Cerebral venous sinus thrombosis with meningitis in a child with disseminated staphylococcal disease

Shalu Gupta; Sanya Chopra

doi:10.4103/jpcc.jpcc_164_20

CASE REPORT

Year : 2021 | Volume : 8 | Issue : 3 | Page : 149-152

Cerebral venous sinus thrombosis with meningitis in a child with disseminated staphylococcal disease

Shalu Gupta, Sanya Chopra
Department of Pediatrics, Kalawati Saran Children's Hospital, New Delhi, India

Date of Submission	17-Oct-2020
Date of Decision	10-Jan-2021
Date of Acceptance	17-Jan-2021
Date of Web Publication	30-Apr-2021

Correspondence Address:
Dr. Sanya Chopra
Kalawati Saran Children's Hospital, Bangla Sahib Road, Connaught Place, New Delhi - 110 001
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jpcc.jpcc_164_20

Abstract

The availability of anti-staphylococcal antibiotics today has revolutionized the treatment strategies to fight Staphylococcus aureus. However, its virulent nature still remains a major cause of morbidity and mortality, especially in the pediatric age group. It presents with a wide spectrum of illnesses ranging from minor skin and soft-tissue infections to fatal necrotizing pneumonia and disseminated disease. However, its presentation as meningitis with septic venous sinus thrombosis in pediatrics remains a rare complication till date. We present the case of an 8-month-old girl child with disseminated staphylococcal disease (DSD) caused by community-acquired methicillin-sensitive S. aureus and complicated by acute mastoiditis, meningitis, and cerebral venous sinus thrombosis. This rare and severe manifestation of DSD was managed successfully with intravenous antibiotics and systemic anticoagulation.

Keywords: Cerebral venous sinus thrombosis, disseminated staphylococcal disease, methicillin-sensitive Staphylococcus aureus

How to cite this article:
Gupta S, Chopra S. Cerebral venous sinus thrombosis with meningitis in a child with disseminated staphylococcal disease. J Pediatr Crit Care 2021;8:149-52

How to cite this URL:
Gupta S, Chopra S. Cerebral venous sinus thrombosis with meningitis in a child with disseminated staphylococcal disease. J Pediatr Crit Care [serial online] 2021 [cited 2023 Jun 2];8:149-52. Available from: http://www.jpcc.org.in/text.asp?2021/8/3/149/315258

Introduction

Staphylococcus aureus is both a commensal and a human pathogen. It is responsible for a wide range of infections ranging from skin and soft-tissue involvement to life-threatening necrotizing pneumonia and disseminated staphylococcal disease (DSD). The disease has been well known in immunocompromised children and infants but now is increasingly being described in healthy children as well, with a rapid progression and a high mortality rate ranging from 30% to 35%.^[1]

DSD is predominantly caused by methicillin-resistant S. aureus (MRSA), where community-acquired MRSA (CA-MRSA) strains are being increasingly isolated.^[2],[3] Lung, bones, and joints are the most common organs involved in DSD, followed by skin, liver, and central nervous system (CNS). Although case reports of invasive CA-MRSA infection causing venous thrombosis have been described in adults,^[4],[5] DSD presenting as septic cerebral venous sinus thrombosis (CVST) has rarely been reported in the pediatric literature.^[6] This clinical vignette describes a case of DSD by community-acquired methicillin-susceptible S. aureus (CA-MSSA) in a child with CVST.

Case Report

A previously healthy and immunized, 8 month-old-female child presented to our hospital with a history of high-grade fever for 10 days, dry cough and bilateral purulent ear discharge for the last 8 days, and one episode of a generalized tonic–clonic seizure 2 days back. She had no significant past history of recurrent infections, hospital admissions, or any recent history of trauma. At presentation, she was febrile, drowsy, sick looking with a heart rate of 150 beats/minute and respiratory rate of 68/min. Detailed clinical examination revealed cellulitis over the dorsum of the right foot, bilateral diffuse crepitation, tender hepatomegaly, and splenomegaly. There were no features suggestive of raised intracranial pressure, seizures, or any focal deficits. Right ear examination revealed central perforation of the tympanic membrane.

Routine blood investigations were suggestive of a hemoglobin of 10.5 g/dl, marked leukocytosis with a white blood cell count of 48.6 × 10⁹ cells/L (73.8% neutrophils and 22.5% lymphocytes), and thrombocytopenia (platelet count of 56 × 10^9/L) with raised serum inflammatory markers. The liver, kidney function tests, coagulation profile (international normalized ratio: 1.56), and blood glucose (5.4 mmol/L) levels at admission were normal. The chest X-ray was suggestive of a necrotizing pneumonia with bilateral pleural effusion. An ultrasound confirmed the presence of bilateral septated collection (pyothorax) in the lungs with multiple well-defined hypoechoic lesions in both lobes of the liver, largest 1.5 cm × 1.5 cm suggestive of multiple liver abscesses. Doppler ultrasound of the limbs ruled out any evidence of deep vein thrombosis (DVT).

Based on the above clinical findings and laboratory evidence, the child was started on broad-spectrum antibiotics (ceftriaxone and vancomycin). Vancomycin was added empirically in view of the fulminant presentation and suspected Staphylococcus infection. She was shifted to the pediatric intensive care unit in view of worsening of respiratory distress and later mechanically ventilated for impending respiratory failure. Bilateral intercostal drainage tubes were inserted for drainage of the pyothorax. The lumbar puncture showed a cloudy cerebrospinal fluid (CSF) with pleocytosis (total leukocyte count: 0.3 × 10⁹/L, 80% neutrophils and 20% lymphocytes) with the sugar at 1.78 mmol/L (serum 5.11 mmol/L) and a protein of 1.2gm/L. The CSF culture isolated S. aureus, resistant to penicillin but sensitive to cefoxitin, clindamycin, vancomycin, linezolid, and ciprofloxacin. The blood and pus culture were sterile. By this time, as the child improved clinically, the initial choice of intravenous (IV) antibiotics was continued.

The child was evaluated extensively for any underlying causes. The serum immunoglobulin (Ig) G levels were 20.15 g/L (20.3–93.4), IgA 1.01 g/L (0.08–9.1), and IgM 1.38 g/L (0.17–1.5). Flow cytometry showed normal expression of T-cell and B-cell markers. Dihydrorhodamine test and the HIV status were negative.

As the poor sensorium persisted despite the use of sensitive antibiotics, a contrast-enhanced computed tomography head was planned. It was suggestive of right otomastoiditis with filling defects in the right transverse sinus [Figure 1] and [Figure 2]. These findings were later confirmed by a contrast-enhanced magnetic resonance (MR) imaging head and an MR venography which revealed acute mastoiditis and thrombosis in the right transverse and sigmoid sinus [Figure 3]. A prothrombotic workup was planned. The child was started on systemic anticoagulation with low-molecular-weight heparin, followed by oral anticoagulation. The patient responded well to treatment and was gradually weaned off the ventilatory support in 8 days. By day 12, her clinical condition stabilized. The oxygen support was gradually tapered over the next week. A bedside echocardiography revealed a normal study. A detailed ear, nose, and throat evaluation and management followed. Repeat sonography confirmed the resolution of the liver abscess and pyothorax. IV antibiotics were continued for a total of 3 weeks followed by 3 weeks of oral antibiotics. The patient improved clinically over a period of time. She was discharged 4 weeks later with a repeat neuroimaging in plan.

Figure 1: Computed Tomography of Temporal bone showing destruction of right sided mastoid air cells with bony erosion [white arrow]

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Figure 2: Contrast enhanced computed tomography of Head showing right oto-mastoiditis with filling defects in right transverse sinus [black arrow]

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Figure 3: Magnetic Resonance Venography of Brain showing decreased flow in the right transverse and sigmoid sinus, indicating thrombus [small black arrow]

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Discussion

DSD is diagnosed by the involvement of at least two distant organs with the presence of Gram-positive cocci in clusters and/or growth of S. aureus from at least one normally sterile body fluid.^[7] An increasing trend of antibiotic-resistant bacteria such as MRSA causing serious illnesses including bacteremia, CNS infections, and DSD has been reported previously.^[8] While CA-MSSA has been mainly known to cause superficial infections, its involvement as a disseminated disease including CNS is rare. Our case highlights how CA-MSSA caused a disseminated disease in a healthy child with meningitis and progressed to CVST.

In a large series from the Indian subcontinent with 53 children presenting as DSD, CNS involvement in the form of meningitis (17%) and brain abscess (6%) was reported.^[1] Another study by Mandal et al. reported meningitis in 5% cases of DSD.^[9] However, none of these studies reported any case of CVST. Even though S. aureus is the most common bacterial pathogen causing septic cavernous sinus thrombosis (CST), it is an infrequent cause of meningitis. The presence of meningitis and mastoiditis both along with the hematogenous spread of the organism was probably responsible for the development of septic sinus thrombosis in our patient. A high incidence (19%) of isolation of S. aureus from CSF in children <2 years of age with a disseminated disease including meningitis and a poor sensorium has been reported.^[10] CSVT is a frequent complication seen in immunocompromised patients and those with a pro thrombotic state. Overlying trauma or infections including mastoiditis may act as a triggering factor for CSVT in children.^[11] CA-MRSA infections, especially osteomyelitis, have been associated with DVT of lower limbs.^[12] There are also few case reports of septic pulmonary embolism, complicating DSD in children.^[12],[13] Similarly, our patient had a risk factor in the form of mastoiditis which led to an extension into intracranial venous sinuses causing thrombosis. CST has been reported in a previously healthy child who developed pansinusitis without known any identifiable risk factors.^[6]

Multiple virulence factors contribute toward the pathogenesis of thrombosis, including alpha-toxin, panton–valentine leukocidin, and various enzymes.^[8] Alpha-toxins lead to platelet aggregation and spasm of smooth muscle while coagulase promotes clot formation due to interaction with fibrinogen.^[8] Considering the high mortality associated with DSD, the favorable recovery in our patient is noteworthy. Our case highlights the occurrence of CVST as a part of DSD caused by MSSA in an apparently immunocompetent child.

Our experience with this case highlights that CVST can present as a rare complication of DSD with meningitis and mastoiditis and requires a high index of suspicion.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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