Via Research Recognition Day 2024 VCOM-Carolinas

Clinical Case-Based Reports

Rapidly Progressive Fatal Pneumococcal Meningitis in a Fully Immunized Child with History of Facial Bone Fractures Brianna N. Stanley, OMS-III 1 ; Haya B. Rizvi, OMS-IV 2 ; Hanna S. Sahhar, MD, FAAP, FACOP 1,3

1 Edward Via College of Osteopathic Medicine, Carolinas Campus, Department of Pediatrics, Spartanburg, SC 2 Edward Via College of Osteopathic Medicine, Virgina Campus, Department of Pediatrics, Blacksburg, VA 3 Spartanburg Regional Healthcare System, Department of Pediatrics, Pediatric Intensive Care Unit, Spartanburg, SC

Abstract # Goes here

Case Presentation Case Presentation

Discussion

Abstract Abstract

Discussion

Pneumococcal bacterial meningitis is commonly caused by Streptococcus pneumonia in children over the age of three months. Although there has been a 50-60 percent decline in infections due to the introduction of the pneumococcal conjugate (PCV) and pneumococcal polysaccharide (PPSV) vaccines, there are still reported cases of invasive pneumococcal infections with non vaccine serotypes. We report a fully immunized 6-year-old male patient with a history of extensive traumatic facial bone fractures six months ago who presented to the hospital with seizure-like activity, fever, nausea, and vomiting. After admission to the pediatric intensive care unit (PICU), he showed evidence of status epilepticus, clinically and by electroencephalography (EEG) and was treated successfully with anti-epileptic medication. Laboratory investigations revealed pneumococcal meningitis which was treated with broad spectrum antibiotics. Nine hours after admission to PICU, the patient underwent a catastrophic incident with a sudden change in mental status, rapid deterioration in pupillary reaction using pupillary reactivity assessment scale called Neurological Pupil index (NPi®) along with respiratory depression and arrest, all indications of sudden increase in intracranial pressure and brain herniation. Initial computed tomography (CT) scan of the brain at admission demonstrated no acute intracranial process but repeat imaging after the incident showed increased intracranial pressure without evidence of infarction or hemorrhage. With persistent Glasgow Coma Scale (GCS) of 3 and isoelectric brain activities on EEG, brain death determination was done in 24 hours and repeated in 12 hours of which both were positive for brain death, the patient pronounced dead and proceeded for organ donation. Our case demonstrates a unique presentation of rapidly progressing pneumococcal meningitis complicated by septic thrombophlebitis and subsequent brain herniation in a fully immunized patient six months after a severe traumatic facial injury.

References 1. Brooke P, Patel A, Agrawal S. Pneumococcal Meningitis in Children. Paediatr and Child Health. 2023; 33(10):289-294 2. Meiring S., Cohen C., de Gouveia L., et al. Case-fatality and sequelae following acute bacterial meningitis in South Africa. Int. J of Infectious Diseases.2022; 122: 1056-1066. https://doi.org/10.1016/j.ijid.2022.07.068 3. Deliran S., Brouwer M., Coutinho J., de Beek D. Bacterial meningitis complicated by cerebral venous thrombosis. Eur Stroke J. 2020; 5(4): 394-401. doi: 10.1177/2396987320971112 4. Privitera, C.M., Neerukonda, S.V., Aiyagari, V. et al. A differential of the left eye and right eye neurological pupil index is associated with discharge modified Rankin scores in neurologically injured patients. BMC Neurol.2022; 273. https://doi.org/10.1186/s12883-022-02801-3 5. Das S., Pal T. Post-Traumatic Meningitis: Case- Based Review of Literature from Internist’ Perspective. Case Rep in Acute Med. 2021; 4. 41-49. DOI: 10.1159/000515540 6. Strandvik G., Shaaban A., Alsaleh A., Khan M. Rapidly fatal pneumococcal meningitis following non penetrating traumatic brain injury. BMJ Case Rep. 2020; 13(2). doi:10.1136/bcr-2019-232692 ​The epidemiology of pneumococcal meningitis has changed since the introduction of the pneumococcal vaccinations. There is decreased incidence of vaccine serotypes and increased prevalence of non-vaccine serotypes. Therefore, it is important to note that pneumococcal meningitis in a vaccinated individual can still result in significant disease and consequences, as seen with our case. Post-traumatic meningitis has been reported in a few cases following head injury where the bacteria possibly traveled to the brain through facial sinuses. Although there was no statistical significance, the literature stressed the importance of pneumococcal vaccine prophylaxis for meningitis in those with facial fractures. The suspected brain matter that was observed in bilateral nostrils supports our theory that the facial fractures played a significant role in the spread and extent of infection. Our case is significant because of the vaccination history, young age, and rapid progression and spread of infection. The uncommon complication of cerebral venous thrombosis can have clinical manifestations like uncomplicated meningitis and can often be a missed or delayed. This complication occurs in 1% of patients and is seen in patients with focal neurologic deficits, coma, and ear-nose-throat infections. Despite the low percentage, there are life threatening consequences in the pediatric population. S. pneumoniae is the most common pathogen associated with cerebral venous thrombosis. Causes of cerebral thrombosis include hypercoagulable states, blood flow disturbances, and infection. Treatment for thrombosis is supportive care and anticoagulation. Although there is little evidence, unfractionated heparin or low molecular weight heparin has been utilized as anticoagulant therapy for acute cerebral venous thrombosis. Our patient’s typical meningeal signs and symptoms along with his history of facial fractures suggest an increased risk and predisposition to develop cerebral venous thrombosis. Resulting in rapid progression to brain death. As such, further evaluation for thrombosis should be encouraged in children with such history and presentation.

Figure 3A. EEG Findings on admission to hospital: Asymmetrical poorly organized background with relative lower amplitudes in right hemisphere, showing mainly high amplitudes slow delta with less abundant theta waves. No epileptiform activities in the right hemisphere. Seizures focus clearly from the left hemisphere despite muscles and other artifacts that show rhythmical 1-2 hz delta of high amplitudes spikes and sharp waves.

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Figure 2A. Initial CT scan of head with no acute changes.

Figure 3B. Clinical Status Epilepticus after hospitalization: Epileptiform activities evolving to secondary generalization (focal to bilateral tonic-clonic seizure).

Case Presentation

6-year-old male with a history of asthma and facial trauma six months prior presented to the emergency department (ED) via emergency medical services (EMS) due to seizure-like activity. His mother reported tonic/clonic like movements on three separate occasions. She reported recent headaches after his head injury (Figure 1). He presented with fever, nausea, and vomiting for the past day. Patient was up to date on all his vaccinations and no known drug allergies. He was febrile while in the ED and other vitals were unremarkable.

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Figure 3C. Ten hours after admission: Diffuse background activities suppression pattern and no electrographic seizures or other epileptiform activities consistent with electro-cerebral silence.

Figure 2B. Repeat CT scan with evidence of increased intracranial pressure.

Figure 1. CT scan of head from six months prior when the patient was injured causing facial fractures. The following findings: left nasal bone fracture, bilateral impacted medial orbital wall fractures with one posteriorly on the right with most prominent fracture, minimally displaced fracture of right inferior temporal fossa, minimally displaced sphenoid bone, fracture of anterior cranial fossa at the cribriform plate, and oblique fracture of left supraorbital frontal bone.

There was a sudden change in his physical examination early the next morning, nine hours after admission, his right pupil became fully dilated and non-reactive. The patient entered respiratory depression and became severely agitated, with an oxygen saturation (SpO2) of 80%. After intubation and stabilization, both pupils were fully dilated and fixed. He was given mannitol and had a decreasing NPi score (Figure 4A,B,C). A second CT without contrast demonstrated an increased intracranial pressure without evidence of infarction or hemorrhage and paranasal sinus disease (Figure 2B). Upon returning, he entered an episode of pulseless ventricular tachycardia that required cardiopulmonary resuscitation, lidocaine, and an increased epinephrine drip to return to sinus rhythm. Roughly one hour later, the patient had a persistent GCS <3. There was noted to be progressive cerebral edema consistent with herniation, along with suspected brain matter that was present in bilateral nostrils. The patient was declared brain dead two days after admission following two brain death examinations.

His initial physical examination was notable for opening his eyes intermittently to voice, moving all extremities, and post-ictal state. Laboratory results were significant for metabolic acidosis and an increased C-reactive protein (CRP) 14.5 mg/dL (0.0 - 0.6 mg/dL). CT scan of the head with and without contrast showed no evidence of acute intracranial process (Figure 2A). Patient was admitted to the PICU, a lumbar puncture was completed showing heavy growth of Streptococcus pneumoniae that was susceptible to ceftriaxone, levofloxacin, penicillin, and vancomycin. Repeat physical examination in the PICU was significant for dry mucous membranes, delayed capillary refill, pale skin, positive neck stiffness, positive Kernig and Brudzinski sign. His GCS was <12 and his left pupil was larger than the right. Patient was sluggish and tachypneic. Additional labs showed an elevated white blood cell (WBC) count 29.2 x 103/µL (5.0 - 14.5 x 103/ µL) and a decreased bicarbonate (HCO3) 17.7 mmol/L (23.0 -32.6 mmol/L). An EEG was obtained pre- and post-witnessed seizure and demonstrated status epilepticus (Figure 3A,B,C). Patient was given fosphenytoin and levetiracetam to manage his seizures.

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No relevant financial affiliations or conflicts of interest. If the authors used any personal details or images of patients or research subjects, written permission or consent from the parent (or legal guardian) was obtained. This work was not supported by any outside funding. The authors would like to acknowledge and thank Dr. Gonzalo F. Pares and Dr. Rowena Emilia Desailly-Chanson for providing the electroencephalographic interpretation for this patient.

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4A

Figure 4A . NPi test at 0031, with a normal NPi scores and right pupil slightly larger than the left (normal > 3.0) Figure 4B. NPi test at 0050, after patient had sudden change in presentation at 0048 with dilated right pupil and respiratory depression showing abnormal NPi score and dilated right pupil, and no change of left pupil. Figure 4C. NPi test at 0134 shown abnormal NPi scores (non-reactive pupils) and dilated both pupils.

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2024 Research Recognition Day