Severe respiratory syncytial virus bronchiolitis complicated by profound hyponatremia and seizures in an infant: a case report

Abstract

Background

Respiratory syncytial virus (RSV) is the leading cause of bronchiolitis in infancy and the most frequent reason for hospitalization in the first months of life. While most infections follow a mild course, a proportion of infants develop severe disease requiring intensive care. Electrolyte disturbances, especially hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH), are a recognized complication and may trigger neurological symptoms. Severe hyponatremia with seizures is rarely documented in otherwise healthy term infants, which makes such cases clinically important. The aim of this report is to describe hyponatremia-induced seizures as a rare but clinically important complication of severe RSV bronchiolitis in a previously healthy infant.

Case Description

We report a 1-month-old previously healthy female infant who presented with cough, rhinorrhea, somnolence, and progressive respiratory distress. On admission, the infant developed generalized tonic seizures, and laboratory tests revealed profound hyponatremia with serum sodium of 113 mmol/L. RSV infection was confirmed by nasopharyngeal swab. The infant required transfer to the intensive care unit (ICU), where she was intubated and mechanically ventilated. Hyponatremia was managed with 3% hypertonic saline, and she received empiric antibiotics, later tailored to ceftazidime and amikacin, along with supportive therapy. Ventilatory support was required for 7 days. Neuropediatric assessment confirmed hyponatremia-related seizures, and no underlying neurological disorder was identified. After normalization of electrolytes and gradual clinical improvement, she was discharged after 20 days in good condition.

Conclusions

This report highlights that RSV bronchiolitis can, in rare cases, present with profound hyponatremia and seizures even in previously healthy infants. Routine monitoring of serum sodium at admission, cautious use of intravenous fluids, and early recognition of neurological symptoms are essential to avoid serious outcomes. Awareness of this potential complication can help clinicians initiate timely management and prevent life-threatening consequences.

Highlight box.

Key findings

• Severe respiratory syncytial virus (RSV) bronchiolitis in an otherwise healthy infant was complicated by profound hyponatremia (sodium 113 mmol/L) and seizures. Treatment with hypertonic saline and supportive care led to recovery.

What is known and what is new?

• RSV bronchiolitis is the leading cause of hospitalization in early infancy and may be associated with hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion, especially in intensive care.

• This case shows that severe hyponatremia with seizures can occur even in a previously healthy term infant, stressing the need for routine sodium checks at admission.

What is the implication, and what should change now?

• Infants with severe bronchiolitis should have regular electrolyte monitoring. Isotonic fluids are recommended, and neurological symptoms must be recognized promptly to avoid complications.

Introduction

Background

Respiratory syncytial virus (RSV) is the most frequent cause of lower respiratory tract infection in infants and small children. Most infections are mild, but in early infancy severe forms often lead to hospital admission and sometimes intensive care. Apart from respiratory failure, electrolyte disturbances may complicate the course. Hyponatremia, usually the result of inappropriate secretion of antidiuretic hormone (ADH), has been described in this setting and can trigger seizures. Although not common, such complications can markedly worsen the condition (1).

Rationale and knowledge gap

Infants carry the greatest risk, making up more than 60% of RSV-related hospitalizations under 5 years of age and almost two-thirds of related deaths. The highest burden is seen in the first months, with a global peak around the second month and more than half of admissions taking place before 6 months. The timing of birth in relation to seasonal circulation also affects the risk (2). Neurological complications are rare but recognized. Seizures occur in fewer than 1% of admitted children, but the proportion rises to over 6% among those in intensive care. Severe hyponatremia is found in about one-third of children in intensive care, and sodium below 130 mmol/L in more than 10%. This has been linked to increased ADH secretion, especially in ventilated patients, and can be aggravated by hypotonic fluid therapy, further raising the risk of seizures (3). While hyponatremia is described in critically ill infants with RSV bronchiolitis, its presentation with seizures at admission in otherwise healthy term infants is rarely reported, which represents a relevant gap in the current literature.

Objective

The aim of this report is to describe hyponatremia-induced seizures as a rare but clinically important complication of severe RSV bronchiolitis in early infancy. We present this case in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-20251-272/rc).

Case presentation

A 1-month-old female infant, born at term in Bosnia and Herzegovina after an uncomplicated pregnancy and spontaneous vaginal delivery (birth weight 2,600 g, Apgar 10/10), was admitted with a 4-day history of cough, rhinorrhea and increasing respiratory distress. The day prior to admission she became lethargic and refused breastfeeding. In the 24 hours before admission, the infant also became increasingly unresponsive, with reduced urine output and a brief nonspecific rash. Neurologically, she showed reduced spontaneous activity and lower muscle tone before the onset of seizures. She was exclusively breastfed and had not received any routine neonatal or infant vaccinations [including Bacillus Calmette-Guérin (BCG) vaccine and the first dose of hepatitis B], and had no previous illnesses. Family history was unremarkable. On admission, the infant was somnolent and dyspneic, with oxygen saturation of 88% on room air and body weight of 3,730 g. She appeared pale and marbled with cyanotic extremities. Auscultation revealed diffuse bilateral crackles, while cardiovascular and abdominal findings were normal. Initial laboratory results showed serum sodium of 113 mmol/L. Before hyponatremia was detected, the infant received an isotonic glucose-electrolyte solution for initial rehydration. The symptoms described earlier preceded this laboratory finding, and the seizures occurred shortly after it was obtained. During assessment the infant developed generalized tonic seizures, which resolved after intravenous midazolam. Other causes of seizures were evaluated. Cranial ultrasound was normal, there were no clinical features of central nervous system (CNS) infection, and glucose, calcium, and magnesium values did not suggest an alternative etiology. The seizures were attributed to severe hyponatremia. A nasopharyngeal swab was positive for RSV. Chest radiograph demonstrated bilateral perihilar infiltrates compatible with pneumonia. Twelve hours after admission the infant developed apnea and acute respiratory failure, requiring transfer to the intensive care unit (ICU). She was intubated, mechanically ventilated and started on 3% NaCl for correction of hyponatremia. Correction was carried out with a target rate below 0.5 mmol/L per hour. Serum sodium was checked every 2–4 hours with continuous neurological monitoring, and levels normalized gradually over the first 48–72 hours. Empiric antibiotics were started and later adjusted to ceftazidime and amikacin. They were indicated due to clinical deterioration with progressive respiratory distress, bilateral infiltrates on chest radiograph, and rising inflammatory markers (C-reactive protein 103 mg/L, procalcitonin 1.07 ng/mL), findings consistent with suspected bacterial superinfection. Additional therapy included transfusion of packed red blood cells, intravenous albumin, magnesium sulfate, corticosteroids, and inhaled bronchodilator and anti-inflammatory treatment. The transfusion was given when hemoglobin had fallen to 94 g/L (hematocrit 0.259), which was below the desired range in the setting of severe respiratory failure. Albumin replacement was indicated for hypoalbuminemia, with levels decreasing to 29 g/L and then 22.8 g/L during the early intensive care course. Magnesium sulfate was added due to hypomagnesemia, with serum magnesium decreasing to 0.57 mmol/L. Corticosteroids were started on day 6 because of ongoing airway obstruction and edema causing difficult ventilation and persistent secretion burden. Mechanical ventilation was required for 7 days. After extubation she briefly received supplemental oxygen, which was discontinued within 24 hours. Antibiotics were continued for 10 days. Electrolytes and inflammatory markers normalized, and oral feeding was well tolerated.

On day 14, she was transferred back to the pulmonology ward in stable condition. Central venous catheter was removed and no further oxygen support was needed. Neuropediatric evaluation confirmed seizures secondary to hyponatremia and noted transient abnormalities in tone and reflexes, for which neurodevelopmental physiotherapy and follow-up were recommended. The patient was discharged after 20 days, afebrile and in good general condition, with a body weight of 4,080 g. Lung auscultation was normal apart from mild hoarseness. She was prescribed vitamin D supplementation and scheduled for follow-up. A follow-up neurological assessment was performed before discharge, showing normal visual tracking, normal response to sound, and no focal deficits, with only mild variability in tone. Cranial ultrasound was without abnormalities, and outpatient neurodevelopmental follow-up was recommended.

Key clinical features and early recognition and management principles for hyponatremia in infants are summarized in Table 1.

Table 1. Key clinical features and early recognition and management of hyponatremia in infants.

Typical clinical features

Lethargy or reduced responsiveness

Poor feeding

Vomiting

Irritability

Somnolence

Apnea

Seizures

Early recognition

Check serum sodium in infants with severe RSV bronchiolitis or any neurological changes

Evaluate fluid balance, urine output, and weight changes

Consider SIADH when sodium is low despite adequate hydration

Monitor serum sodium every 2–4 hours once abnormal values are detected

Initial management

Avoid hypotonic IV fluids; use isotonic solutions for maintenance and resuscitation

If symptomatic hyponatremia (e.g., seizures): consider 3% hypertonic saline according to weight-based dosing and established pediatric guidelines

Correct sodium slowly to avoid osmotic demyelination (target rise ≤8–10 mmol/L per 24 h)

Treat the underlying cause (e.g., RSV bronchiolitis, SIADH triggers)

Maintain strict fluid restriction in SIADH when appropriate

Treat symptomatic hyponatremia with cautious hypertonic saline correction

IV, intravenous; RSV, respiratory syncytial virus; SIADH, syndrome of inappropriate antidiuretic hormone secretion.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parents for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

Our case shows that even in an otherwise healthy young infant, severe RSV bronchiolitis may be complicated by profound hyponatremia and seizures. This underlines the need for early detection of electrolyte imbalance, careful fluid use, and close neurological monitoring in these patients.

Strengths and limitations

The strength of this report is that it documents a rare but clinically important complication in a term infant with no comorbidities, which makes it relevant for everyday pediatric practice. A limitation is that it is a single case, so the findings cannot be generalized, and causality cannot be fully established.

Comparison with similar research

RSV is a leading cause of lower respiratory tract infection in infants, with the highest burden in the first months of life. Certain groups—such as preterm infants or those with underlying conditions—have an increased risk of severe disease and intensive care admission (4). Hyponatremia is a known complication of severe RSV bronchiolitis, particularly in infants admitted to intensive care. In one study, one-third of critically ill children developed hyponatremia, and in 11% sodium dropped below 130 mmol/L. Seizures were seen in 4.4% of cases and resolved after treatment with hypertonic saline and fluid restriction. The main triggers were inappropriate secretion of ADH and use of hypotonic fluids. Neurological signs can resemble worsening respiratory distress, which may delay recognition and treatment (5). Extrapulmonary complications include cardiovascular failure, arrhythmias, apnoea, seizures, hyponatremia, and hepatitis. Neurological involvement is found in up to 39% of intensive care cases, compared with 1–2% on general wards. Seizures occur in about 0.7% of hospitalized children, but in up to 6.6% of those in intensive care, sometimes as status epilepticus. Hyponatremia is usually linked to syndrome of inappropriate antidiuretic hormone secretion (SIADH) and can be aggravated by hypotonic therapy (3,6).

Explanations of findings

Elevated ADH levels have been associated with RSV-positive bronchiolitis, and hyponatremia at admission often indicates more severe disease. For this reason, close monitoring of sodium and neurological status is recommended, especially in neonates and infants under three months (7). RSV can also be linked to encephalopathy, reported in 0.1–10% of infections. This may result from direct viral invasion or cytokine-mediated injury. High interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha (TNF-α) in cerebrospinal fluid have been associated with cerebral edema and neuronal damage. Neuroimaging findings vary, ranging from diffuse edema to changes resembling acute disseminated encephalomyelitis (ADEM) (8). Severe hyponatremia with seizures has been described in several reports, often in infants who received large amounts of hypotonic fluids (8). In this case, SIADH was the main cause of hyponatremia. Although hypotonic fluids were not used before admission, they are a known factor that can aggravate dilutional hyponatremia in bronchiolitis, which supports the use of isotonic solutions in acutely ill infants. Hyponatremic encephalopathy develops when low extracellular tonicity drives water into neurons, leading to cerebral edema. If unrecognised, this may progress to cardiorespiratory arrest and death. Clinical signs such as irritability, somnolence, vomiting, or seizures can be mistaken for worsening respiratory failure. In infants with RSV bronchiolitis, this overlap may mask early neurological deterioration, as symptoms such as lethargy or reduced responsiveness can be misinterpreted as progression of respiratory disease. The main mechanism behind hyponatremia in RSV bronchiolitis is inappropriate ADH secretion. Non-osmotic stimuli such as hypoxemia, hypercapnia, raised airway pressure, stress, and cytokines—especially IL-6—are common triggers (8). This results in water retention and dilutional hyponatremia, worsened when hypotonic fluids are given (5,9). Falling serum sodium lowers extracellular tonicity, causing water to shift into neurons and leading to cerebral edema and seizures if not treated (3).

Implications and actions needed

Prevention requires routine sodium checks and preference for isotonic fluids in at-risk infants (9). Because inappropriate ADH secretion and the use of hypotonic fluids are key contributors to hyponatremia in RSV bronchiolitis, careful fluid selection and avoidance of hypotonic solutions are important parts of preventive management. Prompt recognition of neurological symptoms such as irritability, somnolence, vomiting, or seizures is important to avoid delayed diagnosis of hyponatremic encephalopathy. Early identification and appropriate management can prevent progression to severe complications, including cerebral edema and respiratory failure (10).

Conclusions

Severe RSV bronchiolitis in early infancy may be complicated by profound hyponatremia and seizures, even in previously healthy children. This case highlights the importance of routine electrolyte monitoring, cautious use of intravenous fluids, and early recognition of neurological symptoms to prevent serious outcomes. Clinicians should remain vigilant for these potentially life-threatening complications, as timely intervention can improve prognosis.

Supplementary

The article’s supplementary files as

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient’s parents for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.