P 1103. Fatal Outcome of Metapneumovirus Infection in Patient with 4H Syndrome

Background: Fatal outcome of metapneumovirus infection in patient with 4H syndrome

Goals: To describe the fatal clinical course of a patient with 4H syndrome and metapneumovirus infection which led to perimyocarditis, pericardial effusion, and most likely cerebral edema due to rapid encephalitis.

Leading Question: How do metapneumovirus infections present in children with severe chronic neurological diseases?

Methods/Case Study: We present the case of a 10-year-old female patient with known 4H syndrome and anticonvulsive therapy who was admitted to our hospital due to fever, dyspnoe, vomiting, diarrhea, and reduced vigilance. The physical examination showed bronchiolitis with low oxygen saturation. Rapid testing for influenza and RSV were negative. Laboratory results showed elevated CRP levels of 9.44 mg/dL, procalcitonin of 0.84 ng/mL, but no other significant changes of laboratory parameters., Oxygen supplementation was needed 0.5 L/min. Treatment with cefuroxime, systemic steroids, and inhalation with salbutamol/Atrovent stabilized the patient the next 3 days: oxygen was not more required, CRP levels dropped to 0.87 mg/dL, the fever adjourned, and vigilance improved.

However, within the next 2 days, rapid neurological decline occurred with recurrent focal seizures that were treated with levetiracetam. The EEG developed continuous migrating focal seizure patterns on both hemispheres. During seizures, the eye status showed invert strabismus on left eye, slightly larger pupil on the right eye, and slow light reaction on both sides. After application of anticonvulsive therapy, the eye positions normalized and pupil diameters became isocore on both sides. The two-sided slow light reaction remained stable. Due to the generally very unstable condition of the patient, we decided re-evaluate the clinical situation after a short interval and if stable enough seek emergency cerebral imaging and lumbal puncture. However, due to increased oxygen demand and progressive respiratory failure, the patient was transferred to the intensive care unit and intubated. Laboratory results showed a relapse, CRP increased to 11.96 mg/dL. Additionally, troponin-T levels were significantly elevated at 271 pg/mL and pro-brain natriuretic peptide was >70,000 pg/mL. Multiplex PCR revealed an infection with metapneumovirus, the CT value was significantly increased at 28.17. Chest X-ray showed severe bilateral bronchopneumonia. Cardial sonography showed pericardial effusion of ∼1 cm and the blood pressure dropped. Catecholamine supply was required due to secondary cardiovascular distress. EEG showed an isoelectric line. Transcranial sonography showed oscillatory flow. Ascites or pleural effusion was not detected.

Due to the rapid clinical decline with cardial and cerebral decompensation, an immediate interdisciplinary round table discussion including the parents was set up. All parties agreed to a palliative setting without conducting cerebral imaging, pericardial and lumbal puncture. Exitus letalis occurred soon after.

Results/Conclusion: Metapneumovirus infection is a common but underdiagnosed cause for seasonal respiratory infections. Metapneumovirus infection is a severe threat to children with chronic underlying diseases, especially if they suffer from neurological diseases. Our case shows additional evidence that metapneumovirus infection can cause a severe and rapid cardial and neurological decline in patients with rare neurological disease. In suspected cases, early and rapid metapneumovirus testing is necessary and development of an efficient vaccination is urgently needed.

No conflict of interest has been declared by the author(s).