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Submandibular Lymph Node in Child

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Vol. 16 •Issue 5 • Page 23

Submandibular Lymph Node in Child

Treatment in the Absence of Other Symptoms

"Ella," age 26 months, presented for evaluation of an enlarged left submandibular lymph node.

Ella's parents said she had not experienced or been exposed to fever, chills, night sweats, cough, runny nose, vomiting, diarrhea, mouth sores, animal contacts, foreign travel, weight loss, activity decrease or feeding or elimination changes. Vital signs were within normal limits. An initial physical exam revealed a 1-cm mobile, rubbery, nontender left submandibular lymph node. No hepatospleno-megaly was present. No other lymph nodes were palpable. The initial blood work included a complete blood count (CBC) with differential, sedimentation rate (ESR), C-reactive protein (CRP), cat scratch antibody screen and blood cultures.

Ella's CBC was within normal limits except for decreased polymorphonuclear neutrophil (PMN) at 38.8% (normal range: 50% to 70%), elevated lymphocytes at 52.2 (normal range: 25 to 45) and elevated sedimentation rate at 50 (normal range: 4 to 27). I decided to continue observation with a follow-up visit in 1 week.

Seven days later, the node had increased to about 2.5 cm. No other signs or symptoms of illness were present. I consulted a pediatric infectious disease expert about the possibility of nontuberculosis mycobacterium (NTM). I ordered a computed tomography (CT) scan with contrast, purified protein derivative (PPD), chest radiograph and a trial of clarithromycin (Biaxin). The PPD came back positive at 10 mm, but the chest x-ray was normal. The CT scan identified a 2.4 cm x 1.2 cm necrotic, matted left submandibular lymph node. The radiology report also noted bilateral posterior triangles, jugular chain lymphadenopathy and a mildly enlarged right submandibular lymph node.

At this point, we brought in a pediatric otolaryngology (ENT) surgeon to determine whether the node should be biopsied. The ENT performed an excisional biopsy within a week of the CT scan. The patient had an uneventful 3-day inpatient stay and was discharged with instructions to continue taking clarithromycin (Biaxin) orally twice a day with a follow-up in 1 week.

The biopsy results revealed the causative organism to be Mycobacterium avium. The pediatric infectious disease team recommended the addition of rifampin (Rifadin) to eradicate any remaining NTM. The patient had a CT scan after 2 months of clarithromycin and 1 month of rifampin. Results showed an increase in bilateral jugulodigastric lymphadenopathy (0.8 cm x 1.2 cm on the left and 1.2 cm x 1.8 cm on the right) with possible necrosis. The infectious disease team recommended 4 more months of pharmacotherapy along with a follow-up CT scan. The ENT surgeons agreed.

More than 18 months after starting treatment, the patient remains asymptomatic but continues to have palpable jugulodigastric lymph nodes.

Etiology and Pathophysiology

Among the large genus of Mycobacterium are a group of NTM, some of which cause disease in children. Most NTM infections occur in immunocompetent children younger than 5 years. The most common cause of NTM infection in the United States is M avium.1,2

M avium are considered endemic in certain portions of the United States, especially in the Southeast. Contaminated water, dairy products, eggs and dust have been implicated in M avium infection.2,3

The most common cause of M avium infection is ingesting contaminated material. In children, breaks in the oral mucosa may provide a route for infection.

Clinical Manifestations

Infection generally manifests itself as a firm, nontender and well-circumscribed node that slowly enlarges over several weeks. The submandibular nodes are most commonly affected, but jugulodigastric and preauricular nodes have also been reported. The nodes are usually less than 4 cm in size. In the early stages, the lymph nodes are painless and do not produce the skin erythema and warmth that would suggest suppurative lymphadenitis.1,2

Differential Diagnoses

Acute and chronic forms of unilateral lymphadenitis have many causes. Common infectious causes include Staphylococcus aureus, Group A streptococcus, anaerobic bacteria, NTM and cat scratch disease. Uncommon causes include Group B streptococcus, tularemia, Yersinia pestis, gram-negative bacilli, toxoplasmosis, tuberculosis, actinomycosis and Pasteurella multocida. Rare causes include anthrax, Yersinia enterocolitica, Nocardia brasiliensis, aspergillosis and sporotrichosis. Causes of acute and chronic bilateral lymphadenitis, which are mainly viral in origin, include rhinovirus, Epstein-Barr, cytomegalovirus, herpes simplex and human immunodeficiency virus (HIV). Noninfectious causes must also be considered, such as malignancies, collagen vascular diseases and drugs.1

Diagnostic Approach

Most often, causes of lymphadenopathy are apparent after a thorough history and physical. The persistence of the adenopathy drives the diagnostic approach. Some cases may require the use of diagnostic testing. The history of a patient with lymphadenopathy should focus on the following areas: localizing the history of infection, exposure history, constitutional symptoms and prescribed medications.

The physical exam should look for signs of systemic infection or disease. Vital signs and weight are mandatory. Evaluate the neck mass for the following: location, size, fluctuance, tenderness, consistency, fixation, skin changes and sinus drainage. Inspect the oral cavity for mucosal breaks and signs of infection. Auscultate the lungs for the presence of any abnormalities.2

Diagnostic tests may confirm a diagnosis based on the history and physical. A CBC with differential, ESR, Epstein-Barr virology, PPD, blood cultures, cat scratch antibodies and HIV may also be helpful. A chest x-ray, CT, MRI and ultrasound are tools that can help confirm a suspected diagnosis. Caution is warranted with interpretation of the PPD due to the cross-reactivity between NTM and TB. Chest radiographs are often negative but must be obtained to rule out active TB infection. Definitive diagnosis of NTM is based on histopathologic findings, which are obtained by collecting a specimen of the organism. The specimen can be obtained by fine needle aspiration or open excisional biopsy.1,2,4

Treatment

A complete excisional biopsy of infected lymph nodes appears to be the most effective strategy in NTM lymphadenitis. The success rate with this procedure is about 95% without the use of antibiotics. Pharmacologic treatment for early NTM infection may include macrolide antibiotics such as clarithromycin (7.5 mg/kg/day to 30 mg/kg/day in two divided doses) or azithromycin (Zithromax 10 mg/kg/d). Other common medications are the rifamycins, such as rifampin (10 mg/kg/day to 20 mg/kg/day) or rifabutin (5 mg/kg/day to 20 mg/kg/day). Rifampin and rifabutin are used for the prevention and treatment of M avium complexes (MAC), usually in HIV patients.2,5 Data suggest limited in vitro susceptibility of MAC to rifamycins, but it is unclear whether this is of clinical relevance, because M tuberculosis does respond to rifamycins. There are no data to demonstrate superiority of one macrolide or rifamycin over another. Rifampin is more often advocated because it is associated with fewer adverse events.6 Some researchers recommend a combination of excisional biopsy and medication. The optimum time for surgical intervention is prior to the onset of skin breakdown.2

In early disease or cases in which surgery may be inappropriate, a trial of antibiotics appears to be useful. One study indicated that 96% of patients treated with antibiotics alone will have complete resolution within 6 months of starting the medication. Most patients (77%) had lymph node regression within 2 months of treatment.7

Complications and Prognosis

If an infected lymph node is not treated, progressive lymph node necrosis, overlying skin changes, suppuration and eventual draining of the skin sinus may occur. The literature contains reports of infection, such as NTM sinusitis, spreading to other sites around the head and neck.1,2 After the lymph node surfaces and drains, the infection will resolve or chronic drainage will occur.6

As stated, surgery provides the best cure rate (95%). Often, there are no long-term effects from this infection once treated. If treatment is delayed, the complications can be serious, and the infection can take months to respond. No recommendation for frequency of follow-up or long-term medication need has been published. Each case must be evaluated individually based on clinical response.1

Education

This infection is caused by ingestion of contaminated material. Two primary strategies to prevent this are to provide only pasteurized milk products and to fully cook meat. Monitoring children for nonnutritional eating patterns is important, as well as watching what they place in their mouths. The American Academy of Pediatrics recommends water heater settings of 120 degrees to prevent scalding, but that temperature is too low to suppress NTM. Research shows that raising the water heater temperature to 150 degrees for 1 week suppresses NTM growth. Those who interact with children need to be informed that no human-to-human transmission of NTM has been documented. Once a patient has reacted positively to the PPD skin test, he or she will most likely be a positive responder.2,8

Monitoring and Evaluation

No guidelines have been issued to guide how frequently or in which manner patients should be monitored after resolution. Drug toxicity is the most important component that must be observed for inpatients placed on medications. With clarithromycin and rifampin, liver function is often affected. Azithromycin may affect auditory and vestibular function. Each medication must be evaluated individually for potential adverse effects. Exercise caution when prescribing combination therapy, due to the likelihood of the medications acting synergistically and causing an increased risk for adverse outcomes.5

Putting It Into Practice

Most lymphadenopathy in children is caused by a viral upper respiratory infection (URI) and is self-limited. When the patient does not have URI symptoms but has adenopathy that increases from days to weeks, many possible differential diagnoses must be considered.

Acute unilateral cervical lymphadenopathy is a diagnosis without a clear course of action. Conservative and surgical intervention are each effective, but they are not without risk. Early intervention with education, medications and a referral to a pediatric otolaryngologist is an appropriate management strategy.

References

1. Swanson DS. Etiology and clinical manifestations of cervical lymphadenitis in children. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

2. Albright JT, Pransky SM. Nontuberculous mycobacterial infections of the head and neck. Pediatr Clin North Am. 2003;50(2):503-514.

3. Collins CH, Grange JM, Yates MD. Mycobacteria in water. J Appl Bacteriol. 1984;57(2):193-211.

4. McClain KL, Fletcher RH. Approach to the child with peripheral lymphadenopathy. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

5. American Thoracic Society. Diagnosis and treatment of disease caused by nontuberculosis mycobacteria. Am J Respir Crit Care Med. 1997;156(2 Pt 2):S1-S25.

6. Griffith DE, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberulous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

7. Luong A, et al. Antibiotic therapy for nontuberculous mycobacterial cervicofacial lymphadenitis. Laryngoscope. 2005;115(1):1746-1751.

8. Griffith DE, Wallace RJ. Epidemiology of nontuberculous mycobacterial infections. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

References

1. Swanson DS. Etiology and clinical manifestations of cervical lymphadenitis in children. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

2. Albright JT, Pransky SM. Nontuberculous mycobacterial infections of the head and neck. Pediatr Clin North Am. 2003;50(2):503-514.

3. Collins CH, Grange JM, Yates MD. Mycobacteria in water. J Appl Bacteriol. 1984;57(2):193-211.

4. McClain KL, Fletcher RH. Approach to the child with peripheral lymphadenopathy. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

5. American Thoracic Society. Diagnosis and treatment of disease caused by nontuberculosis mycobacteria. Am J Respir Crit Care Med. 1997;156(2 Pt 2):S1-25.

6. Griffith DE, et al. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberulous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

7. Luong A, et al. Antibiotic therapy for nontuberculous mycobacterial cervicofacial lymphadenitis. Laryngoscope. 2005;115(1):1746-1751.

8. Griffith DE, Wallace RJ. Epidemiology of nontuberculous mycobacterial infections. UpToDate. Available with paid subscription at www.uptodate.com. Accessed Mar 7, 2008.

9. Kubba H. A child with cervical lymphadenopathy. Clin Otolaryngology. 2006;31(5):433-434.

Brad Franklin is a family nurse practitioner at William Beaumont Army Medical Center in El Paso, Texas.




     

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