9 A NÁLISIS EXTENSIVO DE HERRAMIENTAS
9.3 Gestión de proyectos
■ Bony.Injuries
Great advances have been made in recent decades in treating pediatric facial fractures. Specific techniques used for reconstruction in children must accommodate a child’s developing anatomy, rapid healing, psy-chological development, and potential for deformity as a consequence of altered facial growth. The prevalence of CT scans makes accurately diagnosing facial fractures possible in most instances. Rigid internal fixation has been successfully adapted from adults to pediatric patients with careful modification. Open reduction and rigid internal fixation is indicated for severely displaced fractures. Primary bone grafting is preferred over secondary reconstruction. Alloplastic materials should be avoided when possible.
Associated injuries are a common feature of childhood maxil-lofacial trauma. Neurologic and orthopedic injuries are seen in 30%
of children with facial fractures, which reinforces the importance of a complete initial assessment of a child with facial trauma and high-lights the dilemma with regard to the timing of the reconstruction because of the rapid healing of bony injuries in children.
NOSE
Nasal fractures are by far the most common facial bone injuries in children, followed by dentoalveolar injuries. Nose fractures usually are treated in the outpatient setting and do not require surgical inter-vention. Whether treatment is necessary is not dictated by the presence of fracture but by the presence of functional or cosmetic deficits.
The initial examination of a child with nasal fracture may be very limited due to midfacial swelling. Several days are required for the swelling to subside before the true extent of the deformity can be appre-ciated. On the other hand, immediate intranasal examination is impor-tant to detect the presence of septal hematoma (Figure 8-1). Although
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rarely seen, septal hematoma can be observed on anterior rhinoscopy as an obvious purple bulge on one side of the nose. The bulge is com-pressible with a cotton tip applicator and does not shrink with topical vasoconstriction. A septal hematoma requires immediate evacuation on detection. An untreated hematoma can become a thick, fibrotic, and obstructive septum. If the hematoma becomes infected, the result-ing loss of cartilage can cause a saddle nose deformity.
In cases of nasal fracture without septal hematoma, the patient should return 3 to 4 days after injury, when a more accurate examina-tion is possible. If a cosmetic deformity or a fixed nasal obstrucexamina-tion is detected, definitive surgical treatment is undertaken. Closed reduction of the bony fracture can be performed with intranasal instrumentation and bimanual external manipulation. If significant dislocations are present or if the injury is more than 2 weeks old, open reduction may be necessary.
MANDIBLE
Fractures of the mandible are the most common facial fractures requir-ing hospitalization. They account for 30% to 50% of all pediatric facial fractures when nasal fractures are excluded. Because pediatric condyles are highly vascularized and thin necks are poorly resistant to impact forces, the most vulnerable part of the pediatric mandible is the con-dyle. More than 50% of pediatric mandibular fractures involve one of the condyles, whereas only 30% of adult cases show condylar involve-ment. As patients mature, the frequency of symphyseal, body, and ramus fractures increases.
Clinical signs of mandibular fractures may include displace-ment of the fragdisplace-ments, mobility, swelling, mucosal tears, limited mouth opening, malocclusion, and pain. Clinical suspicion of a
Figure.8-1. A, Nasal septal hematoma visible inside the left nostril. B, Nasal septum after drainage of the hematoma in the same patient.
A B
Chapter 8: Pediatric Nasal and Facial Fractures
fracture is confirmed by panorex, a complete mandible series, or CT scans. Computed tomography is especially helpful to help determine 3- dimensional displacement of the condyles.
Immobilization is difficult in patients younger than 2 years because of incomplete eruption of the deciduous teeth, although later growth and remodeling frequently compensate for less than ideal post-injury alignment. The primary teeth, which develop firm roots between 2 and 5 years of age, can be used for splints and arch bars. Deciduous roots are resorbed between 6 and 12 years of age; hence arch bars may need extra support from circummandibular wiring and pyriform aperture suspen-sion. Permanent teeth are safe anchors for fixation after 13 years of age.
The central question when treating pediatric condylar fracture is whether the patient needs immobilization. Although minimally inva-sive endoscopic open reduction with internal fixation (ORIF) is gain-ing popularity for treatgain-ing adult condylar fractures, most authors still advocate conservative measures in pediatric patients. If the patient has normal occlusion and normal mandibular movement, only a soft diet and movement exercises are necessary. However, if open bite deformi-ties with retrusion of the mandible and movement limitation are pres-ent, a brief period of immobilization lasting 2 to 3 weeks followed by the use of guiding elastics can yield normal function in the end.
Displaced symphysis fractures can be treated by ORIF through an intraoral incision after age 6 years, after the permanent incisors have erupted. Open reduction with internal fixation in parasymphysial fractures is possible once buds of the canines have moved up from the mandibular border after age 9 years. In body fractures, the inferior mandibular border can be plated when buds of the permanent premo-lar and mopremo-lar have migrated superiorly toward the alveolus.
Frequent postoperative follow-up visits are necessary to detect and treat early complications such as infection, malocclusion, malunion, and nonunion. Late complications such as damage to permanent teeth, temporomandibular joint dysfunction, or midface deformity with facial asymmetry also need attention and possible treatment.
ORBIT
Fractures of the orbital walls are not infrequent secondary to the very thin bones that are present, accounting for 20% to 25% of pediatric facial fractures. Medial orbital wall and orbital floor fractures are more common for the same reason. The mechanism of injury is often direct trauma to the eye or surrounding structure. Such pressure causes the
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orbital contents to explode beyond the normal boundary, thus fractur-ing the bones.
In assessing orbital injuries, it is important to document visual acuity, ocular pressure, and extraocular movements. Diplopia is a sensi-tive measure of extraocular movement deficit in a cooperasensi-tive patient.
All visual fields need to be inspected before diagnosing diplopia.
The treatment of isolated blowout fractures is symptom dependent.
In an asymptomatic patient, no intervention is necessary because frac-tures will heal spontaneously. If persistent enophthalmos, extraocular muscle restriction, or pain on movement of the eye is present, surgical exploration is indicated. Large fractures also are routinely explored, as are fractures that on CT have obvious muscle entrapment. Absorbable gelatin film usually is sufficient for reconstructing small defects of the floor, although large disruptions are best repaired with calvarial bone grafts.
Orbital roof fractures occur in very young children whose fron-tal sinuses are still underdeveloped. These are often associated with skull injuries.
Pediatric orbital roof fractures are different than those of adults.
They occur more frequently because of the lack of frontal sinus pneu-matization. Children have a craniofacial ratio of 8:1 at birth, compared with 2:1 in adults, thus exposing more of their cranium and skull base to potential injuries. Most orbital roof fractures, particularly those that are non-displaced or with fragments displaced superiorly (blow-out fractures), can be safely observed in the acute setting. Treatment should be directed by the presence of symptoms, such as extraocular muscle entrapment, enophthalmos, exophthalmos, diplopia, vision changes, or dystopia. Large blow-in fractures have a higher chance for late onset complications; therefore, surgical thresholds should be lower.
Depending on the extent and location of the orbital roof fracture, vari-ous approaches are available. Cooperation among neurosurgery, oph-thalmology, and head and neck surgery are essential to ensure optimal care for these patients.
MIDFACE
Midfacial fractures are rare in children and usually result from high-impact, high-velocity forces such as motor vehicle crashes (MVCs).
Zygomaticomalar complex (ZMC) fractures are seen in 10% to 15%, and Le Fort maxillary fractures are seen in 5% to 10%. Free-floating nasal base is a rare injury and indicates a nasoethmoidal fracture.
Chapter 8: Pediatric Nasal and Facial Fractures
Zygomaticomalar complex fractures parallel the pneumatization of the maxillary sinus and are uncommon before the age of 5 years.
Surgical correction of ZMC fractures is indicated when bony displace-ment is present. Adequate exposure is essential, and such correction is achieved by a process called triangulation. Three key sites need to be directly visualized: the frontozygomatic suture, infraorbital rim, and anterior zygomaticomaxillary buttress. Access can be achieved via the lateral upper eyelid incision, lower eyelid infraciliary or transcon-junctival incision, and transoral buccal sulcus incision. Unlike adults, one-point fixation at the frontozygomatic suture may suffice in children because of shorter lever arm forces from the frontozygomatic suture to the infraorbital rim.
In nasoethmoidal fractures, medial canthal ligament integrity must be assessed. This is done by inserting a hemostat into the nose toward the medial orbital rim. The child should be anesthetized for this examination. Mobility of the underlying fragments suggests that the bone with its canthal attachment has been displaced and that recon-struction of the nasal maxillary buttress and possibly transnasal wiring is necessary. Measurement of soft-tissue intercanthal distance is difficult because ethnic, racial, and gender variations can significantly affect its values. Nevertheless, the average intercanthal distance at 4 years of age is approximately 25 mm; by age 12 years, 28 mm; and by adulthood, 30 mm. One can easily see that near-adult intercanthal distance is achieved at a very early age; hence, an easy mistake is to set the inter-canthal distance too wide. Interinter-canthal distances 5 mm more than the average values tend to be indicative of, and 10 mm confirms the diag-nosis of, displaced fractures of the nasoethmoidal complex. Attempts should be made to narrow excessive distance between the eyes and project the nose of a child.
■
■ Conclusion
Children of all ages can be afflicted by ENT trauma, often resulting in functional and cosmetic deficits. A thorough understanding of pedi-atric skull and facial growth enables practitioners to focus the search for subtle fractures in the most age-appropriate locations. Soft tissue injuries often can point out possible locations of fracture and should be carefully treated. Anticipation of mandibular growth facilitates repair because most injuries can be treated with intermaxillary fixation.
Unerupted dentition requires careful selection of fixation methods and cautious screw placement if rigid fixation is ultimately required. Modern
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rigid plating systems have greatly enhanced surgeons’ ability to recon-struct facial fractures in a 3-dimensional fashion. Depending on the site of injury, a multidisciplinary team approach can ensure that injuries to organs systems around the face are cared for in an optimal manner.
■
■ Selected.References
Caldicott WJ, North JB, Simpson DA. Traumatic cerebrospinal fluid fistulas in children.
J Neurosurg. 1973;38(1):1–9
Gussack GS, Luterman A, Powell RW, Rodgers K, Ramenofsky M. Pediatric maxillo- facial trauma: unique features in diagnosis and treatment. Laryngoscope. 1987;97 (8 Pt 1):925–930
Hardt N, Gottsauner A. The treatment of mandibular fractures in children.
J Craniomaxillofac Surg. 1993;21(5):214–219
Hogg NJ, Horswell BB. Soft tissue pediatric facial trauma: a review. J Can Dent Assoc.
2006;72(6):549–552
Holland AJ, Broome C, Steinberg A, Cass DT. Facial fractures in children. Pediatr Emerg Care. 2001;17(3):157–160
Kaban LB. Diagnosis and treatment of fractures of the facial bones in children 1943–
1993. J Oral Maxillofac Surg. 1993;51(7):722–729
Kaban LB, Mulliken JB, Murray JE. Facial fractures in children: an analysis of 122 frac-tures in 109 patients. Plast Reconstr Surg. 1977;59(1):15–20
Koltai PJ. Maxillofacial injuries in children. In: Smith JD, Bumstead RM, eds. Pediatric Facial Plastic and Reconstructive Surgery. New York, NY: Raven Press; 1993
Koltai PJ. Pediatric facial fractures. In: Bailey Head and Neck Surgery-Otolaryngology.
Philadelphia, PA: Lippincott; 2001
Koltai PJ, Rabkin D. Management of facial trauma in children. Pediatr Clin North Am.
1996;43(6):1253–1275
Koltai PJ, Rabkin D, Hoehn J. Rigid fixation of facial fractures in children.
J Craniomaxillofac Trauma. 1995;1(2):32–42
Law RC, Fouque CA, Waddell A, Cusick E. Lesson of the week. Penetrating intra-oral trauma in children. BMJ. 1997;314:50–51
Lee D, Honrado C, Har-El G, Goldsmith A. Pediatric temporal bone fractures.
Laryngoscope. 1998;108(6):816–821
Liu-Shindo M, Hawkins DB. Basilar skull fractures in children. Int J Pediatr Otorhinolaryngol. 1989;17(2):109–117
Marom T, Russo E, Ben-Yehuda Y, Roth Y. Oropharyngeal injuries in children. Pediatr Emerg Care. 2007;23(12):914–918
McGraw BL, Cole RR. Pediatric maxillofacial trauma. Age-related variations in injury.
Arch Otolaryngol Head Neck Surg. 1990;116(1):41–45
McGuirt WF Jr, Stool SE. Cerebrospinal fluid fistula: the identification and management in pediatric temporal bone fractures. Laryngoscope. 1995;105(4 Pt 1):359–364
Chapter 8: Pediatric Nasal and Facial Fractures
McGuirt WF Jr, Stool SE. Temporal bone fractures in children: a review with emphasis on long-term sequelae. Clin Pediatr (Phila). 1992;31(1):12–18
Mitchell DP, Stone P. Temporal bone fractures in children. Can J Otolaryngol.
1973;2:156–162
Nicol JW, Johnstone AJ. Temporal bone fractures in children: a review of 34 cases. J Accid Emerg Med. 1994;11(4):218–222
Pierrot S, Bernardeschi D, Morrisseau-Durand MP, Manach Y, Couloigner V. Dissection of the internal carotid artery following trauma of the soft palate in children. Ann Otol Rhinol Laryngol. 2006;115(5):323–329
Posnick JC, Wells M, Pron GE. Pediatric facial fractures: evolving patterns of treatment.
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Rowe IM, Fonkalsrud EW, O’Neil JA, et al. The injured child. In: Essentials of Pediatric Surgery. St. Louis, MO: Mosby; 1995
Rowe NL. Fractures of the facial skeleton in children. J Oral Surg. 1968;26(8):505–515 Shapiro RS. Temporal bone fractures in children. Otolaryngol Head Neck Surg.
1979;87(3):323–329
Stefanopoulos PK, Tarantzopoulou AD. Facial bite wounds: management update. Int J Oral Maxillofac Surg. 2005;34(5):464–472
Thorén H, Iizuka T, Hallikainen D, Lindgvist C. Different patterns of mandibular frac-tures in children. An analysis of 220 fracfrac-tures in 157 patients. J Craniomaxillofac Surg.
1992;20(7):292–296
Troulis MJ, Kaban LB. Endoscopic approach to the ramus/condyle unit: clinical applica-tions. J Oral Maxillofac Surg. 2001;59(5):503–509
von Domarus H, Poeschel W. Impalement injuries of the palate. Plast Reconstr Surg.
1983;72(5):656–658
Williams WT, Ghorayeb BY, Yeakley JW. Pediatric temporal bone fractures. Laryngoscope.
1992;102(6):600–603
SECTION.3
Oropharynx
Introduction
Functions of Tonsils and Adenoid
Infectious and Inflammatory Diseases of Tonsils and Adenoid
Hyperplasia of Tonsils and Adenoid
Upper Airway Obstruc-tion and Sleep-Related Breathing Disorders Tonsil and Adenoid Surgery
for Airway Obstruction Malignancy of Tonsils or
Adenoid
Other Tonsil and Adenoid Disorders
David H. Darrow, MD, DDS
Chapter 9: Disorders of the Tonsils and Adenoid
■
■ Introduction
Adenotonsillar disorders in children occur as a result of hyperpla-sia, infection, inflammation, or malignancy. Hyperplasia is a natural consequence of immune activity within these tissues but may become problematic when tissue size becomes excessive for the pharyngeal space they occupy. Infection of the tonsils and adenoid is common in this age group because of their participation in immune processes and continuous exposure to inhaled and ingested antigens. Malignancy of the tonsils and adenoid, in contrast, is exceedingly rare. This chapter will review the functions of the tonsils and adenoid, diagnosis and management of diseases of these tissues, and appropriate indications for their surgical removal.
■
■ Functions.of.Tonsils.and.Adenoid
The palatine tonsils and adenoid are tissues of Waldeyer ring, a group of lymphoepithelial tissues that also includes tubal tonsils in the naso-pharynx and the lingual tonsil. Collectively, these tissues participate in the mucosal immune system of the pharynx. Positioned strategically at the entrance of the gastrointestinal and respiratory tracts, the tonsils and adenoid serve as secondary lymphoid organs, initiating immune responses against antigens entering the body through the mouth or nose. The size of the tonsils appears to correlate with their level of immunologic activity, peaking between the ages of 3 and 10 years, and demonstrating age-dependent involution. There is also some evi-dence that their size increases with bacterial load.
Tonsils are covered by a non-keratinizing stratified squamous epi-thelium featuring some 10 to 30 deep crypts that effectively increase the surface area exposed to incoming antigens. The crypts occasionally harbor degenerated cells and debris that give rise to so-called tonsil-loliths, in which the presence of biofilms has also been implicated.
Although tonsils lack afferent lymphatics, the epithelium contains a system of specialized channels lined by M cells that take up antigens into vesicles and transport them to the intraepithelial and subepithe-lial spaces where they are presented to lymphoid cells. The transport function of M cells serves as a portal for mucosal infections and immu-nizations; M cells also can initiate immunologic responses within the epithelium, introducing foreign antigens to lymphocytes and antigen-presenting cells (APCs).
After passing through the crypt epithelium, inhaled or ingested antigens reach the extrafollicular region or lymphoid follicles. In the
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extrafollicular region, APCs process antigens and present them to helper T lymphocytes that stimulate proliferation of follicular B lymphocytes.
B lymphocytes ultimately develop into 1 of 2 types of cell—antibody-expressing B memory cells capable of migration to the nasopharynx and other sites, or plasma cells that produce antibodies and release them into crypt lumen. Tonsillar plasma cells can produce all 5 immu-noglobulin classes helping to combat and prevent infection. In addition, contact of memory B cells in the lymphoid follicles with antigen is an essential part of the generation of a secondary immune response.
Among immunoglobulin isotypes, IgA may be considered the most important product of the adenotonsillar immune system. In its dimeric form, IgA can attach to the transmembrane secretory component (SC) to form secretory IgA (SIgA), a critical component of the mucosal immune system of the upper airway. This component is necessary for binding of IgA monomers to each other and to the SC and is an impor-tant product of B-cell activity in tonsil follicles. While tonsils produce immunocytes bearing the J (joining) chain carbohydrate, SC is pro-duced only in the adenoid and extratonsillar epithelium, and therefore only the adenoid possesses a local secretory immune system.
■
■ .Infectious.and.Inflammatory.Diseases.of.
.Tonsils and.Adenoid
Pharyngotonsillitis is a general term used to describe diffuse inflam-mation of structures of the oropharynx, including the tonsils. The disorder presents with symptoms of sore throat; however, objec-tive signs of inflammation must be present to make the diagnosis.
Pharyngotonsillitis may be classified based on duration of symptoms as acute, subacute, or chronic, with most patients presenting acutely.
Alternatively, inflammatory disease of the nasopharynx may be Pearls
1. Tonsil size peaks between 3 and 10 years of age.
2. The tonsils and adenoid are a secondary source of circulating B lymphocytes.
3. Only the adenoid and extratonsillar lymphoid tissues, not the tonsils, possess a local secretory immune system.
Chapter 9: Disorders of the Tonsils and Adenoid
considered nasopharyngitis, in which common symptoms include rhinor-rhea, nasal congestion, sneezing, and cough. Inflammation limited to the adenoid pad (adenoiditis) is difficult to diagnose in the primary care setting because of inaccessibility of this tissue to direct visualization.
COMMON VIRAL INFECTION
Nasopharyngitis typically occurs in cold weather months among young children during their early exposures to respiratory viruses.
Adenoviruses, influenza viruses, parainfluenza viruses, and entero-viruses are the most common etiologic agents. Rhinovirus and respi-ratory syncytial virus occur almost exclusively in preschool children and are rarely associated with overt signs of pharyngeal inflamma-tion. Adenoviruses are more common among older children and adolescents. Nasopharyngitis of viral etiology may also cause a con-comitant pharyngotonsillitis. The infection is most commonly acute
Adenoviruses, influenza viruses, parainfluenza viruses, and entero-viruses are the most common etiologic agents. Rhinovirus and respi-ratory syncytial virus occur almost exclusively in preschool children and are rarely associated with overt signs of pharyngeal inflamma-tion. Adenoviruses are more common among older children and adolescents. Nasopharyngitis of viral etiology may also cause a con-comitant pharyngotonsillitis. The infection is most commonly acute