CASE REPORT
Obstetric anaesthetics are generally aware of possible airway problems in their patients. Laryngeal oedema is present in a small number of pregnancies and may well be asymptomatic, but it can be life-threatening if it complicates intubation or extubation of the trachea. This case is a second reminder that airway difficulties in pregnant patients are not confined to the intubation and extubation periods. Airway obstruction requiring urgent intervention may occur in late pregnancy and after vaginal delivery. ACKNOWLEDGEMENTS I wish to thank Professor D. A. Rocke and Dr. R. Williamson of the Department of Anaesthesia, and Professor J. Moodley of the Department of Obstetrics and Gynaecology for their comments on this manuscript. REFERENCES 1. Brock-Utne JG, Downing JW, Seedat F. Laryngeal oedema associated with pre-eclamptic toxaemia. Anaesthesia 1977; 32:556-558. 2. Mackenzie AI. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1978; 33:271. 3. C. Dobb G. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1983; 33: 167. 4. Spotoft H, Christensen P. Laryngeal oedema accompanying weight gain in pregnancy. Anaesthesia 1981; 36:71.
367
5. Jouppila R, Jouppila P, Hollmen A. Laryngeal oedema as an obstetric anaesthesia complication. Acta Anaesth Scand 1980; 24:97-98. 6. Helier PJ, Scheider EP, Mark GF. Pharyngolaryngeal edema as a presenting symptom in preeclampsia. Obstet Gynaecol1983; 62:523-525. 7. Proctor AJM, White JB. Laryngeal oedema in pregnancy. Anaesthesia 1983; 38: 167. 8. Keeri-Szanto M. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1978; 33:272. 9. Hein HAT. Cardiorespiratory arrest with laryngeal oedema in pregnancy induced hypertension. Can Anaesth Soc 1984; 31:210-212. 10. Salt PJ, Nutboume PA, Park GR, Glazebrook CW. Laryngeal oedema after caesarean section. Anaesthesia 1983; 38:693-694. 11. Rocke DA, Scoones GP. Rapidly progressive laryngeal edema associated with pregnancy aggravated hypertension. Anaesthesia 1992; 47:141-143. 12. Seager SJ, MacDonald R. Laryngeal oedema and pre-eclampsia. Anaesthesia 1980; 35:360-362. 13. Cooper MG, Feeney EM, Joseph M, McGuinness JJ. Local anaesthetic infiltration for caesarean section. Anaesth Intens Care 1989; 17: 198-212. 14. Brimacombe J. Acute pharyngolaryngeal oedema and pre-eclamptic toxaemia. Anaesth Intens Care 1992; 20:97-98. 15. Brown MA. Pregnancy-induced hypertension: Current concepts. Anaesth Intens Care 1989; 17:185-197.
Respiratory Obstruction with Lingual Tonsillitis R. A. BOURNE,* P. A. CAMERONt AND L. DZIUKASt Emergency Department, Alfred Hospital, Melbourne, Victoria Key Words: ANAESTHESIA, COMPLICATIONS, INTUBATION: lingual tonsillitis
Lingual tonsillitis is an uncommon disease which has been reported mostly in association with infectious mononucleosis.I. 5 We report a case of acute bacterial lingual tonsillitis in a previously well woman presenting with impending respiratory obstruction. The differential diagnosis and management are discussed. ·M.B., B.S. (Hons.), Hospital Senior Medical Officer. tF.A.CE.M., Deputy Director Emergency Services. tF.A.CE.M., F.R.A.CP., Director Emergency Services. Address for Reprints: Dr. L. Dziukas, Emergency Department, Alfred Hospital, Commercial Road, Prahran, Victoria 3181, Australia. Accepted for publication September 30, 1991 Anaesthesia and Intensive Care, Vol. 20, No. 3, August, 1992
CASE REPORT A previously well 51-year-old female presented to the Emergency Department with a 24-hour history of malaise, fever, sore throat and gradually increasing respiratory difficulty associated with difficulty in speaking. She was not taking any medications, and was a nonsmoker. There was no past history of palatine tonsillectomy. On examination she looked unwell and her vital signs were temperature 39.2°C, pulse rate 100 beats/minute, blood pressure 120/60 mmHg and respiratory rate 20/minute. She was sitting upright, was not cyanosed and was not using her accessory muscles of respiration.
368
R. A.
BOURNE ET AL.
FIGURE I.-Lateral soft tissue X-ray of the neck.
A provisional diagnosis of lingual tonsillitis was made. Arterial blood gases taken with the patient breathing room air revealed the following: pH 7.46, P0 2 73 mmHg, Peo2 30 mmHg, HC03 22 mmolll O 2 saturation 96%. The white cell count was 14.8 X 10 9/1 due predominantly to a neutrophilia of 12.9 X 109/1 (without toxic changes). Blood cultures done at the same time failed to isolate an organism. A throat swab grew a mixtue of normal oral flora. Epstein BaIT virus serology was not considered at the time of presentation. The patient was then treated with intravenous ceftriaxone and chloramphenicol. These were continued for one week. An examination under anaesthesia was then performed in the operating theatre with a surgeon present to create a surgical airway if required. Induction of anaesthesia was with halothane and oxygen, and once anaesthesia was adequate the vocal cords were visualised by direct laryngoscopy. Following this a 1.5 mg/kg dose ofsuxamethonium was given intravenously and the trachea initially intubated orally. Following this a 7.0 mm cuffed PVC endotracheal tube was passed nasally and exchanged for the oral tube. Histology of multiple biopsies from the base of the tongue showed a marked inflammatory cell infiltrate with fragments of tonsillar tissue. Culture of the biopsies grew a pure culture of Streptococcus pyogenes which was sensitive to penicillin, erythromycin and tetracycline. She was then transferred to the Intensive Care Unit where there was a slow resolution in the swelling at the base of the tongue. Extubation was possible five days after intubation. Direct laryngoscopy at this time revealed some swelling of the aryepiglottic folds only. At outpatient follow up two weeks later she remained well.
Her neck was diffusely swollen and tender to palpation. There was no discrete lymphadenopathy and the trachea was midline. The jugular veins could not be assessed. Initial inspection of the oropharynx revealed no pooling of saliva but the base of the tongue was noted to be grossly swollen and beefy red in colour with no exudate. There was no clinical evidence of infection in the teeth, gums or palatine tonsils. Auscultation of the chest revealed good symmetrical air entry with no expiratory wheeze or stridor. Two heart sounds were readily audible. but no bruits were present. Physical examination of the DISCUSSION abdomen and periphery failed to detect any further Lingual tonsillitis is an uncommon condition. It abnormality. should be considered however in the differential A lateral soft tissue X-ray of the neck was then diagnosis of a febrile illness presenting with performed demonstrating swelling of the base of symptoms and signs of upper airway obstruction. the tongue encroaching on the upper airway Alternative diagnosis in the febrile patient would (Figure I). include pharyngitis, epiglottitis, Ludwig's angina or A fibreoptic laryngoscopy was performed by the deep neck infections. Epiglottitis and Ludwig's Ear Nose and Throat Registrar confirming the angina were considered as possible causes but X-ray impressions. The epiglottis was not enlarged excluded after physical examination. or inflamed but was pushed back towards the Lingual tonsillitis has been described in laryngeal opening. The arytenoids and posterior association with infectious mononucleosisl- 5 parts of the vocal cords were seen and noted to be usually in the setting of previous palatine normal and mobile. The patency of the tonsillectomy and adenoidectomy. 6-11 It is assumed oropharyngeal airway was estimated to be 50% of that the tonsillitis involves tissue in Waldeyer's ring that has undergone compensatory hypertrophy normal.
Anaesthesia and Intensive Care, Vo!. 20, No. 3, August, 1992
369
CASE REPORT
following these surgical procedures. 6 However the difficulty of making a diagnosis of chronic lingual tonsillitis and its common association with palatine tonsillitis leads one to suspect that many patients who undergo palatine tonsillectomy have preexisting chronic lingual tonsillitis. 6 ,10-12,14 Subsequent acute lingual tonsillitis may simply reflect progression of the existing disease. Lingual tonsillar hypertrophy is a recognised cause of respiratory obstruction, both acutely and chronically where it has been described as a correctable cause of sleep apnoea syndrome. 7,8,14 Stridor is rare 9- 11 and this may be an important sign in distinguishing acute lingual tonsillitis from acute epiglottitis. Of those cases reported in the literature most have been successfully treated with antibiotics, with surgical intervention being restricted to drainage of an associated abscess or tracheostomy where airway integrity has been an issue. 12,13 The organisms isolated from throat swabs in previous case reports oflingual tonsillitis are mixed gram positive aerobic and anaerobic organisms representing the commensal oral flora. We isolated Streptococcus pyogenes, the classic organism of acute palatine tonsillitis, from biopsy material. A throat swab at the same time showed mixed oral flora only. There is no mention previously in the literature of pure culture of Streptococcus pyogenes being isolated in this condition. It is tempting to postulate, as Elfman did, 6 that the most common bacterium producing lingual tonsillitis is the same as that causing palatine tonsillitis, i.e. Streptococcus pyogenes. The finding of mixed bacterial growth after culture of throat swabs probably reflects the difficulty of obtaining proper cultures from the back of the throat, or may indicate that the causative bacteria is located in the deeper tissues. If Streptococcus pyogenes is the main bacterial species causing lingual tonsillitis, then this would make penicillin the antibiotic of choice. The decision to intubate this patient electively was made because of the rapid progression of the disease with evidence of significant airway compromise. The likely response to antibiotic treatment was unpredictable, and rapid improvement in airway patency could not be guaranteed. It is not clear from other case reports how rapidly the obstruction resolves once antibiotic treatment is begun. As the vocal cords were readily visualised by fibreoptic laryngoscopy, it was decided to progress rapidly to intubation under direct vision. If a conservative approach to management had been adopted, there would have been a risk of a difficult emergency cricothyroidotomy or tracheostomy. Our patient was intubated for five days because Anaesthesia and Intensive Care, Vol. 20, No. 3. August, 1992
of slow resolution of the swelling at the base of the tongue. We felt this supported our clinical decision to intubate this patient electively rather than rely on resolution with initiation of antibiotics. In summary, lingual tonsillitis should be considered in the differential diagnosis of acute upper airway obstruction. The initial consideration should be to secure the airway via endotracheal intubation or a surgical airway if this is not possible. Any antibiotic regimen should include penicillin as the likely causative organism is Streptococcus pyogenes. REFERENCES
I. Harel G, Josephson JS. Infectious mononucleosis complicated by lingual tonsillitis. J Laryngol Otol 1990; 104:651-653. 2. Penman HG. Fatal infectious mononucleosis: a critical review. J Clin Path 1970; 23:765-771. 3. Rubuzzi DD. Otolaryngologic aspects of infectious mononucleosis. J Otolaryng 1973; 2:329-336. 4. Synderman NL, Stool SE. Management of airway obstruction in children with infectious mononucleosis. Otolaryngol Head Neck Surg 1982; 90: 168-1 70. 5. Wolfe JA, Rowe LD. Upper airway obstruction in infectious mononucleosis. Ann Otol, Rhinol Laryngol 1980; 9:430-433. 6. Elfman LK. Lingual tonsils. Laryngoscope 1949; 59:1016-1025. 7. Olsen KD, Suh KW, Staats BA. Surgically correctable causes of sleep apnoea syndrome. Otolaryngol Head Neck Surg 1981; 89:726-731. 8. Phillips DE, Rogers JH. Downs Syndrome with lingual tonsil hypertrophy producing sleep apnoea. J Laryngol Otol 1988; 102(11):1054-1055. 9. Joseph M, Reardon E, Goodman M. Lingual tonsillectomy: a treatment for inflammatory lesions of the lingual tonsil. Laryngoscope 1984; 94: 174-184. 10. Golding Wood DG, Whittet HB. The lingual tonsil. A neglected symptomatic structure. J Laryngol Otol 1989; 103:922-925. 11. Krespi YP, Har El G, Levine TM, Ossoff RH, Wurster CF, Paulsen JW. Laser lingual tonsillectomy. Laryngoscope 1989; 99:131-135. 12. Johnson CA, Mehdiabadi RJ, RuffT. Infection and hypertrophy of the lingual tonsil as a cause of airway obstruction. Texas Medicine 1986; 82:29-31. 13. Dindzans U, Irvine BWH, Hayden RE. An unusual case of airway obstruction. Otolaryngol 1984; 13:252-254. 14. Fitzgerald P, O'Connell D. Massive hypertrophy of the lingual tonsils an unusual cause of dysphagia. Br J Radiol 1987; 60:505-506. 15. Fontanarosa PB, Polsky SS, Goldman GE. Adult epiglottitis. J Emerg Med 1989; 7:223-231. 16. Rannery MJ. Radiographs in the diagnosis of epiglottitis. Ann Emerg Med 1991; 20:438-439. 17. Rapkin RH. The diagnosis of epiglottitis: Simplicity and reliability of radiographs of the neck in the differential diagnosis of the croup syndrome. J Pediatr 1972; 80:96-98.
Obstetric anaesthetics are generally aware of possible airway problems in their patients. Laryngeal oedema is present in a small number of pregnancies and may well be asymptomatic, but it can be life-threatening if it complicates intubation or extubation of the trachea. This case is a second reminder that airway difficulties in pregnant patients are not confined to the intubation and extubation periods. Airway obstruction requiring urgent intervention may occur in late pregnancy and after vaginal delivery. ACKNOWLEDGEMENTS I wish to thank Professor D. A. Rocke and Dr. R. Williamson of the Department of Anaesthesia, and Professor J. Moodley of the Department of Obstetrics and Gynaecology for their comments on this manuscript. REFERENCES 1. Brock-Utne JG, Downing JW, Seedat F. Laryngeal oedema associated with pre-eclamptic toxaemia. Anaesthesia 1977; 32:556-558. 2. Mackenzie AI. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1978; 33:271. 3. C. Dobb G. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1983; 33: 167. 4. Spotoft H, Christensen P. Laryngeal oedema accompanying weight gain in pregnancy. Anaesthesia 1981; 36:71.
367
5. Jouppila R, Jouppila P, Hollmen A. Laryngeal oedema as an obstetric anaesthesia complication. Acta Anaesth Scand 1980; 24:97-98. 6. Helier PJ, Scheider EP, Mark GF. Pharyngolaryngeal edema as a presenting symptom in preeclampsia. Obstet Gynaecol1983; 62:523-525. 7. Proctor AJM, White JB. Laryngeal oedema in pregnancy. Anaesthesia 1983; 38: 167. 8. Keeri-Szanto M. Laryngeal oedema complicating obstetric anaesthesia. Anaesthesia 1978; 33:272. 9. Hein HAT. Cardiorespiratory arrest with laryngeal oedema in pregnancy induced hypertension. Can Anaesth Soc 1984; 31:210-212. 10. Salt PJ, Nutboume PA, Park GR, Glazebrook CW. Laryngeal oedema after caesarean section. Anaesthesia 1983; 38:693-694. 11. Rocke DA, Scoones GP. Rapidly progressive laryngeal edema associated with pregnancy aggravated hypertension. Anaesthesia 1992; 47:141-143. 12. Seager SJ, MacDonald R. Laryngeal oedema and pre-eclampsia. Anaesthesia 1980; 35:360-362. 13. Cooper MG, Feeney EM, Joseph M, McGuinness JJ. Local anaesthetic infiltration for caesarean section. Anaesth Intens Care 1989; 17: 198-212. 14. Brimacombe J. Acute pharyngolaryngeal oedema and pre-eclamptic toxaemia. Anaesth Intens Care 1992; 20:97-98. 15. Brown MA. Pregnancy-induced hypertension: Current concepts. Anaesth Intens Care 1989; 17:185-197.
Respiratory Obstruction with Lingual Tonsillitis R. A. BOURNE,* P. A. CAMERONt AND L. DZIUKASt Emergency Department, Alfred Hospital, Melbourne, Victoria Key Words: ANAESTHESIA, COMPLICATIONS, INTUBATION: lingual tonsillitis
Lingual tonsillitis is an uncommon disease which has been reported mostly in association with infectious mononucleosis.I. 5 We report a case of acute bacterial lingual tonsillitis in a previously well woman presenting with impending respiratory obstruction. The differential diagnosis and management are discussed. ·M.B., B.S. (Hons.), Hospital Senior Medical Officer. tF.A.CE.M., Deputy Director Emergency Services. tF.A.CE.M., F.R.A.CP., Director Emergency Services. Address for Reprints: Dr. L. Dziukas, Emergency Department, Alfred Hospital, Commercial Road, Prahran, Victoria 3181, Australia. Accepted for publication September 30, 1991 Anaesthesia and Intensive Care, Vol. 20, No. 3, August, 1992
CASE REPORT A previously well 51-year-old female presented to the Emergency Department with a 24-hour history of malaise, fever, sore throat and gradually increasing respiratory difficulty associated with difficulty in speaking. She was not taking any medications, and was a nonsmoker. There was no past history of palatine tonsillectomy. On examination she looked unwell and her vital signs were temperature 39.2°C, pulse rate 100 beats/minute, blood pressure 120/60 mmHg and respiratory rate 20/minute. She was sitting upright, was not cyanosed and was not using her accessory muscles of respiration.
368
R. A.
BOURNE ET AL.
FIGURE I.-Lateral soft tissue X-ray of the neck.
A provisional diagnosis of lingual tonsillitis was made. Arterial blood gases taken with the patient breathing room air revealed the following: pH 7.46, P0 2 73 mmHg, Peo2 30 mmHg, HC03 22 mmolll O 2 saturation 96%. The white cell count was 14.8 X 10 9/1 due predominantly to a neutrophilia of 12.9 X 109/1 (without toxic changes). Blood cultures done at the same time failed to isolate an organism. A throat swab grew a mixtue of normal oral flora. Epstein BaIT virus serology was not considered at the time of presentation. The patient was then treated with intravenous ceftriaxone and chloramphenicol. These were continued for one week. An examination under anaesthesia was then performed in the operating theatre with a surgeon present to create a surgical airway if required. Induction of anaesthesia was with halothane and oxygen, and once anaesthesia was adequate the vocal cords were visualised by direct laryngoscopy. Following this a 1.5 mg/kg dose ofsuxamethonium was given intravenously and the trachea initially intubated orally. Following this a 7.0 mm cuffed PVC endotracheal tube was passed nasally and exchanged for the oral tube. Histology of multiple biopsies from the base of the tongue showed a marked inflammatory cell infiltrate with fragments of tonsillar tissue. Culture of the biopsies grew a pure culture of Streptococcus pyogenes which was sensitive to penicillin, erythromycin and tetracycline. She was then transferred to the Intensive Care Unit where there was a slow resolution in the swelling at the base of the tongue. Extubation was possible five days after intubation. Direct laryngoscopy at this time revealed some swelling of the aryepiglottic folds only. At outpatient follow up two weeks later she remained well.
Her neck was diffusely swollen and tender to palpation. There was no discrete lymphadenopathy and the trachea was midline. The jugular veins could not be assessed. Initial inspection of the oropharynx revealed no pooling of saliva but the base of the tongue was noted to be grossly swollen and beefy red in colour with no exudate. There was no clinical evidence of infection in the teeth, gums or palatine tonsils. Auscultation of the chest revealed good symmetrical air entry with no expiratory wheeze or stridor. Two heart sounds were readily audible. but no bruits were present. Physical examination of the DISCUSSION abdomen and periphery failed to detect any further Lingual tonsillitis is an uncommon condition. It abnormality. should be considered however in the differential A lateral soft tissue X-ray of the neck was then diagnosis of a febrile illness presenting with performed demonstrating swelling of the base of symptoms and signs of upper airway obstruction. the tongue encroaching on the upper airway Alternative diagnosis in the febrile patient would (Figure I). include pharyngitis, epiglottitis, Ludwig's angina or A fibreoptic laryngoscopy was performed by the deep neck infections. Epiglottitis and Ludwig's Ear Nose and Throat Registrar confirming the angina were considered as possible causes but X-ray impressions. The epiglottis was not enlarged excluded after physical examination. or inflamed but was pushed back towards the Lingual tonsillitis has been described in laryngeal opening. The arytenoids and posterior association with infectious mononucleosisl- 5 parts of the vocal cords were seen and noted to be usually in the setting of previous palatine normal and mobile. The patency of the tonsillectomy and adenoidectomy. 6-11 It is assumed oropharyngeal airway was estimated to be 50% of that the tonsillitis involves tissue in Waldeyer's ring that has undergone compensatory hypertrophy normal.
Anaesthesia and Intensive Care, Vo!. 20, No. 3, August, 1992
369
CASE REPORT
following these surgical procedures. 6 However the difficulty of making a diagnosis of chronic lingual tonsillitis and its common association with palatine tonsillitis leads one to suspect that many patients who undergo palatine tonsillectomy have preexisting chronic lingual tonsillitis. 6 ,10-12,14 Subsequent acute lingual tonsillitis may simply reflect progression of the existing disease. Lingual tonsillar hypertrophy is a recognised cause of respiratory obstruction, both acutely and chronically where it has been described as a correctable cause of sleep apnoea syndrome. 7,8,14 Stridor is rare 9- 11 and this may be an important sign in distinguishing acute lingual tonsillitis from acute epiglottitis. Of those cases reported in the literature most have been successfully treated with antibiotics, with surgical intervention being restricted to drainage of an associated abscess or tracheostomy where airway integrity has been an issue. 12,13 The organisms isolated from throat swabs in previous case reports oflingual tonsillitis are mixed gram positive aerobic and anaerobic organisms representing the commensal oral flora. We isolated Streptococcus pyogenes, the classic organism of acute palatine tonsillitis, from biopsy material. A throat swab at the same time showed mixed oral flora only. There is no mention previously in the literature of pure culture of Streptococcus pyogenes being isolated in this condition. It is tempting to postulate, as Elfman did, 6 that the most common bacterium producing lingual tonsillitis is the same as that causing palatine tonsillitis, i.e. Streptococcus pyogenes. The finding of mixed bacterial growth after culture of throat swabs probably reflects the difficulty of obtaining proper cultures from the back of the throat, or may indicate that the causative bacteria is located in the deeper tissues. If Streptococcus pyogenes is the main bacterial species causing lingual tonsillitis, then this would make penicillin the antibiotic of choice. The decision to intubate this patient electively was made because of the rapid progression of the disease with evidence of significant airway compromise. The likely response to antibiotic treatment was unpredictable, and rapid improvement in airway patency could not be guaranteed. It is not clear from other case reports how rapidly the obstruction resolves once antibiotic treatment is begun. As the vocal cords were readily visualised by fibreoptic laryngoscopy, it was decided to progress rapidly to intubation under direct vision. If a conservative approach to management had been adopted, there would have been a risk of a difficult emergency cricothyroidotomy or tracheostomy. Our patient was intubated for five days because Anaesthesia and Intensive Care, Vol. 20, No. 3. August, 1992
of slow resolution of the swelling at the base of the tongue. We felt this supported our clinical decision to intubate this patient electively rather than rely on resolution with initiation of antibiotics. In summary, lingual tonsillitis should be considered in the differential diagnosis of acute upper airway obstruction. The initial consideration should be to secure the airway via endotracheal intubation or a surgical airway if this is not possible. Any antibiotic regimen should include penicillin as the likely causative organism is Streptococcus pyogenes. REFERENCES
I. Harel G, Josephson JS. Infectious mononucleosis complicated by lingual tonsillitis. J Laryngol Otol 1990; 104:651-653. 2. Penman HG. Fatal infectious mononucleosis: a critical review. J Clin Path 1970; 23:765-771. 3. Rubuzzi DD. Otolaryngologic aspects of infectious mononucleosis. J Otolaryng 1973; 2:329-336. 4. Synderman NL, Stool SE. Management of airway obstruction in children with infectious mononucleosis. Otolaryngol Head Neck Surg 1982; 90: 168-1 70. 5. Wolfe JA, Rowe LD. Upper airway obstruction in infectious mononucleosis. Ann Otol, Rhinol Laryngol 1980; 9:430-433. 6. Elfman LK. Lingual tonsils. Laryngoscope 1949; 59:1016-1025. 7. Olsen KD, Suh KW, Staats BA. Surgically correctable causes of sleep apnoea syndrome. Otolaryngol Head Neck Surg 1981; 89:726-731. 8. Phillips DE, Rogers JH. Downs Syndrome with lingual tonsil hypertrophy producing sleep apnoea. J Laryngol Otol 1988; 102(11):1054-1055. 9. Joseph M, Reardon E, Goodman M. Lingual tonsillectomy: a treatment for inflammatory lesions of the lingual tonsil. Laryngoscope 1984; 94: 174-184. 10. Golding Wood DG, Whittet HB. The lingual tonsil. A neglected symptomatic structure. J Laryngol Otol 1989; 103:922-925. 11. Krespi YP, Har El G, Levine TM, Ossoff RH, Wurster CF, Paulsen JW. Laser lingual tonsillectomy. Laryngoscope 1989; 99:131-135. 12. Johnson CA, Mehdiabadi RJ, RuffT. Infection and hypertrophy of the lingual tonsil as a cause of airway obstruction. Texas Medicine 1986; 82:29-31. 13. Dindzans U, Irvine BWH, Hayden RE. An unusual case of airway obstruction. Otolaryngol 1984; 13:252-254. 14. Fitzgerald P, O'Connell D. Massive hypertrophy of the lingual tonsils an unusual cause of dysphagia. Br J Radiol 1987; 60:505-506. 15. Fontanarosa PB, Polsky SS, Goldman GE. Adult epiglottitis. J Emerg Med 1989; 7:223-231. 16. Rannery MJ. Radiographs in the diagnosis of epiglottitis. Ann Emerg Med 1991; 20:438-439. 17. Rapkin RH. The diagnosis of epiglottitis: Simplicity and reliability of radiographs of the neck in the differential diagnosis of the croup syndrome. J Pediatr 1972; 80:96-98.
