Management of Adenotonsillar Disease.” CURRENT Diagnosis & Treatment in Otolaryngology—Head & Neck Surgery, 3e Lalwani AK. Lalwani A.K. Ed. Anil K. PDF | Adenotonsillar disease (adenoiditis and recurrent tonsillitis) is a prevalent otolaryngologic disorder aetiologically based on chronic inflammation triggered. Adenoiditis; Adenotonsillitis; Nasopharyngitis; Pharyngitis; Pharyngotonsillitis; Tonsillitis Pharyngotonsillitis (tonsillitis, pharyngitis) is a general term used to.

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Arch Otolaryngol Head Neck Surg. Copyright American Medical Association. Adenotonssillar patients had undergone liver transplantation, and 7 had undergone kidney transplantation. Histopathologic examination revealed that 1 kidney transplant recipient had posttransplantation lymphoproliferative disorder. Eleven patients were found to have Epstein-Barr virus—related lymphoid hyperplasia. All patients experienced djsease resolution of their symptoms after surgery.

Early adenotonsillaf of posttransplantation lymphoproliferative disorder in children may be adenotonsillarr by adenotonsillar enlargement. In addition to the role in relieving upper airway obstruction and decreasing upper respiratory tract infection, adenotonsillectomy may be critical in the prompt evaluation and treatment of posttransplantation lymphoproliferative disorder.

This has resulted in increasing numbers of surviving transplant recipients. However, immunosuppression also predisposes the transplant recipient to an increased risk for opportunistic infections and neoplastic disorders, particularly tumors of the lymphoreticular system.

Posttransplantation lymphoproliferative disorder PTLD is characterized by abnormal proliferation of lymphoid tissue. It is an important cause of morbidity and mortality after solid organ transplantation.

Adenotonsillar enlargement may represent the first manifestations of PTLD. It is important for otolaryngologists to consider the diagnosis of PTLD in pediatric transplant recipients who present with adenotonsillar hypertrophy. Posttransplantation lymphoproliferative disorder has been evaluated extensively in the adult population. We seek to examine the association between adenotonsillar hypertrophy and Adenotonzillar in pediatric transplant recipients and to evaluate whether prompt adenotonsillectomy is beneficial in this population.

To our knowledge, this is the first series that examines the significance and management of adenotonsillar hypertrophy in pediatric patients after transplantation.

Adenotonsillar disease.

The subjects of this report are pediatric transplant recipients who presented with adenotonsillar hypertrophy at adenohonsillar University of California, Los Angeles, Medical Center from March 5,to April 22, All patients subsequently underwent tonsillectomy, adenoidectomy, or both. Clinical information was obtained from a retrospective review of their medical records. The medical records of these patients were reviewed for the following information: Symptoms referable to adenotonsillar enlargement were recorded.

The clinical signs associated with PTLD, including fever, impaired general condition, poor appetite, weight loss, and irritability, were also recorded. Risk factors associated with the development of PTLD, such as young age and tacrolimus immunosuppression, were reviewed. The patients’ age at presentation of adenotonsillar hypertrophy and tonsillar size dsease recorded.

Fourteen patients underwent tonsillectomy and adenoidectomy. Two patients underwent adenoidectomy alone. The perioperative hospital course of each patient was examined, with attention given to any postoperative complication. The pathological diagnosis of the tonsil and adenoid specimen was made using standard histological, immunohistochemical, and molecular genetic techniques. All patients were examined at their 1-month postoperative follow-up visit.

Resolution of signs and symptoms secondary to adenotonsillar hypertrophy was noted. Their subsequent medical history and follow-ups with their respective transplantation services were also reviewed, with particular attention given to whether any patient developed lymphoproliferative disorder.


The duration of the follow-up was recorded. There were 11 boys and 5 girls. The clinical characteristics of the patients are given in Table 2.

Adenotonsillar disease.

Patients are listed in Table 2 according to the type of transplantation they underwent and their age. Nine patients had undergone liver transplantation and 7 had undergone kidney transplantation. All 9 liver allograft recipients had developed end-stage liver disease secondary to biliary atresia.

Indications for kidney transplantation included glomerulonephritis, nephric dysplasia, focal segmental glomerulosclerosis, polycystic kidney disease, and Alport syndrome. The immunosuppression regimen of each transplant recipient is listed in Table 2.

The signs and symptoms of adenotonsillar hypertrophy are shown in Table 3. One patient patient 14 presented with a 2-week history of persistent fever, nasal airway obstruction, somnolence, and poor appetite.

He underwent adenotonsillectomy, and PTLD was diagnosed. Of the remaining 15 patients, 13 presented with symptoms of obstructive sleep disorder or nasal airway obstruction. Of the 2 patients who did not have airway obstruction, one had recurrent tonsillitis and a second had asymptomatic, asymmetric tonsillar enlargement. The 2 patients without tonsillar hypertrophy were found intraoperatively to have adenoid hypertrophy. These 2 patients underwent adenoidectomy alone.

There were no perioperative complications in any of the patients. The histopathologic diagnosis and immunohistochemical staining results of each patient are shown in Table 3.

Adherent Biofilms in Adenotonsillar Diseases in Children

Features of PTLD were demonstrated in the adenoid and tonsil specimen in patient His adenoid tissue showed diffuse adenotinsillar of normal adenoid follicles by a polymorphous proliferation of small lymphocytes, immunoblasts, plasma cells, and plasmacytoid lymphocytes Figure 1. Focal necrosis was also demonstrated Figure 1right.

Histopathologic evaluation results were, therefore, consistent with PTLD, polymorphous type. His immunosuppression consisted of cyclosporine and prednisone. He subsequently underwent serologic evaluation for EBV. These results were adenotonsilllar with an acute EBV infection. In addition, polymerase chain reaction was used adenotonsiolar detect viral sequences in circulating lymphocytes.

He underwent computed tomographic scanning of his neck, chest, abdomen, and pelvis. This revealed bilateral cervical lymphadenopathy. The remaining results of his computed tomographic scans were normal. Cyclosporine therapy was discontinued, and low-dose prednisone therapy was maintained. He did not undergo chemotherapy.

This patient was discharged from the hospital 10 days after tonsillectomy and adenoidectomy with resolution of symptoms. Laboratory evaluation on follow-up has not demonstrated evidence of organ adenottonsillar. An example of EBV-related hyperplasia is shown in patient 1, whose adenoid specimen demonstrated diffuse lymphoid proliferation with preservation of lymphoid architecture Figure 3.

All patients, including the one who developed PTLD, had resolution of their preoperative symptoms on follow-up examinations. Those who demonstrated EBV-related hyperplasia underwent a reduction in the level of immunosuppressant medication. None have demonstrated clinical or laboratory evidence of organ rejection. Adenotonsillar hypertrophy in the posttransplantation population has not been previously emphasized in the English-language literature.

The incidence of adenotonsillar hypertrophy in this patient population is not known. The etiology and clinical significance of such hypertrophy in the immunosuppressed patient also have not been examined.

Even in the immunocompetent patient, the role of the adenoids and tonsils is not clearly defined. It is clear, however, that adenotonsillar hypertrophy in an immunosuppressed child can represent PTLD. Posttransplantation lymphoproliferative disorder is defined as the presence of an abnormal proliferation of lymphoid cells and is associated with EBV infection in the setting of immunosuppression. The use of immunosuppressive agents in the setting of solid organ transplantation is associated with a to fold increased risk of lymphoma.


It infects B lymphocytes, immortalizes them, and leads to their polyclonal proliferation. In the immunosuppressed hosts, the cytotoxic T-lymphocyte response that controls the B-cell proliferation is limited. In a review of the literature, several studies have demonstrated that lymphoproliferative disorder can present as enlargement of the adenoid and tonsil tissue. InMyer and Reilly 4 noted a case of PTLD presenting as adenotonsillar hypertrophy in a 2-year-old recipient of a liver allograft.

Fairley et al 13 described 3 cases of oropharyngeal PTLD, 1 of which adenotonsllar in a 6-year-old heart transplant recipient who had presented with adenotonsillar hypertrophy. Lones et al 5 noted 3 cases of PTLD that presented as adenotonsillar hypertrophy and concluded that adenotonsillectomy can be valuable in the early diagnosis of PTLD.

In a adenoonsillar of 18 pediatric liver diseaes recipients who developed PTLD, Sokal et al 2 noted that 6 patients diseasee tonsillar involvement. Dror et al 10 reported that 8 of the 26 patients with PTLD in their series had tonsillar involvement. Adenotonsillar hypertrophy in a diswase who has undergone solid organ transplantation may represent PTLD.

Factors that increase the risk for PTLD include young age, liver as opposed to kidney allograft, EBV seronegativity, and use of tacrolimus as an immunosuppressive agent Table 4. However, all transplant recipients are at notably increased risk of developing lymphoproliferative disorder compared with the general pediatric patient with adenotonsillar hypertrophy.

The patient’s clinical manifestations may also suggest the diagnosis of PTLD. The clinical signs of PTLD in children may include fever, pharyngitis, lymphadenopathy, hepatosplenomegaly, impaired general condition, poor appetite, weight loss, and irritability. However, the absence of such symptoms does not preclude the presence of PTLD. Many patients with PTLD can present without any constitutional symptoms.

The timing of the onset of adenotonsillar hypertrophy may also provide clues for PTLD. Posttransplantation lymphoproliferative disorder is most common during the first year after transplantation.

Overall, the mean age of the patient at the time of organ transplantation was 3 years 1 month in our series. Adenotonsillae mean duration from organ transplantation to adenotonsillectomy was 5 years 1 month.

This suggested that either symptomatic adenotonsillar hypertrophy may not be an immediate finding after organ transplantation or this symptom is not promptly appreciated by physicians and family members.

The management of adenotonsillar hypertrophy in the immunocompetent cisease population has been controversial. No single algorithm for decision making can encompass all clinical scenarios.

Prompt surgical intervention is necessary. Adenotonsillectomy not only evaluates for PTLD but also allows for early intervention.