Uvula in Snoring and Obstructive Sleep Apnea: Role and Surgical Intervention
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Selecting Different Approaches for Palate and Pharynx Surgery
SPECIAL ISSUE 4: INVITED ARTICLE Selecting Different Approaches for Palate and Pharynx Surgery: Palatopharyngeal Arch Staging System Rodolfo Lugo-Saldaña1 , Karina Saldívar-Ponce2 , Irina González-Sáez3 , Daniela Hernández-Sirit4 , Patricia Mireles-García5 ABSTRACT The examination of the anatomical structures involved in the upper airway collapse in patients with the obstructive sleep apnea-hypopnea syndrome (OSAHS) is a key for integrated evaluation of patients. Our proposal is for a noninvasive classification system that guides us about the presence of anatomical differences between the palatopharyngeal muscle (PFM). The functions of the PFM are narrowing the isthmus, descending the palate, and raising the larynx during swallowing; these characteristics give the PFM a special role in the collapse of the lateral pharyngeal wall. Complete knowledge of the anatomy and classification of different variants can guide us to choose the appropriate surgical procedures for the lateral wall collapse. Until now there is not a consensus about description of the trajectory or anatomical variants of the PFM into oropharynx, the distance between both muscles, and the muscle tone. Here we also present the relationship between the lateral wall surgeries currently available (lateral pharyngoplasty by Cahali, expansion sphincteroplasty by Pang, relocation pharyngoplasty by Li, Roman blinds pharyngoplasty by Mantovani, and barbed sutures pharyngoplasty by Vicini) with the proposed classification of the palatopharyngeal arch staging system (PASS). Keywords: -
Surgical Treatment of Snoring and Obstructive Sleep Apnea Syndrome
Medical Policy Surgical Treatment of Snoring and Obstructive Sleep Apnea Syndrome Table of Contents Policy: Commercial Coding Information Information Pertaining to All Policies Policy: Medicare Description References Authorization Information Policy History Policy Number: 130 BCBSA Reference Number: 7.01.101 Related Policies None Policy Commercial Members: Managed Care (HMO and POS), PPO, and Indemnity Medicare HMO BlueSM and Medicare PPO BlueSM Members Uvulopalatopharyngoplasty (UPPP) may be MEDICALLY NECESSARY for the treatment of clinically significant obstructive sleep apnea syndrome (OSAS) in appropriately selected adult patients who have failed an adequate trial of continuous positive airway pressure (CPAP) or failed an adequate trial of an oral appliance (OA). Clinically significant OSA is defined as those patients who have: Apnea/hypopnea Index (AHI) or Respiratory Disturbance Index (RDI) 15 or more events per hour, or AHI or RDI 5 or more events and 14 or less events per hour with documented symptoms of excessive daytime sleepiness, impaired cognition, mood disorders or insomnia, or documented hypertension, ischemic heart disease, or history of stroke. Hyoid suspension, surgical modification of the tongue, and/or maxillofacial surgery, including mandibular- maxillary advancement (MMA), may be MEDICALLY NECESSARY in appropriately selected adult patients with clinically significant OSA and objective documentation of hypopharyngeal obstruction who have failed an adequate trial of continuous positive airway pressure (CPAP) or failed an adequate trial of an oral appliance (OA). Clinically significant OSA is defined as those patients who have: AHI or RDI 15 or more events per hour, or AHI or RDI 5 or more events and 14 or less events per hour with documented symptoms of excessive daytime sleepiness, impaired cognition, mood disorders or insomnia, or documented hypertension, ischemic heart disease, or history of stroke. -
Embryology8 Dr.Ban Facial, Nasal and Palatal Development the External Human Face Develops Between the 4Th and 6Th Weeks of Embryonic Development
Embryology8 Dr.Ban Facial, nasal and palatal development The external human face develops between the 4th and 6th weeks of embryonic development. Facial swellings arise on: -Frontonasal process (2 medial nasal and 2 lateral nasal processes) -First pharyngeal arch (2 mandibular and 2 maxillary processes). By a process of merging and some localized fusion these processes come together to form the continuous surfaces of the external face. Sequence of developmental events : During the 3rd week of development an oropharyngeal membrane (buccopharyngeal ) is first seen at the site of the future face, between the primordium of the heart and the rapidly enlarging primordium of the brain. It is composed of ectoderm externally and endoderm internally. It lies at the beginning of the digestive tract and breaks down during the 4th week in order to form the opening between the future oral cavity (primitive mouth or stomodeum) and the foregut. The oropharyngeal membrane breaks down when it stops growing and it’s non-proliferating cells are gradually pulled apart 1 because they cannot fill the expanding area.The tissues around it expand very rapidly. The face develops from five primordia that appear in the fourth week: the frontonasal prominence, the two maxillary swellings, and the two mandibular swellings. The external face forms from two sources that surround the oropharyngeal membrane 1-Tissues of the frontonasal process that cover the forebrain, predominantly of neural crest origin. 2-The tissues of the first (or mandibular) pharyngeal arch, of mixed mesoderm and neural crest origin Face initially formed by 5 mesenchymal swellings ( prominences): Two mandibular prominences Two maxillary prominences Frontonasal prominence (midline structure is a single structure that is ventral to the forebrain. -
Abbreviations - Diagnosis
Abbreviations - Diagnosis AB abrasion AT attrition CA caries CFL cleft lip CFP cleft palate CLL cervical line lesion - See TR CMO craniomandibular osteopathy DT deciduous (primary) tooth DTC dentigerous cyst E enamel E/D enamel defect E/H enamel hypocalcification or hypoplasia FB foreign body FORL feline odontoclastic resorptive lesion - See TR FX fracture (tooth or jaw) G granuloma G/B buccal granuloma (cheek chewing lesion) G/L sublingual granuloma (tongue chewing lesion) G/E/L eosinophilic granuloma - lip G/E/P eosinophilic granuloma - palate G/E/T eosinophilic granuloma - tongue GH gingival hyperplasia GR gingival recession LAC laceration LAC/B laceration buccal (cheek) LAC/L laceration lip LAC/T laceration tongue MAL malocclusion MAL/1 class 1 malocclusion (neutroclusion - normal jaw relationship, specific teeth are incorrectly positioned) MAL/2 class 2 malocclusion (mandibular distoclusion - mandible shorter than maxilla) MAL/3 class 3 malocclusion (mandibular mesioclusion - maxilla shorter than mandible) BV buccoversion (crown directed towards cheek) CXB caudal crossbite DV distoversion (crown directed away from midline of dental arch) LABV labioversion (crown directed towards lip) LV linguoversion (crown directed towards tongue) MV mesioversion (crown directed towards midline of dental arch) OB open bite RXB rostral crossbite MN mandible or mandibular MN/FX mandibular fracture MX maxilla or maxillary MX/FX maxillary fracture OM oral mass OM/AD adenocarcinoma OM/EPA acanthomatous ameloblastoma (epulis) OM/EPF fibromatous epulis -
Angina Bullosa Haemorrhagica (Oral Blood Blister) (PDF)
Patient Information Maxillo-facial Angina Bullosa Haemorrhagica (Oral Blood Blister) What is Angina Bullosa Haemorrhagica? Angina Bullosa Hemorrhagica (ABH) is a condition where an often painful, but benign blood-filled blister suddenly develops in the mouth. The blisters are generally not due to a blood clotting disorder or any other medical disorder. It is a fairly common, sudden onset and benign blood blistering oral (mouth) disorder. It mainly affects people over 45 years and both males and females are equally affected. Usually there is no family history of the condition. It may be associated with Type 2 Diabetes, a family history of diabetes or Hyperglycaemia. What are the signs and symptoms of ABH? The first indication is a stinging pain or burning sensation just before the appearance of a blood blister The blisters last only a few minutes and then spontaneously rupture (burst), leaving a shallow ulcer that heals without scarring, discomfort or pain They can reach an average size of one to three centimetres in diameter The Soft Palate (back of the mouth) is the most affected site If they occur on the palate and are relatively big, they may need to be de-roofed (cut and drained) to ease the sensation of choking Patient Information Occasionally blisters can occur in the buccal mucosa (cheek) and tongue Approximately one third of the patients have blood blisters in more than one location. What are the causes of ABH? More than 50% of cases are related to minor trauma caused by: hot foods, restorative dentistry (fillings, crowns etc) or Periodontal Therapy (treatment of gum disease). -
Lecture 2 – Bone
Oral Histology Summary Notes Enoch Ng Lecture 2 – Bone - Protection of brain, lungs, other internal organs - Structural support for heart, lungs, and marrow - Attachment sites for muscles - Mineral reservoir for calcium (99% of body’s) and phosphorous (85% of body’s) - Trap for dangerous minerals (ex:// lead) - Transduction of sound - Endocrine organ (osteocalcin regulates insulin signaling, glucose metabolism, and fat mass) Structure - Compact/Cortical o Diaphysis of long bone, “envelope” of cuboid bones (vertebrae) o 10% porosity, 70-80% calcified (4x mass of trabecular bone) o Protective, subject to bending/torsion/compressive forces o Has Haversian system structure - Trabecular/Cancellous o Metaphysis and epiphysis of long bone, cuboid bone o 3D branching lattice formed along areas of mechanical stress o 50-90% porosity, 15-25% calcified (1/4 mass of compact bone) o High surface area high cellular activity (has marrow) o Metabolic turnover 8x greater than cortical bone o Subject to compressive forces o Trabeculae lined with endosteum (contains osteoprogenitors, osteoblasts, osteoclasts) - Woven Bone o Immature/primitive, rapidly growing . Normally – embryos, newborns, fracture calluses, metaphyseal region of bone . Abnormally – tumors, osteogenesis imperfecta, Pagetic bone o Disorganized, no uniform orientation of collagen fibers, coarse fibers, cells randomly arranged, varying mineral content, isotropic mechanical behavior (behavior the same no matter direction of applied force) - Lamellar Bone o Mature bone, remodeling of woven -
Vestibule Lingual Frenulum Tongue Hyoid Bone Trachea (A) Soft Palate
Mouth (oral cavity) Parotid gland Tongue Sublingual gland Salivary Submandibular glands gland Esophagus Pharynx Stomach Pancreas (Spleen) Liver Gallbladder Transverse colon Duodenum Descending colon Small Jejunum Ascending colon intestine Ileum Large Cecum intestine Sigmoid colon Rectum Appendix Anus Anal canal © 2018 Pearson Education, Inc. 1 Nasopharynx Hard palate Soft palate Oral cavity Uvula Lips (labia) Palatine tonsil Vestibule Lingual tonsil Oropharynx Lingual frenulum Epiglottis Tongue Laryngopharynx Hyoid bone Esophagus Trachea (a) © 2018 Pearson Education, Inc. 2 Upper lip Gingivae Hard palate (gums) Soft palate Uvula Palatine tonsil Oropharynx Tongue (b) © 2018 Pearson Education, Inc. 3 Nasopharynx Hard palate Soft palate Oral cavity Uvula Lips (labia) Palatine tonsil Vestibule Lingual tonsil Oropharynx Lingual frenulum Epiglottis Tongue Laryngopharynx Hyoid bone Esophagus Trachea (a) © 2018 Pearson Education, Inc. 4 Visceral peritoneum Intrinsic nerve plexuses • Myenteric nerve plexus • Submucosal nerve plexus Submucosal glands Mucosa • Surface epithelium • Lamina propria • Muscle layer Submucosa Muscularis externa • Longitudinal muscle layer • Circular muscle layer Serosa (visceral peritoneum) Nerve Gland in Lumen Artery mucosa Mesentery Vein Duct oF gland Lymphoid tissue outside alimentary canal © 2018 Pearson Education, Inc. 5 Diaphragm Falciform ligament Lesser Liver omentum Spleen Pancreas Gallbladder Stomach Duodenum Visceral peritoneum Transverse colon Greater omentum Mesenteries Parietal peritoneum Small intestine Peritoneal cavity Uterus Large intestine Cecum Rectum Anus Urinary bladder (a) (b) © 2018 Pearson Education, Inc. 6 Cardia Fundus Esophagus Muscularis Serosa externa • Longitudinal layer • Circular layer • Oblique layer Body Lesser Rugae curvature of Pylorus mucosa Greater curvature Duodenum Pyloric Pyloric sphincter antrum (a) (valve) © 2018 Pearson Education, Inc. 7 Fundus Body Rugae of mucosa Pyloric Pyloric (b) sphincter antrum © 2018 Pearson Education, Inc. -
Head and Neck
DEFINITION OF ANATOMIC SITES WITHIN THE HEAD AND NECK adapted from the Summary Staging Guide 1977 published by the SEER Program, and the AJCC Cancer Staging Manual Fifth Edition published by the American Joint Committee on Cancer Staging. Note: Not all sites in the lip, oral cavity, pharynx and salivary glands are listed below. All sites to which a Summary Stage scheme applies are listed at the begining of the scheme. ORAL CAVITY AND ORAL PHARYNX (in ICD-O-3 sequence) The oral cavity extends from the skin-vermilion junction of the lips to the junction of the hard and soft palate above and to the line of circumvallate papillae below. The oral pharynx (oropharynx) is that portion of the continuity of the pharynx extending from the plane of the inferior surface of the soft palate to the plane of the superior surface of the hyoid bone (or floor of the vallecula) and includes the base of tongue, inferior surface of the soft palate and the uvula, the anterior and posterior tonsillar pillars, the glossotonsillar sulci, the pharyngeal tonsils, and the lateral and posterior walls. The oral cavity and oral pharynx are divided into the following specific areas: LIPS (C00._; vermilion surface, mucosal lip, labial mucosa) upper and lower, form the upper and lower anterior wall of the oral cavity. They consist of an exposed surface of modified epider- mis beginning at the junction of the vermilion border with the skin and including only the vermilion surface or that portion of the lip that comes into contact with the opposing lip. -
Basic Histology (23 Questions): Oral Histology (16 Questions
Board Question Breakdown (Anatomic Sciences section) The Anatomic Sciences portion of part I of the Dental Board exams consists of 100 test items. They are broken up into the following distribution: Gross Anatomy (50 questions): Head - 28 questions broken down in this fashion: - Oral cavity - 6 questions - Extraoral structures - 12 questions - Osteology - 6 questions - TMJ and muscles of mastication - 4 questions Neck - 5 questions Upper Limb - 3 questions Thoracic cavity - 5 questions Abdominopelvic cavity - 2 questions Neuroanatomy (CNS, ANS +) - 7 questions Basic Histology (23 questions): Ultrastructure (cell organelles) - 4 questions Basic tissues - 4 questions Bone, cartilage & joints - 3 questions Lymphatic & circulatory systems - 3 questions Endocrine system - 2 questions Respiratory system - 1 question Gastrointestinal system - 3 questions Genitouirinary systems - (reproductive & urinary) 2 questions Integument - 1 question Oral Histology (16 questions): Tooth & supporting structures - 9 questions Soft oral tissues (including dentin) - 5 questions Temporomandibular joint - 2 questions Developmental Biology (11 questions): Osteogenesis (bone formation) - 2 questions Tooth development, eruption & movement - 4 questions General embryology - 2 questions 2 National Board Part 1: Review questions for histology/oral histology (Answers follow at the end) 1. Normally most of the circulating white blood cells are a. basophilic leukocytes b. monocytes c. lymphocytes d. eosinophilic leukocytes e. neutrophilic leukocytes 2. Blood platelets are products of a. osteoclasts b. basophils c. red blood cells d. plasma cells e. megakaryocytes 3. Bacteria are frequently ingested by a. neutrophilic leukocytes b. basophilic leukocytes c. mast cells d. small lymphocytes e. fibrocytes 4. It is believed that worn out red cells are normally destroyed in the spleen by a. neutrophils b. -
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PEDIATRIC/CRANIOFACIAL Pharyngeal Flap Outcomes in Nonsyndromic Children with Repaired Cleft Palate and Velopharyngeal Insufficiency Stephen R. Sullivan, M.D., Background: Velopharyngeal insufficiency occurs in 5 to 20 percent of children M.P.H. following repair of a cleft palate. The pharyngeal flap is the traditional secondary Eileen M. Marrinan, M.S., procedure for correcting velopharyngeal insufficiency; however, because of M.P.H. perceived complications, alternative techniques have become popular. The John B. Mulliken, M.D. authors’ purpose was to assess a single surgeon’s long-term experience with a Boston, Mass.; and Syracuse, N.Y. tailored superiorly based pharyngeal flap to correct velopharyngeal insufficiency in nonsyndromic patients with a repaired cleft palate. Methods: The authors reviewed the records of all children who underwent a pharyngeal flap performed by the senior author (J.B.M.) between 1981 and 2008. The authors evaluated age of repair, perceptual speech outcome, need for a secondary operation, and complications. Success was defined as normal or borderline sufficient velopharyngeal function. Failure was defined as borderline insufficiency or severe velopharyngeal insufficiency with recommendation for another procedure. Results: The authors identified 104 nonsyndromic patients who required a pharyngeal flap following cleft palate repair. The mean age at pharyngeal flap surgery was 8.6 Ϯ 4.9 years. Postoperative speech results were available for 79 patients. Operative success with normal or borderline sufficient velopharyngeal function was achieved in 77 patients (97 percent). Obstructive sleep apnea was documented in two patients. Conclusion: The tailored superiorly based pharyngeal flap is highly successful in correcting velopharyngeal insufficiency, with a low risk of complication, in non- syndromic patients with repaired cleft palate. -
Cleft Palate/Lip
CLEFT PALATE/LIP WHAT IS A CLEFT? A cleft is a separation in the skin, tissue lining of the mouth, muscle, and bone that is normally fused together; however, no structures are missing. Clefts can be either unilateral (one side) or bilateral (both sides) and may include the lip, soft palate and/or hard palate or any of the structures in isolation. TYPES OF CLEFTS Cleft Lip – separation in the lip and may include the bottom of the nose Cleft Palate – separation in the hard palate and/or soft palate Submucous Cleft – separation in the muscle of the soft palate with the tissue lining of the mouth intact. Often, it is not easily viewed. WHEN DID CLEFTING HAPPEN? During the 4th week of fetal development, the primary palate (line from nostril to upper lip and mucosa behind upper teeth) fuse together. By the 8th week, the tongue drops in the mouth and the secondary palate (hard palate and soft palate) fuse together with the nasal septum. By the 12th week, if the process is not complete, a cleft (separation) will develop. WHAT CAUSED MY CHILD’S CLEFT? The exact cause is not known but theories include: Low intake of Folic Acid (Vitamin B) Large intake of Vitamin A Genetic disposition Syndromes or Sequences (Pierre Robin, Treacher Collins) Drugs, alcohol, medication, and smoking CLEFT PALATE MANAGEMENT You and your child will be in contact with many different healthcare professionals who need to work together. Every case is individualized, therefore your child will need a thorough assessment to the appropriate treatment plan. -
32 Surgical Treatment of Sleep-Related Breathing Disorders Donald M
32 Surgical Treatment of Sleep-Related Breathing Disorders Donald M. Sesso Department of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center, Stanford, California, U.S.A. Nelson B. Powell and Robert W. Riley Department of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center and Department of Behavioral Sciences, Division of Sleep Medicine, Stanford University School of Medicine, Stanford, California, U.S.A. INTRODUCTION Snoring, upper airway resistance syndrome (UARS), obstructive sleep apnea (OSA), and obstructive sleep apnea-hypopnea syndrome (OSAHS) are collectively referred to as sleep- related breathing disorders (SRBD). These terms describe a partial or complete obstruction of the upper airway during sleep. Patency of the pharyngeal airway is maintained by two opposing forces: negative intraluminal pressure and the activity of the upper airway musculature. Anatomical or central neural abnormalities can disrupt this delicate balance and result in compromise of the upper airway. This reduction of airway caliber may cause sleep fragmentation and subsequent behavioral derangements, such as excessive daytime sleepiness (EDS) (1–3). The goal of medical and surgical therapy is to alleviate this obstruction and increase airway patency. The first therapeutic modality employed to treat SRBD was surgery. Kuhlo described placement of a tracheotomy tube in an attempt to bypass upper airway obstruction in Pickwickian patients (4). Although effective, tracheotomy does not address the specific sites of pharyngeal collapse and is not readily accepted by most patients. These sites include the nasal cavity/nasopharynx, oropharynx, and hypopharynx. Often, multilevel obstruction is present. Consequently, the surgical armamentarium has evolved to create techniques that correct the specific anatomical sites of obstruction.