A Young Female with SARS-CoV-2 Infection Presenting with Concurrent Neurological and Pulmonary Manifestations: A Case Report

Coronavirus disease 2019 (COVID-19) is primarily known for its respiratory effects, but neurological manifestations are increasingly recognized, affecting over 35% of patients. These neurological symptoms are more common in older patients with comorbidities and critically ill individuals with severe COVID-19 pneumonia. The etiologies implicated include infectious, cerebrovascular, and hypoxic-toxic-metabolic factors. Poor outcomes, including persistent neurological deficits, are frequently reported. This case report describes a young female patient who presented with concurrent neurological and pulmonary manifestations of COVID-19, highlighting the importance of early diagnosis and appropriate management to improve outcomes. The study aims to demonstrate that early recognition of neurological manifestations and initiation of timely therapies are crucial for positive patient outcomes.

Existing literature indicates that neurological manifestations in COVID-19 patients are multifactorial. Studies have reported a wide range of neurological symptoms, including headache, dizziness, altered consciousness, and epilepsy, with various etiological factors such as viral meningitis/encephalitis, hypoxic encephalopathy, acute cerebrovascular disease, and encephalomyelitis. Neurological manifestations are commonly reported in older patients with comorbidities and severe COVID-19 disease. However, this case presents a younger, relatively healthy individual with severe neurological symptoms alongside moderately severe COVID-19 pneumonia. Several studies have shown the prevalence of delirium and encephalopathy in hospitalized COVID-19 patients, further emphasizing the complexity of the disease's neurological impact. While the role of glucocorticoids in treating encephalopathy remains uncertain, some studies suggest potential benefit in severe cases.

This is a case report detailing the clinical presentation, diagnosis, and management of a single patient. A 35-year-old unvaccinated woman presented with fever, cough, loss of appetite, and respiratory distress. Rapid Antigen Test (RAT) confirmed COVID-19 infection. On admission, she was drowsy, confused, and tachypneic. Initial treatment included oxygen therapy, dexamethasone, enoxaparin, and ceftriaxone. She was transferred to a COVID-ICU, where her neurological symptoms worsened despite improvement in respiratory parameters. Investigations included high-resolution CT (HRCT) of the chest, which showed moderate interstitial pneumonia, and non-contrast CT (NCCT) of the brain, revealing slightly effaced ventricles and early cerebral edema. Cerebrospinal fluid (CSF) analysis was inconclusive. Treatment for suspected encephalopathy included intravenous dexamethasone and mannitol. Acyclovir and vancomycin were also administered for broad-spectrum antiviral and antibacterial coverage. MRI brain and EEG were not deemed necessary. The patient's clinical course, laboratory results, and respiratory support were meticulously documented. The patient's progress was tracked using regular clinical assessments and laboratory parameters, providing a detailed account of her recovery.

The patient presented with moderately severe COVID-19 pneumonia and severe, progressive neurological symptoms, primarily manifested as drowsiness, confusion, and agitation. Initial respiratory support was effective. Neurological deterioration led to a diagnosis of encephalopathy after ruling out other causes such as infection and cerebrovascular events. NCCT brain imaging showed early cerebral edema. Treatment with intravenous dexamethasone and mannitol resulted in a significant improvement in neurological status. The patient’s respiratory parameters initially deteriorated due to sepsis but subsequently improved with treatment. Complete recovery from neurological manifestations occurred by day 12 of her ICU stay. The patient was discharged from the hospital within a week after recovery. Laboratory findings showed elevated inflammatory markers (CRP, LDH, ferritin) and initial metabolic acidosis and ketonuria, which resolved within 24 hours. Complete blood count showed abnormalities in white blood cell count, neutrophils and platelets.

This case highlights the potential for concurrent and severe neurological and pulmonary manifestations in COVID-19, even in relatively young and otherwise healthy individuals. The rapid progression of neurological symptoms underscores the importance of vigilance and prompt investigation. The successful outcome achieved through conservative management emphasizes the significance of early diagnosis and appropriate treatment in improving neurological outcomes in such cases. While the precise mechanism linking COVID-19 to encephalopathy remains unclear, the presence of cerebral edema and elevated inflammatory markers in this case suggests a possible inflammatory-mediated pathogenesis. Further research is needed to elucidate the mechanisms underlying neurological manifestations of COVID-19 and to develop more targeted therapies.

This case report emphasizes the importance of maintaining a high index of suspicion for neurological manifestations in COVID-19 patients, regardless of age or pre-existing comorbidities. Early recognition of these complications and prompt initiation of appropriate supportive and specific therapies are crucial for optimizing patient outcomes. Further research is needed to better understand the pathophysiology and develop more effective treatments for neurological complications associated with COVID-19.

This study is a single case report, limiting its generalizability. The lack of MRI brain and EEG studies might have missed subtle neurological findings. The absence of a control group prevents drawing definitive conclusions regarding the efficacy of the implemented treatment strategy.