International Journal of Pediatric Otorhinolaryngology, 24 (1992) 8.1-W $3 1992 Elsevier Science Publishers B.V. All rights reserved 0165-5876/92/$0.5.00
PEDOT
83
00785
Urgent adenotonsillectomy for upper airway obstruction * Frank G. Shechtman,
Pi Tang Lit-t and Robert
L. Pincus
Department of Otoiaryngology - Head and Neck Surgery, New York Medical College Affiliated Hospitals Program, New York E.ve and Ear Infirmary, New York. NY 10003 (U.S.A.)
(Revised
Kq words: Urgent
(Received 18 June 1991) versions received 25 June and 7 August (Accepted 12 August 199 I )
adenotonsillectomy;
Chronic
upper
airway obstruction:
199 1)
Car pulmonale
Abstract
Adenotonsillar hypertrophy has been documented to cause chronic upper airway obstruction resulting in cardiopulmonary sequelae in children. It has been less recognized that long-term adenotonsillar hypertrophy may additionally cause acute, life-threatening airway obstruction. A review of 5000 adenotonsillectomies performed at 3 New York Medical College affiliated hospitals from 1982 to 1989 showed 6 pediatric patients with progressive upper airway obstruction severe enough to necessitate intubation in the emergency room or operating room, and subsequent urgent adenotonsillectomy after cardiorespiratory stabilization. Patients were monitored in the ICU with pre- and postoperative blood gases. Observations of cyanosis, car pulmonale, and use of accessory respiratory muscles were carefully recorded. This study illustrates that life-threatening upper airway obstruction may be due to chronic adenotonsillar enlargement and require treatment by urgent adenotonsillectomy.
Introduction
Adenotonsillectomy is still among the most commonly performed operations on children in the United States [3,141 but the increasingly cost-conscious environ-
* Presented December
;at the Sixteenth Annual Meeting 1988, New York City, NY.
Society
for Ear, Nose and Throat
C‘orrrspondence to: F.G. Shechtman, Dept. of ORL - Head College, 310 East 14th Street, New York, NY 10003. U.S.A.
and Neck
Surgery.
Advances
in Children.
New York
Medical
84
ment has placed a great deal of scrutiny on surgeons performing it. The number of tonsillectomies, adenoidectomies, and adenotonsillectomies performed in nonfederal, short-stay hospitals in 1971 was 1,019,OOO. By 1987 this number had declined to 259,000 representing a reduction of 80.7% over the 16-year period [14]. Several reasons for this include better antibiotic therapies, and greater understanding of both the natural history of the disease, and the role Waldeyer’s ring plays in host defense immunity [l]. Over two decades ago several papers reported the death of pediatric patients due to adenotonsillar hypertrophy exacerbated by an acute infection [2,91. In 1982, Grundfast reported the reluctance of primary care physicians to refer patients for adenotonsillectomy and an increasing trend for children to develop the sequelae of adenotonsillar hypertrophy [S]. This paper stimulated a medical communication in JAMA describing Grundfast’s work and identifying characteristics of children at risk for developing insidious airway obstruction from adenotonsillar hypertrophy
[61. Fortunately studies such as those carried out by Bluestone et al. [3] have provided well-researched concepts as to indications for the operative procedure. However, as the medical community has decreased the number of referrals for adenotonsillectomy, there has been increasing evidence that adenotonsillar hypertrophy can result in end-stage sleep apnea [7,12,13] and cardiorespiratory distress syndrome [11,16]. As a result, many elegant laboratory studies including polysomnography, pulse oximetry, and computer-aided analysis of respiratory flow and sounds have been developed in the hope of identifying patients before they become irreversibly damaged [15]. A review in 1987 tabulated over 100 cases reported in the literature of cardiorespiratory distress secondary to adenotonsillar hypertrophy [17]. In 1988, Brown et al. [51 reviewed 11 cases of car pulmonale secondary to tonsil and adenoid hypertrophy. These patients presented with a wide spectrum of disease ranging from mild distress to respiratory arrest 36 h after intervention. The authors underscore the importance of screening for car pulmonale and pre- and postoperative ICU management of these patients. The purpose of this paper is to evaluate the records of pediatric patients who underwent emergency intubation and urgent adenotonsillectomy at two city hospitals and one private institution during the period 1982-1989.
Materials
and methods
Over 5000 adenotonsillectomy operations were performed at 3 New York Medical College affiliated hospitals during 1982-1989. Six patients were identified who presented with severe, life-threatening upper airway obstruction which necessitated emergency airway management, cardiac stabilization, and urgent adenotonsillectomy. The patients were evaluated by clinical history and physical examination. Laboratory studies included routine chemistries, CBC, monospot, arterial blood gases, and pulse oximetry. When indicated an EKG, echocardiogram and
chest X-ray were obtained. oximetry and, when indicated,
Representative
Postoperative studies included blood gases, EKG, echocardiography and chest X-ray.
pulse
case presentation
L.P. is a 7-year-old male who presented to the emergency room with a history of increasing somnolence associated with 24 hours of intermittent apnea. He had been treated for 6 episodes of acute tonsillitis in the past year. On physical examination he was found to have enlarged tonsils free of erythema or exudate. There was no leukocytosis or temperature elevation. He appeared somnolent but rousable. There was no evidence of cyanosis. The respiratory rate was 34 and the patient had respiratory retractions including use of accessory muscles of respiration. Lateral neck X-rays confirmed upper airway obstruction due to enlarged adenoids and tonsils (Fig. 1). The chest X-ray showed cardiomegaly and evidence of car pulmonale. Arterial blood gases on room air showed a pCOz of 66.8, ~0, of 81.9 and O2 saturation of 86%. He became increasingly somnolent and apneic and repeated jaw thrust maneuvers were necessary to keep him breathing. The patient was taken to the operating room and a nasophatyngeal airway was placed (Fig. 2). Despite bypassing the
Fig. 1. Soft tissue neck X-ray confirming
adenotonsillar
hypertrophy.
Fig. 2. Hypersomnolent
patient patient
with nasopharyngeal required intubation
airway in place. Due to loss of hypoxic and mechanical ventilation.
drive, the
cause of the obstruction, his respirations became fatigued due to loss of his hypoxic drive and he was then intubated. An adenotonsillectomy was subsequently performed. Postoperatively, the patient required mechanical ventilation for 36 h. After extubation on the second postoperative day he had a pC0, of 40.1 and ~0, of 89.6 on room air. During the two-year follow-up period, the patient has been asymptomatic but an EKG and chest X-ray show persistent cardiomegaly.
Results The ages of our patients ranged from two to 7 years of age with a mean of 5. Four out of 6 of the patients were male. Three patients presented during the winter and two during the summer season. Two of 6 patients were obese and all patients had chronic adenotonsillar hypertrophy. Four patients presented with cyanosis and all patients had respiratory retractions, use of accessory respiratory muscles, and an increase in respiratory rate. Two patients presented with signs and symptoms of congestive heart failure. Four patients had evidence of cardiomegaly and 3 showed evidence of car pulmonale based upon EKG, chest X-rays, and/or echocardiography. One patient required stabilization with digitalis and lasix prior to surgery. All patients required intubation emergently despite nasopharyngeal airway placement. Three patients required assisted ventilation postoperatively up to 36 h. Five patients had normal chemistries. The patient with congestive heart failure had abnormalities in sodium, potassium, CO,, chloride, BUN and creatinine. The
x7 PRE AND POST OPERATIVE ARTERIAL pco2
!m ,,&
Pre-operative Post-operative
ID 80
0 j
60
;; : a
40
20
0 1
2
3
4
6
6
PATIENT NUMBER
Fig. 3. Pre- and postoperative arterial pC0, (mmHg) Patient numbers I. 2, and 3 received 28% humidified oxygen via face mask when blood gases were drawn prc-op. Postoperative blood gases were on room air.
WBC was slightly elevated in 3 patients and markedly elevated in one patient who also had a positive monospot. All patients evaluated with blood gases showed marked CO, retention and acidosis. The preoperative pC0, ranged from 57 mmHg to 108 mmHg. Postoperatively all patients improved with a range of 40-47.3 mmHg (Fig. 3).
Discussion
The decline in the number of adenotonsillectomies performed in the United States has posed new problems relating to the pathophysiology of adenotonsillar hypertrophy. In 1971 Ballantyne and Groves [2] reported the death of two pediatric patients due to adenotonsillar hypertrophy complicated by an acute infection. In 1974, Jaffee [lo] described 5 cases of adenotonsillectomy performed as emergency medical treatment for chronic respiratory disease (i.e. car pulmonale, congestive heart failure) or acute respiratory disease (i.e. strider). Our paper describes 6 patients with exacerbations of chronic adenotonsillar hypertrophy. Due to these reports, it has been necessary to design studies to identify patients at risk for developing life threatening upper airway obstruction. Mangat [13] reported the use of all night polygraphic monitoring of sleep and respiration in patients with intermittent upper airway obstruction. After adenotonsillectomy, these patients showed improvement of sleep and breathing patterns.
88
By 1982, a pattern of insidious upper airway obstruction in patients with adenotonsillar hypertrophy emerged. Grundfast [8] called this an evolutionary process resulting from decreasing operative intervention. This paper described a constellation of symptoms and physical findings in these patients and called for the development of more sensitive methods of respiratory monitoring in order to identify children at risk for developing the sequelae of adenotonsillar hypertrophy. During the next decade, symptoms of sleep apnea and subsequent polysomnographic monitoring were evaluated as a means for determining which patients might benefit from adenotonsillectomy [13,15]. In addition, cardiopulmonary distress syndrome secondary to adenotonsillar hypertrophy became well documented [.5,11,16]. Finally, even the microbiology of chronic tonsillar hypertrophy appeared to be changing. A study in 1988 [4] suggested that Haemophilus injluenzae played an important part in the pathogenesis of tonsillar hypertrophy. In our study, 6 patients with histories of chronic adenotonsillar hypertrophy required urgent adenotonsillectomy after stabilization of their cardiorespiratory status. One patient had infectious mononucleosis with resulting obstructive adenotonsillitis. Our data show the reversal of CO, retention states as well as partial to complete resolution of apnea, failure to thrive, and airway obstruction. To our knowledge, this is the largest recent individual series of patients with adenotonsillar hypertrophy requiring emergency cardiorespiratory stabilization followed by urgent adenotonsillectomy. Despite advances in technology geared toward identifying these patients, it is clear that the trend toward decreasing adenotonsillectomy operations still continues to pose an evolutionary problem as described by Grundfast. In addition, the recent trend toward outpatient adenotonsillectomy emphasizes the need for identification of patients with car pulmonale who may develop respiratory arrest and congestive heart failure up to 36 h postoperatively due to removal of their hypoxic drive.
Conclusion
Over a decade ago several cases of pediatric mortality had been attributed to adenotonsillar enlargement with an acute infection. During the past decade, considerable research has been undertaken to develop appropriate criteria for adenotonsillectomy in an increasingly skeptical medical and public community. The cases evaluated in this review illustrate the immediate alleviation of lifethreatening upper airway obstruction by urgent adenotonsillectomy. They serve to remind us that adenotonsillar hypertrophy is not a relatively benign entity and can result in a potentially disastrous medical emergency.
References 1 Avery, A.D. and Harris, L.J., Tonsillectomy, adenoidectomy and tonsillectomy with adenoidectomy: assessing the quality of medical care using short-term outcome measures: eight disease-specific applications. In Rand Report R-2021/2-HEW, Rand Corporation, Santa Monica, CA, 1976, pp. 651-757.
2 Ballantyne J. and Groves, T., Scott Brown’s Disease of the Ear. Nose and Throat, Vol. 3, Lippincott, Philadelphia, 1971, pp. 103-145. 3 Bluestone. C.D., Status of tonsillectomy and adenoidectomy, Laryngoscope, X7 (lY77) 1233-1243. 4 Brodsky. L.. Moore, L. and Stanievich, J.. The role of Huemophilus influerzme in the pathogencsis ot tonsillar hypertrophy in children, Laryngoscope, 9X (198X) 1051;-1060. 5 Brown, 0.13.. Manning, S.C. and Ridenour B.. Cor pulmonale secondary to tonsillar and adenoidal hypertrophy: management considerations. Int. J. Ped. Otorhinolaryngol., I6 (19X8) 13 I - 139. 6 Chech. W..4.. Does drop in T and A’s pose new issue of adenotonsillar hypertrophy’! J. Am. Med. Assoc.. 747 (1982) 122991230. 7 Eliascher. I., Peretz, L., Halperin, E.. Gordon, C. and Alroy. G.. sleep apneic episode\ as indications for adenotonsillectomy, Arch. Otolaryngol.. 106 (1980) 4Y2-496. X Grundfast. K.M.. Wittich, D.J., Adenotonsillar hypertrophy and upper airway obstruction in evolutionary perspective, Laryngoscope, 92 (1982) 650-656. Y liaydon-Baillie, J., Tonsilloadenoidectomy, Ann. R. CoII. Surg. Engl.. 5Y (1977) 12X. 10 Jaffee. I..?., Adenotonsillectomy as the treatment of serious medical conditions: five case reports, Laryngoscclpe, X4 (lY74) 1135-l 141. 1 I Levy, A.M . Tabakin, B.S.. Hanson, J.S., et al.. Hypertrophied adenoids causing pulmonary hypertension and severe congestive heart failure, N. Engl. J. Med., 227 (lYh7) 506-51 I. 12 Mandel, E M. and Reynolds, C.F.. Sleep disorders with upper airway obstruction in children. Ped Clin. N. Am., 2X (1981) X97-903. I3 Mangat. P., Orr. W.C. and Smith, R.O., Sleep apnea hypersomnolence and upper airway ohstruction secondary to adenotonsillar enlargement, Arch. Otolaryngol.. 103 (1977) 3833380. 14 Paradise, J.L., Tonsillectomy and adenoidectomy. In C.D. Blucstone, S.E. Stool and M.D. Scheetz (eds.). Pedtatric Otolaryngology, 2nd edn. Saunders, Philadelphia, 1990. pp. Y15-024. 15 Potsic, W.P.. Pasquariello. P.S., Buranch. C.C., et al.. Relief of upper ainvay obstruction by adenotonsillcctomy. Otolaryngol. Head Neck Surg., 94 (1986) 476-480 16 Spaur. R.L.. The cardiorespiratory - car pulmonale syndrome secondary to chronic upper airway obstruction from hypertrophied tonsils and adenoids. A review. E.N.T J.. 62 (1982) 562-570. I7 Yonkers. A.J. and Spaur. R.C., Upper airway obstruction and the pharyngeal lymphoid tissue. Otolaryngol. Clin. N. Am.. 20 (1987) 235-239.
PEDOT
83
00785
Urgent adenotonsillectomy for upper airway obstruction * Frank G. Shechtman,
Pi Tang Lit-t and Robert
L. Pincus
Department of Otoiaryngology - Head and Neck Surgery, New York Medical College Affiliated Hospitals Program, New York E.ve and Ear Infirmary, New York. NY 10003 (U.S.A.)
(Revised
Kq words: Urgent
(Received 18 June 1991) versions received 25 June and 7 August (Accepted 12 August 199 I )
adenotonsillectomy;
Chronic
upper
airway obstruction:
199 1)
Car pulmonale
Abstract
Adenotonsillar hypertrophy has been documented to cause chronic upper airway obstruction resulting in cardiopulmonary sequelae in children. It has been less recognized that long-term adenotonsillar hypertrophy may additionally cause acute, life-threatening airway obstruction. A review of 5000 adenotonsillectomies performed at 3 New York Medical College affiliated hospitals from 1982 to 1989 showed 6 pediatric patients with progressive upper airway obstruction severe enough to necessitate intubation in the emergency room or operating room, and subsequent urgent adenotonsillectomy after cardiorespiratory stabilization. Patients were monitored in the ICU with pre- and postoperative blood gases. Observations of cyanosis, car pulmonale, and use of accessory respiratory muscles were carefully recorded. This study illustrates that life-threatening upper airway obstruction may be due to chronic adenotonsillar enlargement and require treatment by urgent adenotonsillectomy.
Introduction
Adenotonsillectomy is still among the most commonly performed operations on children in the United States [3,141 but the increasingly cost-conscious environ-
* Presented December
;at the Sixteenth Annual Meeting 1988, New York City, NY.
Society
for Ear, Nose and Throat
C‘orrrspondence to: F.G. Shechtman, Dept. of ORL - Head College, 310 East 14th Street, New York, NY 10003. U.S.A.
and Neck
Surgery.
Advances
in Children.
New York
Medical
84
ment has placed a great deal of scrutiny on surgeons performing it. The number of tonsillectomies, adenoidectomies, and adenotonsillectomies performed in nonfederal, short-stay hospitals in 1971 was 1,019,OOO. By 1987 this number had declined to 259,000 representing a reduction of 80.7% over the 16-year period [14]. Several reasons for this include better antibiotic therapies, and greater understanding of both the natural history of the disease, and the role Waldeyer’s ring plays in host defense immunity [l]. Over two decades ago several papers reported the death of pediatric patients due to adenotonsillar hypertrophy exacerbated by an acute infection [2,91. In 1982, Grundfast reported the reluctance of primary care physicians to refer patients for adenotonsillectomy and an increasing trend for children to develop the sequelae of adenotonsillar hypertrophy [S]. This paper stimulated a medical communication in JAMA describing Grundfast’s work and identifying characteristics of children at risk for developing insidious airway obstruction from adenotonsillar hypertrophy
[61. Fortunately studies such as those carried out by Bluestone et al. [3] have provided well-researched concepts as to indications for the operative procedure. However, as the medical community has decreased the number of referrals for adenotonsillectomy, there has been increasing evidence that adenotonsillar hypertrophy can result in end-stage sleep apnea [7,12,13] and cardiorespiratory distress syndrome [11,16]. As a result, many elegant laboratory studies including polysomnography, pulse oximetry, and computer-aided analysis of respiratory flow and sounds have been developed in the hope of identifying patients before they become irreversibly damaged [15]. A review in 1987 tabulated over 100 cases reported in the literature of cardiorespiratory distress secondary to adenotonsillar hypertrophy [17]. In 1988, Brown et al. [51 reviewed 11 cases of car pulmonale secondary to tonsil and adenoid hypertrophy. These patients presented with a wide spectrum of disease ranging from mild distress to respiratory arrest 36 h after intervention. The authors underscore the importance of screening for car pulmonale and pre- and postoperative ICU management of these patients. The purpose of this paper is to evaluate the records of pediatric patients who underwent emergency intubation and urgent adenotonsillectomy at two city hospitals and one private institution during the period 1982-1989.
Materials
and methods
Over 5000 adenotonsillectomy operations were performed at 3 New York Medical College affiliated hospitals during 1982-1989. Six patients were identified who presented with severe, life-threatening upper airway obstruction which necessitated emergency airway management, cardiac stabilization, and urgent adenotonsillectomy. The patients were evaluated by clinical history and physical examination. Laboratory studies included routine chemistries, CBC, monospot, arterial blood gases, and pulse oximetry. When indicated an EKG, echocardiogram and
chest X-ray were obtained. oximetry and, when indicated,
Representative
Postoperative studies included blood gases, EKG, echocardiography and chest X-ray.
pulse
case presentation
L.P. is a 7-year-old male who presented to the emergency room with a history of increasing somnolence associated with 24 hours of intermittent apnea. He had been treated for 6 episodes of acute tonsillitis in the past year. On physical examination he was found to have enlarged tonsils free of erythema or exudate. There was no leukocytosis or temperature elevation. He appeared somnolent but rousable. There was no evidence of cyanosis. The respiratory rate was 34 and the patient had respiratory retractions including use of accessory muscles of respiration. Lateral neck X-rays confirmed upper airway obstruction due to enlarged adenoids and tonsils (Fig. 1). The chest X-ray showed cardiomegaly and evidence of car pulmonale. Arterial blood gases on room air showed a pCOz of 66.8, ~0, of 81.9 and O2 saturation of 86%. He became increasingly somnolent and apneic and repeated jaw thrust maneuvers were necessary to keep him breathing. The patient was taken to the operating room and a nasophatyngeal airway was placed (Fig. 2). Despite bypassing the
Fig. 1. Soft tissue neck X-ray confirming
adenotonsillar
hypertrophy.
Fig. 2. Hypersomnolent
patient patient
with nasopharyngeal required intubation
airway in place. Due to loss of hypoxic and mechanical ventilation.
drive, the
cause of the obstruction, his respirations became fatigued due to loss of his hypoxic drive and he was then intubated. An adenotonsillectomy was subsequently performed. Postoperatively, the patient required mechanical ventilation for 36 h. After extubation on the second postoperative day he had a pC0, of 40.1 and ~0, of 89.6 on room air. During the two-year follow-up period, the patient has been asymptomatic but an EKG and chest X-ray show persistent cardiomegaly.
Results The ages of our patients ranged from two to 7 years of age with a mean of 5. Four out of 6 of the patients were male. Three patients presented during the winter and two during the summer season. Two of 6 patients were obese and all patients had chronic adenotonsillar hypertrophy. Four patients presented with cyanosis and all patients had respiratory retractions, use of accessory respiratory muscles, and an increase in respiratory rate. Two patients presented with signs and symptoms of congestive heart failure. Four patients had evidence of cardiomegaly and 3 showed evidence of car pulmonale based upon EKG, chest X-rays, and/or echocardiography. One patient required stabilization with digitalis and lasix prior to surgery. All patients required intubation emergently despite nasopharyngeal airway placement. Three patients required assisted ventilation postoperatively up to 36 h. Five patients had normal chemistries. The patient with congestive heart failure had abnormalities in sodium, potassium, CO,, chloride, BUN and creatinine. The
x7 PRE AND POST OPERATIVE ARTERIAL pco2
!m ,,&
Pre-operative Post-operative
ID 80
0 j
60
;; : a
40
20
0 1
2
3
4
6
6
PATIENT NUMBER
Fig. 3. Pre- and postoperative arterial pC0, (mmHg) Patient numbers I. 2, and 3 received 28% humidified oxygen via face mask when blood gases were drawn prc-op. Postoperative blood gases were on room air.
WBC was slightly elevated in 3 patients and markedly elevated in one patient who also had a positive monospot. All patients evaluated with blood gases showed marked CO, retention and acidosis. The preoperative pC0, ranged from 57 mmHg to 108 mmHg. Postoperatively all patients improved with a range of 40-47.3 mmHg (Fig. 3).
Discussion
The decline in the number of adenotonsillectomies performed in the United States has posed new problems relating to the pathophysiology of adenotonsillar hypertrophy. In 1971 Ballantyne and Groves [2] reported the death of two pediatric patients due to adenotonsillar hypertrophy complicated by an acute infection. In 1974, Jaffee [lo] described 5 cases of adenotonsillectomy performed as emergency medical treatment for chronic respiratory disease (i.e. car pulmonale, congestive heart failure) or acute respiratory disease (i.e. strider). Our paper describes 6 patients with exacerbations of chronic adenotonsillar hypertrophy. Due to these reports, it has been necessary to design studies to identify patients at risk for developing life threatening upper airway obstruction. Mangat [13] reported the use of all night polygraphic monitoring of sleep and respiration in patients with intermittent upper airway obstruction. After adenotonsillectomy, these patients showed improvement of sleep and breathing patterns.
88
By 1982, a pattern of insidious upper airway obstruction in patients with adenotonsillar hypertrophy emerged. Grundfast [8] called this an evolutionary process resulting from decreasing operative intervention. This paper described a constellation of symptoms and physical findings in these patients and called for the development of more sensitive methods of respiratory monitoring in order to identify children at risk for developing the sequelae of adenotonsillar hypertrophy. During the next decade, symptoms of sleep apnea and subsequent polysomnographic monitoring were evaluated as a means for determining which patients might benefit from adenotonsillectomy [13,15]. In addition, cardiopulmonary distress syndrome secondary to adenotonsillar hypertrophy became well documented [.5,11,16]. Finally, even the microbiology of chronic tonsillar hypertrophy appeared to be changing. A study in 1988 [4] suggested that Haemophilus injluenzae played an important part in the pathogenesis of tonsillar hypertrophy. In our study, 6 patients with histories of chronic adenotonsillar hypertrophy required urgent adenotonsillectomy after stabilization of their cardiorespiratory status. One patient had infectious mononucleosis with resulting obstructive adenotonsillitis. Our data show the reversal of CO, retention states as well as partial to complete resolution of apnea, failure to thrive, and airway obstruction. To our knowledge, this is the largest recent individual series of patients with adenotonsillar hypertrophy requiring emergency cardiorespiratory stabilization followed by urgent adenotonsillectomy. Despite advances in technology geared toward identifying these patients, it is clear that the trend toward decreasing adenotonsillectomy operations still continues to pose an evolutionary problem as described by Grundfast. In addition, the recent trend toward outpatient adenotonsillectomy emphasizes the need for identification of patients with car pulmonale who may develop respiratory arrest and congestive heart failure up to 36 h postoperatively due to removal of their hypoxic drive.
Conclusion
Over a decade ago several cases of pediatric mortality had been attributed to adenotonsillar enlargement with an acute infection. During the past decade, considerable research has been undertaken to develop appropriate criteria for adenotonsillectomy in an increasingly skeptical medical and public community. The cases evaluated in this review illustrate the immediate alleviation of lifethreatening upper airway obstruction by urgent adenotonsillectomy. They serve to remind us that adenotonsillar hypertrophy is not a relatively benign entity and can result in a potentially disastrous medical emergency.
References 1 Avery, A.D. and Harris, L.J., Tonsillectomy, adenoidectomy and tonsillectomy with adenoidectomy: assessing the quality of medical care using short-term outcome measures: eight disease-specific applications. In Rand Report R-2021/2-HEW, Rand Corporation, Santa Monica, CA, 1976, pp. 651-757.
2 Ballantyne J. and Groves, T., Scott Brown’s Disease of the Ear. Nose and Throat, Vol. 3, Lippincott, Philadelphia, 1971, pp. 103-145. 3 Bluestone. C.D., Status of tonsillectomy and adenoidectomy, Laryngoscope, X7 (lY77) 1233-1243. 4 Brodsky. L.. Moore, L. and Stanievich, J.. The role of Huemophilus influerzme in the pathogencsis ot tonsillar hypertrophy in children, Laryngoscope, 9X (198X) 1051;-1060. 5 Brown, 0.13.. Manning, S.C. and Ridenour B.. Cor pulmonale secondary to tonsillar and adenoidal hypertrophy: management considerations. Int. J. Ped. Otorhinolaryngol., I6 (19X8) 13 I - 139. 6 Chech. W..4.. Does drop in T and A’s pose new issue of adenotonsillar hypertrophy’! J. Am. Med. Assoc.. 747 (1982) 122991230. 7 Eliascher. I., Peretz, L., Halperin, E.. Gordon, C. and Alroy. G.. sleep apneic episode\ as indications for adenotonsillectomy, Arch. Otolaryngol.. 106 (1980) 4Y2-496. X Grundfast. K.M.. Wittich, D.J., Adenotonsillar hypertrophy and upper airway obstruction in evolutionary perspective, Laryngoscope, 92 (1982) 650-656. Y liaydon-Baillie, J., Tonsilloadenoidectomy, Ann. R. CoII. Surg. Engl.. 5Y (1977) 12X. 10 Jaffee. I..?., Adenotonsillectomy as the treatment of serious medical conditions: five case reports, Laryngoscclpe, X4 (lY74) 1135-l 141. 1 I Levy, A.M . Tabakin, B.S.. Hanson, J.S., et al.. Hypertrophied adenoids causing pulmonary hypertension and severe congestive heart failure, N. Engl. J. Med., 227 (lYh7) 506-51 I. 12 Mandel, E M. and Reynolds, C.F.. Sleep disorders with upper airway obstruction in children. Ped Clin. N. Am., 2X (1981) X97-903. I3 Mangat. P., Orr. W.C. and Smith, R.O., Sleep apnea hypersomnolence and upper airway ohstruction secondary to adenotonsillar enlargement, Arch. Otolaryngol.. 103 (1977) 3833380. 14 Paradise, J.L., Tonsillectomy and adenoidectomy. In C.D. Blucstone, S.E. Stool and M.D. Scheetz (eds.). Pedtatric Otolaryngology, 2nd edn. Saunders, Philadelphia, 1990. pp. Y15-024. 15 Potsic, W.P.. Pasquariello. P.S., Buranch. C.C., et al.. Relief of upper ainvay obstruction by adenotonsillcctomy. Otolaryngol. Head Neck Surg., 94 (1986) 476-480 16 Spaur. R.L.. The cardiorespiratory - car pulmonale syndrome secondary to chronic upper airway obstruction from hypertrophied tonsils and adenoids. A review. E.N.T J.. 62 (1982) 562-570. I7 Yonkers. A.J. and Spaur. R.C., Upper airway obstruction and the pharyngeal lymphoid tissue. Otolaryngol. Clin. N. Am.. 20 (1987) 235-239.
