Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

 

PART THREE – Clinical Management of Special Surgical Problems

Chapter 23 – Anesthesia for Pediatric Otorhinolaryngologic Surgery

Ira S. Landsman,Jay A. Werkhaven,
Etsuro K. Motoyama

  

 

Anesthesia for Otologic Procedures, 789

  

 

Myringotomy and Insertion of Tympanostomy Tubes,790

  

 

Mastoidectomy and Tympanoplasty, 790

  

 

Cochlear Implant, 791

  

 

Otoplasty, 791

  

 

Anesthesia for Rhinologic Procedures, 791

  

 

Reduction of Nasal Fracture,791

  

 

Nasal Polypectomy, 791

  

 

Sinus Surgery, 793

  

 

Choanal Atresia, 794

  

 

Anesthesia for Pharyngeal and Laryngeal Procedures, 794

  

 

Tonsillectomy and Adenoidectomy,794

  

 

Laser Surgery of the Larynx, 800

  

 

Tracheostomy, 805

  

 

Laryngeal Stenosis, 807

  

 

Anesthesia for Endoscopy, 812

  

 

Laryngoscopy and Bronchoscopy for Stridor,815

  

 

Bronchoscopy for Foreign Body Aspiration,816

  

 

Endoscopy for Foreign Body Ingestion, 818

  

 

Summary, 818

The care of children requiring anesthesia for otorhinolaryngology or ear, nose, and throat (ENT) surgery is described in this chapter. Most pediatric otorhinolaryngologic surgical procedures are of short to intermediate duration, and most of the children in whom they are performed are in reasonably good health. However, the anesthesiologist often encounters children with potentially life-threatening upper airway obstruction (e.g., acute epiglottitis) or with severe pulmonary insufficiency requiring diagnostic or therapeutic ENT procedures. New surgical techniques, such as laryngeal laser surgery, have challenged pediatric anesthesiologists to develop innovative approaches for the protection and maintenance of the patent upper airway.

The art and science of anesthesia must be well integrated in caring for the child undergoing ENT anesthesia. Many procedures, including adenoidectomy, rigid bronchoscopy, and laser removal of papillomas, require short intervals of deep planes of anesthesia and limited movement of the patient. To effectively manage operating room services, the patient must awake in a timely manner without airway irritability. Some of the major changes in pediatric anesthesia over the past decade include the abandonment of halothane in favor of sevoflurane. Although sevoflurane appears to be a safer anesthetic agent than halothane, sevoflurane-induced postoperative delirium continues to challenge the pediatric anesthesiologist.

Propofol has many properties that make it a useful anesthetic agent for ENT surgery. Propofol causes less airway irritability than thiopental. Propofol may be protective against and therapeutic for laryngospasm ( Brown et al., 1991 ; Scanlon et al., 1993 ; Allsop et al., 1995 ; Afshan et al., 2002 ). Propofol also has useful antiemetic properties and a low incidence of emergence delirium ( Uezono et al., 2000 ; Moore et al., 2003 ; Voepel-Lewis et al., 2003 ), making this anesthetic a good choice for ENT anesthesia.

▪ ANESTHESIA FOR OTOLOGIC PROCEDURES

Otitis media is the most frequently diagnosed childhood malady, with the highest incidence occurring among children between the ages of 6 and 18 months. The frequency of otitis media decreases after the first year of life. By age 7 years, otitis media becomes a less frequent pediatric diagnosis. Otitis media is inflammation of the middle ear, without reference to pathogenesis or cause. The other areas of the temporal bone that are contiguous with the middle ear, including the mastoid, petrous apex, and perilabyrinthine air cells, also may be involved. Statistically, in those who have had a single episode of acute otitis media, residual middle ear fluid remains in up to 40% of patients at 1 month, 20% at 2 months, and 10% at 3 months ( Pelton et al., 1977 ; Teele et al., 1980 ; Gluckman, 1990 ).

Many children with persistent middle ear effusion continue to be clinically symptomatic with recurrent acute otitis media, pain, fever, vertigo, disturbed sleep, or significant hearing loss. These symptoms are the most common indications for middle ear effusion drainage by myringotomy and tympanostomy tubes. Myringotomy and insertion of tympanostomy tubes may also be helpful in patients with recurrent acute otitis or atelectasis of the tympanic membrane. Tympanostomy tubes may prevent permanent structural damage and/or cholesteatoma. Myringotomy with aspiration of the middle ear effusion but without tube placement may be appropriate in children with severe otalgia or when culture of the middle ear fluid is required in the evaluation of a child with fever of unknown origin. If the patient will require multiple myringotomy procedures, placement of a tympanostomy tube may be considered.

Many patients with congenital anomalies are candidates for myringotomy tubes. Patients with cleft palate, craniofacial malformations, Down syndrome, Turner's syndrome, and human immunodeficiency virus (HIV) infection have a higher incidence of otitis media and therefore have a greater need for myringotomy and insertion of tympanostomy tubes than the general population ( Bluestone and Klein, 2001 ). These children have other airway and medical issues that complicate the usual approach to the healthy child requiring myringotomy tubes. Critically ill patients with a history of prolonged nasotracheal intubation have a high incidence of persistent middle ear effusions requiring middle ear ventilation.

Adenoidectomy for chronic otitis media with effusion may benefit some children. The effectiveness of adenoidectomy for chronic otitis media with effusion is not directly related to adenoid size. For children who have recurrent or chronic otitis media with effusion and who had one or more myringotomy and tympanostomy tube insertion procedures in the past, adenoidectomy may be a reasonable option ( Paradise et al., 2003 ). Upper airway obstruction, recurrent acute or chronic adenoiditis, and sinusitis are additional indications for adenoidectomy in children who have chronic otitis media with effusion.

▪ MYRINGOTOMY AND INSERTION OF TYMPANOSTOMY TUBES

Candidates for myringotomy and tube insertion can present with subacute or chronic upper respiratory tract infection with or without fever. In these children, surgical intervention appears to improve the symptoms of upper respiratory infection postoperatively ( Tait and Knight, 1987 ). However, the finding by these investigators is applicable only to myringotomy for children with middle ear effusion; it should not be generalized or applied to children with upper respiratory infection (especially in its acute phase with fever) who are scheduled for other surgical procedures ( Hinkle, 1989 ).

In expert hands, the performance of uncomplicated bilateral myringotomies and tube insertions requires only 5 to 10 minutes of operating time; the procedure, however, may take considerably more time when performed by inexperienced trainees or in patients with narrow ear canals. Myringotomy is almost exclusively performed on an outpatient basis.

Preoperative sedation should be administered based on the child's anxiety level. Mask induction of anesthesia with nitrous oxide, oxygen, and sevoflurane (or halothane) provides effective and smooth induction and maintenance anesthesia with prompt emergence. Preoperative or intraoperative analgesia is advocated for early postoperative pain relief. Because these children are usually anesthetized without intravascular access, preoperative administration of oral acetaminophen or nonsteroidal antiinflammatory drugs (NSAIDs) ( Watcha et al., 1992 ) and intraoperative intranasal fentanyl or butorphanol ( Bennie et al., 1998 ; Galinkin et al., 2000 ; Finkel et al., 2001 ) or intramuscular ketorolac ( Pappas et al., 2003 ) has been studied and recommended. It appears intraoperative ketorolac (1 mg/kg, up to 30 mg) administered by the intramuscular route provides superior analgesia than oral or rectal acetaminophen. Ketorolac is associated with less vomiting and minimal sedation compared with intranasal butorphanol and perhaps with fentanyl. However, ketorolac, along with other NSAIDs, should be used with caution because ketorolac affects platelet function, and increased postoperative bleeding during adenoidectomy has been reported ( Dahl and Kehlet, 1994 ; Nikanne et al., 1997 ).

Because children undergoing myringotomy commonly have adenoidal hypertrophy, they may exhibit signs of nasal and upper airway obstruction ( Bluestone and Klein, 2001 ). These children may require continuous positive airway pressure (CPAP) during inhalational induction and an oropharyngeal airway after reaching a surgical plane of anesthesia to maintain a patent airway (see Chapter 2 , Respiratory Physiology, and Chapter 10 , Induction of Anesthesia). Although myringotomy and tube insertion may last less than 10 minutes, it should be performed with standard monitoring (i.e., using a precordial stethoscope, pulse oximeter, electrocardiogram, thermometer, and automated blood pressure cuff). Myringotomy is one of few exceptions in modern pediatric anesthesia practice in the United States for which intravenous infusion is not routinely administered.

Postoperative hypoxemia occurs frequently in infants and children during transport ( Patel et al., 1988) and in the recovery room, even after minor surgical procedures such as myringotomy ( Motoyama and Glazener, 1986 ). After myringotomy, patients are prone to upper airway obstruction, and these children should be transferred to the recovery room in the lateral position while receiving supplemental oxygen (see Chapter 11 , Intraoperative and Postoperative Management).

▪ MASTOIDECTOMY AND TYMPANOPLASTY

The clinical importance of the mastoid process is related to its contiguous structures, which include the posterior and middle cranial fossa, the sigmoid and lateral sinuses, the facial nerve, the semicircular canals, and the petrous tip of the temporal bone. The distal part of the middle ear and mastoid are connected by the aditus ad antrum, making the mastoid susceptible to infection by infectious processes from the middle ear. With improved medical and surgical management of otitis media, mastoidectomy for mastoiditis has declined considerably over the past several decades. However, mastoidectomies may also be performed in association with cholesteatoma removal and tympanoplasty. Tympanoplasty is performed in patients with chronic perforation or atelectasis of the tympanic membrane ( Bluestone and Klein, 2003 ). Deep retraction pockets may lead to squamous epithelium within the middle ear and mastoid cavities, causing a cholesteatoma that may grow by the enzymatic activity of the skin tissues and accumulation of squamous debris.

Tympanoplasty is an operation to reconstruct the tympanic membrane with or without grafting. The primary indications for tympanoplasty are repair of tympanic perforation; stabilization or improvement of hearing; removal or prevention of congenital, iatrogenic, or primary or secondary acquired cholesteatoma; and removal of atelectatic or diseased areas of the tympanic membrane ( Haynes and Harley, 2002). Grafting materials include fat, fascia, perichondrium, periosteum, cartilage, vein, and paper patch.

Mastoidectomy involves the surgical exposure and removal of mastoid air cells. There are several types of mastoidectomy ( Bluestone and Klein, 2003 ). In a complete simple “cortical” mastoidectomy, the mastoid air-cell system is removed, but the canal wall is left intact. The operation is performed for acute or chronic mastoid osteitis, and it is frequently part of the surgical procedure advocated by some surgeons for cholesteatoma.

Posterior tympanotomy or facial recess tympanotomy involves removal of mastoid air cells, followed by formation of an opening between the mastoid and middle ear created in the posterior wall of the middle ear lateral to the facial nerve and medial to the chorda tympani. This procedure allows better visualization of the facial recess without removing the canal wall, and it is primarily advocated for ears in which a cholesteatoma has formed.

With a modified radical mastoidectomy, a portion of the posterior ear canal wall is removed, and a permanent mastoidectomy cavity is created, but the tympanic membrane and some or all of the ossicles are left intact. The procedure is usually performed when a cholesteatoma cannot be removed without removing the canal wall; some function may be preserved.

Radical mastoidectomy involves removal of all mastoid air cells, the posterior ear canal wall, the tympanic membrane, and the ossicles except part or all the stapes. No attempt is made to preserve function. Removal of the posterior ear canal wall allows communication among the exenterated mastoid cellular area, middle ear, and external auditory canal, forming a common single cavity. The procedure is indicated when there is extensive cholesteatoma in the middle ear and mastoid that cannot be removed by a less radical procedure. The operation may be indicated for a suppurative complication of otitis media.

Tympanomastoidectomy with tympanoplasty is the term used when a tympanoplasty is performed in conjunction with a mastoidectomy. Mastoidectomies that leave the posterior ear canal wall intact are closed cavity, canal wall up, or intact canal wall procedures, whereas those in which the posterior canal is partially removed are open cavity or canal wall down procedures.

Anesthetic Management

All children should be monitored with the standard monitoring that includes a pulse oximeter, end-tidal carbon dioxide (CO2) monitor, precordial stethoscope, electrocardiogram, thermometer, and automated blood pressure cuff. Often, electromyography is used to avoid injury to the facial nerve. In these circumstances, neuromuscular blockade is avoided. Standard no oral intake (NPO) guidelines should be followed in nonemergent situations.

For mastoidectomy and tympanoplasty, the patient is positioned supine, with the head laterally rotated away from the affected side. It is important to carefully rotate the neck of a patient under general anesthesia because of the risk of atlantoaxial rotational subluxation ( Brisson et al., 2000 ). Induction of anesthesia may proceed by inhalational or intravenous induction. The anesthesiologist should consider endotracheal intubation without muscle relaxation or with short-acting muscle relaxation so the facial nerve can be monitored during surgery. The use of nitrous oxide may be contraindicated during and after placement of the tympanic graft, because nitrous oxide accumulates in a closed gas space and increases the ambient pressure; some surgeons believe this tends to lift the graft away from its new site ( Koivunen et al., 1996 ; Doyle and Banks, 2003 ).

The most common postoperative complication requiring unscheduled admission to the hospital for children undergoing tympanomastoidectomy is postoperative nausea and vomiting (PONV) ( Megerian et al., 2000 ). PONV has been attributed to surgical stimulation of the vestibular labyrinth, anesthetic techniques, or a combination of the two ( Jellish et al., 1995 ; Dornhoffer and Manning, 2000 ). Propofol has antiemetic properties ( Ved et al., 1996 ; Erb et al., 2002b ). It appears that propofol used for induction and maintenance of anesthesia is superior to isoflurane or sevoflurane in reducing PONV after middle ear surgery (Jellish et al., 1995, 1999 [98] [99]; Moore et al., 2003 ). The use of intravenous dexamethasone during surgery appears to decrease PONV in patients after undergoing tympanomastoid surgery ( Liu et al., 2001 ).

▪ COCHLEAR IMPLANTS

Cochlear implantation has become a feasible choice for profoundly hearing-impaired children (Figs. 23-1 and 23-2 [1] [2]). Profoundly deaf children's auditory nerve fibers remain intact, but the sensory neuroepithelium in the cochlea is absent. This damage occurs because of a genetic defect, infection, cochlear ossification, or aging ( Fischetti, 2003 ). Cochlear implants bypass the damage by receiving and converting sound into signals sent along electrodes to cells adjacent to the auditory nerve. Hearing aids are ineffective because sound cannot be converted into an electrical impulse. Cochlear implants have 8 to 22 electrodes that are placed through a cochleostomy. Sounds received from an external microphone are converted to an electric signal that is received and transmitted by the cochlear nerve ( Balkany et al., 2001 ; Miyamoto and Kirk, 2003 ). Because the cochlea is full size at birth, there is no anatomic difficulty with electrode insertion in very young children.

 
 

FIGURE 23-1  The outer ear collects the pressure waves of a sound, which the eardrum converts into mechanical vibrations in tiny bones in the middle ear. The oscillating stapes sets off pressure waves within the fluid in the cochlea, which stimulates nerve cells on the auditory nerve that leads to the brain. The cochlea transmits pressure waves through its duct fluid, displacing the basilar membrane, which bends hair cells to various degrees. The cells release neurotransmitters that cause attached neurons to fire, telling the brain where along the duct the bending has occurred, which corresponds to the frequency of the original sound, and communicating the amplitude of the bending, which indicates the loudness. The cochlear implant uses a microphone worn behind the ear to pick up sound and send it to a processor, where integrated circuits and algorithms amplify, digitize, and filter the sound into a coded signal sent to the transmitter coil. The coil sends the signal by radio waves through the skin to an implanted receiver. The receiver converts the waves into electrical impulses that travel along electrodes that end at cells at certain points along the cochlea. A magnet in the transmitter holds it against the implanted receiver.  (From Fischetti M: Cochlear implants. To hear again. Sci Am 288:82-83, 2003.)

 

 

 

 
 

FIGURE 23-2  In the Nucleus 24 Counter implant, the active intracochlear electrode array is precurved to wrap around the modiolus. A stylus is used to straighten the electrode during insertion.  (From Miyamoto RT, Kirk KI: Cochlear implants in children. In Bluestone CD, Stool SE, Alper CM, et al., editors: Pediatric otolaryngology, 4th ed. Philadelphia, 2003, WB Saunders, p 809.)

 



Surgery requires 2 to 3 hours, and it is performed through an extended postauricular incision along with a mastoidectomy. Anesthetic considerations are the same as for mastoidectomy, including the avoidance of the muscle relaxants so the facial nerve can be monitored. The anesthesiologist should establish the patient's level of hearing dysfunction so that a method of communication can be established. It is helpful to have a parent or sign language specialist accompany the child to the operating room. If the child reads lips, masks should be kept down from the anesthesiologist's lips until after induction of anesthesia.

▪ OTOPLASTY

Otoplasty is a cosmetic procedure to reconstruct or restructure the auricle. Anesthetic considerations are similar to those in other head and neck cosmetic procedures, with one minor modification. Otoplasty is frequently bilateral, requiring both sides to be simultaneously prepared and draped. To ensure symmetry, simultaneous visualization requires frequent head motion and the endotracheal tube must be well secured.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier

▪ ANESTHESIA FOR RHINOLOGIC PROCEDURES

▪ REDUCTION OF NASAL FRACTURE

A nasal fracture may cause considerable bleeding, and the blood may be swallowed into the stomach. These patients therefore are assumed to have a full stomach, regardless of the time of last food intake. Reduction of a nasal fracture may take only a few moments, but in the acute situation, an oral endotracheal tube is mandatory to protect the airway from pulmonary aspiration. More commonly, surgery is delayed for several days after an isolated nasal fracture to allow swelling to subside. In these cases, a flexible laryngeal mask airway (LMA) can be substituted for an endotracheal tube. The LMA cannot prevent aspiration of stomach contents into the lungs, but it can prevent blood from the nose passing through the vocal cords ( John et al., 1991 ; Williams and Bailey, 1993 ). The LMA may be removed either when the patient is deeply anesthetized or when awake.

▪ NASAL POLYPECTOMY

This procedure is performed under general anesthesia, often using a preformed RAE endotracheal tube, which was originally developed by Ring and colleagues (1975) (see Chapter 9 , Anesthetic Equipment and Monitoring). Packing of the pharynx is indicated in most intranasal procedures. One end of the oropharyngeal gauze packing should be tagged with a hemostat and left hanging externally at one corner of the mouth. A note should be prominently placed in the room for all to see, or a labeled tape should be placed across the exit door, reminding all operating room personnel that a throat pack is in place and needs to be removed. Historically, as much as 10 mcg/kg of epinephrine, usually in a 1:200,000 solution (5 mcg/mL), can be used in children for homeostasis under halothane anesthesia without apparent myocardial irritability ( Karl et al., 1983 ; Ueda et al., 1983 ). However, most clinicians have changed their choice of maintenance anesthetic to isoflurane, sevoflurane, desflurane, propofol, or remifentanil, regardless of the epinephrine dose (see Chapter 11 , Intraoperative and Postoperative Management).

Special consideration should be given to the management of children with cystic fibrosis, in whom nasal polyps often occur ( Hulka, 2000 ) (see Chapter 32 , Systemic Disorders). The polyps are multiple and recur after removal. These children often have severe obstructive lung disease with recurrent pulmonary infection and thick, tenacious secretions. They are frequently hypoxemic in room air. During general anesthesia, the cystic fibrosis patient may require frequent endotracheal lavage with saline and deep suctioning. Secretions can hamper oxygenation and ventilation; a rise in the peak inspiratory pressure intraoperatively may indicate that the endotracheal tube requires suctioning. An inhaled bronchodilator should be immediately available to treat bronchospasm. Inhaled anesthetics and nitrous oxide or opioids and a relaxant may be used for patients with mild to moderate airway obstruction. Nitrous oxide should be avoided in those with severe lower airway obstruction with air trapping because of possible hyperinflation of trapped air spaces and alveolar rupture.

In addition to pulmonary pathology, upper airway obstruction frequently occurs in these patients. During induction, the mouth must be kept open because nasal air passages may be completely blocked by the polyp. Nasal packing, usually placed at the completion of the surgical procedure, may lead to further problems in ventilation and oxygenation in the postoperative period. This situation is partially relieved if the surgeon first introduces a nasopharyngeal airway and then packs around it. If preoperative pulmonary function is poor, the physician should consider transferring the patient to the intensive care unit, with the endotracheal tube in place, for immediate postoperative respiratory care.

▪ SINUS SURGERY

Sinus surgery is indicated for children who have failed maximum medical therapy. Children with allergy or gastroesophageal reflux disease should receive maximal medical therapy and should rarely require surgery ( Goldsmith and Rosenfeld, 2003 ). Children with immune deficiency, immotile cilia syndrome (i.e., Kartagener's syndrome), or cystic fibrosis ( Gysin et al., 2000 ) are at high risk for chronic sinusitis. Unfortunately, because of their underlying disease, these children have a significant surgical failure rate ( Herbert and Bent, 1998 ).

In children with recurrent sinusitis without chronic disease, adenoidectomy should be the initial procedure if the quantity of adenoid tissue visualized on endoscopy is considered sufficient to serve as a reservoir of bacterial pathogens. Adenoidectomy or adenotonsillectomy is usually the first-line surgical intervention for preschoolers, and it is often appropriate in older children. The expected rate of improvement is 70% to 80% ( Goldsmith and Rosenfeld, 2003 ).

Endoscopic sinus surgery (ESS) should be performed only when children have failed previous therapies. In contrast to older traditional techniques of sinus surgery, ESS focuses on enlarging the natural ostia of the maxillary and ethmoid sinuses, while preserving most or all of the sinus mucosa ( Goldsmith and Rosenfeld, 2003 ). In addition to children with chronic sinusitis who fail medical management, Lusk (2003) lists the accepted indications for ESS as complete nasal obstruction in patients with cystic fibrosis, antrochoanal polyp, intracranial complications, mucoceles and mucopyoceles, orbital abscess, traumatic injury in the optic canal, dacrocystorhinitis due to sinusitis, fungal sinusitis, certain neoplasms, and meningoencephalocele. In properly selected children, the results are good, with an expected improvement of 80% ( Lusk, 2003 ). Preoperative computed tomography (CT) is essential in defining the specific diseased sinuses and in looking for anatomic abnormalities that need to be addressed, including septal deviation, concha bullosa cells, obstructing Haller air cells, and abnormal middle turbinates ( Goldsmith and Rosenfeld, 2003 ).

ESS is performed under general anesthesia using an oral preformed (RAE) or standard endotracheal tube. Many of these children have chronic disease or upper airway obstruction. The anesthetic approach is similar to that described for nasal polypectomy and adenotonsillectomy. The surgeon may elect to use topical oxymetazoline (0.25% to 0.50%) for initial vasoconstriction and then infiltrate the tissue with lidocaine (0.5%) and epinephrine (1:100,000 solution) for hemostasis. The surgeon and the anesthesiologist should be aware that the duration of vasoconstriction usually does not last longer than 1.5 hours, and when surgical procedures are not completed within this period, mild bleeding may make visualization of the surgical site difficult and present a potential problem postoperatively. Some surgeons routinely pack the nose with gauze after the procedure for hemostasis, and the patient becomes an obligate mouth breather. Other surgeons may elect to use Surgicel or FloSeal to obtain hemostasis, and each of these may have the potential for migration into the lower airway.

▪ CHOANAL ATRESIA

Choanal atresia is a congenital malformation in which no connection exists between the nasal cavity and the aerodigestive tract ( Prasad et al., 2002 ); it has an incidence of 1 in 7000 births. The atresia is bony (30%) or mixed membranous and bony (70%). The existence of purely membranous atresia has come into question ( Brown et al., 1996 ). Choanal atresia is unilateral in 50% to 60% of patients. Syndromes associated with choanal atresia include Apert's syndrome, DiGeorge syndrome, trisomy 18, Treacher Collins syndrome, camptomelic dysplasia, and CHARGE association (i.e., coloboma, heart defects, atresia choanae, retardation of growth and development, genitourinary problems, and ear anomalies) ( Telfick et al., 1997) .

The symptoms caused by choanal atresia depend on whether the obstruction is unilateral or bilateral. Because neonates are obligatory nasal breathers, those with bilateral disease present with acute respiratory distress. Respiratory distress can be attenuated if the mouth is kept open with an oral airway strapped in place or by a large rubber nipple with a large hole cut in it and kept in place with an umbilical tape around the neck ( McGovern, 1961 ; Hengerer and Wein, 2003 ). For the neonate with bilateral choanal atresia, surgical nasal correction or tracheostomy must be performed within the first few days of life. Other infants may have only unilateral atresia, with minimal symptoms that can go undiagnosed for months or even years. The most common complaint is intractable unilateral anterior nasal discharge.

A number of surgical procedures have been described for the correction of choanal atresia, including endoscopic, transnasal, transseptal, and transpalatal procedures ( Holland and McGuirt, 2001 ). Timing of surgery for bilateral choanal atresia varies, and it depends on the infant's ability to adapt to oral breathing and acquire adequate nutrition. Hengerer and Wein (2003) state that some surgeons advocate “a rule of tens” to guide the timing of surgical intervention. The child must reach 10 weeks of age, weigh 10 pounds, and have a hemoglobin level of 10 g. Other surgeons have demonstrated routine success in newborns 48 to 72 hours old and weighing as little as 1900 g (Werkhaven J, personal communication, 2003).

The anesthetic approach depends on the child's condition. In general, intravenous induction with a muscle relaxant of intermediate duration, endotracheal intubation with an oral RAE tube, and maintenance with an inhaled agent and opioid or propofol and remifentanil infusion suffice. Rarely, algorithms for difficult neonatal intubation must be used for securing the airway in infants with bilateral choanal atresia. After the atresia is surgically corrected, the surgeon is often faced with the problem of restenosis ( Pirsig, 1986 ). Two innovations have created optimism that the restenosis rate can be reduced. Newer endoscopic techniques with powered instrumentation have enhanced safety and efficacy for choanal atresia repair ( Prasad et al., 2002 ). Mitomycin-C, an aminoglycoside and alkylating agent used as an intravenous antineoplastic agent, can be used topically after choanal atresia repair. Topical application inhibits fibroblast growth and migration and granulation tissue formation responsible for restenosis ( Holland and Mcguirt, 2001 ). Topical mitomycin has not caused systemic effects and has not contributed to anesthetic complications.

Postoperatively, patients with unilateral obstruction usually do well and require no special monitoring. However, infants undergoing bilateral repair can exhibit partial or intermittent upper airway obstruction that persists for some time. The infant should be observed closely in the intensive care unit with appropriate monitoring until breathing dynamics have normalized.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier

▪ ANESTHESIA FOR PHARYNGEAL AND LARYNGEAL PROCEDURES

▪ TONSILLECTOMY AND ADENOIDECTOMY

Tonsillectomy and adenoidectomy (perhaps with the exception of myringotomies) are the most common pediatric surgical procedures performed in the United States. Although tonsillectomy and adenoidectomy are frequently performed procedures, the benefits in relation to cost and risk are still hotly debated ( Paradise, 2003 ). Just about every indication has its advocates and detractors ( Bluestone, 2001 ; Paradise, 2003 ).

Nocturnal upper airway obstruction, with or without obstructive sleep apnea, is a common indication for adenotonsillectomy. A mild, partial obstruction in otherwise healthy children is exacerbated by conditions such as achondroplasia, Down syndrome, mucopolysaccharidosis, and obesity. Adenotonsillectomy is considered curative when adenotonsillar hypertrophy is the primary cause of childhood sleep-related breathing disorders ( Schechter, 2002 ). Indications for tonsillectomy include recurrent pharyngotonsillitis, chronic tonsillitis, hemorrhagic tonsillitis, peritonsillar abscess, streptococcal carriage, dysphagia, abnormal dentofacial growth, halitosis, and suspicion of malignant disease (i.e., tonsil asymmetry) ( Darrow and Siemans, 2002) . Additional indications for adenoidectomy include recurrent or chronic rhinosinusitis or adenoiditis, and recurrent otitis media ( Darrow and Siemans, 2002) . Adenotonsillar hypertrophy with resultant upper airway obstruction is the most frequent cause of obstructive sleep apnea in children ( Fig. 23-3 ).

 
 

FIGURE 23-3  Adenoidal and tonsillar hypertrophy. A, Dull expression of a child with marked adenotonsillar hypertrophy and nasal obstruction (i.e., adenoid facies). He must keep his mouth open to breathe and shows signs of fatigue as a result of obstructive sleep apnea caused by upper airway obstruction. B, On examination of the pharynx, his enlarged tonsils are seen meeting in the midline.  (From Yellon RB, McBride TP, Davis HW: Otolaryngology. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, 4th ed. St. Louis, 2002, Mosby, p 836.)

 



Obstructive Sleep Apnea Syndrome

Obstructive sleep apnea syndrome (OSAS) is a disorder of breathing during sleep characterized by prolonged partial upper airway obstruction or intermittent complete obstruction (i.e., obstructive apnea) that disrupts normal sleep-time breathing and normal sleep patterns ( American Thoracic Society, 1996 ). OSAS also occurs in children with upper airway narrowing due to craniofacial anomalies and in those with neuromuscular diseases, including cerebral palsy and muscular dystrophy ( Marcus, 2001 ).

Adenotonsillar hypertrophy is the most common cause of OSAS in children. Many published papers, primarily case reports and case series, support the idea that tonsillectomy with or without adenoidectomy is often the cure for OSAS ( Schechter et al., 2002) .

The peak prevalence of OSAS occurs at 2 to 8 years, which is the age the tonsils and adenoids are proportionately large in relation to the child's upper airways. The site of collapse is most commonly at the level of the adenoids or velopharynx ( Isono et al., 1998 ). Although OSAS is associated with adenotonsillar hypertrophy, there must be other neuromuscular factors involved. These patients usually do not obstruct while awake, implying sleep induces another dimension to OSAS. Some otherwise normal children with OSAS with smaller tonsils and adenoids are cured by adenotonsillectomy, whereas others with larger tonsils and adenoids are not ( Marcus, 2001 ). The patency of pharyngeal airway is maintained by tonic and phasic contractions of the upper airway dilator muscles, such as the genioglossus, geniohyoid, and velopalatine muscles. Compared with other inspiratory muscles (i.e., diaphragm and intercostal muscles), these upper airway muscles are preferentially depressed with sleep, sedatives, and general anesthetics (Ochiai, Guthrie, Motoyama, 1989, 1992 [152] [153]) (see Chapter 2 , Respiratory Physiology). It is hypothesized that children with OAS may have abnormal centrally mediated activation of their airway muscles, leading to a more collapsible upper airway ( Marcus et al., 1994 ).

Symptoms of OSAS include nocturnal snoring, breathing pauses, gasping, use of accessory muscles of respiration, enuresis, and excessive sweating ( Messner, 2003 ). The diagnosis of OSAS is based on a thorough history and physical examination along with appropriate sleep studies, including polysomnography. Snoring, increased respiratory efforts, periodic obstructive apnea, and oxygen desaturation while sleeping are the universal features of OSAS, which must be differentiated from the benign condition referred to as primary snoring. Although definitive diagnosis of OSAS is made by a positive polysomnogram, many children are not tested because the polysomnography laboratories specializing in children are few in number, and the tests are expensive and require an overnight stay ( Sterni and Tunkel, 2003 ). Most children are diagnosed by recommendations set forth by the section of Pediatric Pulmonology Subcommittee on Obstructive Sleep Apnea, sans Polysomnography. This committee's recommendations for otherwise healthy children older than 1 year are as follows ( Schechter, 2002 ):

  

1.   

All children should be screened for snoring. As part of routine health care maintenance for all children, pediatricians should ask whether the patient snores. An affirmative answer should be followed by a more detailed evaluation.

  

2.   

Complex, high-risk patients should be referred to a specialist.

  

3.   

Patients with cardiorespiratory failure cannot await elective evaluation. It is expected that these patients will be in an intensive care setting and will be treated by a specialist; these patients are not covered in this practice guideline.

  

4.   

Thorough diagnostic evaluation should be performed. History and physical examination have been shown to be poor in discriminating between primary snoring and OSAS. Polysomnography is the only method that quantifies ventilatory and sleep abnormalities, and it is recommended as the diagnostic test of choice. Other diagnostic techniques, such as videotaping, nocturnal pulse oximetry, and daytime nap studies, may be useful in discriminating between primary snoring and OSAS. However, they do not assess the severity of OSAS, which is useful for determining treatment and follow-up.

  

5.   

Adenotonsillectomy is the first line of treatment for most children. CPAP is an option for those who are not candidates for surgery or do not respond to surgery.

Children with OSAS have a host of sequelae, which are usually reversible after adenotonsillectomy but can lead to perioperative complications during and after surgery. Children with OSAS may present with failure to thrive, although the cause of this growth failure is unclear ( Sterni and Tunkel, 2003 ). Many of these children experience a growth spurt after surgery. Children with OSAS may have neurocognitive deficits such as poor learning, behavioral problems, and lower grades in school than non-OSAS children. Adenotonsillectomy improves functioning in these children ( Marcus, 2001 ).

Severe, untreated OSAS may lead to pulmonary hypertension and cor pulmonale caused by nocturnal hypoxia and hypercarbia resulting in compensatory changes in the pulmonary vasculature. Pulmonary vascular resistance increases, causing increased right ventricular strain. Severe cases may progress to pulmonary hypertension, arrhythmias, and cor pulmonale, which are reversible by performing early adenotonsillectomy ( Miman and Kirazli, 2000) . Children with OSAS also tend to have higher diastolic blood pressures. The cardiovascular changes appear to be the result of an increase in sympathetic tone that results from obstructive respiratory events ( Marcus et al., 1998 ). Fortunately, few children develop clinically significant heart failure. It is prudent to pursue an aggressive cardiac evaluation if the child has a loud second heart sound, has exercise intolerance, or has diastolic hypertension. Because children are diagnosed earlier today, significant heart disease is rarely an issue ( Marcus, 2001 ). Tonsillectomies, adenoidectomies, and adenotonsillectomies are performed on an outpatient basis, except for patients with a history of OSAS.

Preoperative Preparations

A careful review of the history, laboratory data, and physical examination results are essential for the optimal outcome of adenotonsillectomy. Careful evaluation of coagulation status is important before performing this procedure. If there is a history of easy bruisability, frequent epistaxis, or positive family history, the prothrombin time (PT), partial thromboplastin time (PTT), and platelet count should be obtained to rule out coagulopathies. In many pediatric institutions, a coagulation profile is obtained routinely for patients scheduled for adenotonsillectomy. However, in a prospective study of hemostatic assessment of patients before tonsillectomy, routine measurements of a coagulation profile were not useful predictors of postoperative bleeding ( Close et al., 1994 ).

Although relatively mild, von Willebrand's disease (i.e., reduced factor VIII, decreased platelet adhesiveness because of deficient von Willebrand factor) is the most common coagulopathy seen among patients scheduled for adenotonsillectomy. Children with von Willebrand's disease or mild hemophilia A are treated preoperatively with desmopressin (1-desamino-8-D-arginine vasopressin [DDAVP]) (Prinsley et al., 1993 ). DDAVP is a synthetic analogue of vasopressin, which, in addition to its antidiuretic effect, stimulates endothelial cells and releases stored factor VIII and von Willebrand factor (Mannucci, 1988) . The intravenous dose of DDAVP is 0.3 mcg/kg, given over 20 minutes before anesthetic induction.

The examiner should elicit a history of drug ingestion, especially acetylsalicylic acid (ASA). If the patient was given ASA-containing drugs recently, surgery should be postponed, because these drugs cause platelet dysfunction for as long as 10 days and may cause excessive bleeding intraoperatively and postoperatively ( Davies and Steward, 1977 ; Paradise, 2003 ).

During the preoperative visit, the patency of oral and nasal air passages is carefully examined. The patient's mouth should be inspected for the degree of tonsillar hypertrophy or inflammation. The examiner should also have the child breathe with the mouth closed to evaluate the degree of nasal airway obstruction and estimate adenoidal hypertrophy. It is important to inspect the teeth routinely, because tonsillectomy is often performed on children who are losing their primary dentition. Any teeth missing preoperatively should be noted carefully. A tooth that is loose should be pointed out to the parent and child, with the explanation that it may be necessary to remove it while the child is anesthetized (it must then be saved). It is also possible for the surgeon to dislodge or chip teeth in the application of a mouth gag or during other intraoperative manipulations.

Anesthetic Management

All children should be monitored with a pulse oximeter, end-tidal CO2 precordial stethoscope, electrocardiogram, thermometer, and automated blood pressure. Oxygen saturation is determined in room air before the induction of anesthesia to establish the baseline value. If neuromuscular blockade is required, a nerve stimulator should be used to track the depth of paralysis. Standard NPO guidelines should be followed in nonemergent situations.

Children who are anxious preoperatively may receive sedation with oral midazolam. In older children scheduled for intravenous induction, EMLA cream (i.e., eutectic mixture of local anesthetics, 2.5% lidocaine and 2.5% prilocaine) is applied to the dorsum of both hands and sealed with plastic adhesives at least 1 hour before intravenous catheter insertion (see Chapter 8 , Preoperative Preparation, andChapter 10 , Induction of Anesthesia).

The anesthetic approach to tonsillectomy or adenoidectomy is similar to the methods described for myringotomies. Adenoidectomy is a relatively short procedure (15 to 45 minutes), and many centers perform anesthesia without neuromuscular blockade and with less opioid than suggested in the following descriptions. Anesthesia is induced most commonly with oxygen and nitrous oxide followed by sevoflurane. As with those undergoing myringotomies, children with adenotonsillar hypertrophy often have partial or complete nasal airway obstruction. The mouth must be kept open during the induction of anesthesia until the gag reflex is abolished and the oral airway is inserted. Moderate CPAP (10 to 15 cm H2O) during induction before the oral airway insertion helps to prevent pharyngeal airway collapse as a result of the relaxation of upper airway muscle tone ( Reber et al., 2001 ; Bruppacher et al., 2003 ) (see Chapter 2 , Respiratory Physiology, and Chapter 10 , Induction of Anesthesia).

After the intravenous route is established, atropine or glycopyrrolate may be given for its anticholinergic effects. The patient's trachea is intubated with a preformed oral (RAE) tube under deep inhalational anesthesia, inhalational anesthesia supplemented with propofol, or with the aid of an intermediate-acting, nondepolarizing muscle relaxant (e.g., cisatracurium, vecuronium). In older children, anesthesia may be induced intravenously with propofol (2 to 3 mg/kg) mixed with lidocaine (1 to 2 mg/mL of propofol) to reduce pain at injection site, with or without anticholinergic agent or a muscle relaxant. If thiopental is used for induction then it must be supplemented with an inhaled anesthetic or muscle relaxant before intubating the trachea. Inhalation anesthetic or propofol infusion is continued thereafter with spontaneous or controlled ventilation. A cuffed endotracheal tube is preferred to reduce the chance of aspiration of blood and secretions and to reduce gas leaks around the tube. A cuffed endotracheal tube, 0.5 to 1.0 mm ID smaller than the age-appropriate size, should be chosen to accommodate the passage of the cuff through the subglottis ( Khine et al., 1997 ; James, 2001 ; Fine and Borland, 2004 ). The endotracheal tube is immobilized with adhesive tape over the middle of the lower lip ( Fig. 23-4 ). The breath sounds on both sides of the chest should be auscultated carefully to avoid endobronchial intubation. The endotracheal tube is then held in place by the groove-bladed tongue depressor that is a part of the Ring adaptation of the Brown-Davis mouth gag ( Fig. 23-5 ).

 
 

FIGURE 23-4  For tonsillectomy or adenoidectomy, an oral RAE endotracheal tube is fixed over the middle of the lower lip.

 

 

 
 

FIGURE 23-5  Patient in position for tonsillectomy. A Brown-Davis mouth gag holds the mouth open. An oral RAE endotracheal tube is fixed to the middle of the lower lip and is held in the groove of the tongue blade.

 

 

Anesthesia is maintained with supplemental opioids to reduce the requirement of the anesthetic maintenance agent and to provide postoperative analgesia. The physician may start with a loading dose of 1 to 2 mcg/kg of fentanyl, 50 to 100 mcg/kg of morphine, or 10 to 20 mcg/kg of hydromorphone given intravenously, with additional doses administered as needed. There is evidence that high doses of dexamethasone (up to 1 mg/kg, 25 mg maximum) reduce postoperative swelling and pain and decrease the incidence of PONV without apparent adverse effects attributable to dexamethasone ( Pappas et al., 1998 ). Children receiving dexamethasone are more likely to advance to a soft-solid diet on the first postoperative day ( Steward et al., 2003 ).

Bleeding during tonsil and adenoid surgery seldom is excessive, but massive hemorrhage has occurred with tearing of the carotid vessels (Smith, 1972, 1980 [193] [194]). Homeostasis is usually obtained using electrocautery. There have been several reports of fires due to electrocautery-induced ignition of the endotracheal tube or packing during tonsillectomy. Fires are caused by combustible material in an oxygen-rich environment ( Mattucci and Militana, 2003 ); management of airway fires is discussed in a later section.

At the conclusion of surgery, the surgeon usually suctions the pharynx and larynx under direct vision to prevent bleeding caused by agitation of raw mucosal surfaces by a suction catheter. Some surgeons elect to superficially infiltrate 0.25% bupivacaine into the tonsillar fossa to aid in postoperative pain relief. This practice, however, has been associated with airway obstruction after extubation. The anesthesiologist should always use a plastic tonsil suction tip and should never blindly suction the nasopharynx or oropharynx after adenoidectomy or tonsillectomy. Before a child regains active reflexes toward the completion of surgery, the anesthesiologist should auscultate both sides of the chest to rule out the presence of aspirated blood or secretions and, under direct laryngoscopic visualization, examine the mouth and pharynx for blood and other debris that could cause irritation after extubation.

Laryngospasm may occur when the patient is extubated after tonsillectomy. Methods for avoiding this problem include extubating the trachea while the child is deeply anesthetized (not recommended for children with OSAS) or almost completely awake (see Chapter 11 , Intraoperative and Postoperative Management). Although intravenous lidocaine has not consistently proved helpful in preventing laryngospasm, application of local anesthetic before intubation or manipulation of the airway can reduce the incidence of laryngospasm during intubation and after extubation ( Leicht et al., 1985 ;McCulloch et al., 1992 ; Landsman, 1997 ). It appears that lidocaine deposited locally in the laryngeal area suppresses laryngeal mucosa neuroreceptor transmission. However, lidocaine's duration of action at laryngeal receptor sites is only 30 minutes, and its administration before intubation may not protect against laryngospasm at the time of extubation ( Warner, 1996 ).

Conventional “preoxygenation” with 100% oxygen before extubation, which has been practiced for decades, may cause more atelectasis than breathing oxygen mixed with air. An air mix (FIO2 of 0.5 to 0.7) together with slow deep sighs (or vital capacity maneuvers) before extubation can minimize the development of atelectasis after general anesthesia ( Benoit et al., 2002 ; Tusman et al., 2003 ). These authors suggest that the patient should breathe a 1:1 to 1:2 air-oxygen mixture (60% to 73% oxygen) instead of 100% oxygen. The lungs are then slowly inflated to a peak pressure of 30 to 35 cm H2O several times (i.e., vital capacity maneuvers) to eliminate atelectasis that has developed during the course of general anesthesia. This can be achieved by closing and reopening the exhaust valve of the anesthesia circuit while the patient breathes spontaneously against CPAP. The endotracheal tube is left in place until the child reestablishes adequate rhythmic breathing on air-oxygen mixture. The child is then extubated as the anesthesiologist squeezes the bag by hand with the exhaust valve nearly closed, so that a moderate positive pressure (15 to 20 cm H2O) is maintained to the endotracheal tube and the lungs. Positive extending pressure on the airway walls also attenuates the excitation of the superior laryngeal nerve and may diminish the risk of laryngospasm ( Suzuki and Sasaki, 1977 ; Sasaki, 1979 ) (see Chapter 2 , Respiratory Physiology). Positive airway pressure at the moment of extubation causes a coughing motion, which helps expel secretions around the vocal cords; lungs filled with a high concentration of oxygen maintain oxygenation of the child for several minutes in the event of laryngospasm. The mouth is suctioned again to remove blood and secretions brought up by the endotracheal tube during its removal. For the management of laryngospasm, see Chapter 10 (Induction of Anesthesia) and Chapter 11 (Intraoperative and Postoperative Management).

Postoperative Management

Children with hypertrophic tonsils and adenoids tend to have increased airway obstruction immediate postoperatively. The presence of blood and secretions in the pharynx and larynx may provoke upper airway reflexes. These patients tend to become hypoxemic more often and perhaps more severely during the first several hours after surgery than patients undergoing procedures not involving the upper airways ( Motoyama and Glazener, 1986 ). However, they seem to maintain their preoperative levels of oxygen saturation in room air thereafter, as determined with pulse oximetry (Motoyama and Borland, unpublished observations). Fortunately, serious complications after adenotonsillectomy are infrequent. Postoperative hemorrhage, however, does occur and can become a life-threatening catastrophe (discussed later). Postoperative emesis is relatively common because of pharyngeal mucosal irritation from surgery and bloody secretions that are swallowed. It is therefore prudent for the anesthesiologist to administer antiemetics (i.e., ondansetron or metoclopramide) prophylactically in addition to dexamethasone before the end of surgery ( Pappas et al., 1998 ). Pain after tonsillectomy is mild to moderate and may be controlled by opioids given intraoperatively as part of anesthetic management or by supplementation (morphine, 50 mcg/kg; fentanyl, 0.5 to 1.0 mcg/kg; hydromorphone, 10 mcg/kg) in the postanesthetic care unit. Postoperative pain after adenoidectomy is relatively mild. Acetaminophen is a good adjunct to pain control in these patients.

Children undergoing adenotonsillectomy for OSAS require close observation after surgery and are not candidates for same-day surgery. These children have a higher incidence of postoperative respiratory complications, including prolonged oxygen requirements, airway obstruction requiring nasal airway, and major respiratory compromise requiring airway instrumentation ( Biavati et al., 1997 ; Wilson et al., 2002) . Because OSAS is a disorder of anatomic and dynamic factors of upper airway function, it is not surprising a procedure that is curative in many of these children would cause significant postoperative respiratory complications. Because these children are presumed to have impaired neuromuscular control of upper airway patency, residual anesthetic effects combined with blood, edema and residual lymphoid tissue obstructing the postsurgical airway can lead to postoperative respiratory events ( Wilson et al., 2002) . McColley and others (1992) reported a 58% incidence of severe respiratory compromise in children younger than 3 years that was associated with severe oxygen desaturation (SpO2 < 70%) or hypoventilation from upper airway obstruction. Among children with obstructive sleep apnea undergoing adenotonsillectomy (mean age, 5 years), intraoperative and postoperative complications are particularly high among those who were born prematurely (85% versus 25% to 34% in full-term infants). Children with OSAS tend to emerge from anesthesia slower than children without OSAS. This may be explained by their deficit in sleep arousal mechanisms. They seem to have elevated sleep arousal mechanisms in response to hypercarbia and increased upper airway obstruction (Marcus et al., 1998, 1999 [122] [123]). Other subtle disturbances of sleep architecture may be present ( Bandla et al., 1999 ).

A rare complication of adenotonsillectomy in children with severe OSAS is pulmonary edema resulting from relief of upper airway obstruction. The exact cause is unknown. Galvis and others (1980)hypothesized that during obstructed breathing, extreme negative pressures occur in the intrapleural and intrathoracic compartments. Intubation results in sudden equalization of pressure. The pulmonary venous pressure is suddenly much higher than intrathoracic pressure, resulting in pulmonary hyperemia and edema. Furuhashi-Yanaha and colleagues (2000) hypothesized that the abrupt switch from nasal to oral breathing during emergence from anesthesia might create acute obstruction, which creates an increase in negative intrapleural pressure leading to pulmonary edema. Regardless of the cause, these children require oxygen, diuretic therapy, and possible reintubation to provide CPAP or positive end-expiratory pressure (PEEP). This condition usually resolves in 24 to 48 hours ( Carcillo, 2003 ).

Posttonsillectomy Bleeding

Occasionally, bleeding continues or recurs after tonsillectomy, and the child must be anesthetized to suture or pack the bleeding area. Posttonsillar bleeding is classified as primary or secondary bleeding. Primary bleeding occurs within the first 24 hours after surgery; primary bleeding is usually more brisk and profuse than secondary bleeding. Most fatal hemorrhages occur within the first 24 hours after surgery ( Randall and Hoffer, 1998 ). Most posttonsillectomy bleeding occurred within the first 6 hours after surgery ( Crysdale and Russel, 1986 ; Carithers et al., 1987 ; Guida and Mattucci, 1990 ). It is therefore desirable to keep the patients undergoing tonsillectomy and adenoidectomy in the same-day surgery setting for up to 6 to 8 hours to minimize the risk of hemorrhage after discharge from the hospital ( Carithers et al., 1987 ; McGoldrick, 1993 ).

Secondary bleeding usually occurs 24 hours to 5 to 10 days after surgery, when the eschar covering the tonsillar bed sloughs ( Verghese and Hannallah, 2001 ). Allen and others (1973) reported a 0.1% incidence of posttonsillectomy bleeding necessitating repeat exploration in the operating room. Crysdale and Russel (1986) reported a 2.15% incidence of bleeding during the overnight stay in the hospital for 9400 children undergoing tonsillectomy with or without adenoidectomy. Of these, 3% (0.06% of all patients) required reexploration under general anesthesia.

The child with tonsillar bleeding may be brought back to the anesthesia service several hours postoperatively or even days or weeks after the surgery. Because primary bleeding tends to be more rigorous, bleeding may obstruct the view of the larynx and emergent tracheostomy may be needed. The otolaryngologist should be present before anesthetic induction. Whether the bleeding is primary or secondary, the following issues must be addressed before induction of anesthesia. The child usually is hypovolemic, anemic, agitated, or in shock, with a stomach full of blood clots and often without an intravenous catheter. This is one of the most dangerous and challenging situations in pediatric anesthesia practice, and the failure to initiate prompt action has been one of the main causes of death associated with tonsillectomy ( Alexander et al., 1965 ).

Under these circumstances, intravenous access must be reestablished, unless it is still in place to rehydrate or transfuse without delay. It is frequently difficult to find a suitable vein for insertion of a large enough catheter (at least 22 gauge for infants, 20 gauge for children) for rapid hydration and transfusion in an agitated and hypovolemic child with extreme cutaneous vasoconstriction. An intraosseous infusion or surgical cutdown may be indicated in some patients.

It may be difficult to estimate the extent of blood loss and dehydration. The patient may be tachycardic and have an elevated blood pressure caused by the release of endogenous catecholamines from hemorrhage, hypovolemia, or fear and excitement. If the child is sitting up and talking without feeling dizzy, hypovolemia is only mild to moderate; there is enough time to evaluate his or her volume status with the determination of hemoglobin, hematocrit, and urine specific gravity and to obtain additional information on his or her overall physical status. If the child is lying down and has pale conjunctivae, hypotension, and diminished consciousness, he or she may be on the verge of hypovolemic shock and volume resuscitation must begin without delay. In most cases, tonsillar bleeding is not massive, and the child should be rehydrated and transfused as needed before the induction of anesthesia. Hematocrit values should be rechecked after rehydration to have a more accurate estimate of blood loss.

The anesthesiologist must be aware that the child and parents are extremely frightened. If the patient's condition permits, he or she may be sedated with intravenous midazolam to relieve anxiety. Before the induction of anesthesia, all the precautions and preparations for the patient with a full stomach should be made. These include at least one, but preferably two, well-functioning suction apparatuses with large-bore suction tubes, extra laryngoscope handles and blades, and several cuffed endotracheal tubes with lubricated stylets in place. An experienced assistant should always be available to help the anesthesiologist and to apply cricoid pressure during the rapid-sequence induction (see Chapter 10 , Induction of Anesthesia).

After preoxygenation, atropine (0.02 mg/kg) and a defasciculating dose of nondepolarizing muscle relaxant in older children, the child is intubated most commonly with a rapid sequence technique using sodium thiopental (3 to 6 mg/kg), propofol (2 mg/kg), etomidate (0.3 to 0.4 mg/kg), or ketamine (2mg/kg), with doses guided by the patient's hemodynamic status, and succinylcholine (2 mg/kg), with cricoid pressure. Alternatively, rocuronium (1.2 mg/kg) may be used. When using thiopental and rocuronium for induction, significant precipitation will occur if they are given together without flushing the intravenous tubing between the two drugs. If the child is still anemic or dehydrated before induction, ketamine (2 mg/kg) may be used instead of propofol or thiopental, because the latter two drugs may cause profound myocardial depression and hypotension. A cuffed endotracheal tube is used in these cases to prevent blood from entering the trachea around the uncuffed tube ( Berry, 1982 ).

Management of anesthesia during maintenance and emergence in these patients focuses on hypovolemia and a full stomach. A large-bore gastric tube is introduced through the mouth to decompress the stomach, although it is not possible to evacuate all blood clots and solid food. Both sides of the chest are carefully auscultated, and the endotracheal tube is suctioned to rule out aspiration of blood or gastric contents. When there is doubt, fiberoptic bronchoscopy may be performed before extubation, and a portable chest radiograph is taken in the operating room or in the postanesthetic care unit. The endotracheal tube is left in place until the child is fully awake and normal gag and cough reflexes have returned.

The death of a child as a consequence of tonsil and adenoid surgery is particularly tragic because the operation in most cases is elective in nature and the child is in relatively good health. Mortality rates reported in the literature range from 1 in 1000 to 1 in 27,000 ( Bluestone et al., 1975 ; Avery and Harris, 1976 ). The anesthesia-related mortality unadjusted for age is reported to be 1 in 14,000 ( Avery and Harris, 1976 ).

Peritonsillar Abscess

Peritonsillar cellulitis and abscess occur more frequently in older children and adults than in young children. Most infections appear to originate in the tonsil and spread to the peritonsillar space between the tonsillar capsule and the superior constrictor muscle. The infection may spread upward into the palate but usually does not invade the posterior tonsillar pillar or the posterior pharyngeal wall ( Teele, 1983 ). The patient presents with complaints of severe sore throat, difficulty in swallowing, and high fever. Progressive difficulty in opening the mouth may develop because of spasm of the pterygoid muscles. It is therefore imperative to determine the extent of limitation of mouth opening preoperatively. The affected tonsillar area is markedly inflamed and swollen, and the uvula is displaced to the opposite side (Cook, 1982 ). In older children and adolescents, it is possible to perform incision and drainage of a peritonsillar abscess with intravenous sedation using an opioid and topical or local anesthesia, with the patient in a head-down position and his or her head turned to the side of the abscess. If this is not possible, general endotracheal anesthesia is necessary.

The child should be well sedated. Anesthesia is induced with oxygen, nitrous oxide, and sevoflurane by mask or with intravenous sodium thiopental or propofol. Anesthesia is deepened in oxygen without nitrous oxide while spontaneous breathing is maintained and assisted in a head-down tilt with the head turned toward the affected side. Under deep inhalational anesthesia, the larynx is exposed carefully with the laryngoscope blade for intubation with a cuffed endotracheal tube. It is advantageous to let the patient breathe spontaneously and maintain the upper airway muscle tone and airway patency. Muscle relaxants should not be given until the anesthesiologist is certain that the airway can be maintained by mask and bag. Two large-bore suction catheters and tonsil suction tips should be on hand in case the abscess ruptures during the process of laryngoscopy and intubation.

Use of the Laryngeal Mask Airway During Adenotonsillectomy

Since the early 1990s, there have been several reports (but no scientific studies) describing the use of the armored LMA rather than an endotracheal tube for airway support during tonsil or adenoid surgery. The armored LMA can be held within the Boyle-Davis gag and remain patent ( Alexander, 1990 ) ( Fig. 23-6 ). The reported benefits of using the LMA are avoiding tracheal intubation with its associated complications of trauma, cardiovascular stimulation, endobronchial intubation, coughing, laryngospasm, and subglottic edema ( Hatcher and Stack, 1999 ). The disadvantages of the armored LMA include the risk of aspiration of stomach contents and the risk of inadequate positioning ( Hatcher and Stack, 1999 ).

 
 

FIGURE 23-6  Armored laryngeal mask airway is used for adenotonsillectomy in a child.  (From Kretz FJ, Reimann B, Stelzner J, et al.: The laryngeal mask in pediatric adenotonsillectomy. A meta-analysis of medical studies [in German]. Anaesthesist 49:706, 2000. With permission of Springer Science and Business Media.)

 

 

 

Hern and others (1999) reported the surgeon's perspective on the use of LMA for tonsillectomy. In their study, 44 children were anesthetized using an LMA, and 47 patients were anesthetized using an endotracheal tube before tonsillectomy. There was an 11.4% failure rate for the LMA, requiring change to an endotracheal tube before the end of the procedure. The LMA was reported to hamper the surgeon's visualization of the field and might have led to removal of less tonsillar tissue in the LMA group. It is difficult to suggest that the LMA is a superior choice for airway management during tonsillectomy. Additional objective data must be accumulated before recommending this technique.

▪ LASER SURGERY OF THE LARYNX

The laser (light amplification by the stimulated emission of radiation) has been used increasingly in otolaryngology since the introduction of the CO2 laser for laryngeal surgery ( Strong et al., 1973 ). The laser is a beam of coherent electromagnetic radiation that can be focused to a very small spot with precision, resulting in controlled coagulation, incision, or vaporization of the target tissue without it affecting the neighboring tissues ( Geffin et al., 1986 ; Keon, 1988 ). Clinical uses of the laser for upper and lower airways and its anesthetic implications have been reviewed elsewhere ( Beamis et al., 1991; Rampil, 1992 ; Pashayan, 1994 ).

The principal components of a laser system include a lasing medium (gaseous or solid) that holds the molecules whose electrons create the laser light, resonating mirrors to boost lasing efficiency, and an energy source that pumps the lasing molecules into producing laser light ( Fig. 23-7 ) ( Rampil, 1992 ). Some lasers use a gaseous lasing media, such as CO2, argon, or helium-neon, whereas other lasers use solid rods of laser-passive material that contain small quantities of ionic impurities, such as chromium (for ruby laser) and neodymium (Nd). A synthetic gem crystal, yttrium-aluminum-garnet (YAG), is commonly used as a passive host matrix ( Rampil, 1992 ). Fiberoptic bundles are used for beam delivery of lasers of visible and near-infrared wavelength. For the CO2 laser with invisible far-infrared wavelength, an articulated arm containing front-surface mirrors at each junction is used together with a low-powered visible helium-neon gas laser beam through the same optical path as a guide ( Rampil, 1992 ; Pashayan, 1994 ). Physical characteristics of commonly used lasers are described in Table 23-1 .

 
 

FIGURE 23-7  The central component is the lasing medium itself. This may, for example, be a solid crystal of yttrium-aluminum-garnet (YAG) with a small concentration of neodymium (Nd) or a tube containing carbon dioxide. The energy pump provides the means of obtaining a population inversion of orbital electrons. It may consist of a xenon flash lamp or an electric spark generator. A pair of axial mirrors allows separated passes of collimated photons through the media, enabling maximum amplification by stimulated emission. The mirror on the right is not 100% reflective, allowing the beam to escape eventually. The optional Q-switch increases efficiency of pulsed lasers by allowing a small delay to increase the pumping.  (Adapted from Rampil IJ: Anesthetic considerations for laser surgery. Anesth Analg 74:424, 1992.)

 

 

 


TABLE 23-1   -- Lasers commonly used for airway surgery

Laser Medium

Color

Wavelength (nm)

Tissue Penetration (mm)

CO2

Far infrared

10,600

<0.25

Nd:YAG

Near infrared

1064

2 to 6

KTP

Green

532

0.5 to 2

Argon

Blue/green

488/515

0.5 to 2

Adapted from Rampil IJ: Anesth Analg 74:424, 1992; and Pashayan AG: Anesthesia for laser surgery, Annual Refresher Courses, No. 221, 1994, ASA.

 

 

 

The most commonly used laser for laryngeal surgery is the CO2 laser. The CO2 laser, which has a long, far-infrared wavelength, is completely absorbed by the bending frequency of the water molecules; it is absorbed completely in the first few layers of cells and produces very little scatter of energy. The powerful, focused CO2 laser beam therefore produces explosive vaporization of the target tissue surface with minimal damage to the underlying tissues ( Beamis et al., 1991 ; Rampil, 1992 ). The thermal effect (i.e., coagulation lateral to the zone of vaporization) can be varied between 80 and 400 μm. The thermal effect is diminished with increasing water content or vascularity of the tissue or by the use of less power. Thermal coagulation also decreases with shorter pulse duration. The CO2 laser beam is delivered to the target tissue by means of an articulated arm and a micromanipulator attached to the microscope or a bronchoscope coupler for tracheobronchial applications ( Werkhaven, 1995 ). The micromanipulator allows surgical precision on the order of 250 μm.

The potassium (kalium) titanyl phosphate (KTP) laser and argon laser operate in the green and blue-green wavelength range of the spectrum. The KTP and argon laser beams are transmitted through clear substances and are well absorbed by pigments in the tissues, especially melanin and hemoglobin. They therefore have widespread applications for certain lesions, such as hemangiomas and granulation tissue ( Werkhaven, 1995 ). The energy scatter is intermediate between the CO2 and Nd:YAG laser beams. Because the depth of thermal damage produced by a laser beam beyond the immediate vaporization site partially depends on scatter, it produces vaporization (but less than that of the CO2 laser) in addition to coagulation and cutting ( Beamis et al., 1991 ). The depth of tissue penetration is 0.5 to 2 mm ( Pashayan, 1994 ). KTP and argon laser beams, as well as the Nd:YAG beam, can be transmitted by means of fiberoptic bundles through the rigid or flexible bronchoscope to vaporize or coagulate lesions in the tracheobronchial lumen ( Geffin et al., 1986 ; Ward, 1992 ).

The Nd:YAG laser has a near-infrared wavelength, is transmitted through clear fluids, and is readily absorbed by proteins. It is absorbed much less by water, and the beam is transmitted and scattered through much larger volumes of tissue. The energy of the Nd:YAG laser beam is therefore widely disseminated and produces less vaporization and more thermal coagulation. The depth of tissue penetration may range from 2 to 6 mm ( Pashayan, 1994 ). The Nd:YAG laser is transmitted by means of flexible optic fibers that can be directed through the side suction port of ventilating bronchoscope. The ablation of granulation tissue, mixed capillary-cavernous hemangioma, or obstructive vascular tumor in the tracheobronchial wall may be accomplished successfully with the Nd:YAG laser ( Werkhaven, 1995 ).

Risks Associated with Laser Surgery

Because of potential danger with the use of laser beams in the operating room, the users and other operating room personnel should follow the safety guidelines established by the American National Standard for the Safe Use of Laser in Health Care Facilities and published by the American National Standard Institute (ANSI, 1430 Broadway, New York, NY 10018; ANSI Z136). Doors to operating rooms where laser surgery is in progress should be clearly marked to prevent unprotected personnel from accidentally straying into the path of laser beams. Warning signs should specify the class and type of the laser being used as well as appropriate protective measures specific for the wavelength ( Rampil, 1992 ; Pashayan, 1994 ).

All laser beams for medical use are transmitted through air and are well reflected by smooth metal surfaces. Patients and health care personnel involved in laser surgery are at risk for laser injury, particularly of the eyes. The nature and extent of eye injury depend on the wavelength of the laser beam and its energy. Because the laser beam of far-infrared wavelength is absorbed by the surface it first encounters, errant CO2 laser beams can cause serious cornea ulcerations and scar formation ( Liebowitz and Peacock, 1980 ). Visible and near-infrared lasers (e.g., KTP, argon, Nd:YAG) penetrate through the transparent cornea and anterior chamber of the eye, are absorbed by the retina, and cause serious damage. The anesthetized patient's eyes should be taped closed and covered with saline-soaked eye pads or metal shields, or both ( Keon, 1988 ). Operating room personnel must wear safety goggles that are specific for the laser wavelength in use. Safety goggles should provide wrap-around protection from reflected beams ( Rampil, 1992 ). For CO2 lasers, any plastic or regular eyeglasses (not contact lenses nor thin plastic splash protection shields) will suffice as protection (provided that lateral aspects of the eye are also covered), because far-infrared beams are completely absorbed. Visible and near-infrared lasers require specific filters for particular laser wavelengths.

Incandescent debris resulting from the explosive vaporization of the tissue in contact with the laser beam produces a plume of smoke with fine particulates (0.1 to 0.8 μm), which may contain infectious or mutagenic viral particles ( Nezhat et al., 1987 ; Kokosa and Eugene, 1989 ). Fragments of DNA have been found in the smoke plume, but only one study has found viral transmission from the laser plume (Garden, 2002) . The same risk actually exists for the smoke plume from electrocautery. Ordinary surgical masks do not effectively filter particles smaller than 3.0 μm; special high-efficiency masks are therefore needed to filter laser plume particles ( Rampil, 1992 ).

A laser beam can ignite inflammable materials used for general anesthesia, such as endotracheal tubes, anesthesia circuits, oil-based lubricants, ointments, sponges, and drapes ( Snow et al., 1976 ; Cozine et al., 1981 ; Hermens et al., 1983 ). All materials used for endotracheal tubes, with the exception of special metallic tubes, are quite vulnerable to laser impact ( Geffin et al., 1986 ; Sosis, 1989a, 1989b [198] [199]). Polyvinyl chloride (PVC) tubes appear to be more easily punctured and ignited by CO2 laser than red-rubber tubes, and to produce more toxic combustion fumes ( Ossoff et al., 1983) , although black smoke from burning rubber is probably just as damaging to the airway mucosa. Wolf and Simpson (1987) found that once PVC is ignited, it is less flammable than silicone or red rubber, with a flammability index (i.e., FIO2 at which the material ignites) of 0.26, compared with silicone (0.19) and red rubber (0.18); this means silicone and rubber tubes continue to burn in room air, whereas PVC tubes do not. Red-rubber tubes, however, are more resistant to puncture than PVC tubes (41 versus 0.8 seconds with PVC at the same power density) and intramural fires are less likely to occur ( Ossoff, 1989) . For these reasons, metal tubes are preferred overall.

During laser surgery, when a nonmetallic endotracheal tube is used, the inspired concentration of oxygen should be reduced to 30% or less, as long as the patient is adequately oxygenated, to reduce combustibility of endotracheal tubes ( Hermens et al., 1983 ). Oxygen may be diluted by nitrogen or helium to reduce inflammability of endotracheal tubes ( Pashayan and Gravenstein, 1985 ; Simpson et al., 1990 ). Oxygen concentrations up to 60% may be used if helium is the diluent gas. Nitrous oxide supports combustion above 450°C and should therefore be avoided ( Wolf and Simpson, 1987 ; Keon, 1988 ). It is imperative that the patient be immobilized during laser surgery. The choice of anesthetics depends largely on the technique of ventilation during the laser surgery.

Airway Fire

An airway fire is potentially the worst complication to occur with the use of the laser. Although uncommon, the risk should be appreciated by the anesthesiologist and surgeon, and appropriate responses should be planned before the procedure. Airway fires also have been reported with the use of electrocautery for tonsillectomy and tracheotomy.

Although fires can occur in the operating room environment if the laser accidentally contacts flammable material, airway fires may occur only if flammable materials are present within the airway. Materials such as endotracheal tubes or cottonoid pledgets within the airway are the most common sources of combustion. In the absence of flammable materials, an airway fire cannot be sustained. Although the use of the laser on tissue may generate combustible breakdown products such as methane, the amounts are too small to produce enough heat to self-generate other combustible products. As noted, the concentration of oxygen should be kept as low as possible in the presence of combustible materials.

In the unfortunate event of an airway fire, a mnemonic of the four Es—extract, eliminate, extinguish, and evaluate—may help guide management. In the event of an airway fire, immediately extract all combustible materials from the airway such as pledgets or endotracheal tubes, even if they are still burning. Second, eliminate the source of oxygen being delivered to the endotracheal tube. The continued delivery of oxygen to a combustible source produces a blowtorch effect that can further ignite material in the vicinity. Third, extinguish any other fires in the vicinity. If a combustible material such as a pledget is still in the airway and cannot be removed, saline flush should be used to extinguish the fire. Fourth, evaluate any damage that may have been caused by the fire or the combustion byproducts. The operative field needs to be examined along with the lower tracheobronchial tree. Standards and guidelines for the management of surgical fires, including airway fires, have been published ( A clinician's guide to surgical fires, 2003 ).

Ventilatory Management During Laser Surgery

Numerous anesthetic approaches have been reported for airway management during laryngeal laser surgery. Transtracheally, general anesthesia through a preexisting tracheostomy is the easiest and probably the safest method. It is performed by replacing the preexisting tracheostomy cannula with a metal tracheostomy tube. Manually operated intermittent jet ventilation ( Rontal et al., 1980 ; Scamman and McCabe, 1986 ; Ravussin et al., 1987 ) or high-frequency jet ventilation ( Smith et al., 1975 ) by means of a needle or a catheter through the cricothyroid membrane has been used. These techniques, however, have a potential risk of barotrauma to the upper airways and overdistension of lungs (e.g., pneumothorax, pneumomediastinum), particularly when the laryngeal airway is obstructed. Subcutaneous emphysema and pneumomediastinum also may occur because of needle misplacement or a direct leak at the tracheal puncture site ( Borland and Reilly, 1987 ). Without tracheostomy or transtracheal puncture, the maintenance of airways and pulmonary ventilation during laser surgery can be accomplished by means of manual jet ventilation (i.e., Saunder's jet) without an endotracheal tube. A combination of intravenous propofol, topical lidocaine, and small doses of opioids (i.e., fentanyl or remifentanil infusion) has been used successfully with the patient breathing spontaneously (Borland LM, unpublished data).

Nonflammable Endotracheal Tubes

Red-rubber tubes wrapped with reflective aluminum or copper adhesive-backed tape, originally described by Snow and others (1974) , have been used effectively ( Norton et al., 1976 ), but the use of these homemade, laser-resistive tubes has decreased considerably over the past decade with the advent of commercially available nonflammable endotracheal tubes. Before wrapping a red-rubber tube with a metal tape, the tube should be wiped with alcohol to remove greasy or oily residues that interfere with adhesion. It should also be wiped with tincture of benzoin or an equivalent before spiral wrapping with a metal tape ( Rampil, 1992 ). There should be no windows of exposed tube; care should be taken to prevent wrinkles, which may cause abrasion of the laryngotracheal mucosa.

Certain metallic tapes do not sufficiently prevent the CO2, Nd:YAG, or KTP laser beams from penetrating the endotracheal tube and igniting a blowtorch fire. The CO2 laser can ignite the adhesive backing of all these tapes and perforate the aluminum tapes within 0.1 second ( Sosis, 1989a ). Other aluminum tapes (3M No. 425 and 433, 3M Corp., St. Paul, MN) and a copper foil tape (Venture Tape Corp, Rockland, MA; 3M Corp.) are effective in shielding at least 60 seconds of direct exposure (ECRI, 1990; Sosis and Dillon, 1990 ). A metallic foil wrap for endotracheal tubes, specifically manufactured for the laser, is also available (Laser Guard, Merocel Corp., Mystic, CT) and is approved by the U.S. Food and Drug Administration (FDA). This metal-based surgical sponge provides protection against CO2, argon, and KTP lasers but not against Nd:YAG lasers, according to the study by the Emergency Care Research Institute (ECRI, 1990). It also provides a smoother surface than metal tapes on the endotracheal tube for better airway mucosal protection but is bulky, adding about 2 mm to the diameter of the endotracheal tube.

A number of laser-resistant endotracheal tubes with metal exteriors have become available for clinical use. The Laser Flex tube (Mallinckrodt, St. Louis, MO; Bivona, Gary, IN) is a stainless steel spiral with a PVC tip, with or without two distal saline-inflatable cuffs ( Fig. 23-8 ). This tube is resistant to CO2 and the Nd:YAG laser (ECRI, 1990, 1992). The Fome Cuff tube (Bivona, Gary, IN) is an aluminum spiral tube with an outer coating of silicone that is approved by the manufacturer for the CO2 laser only. This tube has a self-inflating foam sponge-filled cuff. The foam in the cuff prevents deflation of the cuff after puncture, but damage to the filling tube may cause difficulty in deflating the cuff ( Rampil, 1992 ). The Laser Shield II (Medtronic/Xomed, Jacksonville, FL) is silicon-based endotracheal tube wrapped with metal foil and then wrapped in polytetrafluoroethylene tape to smooth the tube. These tubes are available only in two sizes, and the smallest size (5.0) has an outside diameter with cuff roughly equivalent to a size 5.5 endotracheal tube.

 
 

FIGURE 23-8  Flexible stainless steel (Laser Flex) tubes. Top to bottom, A 3.5-mm-ID, uncuffed tube; a 4.0-mm-ID, uncuffed tube; and a 5.0-mm, double-cuffed tube.  (Courtesy of Mallinckrodt Medical Inc., St. Louis, MO.)

 



Anesthesia with Nonflammable Endotracheal Tubes

For laser resections of laryngeal papillomas in a child, anesthesia may be induced by mask with nitrous oxide and sevoflurane with the standard monitors, including a precordial stethoscope, pulse oximeter, a capnograph, electrocardiogram, blood pressure cuff, and nerve stimulator. After intravenous access is secured and an intermediate-acting muscle relaxant is given, the child is intubated with a laser-resistant endotracheal tube. Nitrous oxide is then replaced with air or a helium-oxygen mixture (i.e., heliox). Anesthesia is maintained with a volatile anesthetic or propofol infusion with nitrogen and oxygen, and inspired oxygen concentration is kept at 30% or less as long as oxygen saturation can be maintained at or above 98%. The patient's eyes are taped closed and then covered with saline-soaked gauze pads; the portion of the endotracheal tube not metal coated is also covered with saline-soaked towels to avoid the fire hazard of the laser beam while a Jako-type suspension laryngoscope is being positioned. The child is paralyzed, and ventilation is controlled manually or mechanically with a ventilator. Supplemental opioids may be added intravenously to reduce the need for the inhaled anesthetic. Dexamethasone (0.4 mg to 1 mg/kg) may be used prophylactically to minimize postoperative mucosal swelling.

Anesthesia with Manual Jet Ventilation

A more commonly accepted and practiced method for ventilation during laryngeal laser surgery is the use of a Venturi apparatus (i.e., Sanders—jet injector), originally described by Sanders (1967) andSpoerel and others (1971) and applied in pediatric patients by Miyasaka and others (1980) as well as others ( Johans and Reichert, 1984 ; Scamman and McCabe, 1986 ; Borland and Reilly, 1987 ). The apparatus consists of an injector and tubing, a toggle switch, a reducing valve or regulator, and a tubing and connector to a high-pressure wall oxygen supply (50 psi) (Figs. 23-9 and 23-10 [9] [10]). After a precordial stethoscope, a pulse oximeter sensor, electrocardiogram leads, and a blood pressure cuff are positioned on the child, anesthesia is induced usually by mask with nitrous oxide, sevoflurane, and oxygen. An intravenous catheter is inserted, an axillary or rectal temperature probe is placed, and a nerve stimulator is positioned. Cisatracurium (or other intermediate-acting muscle relaxant), fentanyl (2 to 3 mcg/kg), and lidocaine (1 mg/kg) are injected intravenously. Midazolam may be given to ensure amnesia during the laser surgery. Alternatively, anesthesia may be switched to intravenous propofol with or without a small dose of fentanyl. Nitrous oxide is discontinued, and the patient is ventilated with 100% oxygen for several minutes before the mask is removed. The surgeon positions the child's head and inserts a Jako suspension laryngoscope to secure a patent laryngeal airway.

 
 

FIGURE 23-9  The Venturi ventilation apparatus with injector needle-on-clamp. A, High-pressure gas source with optional oxygen-nitrous oxide or helium blender. B, High-pressure tubing. C, Reducing valve and pressure gauge. D, Short piece of high-pressure tubing. E, Manual, all-or-none trigger valve. F, Tapered metal connector of the pop-off type. G, Low-pressure plastic tubing. H, Optional Luer-Loc fitting on tapered metal connector of the pop-off type. I, An adapted, curved stainless steel needle, 12 to 18 gauge. J, Screw clamp to fit on the edge of the operating laryngoscope. K, Schematic outline of the operating laryngoscope. L, Laryngoscope handle that fits the suspension apparatus. It should be possible for fittings F and H to pop off when high-pressure is inadvertently transmitted through the low-pressure tubing (i.e., when C or E, or both, are failing) or when an obstruction occurs distally.  (Adapted from Van Der Spek AF, Spargo PM, Norton ML: The physics of lasers and implications for their use during airway surgery. Br J Anaesth 60:709, 1988.)

 

 

 

 
 

FIGURE 23-10  A Saunders-type, hand-held jet ventilation apparatus.  (Courtesy of Manujet III, VBM Medizintechnik, Sulz am Neckar, Germany.)

 



In children, supraglottic jet ventilation is used. Subglottic jet ventilation is rarely used in children, because it requires extremely delicate skills to assess adequate egress of air between pulses, or pneumothorax or pneumomediastinum results ( Fumsaker, 1944) .

For supraglottic ventilation, a 10-French metal injector is inserted into the side channel of the suspension laryngoscope and is secured with the distal end 1 to 2 cm above the glottic opening; the metal injector is readjusted as needed to obtain the optimal distance and direction. Oxygen concentration of the jet injector is adjusted with an oxygen blender to reduce the inspired oxygen concentration with room air entrainment to 30% or less, provided that oxygen saturation on the pulse oximeter is 98% or higher. The anesthesiologist begins jet ventilation by intermittently squeezing the toggle switch. Short bursts of inspiration with air entrainment (1 to 2 seconds) with the driving pressure of 15 psi or less (the pressure may vary with different setups), followed by enough expiration time (2 to 4 seconds) to complete exhalation, provides adequate pulmonary ventilation. Close observation of the child's chest motion during each breath is crucial to prevent air trapping, hyperinflation, and volutrauma to the lungs ( Borland and Reilly, 1987 ). Inspired oxygen concentration is decreased as low as possible by adjusting the oxygen-blender to maintain SpO2 between 98% and 100% throughout the procedure. If passive exhalation is unusually prolonged, measures to improve airway patency must be taken immediately. This can usually be accomplished by readjusting or redirecting the injector. Occasionally, when papillomatous growth about the glottis is extensive, the child may require intubation with a small tube and manual ventilation while the surgeon improves the glottic aperture by debulking papillomas on and around the vocal cords.

After the laryngeal surgery is completed, ventilation is maintained with 100% oxygen by mask and bag, or the airway is secured by intubation with a small cuffed or uncuffed orotracheal tube. Neuromuscular blockade is reversed in the usual manner. The endotracheal tube is removed after neuromuscular blockade is completely reversed and the child is breathing satisfactorily.

The manual jet ventilation technique offers several advantages in laryngeal laser surgery, including adequate ventilation, excellent surgical access to the larynx (especially to the anterior and posterior commissures where an endotracheal tube obliterates the exposure), and the absence of ignitable material in the surgical field ( Norton et al., 1976 ; Goforth et al., 1983 ). Potential risks of this technique include pneumothorax, pneumomediastinum, distension of the stomach and regurgitation, aspiration of resected material, and dehydration of mucosal surface ( Lines, 1973 ; Norton et al., 1976 ; Rontal et al., 1980 ; Ruder et al., 1981 ; Keon, 1988 ).

Anesthesia with Spontaneous Breathing

Anesthesia for airway laser surgery can be managed by experts with a combination of carefully administered intravenous anesthesia and topical lidocaine. Anesthesia may be induced with inhalation of sevoflurane with a nitrous oxide-oxygen mixture while the patient is allowed to breathe spontaneously. After an intravenous catheter is inserted and the patient positioned with a suspension laryngoscope, topical lidocaine is sprayed under the direct vision. Inhaled anesthetics are turned off and an infusion of propofol is started. During laser surgery, high-dose propofol (300 to 400 mcg/kg per minute) is supplemented with intermittent doses of morphine (up to 0.1 mg/kg) or an infusion of fentanyl (2 to 3 mcg/kg per hour) to prevent tachypnea. The concentration of oxygen insufflations should be limited to less than 30% for safety while the patient's breathing is continuously monitored with a precordial stethoscope and oxygen saturation is monitored with a pulse oximeter. A manual jet ventilator (Sanders) should be readily available for supraglottic jet ventilation as needed if the patient's breathing is too depressed or he or she becomes apneic. Alternatively, total intravenous anesthesia (TIVA) may be administered with a combination of remifentanil and propofol infusions. This combination appears to make spontaneous breathing more difficult to maintain.

Laser Bronchoscopy

The laser may be used coupled to a ventilating bronchoscope. If the CO2 laser is used, higher oxygen concentrations may be employed, because there is no flammable material within the airway. The fibers used for KTP and Nd:YAG laser delivery may support combustion, and when used through a bronchoscope, the inspired oxygen concentration should be less than 40%.

▪ TRACHEOSTOMY

Tracheostomy is indicated in numerous situations before development of respiratory distress ( Stool and Eavey, 1990 ). The three primary indications for the creation of an artificial airway are airway obstruction, chronic assisted ventilation, and pulmonary toilet ( Wetmore et al., 1999 ; Carron et al., 2000 ). Table 23-2 lists conditions for which tracheotomy has been advocated in pediatric patients (Wetmore, 2003 ).


TABLE 23-2   -- Conditions for which tracheotomy has been advocated

 

Allergy

Metabolic

Prophylactic

Degenerative; Idiopathic

Sleep Disorders

Upper airway obstruction

  

 

Angioneurotic edema

  

 

Anaphylaxis

 

  

 

Head and neck surgery

  

 

Neurosurgery

  

 

Cardiac surgery

  

 

Prolonged endotracheal tube placement

Vocal cord paralysis

  

 

Pharyngeal musculature collapse

  

 

Tonsilloadenoid hypertrophy

Pulmonary toilet assisted ventilation

Asthma

  

 

Cystic fibrosis

  

 

Coma due to diabetes, Reye syndrome, uremia, etc.

  

 

Respiratory distress syndrome

 

Central nervous system or neuromuscular failure as in Guillain-Barré syndrome, polymyositis, myasthenia gravis, botulism, cardiac arrest, respiratory arrest

 

 

Congenital

Trauma

Toxic

Infection

Neoplastic

Upper airway obstruction

  

 

Choanal atresia

  

 

Macroglossia

  

 

Cleft palate

  

 

Pierre Robin anomaly

  

 

Laryngomalacia

  

 

Laryngeal stenosis

  

 

Vocal cord paralysis

  

 

Laryngeal webs, cysts

  

 

Subglottic stenosis

  

 

Vascular ring

  

 

Tracheal hypoplasia

  

 

Facial injury

  

 

Oral injury

  

 

Foreign body

  

 

Burns (steam, smoke, thermal)

  

 

Laryngeal edema

  

 

Recurrent laryngeal nerve injury

  

 

Laryngeal fracture

Corrosives

  

 

Epiglottitis

  

 

Laryngotracheitis (croup)

  

 

Gingivostomatitis

  

 

Diphtheria

  

 

Retropharyngeal abscess

  

 

Ludwig angina

  

 

Neek cellulitis

  

 

Tetanus

  

 

Rabies

  

 

Plague

  

 

Laryngeal tumors

  

 

Tracheal tumors

  

 

Tumors of pharynx and tongue: papilloma, hemangioma, lymphangioma, sarcoma

Pulmonary toilet, assisted ventilation

  

 

Congenital heart disease

  

 

Congenital heart failure

  

 

Esophageal atresia due to tracheoesophageal fistula

  

 

Hypoplastic lung due to diaphragmatic hernia

  

 

Adjunct to craniofacial surgery

  

 

Head trauma

  

 

Crushed chest

  

 

Shock lung

  

 

Intrapulmonary hemorrhage

  

 

Pneumothorax

  

 

After lung bypass

  

 

Coma due to toxins (e.g., phenobarbital)

  

 

Hydrocarbon lung

  

 

Aspiration syndromes such as from meconium

  

 

Meningitis

  

 

Encephalitis

  

 

Brain abscess

  

 

Pneumonia

  

 

Bronchiolitis

  

 

Poliomyelitis

  

 

Pulmonary aspiration necessitating laryngeal closure

  

 

Brain tumors

  

 

Spinal cord tumors

From Werkhaven J: Laser surgery. In Bluestone CD, Stool SE, Alper CM, et al., editors. Pediatric otolaryngology, 4th edition. WB Saunders, 2003, Philadelphia, pp 1573–1598, Table 93–1.

 

 

The ideal tracheotomy tube conforms to the trachea and neck without causing undo pressure or injury to the skin or tracheal mucosa. Plastic tracheotomy tubes are commonly used because they cause minimal tissue reaction. Tracheotomy tubes should be manufactured in metric sizes that correspond to endotracheal tube sizes. However, metal tracheotomy tubes are still measured in French sizes (Wetmore, 2003 ). Table 23-3 compares the sizes of the endotracheal tubes and commonly used tracheotomy tubes in infants and children ( Wetmore, 2003 ).


TABLE 23-3   -- Size comparison of endotracheal and plastic tracheostomy tubes

Cannula

Approx. French

Inner Diameter (mm)

Outer Diameter (mm)

Overall Length

Endotracheal Tube[*]

 2.5

 

2.5

3.6

12 cm

 3.0

 

3.0

4.3

14 cm

 3.5

 

3.5

4.9

16 cm

 4.0

 

4.0

5.6

18 cm

 4.5

 

4.5

6.2

20 cm

 5.0

 

5.0

6.9

22 cm

 5.5

 

5.5

7.5

25 cm

 6.0

 

6.0

8.2

26 cm

Bivona[†]

 2.5

12

2.5

4.0

30 mm

 2.5

12

2.5

4.0

38 mm

 3.0

14

3.0

4.7

32 mm

 3.0

14

3.0

4.7

39 mm

 3.5

16

3.5

5.3

34 mm

 3.5

16

3.5

5.3

40 mm

 4.0

18

4.0

6.0

36 mm

 4.0

18

4.0

6.0

41 mm

 4.5

20

4.5

6.7

42 mm

 5.0

22

5.0

7.3

44 mm

 5.5

24

5.5

8.0

46 mm

Franklin[‡]

 3.5

 

3.5

5.0

44 mm

 4.0

 

4.0

6.0

44 mm

 4.5

 

4.5

6.7

48 mm

 5.0

 

5.0

8.0

51 mm

 5.5

 

5.5

8.5

54 mm

 6.0

 

6.0

9.3

57 mm

Portex

 3.0

 

3.0

5.0

36 mm

 3.5

 

3.5

5.8

40 mm

 4.0

 

4.0

6.5

44 mm

 4.5

 

4.5

7.1

48 mm

 5.0

 

5.0

7.7

50 mm

 5.5

 

5.5

8.3

52 mm

Shiley[‖]

 00 Neonatal

 

3.1

4.5

30 mm

 00 Pediatric

 

3.1

4.5

39 mm

 0 Neonatal

 

3.4

5.0

32 mm

 0 Pediatric

 

3.4

5.0

40 mm

 1 Neonatal

 

3.7

5.5

34 mm

 1 Pediatric

 

3.7

5.5

41 mm

 2 Pediatric

 

4.1

6.0

42 mm

 3 Pediatric

 

4.8

7.0

44 mm

 4 Pediatric

 

5.5

8.0

46 mm

From Werkhaven J: Laser surgery. In Bluestone CD, Stool SE, Alper CM, et al., editors. Pediatric otolaryngology, 4th edition. WB Saunders, 2003, Philadelphia, pp 1573–1598, Table 93–3.

*

The endotracheal tubes are marked with the inner diameter, usually with the outer diameter, and with the length.

The Bivona tube is manufactured by the Bivona Corporation of Gray, IN. Both the inner and outer diameters are marked on the tubes.

The Franklin tube is of the Great Ormond Street design, manufactured in England and distributed by Inmed Corporation, Norcross, GA. The tubes are stamped with just the inner diameter.

The Shiley tube is manufactured by Shiley Laboratories, Irvine, CA. The tubes are stamped with the size and inner and outer diameters.

 

Anesthetic Approach for Tracheostomy

The need for tracheotomy may occur emergently, urgently, or electively. It is essential for the surgeon and anesthesiologist to establish a plan before surgery. Some situations, including laryngeal trauma, massive facial injuries, upper airway obstruction, and oropharyngeal distortion, require emergency tracheostomy for airway management. This procedure is usually performed outside the operating room and fortunately rarely in the pediatric population.

Urgent tracheotomy may be required in neonates for congenital airway defects and for older children because of upper airway trauma, corrosive ingestion, infections, and tumors (see Table 23-2 ). Although these children may initially maintain oxygenation and ventilation, they are at risk for acute respiratory failure. They may have airway anomalies that contribute to difficult or impossible tracheal intubation. The location of the obstruction will dictate the surgical and anesthetic approach. The anesthesiologist must establish whether the child can maintain a patent airway under anesthesia and whether they can be intubated by standard laryngoscopy or fiberoptic bronchoscopy. Sedation with ketamine may also be an option. Otherwise, anesthesia is induced with an inhaled anesthetic agent (i.e., propofol or ketamine) after preoxygenation in the position in which the child is most comfortable, often the sitting position. If there is no intravenous catheter in place an intravenous catheter is inserted, and atropine (0.01 to 0.02 mg/kg) or glycopyrrolate (0.01 mg/kg) is injected intravenously after induction of anesthesia. Unless a normal, unobstructed airway can be maintained, muscle relaxants should not be used because total upper airway obstruction may result. After the child is anesthetized but spontaneously breathing, topical lidocaine (up to 5 mg/kg) may be sprayed on the larynx to ablate laryngeal reflexes before laryngoscopy. If intubation is impossible, an LMA may be used to maintain an airway until the tracheotomy is performed. Tracheotomy is best performed in infants with an endotracheal tube or a rigid bronchoscope in place to ensure adequate pulmonary gas exchange. The endotracheal tube also helps the surgeon to identify the trachea. Many surgeons prefer to use a rigid bronchoscope held in place rather than an endotracheal tube. The rigid bronchoscope allows for a firmer anatomic reference for the trachea, but it cannot be taped in place and must be held by hand. Elective tracheotomy is usually performed in children already intubated for chronic ventilation or pulmonary toilet or performed in combination with tumor removal or repair of tracheal abnormalities.

For tracheotomy, the patient is positioned with the shoulders elevated by placing a roll underneath the neck so that the neck is hyperextended. Some surgeons request that the anesthesiologist hold the chin with the left hand to keep the neck stretched so that soft tissue over the trachea is stabilized ( Fig. 23-11 ) ( Stool and Eavey, 1990 ). The surgeon palpates the neck to identify the thyroid and cricoid cartilages, sometimes with difficulty. The trachea is palpated down to the sternal notch, guided by the presence of an endotracheal tube. A skin incision is made about1 fingerbreadth above the sternal notch, either horizontally or vertically. When the fascial layer is incised under the subcutaneous fat and the trachea is identified, a pair of stay sutures, one on each side of the tracheal incision, is placed for traction during the cannulation of the tracheotomy tube. The stay sutures also serve to prevent asphyxiation in the event that the tracheotomy tube becomes displaced in the immediate postoperative period before the tract has formed ( Myers et al., 1985 ). Before the tracheotomy cannula is inserted in the tracheal incision, the endotracheal tube or bronchoscope is slowly pulled back to accommodate the insertion. The endotracheal tube or bronchoscope should not be removed completely until successful ventilation is demonstrated through the tracheotomy. The anesthesia delivery tube is then disconnected from the endotracheal tube under the drapes and reconnected to the proximal universal adapter end of the tracheotomy tube over the operative field.

 
 

FIGURE 23-11  Schematic of a child positioned for tracheostomy with the shoulders elevated, the neck hyperextended, and the chin pulled up by hand.

 

 

An esophageal stethoscope or a nasogastric tube has occasionally been misidentified as an endotracheal tube in the trachea by the surgeon, and inadvertent esophageal incision has been made ( Schwartz and Downes, 1977 ); esophageal stethoscopes therefore should be avoided during tracheotomy. The child is monitored with a precordial stethoscope, pulse oximeter, capnograph, electrocardiogram, automated blood pressure cuff, and rectal or skin thermometer.

Major intraoperative and postoperative complications of tracheotomy include hemorrhage, subcutaneous emphysema, pneumothorax, and pneumomediastinum. The neck and shoulders of the child should be palpated for the typical crepitus to rule out subcutaneous emphysema. Then both sides of the chest are auscultated. In most hospitals, the patient is transferred to the intensive care unit for observation and a chest radiograph to ensure proper tracheotomy tube positioning and the absence of pneumothorax.

▪ LARYNGEAL STENOSIS

Laryngeal stenosis may occur in the supraglottis, glottis, or subglottis. Clinically, subglottic stenosis is most common. Supraglottic stenosis is rare in children. It usually is a consequence of thermal or chemical injury or iatrogenic injury after previous reconstructive airway surgery.

Subglottic Stenosis

Neonatal subglottic stenosis can be categorized as congenital or acquired. The incidence of congenital subglottic stenosis is 5%; the remaining cases are acquired. Subglottic stenosis in the full-term infant is defined as a subglottic airway diameter of less than 4 mm at the level of the cricoid cartilage and less than 3 mm in the premature infant ( Walner et al., 2001 ). This narrowing can be compared with the reference point of a neonatal endotracheal tube. The outer diameter of a 2.5 endotracheal tube is 3.6 mm, and the outer diameter of a 3.0 endotracheal tube is 4.2 mm ( Rutter et al., 2003 ). The diagnosis of subglottic stenosis is made by rigid endoscopy while the patient is anesthetized. The extent of the subglottic stenosis is determined by placement of an endotracheal tube that allows an airway leak between 10 and 25 cm H2O ( Table 23-4 ). This leak allows accurate measure of the airway size. The airway stenosis is then graded as follows: grade I, less than 50% obstruction; grade II, 51% to 70% obstruction; grade III, 71% to 91% obstruction; and grade IV, no detectable lumen ( Gerber and Holinger, 2003 ).


TABLE 23-4   -- Obstruction of laryngotracheal stenosis estimated by endotracheal tube sizing

Age of Patient

ID 2.0

ID 2.5

ID 3.0

ID 3.5

ID 4.0

ID 4.5

ID 5.0

ID 5.5

Premature

40[*]

 

58

30

0-3 mo

68

48

26

3-9 mo

75

59

41

22

9 mo to 2 yr

80

67

53

38

20

2 yr

84

74

62

50

35

19

4 yr

86

78

68

57

45

32

17

6 yr

89

81

73

64

54

43

30

16

Adapted from Gerber ME, Holinger LD: Congenital laryngeal anomalies. In Bluestone CD, Stool SE, editors: Pediatric otolaryngology. New York, 2003, WB Saunders, pp 1460–1472.

ID, internal diameter of the endotracheal tube.

 

*

Endotracheal tube sizing is used for characterizing firm, mature subglottic stenosis. The size is determined by placement of an endotracheal tube that leaks 10 to 25 cm H2O. The numbers in the columns indicate the percent of obstruction.

 

In the absence of trauma, an abnormality of the cartilage or subglottic tissues is usually considered congenital. The cause of congenital subglottic stenosis is thought to be a failure of the laryngeal lumen to recanalize after completion of normal epithelial fusion at the end of the third month of gestation ( Walander, 1955 ). Congenital subglottic stenosis lies on a continuum of embryologic failure that includes laryngeal atresia, stenosis, and webs. In its mildest form, congenital subglottic stenosis merely represents a normal appearing cricoid with a smaller-than-average diameter, usually with an elliptical shape. Infants and children with mild subglottic stenosis may present with a history of recurrent upper respiratory infections, often diagnosed as croup, in which minimal glottic swelling precipitates airway obstruction. The location of the stenosis is usually 2 to 3 mm below the true vocal cords ( Rutter et al., 2003 ).

Severe congenital subglottic stenosis can be a life-threatening airway emergency manifesting immediately after the infant is delivered. If endotracheal intubation is successful, the patient may require intervention before extubation. In more severe cases, tracheotomy can be life saving at the time of delivery. Infants with congenital subglottic stenosis may have surprisingly few symptoms and may not present for treatment for weeks or months after birth ( Rutter et al., 2003 ). After the initial management of congenital subglottic stenosis, the larynx will grow with the patient and may not require further surgical intervention.

Laryngomalacia is a congenital condition of excessive flaccidity of the laryngeal structures, especially the epiglottis and arytenoids, most likely caused by the lack of neural control of laryngeal muscles. Laryngomalacia accounts for more than 70% of persistent stridor in neonates and young infants ( Fig. 23-12 ); the remaining 10% of neonatal stridor is caused by vocal cord paralysis ( Fig. 23-13 ) ( Yellon et al., 2002 ).

 
 

FIGURE 23-12  Laryngomalacia. A, The larynx during expiration; the omega-shaped epiglottis and the arytenoid cartilages appear normal. B, The larynx during inspiration; the force of the inspiratory airflow leads to collapse of the laryngeal inlet. Infolding of the epiglottic surface and the arytenoids causes severe upper airway obstruction.  (From Yellon RF, McBride TP, et al.: Otolaryngology. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, 4th ed. St. Louis, 2002, Mosby, p 863.)

 



 
 

FIGURE 23-13  A, Congenital bilateral vocal cord paralysis. The marked narrowing of the aperture between the vocal cords stems from the loss of ability to abduct on inspiration. B, Normal neonatal vocal cords with a wide opening during inspiration.  (From Yellon RF, McBride TP, Davis HW: Otolaryngology. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, 4th ed. St. Louis, 2002, Mosby, p 863.)

 



In the mid-1960s, long-term intubation was introduced as the preferred artificial airway in neonates ( McDonald and Stocks, 1965 ). With increasing neonatal survival rates, subglottic stenosis occurred as a frequent morbidity caused by long-term tracheal intubation. Acquired subglottic stenosis results from intubation trauma and accompanying inflammatory responses. Factors suspected in contributing to this problem include prematurity, the size and amount of movement of the endotracheal tube, duration of intubation, laryngeal or tracheal injury during intubation, and presence of infection during the course of tracheal intubation. The incidence of acquired subglottic stenosis has decreased over the past decade by minimizing the issues known to exacerbate subglottic injury ( Walner et al., 2001 ). Patients presenting to the otolaryngologist for diagnosis or treatment for subglottic stenosis are intubated in the neonatal intensive care unit, have a tracheotomy in place with an established diagnosis, or are examined on an outpatient basis for symptoms suggesting subglottic stenosis ( Cotton, 2000 ).

Surgical Management of Acquired Subglottic Stenosis in the Neonate

Neonatal subglottic stenosis unresponsive to nonoperative therapy may require tracheotomy or an anterior cricoid split procedure. Tracheotomy is performed if in addition to severe subglottic injury there is substantial glottic and/or tracheal involvement. After tracheotomy and without the endotracheal tube to act as a stent, the stenosis becomes more severe. Over the next 2 years, the airway may heal, allowing for decannulation, but more often, surgical reconstruction of the trachea will be necessary ( Rutter et al., 2003 ).

The anterior cricothyroidotomy or cricoid split is an effective treatment for some cases of acquired neonatal subglottic stenosis in the absence of substantial glottic or tracheal or pulmonary pathology (Rutter et al., 2003 ). The neonate must meet the following criteria ( Cotton, 2000 ):

  

1.   

Failure of extubation on at least two occasions

  

2.   

Body weight greater than 1500 g

  

3.   

Absence of assisted ventilation for 10 days

  

4.   

Supplemental oxygen requirement less than 30%

  

5.   

Absence of heart failure for at least 1 month

  

6.   

No evidence of an upper or lower respiratory infection

  

7.   

No antihypertensive medication required

The procedure is performed under general anesthesia with muscle relaxation. The shoulders are elevated, and the neck is extended as in the tracheotomy position (see Fig. 23-11 ). A horizontal incision is made in the skin over the cricoid cartilage. The cricoid cartilage, upper trachea, and lower edge of the thyroid cartilage are exposed. An incision is made through the cricoid ring and underlying mucosa through the first two tracheal rings and the lower one third of the thyroid cartilage. Stay sutures are placed on both severed edges of the cricoid cartilage, as in a tracheotomy ( Healy, 1995b ). The endotracheal tube, which has been used for anesthesia and airway management is then removed. It is replaced while the larynx is still split with a nasotracheal tube, which is one size (0.5 mm) larger than that predicted for the patient's age and body size. The surgeon helps guide the nasotracheal tube into position through the open incision. The wound is closed loosely with a drain. The nasotracheal tube is left in place for 7 days to stent the subglottic aperture. The patient is kept well sedated with or without mechanical ventilation in the pediatric intensive care unit. A modification of the anterior cricoid split is to place a cartilage graft over the split in an effort to allow the airway to seal more rapidly, leading to earlier extubation. Thyroid alar cartilage and occasionally auricular cartilage are used ( Rutter et al., 2003 ).

Laryngotracheal Reconstruction in Children

Chronically ventilated infants who have undergone tracheotomy because of prolonged intubation and subglottic stenosis most likely will require laryngeal reconstructive surgery. Children with greater than 70% obstruction of their laryngeal lumen usually require this surgery to allow for decannulation ( Rutter et al., 2003 ).

Laryngotracheal reconstruction has become the standard of care for symptomatic subglottic stenosis in the pediatric age group. The five stages involved with laryngotracheal reconstruction are characterization of the stenosis, expansion of the tracheal lumen, stabilization of the framework, healing of the airway, and decannulation ( Rothschild et al., 1995 ). The procedure has evolved to include a variety of techniques for expanding the laryngotracheal complex to provide a stable airway of sufficient size. These include, but are not limited to, anterior cartilage graft with the tracheotomy left in place without stent; long-term (several months) stenting with or without cartilage grafts; and short-term (4 to 6 weeks) stenting with anterior or posterior cartilage grafts ( Cotton, 2000 ).

Anterior cartilage graft with a tracheotomy left in place without a stent is indicated primarily for isolated anterior subglottic stenosis with no or relatively mild posterior subglottic components. A variation of this procedure is to remove the tracheotomy at the time of surgery and perform a single stage laryngotracheoplasty. Posterior division of the cricoid plate and the introduction of a cartilage graft in between the cut ends are indicated particularly for children with persistent posterior glottic pathology or primarily posterior subglottic pathology ( Cotton, 2000 ).

Single-stage laryngotracheal reconstruction (LTR) uses cartilage grafts to obtain stability of the reconstructed airway. Single-stage LTR may include an anterior cartilage graft, a posterior cartilage graft, or both, and reconstruction often includes a cartilage graft at the former stoma site. The grafts are supported temporarily by a full-length endotracheal tube fixed in position through the nasal route ( Cotton et al., 2000) . The optimal time for extubation has not been established definitively. In general, children remain intubated for 7 to 10 days for anterior cartilage grafts alone, and 12 to 14 days if a posterior and anterior graft is required ( Cotton, 2000 ).

The patient may be anesthetized by the intravenous route or through a tracheotomy cannula. Standard monitoring includes pulse oximetry, precordial stethoscope, capnography, anesthetic gas monitoring, electrocardiogram, blood pressure apparatus, peripheral nerve stimulator, and axillary or rectal temperature monitor. The patient is placed in the tracheotomy position with the shoulders elevated and the neck hyperextended. A tracheotomy tube is replaced with a sterile cuffed armored (anode) endotracheal tube through the tracheostomy stoma and is covered under an adhesive drape to minimize contamination of the surgical field.

Through a horizontal skin incision over the cricoid cartilage, laryngeal structures are exposed. A vertical incision is made through the lower thyroid cartilage, the cricoid cartilage, and the upper tracheal rings ( Fig. 23-14A ). The rib cartilage graft, which had been taken from the anterior chest wall with the external perichondrium intact, is used for the anterior or posterior grafts (see Fig 23-14B ). Auricular cartilage and septal cartilage have also been used as graft materials. Toward the conclusion of surgery, the armored tube is removed from the tracheotomy stoma and replaced with a cuffed nasotracheal tube, one size larger than is appropriate for the patient's age and size, to stent the larynx. This intraoperative transition needs to be carefully coordinated between the anesthesiologist and the surgeon.

 
 

FIGURE 23-14  Schematic of laryngotracheoplasty for subglottic stenosis. A, Laryngotracheal incision with upper and lower extension, depending on the extent of stenosis, and a cartilage graft. B, Cartilage graft is shown with the perichondrium internalized. A graft is sutured in position.  (From Healy GB: Surgery of the larynx and trachea. In Bluestone CD, Stool SE, editors: Atlas of pediatric otolaryngology. Philadelphia, 1995b, WB Saunders.)

 



One requirement of single-stage LTR is meticulous postoperative management of the patient's condition in the intensive care unit. The nasotracheal airway must be maintained securely during the time of extended stenting without accidental extubation. The postoperative management of single-stage LTR patients is not standardized ( Cotton, 2000 ). Some centers use sedation to prevent agitation and accidental self-extubation and to avoid pharmacologic paralysis ( Rothschild et al., 1995 ). However, many children do not tolerate nasotracheal intubation and require prolonged sedation and neuromuscular blockade to ensure maintenance of an airway with minimal trauma during healing ( Brandom, 1997 ; Yellon et al., 1997 ). If neuromuscular blockade is used, daily recovery of neuromuscular function and the avoidance of prolonged use of corticosteroids will be associated with less muscle weakness after extubation ( Yellon et al., 1997 ). Prolonged sedation with benzodiazepines or opioids can lead to withdrawal syndrome, and close observation after weaning these agents is paramount.

Acute Supraglottitis or Epiglottitis

Acute infectious epiglottitis or supraglottitis is a relatively uncommon but truly life-threatening disease of childhood. Acute epiglottitis is an acute bacterial infection principally involving supraglottic structures, including the lingular surface of the epiglottis, the aryepiglottic folds, and the arytenoids, with little or no involvement of subglottic structures, including the laryngeal surface of the epiglottis. It is therefore more appropriate to call it supraglottitis. Until the late 1980s, before the vaccination became available, Haemophilus influenzae type b (Hib) was the causative organism in more than 75% of cases. Group A β-hemolytic streptococci account for most of the rare cases of epiglottitis ( Gorelick and Baker, 1994 ). With the advent of effective Hib conjugate vaccines in 1988, the incidence of Hib disease has declined dramatically in the United States ( Adams et al., 1993 ; Hoekelman, 1994 ). The age-specific incidence of Hib disease among children younger than 5 years old decreased by 71% and that of Hib meningitis by 82% between 1985 and 1991 ( Adams et al., 1993 ). Similarly, the incidence of acute epiglottitis, one of the most dreaded childhood emergencies, has declined by 84% ( Gorelick and Baker, 1994 ).

Until the late 1980s, before the era of Hib conjugate vaccination, preschool children between the ages of 2 and 6 years had the highest incidence of supraglottitis, although it occurred in infants, in older children, and occasionally in adults ( Schloss et al., 1979 ; Blackstock et al., 1987 ; Crysdale and Sendi, 1988 ). The highest number of cases is reported in the spring and fall, but sporadic cases are reported in other seasons. The condition usually begins with complaints of severe sore throat associated with dysphagia and a thick, muffled voice without a preceding history of runny nose. Rarely is there a croupy or barking cough, except in atypical cases in infants ( Blackstock et al., 1987 ). The symptoms rapidly progress, and typical pathognomonic signs of dysphagia, dysphonia, dyspnea, and drooling (i.e., the four Ds) appear ( Diaz, 1985 ).

In most children presenting with stridor in the emergency room, the most common symptoms found in those with acute epiglottitis are drooling, agitation, and absence of spontaneous cough ( Mauro et al., 1988 ). The child looks toxic and usually has a high fever and tachycardia. The disease progresses very rapidly and may be fatal, with severe airway obstruction within 6 to 12 hours, unless immediate steps are taken to restore the patient's upper airway patency. Classically, the child is sitting up, is dyspneic with the mouth open and drooling, and resists attempts to get him or her to lie down. There is forward chin thrust, slight cervical flexion, and forward flexion at the waist, together with tripod placement of the arms to support this posture. The inspiratory phase is slow, with stridor and retraction, whereas the expiratory phase is unobstructed. The inspiratory sound has been compared with that of a quacking duck.

As soon as acute supraglottitis is diagnosed in the emergency room, a pediatric anesthesiologist or intensive care staff and otolaryngologist should be called. The child should never be left unattended by one of these physicians, because the disease can progress so rapidly that complete upper airway obstruction may ensue within minutes. The patient is kept in a sitting or tripod position with an oxygen mask in place and with a pulse oximeter monitoring. The child is transferred to the operating room without delay and is accompanied by an anesthesiologist or an intensivist and an otolaryngologist.

A laryngoscope with several blades, endotracheal tubes with stylets, a bronchoscope, and a self-inflating bag with facemask and oxygen must accompany the patient for emergency intubation ( Oh and Motoyama, 1977 ). Throat examination should not be attempted in the emergency room, because the risk of complete airway obstruction is great. If the child's condition permits or when the diagnosis is questionable, the patient may be transferred to the pediatric intensive care unit, where a radiograph of the lateral neck is taken with a portable x-ray machine ( Butt et al., 1988 ). In the intensive care unit, all the help and expertise needed for an emergency should be readily available. In most patients, a swollen epiglottis obstructing the air (shadow) is seen on the lateral neck radiograph ( Fig. 23-15A ). Negative radiographs, however, do not necessarily rule out supraglottitis.

 
 

FIGURE 23-15  Radiographs of the lateral area of the neck. A, Supraglottitis. The upper airway is obstructed by marked swelling of the epiglottis and other supraglottic structures. Notice the loss of normal curvature of the cervical spine. B, Laryngotracheitis. Arrows point to airway constriction below the vocal cords.  (Courtesy of Dr. K.S. Oh, Department of Radiology, The Children's Hospital of Pittsburgh, PA.)

 



Compared with acute supraglottitis, the onset of laryngotracheobronchitis (subglottic croup) is insidious. The child starts with the symptoms of upper respiratory infection, with rhinorrhea, cough, sore throat, and low-grade fever for several days before developing the symptoms of upper airway obstruction characterized by inspiratory stridor and barky or seal-like coughs (i.e., croup). The symptoms may last from a few days to more than a week, with various degrees of severity that is worse at night in the supine position. In severe cases, endotracheal intubation under general anesthesia is required.

A lateral neck radiograph typically shows a narrowing of the airway shadow below the vocal cords (see Fig. 23-15B ). An anteroposterior radiograph of the neck may show a long area of airway narrowing resembling a steeple of a church (“steeple sign”) ( Fig. 23-16 ).

 
 

FIGURE 23-16  Subglottic croup (i.e., laryngotracheobronchitis). A, Antero-posterior radiograph of the neck reveals a long area of the airway (shadow) narrowing and extending well below the normally narrowed area at the level of the vocal cords. This finding often is called the steeple signB, In this child, direct visualization using a bronchoscope revealed subglottic narrowing that was so severe that it would require endotracheal intubation or tracheostomy to establish an adequate airway.  (Courtesy of Sylvan Stool, M.D., Children's Hospital of Pittsburgh, PA.) (From Yellon RF, McBride TP, Davis HW: Otolaryngology. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, 4th ed. St. Louis, 2002, Mosby, p 860.)

 



Anesthetic Management of Acute Supraglottitis

In the operating room, anesthesia is induced with halothane (historically) or sevoflurane and oxygen in a sitting position while the child is monitored with a precordial stethoscope, pulse oximeter, and electrocardiogram. The child in respiratory distress usually breathes continually, uninterrupted by breath holding. A moderate continuous positive pressure (10 to 15 cm H2O) must be maintained to minimize the inspiratory collapse of laryngeal airways by the Venturi effect, and ventilation must be assisted with moderate continuous positive airway pressure while avoiding inflating the stomach with excessive pressure. An intravenous access is established as soon as the child is sufficiently obtunded, and atropine (0.02 mg/kg) is given to block vagally mediated slowing of the heart; bradycardia in an atropinized child is a sign of severe hypoxia.

The induction may take much longer, even with a higher concentration of an anesthetic, to reach the state where relaxation and centrally fixed pupils indicate that the child is ready for intubation. The use of muscle relaxants is contraindicated, even when the maintenance of the airway with mask and bag seems reasonable, because their use often results in the relaxation of pharyngeal muscles and complete obstruction of the laryngeal airway; frantic attempts to ventilate the child with high pressure cause gastric distension, regurgitation, and further asphyxia.

Endotracheal intubation is performed orally with a styletted tube one or two sizes smaller than usual. Visualization of the classic cherry-red epiglottis under direct laryngoscopy confirms the diagnosis ( Fig. 23-17 ). However, the picture may be atypical or only part of the epiglottis may be inflamed or swollen. Inflammatory swelling of other supraglottic structures, including the uvula, arytenoids, aryepiglottic folds, and false vocal cords, also causes severe obstruction. To visualize the vocal cords for intubation, the epiglottis is lifted by the curved tip of a straight laryngoscope blade (e.g., Phillips 1). In children with severe obstruction and mucosal swelling, identification of supraglottic structures and glottic opening with a laryngoscope blade may be extremely difficult. Under these circumstances, forcible manual chest compression by the assistant may open up the expiratory passages momentarily (or produce a few bubbles of expired air). By aiming the tip of the endotracheal tube at that spot and advancing the tube with a gentle twisting motion, the physician may be successful in inserting the tube in the glottis ( Smith, 1980 ). In case intubation proves to be impossible, a surgeon who can perform an emergency tracheotomy in the operating room with the surgical instruments and various tracheotomy tubes should be immediately available.

 
 

FIGURE 23-17  A bright red and swollen epiglottis in a patient with acute supraglottitis. It may retain its omega shape (A) or resemble a cherry (B).  (From Yellon RF, McBride TP, Davis HW: Otolaryngology. In Zitelli BJ, Davis HW, editors: Atlas of pediatric physical diagnosis, 4th ed. St. Louis, 2002, Mosby, p 858.)

 



After the endotracheal tube is in place, breath sounds are checked on both sides of the chest, and the tube is fixed with adhesive tapes. The breath sounds are monitored carefully with the precordial stethoscope while continuous positive pressure (10 to 15 cm H2O) is maintained, because pulmonary edema may occur after the relief of severe upper airway obstruction ( Travis et al., 1977 ; Galvis et al., 1980 ), with an incidence of about 7% ( Davis et al., 1981 ). Throat and blood cultures are taken during this period of stabilization but not before the intubation and restoration of adequate pulmonary gas exchange.

After the child's condition is stabilized after the restoration of adequate alveolar ventilation, some anesthesiologists replace the orotracheal tube by a nasotracheal tube that has a leak at or below 30 cm H2O ( Oh and Motoyama, 1977 ). This is not a necessary step, and the physician should be confident that the switch could be made without losing the airway. Because acute epiglottitis has become an uncommon phenomenon, many anesthesiologists are happy with the oral intubation and leave the tube in place. The child can be deeply sedated for 24 hours to avoid premature extubation.

Since the mid-1970s, the management of epiglottitis with tracheotomy has been replaced by the less invasive long-term nasotracheal or orotracheal intubation as the standard treatment of choice. This has significantly reduced the duration of hospital stay for children with acute supraglottitis ( Oh and Motoyama, 1977 ; Schloss et al., 1983 ). Accidental or self-extubation is a potentially disastrous complication. Careful taping of the tube and proper restraint of elbows and hands can prevent untimely extubation. Because most children are bacteremic, antimicrobial therapy, consisting of ampicillin with sulbactam, cefotaxime, or ceftriaxone, is started after blood and throat cultures are obtained. Any fluid deficits should be corrected parenterally. After the emergence from anesthesia, the child often falls back to sleep for some time because of sleep deprivation and exhaustion. After this period, most patients require minimal or no sedation ( Oh and Motoyama, 1977 ), although deep sedation has been used in some centers. Usually, it is possible to extubate these patients in 24 to 48 hours. A return of normal body temperature and increased leaks around the nasotracheal tube are major signs of recovery. The epiglottis may be examined under direct vision, with intravenous propofol or thiopental to determine the time for extubation. Alternatively, a flexible fiberoptic bronchoscope may be used transnasally with intravenous sedation.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier

▪ ANESTHESIA FOR ENDOSCOPY

Anesthesia for rigid and flexible bronchoscopy in infants and children requires meaningful cooperation and communication between the endoscopist and anesthesiologist ( Donlon, 1996) . The surgeon and the anesthesiologist are both working in the same anatomic field. The anesthesiologist is concerned about maintaining a patent airway, oxygenation, adequate ventilation, preventing aspiration, minimizing laryngeal motion, and preventing cardiac dysrhythmias, and the surgeon needs a clear view of a motionless field for a reasonable time. Sometimes, these goals may conflict. Donlon (1996) has eloquently described the anesthetic goals during bronchoscopy:

  

   

Control of the airway

  

   

Decreased airway reflexes

  

   

Topical anesthesia

  

   

Amnesia

  

   

Unobstructed view of immobile surgical field

  

   

No time restriction on surgeon inherent in the anesthetic technique

  

   

Prevention of aspiration

  

   

Smooth emergence

  

   

Safe extubation

  

   

Minimization of secretions

  

   

Prevention of adrenergic reflexes

To achieve these goals, anesthetic management must be individualized based on the patient's age, concurrent illnesses, goals of endoscopy, skill of the anesthesiologist, and the proven track record of the anesthetic technique.

Rigid bronchoscopy has broad applications in the diagnostic and therapeutic arenas. Common indications for pediatric patients include investigation of stridor, upper and central airway obstruction, gastroesophageal reflux disease, and removal of airway foreign bodies ( Hoeve and Rombout, 1992 ; Cohen et al., 2001 ). Flexible bronchoscopy is frequently used for examination of the nasal cavity, nasopharynx, larynx, trachea, and bronchi in motion. Technological advances, such as smaller instruments and improved forceps, will continue to expand the diagnostic and therapeutic role of the flexible bronchoscopy ( Cohen et al., 2001 ). Flexible and rigid bronchoscopies are used complementarily, and these procedures are often performed during the same examination. Table 23-5 lists the common indications for fiberoptic and rigid bronchoscopy. Many scenarios exist when either instrument can be used for the same indication.

TABLE 23-5   -- Indications for flexible or rigid bronchoscopy

Indications for Fiberoptic Laryngoscopy

Indications for Fiberoptic Bronchoscopy

Evaluation of stridor

Diagnostic

Hoarseness or weak cry

 

Difficult preextubation of epiglottitis

Stridor

 

Tracheotomy surveillance

Indications for Rigid Microlaryngoscopy and Bronchoscopy

Persistent wheezing

 

Persistent atelectasis

Stridor

Persistent pneumonia/diffuse infiltrates

Tracheotomy surveillance

Chronic cough

Foreign body evaluation/management

Infiltrates in the immunocompromised host bronchoalveolar lavage

Interval evaluation following laryngotracheal reconstruction

Mild hemoptysis

Chronic cough

Lung lesion of unknown cause

Severe hemoptysis

Selective bronchography

Management of severe laryngotracheal infections

Assessment of toxic inhalation/aspiration

Airway trauma

Monitor after lung transplantation

Assessment of toxic inhalation/aspiration

 

Evaluation of laryngeal pathology

Therapeutic

Management of mass lesions of the airway, including recurrent respiratory papillomatosis

Confirmation of endotracheal tube position

 

Acute lobar aelectasis

 

Cystic fibrosis management

 

Removal of mucous plugs

From Hartnick CJ, Cotton RT: Stridor and airway obstruction. In Bluestone CD, Stool SE, Alper CM, et al., editors. Pediatric otolaryngology, 4th edition. WB Saunders, 2003, Philadelphia, pp 1437–1447, Table 81–4.

 

 

The Storz-Hopkins rigid bronchoscope, with a ventilating sidearm, provides excellent visibility for pediatric bronchoscopy ( Szekely and Farkas, 1978 ; Johnson et al., 1986 ). This bronchoscope consists of several components: Storz bronchoscope (sizes 3.0 to 6.0); Hopkins glass rod telescope (2.8 and 4.0 mm ED); antifog sheath for the telescope; adapter for anesthesia circuit connecting to the sidearm, which shares the same narrow channel for aspiration and instrumentation; glass obturator cap; and the light source attached to the telescope and prism ( Fig. 23-18 ). The pediatric Storz rigid bronchoscopes are available in three lengths and various diameters ( Fig. 23-19 ). A variety of forceps is available for biopsy and foreign body removal.

 
 

FIGURE 23-18  Storz-Hopkins pediatric bronchoscopy assembly. 1, Hopkins glass rod telescope. 2, Antifog sheath for the telescope shown in 1. 3, Storz ventilation bronchoscope, which accommodates the telescope and antifog sheath. 4, Adapter for the anesthesia circuit. 5, Prism. 6, Glass obturator cap.

 

 

 
 

FIGURE 23-19  Different bronchoscope sizes (3.5 to 6.0) (left) and lengths (20, 26, and 30 cm) (right) are shown.  (From Casselbrant ML, Alper CM: Methods of examination. In Bluestone CD, Stool SE, editors: Pediatric otolaryngology, 4th ed. New York, 2003, WB Saunders, pp 1379-1394.)

 



It is important to use the smallest optical telescope through the rigid bronchoscope to not completely occlude or unduly increase airflow resistance. For example, use of the standard optical telescope (4 mm OD), as recommended in the literature ( Szekely and Farkas, 1978) , almost completely occludes the lumen of small bronchoscopes (size 3.5 and smaller). The total airway resistance increases six to sevenfold ( Widlund, et al., 1982) unless a smaller telescope (2.8 mm OD) is used ( Table 23-6 ). When airway resistance is too high, neither spontaneous nor controlled ventilation is sufficient for adequate gas exchange during rigid bronchoscopy. High airway resistance would be expected to cause hyperinflation of the lungs and respiratory acidosis ( Rah et al., 1979 ). Spontaneous breathing during rigid bronchoscopy, especially in neonates and infants, should be limited primarily to evaluations of the larynx and documentation of tracheobronchomalacia in the patient with stridor. The high resistance caused by the telescope within the bronchoscope, together with central respiratory depression caused by general anesthesia, makes spontaneous breathing nearly impossible in these young children ( Motoyama, 1992 ).


TABLE 23-6   -- Flow resistance of Storz bronchoscope in relation to estimated airway resistance (cm H2O/L/sec) in infants and children

Age

Airway Resistance (Raw)

Bronchoscope Size

BRONCHOSCOPE RESISTANCE

Ratio Rsa-2/Raw

Rsa-1[*]

Rsa-2[†]

1 wk

29

3.0

17

31

4.1

6 mo

19

3.5

12

134

7.0

3 yr

10

4.0

14

37

5.7

5 yr

8

5.0

10

17

3.1

10 yr

5

6.0

16

19

4.3

Based on data from Widlund B, Walczak S, Motoyama EK: Flow-pressure characteristics of pediatric Storz-Hopkins bronchoscopes. Anesthesiology 57:A417, 1982.

*

Flow resistance through breathing sidearm (Rsa) at 0.4 L/sec without telescope.

Rsa at 0.4 L/sec with telescope (4.0 mm OD) engaged in bronchoscope.

 

 

With the advances in fiberoptic technology, diagnostic bronchoscopy can be performed with a flexible fiberoptic bronchoscope during spontaneous breathing with topical anesthesia and minimal sedation even in the sick premature infant. Bronchoscopy also may be performed under general anesthesia through an endotracheal tube or LMA by means of a right-angle adapter with a diaphragm ( Maekawa et al., 1981 ; Wood and Postma, 1988 ). The use of the flexible fiberoptic bronchoscope for difficult intubation is described in Chapter 10 (Induction of Anesthesia).

▪ LARYNGOSCOPY AND BRONCHOSCOPY FOR STRIDOR

Stridor in pediatric patients may have a congenital or acquired cause. Most cases are of extrathoracic origin, but some originate in the large intrathoracic airways (i.e., trachea and major bronchi) ( Box 23-1) ( Maze and Bloch, 1979 ). Stridor may be caused by fixed obstruction (i.e., airway cross section does not change with transmural pressure) or various degrees of obstruction (i.e., airway caliber responds to changes in transmural pressure). These children must be examined while they are actively breathing to document underlying pathophysiology.

BOX 23-1 

Causes of Stridor in the Pediatric Patient

Congenital Stridor

Craniofacial dysmorphology (with micrognathia and glossoptosis)

  

 

Pierre Robin syndrome

  

 

Treacher Collins syndrome (mandibulofacial dysostosis)

  

 

Hallermann-Streiff (oculomandibular) syndrome

  

 

Moebius syndrome

  

 

De Lange's syndrome

  

 

Freeman-Sheldon syndrome (whistling face)

Macroglossia

  

 

Beckwith's syndrome

  

 

Congenital hypothyroidism

  

 

Glycogen storage diseases

  

 

Down syndrome

  

 

Diffuse muscular hypertrophy of the tongue

  

 

Localized lingual tumors

  

 

Laryngomalacia

Congenital subglottic stenosis

Congenital laryngeal webs

Laryngotracheoesophageal cleft

Congenital vocal cord paralysis

Vascular rings and slings

Congenital tracheal anomalies

Congenital tumors and cysts

  

 

Congenital subglottic hemangroma

  

 

Laryngeal lymphangioma and cystic hygroma

  

 

Cysts and laryngoceles

  

 

Miscellaneous congenital tumors

Birth trauma: edema

Metabolic stridor: laryngismus stridulus

Immunologic stridor: hereditary angioneurotic edema

Neurogenic stridor: reflex laryngospasm

Acquired Stridor

Infectious stridor

  

 

Supraglottitis

  

 

Subglottic group

  

 

Acute spasmodic laryngitis

  

 

Diphtheria

  

 

Retropharyngeal abscess

Immunologic stridor—juvenile rheumatoid arthritis

Foreign bodies

Postintubation stridor

Laryngeal trauma: mechanical, thermal, chemical

Neoplasia

  

 

Laryngeal papillomatosis

  

 

Miscellaneous tumors and nodes

Modified from Maze A, Bloch E: Stridor in pediatric patients. Anesthesiology 50:132, 1979.

 

The anesthetic approach should be individualized, with good communication between the endoscopist and anesthesiologist. All children should be monitored with a pulse oximeter, end-tidal CO2 monitor, precordial stethoscope, electrocardiogram, and automated blood pressure and thermometer. Oxygen saturation is determined in room air before the induction of anesthesia to establish the baseline value. If neuromuscular blockade is required, a nerve stimulator should be used to track the depth of paralysis. Standard NPO guidelines should be followed.

In the newborn infant, flexible and rigid forms of bronchoscopy are used to determine the cause of stridor. Flexible bronchoscopic examination of the infant's larynx by the nasal approach is possible when the child is awake. The infant should be swaddled for restraint. Information about cord mobility and laryngeal dynamics can be made without much stress to the infant. Atropine or glycopyrrolate can be used as an antisialogue and to prevent vagally mediated bradycardia. The nasal mucosa can be anesthetized with topical lidocaine to prevent discomfort during the transnasal approach, but the vocal cords should not be sprayed, because topical anesthesia affects their motion. Midazolam or low-dose propofol may be helpful to reduce the infant's excessive movement while still maintaining breathing dynamics. Because the upper airway muscles, including the vocal cords (i.e., cricoarytenoid muscles), are extremely sensitive to the depressant effect of sedatives and anesthetics (Ochiai et al., 1989, 1992 [153] [152]), anesthesia should be maintained at a minimal level. Otherwise, the vocal cord motions will cease.

Alternatively, anesthesia is induced with an inhaled agent (i.e., sevoflurane or halothane) without assisting ventilation and intravenous access is established. After atropine or glycopyrrolate is infused and a nasal topical decongestant (i.e., oxymetazoline) and lidocaine is sprayed, the anesthetic is discontinued while flexible nasopharyngoscopy is performed as the infant starts to wake up and the motion of the vocal cords return before the diagnosis of vocal cord paralysis is made. This approach is superior, especially for the diagnosis of laryngomalacia. The infant breathes actively and may move, but he or she is still unconscious during the flexible laryngoscopy. The patient is then reanesthetized with an inhaled anesthetic or with propofol for rigid tracheobronchoscopy.

Only by rigid bronchoscopy under the controlled conditions of general anesthesia can a magnified clear view of the larynx and lower airways be achieved ( Hartnick and Cotton, 2003 ). The use of the rigid bronchoscope allows for lower airway inspection while maintaining complete and secure control over oxygenation and ventilation. After airway dynamics are inspected by fiberoptic or rigid bronchoscopy, the child can be paralyzed with an intermediate muscle relaxant. Anesthesia can be maintained with an inhaled anesthetic agent or total intravenous anesthesia. Communication must continue with the bronchoscopist to maintain adequate oxygenation and ventilation. When the lower airways are explored, the endoscopist may need to be reminded to intermittently to return above the carina for the anesthesiologist to ventilate and oxygenate both lungs.

In older infants and children, spontaneous breathing may be maintained during the entire procedure. This technique for laryngoscopy and bronchoscopy with spontaneous breathing is useful for the evaluation of stridor, laryngomalacia, and tracheobronchomalacia. It is also a technique some anesthesiologists advocate for foreign body removal from the airway. Maintenance of spontaneous breathing can be achieved with an inhalational or an intravenous anesthetic technique. For example, after inhalational induction, the concentration of sevoflurane in oxygen is maintained at 2 or 3 minimum alveolar concentration (MAC) for about 5 minutes to establish a sufficient tissue level of anesthesia to allow endotracheal instrumentation ( Smith, 1980 ). An alternative is to discontinue the inhaled anesthetic, slowly provide a bolus (2 to 3 mg/kg) of propofol, and begin a propofol infusion between 200 and 400 mcg/kg per minute while maintaining spontaneous breathing. Supplementation with fentanyl or morphine can further ablate laryngeal responses. Before endoscopy, the glottis and trachea are topically anesthetized with 2% to 4% lidocaine (up to 5 mg/kg) under the direct vision.

The otolaryngologist then proceeds, using a ventilating bronchoscope and a telescope in situ. Initially, the endoscopist inspects the appearance and motion (widening) of vocal cords with inspiration and the motion of the soft tissues surrounding the inlet to the larynx. The tip of the bronchoscope is held above the inlet to the larynx without touching the pharyngeal or laryngeal soft tissues. After the bronchoscope is introduced past the vocal cords, the anesthesia circuit is connected to the side arm of the bronchoscope allowing for continued spontaneous ventilation or supplemental controlled ventilation. At the end of bronchoscopy, the bronchoscope is removed, and the anesthetic agents are discontinued. If the patient has been spontaneously breathing throughout the anesthesia, the patient can be maintained with oxygen by means of a mask and CPAP. If the patient is apneic or neuromuscular blockade was required, the child may be intubated and ventilated until clinically ready for extubation.

▪ BRONCHOSCOPY FOR FOREIGN BODY ASPIRATION

Foreign body aspiration occurs most frequently in children between 1 and 3 years of age. Common aspirated objects include peanuts, seeds, and other food particles and less frequently plastic and metal particles ( Baraka, 1974 ; Blazer et al., 1980 ). Foreign bodies are embedded more commonly in the right main bronchus than in the left and less frequently in the larynx and trachea ( Blazer et al., 1980 ;Cohen et al., 2001 ). Symptoms and signs associated with bronchial aspiration include coughing, wheezing, dyspnea, and decreased air entry in the affected side, whereas dyspnea, stridor, coughing, and cyanosis are more common with laryngeal or tracheal foreign bodies ( Blazer et al., 1980 ).

In addition to the usual preoperative assessment, physical examination should focus on the location, degree of airway obstruction, and gas exchange. A review of the latest chest radiographs is helpful in determining the location of the foreign body and for evidence of secondary pathologic changes such as atelectasis, air trapping, or pneumonia ( Fig. 23-20 ). If significant hyperinflation of one lung or lobe exists, nitrous oxide should be withheld because of the potential danger of further increase in gas volume and possible rupture of the affected lung. Although it is desirable to keep the child NPO 6 or more hours for solids and 2 hours for clear liquids, the patient's condition determines the timing of the bronchoscopic examination. If foreign body aspiration causes life-threatening respiratory distress, its removal takes precedence over NPO guidelines.

 
 

FIGURE 23-20  Foreign body in the left bronchus with hyperinflation of the ipsilateral portion of the lung.  (Courtesy of Dr. K.S. Oh, Department of Radiology, The Children's Hospital of Pittsburgh, PA.)

 



A major controversy in the anesthetic management of patients undergoing bronchoscopy for foreign body removal is whether to control ventilation or to maintain spontaneous ventilation ( Verghese and Hannallah, 2001 ). There are few data to justify one technique over the other. Woods (1990) prefers spontaneous ventilation, and Kosloske (1982) advocates neuromuscular blockade and controlled ventilation. The risk of controlled ventilation is to force the foreign body deeper into the small airways, and the risk for the spontaneously breathing patient is unexpected movement or cough ( Donlon, 1996) . In a report of four patients in whom the bronchoscopist had the foreign body slip from the forceps back into the airway, neither controlled ventilation with muscle paralysis nor spontaneous breathing under a deep plane of anesthesia played a role in the mishaps. It was thought that the experience of the endoscopist and the availability of proper equipment were more important factors than the method of ventilation ( Pawar, 2000 ).

Muscle relaxation is particularly useful for bronchoscopy involving the removal of a foreign body distal to the carina especially because the duration of these procedures can extend to more than an hour. If the spontaneous ventilation technique is employed, meticulous topical anesthesia of the vocal cords with lidocaine can decrease the risk of coughing and laryngospasm. Propofol-based total intravenous anesthesia would be a superior choice over inhalational anesthesia because propofol provides a steady level of anesthesia regardless of ventilation and perfusion mismatches ( Verghese and Hannallah, 2001).

The anesthetic approach to the child who has aspirated a foreign body must be individualized. All children should be monitored with a pulse oximeter, end-tidal CO2 precordial stethoscope, electrocardiogram, thermometer, and automated blood pressure. Oxygen saturation is determined in room air before the induction of anesthesia to establish the baseline value. If neuromuscular blockade is required, a nerve stimulator should be used to track the depth of paralysis.

Foreign bodies in the larynx are more likely to cause total airway obstruction than are foreign bodies below the glottis. Foreign bodies located in the bronchi may dislodge from cough or change in position and cause total obstruction ( Woods, 1990 ). In case of acute respiratory distress and hypoxemia with a laryngeal foreign body, anesthesia is induced with the patient in a sitting position with an inhaled anesthetic and oxygen while the patient is monitored with a precordial stethoscope, pulse oximeter, and electrocardiogram. Spontaneous breathing is preferable; positive pressure ventilation may cause the foreign body to be displaced and further obstruct the airway ( Darrow and Holinger, 2003 ). After inhalational induction, intravenous access is established (if not already available), and a vagolytic dose of atropine (0.02 to 0.03 mg/kg) is administered. After intravascular access is established, inhalational anesthesia may be switched to total intravenous anesthesia with propofol with or without opioids (e.g., fentanyl, remifentanil). For children in stable condition with foreign body aspiration presumed to be in the bronchus, an intravenous catheter is inserted before the induction, and the child is monitored in the usual manner. If a full stomach is suspected, the physician must weigh the risk of aspiration against loss of a patent airway before rapid sequence with succinylcholine and cricoid pressure is considered.

As soon as the child is anesthetized, the endoscopist must ensure that no foreign body is present above the vocal cords. If the laryngeal outlet is clear, the larynx is sprayed with 2% to 4% lidocaine, and a bronchoscope is inserted through the laryngeal inlet. Fortunately, it is rare for an anesthesiologist to encounter a foreign body in the larynx and upper trachea that causes dyspnea and life-threatening hypoxia.

Immediately after the bronchoscope passes the glottis, the anesthesia circuit is connected to the breathing sidearm of the bronchoscope, and manual ventilation or spontaneous breathing with manual assist is resumed. It is important to remember that, with extremely high flow resistance through the side arm of the bronchoscope, spontaneous breathing is all but ineffective and the respiratory rate (especially the expiratory phase) must be kept very slow to allow sufficient time for passive exhalation. Inspiratory gas flow is adjusted to accommodate for the leak around the bronchoscope.

During the procedure, the anesthesiologist's attention should be focused on the breath sounds detected by the precordial stethoscope, the symmetry of respiratory excursion, and oxygen saturation measured by a pulse oximeter. Close communication and cooperation between the bronchoscopist and the anesthesiologist are essential throughout bronchoscopy. It is important to remember that the lumen of the bronchoscope is narrowed by the telescope and the use of instruments, especially when a suction catheter is inserted through the side port, the same narrow channel through which the patient must be ventilated ( Cotton and Reilly, 1990 ). The rate of rise in end-tidal PCO2 in apneic infants and young children is extremely high, at the rate of approximately 9 mm Hg/min ( Motoyama et al., 2001 ). The period of apnea or severe hypoventilation therefore should be closely observed and communicated with the endoscopist. The physician must make sure that after each period of hypoventilation or apnea the telescope, forceps, or endobronchial suction catheter through the bronchoscope's side arm is removed. The distal end of the bronchoscope should be pulled above the carina, and the proximal open end of the bronchoscope is occluded with the endoscopist's thumb or a glass obturator cap (see Fig. 23-18 ), so that the child can be hyperventilated before instrumentation is resumed. Keep in mind that during the crucial moment of foreign body retrieval, ventilation sometimes must be held until the oxygen saturation begins to fall.

When the foreign body or its fragment is successfully grasped with the forceps, the forceps and the bronchoscope are carefully pulled out of the trachea and the larynx together as a single unit. It is imperative that the upper airway and glottis are totally relaxed allowing the foreign body to pass through without being dislodged prematurely. The patient is mask ventilated until the bronchoscope is reintroduced into the trachea. This maneuver may be repeated when the foreign body is fragmented. If a large, obstructive foreign body is removed from the bronchus but is dislodged in the trachea or larynx during the process of retrieval, it can cause serious obstruction of the entire respiratory system unless it is removed immediately. If prompt removal is not possible, the foreign body should be pushed back into one of the main bronchi so that ventilation can be resumed with at least one lung.

Intraoperative complications include laryngospasm, bronchospasm, hypoxia, arrhythmias, and pneumothorax. They are preventable by maintaining adequate anesthesia, oxygenation, ventilation, and muscle relaxation. Premature ventricular contraction, although rare, can usually be treated with hyperventilation, intravenous lidocaine (1 mg/kg), and by avoiding halothane. Pneumothorax, although infrequent, must be kept in mind if acute deterioration of ventilation and gas exchange occurs. A portable chest radiograph is diagnostic, and a chest tube is inserted to reexpand the lung.

After the completion of bronchoscopy for foreign body retrieval, the child is usually intubated with an endotracheal tube. Tracheal intubation allows for tracheobronchial suction, lung expansion, and for oxygenation and ventilation until adequate reversal of muscle relaxation and return to spontaneous breathing. Dexamethasone (0.4 to 1.0 mg/kg, up to 20 mg/kg) is given prophylactically to prevent laryngeal edema ( Tunnessen and Feinstein, 1980 ; Postma et al., 1987 ). Postoperative croup is treated with inhalation of racemic epinephrine (0.5 mL of 2.25% solution diluted in 3 mL of saline solution) (Adair et al., 1971 ).

▪ ENDOSCOPY FOR FOREIGN BODY INGESTION

According to the National Safety Council, suffocation from foreign body ingestion and aspiration is the third leading cause of accidental death in children younger than 1 year and the fourth leading cause in children between 1 and 6 years old. Ingestions are often asymptomatic, unrecognized, and self-resolving. Because retained esophageal foreign bodies are so much more common than aspirations, procedures for removal outnumber those for aspirated foreign bodies ( Manning and Stool, 2003 ). The most commonly ingested foreign body is a coin followed by food or bones. Other foreign bodies include buttons, batteries, pins, safety pins, thumbtacks, and small toys ( McGahren, 1999 ). Once in the stomach or bowel, coins usually pass through the remainder of the gastrointestinal tract. Many coins, however, become lodged in the esophagus. The most frequent symptoms of upper esophageal foreign body include dysphagia, drooling, gagging, retching, and vomiting. The child may also experience coughing, choking, and significant airway compromise. Serious complications, such as esophageal erosion, caused by retained esophageal coins are rare and occur only after a coin has been lodged more than 24 hours. Soprano and others (1999) recommend that children with a single coin in any part of the esophagus who have no history of esophageal disease, or respiratory compromise on presentation to the emergency department, be observed for 12 to 24 hours. These authors found that within 24 hours there is a 28% chance of spontaneous passage of the coin into the stomach, regardless of esophageal location ( Soprano et al., 1999 ).

A chest radiograph should be obtained in all cases of suspected foreign body ingestion. Ingested foreign bodies are predisposed to lodge in three areas of anatomic constriction in the esophagus: the proximal esophagus at the level of the cricopharyngeal muscle and thoracic inlet (the foreign body is seen at the level of the clavicles on chest radiograph), the middle esophagus at the level of the carina and the aortic arch, and the distal esophagus just proximal to the esophageal gastric junction (the foreign body is seen two to four vertebral bodies above the stomach bubble on chest radiography). The most common site for foreign bodies to lodge is at the upper esophagus at the level of the thoracic inlet. If the foreign body is a coin, it will be oriented in a transverse position because the opening of the esophagus is widest in a transverse position ( McGahren, 1999 ).

Removal of a foreign body from the esophagus is not usually a complicated procedure. As long as the child is not dyspneic, the physician should wait 4 to 6 hours after the last meal, depending on the child's age, until the stomach is empty. The child should be well sedated, and anesthesia is induced with inhaled or intravenous anesthetics. During esophagoscopy, the mucosa over the cricoid cartilage may be traumatized by compression between the endotracheal tube anteriorly and the rigidesophagoscope posteriorly. A prospective review involving more than 50,000 general pediatric anesthetic cases revealed that the incidence of postintubation croup after esophagoscopy was 20 times higher than that of the general pediatric surgical population during the same time period (Moro, Borland, and Motoyama, unpublished observations). A reduced-size endotracheal tube may be helpful to minimize subglottic swelling ( Smith, 1980 ). Dexamethasone (0.4 to 1 mg/kg up to 20 mg) may also reduce the incidence of postoperative stridor.

The only potential and major hazard with foreign body ingestion is the situation in which the foreign body, usually a coin, is held in the hypopharynx, and on gagging and coughing, it dislodges and slips into the larynx, completely occluding the airway. When a radiograph of the neck demonstrates a foreign body high in the esophagus ( Fig. 23-21 ), the child is sedated heavily with an opioid and a sedative to avoid excitement, gagging, and coughing. After intravenous access is established and atropine is given, the trachea is intubated under deep inhalational anesthesia or propofol with or without muscle relaxation. The use of neuromuscular blockade is determined by the ability to ventilate the child with positive pressure. Cricoid pressure is avoided under these circumstances because it may irritate the upper airway or dislodge the foreign body.

 
 

FIGURE 23-21  A jack is lodged high in the esophagus of a 4-year-old boy.  (Courtesy of Dr. J. Medina, Department of Radiology, The Children's Hospital of Pittsburgh, PA.)

 



Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier

▪ SUMMARY

Surgical procedures involving the ear, nose, and throat are the most frequently performed procedures requiring general anesthesia in infants and children. Most procedures are of short duration and involve relatively healthy patients. However, there is a subset of patients with congenital abnormalities and OSAS that presents with difficult airways and significant upper airway obstruction. Improved monitoring technology, newer anesthetic agents (e.g., sevoflurane, propofol), and shorter-acting muscle relaxants have made care of these patients safer and more efficient.

Over the past 2 decades, a drastic decline of acute supraglottitis, the most dreaded of childhood emergencies for pediatric anesthesiologists, has been witnessed with the development of the Hib vaccine. Technological advances in laser surgery and laryngoplasty have continued to challenge pediatric anesthesiologists to develop approaches to meet the needs of advancing otolaryngologic technology.

Copyright © 2008 Elsevier Inc. All rights reserved. - www.mdconsult.com

Motoyama & Davis: Smith's Anesthesia for Infants and Children, 7th ed.

Copyright © 2005 Mosby, An Imprint of Elsevier

REFERENCES

A clinician's guide to surgical fires, 2003. A clinician's guide to surgical fires : How they occur, how to prevent them, how to put them out.  Health Devices  2003; 32:5.

Aberdeen and Downes, 1974. Aberdeen E, Downes JJ: Artificial airways in children.  Surg Clin North Am  1974; 54:1155.

Adair et al., 1971. Adair JC, Ring WH, Jordan WS, et al: Ten-year experience with IPPB in the treatment of acute laryngotracheobronchitis.  Anesth Analg  1971; 50:649.

Adams et al., 1993. Adams WG, Deaver KA, Cochi SL, et al: Decline of childhood Haemophilus influenzae type b (Hib) disease in the Hib vaccine era.  JAMA  1993; 269:221.

Afshan et al., 2002. Afshan G, Chohan U, Qamar UL, et al: Is there a role of a small dose of propofol in the treatment of laryngeal spasm?.  Paediatr Anaesth  2002; 12:625.

Airway fires, 1990. Airway fires : Reducing the risk during laser surgery.  Health Devices  1990; 19:109.

Alexander, 1990. Alexander CA: A modified Intravent laryngeal mask for ENT and dental anaesthesia.  Anaesthesia  1990; 45:892.

Alexander et al., 1965. Alexander DW, Graff TW, Kelley E: Factors in tonsillectomy mortality.  Arch Otolaryngol  1965; 82:409.

Allen et al., 1973. Allen TH, Steven IM, Sweeney DB: The bleeding tonsil: Anesthesia for control of haemorrhage after tonsillectomy.  Anaesth Intensive Care  1973; 1:517.

Allsop et al., 1995. Allsop E, Innes P, Jackson M, et al: Dose of propofol required to insert the laryngeal mask airway in children.  Paediatr Anaesth  1995; 5:47.

American Thoracic Society, 1996. American Thoracic Society : Standards and indications for cardiopulmonary sleep studies in children.  Am J Respir Crit Care Med  1996; 153:866.

Avery and Harris, 1976.   Avery AD, Harris LJ: Tonsillectomy, adenoidectomy, and tonsillectomy with adenoidectomy: Assessing the quality of care using short-term outcome measures. Quality of medical care assessment using outcome measures: Eight disease-specific applications. Santa Monica, CA, 1976, Rand Corp.

Balkany et al., 2001. Balkany TJ, Hodges A, Miyamoto RT, et al: Cochlear implants in children.  Otolaryngol Clin North Am  2001; 34:455.

Bandla et al., 1999. Bandla HP, Hopkins RL, Beckerman RC, et al: Pulmonary risk factors compromising postoperative recovery after surgical repair for congenital heart disease.  Chest  1999; 116:740.

Baraka, 1974. Baraka A: Bronchoscopic removal of inhaled foreign bodies in children.  Br J Anaesth  1974; 46:124.

Beamis et al., 1991. Beamis JE, Vergos K, Rebeiz EE, et al: Endoscopic laser therapy for obstructive tracheobronchial lesions.  Ann Otol Rhinol Laryngol  1991; 100:413.

Benoit et al., 2002. Benoit Z, Wicky S, Fischer J-F, et al: The effect of increased FIO2 before tracheal extubation on postoperative atelectasis.  Anesth Analg  2002; 95:1477.

Bennie et al., 1998. Bennie RE, Boehringer LA, Dierdorf SF, et al: Transnasal butorphanol is effective for postoperative pain relief in children undergoing myringotomy.  Anesthesiology  1998; 89:385.

Berry, 1982. Berry FA: Post-tonsillectomy bleeding.  Common problems in pediatric anesthesia,  Chicago, Year Book Medical Publishers, 1982.

Biavati et al., 1997. Biavati MJ, Manning SC, Phillips DL: Predictive factors for respiratory complications after tonsillectomy and adenoidectomy in children.  Arch Otolaryngol Head Neck Surg  1997; 123:517.

Blackstock et al., 1987. Blackstock D, Adderley RJ, Steward DJ: Epiglottitis in young infants.  Anesthesiology  1987; 67:97.

Bland and Edwards, 1969. Bland Jr JW, Edwards FK: Pulmonary hypertension and congestive heart failure in children with chronic upper airway obstruction. New concepts of etiologic factors.  Am J Cardiol  1969; 23:830.

Blazer et al., 1980. Blazer S, Naveh Y, Friedman A: Foreign body in the airway. A review of 200 cases.  Am J Dis Child  1980; 134:68.

Bluestone, 2001. Bluestone CD: Controversies in tonsillectomy, adenoidectomy and tympanostomy tubes.   In: Bailey B, ed. Head and neck surgery—otolaryngology,  Philadelphia: Lippincott Williams & Wilkins; 2001:993-1006.

Bluestone and Klein, 2003. Bluestone CD, Klein JO: Intracranial Complications of otitis media.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:765-778.

Bluestone and Klein, 2001. Bluestone CD, Klein JO: Pediatric otolaryngology,  Philadelphia, WB Saunders, 2001.

Bluestone and Klein, 2003. Bluestone CD, Klein JO: Pediatric otolaryngology,  Philadelphia, WB Saunders, 2003.

Bluestone et al., 1975. Bluestone CD, Paradise JL, Kass EH, et al: The workshop on tonsillectomy and adenoidectomy.  Ann Orol Rhinol Laryngol suppl  1975; 19:84.

Borland and Reilly, 1987. Borland LM, Reilly IS: Jet ventilation for laser laryngeal surgery in children. Modification of the Saunders jet ventilation technique.  Int J Pediatr Otorhinolaryngol  1987; 14:65.

Brandom, 1997. Brandom BW: Postoperative management of laryngotracheal reconstruction.  Int Anesthesiol Clin  1997; 35:127.

Brisson et al., 2000. Brisson P, Patel H, Scorpio R, et al: Rotary atlanto-axial subluxation with torticollis following central-venous catheter insertion.  Pediatr Surg Int  2000; 16:421.

Brown et al., 1991. Brown GW, Patel N, Ellis FR: Comparison of propofol and thiopentone for laryngeal mask insertion.  Anaesthesia  1991; 46:771.

Brown et al., 1996. Brown OE, Pownell P, Manning SC: Choanal atresia: A new anatomic classification and clinical management applications.  Laryngoscope  1996; 106:97.

Bruppacher et al., 2003. Bruppacher H, Reber A, Keller JP, et al: The effects of common airway maneuvers on airway pressure and flow in children undergoing adenotonsillectomies.  Anesth Analg  2003; 97:29.

Butt et al., 1988. Butt W, Shann F, Walker C, et al: Acute epiglottitis: A different approach to management.  Critical Care Medicine  1988; 16:43.

Carcillo, 2003. Carcillo J: Intensive care management of infection-related acute upper airway obstruction in children.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1599-1604.

Carithers et al., 1987. Carithers JS, Gebhart DE, Williams JA: Postoperative risks of pediatric tonsilloadenoidectomy.  Laryngoscope  1987; 97:422.

Carron et al., 2000. Carron JD, Derkay CS, Strope GL, et al: Pediatric tracheotomies: Changing indications and outcomes.  Laryngoscope  2000; 110:1099.

Casselbrant and Alper, 2003. Casselbrant ML, Alper CM: Methods of examination.   In: Bluestone CD, Stool SE, Alper CM, et al ed. Pediatric otolaryngology,  4th ed.. Philadelphia: WB Saunders; 2003:1379-1394.

Cayler et al., 1969. Cayler GG, Johnson EE, Lewis BE, et al: Heart failure due to enlarged tonsils and adenoids. The cardiorespiratory syndrome of increased airway resistance.  Am J Dis Child  1969; 118:708.

Close et al., 1994. Close HL, Kryzer TC, Nowlin JR, et al: Hemostatic assessment of patients before tonsillectomy: A prospective study.  Otolaryngol Head Neck Surg  1994; 111:733.

Cohen et al., 2001. Cohen S, Pine H, Drake A: Use of rigid and flexible bronchoscopy among pediatric otolaryngologists.  Arch Otolaryngol Head Neck Surg  2001; 127:505.

Cook, 1982. Cook DR: Peritonsillar abscess and hyperthyroidism.   In: Sterling LC, ed. Common problems in pediatric anesthesia,  Chicago: Year Book Medical Publishers; 1982.

Coté et al., 1988. Coté CJ, Goldstein EA, Coté MA, et al: A single-blind study of pulse oximetry in children.  Anesthesiology  1988; 68:184.

Coté et al., 1991. Coté CJ, Roll N, Liu LMP, Gousouzian NG: A single-blind study of pulse oximetry and capnography in children.  Anesthesiology  1991; 74:984.

Cotton, 1990. Cotton RT: Advancing the quality of care for children.  Arch Otolaryngol Head Neck Surg  1990; 116:33.

Cotton, 2000. Cotton RT: Management of subglottic stenosis.  Otolaryngol Clin North Am  2000; 33:111.

Cotton and Reilly, 1990. Cotton RT, Reilly JS: Congenital malformations of the larynx.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  2nd ed.. Philadelphia: WB Saunders; 1990:1121-1128.

Cozine et al., 1981. Cozine K, Rosenbaum LM, Askanazi J, et al: Laser-induced endotracheal tube fire.  Anesthesiology  1981; 55:583.

Crysdale and Russel, 1986. Crysdale WS, Russel D: Complications of tonsillectomy and adenoidectomy in 9,409 children observed overnight.  Can Med Assoc J  1986; 135:1139.

Crysdale and Sendi, 1988. Crysdale WS, Sendi K: Evolution in the management of acute epiglottitis: a 10-years experience with 242 children.  Int Anesthesiol Clin  1988; 26:32-38.

Crysdale et al., 1991. Crysdale WS, Sendi KS, Yoo J: Esophageal foreign bodies in children: 15-year review of 484 cases.  Ann Otol Rhinol Laryngol  1991; 100:320.

Dahl and Kehlet, 1994. Dahl JB, Kehlet H: Non-steroidal anti-inflammatory drugs: Rationale for use in severe postoperative pain.  Br J Anaesth  1994; 72:375.

Darrow and Holinger, 2003. Darrow DH, Holinger LD: Foreign bodies of the larynx, trachea, and bronchi.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1543-1557.

Darrow and Siemens, 2002. Darrow DH, Siemens C: Indications for tonsillectomy and adenoidectomy.  Laryngoscope  2002; 112:6.

Davies and Steward, 1977. Davies DW, Steward DJ: Unexpected excessive bleeding during operation: Role of acetylsalicylic acid.  Can Anaesth Soc J  1977; 24:452.

Davis et al., 1981. Davis HW, Gartner JC, Galvis AG, et al: Acute upper airway obstruction: Croup and epiglottitis.  Rev Pediatr Clin North Am  1981; 28:859.

Diaz, 1985. Diaz JH: Croup and epiglottitis in children: The anesthesiologist as diagnostician.  Anesth Analg  1985; 64:621.

Donlon and Benumof, 1996. Donlon JV, Benumof JL: Anesthetic and airway management of laryngoscopy and broncoscopy,  St Louis, Mosby, 1996.

Dornhoffer and Manning, 2000. Dornhoffer J, Manning L: Unplanned admissions following outpatient otologic surgery: The University of Arkansas experience.  Ear Nose Throat J  2000; 79:710.

Doyle and Banks, 2003. Doyle WJ, Banks JM: Middle ear pressure change during controlled breathing with gas mixtures containing nitrous oxide.  J Appl Physiol  2003; 94:199.

Emhardt et al., 1988. Emhardt JD, Weisberger ED, Dierdorf SF, et al: The rise of arterial carbon dioxide during apnea in children.  Anesthesiology  1988; 69:779.

Erb et al., 2002b. Erb TO, Hall JM, Ing RJ, et al: Postoperative nausea and vomiting in children and adolescents undergoing radiofrequency catheter ablation: A randomized comparison of propofol- and isoflurane-based anesthetics.  Anesth Analg  2002; 95:1577.

Erb et al., 2002a. Erb TO, Schulman SR, Sugarman J: Permission and assent for clinical research in pediatric anesthesia.  Anesth Analg  2002; 94:1155.

Fine and Borland, 2004. Fine GF, Borland LM: The future of the cuffed endotracheal tube.  Paediatr Anaesth  2004; 14:38-42.

Finkel et al., 2001. Finkel JC, Cohen IT, Hannallah RS, et al: The effect of intranasal fentanyl on the emergence characteristics after sevoflurane anesthesia in children undergoing surgery for bilateral myringotomy tube placement.  Anesth Analg  2001; 92:1164.

Fischetti, 2003. Fischetti M: Cochlear implants. To hear again.  Sci Am  2003; 288:82.

Fumsaker, 1944. Funsaker DH: Anesthesia for microlaryngeal surgery: The case for subglottic jet ventilation.  Laryngoscope  1944; 104:1-30.

Furuhashi-Yanaha et al., 2000. Furuhashi-Yanaha A, Dohi S, Oshima T, et al: Acute pulmonary edema caused by impaired switching from nasal to oral breathing in the emergence from anesthesia.  Anesthesiology  2000; 92:1209.

Galinkin et al., 2000. Galinkin JL, Fazi LM, Cuy RM, et al: Use of intranasal fentanyl in children undergoing myringotomy and tube placement during halothane and sevoflurane anesthesia.  Anesthesiology  2000; 93:1378.

Galvis et al., 1980. Galvis AG, Stool SE, Bluestone CD: Pulmonary edema following relief of acute upper airway obstruction.  Ann Otol Rhinol Laryngol  1980; 89:124.

Garden et al., 2002. Garden JM, O'Banion MK, Bakus AD, et al: Viral disease transmitted by laser-generated plume (aerosol).  Arch Dermatol  2002; 138:1303.

Geffin et al., 1986. Geffin B, Shapshay SM, Bellack GS, et al: Flammability of endotracheal tubes during Nd-YAG laser application in the airway.  Anesthesiology  1986; 65:5-11.

Gerber and Holinger, 2003. Gerber ME, Holinger LD: Congenital laryngeal anomalies.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1460-1472.

Gluckman, 1990. Gluckman IL: Inflammatory diseases of the mouth and pharynx.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  2nd ed.. Philadelphia: WB Saunders; 1990.

Goforth et al., 1983. Goforth AJ, Cooke JE, Putney FJ: An anesthesia technique for laser surgery of the larynx.  Laryngoscope  1983; 93:822.

Goldsmith and Rosenfeld, 2003. Goldsmith AJ, Rosenfeld RM: Treatment of pediatric sinusitis.  Pediatr Clin North Am  2003; 50:2.

Gorelick and Baker, 1994. Gorelick MH, Baker MD: Epiglottitis in children, 1979 through 1992. Effects of Haemophilus influenzae type b immunization.  Arch Pediatr Adolesc Med  1994; 148:47.

Guida and Mattucci, 1990. Guida RA, Mattucci KF: Tonsillectomy and adenoidectomy: An inpatient or outpatient?.  Laryngoscope  1990; 100:491.

Gysin et al., 2000. Gysin C, Alothman GA, Papsin BC: Sinonasal disease in cystic fibrosis: Clinical characteristics, diagnosis, and management.  Pediatr Pulmonol  2000; 30:481.

Hartnick and Cotton, 2003. Hartnick CJ, Cotton RT: Stridor and airway obstruction.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1437-1447.

Hatcher and Stack, 1999. Hatcher IS, Stack CG: Postal survey of the anaesthetic techniques used for paediatric tonsillectomy surgery.  Paediatr Anaesth  1999; 9:311.

Haynes and Harley, 2002. Haynes DS, Harley DH: Surgical management of chronic otitis media: Beyond tympanotomy tubes.  Otolaryngol Clin North Am  2002; 35:827.

Healy, 1995a. Healy GB: The appropriateness of tympanostomy tubes for children.  JAMA  1995; 273:700.

Healy, 1995b. Healy GB: Surgery of the larynx and trachea.   In: Bluestone CD, Stool SE, ed. Atlas of pediatric otolaryngology,  Philadelphia: WB Saunders; 1995.

Hengerer and Wein, 2003. Hengerer AS, Wein RO: Congenital malformations of the nose and paranasal sinuses.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:979-994.

Herbert and Bent, 1998. Herbert RL, Bent JP: Meta-Analysis of outcomes of pediatric functional endoscopic sinus surgery.  Laryngoscope  1998; 108:796.

Hermens et al., 1983. Hermens JM, Bennett MJ, Hirshman CA: Anesthesia for laser surgery.  Anesth Analg (Paris)  1983; 62:218.

Hern et al., 1999. Hern JD, Jayaraj SM, Sidhu VS, et al: The laryngeal mask airway in tonsillectomy: The surgeon's perspective.  Clin Otolaryngol Allied Sci  1999; 24:122.

Hinkle, 1989. Hinkle AJ: What wisdom is there in administering elective general anesthesia to children with active upper respiratory tract infection?.  Anesth Analg  1989; 68:413.

Hoekelman, 1994. Hoekelman RA: Epiglottitis: Another dying disease?.  Pediatr Ann  1994; 23:229.

Hoeve and Rombout, 1992. Hoeve LJ, Rombout J: Pediatric laryngobronchoscopy: 1332 procedures stored in a database.  Int J Pediatr Otorhinolaryngol  1992; 24:73.

Holland and McGuirt, 2001. Holland BW, McGuirt Jr WF: Surgical management of choanal atresia: Improved outcome using mitomycin.  Arch Otolaryngol Head Neck Surg  2001; 127:1375.

Hulka, 2000. Hulka GF: Head and neck manifestations of cystic fibrosis and ciliary dyskinesia.  Otolaryngol Clin North Am  2000; 33:1333.

Hwang et al., 1983. Hwang J, St John WM, Bartlett D: Respiratory related hypoglossal nerve activity: Influence of anesthetics.  J Appl Physiol  1983; 55:785.

Isono et al., 1998. Isono S, Shimada A, Utsugi M, et al: Comparison of static mechanical properties of the passive pharynx between normal children and children with sleep-disordered breathing.  Am J Respir Critical Care Med  1998; 157:1204.

James, 2001. James I: Cuffed tubes in children.  Paediatr Anaesth  2001; 11:259.

Jellish et al., 1999. Jellish WS, Jensen RL, Anderson DE, et al: Intraoperative electromyographic assessment of recurrent laryngeal nerve stress and pharyngeal injury during anterior cervical spine surgery with Caspar instrumentation.  J Neurosurg  1999; 91:170.

Jellish et al., 1995. Jellish WS, Leonetti JP, Murdoch JR, et al: Propofol-based anesthesia as compared with standard anesthetic techniques for middle ear surgery.  J Clin Anesth  1995; 7:292.

Johans and Reichert, 1984. Johans TG, Reichert TI: An insufflation device for anesthesia during subglottic carbon dioxide laser microsurgery in children.  Anesth Analg  1984; 63:368.

John et al., 1991. John RE, Hill S, Hughes TJ: Airway protection by the laryngeal mask: A barrier to dye placed in the pharynx.  Anaesthesia  1991; 46:366.

Johnson et al., 1986. Johnson JT, Schuller DE, Silver F, et al: Antibiotic prophylaxis in high-risk head and neck surgery: One-day vs. five-day therapy.  Otolaryngol Head Neck Surg  1986; 95:554.

Karl et al., 1983. Karl HW, Swedlow DB, Lee KW, Downes JJ: Epinephrine interactions in children.  Anesthesiology  1983; 58:142.

Keon, 1988. Keon TP: Anesthetic considerations for laser surgery.  Int Anesthesiol Clin  1988; 26:50.

Khine et al., 1997. Khine HH, Corddry DH, Kettrick RG, et al: Comparison of cuffed and uncuffed endotracheal tubes in young children during general anesthesia.  Anesthesiology  1997; 86:627.

Koivunen et al., 1996. Koivunen P, Alho OP, Uhari M, et al: General anesthesia with and without nitrous oxide (N2O) and the weight of middle ear effusion in children undergoing adenoidectomy and tympanostomy.  Laryngoscope  1996; 106:724.

Kokosa and Eugene, 1989. Kokosa I, Eugene I: Chemical composition of laser-tissue interaction smoke plume.  J Laser Appl  1989; 2:59.

Kosloske, 1982. Kosloske AM: Bronchoscopic extraction of aspirated foreign bodies in children.  Am J Dis Child  1982; 136:924.

Kretz et al., 2000. Kretz FJ, Reimann B, Stelzner J, et al: The laryngeal mask in pediatric adenotonsillectomy. A meta-analysis of medical studies [in German].  Anaesthesist  2000; 49:706.

Krishna, 2001. Krishna P: Post-tonsillectomy bleeding: A meta-analysis.  Laryngoscope  2001; 111:1358.

Landsman, 1997. Landsman IS: Mechanisms and treatment of laryngospasm.  Int Anesthesiol Clin  1997; 35:67.

Health Devices, 1992. Laser-resistant tracheal tubes.  Health Devices  1992; 21:4.

Leicht et al., 1985. Leicht P, Wisborg T, Chraeinrner-Jorgensen B: Does intravenous lidocaine prevent laryngospasm after extubation in children?.  Anesth Analg  1985; 64:1193.

Liebowitz and Peacock, 1980. Liebowitz HM, Peacock GR: Cortical injury produced by carbon dioxide laser radiation.  Arch Ophthalmol  1980; 52:993.

Lines, 1973. Lines V: Anaesthesia for laryngoscopy and microlaryngeal surgery in children.  Anaesth Intensive Care  1973; 1:507.

Liu et al., 2001. Liu YH, Li MJ, Wang PC, et al: Use of dexamethasone on the prophylaxis of nausea and vomiting after tympanomastoid surgery.  Laryngoscope  2001; 111:1271.

Lusk, 2003. Lusk R: Surgical management of chronic rhinosinusitis.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1013-1020.

Maekawa et al., 1981. Maekawa S, Fukuda K, Yamauchi T, et al: Follow-up study of pharyngeal carriers of beta-hemolytic streptococci among school children in Sapporo City during a period of 2 years and 5 months.  J Clin Microbiol  1981; 13:1017.

Manning and Stool, 2003. Manning SC, Stool SE: Foreign bodies of the pharynx and esophagus.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1324-1337.

Mannucci, 1988. Mannucci PM: Desmopressin: A non-transfusional form of treatment for congenital and acquired bleeding disorders.  Blood  1988; 72:1449.

Marcus, 2001. Marcus CL: Sleep-disordered breathing in children.  Am J Respir Crit Care Med  2001; 164:16.

Marcus et al., 1998. Marcus CL, Greene MG, Carroll JL: Blood pressure in children with obstructive sleep apnea.  Am J Respir Crit Care Med  1998; 157:1098.

Marcus et al., 1999. Marcus CL, Lutz J, Hamer A, et al: Developmental changes in response to sub atmospheric pressure loading of the upper airway.  J Appl Physiol  1999; 87:626.

Marcus et al., 1994. Marcus CL, McColley SA, Carroll JL, et al: Upper airway collapsibility in children with obstructive sleep apnea syndrome.  J Appl Physiol  1994; 77:918.

Mattucci and Militana, 2003. Mattucci KF, Militana CJ: The prevention of fire during oropharyngeal electrosurgery.  Ear Nose Throat J  2003; 82:107-109.

Mauro et al., 1988. Mauro RD, Poole SR, Lockhart CH: Differentiation of epiglottitis from laryngotracheitis in the child with stridor.  Am J Dis Child  1988; 142:679.

Maze and Bloch, 1979. Maze A, Bloch E: Stridor in pediatric patients.  Anesthesiology  1979; 50:132.

McColley et al., 1992. McColley SA, April MM, Carroll JL, et al: Respiratory compromise after adenotonsillectomy in children with obstructive sleep apnea.  Arch Otolaryngol Head Neck Surg  1992; 118:940.

McCulloch et al., 1992. McCulloch TM, Richardson MA, Flint PW, et al: Lidocaine effects on the laryngeal chemoreflex, mechanoreflex, and afferent electrical stimulation reflex.  Ann Otol Rhinol Laryngol  1992; 101:583.

McDonald and Stocks, 1965. McDonald IH, Stocks JG: Prolonged nasotracheal intubation: A review of its development in a pediatric hospital.  Br J Anaesth  1965; 37:161.

McGahren, 1999. McGahren ED: Esophageal foreign bodies.  Pediatr Rev  1999; 20:129.

McGoldrick, 1993. McGoldrick KE: Tonsillectomy and adenoidectomy: Avoiding complications.  Day Surg Patient  1993; 2:1.

McGovern, 1961. McGovern PH: Bilateral choanal atresia in newborns: A new method of medical management.  Laryngoscope  1961; 71:480.

McGowan et al., 1992. McGowan FX, Kenna MA, Fleming JA, et al: Adenotonsillectomy of upper airway obstruction carries increased risk in children with a history of prematurity.  Pediatr Pulmonol  1992; 13:222.

Megerian et al., 2000. Megerian CA, Reily J, O'Connell FM, et al: Outpatient tympanomastoidectomy: Factors affecting hospital admission.  Arch Otolaryngol Head Neck Surg  2000; 126:1345.

Messner, 2003. Messner AH: Treating pediatric patients with obstructive sleep disorders: An update.  Otolaryngol Clin North Am  2003; 36:519.

Miman et al., 2000. Miman MC, Kirazli T, Ozyurek R: Doppler echocardiography in adenotonsillar hypertrophy.  Int J Pediatr Otorhinolaryngol  2000; 54:21.

Miyamoto and Kirk, 2003. Miyamoto RT, Kirk KI: Cochlear implants in children.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:808-816.

Miyasaka et al., 1980. Miyasaka K, Sloan IA, Froese AB: An evaluation of the jet injector (Sanders) technique for bronchoscopy in paediatric patients.  Can Anaesth Soc J  1980; 27:117.

Moore et al., 2003. Moore JK, Moore EW, Elliott RA, et al: Propofol and halothane versus sevoflurane in paediatric day-case surgery: Induction and recovery characteristics.  Br J Anaesth  2003; 90:461.

Motoyama, 1992. Motoyama EK: Anesthesia and the upper airway in infants and children.  Int Anesthesiol Clin  1992; 30:17.

Motoyama et al., 2001. Motoyama EK, Fine GF, Jacobson KH, et al: Accelerated increases in end-tidal CO2 (PETCO2) in anesthetized infants and children during rebreathing.  Anesthesiology  2001; 94:A1276.

Motoyama and Glazener, 1986. Motoyama EK, Glazener CI: Hypoxemia after general anesthesia in children.  Anesth Analg  1986; 65:267.

Myers et al., 1985. Myers EN, Stool SE, Johnson JT: Technique of tracheotomy.   In: Myers EN, Stool SE, Johnson JT, ed. Tracheotomy,  New York: Churchill Livingstone; 1985.

Nezhat et al., 1987. Nezhat C, Winen WK, Nezhat C, et al: Smoke from laser surgery: Is there a health hazard?.  Laser Surg Med  1987; 7:376.

Nikanne et al., 1997. Nikanne E, Kokki H, Tuovinen K: Perioperative ketoprofen in small children during adenoidectomy.  Br J Anaesth  1997; 78:24.

Noonan, 1965. Noonan JA: Reversible cor pulmonale due to hypertrophied tonsils and adenoids; studies in two cases.  Circulation  1965; 32:164.

Norton, 1983. Norton ML: Anesthesia for laser surgery in laryngobronchoesophagology.  Otolaryngol Clin North Am  1983; 16:785.

Norton and deVos, 1978. Norton ML, deVos P: New endotracheal tube for laser surgery of the larynx.  Ann Otol Rhinol Laryngol  1978; 87:554.

Norton et al., 1976. Norton MI, Strong MS, Baughan CW, et al: Endotracheal intubation and Venturi (jet) ventilation for laser microsurgery of the larynx.  Ann Otol Rhinol Laryngol  1976; 85:656.

Nowill and Ridall, 1969. Nowill WK, Ridall EG: Blood loss during adenotonsillectomy.  Surgery  1969; 66:856.

Ochiai et al., 1992. Ochiai R, Guthrie RD, Motoyama EK: Differential sensitivity to halothane anesthesia of the genioglossus, intercostals and diaphragm in kittens.  Anesth Analg  1992; 74:338.

Ochiai et al., 1989. Ochiai R, Guthrie RD, Motoyama EK: Effects of varying concentrations of halothane on the activity of the genioglossus, intercostals, and the diaphragm in cats: An electromyographic study.  Anesthesiology  1989; 70:812.

Oh and Motoyama, 1977. Oh TH, Motoyama EK: Comparison of nasotracheal intubation and tracheostomy in management of acute epiglottitis.  Anesthesiology  1977; 46:214.

Ossoff, 1989. Ossof RH: Laser safety in otolaryngology—head and neck surgery: Anesthetic and educational considerations for laryngeal surgery.  Laryngoscope  1989; 99:1.

Ossof et al., 1983. Ossof RH, Duncavage IA, Eisenman TS, et al: Comparison of tracheal damage from laser-ignited endotracheal tube fires.  Ann Otol Rhinol Laryngol  1983; 92:333.

Patel et al., 1988. Palel R, Norden J, Hannallah RS: Oxygen administration prevents hypoxemia during postanesthetic transport in children.  Anesthesiology  1988; 69:616-618.

Pappas et al., 2003. Pappas AL, Fluder EM, Creech S, et al: Postoperative analgesia in children undergoing myringotomy and placement equalization tubes in ambulatory surgery.  Anesth Analg  2003; 96:1621.

Pappas et al., 1998. Pappas AL, Sukhani R, Hotaling AJ, et al: The effect of preoperative dexamethasone on the immediate and delayed postoperative morbidity in children undergoing adenotonsillectomy.  Anesth Analg  1998; 87:57.

Paradise, 2003. Paradise JL: Tonsillectomy and adenoidectomy.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1210-1222.

Paradise et al., 1990. Paradise JL, Bluestone CD, Rogers KD, et al: Efficacy of adenoidectomy for recurrent otitis media in children previously treated with tympanostomy-tube placement results of parallel randomized and nonrandomized trials.  JAMA  1990; 263:2066.

Paradise et al., 2003. Paradise JL, Feldman HM, Campbell TF, et al: Early versus delayed insertion of tympanostomy tubes for persistent otitis media: Developmental outcomes at the age of three years in relation to prerandomization illness patterns and hearing levels.  Pediatr Infect Dis J  2003; 22:309.

Pashayan, 1994. Pashayan AG: Anesthesia for laser surgery. ASA Refresher Course, No. 221,  Park Ridge, IL, American Society of Anesthesiologists, 1994.

Pashayan and Gravenstein, 1985. Pashayan AG, Gravenstein JS: Helium retards endotracheal tube fires from carbon dioxide lasers.  Anesthesiology  1985; 62:274.

Pawar, 2000. Pawar DK: Dislodgement of bronchial foreign body during retrieval in children.  Paediatr Anaesth  2000; 10:333.

Pelton et al., 1977. Pelton SI, Shurin PA, Klein JO: Persistence of middle ear effusion after otitis media.  Pediatr Res  1977; 11:504.

Pirsig, 1986. Pirsig W: Surgery of choanal atresia in infants and children: Historical notes and updated review.  Int J Pediatr Otorhinolaryngol  1986; 11:153.

Postma et al., 1987. Postma DS, Prazma J, Woods CI, et al: Use of steroids and a long-acting vasoconstrictor in the treatment of postintubation croup. A ferret model.  Arch Otolaryngol Head Neck Surg  1987; 113:844.

Prasad et al., 2002. Prasad M, Ward RF, April MM, et al: Topical mitomycin as an adjunct to choanal atresia repair.  Arch Otolaryngol Head Neck Surg  2002; 128:398.

Prinsley et al., 1993. Prinsley P, Wood M, Lee CA: Adenotonsillectomy in patients with inherited bleeding disorders.  Clin Otolaryngol  1993; 18:206.

Rah et al., 1979. Rah KH, Salzberg AM, Boyan CP, et al: Respiratory acidosis with the small Storz-Hopkins bronchoscopes: Occurrence and management.  Ann Thorac Surg  1979; 27:197.

Rampil, 1992. Rampil IJ: Anesthetic considerations for laser surgery.  Anesth Analg  1992; 74:424.

Randall and Hoffer, 1998. Randall DA, Hoffer ME: Complications of tonsillectomy and adenoidectomy.  Otolarygol Head Neck Surg  1998; 118:61.

Ravussin et al., 1987. Ravussin P, Bayer-Berger M, Monnier P, et al: Percutaneous transtracheal ventilation for laser endoscopic procedures in infants and small children with laryngeal obstruction: Report of two cases.  Can J Anaesth  1987; 34:83.

Reber et al., 2001. Reber A, Pagonini R, Frei FJ: Effect of common airway manoeuvres on upper airway dimensions and clinical signs in anaesthetized, spontaneously breathing children.  Br J Anaesth  2001; 86:217.

Ring et al., 1975. Ring WH, Adair JC, Elwyn RA: The new pediatric endotracheal tube.  Anesth Analg  1975; 54:237.

Rontal et al., 1980. Rontal M, Rontal E, Wenokur M: Jet insufflation anesthesia for endolaryngeal surgery.  Laryngoscope  1980; 90:1162.

Rothschild et al., 1995. Rothschild MA, Cotcamp D, Cotton RT: Postoperative medical management in single-stage laryngotracheoplasty.  Arch Otolaryngol Head Neck Surg  1995; 121:1175.

Ruder et al., 1981. Ruder CB, Raphael NL, Abramson AL, et al: Anesthesia for carbon dioxide laser microsurgery of the larynx.  Otolaryngol Head Neck Surg  1981; 89:732.

Rutter et al., 2003. Rutter MJ, Yellon RF, Cotton RT: Management and prevention of subglottic stenosis in infants and children.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1519-1542.

Sanders, 1967. Sanders RD: Two ventilating attachments for bronchoscopes.  Del Med J  1967; 39:170.

Sasaki, 1979. Sasaki CT: Development of laryngeal function: Etiologic significance in the sudden infant death syndrome.  Laryngoscope  1979; 89:1964.

Scamman and McCabe, 1986. Scamman FL, McCabe BF: Supraglottic jet ventilation for laser surgery of the larynx in children.  Ann Otol Rhinol Laryngol  1986; 95:142.

Scanlon et al., 1993. Scanlon P, Carey M, Power M, et al: Patient response to laryngeal mask insertion after induction of anaesthesia with propofol or thiopentone.  Can J Anaesth  1993; 40:816.

Schechter, 2002. Schechter MS: Section on pediatric pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. Technical report: Diagnosis and management of childhood obstructive sleep apnea syndrome.  Pediatrics  2002; 109:69.

Schloss et al., 1979. Schloss MD, Hannallah R, Baxter JD: Acute epiglottitis: 26 years' experience at the Montreal Children's Hospital.  J Otolaryngology  1979; 8:259.

Schloss et al., 1983. Schloss MD, Pham-Dang H, Rosales JK: Foreign bodies in the tracheobronchial tree—a retrospective study of 217 cases.  J Otolaryngol  1983; 12:212.

Schwartz and Downes, 1977. Schwartz AJ, Downes JJ: Hazards of a simple monitoring device, the esophageal stethoscope.  Anesthesiology  1977; 47:64.

Seliman et al., 1986. Seliman OL, Patel RI, Hannallah RS: Change in arterial oxygen saturation in the pediatric patient during postoperative transport.  Anesthesiology  1986; 65:447.

Shprintzen, 1988. Shprintzen RJ: Pierre Robin, micrognathia, and airway obstruction: The dependency of treatment on accurate diagnosis.  Int Anesthesiol Clin  1988; 26:64.

Simpson et al., 1990. Simpson JI, Schiff GA, Wolf GL: The effect of helium on endotracheal to be flammability.  Anesthesiology  1990; 73:538.

Smith et al., 1975. Smith RB, Schaer WB, Pfaeffle H: Percutaneous transtracheal ventilation for anesthesia and resuscitation: a review and report of complications.  Can Anesth Soc J  1975; 22:607-612.

Smith, 1972. Smith RM: Anesthesia for pediatric otolaryngology.   In: Ferguson CE, Kendig Jr EL, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 1972.

Smith, 1980. Smith RM: Anesthesia for infants and children,  4th ed.. St Louis, CV Mosby, 1980.

Snow et al., 1974. Snow JC, Kripke BJ, Strong MS, et al: Anesthesia for carbon dioxide laser microsurgery on the larynx and trachea.  Anesth Analg (C/eve)  1974; 53:507.

Snow et al., 1976. Snow JC, Norton ML, Suluja IS, et al: Fire hazard during CO2, laser microsurgery on the larynx and trachea.  Anesth Analg  1976; 55:146T.

Soprano et al., 1999. Soprano JV, Fleisher GR, Mandl KD: The spontaneous passage of esophageal coins in children.  Arch Pediatr Adolesc Med  1999; 153:1073.

Sosis, 1989a. Sosis MB: Evaluation of five metallic tapes for protection of endotracheal tubes during CO laser surgery.  Anesth Analg  1989; 68:392.

Sosis, 1989b. Sosis MB: What is the safest endotracheal tube for Nd-YAG laser surgery? A comparative study.  Anesth Analg  1989; 69:802.

Sosis and Dillon, 1990. Sosis M, Dillon F: What is the safest foil tape for endotracheal tube protection during Nd-YAG laser surgery? A comparative study.  Anesthesiology  1990; 72:553.

Spoerel et al., 1971. Spoerel WE, Narayanan PS, Singh NP: Transtracheal ventilation.  Br J Anaesth  1971; 43:932.

Sterni and Tunkel, 2003. Sterni LM, Tunkel DE: Obstructive sleep apnea in children: An update.  Pediatr Clin North Am  2003; 50:427.

Steward et al., 2003. Steward DL, Welge JA, Myer CM: Steroid for improving recovery following tonsillectomy in children.  Cochrane Database Syst Rev  2003; 1:CD003997

Stool and Eavey, 1990. Stool SE, Eavey R: Tracheostomy.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  2nd ed.. Philadelphia: WB Saunders; 1990.

Stool and Eavey, 2003. Stool SE, Eavey RD: Tracheotomy.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1226-1243.

Strong et al., 1973. Strong MS, Jako EJ, Polyani T, et al: Laser surgery in the aerodigestive tract.  Am J Surg  1973; 126:529.

Suzuki and Sasaki, 1977. Suzuki M, Sasaki CT: Laryngeal spasm: A neurophysiologic redefinition.  Ann Otol Rhinol Laryngol  1977; 86:150.

Szekely et al., 1978. Szekely E, Farkas E, Matyas G, et al: Comparative studies of the IgA content of bronchial secretion, nasal secretion and serum in children with chronic respiratory tract diseases.  Kinderarztl Prax  1978; 46:67.

Tagaito et al., 1998. Tagaito Y, Isono S, Nishino T: Upper airway reflexes during a combination of propofol and fentanyl anesthesia.  Anesthesiology  1998; 88:1459.

Tait and Knight, 1987. Tait AR, Knight PR: The effects of general anesthesia on upper respiratory tract infections in children.  Anesthesiology  1987; 67:930.

Teele, 1983. Teele DW: Inflammatory diseases of the mouth and pharynx.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 1983.

Teele et al., 1980. Teele DW, Healy GB, Tally FP: Persistent effusions of the middle ear: Cultures for anaerobic bacteria.  Ann Otol Rhinol Laryngol  1980; 89:102.

Telfick and Kaloustian, 1997. Telfik TL, Kaloustian VM: Congenital anomalies of the ear, nose and throat,  New York: Oxford Press; 1997:218-219.

Travis et al., 1977. Travis KW, Todres ID, Shannon DC: Pulmonary edema associated with croup and epiglottitis.  Pediatrics  1977; 59:695.

Tunnessen and Feinstein, 1980. Tunnessen Jr WW, Feinstein AR: The steroid-croup controversy: An analytic review of methodologic problems.  J Pediatr  1980; 96:751.

Tusman et al., 2003. Tusman G, Bohn SH, Tempra A, et al: Effect of recruitment maneuver on atelectasis in anesthetized children.  Anesthesiology  2003; 98:14.

Ueda et al., 1983. Ueda W, Hirakawa M, Mae O: Appraisal of epinephrine administration to patients under halothane anesthesia for closure of cleft palate.  Anesthesiology  1983; 58:574.

Uezono et al., 2000. Uezono S, Goto T, Terui K, et al: Emergence agitation after sevoflurane versus propofol in pediatric patients.  Anesth Analg  2000; 91:563.

Van Der Spek et al., 1988. Van Der Spek AF, Spargo PM, Norton ML: The physics of lasers and implications for their use during airway surgery.  Br J Anaesth  1988; 60:709.

Ved et al., 1996. Ved SA, Walden TL, Montana J, et al: Vomiting and recovery after outpatient tonsillectomy and adenoidectomy in children. Comparison of four anesthetic techniques using nitrous oxide with halothane or propofol.  Anesthesiology  1996; 85:4.

Verghese and Hannallah, 2001. Verghese ST, Hannallah RS: Pediatric otolaryngologic emergencies.  Anesthesiol Clin North Am  2001; 19:237.

Voepel-Lewis et al., 2003. Voepel-Lewis T, Malviya S, Tait AR: A prospective cohort study of emergence agitation in the pediatric postanesthesia care unit.  Anesth Analg  2003; 96:1625.

Walander, 1955. Walander A: The mechanism of origin of congenital malformation of the larynx.  Acta Otolaryngol  1955; 45:426.

Walner et al., 2001. Walner DL, Loewen MS, Kimura RE: Neonatal subglottic stenosis–incidence and trends.  Laryngoscope  2001; 111:48.

Ward, 1992. Ward RF: Treatment of tracheal and endobronchial lesions with the potassium titanyl phosphate laser.  Ann Otol Rhinol Laryngol  1992; 10:205.

Warner, 1996. Warner DO: Airway pharmacology.   In: Benumof JL, ed. Airway management,  Boston: Mosby; 1996:74.

Watcha et al., 1992. Watcha MF, Ramirez-Ruiz M, White PF, et al: Perioperative effects of oral ketorolac and acetaminophen in children undergoing bilateral myringotomy.  Can J Anaesth  1992; 39:649.

Werkhaven, 1995. Werkhaven JA: Laryngotracheal laser surgery.   In: Bluestone CD, Stool SE, ed. Atlas of pediatric otolaryngology,  Philadelphia: WB Saunders; 1995.

Wetmore, 2003. Wetmore RF: Tracheotomy.   In: Bluestone CD, Stool SE, ed. Pediatric otolaryngology,  Philadelphia: WB Saunders; 2003:1583-1598.

Wetmore et al., 1999. Wetmore RF, Marsh RR, Thompson ME, et al: Pediatric tracheostomy: A changing procedure?.  Ann Otol Rhinol Laryngol  1999; 108:695.

Widlund et al., 1983. Widlund B, Vlaczak S, Motoyama E: Flow pressure characteristics of pediatric Storz-Hopkins bronchoscope.  Anesthesiology  1983; 54:341.

Widlund et al., 1982. Widlund B, Walczak S, Motoyama E: Flow-pressure characteristics of pediatric Storz-Hopkins bronchoscopes.  Anesthesiology  1982; 57:A417.

Williams and Bailey, 1993. Williams PJ, Bailey PM: Comparison of the reinforced laryngeal mask airway and tracheal intubation for adenotonsillectomy.  Br J Anaesth  1993; 70:30.

Wilson and Robertson, 2002. Wilson JW, Robertson CF: Angiogenesis in paediatric airway disease.  Paediatr Respir Rev  2002; 3:219.

Wolf and Simpson, 1987. Wolf GL, Simpson II: Flammability of endotracheal tubes in oxygen and nitrous oxide-enriched atmosphere.  Anesthesiology  1987; 67:236.

Wood and Postma, 1988. Wood RE, Postma D: Endoscopy of the airway in infants and children.  J Pediatr  1988; 112:1.

Woods, 1990. Woods AM: Pediatric endoscopy.   In: Berry FA, ed. Anesthetic management of difficult and routine pediatric patients,  2nd ed.. New York: Churchill Livingstone; 1990:199-242.

Yellon et al., 2002. Yellon RF, McBride TP, Davis HW: Otolaryngology.   In: Zitelli BJ, Davis HW, ed. Atlas of pediatric physical diagnosis,  4th ed.. St Louis: Mosby; 2002:818-865.

Yellon et al., 1997. Yellon RF, Parameswaran M, Brandom BW: Decreasing morbidity following laryngotracheal reconstruction in children.  In Anesthesiol Clin  1997; 35:145.