Case Presentation: Respiratory Synctial Virus (RSV) Infection -
May 2003
As the winter RSV season winds down, we would like to share with you a case from California Pacific’s Pediatric Unit. As pediatricians, we see many cases of RSV bronchiolitis every year; one of the more unusual presentations of RSV is encephalitis or encephalopathy. A discussion follows the case:
Case History:
Our patient is an ex-36 wk, now 1-month old (twin A) girl with a 3-day h/o cough and nasal congestion. She presented to her PMD with decreased activity, sleepiness and 2 episodes of jerking movements in the last 24 hrs. These episodes lasted several seconds. On the day of her admission, she was seen by her doctor and noted to be hypothermic to 35.8 C, lethargic and had a leg stiffness episode lasting about one minute. She was admitted for further evaluation and treatment.
Hospital Course:
Upon admission, the child appeared slightly lethargic. The Pediatric Team did a complete septic w/u. UA, CSF and CBC were all with in normal limits. Urine, CSF and blood were sent for culture. The child was started on ampicillin and gentamicin pending cultures. Because of her nasal discharge and cough, RSV and Flu-A nasal washings were also sent. CXR revealed R middle lobe infiltrate and hyperinflation. Nasopharyngeal washing for RSV was positive. The team initiated racemic epinephrine and nasal suctioning.
Shortly after her admission, the child had a couple more episodes of jerking and stiffness, prompting further w/u including CT of head (which was normal) and initiation of Acyclovir therapy pending HSV testing. She had 2 more episodes of tonic clonic activity the next day. We obtained a neurology consult and EEG that revealed rhythmic spikes consistent with epileptic activity originating from right hemisphere. Dilantin® was initiated and seizures subsided. The child remained afebrile; all cultures remained negative x5 days and Acyclovir was stopped after negative HSV PCR. Her respiratory symptoms also resolved over the course of a week. No further seizures were noted.
The child was discharged home after Dilantin was stopped with follow-up in Neurology Clinic and an outpatient Head MRI. This MRI (performed a few weeks later) was within normal limits.
Discussion:
Estimates link RSV to 100,000 pediatric admissions and 2,000 deaths annually in the US alone.(1) Apnea is a known complication of RSV infection, with some studies showing an incidence as high as 25% in hospitalized neonates and infants.(2)
An association is now recognized between RSV infection and encephalopathy (with seizures as the most common manifestation) in young infants. In the few articles describing this, the incidence of seizures was reported at 7% for children and 12% for infants with RSV infection. (3)
An article published in Child Neurology by Ng et al(4) found an incidence of 1.8% of encephalopathy in children and infants with RSV infection. Most commonly, the encephalopathic patients had tonic clonic seizures. The spectrum included focal and generalized seizures and status epilepticus. One patient had hypotonia and another had transient loss of developmental milestones. All these patients had normal head MRIs and 6 out of 9 had abnormal EEGs. There did not seem to be a correlation between severity of lung disease and neurological symptoms. Of note this study excluded patients with prior seizure disorder or other neurological problems. Therefore, it is unclear as to the effect of RSV infection on children with underlying seizure disorders. Animal studies have shown that some cellular and biochemical changes are associated with RSV infection in the brain. Humoral mediators are thought to mediate these changes. The authors postulate that RSV, through direct and indirect inflammatory processes, may cause specific neurotoxic effects causing encephalopathy during acute RSV infection. The value of RSV cultures or testing on the CSF is currently unknown.
In a case report form Japan, Hirayama et al 5 described a 3-year old girl with RSV infection who developed changes in mental status, conjugate eye deviation, truncal ataxia and intention tremors. T2 weighted MRI showed hyperintense areas in the cerebellar cortex. These hyperintense areas resolved 2 months after the acute illness. SPECT and PET scans 3 months post acute infection showed areas of hypoperfusion and hypometabolism in the same sites shown on MRI. One year post infection, MRI showed mild atrophy of the cerebellum and SPECT and PET scan findings remained. This patient was thought to have cerebellitis caused by RSV.
There has been little discussion in the literature regarding follow-up and treatment of seizures for this group. However, it is expected that there will be no long-term issues or increased risk of epilepsy.
For the child treated at California Pacific, she is doing very well as of her visit three weeks following discharge. The Pediatric Team has found no evidence of neurologic or developmental sequelae.
References:
1.Ruuskanen O, Ogra PL – Respiratory Syncytial Virus. Curr Probl Pediatr 1993; 23; 50-79
2.Anas N. Boertich C. Hall et al: The Association of Apnea and RSV Infection in Infants. J Peds 1982; 101:65-66
3. Gouyon JB, Fantino M et al: RSV in Neonates. Arch Fr Pedi 1986;43:93-97.
4. Ng Y, Cox C. et al: Encephalopathy Associated with RSV Bronchiolitis. J Child Neuro .2001; 16(2):105-8, eb
5. Hirayama K et al: Sequential MRI, SPECT and PET in RSV Encephalitis. Pedi Radiology. 1999;29(4):282-6