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Pediatric Surgical Procedures – An Updated Guide – Volume I
Tailoring personalized analgesic strategies, considering the age and individual char-
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acteristics of each patient, reinforces the integral role of pediatric anesthesiologists in postoperative care. Interdisciplinary collaboration and specific expertise in pediatrics anesthesiology are essential to address the unique challenges of laparoscopic surgery in children. The presence of pediatric anesthesiologists not only ensures safety and stability during the procedure but also contributes significantly to a more comfort­able and satisfactory recovery for the pediatrics patient undergoing laparoscopic procedures.
Importance of Anesthesia in Pediatric Laparoscopic Procedures DOI: http://dx.doi.org/10.5772/intechopen.115024
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References
[1] Pelizzo G, Carlini V, Iacob G,
Pasqua N, Maggio G, Brunero M, et al. Pediatric laparoscopy and adaptive oxygenation and hemodynamic changes. Pediatric Reports. 2017;(2):7214
[2] Jiang R, Sun Y, Wang H, Liang M,
Xie X. Effect of different carbon dioxide (CO2) insufflation for laparoscopic colorectal surgery in elderly patients. Medicine. 2019;(41):e17520
[3] Kim SJ, Barlog JS, Akhavan A.
Robotic-assisted urologic surgery in infants: Positioning, trocar placement, and physiological considerations. Frontiers in Pediatrics. 2019;:411
[4] Brady MC, Kinn S, Ness V, O'Rourke K,
Randhawa N, Stuart P. Preoperative fasting for preventing perioperative complications in children. Cochrane Database of Systematic Reviews. 2009;:CD005285
[5] Li-Wei L. y cols, influence
of laparoscopic carbon dioxide pneumoperitoneum on neonate circulation and respiration. Journal of International Medical Research. 2013;(3):889-894
[6] Jackson HT, Kane TD. Advances in
minimally invasive surgery in pediatric patients. Advances in Pediatrics. 2014;(1):149-195
[7] Tuna AT, Akkoyun I, Darcin S,
Palabiyik O. Effects of carbon dioxide insufflation on regional cerebral oxygenation during laparoscopic surgery in children: A prospective study. Brazilian Journal of Anesthesiology. 2016;(3):249-253
[8] Heuttemann E, Sakka SG, Petrat G,
Schier F, Reinhart K. Left ventricular regional wall qqmotion abnormalities
during pneumoperitoneum in children, British. Journal of Anesthesia. 2003;:773-776
[9] Chou CM, Yeh CM, Huang SY, Chen HC.
Perioperative parameter analysis of neonates and infants receiving laparoscopic surgery. Journal of the Chinese Medical Association. 2016;(10):559-564
[10] Fujimoto T, Segawa O, Lane GJ,
Esaki S, Niyano T. Laparoscopic surgery in newbonrs infants. Surgical Endoscopy. 1999;:773-777
[11] Shi Y, Hanson AC, Schroeder DR,
Haines KM, Kirsch AC, Macoun S, et al. Longitudinal assessment of cognitive function in young children undergoing general anaesthesia. British Journal of Anaesthesia. 2022;(2):294-300
[12] Kangralkar G, Jamale P. Sevoflurane
versus halothane for induction of anesthesia in pediatric and adult patients. Medical Gas Research. 2021;(2):53
[13] Brown EN, Lydic R, Schiff ND.
General anesthesia, sleep, and coma. New England Journal of Medicine. 2010;(27):2638-2650
[14] Fiadjoe J, Nishisaki A. Normal and
difficult airways in children: "What's new"-current evidence. Pediatric Anesthesia. 2020;(3):257-263
[15] Bai W, Golmirzaie K, Burke C, Van
Veen T, Christensen R, Voepel-Lewis T, et al. Evaluation of emergency pediatric tracheal intubation by pediatric anesthesiologists on inpatient units and the emergency department. Pediatric Anesthesia. 2016;(4):384-391
[16] Napolitano N, Laverriere EK,
Craig N, Snyder M, Thompson A,
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Pediatric Surgical Procedures – An Updated Guide – Volume I
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Davis D, et al. Apneic oxygenation As a quality improvement intervention in an academic PICU*. Pediatric Critical Care Medicine. 2019;(12):e531-e537
[17] Crulli B, Kawaguchi A, Praud JP,
Petrof BJ, Harrington K, Emeriaud G. Evolution of inspiratory muscle function in children during mechanical ventilation. Critical Care. 2021;(1):229
[18] Emeriaud G, Larouche A,
Ducharme-Crevier L, Massicotte E, Fléchelles O, Pellerin-Leblanc AA, et al. Evolution of inspiratory diaphragm activity in children over the course of the PICU stay. Intensive Care Medicine. 2014;(11):1718-1726
[19] Dmytriiev D,Melnychenko M,
Dobrovanov O,Nazarchuk O, Vidiscak M. Perioperative haemodynamic protective assessment of adaptive support ventilation usage in paediatric surgical patients. Acute and Critical Care. 2022;(4):636-643
et al. Pneumoperitoneum modifies serum and tissue CCL2-CCL5 expression in mice. JSLS: Journal of the Society of Laparoscopic & Robotic Surgeons. 2020; (2):e2020
[24] Umano GR, Delehaye G,
Noviello C, Papparella A. The "dark side" of Pneumoperitoneum and laparoscopy. Minimally Invasive Surgery;:1-9
[20] Lloyd TC. Mechanical
cardiopulmonary interdependence. Journal of Applied Physiology. 1982;(2):333-339
[21] Peng Z, Xia J, Yin N, Xue H. The
effects of volume-controlled ventilation versus pressure-controlled ventilation on hemodynamic and respiratory parameters in patients undergoing lumbar spine fusion surgery: A randomized controlled trial. Annals of Palliative Medicine. 2021;(9):9553-9563
[22] Groene P, Gündogar U,
Hofmann-Kiefer K, Ladurner R. Influence of insufflated carbon dioxide on abdominal temperature compared to oesophageal temperature during laparoscopic surgery. Surgical Endoscopy. 2021;(12):6892-6896
[23] Papparella A, Noviello C, Ranucci S,
Paciello O, Papparella S, De Biase D,
Chapter 2
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Cleft Lip/Palate: Hidden Aspects beyond the Gap
ShilpiKarmakar and Pawan KumarDixit
Abstract
Cle
ft lip/palate is a common congenital anomaly, with 1 in 700 newborns afflicted. Most surgery textbooks teach standard techniques for cleft lip/palate repair. However, there is much deeper science and art behind eradicating the stigma of the cleft. The cleft nose, vermillion, maxilla, and voice are giveaways of a good-but-not-great surgery. Similarly, the failure to address the maxillary hypoplasia, the dentition, themaxillary arches, the hearing, and the speech are common occurrences. This chapter will highlight the broad spectrum of cleft lip/palate conditions and the “why,” “when”, and “how” to address these deformities. Management of cleft lip/palate is a multidisciplinary task, with the child’s welfare at its center.
Keywords: maxilla, cleft lip, cleft palate, rhinoplasty, nasal bone, nasoalveolar molding, orthopedics, malocclusion
. Introduction
Werner Hagedorn said, “Great things are done when art and science meet.” Cleft care is a discipline where art and science blend to create magic. Adding the elixir of “timing” and “dedicated teamwork” leads to mesmerizing magic of galactic proportions.
One in 700 newborn babies are born with cleft lip and palate (CLP) worldwide. The numbers vary for sex, race, and region [1]. The multifactorial etiology occurs due to variations during the embryo’s normal development. The regular events of the development of the face are well described in the literature, and the reader is referred elsewhere to understand the same.
Besides the visibly apparent defects of the lip and palate, children affected with CLP also have distortion and dysfunction of the velum, eustachian tubes, hearing apparatus, speech apparatus, nose, maxilla, and dentition. These all cumulatively lead to inadequate physical development and psychological trauma. The malady affects not only the child but also the parents and the family, who struggle with a sense of guilt and helplessness. The management of CLP, thus, requires a dedicated team of health­care providers and interventions that are timely and intelligent. The skilled care of the CLP child occurs throughout the individual’s growth period.
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. Health concerns in a child born with CLP
. Lip defect
There is a deficiency of upper lip tissue comprising orbicularis oris, skin, mucosa, and vermillion. The fibers of orbicularis oris are discontinuous and abnormally attached to the cleft margin, maxilla, and alar base. These abnormal attachments lead to widening of the cleft gap as the child grows. The bilateral cleft lip has a deficiency of orbicularis oris in the central premaxilla segment. Thus, the absence of muscular reining forces manifests in the protrusion of the premaxilla.
During the repair of the cleft lip, the orbicularis oris is freed from all anomalous attachments and sutured across the cleft. The height and thickness of the orbicularis need to be maintained while repairing for adequate cosmesis.
. Defect in palate
There is a deficiency of palate tissue, comprising horizontal plate of maxilla bone, palatine bone, oral mucosa, nasal mucosa, muscles of soft palate (levator veli palatine (LVP), tensor veli palatini (TVP), musculus uvula, palatopharyngeus and palatoglos­sus). As in the cleft lip, the fibers of these muscles are abnormally attached to the cleft margin and posterior border of the hard palate. During the repair of the hard palate, closure of oral and nasal mucosa is not enough. The abnormal attachments of the muscles must be released, and the LVP of both sides must be repaired.
The LVP is a crucial member of the velopharyngeal sphincter complex. While repairing the LVP, it must also be positioned in the more anatomical posterior part of the velum. Positioning is vital to prevent nasal air leaks while speaking and fluids while swallowing.
. Nutrition
Feeding is a significant challenge for the parents of CLP babies. In normal children, during sucking, the lips form a seal over the mother’s breast as the velum closes the nasopharynx. In this closed cavity, movements of the tongue and mandible in relation to the palate generate a suction force. The cleft in the lip prevents the formation of the lip seal [2]. This is overcome by a child with a cleft lip (CL) by using the alveolar arch. A cleft palate (CP) precludes the formation of the velopharyngeal seal. This leads to weak suction pressure while feeding and milk regurgitation through the nose. The attempts at breastfeeding are also exhausting for the CLP baby. Over time, with inadequate breast milk expression, there is gradual lactation suppression. The parents resort to formula feeding or diluted cow’s milk, which does not have sufficient nutrient value.
The CLP child, thus, gets entangled in a vicious circle, where the result is malnutri­tion, failure to thrive, anemia, hypoproteinemia, and low weight gain. All this is happen­ing while the infant’s brain is undergoing maximal development. Nutritional insult at this stage has devastating consequences for the physical and mental growth of the child.
. Hearing
The eustachian tube connects the nasopharynx to the tympanic cavity, and its nasopharyngeal opening is regulated mainly by the TVP. The LVP functions as a tube dilator. The eustachian orifices usually are closed at rest and open with yawning,
Cleft Lip/Palate: Hidden Aspects beyond the Gap DOI: http://dx.doi.org/10.5772/intechopen.115578
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swallowing, and speech. In CP children, the anomalous insertions of the TVP and LVP result in the replacement of the isotonic contractions by isometric contractions. Thus, the eustachian tube opening and middle ear ventilation are affected [3, 4]. The abnormal nasal reflux of feeds instigates an inflammatory reaction, resulting in edema around the tubal orifice. The variations of the craniofacial skeleton, intrin­sic abnormalities of the tubal cartilage framework, misaligned and dysfunctional peritubal musculature, repeated respiratory infections, and hypertrophied adenoids all add insult to injury and further block the orifice of the eustachian tube [5–7].
Thus, when absorbed, the gases in the middle ear are not replaced, resulting in a negative pressure and tympanic membrane retraction. The negative pressure leads to fluid secretion from the mucous membrane into the middle ear, causing an effusion. Recurrent effusions may get infected and lead to suppurative otitis media. Recurrent or chronic middle ear disease can eventually result in conductive hearing loss [2]. Conductive hearing loss further exacerbates speech and learning problems in CLP children.
The incidence of middle ear disease is as high as 90% in children with CP, 45% of whom suffer from recurrent ear infections [8]. More than 50% of adolescents and adults with unoperated CP have developed a hearing loss of more than 15dB [8].
. Speech
The motor aspect of speech includes phonation (involving the larynx), articula­tion, and resonance. Articulation results from muscular activity of the lip, tongue, and soft palate. Resonance involves the mouth, nose, paranasal sinuses, pharynx, and chest cavity [2]. The consonants are categorized depending on whether the articula­tors are closed (plosives) or narrowed (fricatives) at a specific point.
The cleft of the lip and alveolus only affects the related consonants. The gap in the palate results in nasal emission of air, incompetence of the velopharyngeal sphincter, and defects in articulation. This is responsible for the nasal intonation, primarily of the vowels—the typical hypernasal cleft palate speech or audible nasal emissions or frictations [2, 9]. Extensive scars (due to messy surgery) in the soft palate also inter­fere with the closure of the velopharyngeal apparatus. The fistula in the hard or soft palate allows nasal air to escape with speech, leading to altered vowel quality, audible nasal emission, indistinct consonant production, and substitution mechanisms [10].
. Maxilla and alveolus
The affected side maxilla is generally underdeveloped and hypoplastic, and surgi­cal intervention negatively influences further growth. InCLP, the alveolar segment is displaced laterally—pushed by the tongue and pulled by the anteriorly attached muscle. In addition, the posterior arch is pushed posteromedially by cheek pressure. These forces misalign the alveolar arch [11]. Thus, the maxillary segment is displaced in the frontal, sagittal, and vertical planes, with the larger segment retroposition upward and outward and the lateral segment collapsing and displaced medially [2].
In bilateral CLP, the excessive premaxillary protrusion is directed more horizon­tally, resulting in a prominent central prolabial segment of the lip. This is due to the forward expansion of the alveolar process by unrestrained bone growth at the suture between the vomer and premaxilla, the growth of cartilaginous nasal septum due to facial muscle and maxillary bone disruption, and associated underdevelopment of the maxillary segments [2].
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Cleft of the alveolus affects the number, position, shape, size, time of eruption, and crown/ root formation of the deciduous and permanent teeth in and adjacent to the cleft. Also, the alveolar cleft between the maxillary lateral incisor and the canine tooth roots increases from the incisal edge to the apices of the teeth and is widest at the nasal cavity [2].
. Dentition
InCL, the incisors may be excessively proclined due to incontinence of the orbicu­laris muscle or retroclined due to “too tight” lip closure [2]. The number and position of teeth are affected. CLP children are more prone to develop caries. Compounded to it is the insult induced by surgical procedures. Palate repair procedures are known to reduce the vascularity of the alveolar mucoperiosteum.
Malocclusion is common in CLP patients and is somewhat related to the severity of the cleft and alignment of the arches. Intrinsic maxillary sagittal growth inhibi­tion leads to anterior crossbite. Transverse deficiency presents with crowding, lateral crossbite, and open bite. Surgical scars greatly restrict the sagittal and transverse growth [2].
. Nose
Along with CLP, there is an innate deficiency of the maxilla and cleft in the floor of the nose. The bone platform, cartilage support, lining, and skin are inherently dissimilar. There is an inherent discrepancy in the skin cover, cartilage support, nasal lining, and bony platform. Added to it is the anomalous insertion of the transverse muscle of the nose and the orbicularis oris around the nasal septum and nasal spine and the contractions of the contralateral normal muscle [2]. These cause the develop­ment of a peculiar set of nasal abnormalities, described below. To these deficiencies is added the insult of growth.
In unilateral CLP, the nasal tip is deviated to the non-cleft side (
Figure ). The nasal spine is positioned on the floor of the normal nostril, as the inferior edge of the nasal septum may be anteriorly dislocated from the vomerine groove. The vertical height of the columella on the cleft side is reduced and is slanted obliquely. The alar cartilage is attenuated, flattened, and dislocated from the tip [2]. The lateral crus is spread at an obtuse angle with respect to the medial crus. The medial crus lies lower in the columella. The dome is retroplaced. The overhanging alar rim forms a web as it lacks cartilage. Due to a lack of bony support, the alar base is asymmetrical, lying inferior and posterior, with an outward flare and no alar-facial groove definition. The cleft side nostril has a trans­verse axis and a circumference greater than the normal nostril [2, 12].
In bilateral cleft lip nasal deformity, the nose is flared with a broad, depressed, flat nasal tip and a markedly shortened columella (Figure ) [11]. The columella, caudal end of the septum, and the anterior nasal spine are displaced inferiorly in relation to the level of the alar bases. The bilateral alar cartilages are severely deformed and dislocated off the septum [11]. The medial crura is short and widely separated at the tip, the lateral crura is flat and elongated, and there is an obtuse angle between the crura and the dome [2, 12]. The alar bases are displaced laterally and sometimes inferiorly and posteriorly. The often asymmetric nostrils are horizontally oriented, and the nasal floor may be absent [2].
Cleft Lip/Palate: Hidden Aspects beyond the Gap DOI: http://dx.doi.org/10.5772/intechopen.115578
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Figure 1. Nasal deformity in unilateral cleft lip.
Figure 2. Nasal deformity in bilateral cleft lip.
Pediatric Surgical Procedures – An Updated Guide – Volume I
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. Growth of the child
Poor feeding, recurrent ear and airway infections, intrinsic growth deficiency, decreased levels of growth hormone, and repeated surgeries contribute to unsatisfac­tory growth of the child. There is poor weight gain in early life and a general lag in the growth curve, with a transient growth retardation. In late childhood, the height and weight are decreased compared with normal children, and puberty is delayed by 6months with reduced velocity of skeletal growth [11]. However, longitudinal studies reveal that the average growth usually returns to normal by 4years of age initially and again after puberty, which may be prolonged by up to 1year [2].
. Confidence
Teasing over facial appearance is commonly reported and has been found to result in poor psychological functioning in individuals with CLP [13]. Anxiety, depression, and low self-esteem are common among affected adult individuals [14]. Job oppor­tunities and the marriage market are relatively constricted for CLP individuals when compared to the average population [14].
. Parental distress
After the birth of an infant with CLP, the parents are usually shocked at the first sight of their child’s face [15]. The family’s situation is classified as a “psychosocial emergency,” characterized by disappointment, helplessness, and desperation, which may lead to a period of severe emotional crisis for the parents [15]. Parents often feel guilty about the malformation and are concerned about their child’s future. Parents of CLP may develop a feeling of chronic disappointment, which parents of physically disabled children are often seen to struggle with [15].
. Classification systems of CLP
Davis and Ritchie gave the first classification for CLP, considering the alveolar process as the foundation. Group I was Prealveolar, Group II was Postalveolar, Group III was Unilateral alveolar cleft, and Group IV was Bilateral alveolar cleft. This clas­sification was neither based on anatomy nor embryological development. Kernahan and Stark designated the incisive foramen as the dividing point between primary and secondary palates. This correctly described the deformity. Vilar-Sancho classified clefts based on Greek nomenclature. Lip was shown by “K” (keilos), alveolus by “G” (gnato), hard palate by “U” (urano), and soft palate by “S” (stafilos). Complete cleft was represented in capitals and partial in small letters. “2” was used to represent bilateral, “d” indicated right, “l” indicated left, an “I” indicated incomplete, and “o” indicated operated. Being in Greek, it could not be used by the rest of the world [16].
Spina used the incisive foramen as a reference point and divided clefts into four groups: Group I – Preincisive foramen clefts, Group II – Transincisive foramen clefts, Group III – Postincisive foramen clefts and Group IV – Rare facial clefts. Each group had unilateral, bilateral, and median; each group was subdivided into total and partial. The International Society adopted this for Plastic and Reconstructive Surgery. Kernahan proposed the “Y” classification, drawing nine boxes with nasopalatine foramen as the central point. This classification was a
Cleft Lip/Palate: Hidden Aspects beyond the Gap DOI: http://dx.doi.org/10.5772/intechopen.115578
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diagrammatic or symbolic representation of the cleft deformity and was used very effectively for documentation or charting. It could not be used for writing the diag­nosis in the case file, verbal communication for the text’s description, or computer archiving [16].
In 1989, Kriens proposed LAHSHAL, an abbreviated documentation system. Lip (L), alveolus (A), hard palate (H), and soft palate (S) were used to form LAHSHAL. The Indian classification was given by Balakrishnan and is widely accepted now. It classifies almost all the combinations of clefts encountered, and a brief notation can represent it. Gp 1 indicates cleft lip, with the suffix “a” indicates cleft alveolus. Gp 2 indicates cleft palate. Gp 3 indicates cleft of lip and palate.
. Management of CLP
A specialized team manages the CLP throughout the individual’s growth period. The team of healthcare providers for the CLP child incorporates many specialists, including a counselor, pediatrician, nutritionist, geneticist, plastic surgeon, maxil­lofacial surgeon, ear, nose and throat specialist, orthodontist, prosthodontist, speech pathologist, speech therapist, social worker and nurse (Table ) [17]. The quality of life of the family on the whole, as measured by the “Impact on Family Scale”, is
Age Issues Management Specialities
Antenatal Detection Family and genetic counseling Pediatrician
Parental distress Geneticist
Counselor
Birth to 1month
0 to 3months Feeding Feeding and growth assessment Pediatrician
3 to 6months Cleft lip Cheiloplasty, primary rhinoplasty and anterior
6 to 12months Cleft palate Cleft palatoplasty with soft palate muscle
1 to 5years Speech and language
Parental adaptation Family and genetic counseling Pediatrician
Feeding Feeding counseling Geneticist
Other congenital malformations
Growth and development
Gap in lip tissues and nasal deformity
Speech development Speech evaluation Speech therapist
Middle ear effusion Hearing evaluation =/− ventilatory tube
development
Dental abnormalities Velopharnygeal dysfunction assessment and
Hearing abnormalities Dental evaluation Ent surgeon
Complete medical assessment Counselor
Nasoalveolar molding Orthodontist
Presurgical orthopedics Plastic surgeon
Nutritional assessment Nutritionist
Plastic surgeon
palatoplasty (or gingivoperiosteoplasty)
Plastic surgeon
repair
ENT surgeon
insertion
Speech and language evaluation Speech therapist
Plastic surgeon
management
Hearing evaluation Orthodontist