April 22, 2005
A Swollen Neck/Commentary
Ylva Bengtsson, MD
Raja Mouallem, MD
The following Brief Report was written by a resident. A discussion by a member of the resident's faculty follows. We invite any resident to submit such articles, together with commentary by a faculty member.
A 12-year-old boy presented to this pediatrie emergency department (PED) with tender swelling of his neck. The swelling had slowly developed over the previous 2 days. There was no history of bites, trauma to the neck, or exposure to kittens, and he denied toothache. He was diagnosed with cervical lymphadenitis and treatment with oral clindamycin was initiated. The following day, because he was febrile and the swelling had progressed to where he was unable to open his mouth, he returned to the PED. His oral intake had decreased, but he maintained a normal urine output. He denied shortness of breath and the review of systems was otherwise negative.
His previous medical history was remarkable only for recurrent herpes labialis. There was no history of dental caries or abscess. The family history was also unremarkable. He lives with his mother, and there are no pets. Immunizations were up to date, and he did not have any allergies. He was not taking any medicines except for clindamycin.
Physical examination revealed an alert boy in no acute distress but with significant swelling of his neck (Figure 1). There was no stridor. His temperature was 37.5C, heart rate, 102 beats/minute, respiratory rate 24 breaths/minute, and blood pressure was 132/79 mm Hg. Pulse oximetry was 100% on room air. A crusted lesion was noted on the left side of his lower lip. Neck swelling extended from the angle of the mandible to the middle of the neck (zone 2) and was indurated and warm but not fluctuant. The left side was somewhat more swollen than the right. He was unable to open his mouth more than minimally secondary to pain. His mouth could, however, be opened passively. The teeth were intact and there was no gingival swelling. The floor of the mouth was tender anteriorly and his voice was muffled, but he was not drooling. The tympanic membranes were pale and intact bilaterally. The neck was supple with full range of motion, and he did not have torticollis. He was tachycardie. The remainder of the physical examination findings was normal.
Initial laboratory investigation included an elevated WBC count of 19,100/mm^sup 3^ The differential showed 84% neutrophils, 11% lymphocytes, and 5% monocytes. A basic metabolic panel was within normal limits. Screen for Epstein Barr Virus (EBV-monospot) and a blood culture were obtained.
At this point the diagnosis of Ludwig angina was suspected. Owing to concern about the continued patency of his airway he was given intravenous dexamethasone and placed on continuous cardiorespiratory monitoring. ENT was consulted.
Computed tomography (CT) of the neck with contrast revealed a 1.3 0.9 cm hypodense area posterior to the symphysis of the mandible, likely representing a necrotic lymph node (Figure 2). There was diffuse density of the subcutaneous fat in the submental region consistent with cellulitis and there were additional prominent lymph nodes in the submental and submandibular regions interpreted as reactive lymph nodes. The airway was patent and there were no abnormal neck masses.
Figure 1. 12-year-old boy with marked swelling of the neck extending from the mandible to just above the clavicle.
Diagnosis: Cervical Lymphadenitis Presenting as Ludwig Angina
He was admitted to the pediatrie intensive care unit for close monitoring of his airway and was continued on intravenous dexamethasone clindamycin. Over the next two days, the swelling improved and he did not require surgical drainage. The screen for EBV (monospot) was negative as was the blood culture. He was discharged home to finish a ten-day course of oral clindamycin.
Department of Pediatrics, Division of Emergency Medicine. LSU Health Sciences Center, New Orleans, Louisiana.
Reprint requests and correspondence to: Ylva Bengtsson, MD, Children's Hospital, 200 Henry clay Avenue. New Orleans, LA 70118.
2005 Westminster Publications, Inc., 708 Glen Cove Avenue, Glen Head, NY 11545, U.S.A.
Raja Mouallem, MD
Department of Pediatrics, Division of Emergency Medicine, LSU Health Sciences Center, New Orleans, Louisiana
Ludwig angina was first described in 1836 by Wilhelm Frederick von Ludwig and is a potentially serious condition in which there is a bilateral infection of the sublingual and submandibular area that can lead to airway obstruction. The infection begins in the floor of the mouth and induces a rapidly spreading gangrenous cellullitis. It is spread along the fascial planes, not propagated by the lymphatic system. The rapid spread causes edema of the neck and glottis and, thus, may cause airway obstruction.
Patients typically present with bilateral submandibular swelling, neck pain, fever and elevation of the tongue. Other common symptoms are toothache, trismus, dysphagia, and breathing difficulties.1 The submandibular swelling is characteristically firm and painful. There is usually tenderness of the floor of the mouth causing elevation of the tongue. If swelling is bilateral, the tongue is displaced upward and backward forcing the mouth open and occasionally interfering with breathing.2 The lymph nodes are unaffected.
The majority of cases are caused by dental infections, most commonly from the second or third mandibular molars. Other causes include peritonsillar and parapharyngeal abscesses, oral lacerations, mandibular fractures, submandibular sialadentitis,3 and intravenous drug injection into neck veins.4
Infection is usually polymicrobial with pathogens consisting of normal mouth flora such as Streptococcus viridans, Staphylococcus aureus, Staphylococcus epidermidis, and anaerobes, particularly Bacteroides.5
Plain radiographs, CT, and magnetic resonance imaging (MRI) of the neck and chest should be obtained to demonstrate the extent of the soft tissue swelling and intrathoracic extension.
Early administration of parenteral antibiotics, careful monitoring of the airway, and surgical drainage if there are any signs of fluctuance or abscess are the cornerstones of treatment.6,7 Initial antibiotic coverage is usually with penicillin, clindamycin, and metronidazole to cover for grampositive cocci and anaerobes.7 Some experts recommend the use of dexamethasone to decrease the inflammation and thus reduce the risk of airway compromise and improve antibiotic penetration.8 Complications, in addition to airway compromise, are mediastinitis, subphrenic abscess, pericardial/pleural effusion, empyema, abscess of the mandible, infection of the carotid sheath, rupture of the carotid artery, and thrombophlebitis of the internal jugular vein.7 The mortality rate exceeded 50% in the preantibiotic era but currently is reported to be fewer than 5%.5
Figure 2. Computerized tomography with contrast of the neck, showing a 1.3 0.9 cm hypodense area posterior to the symphysis of the mandible, likely representing a necrotic lymph node.
The differential of neck masses includes congenital, inflammatory, neoplastic, and traumatic processes. The most common are thyroglossal duct cysts, dermoid cysts, branchial cleft cysts, and cystic hygroma. Thyroglossal duct cysts can be recognized by their midline location between the hyoid bone and the suprasternal notch and by their upward movement with swallowing. Dermoid cysts are also in the midline and contain both solid and cystic components. A branchial cleft cyst feels smooth and fluctuant and is located along the lower anterior border of the sternocleidomastoid muscle. Cystic hygroma is a mutiloculated cyst that is diffuse, soft, and compressible and contains lymphatic fluid.
Lymphadenopathy accounts for the majority of neck masses in children and is most often of infectious etiology, either caused by a reaction to a local or systemic infection or involved in the infection itself. Causes of reactive lymphadenopathy in the cervical area are upper respiratory tract infections, pharyngitis, dental infections, and HIV. Pathogens that directly involve the nodes are mycobacterial organisms, cat scratch disease (Barlonella henselae), toxoplasmosis, and pyogenic bacteria (usually group A beta- hemolytic streptococci and Staphylococcus aureus).
The location of the lymphadenopathy may be helpful for differentiating the site of primary infection. Submandibular nodes are enlarged in diseases involving the oral cavity and the sinuses. Midjugular nodes are associated with hypopharyngeal and laryngeal infection while upperjugular nodes drain infection in the oropharynx and oral cavity. Supraclavicular nodes are usually involved in processes that originate below the clavicles including the lungs.
Sialoadenitis is most often caused by an infection of the parotid or submandibular glands but may result from reactive lymphadenopathy within the gland. Infections typically are associated with obstruction of the salivary flow due to dehydration, salivary stone, or sludge.
Tumors that present as neck masses include thyroid adenoma, lymphoma, thyroid cancer, metastases from squamous cell carcinoma, and adenocarcinoma. Neuroblastoma and leukemia are the most commontumors with cervical lymphadenopathy in patients less than 6 years of age. After 6 years, the most common tumor to present with cervical lymphadenopathy is Hodgkin's lymphoma, followed by non- Hodgkin's lymphoma and rhabdomyosarcoma.
In children, deep neck space infections are caused by acute tonsillitis with involvement of the peritonsillar space, whereas in adults they usually result from dental infections.4
Retropharyngeal abscesses (RPA) are infections in the space anterior to the prevertebral layer of the deep cervical fascia, most commonly seen in patients younger than 5 years of age because they have a greater number of lymph nodes in this region. In a retrospective review of patients with RPA,9 the most common presenting symptom was limitation of neck movement; 45% had limitation of neck extension, 36% had torticollis, and 12% had limited neck flexion. Other common presenting symptoms were the following: neck pain (38%), fever (17%), sore throat (17%), neck mass (16%), and respiratory distress or stridor (5%).
On examination, an asymmetric swelling of the posterior pharyngeal wall is highly suspicious of RPA, but such swelling may be absent in smaller children. RPA can also present as a neck mass. Streptococcus pyogenea, Staphylococcus aureus, and anaerobic bacteria are the most common etiologic agents. Radiographie findings include thickening of the retropharyngeal soft tissue (defined as more than 50% of the width of the vertebral body), loss of the normal cervical lordosis, and air in the retropharyngeal space. CT with contrast is the preferred diagnostic test. A chest radiograph should be performed as the RPA can extend into the mediastinum. Treatment should include parenteral antibiotics that are active against common oral facultative and anaerobic bacteria. The benefit of surgical drainage is determined by the maturity of the infection and the degree of airway compromise. Studies have shown that medical treatment alone can be curative in well over 50% of the patients.10,11 Late complications include rupture of the abscess with aspiration, asphyxiation, or pneumonia; empyema; and mediastinitis.9
1. Hartmann RWJr. Ludwig's angina in children. Am Earn Phys. 1999;60:109-112.
2. Weisengreen HH. Ludwig's angina: historical review and reflections. Ear Nose Throat J. 1986;65:457-461.
3. Kurien M, MathewJ, Job A, et al. Lugwig's angina. Clin Otolaryngol. 1997;22:263-265.
4. Nguyen VD, Potter JL, Hersh-Schick MR. Ludwig angina: uncommon and potientially lethal neck infection. AJNR. 1992;13:215-219.
5. Beasley DJ, Amedee RG. Deep neck space infections. / La State Med Soc. 1995;147:181-184.
6. Srirompotong S, Art-smart T. Ludwig's angina: a clinical review. Eur Arch Oto-Rhino-Laryngol. 2003:1-4.
7. Barakate MS, Hemli (M, Jenscn MJ, et al. Ludwig's angina: report of a case and review of management issues. Ann Otol Rhinol Laryngol. 2001;110:453-456.
8. Busch RF, Shah D. Ludwig's angina: improved treatment. Otolaryngol Head Neck Surg. 1997; 117:S172-S175.
9. Lee SS, Schwartz RH, Bahadori RS. Retropharyngeal abscess: epiglottits of the new millennium. J Pediatr. 2001;138:435-437.
10. Craig FW, Schunk JE. Retropharyngeal abscess in children: clinical presentation, utility of imaging, and current management. Pediatrics. 2003;111:1394-1398.
11. Albright JT, Pransky SM. Nontuberculous mycobacterial infections of the head and neck. Pediatr Clin North Am. 2003;50:503- 514.
Copyright Westminster Publications, Inc. Apr 2005