels were recovered fully. Notably, postural tremor remained for 2 weeks to 7 months.LessonsIn our patients, DE after COVID-19 was characterized by symptoms of acute encephalopathy accompanied with tremor in the absence of worsening pneumonitis after the fourth week of COVID-19 onset. Our findings indicate blood-brain barrier dysfunction may contribute to the pathogenesis of DE after COVID-19.
| S-EPMC9592135 | biostudies-literature
Project description:IntroductionAn increasing number of published reports on SARS-CoV-2 neurological manifestations have revealed a wide spectrum of symptoms, diagnostic features, and outcomes. We report a fatal case of a COVID-19-associated acute necrotizing encephalopathy (ANE).Case reportWe report a 70-year-old man brought to the hospital after a generalized tonic-clonic seizure. He was confused and disoriented. Nasopharyngeal swab testing for SARS-CoV-2 was positive. A head computed tomography (CT) scan and cerebrospinal fluid (CSF) analysis showed no signs of acute pathology. After recurrent seizures, he was sedated and intubated. Throughout the days that followed he remained in a therapeutic coma. After discontinuation of sedatives, he remained unconscious. A repeated head CT scan showed signs of pontine edema, and brain magnetic resonance imaging (MRI) revealed inhomogeneous hyperintensities with microhemorrhages and small autonecrotic cavities in both thalami, brain stem, and cerebellar peduncles. With a high suspicion of a COVID-19-associated ANE, the patient was started on high-dose glucocorticoids; however, he died the next day. The CSF tested negative for SARS-CoV-2.DiscussionA variety of COVID-19 neurological manifestations have been reported to date, including various forms of encephalitis and encephalopathy. In our patient, encephalopathy with seizures was the presenting symptom of SARS-CoV-2 infection. The radiological findings on days 8 and 9 were consistent with an ANE. The precise pathogenesis of ANE remains unclear; however, an immune-mediated mechanism is suspected. Early diagnostics with prompt administration of immunomodulators may be lifesaving. Suspicion of a COVID-19-related encephalopathy/encephalitis should be raised in all patients with altered mental status, seizures, and/or coma.
| S-EPMC8653160 | biostudies-literature
Project description:The majority of patients with severe COVID-19 suffer from delirium as the main sign of encephalopathy associated with this viral infection. The aim of this study was to identify early markers of the development of this condition. The prospective cohort-based study included patients with community-acquired pneumonia and confirmed pulmonary tissue infiltration based on CT data, with a lesion consisting of at least 25% of one lung. The main group included patients who have developed acute encephalopathy (10 patients, 3 (30%) women; average age, 47.9 ± 7.3 years). The control group included patients who at discharge did not have acute encephalopathy (20 patients, 11 (55%) women; average age, 51.0 ± 10.5 years). The study collected clinical examination data, comprehensive laboratory data, neurophysiological data, pulse oximetry and CT data to identify the predictors of acute encephalopathy (study ClinicalTrials.gov identifier NCT04405544). Data analysis showed a significant relationship between encephalopathy with the degree of lung tissue damage, arterial hypertension, and type 2 diabetes mellitus, as well as with D-dimer, LDH, and lymphopenia. The development of encephalopathy is secondary to the severity of the patient's condition since a more severe course of the coronavirus infection leads to hypoxic brain damage.
| S-EPMC8584437 | biostudies-literature
Project description:Severe acute respiratory coronavirus 2 (SARS-CoV-2) has been associated with neurological complications, including acute encephalopathy. To better understand the neuropathogenesis of this acute encephalopathy, we describe a series of patients with coronavirus disease 2019 (COVID-19) encephalopathy, highlighting its phenomenology and its neurobiological features. On May 10, 2020, 707 patients infected by SARS-CoV-2 were hospitalized at the Geneva University Hospitals; 31 (4.4%) consecutive patients with an acute encephalopathy (64.6 ± 12.1 years; 6.5% female) were included in this series, after exclusion of comorbid neurological conditions, such as stroke or meningitis. The severity of the COVID-19 encephalopathy was divided into severe and mild based on the Richmond Agitation Sedation Scale (RASS): severe cases (n = 14, 45.2%) were defined on a RASS < -3 at worst presentation. The severe form of this so-called COVID-19 encephalopathy presented more often a headache. The severity of the pneumonia was not associated with the severity of the COVID-19 encephalopathy: 28 of 31 (90%) patients did develop an acute respiratory distress syndrome, without any difference between groups (p = .665). Magnetic resonance imaging abnormalities were found in 92.0% (23 of 25 patients) with an intracranial vessel gadolinium enhancement in 85.0% (17 of 20 patients), while an increased cerebrospinal fluid/serum quotient of albumin suggestive of blood-brain barrier disruption was reported in 85.7% (6 of 7 patients). Reverse transcription-polymerase chain reaction for SARS-CoV-2 was negative for all patients in the cerebrospinal fluid. Although different pathophysiological mechanisms may contribute to this acute encephalopathy, our findings suggest the hypothesis of disturbed brain homeostasis and vascular dysfunction consistent with a SARS-CoV-2-induced endotheliitis.
| S-EPMC8251282 | biostudies-literature
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| S-EPMC8680876 | biostudies-literature
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| S-BSST677 | biostudies-other
Project description:Neurological complications are frequent non-respiratory complications associated with coronavirus disease 2019 (COVID-19), and acute encephalopathy (AE) has been reported to occur in 2.2% of patients. Among many phenotypes of AEs, acute necrotizing encephalopathy (ANE) is associated with multiple organ failure (MOF), leading to severe neurological morbidity and mortality. A previously healthy seven-year-old girl presented with a one-day history of fever followed by 12 hours of vomiting and altered consciousness. On arrival, the patient was in shock. Blood tests revealed severe acute liver failure and kidney injury, accompanied by coagulopathy. The serum interleukin-6 levels were also elevated. PCR testing for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was positive. A head CT scan showed heterogeneous low-density areas in the bilateral thalamus, without brainstem involvement. She was diagnosed as ANE complicated with MOF (ANE severity score = 6). Intravenous methylprednisolone and therapeutic plasma exchange (TPE) were initiated with neurocritical care. After the introduction of TPE, hemodynamics improved rapidly, followed by gradual improvement in neurological manifestations. Upon follow-up after two months, no neurological or systemic sequelae were noted. Although further studies are needed, our case suggests that early immunomodulatory therapy and TPE may have contributed to the improvement in ANE and MOF associated with COVID-19.
| S-EPMC10838156 | biostudies-literature
Project description:Severe forms of COVID-19 infection are associated with the need for invasive mechanical ventilation and thromboembolic complications; those can affect the cardiac function especially the right ventricle performance. Critical care echocardiography has rapidly evolved as the election technique in the evaluation of the critically ill patients. This technique has the advantage that it can be done at patient´s bedside and helps to provide the appropriate treatment and to monitoring maneuver's response. We present 4 patients with a confirmed COVID-19 infection who presented with sudden hemodynamic and / or respiratory deterioration, in which transthoracic echocardiogram showed acute right ventricular failure as the trigger for the event and helped to guide an early therapeutic intervention. <Learning objective: Routine echocardiographic evaluation must be mandatory in patients with COVID-19 infection. The presence of refractory hypoxemia and/or hypotension should raise the suspicion of right ventricle failure and must be evaluated with transthoracic echocardiogram. In the clinical scenario of acute right ventricular failure, rising D-dimer and suspected pulmonary embolism, thrombolysis must be considered even without tomographic confirmation.>.
| S-EPMC7832825 | biostudies-literature
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| S-EPMC7159872 | biostudies-literature
Project description:BackgroundSARS-coronavirus-2 [coronavirus disease 2019 (COVID-19)] infection is a public health issue affecting millions of people. It started in Wuhan in China in December 2019 spreading rapidly worldwide.Case summaryThree patients aged 51-84 developed a pericarditis related to COVID-19, associated for two of them with a myocarditis. Case 1 was a COVID-19 cardiac tamponade without myocarditis, confirmed by a positive chest computed tomography (CT) scan. Case 2 showed a COVID-19 myopericarditis, confirmed by a positive chest CT scan and a SARS-coronavirus-2 positive swab. Case 3 was a cardiac tamponade due to COVID-19 pericarditis, with a positive polymerase chain reaction on pericardial fluid. They were all treated by colchicine and their condition improved rapidly.DiscussionPresumably rare, we reported three cases of pericardial effusions (PEs) occurring in a single cardiology centre. There is a higher incidence of COVID-19-related cardiac diseases such as pericarditis that can manifest as a minimal PE to a cardiac tamponade, which should result in a higher awareness of cardiologists. A systematic measure of the high-sensitivity troponin kinetic in patients affected by COVID-19 could be interesting in order to screen for potential myocarditis. Any unexplained haemodynamic failure or increased cardiac biomarkers should make the medical team search for myopericarditis by a transthoracic echocardiography.
| S-EPMC7499573 | biostudies-literature