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

COVID-19 is predominantly recognized for its respiratory involvement, but more than 35% of patients may initially present with neurological manifestations of varied etiologies. CNS involvement is more common in patients older than 50 years, those with co-morbidities, and in the critically ill, which complicates recognition and delays treatment. This case report describes a relatively young adult with moderately severe COVID-19 pneumonia who concurrently developed significant neurological symptoms consistent with acute encephalopathy and subsequently achieved complete recovery with timely supportive and targeted management.

Neurological manifestations are reported in over one-third of hospitalized COVID-19 patients and may occur during the disease course or as the initial/only presentation. Proposed mechanisms include direct infection, toxic–metabolic encephalopathy, cerebrovascular events (thromboembolic/hemorrhagic related to ACE2 dysfunction and hypertension), and immune-mediated processes. In a systematic review (n=407), incidences of neurological symptoms included headache 16.8%, dizziness 13.9%, altered consciousness 11.2%, and epilepsy 1.7%; associated etiologies included viral meningitis/encephalitis 6.1%, hypoxic encephalopathy 5.6%, acute cerebrovascular disease 1.4%, and encephalomyelitis 0.2%. Delirium has been reported in 55% of critically ill patients in a large cohort, and encephalopathy in 31.8% of hospitalized patients. Neurological complications tend to be more frequent and severe among elderly patients with co-morbidities and those with severe COVID-19.

Case report and clinical management: An unvaccinated 35-year-old woman presented on day 17 of illness with fever, cough, anorexia, respiratory distress, and a positive COVID-19 rapid antigen test. On admission: drowsy but conscious, RR 60/min, SpO2 84% on room air. Initial management: oxygen via non-rebreathing mask (NRBM) 15 L/min, IV dexamethasone 6 mg, SC enoxaparin 40 mg, IV ceftriaxone 2 g; stabilized (SpO2 96% on NRBM) and transferred to COVID-ICU. Past history notable only for gestational diabetes. In ICU: afebrile, drowsy/confused (GCS 14/15), no focal deficits; RR 35–40/min, SpO2 96% on NRBM; mild tachycardia; random blood sugar 500 mg/dL with ketonuria; glycemic control achieved with IV soluble insulin sliding scale. HRCT chest showed moderately severe interstitial pneumonia with minimal ground-glass opacities (CT severity score 15/25). Neurological status worsened with increasing drowsiness, confusion, and agitation. Non-contrast CT brain showed slightly effaced ventricles suggestive of early cerebral edema. CSF studies were inconclusive for infection/inflammation. Working diagnosis: acute encephalopathy after excluding infective and cerebrovascular etiologies. Empirical therapy: IV dexamethasone 8 mg every 8 hours for 48 hours, IV mannitol 20% 250 mL for 3 days; antiviral and antibacterial cover with IV acyclovir 500 mg every 8 hours and IV vancomycin 1 g every 12 hours. MRI brain and EEG were deferred in the absence of focal signs or seizures. On ICU day 2, respiratory parameters deteriorated due to sepsis but subsequently improved with supportive care. CT pulmonary angiogram excluded pulmonary embolism. Respiratory support was stepped down gradually (from NRBM/CPAP to Venturi mask and then nasal prongs). By ICU day 12, CNS manifestations had resolved completely; patient was transferred to a ward on nasal oxygen 2 L/min and discharged home within a week. Laboratory trends showed elevated inflammatory markers (e.g., CRP up to 200 mg/L, LDH up to 807 IU/L, ferritin 500 ng/mL), initial metabolic acidosis (base deficit −15) and ketonuria that normalized within 24 hours, stable renal and hepatic function, and arterial blood gases showing hypoxemia during acute illness (PaO2 approximately 52–80 mmHg; SpO2 92–96%).

A young, previously healthy, unvaccinated woman with moderately severe COVID-19 pneumonia developed acute encephalopathy without evidence of CNS infection or stroke. Neuroimaging (NCCT) suggested early cerebral edema; CSF was inconclusive for infection. Likely contributors included hypoxemia (PaO2 ~52–80 mmHg; SpO2 ~92–96%) and systemic inflammation (elevated CRP/LDH/ferritin), with transient metabolic derangements (ketonuria, base deficit −15) that resolved rapidly. Management with optimized respiratory support, glycemic control, empirical antimicrobials/antiviral, osmotherapy (mannitol), and short-course corticosteroids (dexamethasone) was associated with full neurological recovery within approximately 12 ICU days and hospital discharge within 3 weeks. CTPA excluded pulmonary embolism; HRCT chest showed CT severity score 15/25. The case underscores that significant CNS involvement can occur in younger adults with COVID-19 and that early recognition and supportive care can lead to complete recovery.

This case illustrates concurrent pulmonary disease and acute encephalopathy in COVID-19. The absence of focal deficits, inconclusive CSF, and CT evidence of diffuse cerebral edema supported a diagnosis of encephalopathy rather than encephalitis or cerebrovascular disease. Encephalopathy in COVID-19 is multifactorial, often driven by hypoxemia, toxic–metabolic disturbances, and systemic inflammation; in this patient, hypoxemia and elevated inflammatory markers were likely predominant factors, while initial metabolic acidosis and ketonuria resolved quickly and were unlikely sustained contributors. Although the benefit of glucocorticoids and other immunomodulators for encephalopathy is uncertain, limited reports suggest potential improvement in select cases; a brief course of dexamethasone and osmotherapy was used here alongside comprehensive supportive care. Despite encephalopathy being associated with poorer outcomes and functional/cognitive impairment in a substantial proportion of patients, this patient achieved full recovery, emphasizing the importance of early identification of neurological manifestations and prompt, targeted supportive management.

Clinicians should maintain high vigilance for CNS manifestations of SARS-CoV-2 infection to expedite diagnosis and initiate appropriate supportive and specific therapies. Early recognition and management of COVID-19–associated encephalopathy can facilitate recovery and favorable outcomes, even in patients presenting with concurrent moderate-to-severe pneumonia.

Single-patient case report limits generalizability. Advanced neurodiagnostics (MRI, EEG) were not performed, and CSF analysis was inconclusive, leaving some diagnostic uncertainty regarding encephalitis vs. encephalopathy. Long-term neurocognitive follow-up was not reported.