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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 19, Number 2 • March 2001

to light. There was fight-sided hyperreflexia with unilateral Babinski's sign. There was left sided facial droop, and no fight-sided motor or sensory activity was appreciated. Administration of 30 mg/kg of methylprednisolone, followed by an infusion of 5.4 mg/kg/hr was given intravenously. Cervical spine radiographs were obtained which were interpreted as normal. Brain computed tomography (CT) was normal. A magnetic resonance angiography (MRA) was obtained, revealing a left pontine infarct with vertebral artery dissection. Several weeks after the incident, the patient began to regain only minimal motor activity in her fight arm. She is now in the care of a rehabilitation facility, and her neurologic deficits are only minimally improved. The technique of spinal adjustment initially used was a high cervical, high-velocity-low amplitude method (sudden thrust delivered to involved vertebrae). The occurrence of neurologic symptoms after cervical manipulation is an uncommon event in relation to the large number of manipulations performed. The risk of neurologic complications after spinal manipulation is as low as 1 case per million treatments. 2 There are only 2 cases of vertebral or basilar artery injury associated with chiropractic manipulation in the emergency medicine literature, and neither resulted in a stroke or caused permanent neurologic sequelae. 3,4 The most common site of injury to the vertebral artery appears to be the atlantoaxial joint where the artery changes from a vertical to a horizontal course. Rotating and hyperextending the neck may produce a sheafing force on the atlantoaxial joint producing intimal tearing, dissection, and thrombus formation.5 Conditions such as a vertebral bony abnormality, symptoms of vertebrobasilar insufficiency, cervical spondlyosis, myelopathy, hypermobility syndrome, infection, malignancy, and anticoagulation therapy are absolute contraindications for chiropractic intervention. 5 These conditions need to be carefully screened for before manipulation. In addition, a careful history should include the presence or absence of recent manipulations when faced with a patient with new onset vertigo. The patient in our case discussion had no known contraindications to spinal manipulation. Even admitting chiropractic's low incidence of injury, this article is important in divulging the vulnerability an average person has to such interventions. Patients, chiropractors, and physicians should all be aware of the potentially devastating neurologic outcomes possible from chiropractic manipulations. DAVID SIEGEL, MD TINA NEIDERS, MD Madigan Army Medical Center Tacoma, WA

References 1. Horn SW: The "Locked-In syndrome following chiropractic manipulation of the cervical spine. Ann Emerg Met 1983;12:648-50 2. Hosek RS, Schram SB, Silverman H, et al: Cervical manipulation. JAMA 1981 ;245:922 3. Showalter W, Esekogwu V, Newton K, et al: Vertebral artery dissection. Acad Emerg Met 1997;4:991-5 4. Cortazzo JM, Tom KB: Vertebral artery dissection following chiropractic manipulation. Am J Emerg Met 1998;16:619-20

5. Lee KP, Carlini WG, McCormick GF, et al: Neurologic complications following chiropractic manipulation: A survey of California neurologist. Neurology 1995;45:1213-5

INADVERTENT ADMINISTRATION OF NEBULIZED ACETIC ACID To the Editor:--Acetic acid ( C H 3 COOH) has many uses, including: a manufacturing component of various acetates and plastics, a preservative in foods, a solvent for gums and oils, and a pharmaceutical acidifier.1 Inhalation of acetic acid has caused reactive airway disease, pulmonary edema, pneumonitis, asthma exacerbation, and other respiratory problems. 2-4 We report a case where inhaled acetic acid produced relatively significant respiratory effects (respiratory acidosis, hypercapnea, tachypnea, and increased respiratory effort) in a 10-month old girl. The child was initially hospitalized for respiratory syncytial virus (RSV) pneumonia and started on ceftriaxone 160mg IV every 6 hours, albuterol nebulization treatments every 4 hours, and supplemental oxygen. Approximately 12 hours after admission, one of her albuterol treatments was inadvertently diluted in a 1:1 ratio, with 5% acetic acid, instead of the intended 0.9% sodium chloride diluent and administered via nebulizer for less than 30 minutes at which time the error was discovered.. The acetic acid solution was located in the patient's room on a bedside cart. It was intended to be used to cleanse and disinfect her roommate's tracheotomy site. After the respiratory therapist inadvertently administered the albuterol treatment mixed with acetic acid, the child developed an immediate cough, tachypnea, and a mild respiratory acidosis. Shortly after the accident, her arterial blood gas (ABG): pH=7.35, pCOe=59.8 mgHg, pOe=66.9 mmHg, HCO3=32.3 mmol/L, base excess=+4.8, and 02 saturation=92.2% on FiO2= 100% and continuous albuterol nebulization treatments. On her admission ABG 12 hours before this error her pCO 2 was 42 mmHg. Over the 12 hours, she received continuous albuterol nebulizer treatments while her respiratory rate increased from 40 to 65 per minute and became more labored. Her repeat ABG, 6 hours after the incident showed pH=7.30, pCO2=67.4 mmHg, pO~=71.9 mmHg, HCO3=32.9 m m o l / L base excess= +3.8, and 02 saturation=92.5% on 100% oxygen. Her vital signs at this time were: blood pressure 111/60 mmHg, pulse 143 beats/min, respiratory rate 40 breaths/rain, and a temperature of 97.2°F. The child appeared to have labored breathing and was in obvious respiratory discomfort. Seventeen hours after the incident her vital signs were: blood pressure 99/60 mmHg, pulse 159beats/rain, respiratory rate 60 breaths/min, and a temperature of 98.6°F. She required frequent suctioning of secretions, with no significant increase after the incident. Also, bilateral rales and rhonchi were unchanged from baseline. All chest radiographs obtained were significant for RSV pneumonia and showed no new infiltrates after the accident. The next morning, she became more playful and alert, the albuterol administration was changed to every 2 hours, and her vital signs were: blood pressure 118/80 mmHg, pulse 147 beats/rain, temperature of 98.0°F, and her respiratory rate decreased back to 40 breaths/min while 02 saturation on 30% oxygen was 95%. The child developed transient hypercapnea, cough, respiratory difficulty, and increased respiratory effort after the inadvertent administration of nebulized acetic acid. She was treated for approximately 24 hours with 100% oxygen and intermittent administration of nebulized albuterol. Her acute symptoms resolved within 36 hours of the accident. No metabolic consequences were seen, probably showing a lack of systemic absorption. Treatment consisted of oxygen and bronchodilators; resolution was complete

Copyright © 2001 by W.B. Saunters Company 0735-6757/01/1902-0024535.00/0 doi:l 0.1053/ajem.2001.21309

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within 36 hours with no permanent sequelae noted. Subsequently, she was discharged home when the RSV pneumonia resolved. This case shows that inhalation with a significant concentration of acetic acid through nebulization can be treated with conventional supportive respiratory therapy. TODD SIGG, PHARMD ERIN PALLASCH, PHARMD JERROLD B. LEIKIN,MD Illinois Poison Center and Rush-Presbyterian-St. Medical Center

Luke's

Chicago, IL

References 1. The Merck Index (ed 11), Monograph 47. Rahway, NJ, Merck & Co., Inc, 1989 2. Kivity S, Fireman E, Lerman Y: Late asthmatic response to inhaled glacial acetic acid. Thorax 1994;49:727-8 3. Shimizu T, Mochizuki H, Tokuyama K, et al: Relationship between the acid-induced cough response and airway responsiveness and obstruction in children with asthma. Thorax 1996;51:284-7 4. Mochizuki H, Shimizu T, Maeda S, et al: Relationship between ultrasonically nebulized distilled water-induced bronchoconstriction and acetic acid-induced cough in asthmatic children. J Allergy Clin Immunol 1995;96:193-9

LINGUAL TONSILLITIS: AN UNUSUAL PRESENTATION OF MONONUCLEOSIS To the E d i t o r : - - W e recently saw a 12-year-old girl in our emergency department (ED) with a week's complaint of a sore throat preceded by a dry cough over the antecedent 3 weeks. Oropharyngeal symptoms had worsened on the day of presentation to the point that the child was having increased difficulty swallowing liquids. The prior medical history was unremarkable, immunizations were up-to-date and the patient was taking no medications. Vital signs were: temperature 37°C (oral), pulse 100 beats/min and regular, respirations 20 breaths/min, blood pressure 110/70 mmHg, and oxygen saturation 100% (ambient oxygen). The head and neck examination was remarkable for multiple tender lymph nodes in the posterior cervical triangle region bilaterally and mildly muffled phonation, although articulation was normal. The oropharyngeal examination revealed small palatine tonsils and no evidence of erythema or exudates. The lungs were clear to auscultation and the heart sounds were normal The abdomen was nontender and organomegaly was not palpated. No skin lesions were noted. Hemogram parameters included: hemoglobin 14.3 grams, hematocrit 41.4%, white blood cell count 5,400cc 3 (39% polymorphonuclear leukocytes, 5% band forms, 49% lymphocytes with a moderate amount of atypical lymphocytes, 6% monocytes) and platelet count of 154,00cc 3. Serum chemistries were normal and a heterophile antibody screen for mononucleosis was positive. Throat cultures were not obtained. A lateral radiograph of the neck was interpreted by attending staff radiologists as showing adenoidal prominence and swelling at the base of the tongue, causing some effacement of the valleculae and consistent with lingual tonsil enlargement. The epiglottis was of normal size and shape (Fig 1). The patient was able to tolerate small amounts of liquids in the ED and was started on prednisolone syrup (2 mg/kg/day in 2 divided doses) tapered over a 3-week period. On telephone follow-up at 3

Copyright © 2001 by W.B. Saunders Company 0735-6757/01/1902-0025535.00/0 doi:10.1053/ajem.2001.21301

FIGURE 1. Lateral radiograph of the neck showing adenoidal and lingual tonsil enlargement.

days, there was symptomatic improvement and increased alimentation. At 2-week and 1-month follow-up, the patient was asymptomatic. Infectious mononucleosis (IM) is an acute viral disease classically defined by the clinical triad of fever, lymphadenopathy, and pharyngitis, associated with laboratory findings of transient heterophile antibodies and atypical lymphocytes. 1 The causative agent is the Epstein-Barr virus (EBV), a B-lymphotropic herpesvirus with worldwide distribution. 1,2 Severe pharyngitis is the most common reason for medical evaluation of mononucleosis. 1 Lingual, pharyngeal (adenoids), and palatine tonsils, known collectively as Waldeyer's ring, are masses of similar lymphoid tissue. 3 The adenoids and palatine tonsils gradually atrophy after puberty, but the lingual tonsils (LT) persist into adulthood. 4.5 Located at the base of the tongue and extending downward from the circumvallate papillae to the root of the epiglottis, LT may become enlarged or hypertrophied as a result of numerous processes (Table 1). 6-13 Radiographically, the nondiseased LT can manifest a range of sizes and appearance, and no criteria exist regarding the normal limits of these parameters.14 However, radiographic findings of distal lingual encroachment on the epiglottis, effacement of the vallecula and impingement on the aryepiglottic folds are suggestive of LT enlargement. 14 Because of their distal pharyngeal location, acute inflammation of LT can cause moderate-to-severe dysphagia, odynophagia, and speech alteration, as noted in our patient. 8.1° Using a computerized search (MEDLINE) of the medical literature, spanning the past 35 years, we were unable to find any report of uncomplicated lingual tonsillitis as a presentation of 1M. One case of bacterial lingual tonsillitis in association with a concomitant IM has been reported in a patient who presented febrile with