Volume 1, Issue 4 , Pages 271-273, December 2006
Adenoidectomy due to obstructive neonatal adenoid hypertrophy secondary to cytomegalovirus infection in an 8-week-old infant
Article Outline
Summary
Adenoid hypertrophy is a common feature of childhood. It is thought to be caused by the antigen stimulated increased activity of B lymphocytes. Obstructive adenoid hypertrophy on the other hand is extremely rare in the neonatal period. We present a 2-month-old female patient with difficulty in nasal breathing due to obstructive adenoid hypertrophy. Endoscopic examination, tissue removal and biopsy was performed. Lymphoid hyperplasia and inclusion-bearing cytomegalic cells within the endothelium were seen in the histopathologic examination. Cytomegalovirus (CMV) infection of the nasopharynx is very rare. An adenoidectomy was performed and the symptoms of the patients were immediately disappeared. To our knowledge this is the youngest case with CMV related adenoid hypertrophy necessitating adenoidectomy.
Keywords: Neonatal adenoid hypertrophy, Cytomegalovirus (CMV), Adenoidectomy
1. Introduction
Adenoid tissue, as a part of Waldeyer's ring, belongs to the lymphoepithelial system. Adenoid hypertrophy is a common feature of childhood with a peak age of 3–6 years. Obstructive adenoid hypertrophy necessitating surgical treatment is extremely un-common in the neonatal period. It is thought to be caused by the antigen stimulated increased activity of B lymphocytes [1]. Adenoidectomy is the only effective therapy. Cytomegalovirus (CMV) infection of the nasopharynx is also very rare. To our knowledge this is the youngest case with CMV related adenoid hypertrophy treated with adenoidectomy.
2. Case report
A 2-month-old female patient was referred to our center with a history of difficult breast-feeding and stridor, suggestive of progressive nasal obstruction. She was born at 35 weeks of gestation with a birth weight of 2400
g and Apgar score of 7/9. She stayed 7 days in the neonatal ward, then discharged without any difficulty of breast feeding and nasal breathing. ENT examination revealed unremarkable nasal findings, no signs of nasal or nasopharyngeal infection, but the uvula was edematous. In her physical examination there was neither hepatomegaly, nor splenomegaly. Fundoscopic examination was normal. During bad-side fiberoptic nasopharyngolaryngologic examination the patient had apnea and cyanosis and the procedure had to be stopped. Cranial computerized tomography showed hypertrophic adenoid tissue in the nasopharynx, obliterating choanae (Fig. 1).
Fig. 1.
Hypertrophic adenoid tissue in the nasopharynx obliterating choanae.
Under general anesthesia, endoscopic nasopharyngolaryngologic examination was performed. Hypertrophic adenoid tissue resembling adenoid vegetation, obliterating choanae and nasal cavities, and also extending to oropharynx was observed. Since adenoid hypertrophy in the very first weeks of life is very uncommon, endoscopic tissue removal, and biopsy was performed. Difficulty in nasal breathing and stridor were increased in the postoperative first week, and fiberoptic nasopharyngolaryngologic examination was repeated. Residual adenoid tissue at the junction of nasopharynx and oropharynx, which was not seen with rigid endoscope during the first procedure was observed when the patient was 8-week old. Conventional adenoidectomy, with the smallest size adenoid curette was performed. Symptoms were disappeared immediately after the operation. Histopathologic examination of both specimens revealed lymphoid hyperplasia and cytomegalic cells with intranuclear and/or intracytoplasmic inclusions mostly in the endothelium (Fig. 2). The second biopsy also showed focal acute inflammation and some granulation tissue, probably due to the previous procedure. Immunohistochemistry confirmed the presence of CMV and most of the lymphoid cells were CD20(+) B cells. Laboratory investigation including complete blood count and liver function tests were within normal limits. Serology for TORCH, as well as urine and blood CMV load was negative. A search for immunodeficiency did not show any pathology. Lateral cranial X-ray did not show calcification. Since a localized CMV infection was considered, systemic anti-CMV therapy was not given. As her symptoms were resolved, she was discharged after 2 weeks. Her physical growth and nasal potency were normal during her follow-up visits in the third, sixth and ninth months.
Fig. 2.
Inclusion-bearing cytomegalic cells in the endothelium. 400×, HE.
3. Discussion
Neonates are obligatory nasal breathers until 6–8 weeks of life. It is important that the nasal airway be patent during this crucial time. In the absence of correct diagnosis and treatment, nasal obstruction may cause serious respiratory distress and feeding difficulties. A particular anatomic configuration, combined with immaturity of the neuromuscular responses, impedes conversion to oral breathing in case of nasal obstruction [2].
Nasal airway obstruction in the neonate can result from several causes. Some of the more common ones include mucosal edema, neonatal rhinitis (adenoiditis), septal displacement or hematoma, displaced nasal bone fractures and choanal atresia or stenosis [3].
A small number of anomalies can present with acute respiratory problems either immediately at birth or within the first few days or weeks of life. One of the most common anomalies is choanal atresia or stenosis. The incidence is thought to be about 1 in 8000 live births [4]. Bilateral choanal atresia causes immediate respiratory distress at birth, and these babies require support with an oral airway until urgent remedial treatment can be undertaken. Some children with unilateral atresia present with feeding difficulties and persistent rhinorrhoea, especially when the patent nostril is partially blocked because of an infection [4]. Sixty to seventy per cent of choanal atresia patients have other associated congenital anomalies [5]. The most common and most serious of these is the CHARGE association. Congenital anomalies of the choanae can best be imaged by computed tomography scan. This can show the exact site of obstruction and also whether it is bony or membranous.
Nasal obstruction without choanal atresia has also been recognized in infants between 3 and 6 weeks of life, which is associated with a snorting respiratory pattern. The underlying causes [6], [7], [8], [9] include edema of the nasal mucosa, obstruction of the nasal passage by a nasolacrimal duct cyst, congenital mass lesions or adenoid tissue, decreased width of the bony nose, pyriform aperture stenosis, a rare cause of airway obstruction in the newborn and is easily mistaken for choanal stenosis or atresia, and hypoplasia of the nasal alae. Inflammatory edema of the nasal and nasopharyngeal mucosa due to neonatal rhinitis was stated as the most common causative factor [6]. Obstructive adenoid hypertrophy necessitating surgical treatment in the neonatal period is extremely rare. The peak age for adenoid hypertrophy is 3–6 years [10]. Neither related prevalence, nor information about the youngest age of adenoidectomy was present in the literature, although there are personal notes, about the youngest patient to whom an adenoidectomy had been performed was 4-day old.
Several studies have demonstrated EBV related lymphoid hyperplasia is frequently found in adenotonsillar tissue after removal. Post-transplantation lymphoproliferative disorder (PTLD), or its precursor EBV-related lymphoid hyperplasia, may first present in tonsils and adenoids in the pediatric solid organ transplant population [11].
CMV related adenotonsillar tissue hypertrophy has not been established in congenital, opportunistic infections. CMV infection of the nasopharynx in an otherwise healthy man as the only case was reported [12].
4. Conclusion
Although obstructive adenoid hypertrophy is extremely rare in the neonatal period, when dealing with a neonate presenting with progressive nasal obstruction, adenoid hypertrophy related viral infections should be kept in mind.
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PII: S1871-4048(06)00071-2
doi:10.1016/j.pedex.2006.06.004
© 2006 Elsevier Ireland Ltd. All rights reserved.
Volume 1, Issue 4 , Pages 271-273, December 2006
