Respiratory Compromise After Adenotonsillectomy in Children With Obstructive Sleep Apnea Susanna A. \s=b\
A
tive
McColley, MD; Max M. April, MD; John
L.
Carroll, MD; Robert M. Naclerio, MD; Gerald M. Loughlin,
retrospective study of pediatric patients with obstrucsleep apnea who underwent adenotonsillectomy be-
was undertaken to determine the freof postoperative respiratory compromise and to quency determine if risk factors for its development could be identified. Sixty-nine patients less than 18 years old had polysomnographically documented obstructive sleep apnea and were observed postoperatively in the pediatric intensive care unit. Of these, 16 (23%) had severe respiratory compromise, defined as intermittent or continuous oxygen saturation of 70% or less, and/or hypercapnia, requiring intervention. Compared with patients without respiratory compromise, these patients were younger (3.4\m=+-\4vs 6.1 \m=+-\4 years) and had more obstructive events per hour of sleep on the polysomnogram (49\m=+-\41vs 19\m=+-\30).They were more likely to weigh less than the fifth percentile for age (odds ratio [OR], 5.1; 95% confidence interval [CI], 1.4 to 18.7), to have an abnormal electrocardiogram and/or echocardiogram (OR, 4.5; 95% CI, 1.3 to 15.1), and to have a craniofacial abnormality (OR, 6.2; 95% CI, 1.5 to 26). Multiple logistic regression analysis revealed the most significant risk factors were age below 3 years and an obstructive event index greater than 10. Children with obstructive sleep apnea are at risk for respiratory compromise following adenotonsillectomy; young age and severe sleep-related upper airway obstruction significantly increase this risk. We recommend in-hospital postoperative monitoring for children undergoing adenotonsillectomy for obstructive sleep apnea. (Arch Otolaryngol Head Neck Surg. 1992;118:940-943)
tween 1987 and 1990
sleep apnea (OSA) increasing impor¬ Obstructive adenotonsillectomy children.1
is in indication for in Children with OSA may be at risk for postoper¬ ative respiratory compromise for several reasons. Anes¬ thetic agents, including inhalational anesthetics and nar¬ cotics, lead to upper airway collapse by decreasing the activity of pharyngeal dilator muscles2; this occurs even in subanesthetic doses3 and thus may persist once other effects of anesthesia have abated. Pulmonary edema may complicate adenotonsillectomy,4 possibly through the mechanism that leads to pulmonary edema following re¬ lief of acute upper airway obstruction.5 Children with OSA may have impaired ventilatory responses to carbon diox¬ ide.6 Finally, the cardiopulmonary consequences of OSA, which include cor pulmonale,7 may place these children at increased risk for postoperative complications. tance as an
Accepted for publication
November 5, 1991. From the Eudowood Division of Pediatric Respiratory
Sciences,
De-
partment of Pediatrics (Drs McColley, Carroll, and Loughlin), and the Division of Pediatric Otolaryngology, Department of Otolaryngology, Head and Neck Surgery (Drs April and Naclerio), The Johns Hopkins University School of Medicine, Baltimore, Md.
Presented at the American Society of Pediatric Otolaryngology meeting, Waikaloa, Hawaii, May 11, 1991. Reprint requests to The Johns Hopkins Medical Institutions, 600 N Wolfe St, Park 316, Baltimore, MD 21205 (Dr McColley).
Between 1987 and 1990,
we
observed
severe
compromise following adenotonsillectomy
MD
respiratory
in several chil¬
dren with OSA. We therefore undertook a retrospective study of children undergoing adenotonsillectomy for OSA to determine the frequency of postoperative respiratory com¬ promise in this population. We examined patient character¬ istics and operative and anesthetic factors to determine whether patients at increased risk could be identified. PATIENTS AND METHODS The charts of all patients below 18 years old who underwent ad¬ enotonsillectomy for a clinical diagnosis of OSA between May 1987 and lune 1990 were reviewed. To confirm the diagnosis and stan¬ dardize postoperative monitoring, only patients who had OSA doc¬ umented by polysomnography (PSG) and who underwent intensive postoperative monitoring in the pediatrie intensive care unit (PICU) were included in the statistical analysis. The remaining charts were reviewed to determine whether there was a significant incidence of respiratory compromise in patients not meeting these criteria. Patient characteristics, PSG results, operative and anesthetic factors, and postoperative course were examined. Patient charac¬ teristics included age, gender, weight percentile for age, cranio¬ facial anomalies, and laboratory data. For most patients, severity of OSA was expressed as an obstructive event index (OEI), the number of episodes of obstructive apnea and obstructive hypoventilation per hour of sleep during PSG. A small number of pa¬ tients did not have an OEI generated during initial PSG scoring and did not have records available for reexamination. Operative and anesthetic factors included anesthem. ugeius administered, duration of anesthesia, operative time, and type of tonsillar dis¬ section (sharp vs cautery). Immediate postoperative course in¬ cluded documentation of hypoxia, hypercapnia, and inter¬ vention. Severe respiratory compromise was defined as oxyhemoglobin desaturation (arterial oxygen saturation [Sa02], 45 mm Hg), requiring nurse or physician intervention. Follow-up PSG was performed at least 6 weeks postoperatively at the discretion of each patients' physician. Patients with tracheotomies or concurrent surgical procedures that might increase the likelihood of respiratory compromise were excluded. Polysomnograms were performed at The Johns Hopkins Medical Institutions, Baltimore, Md, using standard techniques. Measure¬ ments included recording of two electroencephalographic and right and left electro-oculographic leads for sleep staging, electrocardio¬ gram, and tibial and submental surface electromyograms for mea¬ suring muscle activity. Arterial oxyhemoglobin saturation was measured by pulse oximetry (Nellcor N-200 or N-1000, Nellcor Ine, Hayward, Calif). Respiratory effort was measured by mercuryfilled strain gauges placed across the thorax and abdomen. Oronasal airflow was measured by a three-pronged nasal thermistor. All measurements were made during natural sleep, usually nocturnal, and were continuously recorded on an 18-channel polygraphic re¬ corder (Grass model 18D, Grass Instruments Ine, Quincy, Mass). Obstructive apnea was defined as cessation of oronasal airflow with continued respiratory effort for at least 5 seconds, accompanied by a 4% or greater decrease in arterial oxygen saturation. Obstructive hypoventilation was defined as a decrease in amplitude of oronasal airflow of at least 50%, with no decrease in respiratory effort, for at least 5 seconds and accompanied by a 4% or greater decrease in ar¬ terial oxygen saturation.
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Table 1.—Patients With Patient No./
Age,y/mo/Sex 1/0/9/F 2/1/10/M 3/2/0/M 4/2/5/F 5/9/9/M 6/16/5/F 7/1/7/M 8/2/4/M 9/4/0/M 10/3/9/M 11/1/0/M 12/1/11/M
Respiratory Compromise*
Weight (Percentile for Age)
OEI
A
tive
McColley, MD; Max M. April, MD; John
L.
Carroll, MD; Robert M. Naclerio, MD; Gerald M. Loughlin,
retrospective study of pediatric patients with obstrucsleep apnea who underwent adenotonsillectomy be-
was undertaken to determine the freof postoperative respiratory compromise and to quency determine if risk factors for its development could be identified. Sixty-nine patients less than 18 years old had polysomnographically documented obstructive sleep apnea and were observed postoperatively in the pediatric intensive care unit. Of these, 16 (23%) had severe respiratory compromise, defined as intermittent or continuous oxygen saturation of 70% or less, and/or hypercapnia, requiring intervention. Compared with patients without respiratory compromise, these patients were younger (3.4\m=+-\4vs 6.1 \m=+-\4 years) and had more obstructive events per hour of sleep on the polysomnogram (49\m=+-\41vs 19\m=+-\30).They were more likely to weigh less than the fifth percentile for age (odds ratio [OR], 5.1; 95% confidence interval [CI], 1.4 to 18.7), to have an abnormal electrocardiogram and/or echocardiogram (OR, 4.5; 95% CI, 1.3 to 15.1), and to have a craniofacial abnormality (OR, 6.2; 95% CI, 1.5 to 26). Multiple logistic regression analysis revealed the most significant risk factors were age below 3 years and an obstructive event index greater than 10. Children with obstructive sleep apnea are at risk for respiratory compromise following adenotonsillectomy; young age and severe sleep-related upper airway obstruction significantly increase this risk. We recommend in-hospital postoperative monitoring for children undergoing adenotonsillectomy for obstructive sleep apnea. (Arch Otolaryngol Head Neck Surg. 1992;118:940-943)
tween 1987 and 1990
sleep apnea (OSA) increasing impor¬ Obstructive adenotonsillectomy children.1
is in indication for in Children with OSA may be at risk for postoper¬ ative respiratory compromise for several reasons. Anes¬ thetic agents, including inhalational anesthetics and nar¬ cotics, lead to upper airway collapse by decreasing the activity of pharyngeal dilator muscles2; this occurs even in subanesthetic doses3 and thus may persist once other effects of anesthesia have abated. Pulmonary edema may complicate adenotonsillectomy,4 possibly through the mechanism that leads to pulmonary edema following re¬ lief of acute upper airway obstruction.5 Children with OSA may have impaired ventilatory responses to carbon diox¬ ide.6 Finally, the cardiopulmonary consequences of OSA, which include cor pulmonale,7 may place these children at increased risk for postoperative complications. tance as an
Accepted for publication
November 5, 1991. From the Eudowood Division of Pediatric Respiratory
Sciences,
De-
partment of Pediatrics (Drs McColley, Carroll, and Loughlin), and the Division of Pediatric Otolaryngology, Department of Otolaryngology, Head and Neck Surgery (Drs April and Naclerio), The Johns Hopkins University School of Medicine, Baltimore, Md.
Presented at the American Society of Pediatric Otolaryngology meeting, Waikaloa, Hawaii, May 11, 1991. Reprint requests to The Johns Hopkins Medical Institutions, 600 N Wolfe St, Park 316, Baltimore, MD 21205 (Dr McColley).
Between 1987 and 1990,
we
observed
severe
compromise following adenotonsillectomy
MD
respiratory
in several chil¬
dren with OSA. We therefore undertook a retrospective study of children undergoing adenotonsillectomy for OSA to determine the frequency of postoperative respiratory com¬ promise in this population. We examined patient character¬ istics and operative and anesthetic factors to determine whether patients at increased risk could be identified. PATIENTS AND METHODS The charts of all patients below 18 years old who underwent ad¬ enotonsillectomy for a clinical diagnosis of OSA between May 1987 and lune 1990 were reviewed. To confirm the diagnosis and stan¬ dardize postoperative monitoring, only patients who had OSA doc¬ umented by polysomnography (PSG) and who underwent intensive postoperative monitoring in the pediatrie intensive care unit (PICU) were included in the statistical analysis. The remaining charts were reviewed to determine whether there was a significant incidence of respiratory compromise in patients not meeting these criteria. Patient characteristics, PSG results, operative and anesthetic factors, and postoperative course were examined. Patient charac¬ teristics included age, gender, weight percentile for age, cranio¬ facial anomalies, and laboratory data. For most patients, severity of OSA was expressed as an obstructive event index (OEI), the number of episodes of obstructive apnea and obstructive hypoventilation per hour of sleep during PSG. A small number of pa¬ tients did not have an OEI generated during initial PSG scoring and did not have records available for reexamination. Operative and anesthetic factors included anesthem. ugeius administered, duration of anesthesia, operative time, and type of tonsillar dis¬ section (sharp vs cautery). Immediate postoperative course in¬ cluded documentation of hypoxia, hypercapnia, and inter¬ vention. Severe respiratory compromise was defined as oxyhemoglobin desaturation (arterial oxygen saturation [Sa02], 45 mm Hg), requiring nurse or physician intervention. Follow-up PSG was performed at least 6 weeks postoperatively at the discretion of each patients' physician. Patients with tracheotomies or concurrent surgical procedures that might increase the likelihood of respiratory compromise were excluded. Polysomnograms were performed at The Johns Hopkins Medical Institutions, Baltimore, Md, using standard techniques. Measure¬ ments included recording of two electroencephalographic and right and left electro-oculographic leads for sleep staging, electrocardio¬ gram, and tibial and submental surface electromyograms for mea¬ suring muscle activity. Arterial oxyhemoglobin saturation was measured by pulse oximetry (Nellcor N-200 or N-1000, Nellcor Ine, Hayward, Calif). Respiratory effort was measured by mercuryfilled strain gauges placed across the thorax and abdomen. Oronasal airflow was measured by a three-pronged nasal thermistor. All measurements were made during natural sleep, usually nocturnal, and were continuously recorded on an 18-channel polygraphic re¬ corder (Grass model 18D, Grass Instruments Ine, Quincy, Mass). Obstructive apnea was defined as cessation of oronasal airflow with continued respiratory effort for at least 5 seconds, accompanied by a 4% or greater decrease in arterial oxygen saturation. Obstructive hypoventilation was defined as a decrease in amplitude of oronasal airflow of at least 50%, with no decrease in respiratory effort, for at least 5 seconds and accompanied by a 4% or greater decrease in ar¬ terial oxygen saturation.
Downloaded From: http://archotol.jamanetwork.com/ by a New York University User on 05/29/2015
Table 1.—Patients With Patient No./
Age,y/mo/Sex 1/0/9/F 2/1/10/M 3/2/0/M 4/2/5/F 5/9/9/M 6/16/5/F 7/1/7/M 8/2/4/M 9/4/0/M 10/3/9/M 11/1/0/M 12/1/11/M
Respiratory Compromise*
Weight (Percentile for Age)
OEI
