Code Label Code Label NERVOUS SYSTEM DEFECTS ICD-9-CM ICD-10-CM
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Periodontal Assessment and Treatment Planning Gingival description Color: o pink o erythematous o cyanotic o racial pigmentation o metallic pigmentation o uniformity Contour: o recession o clefts o enlarged papillae o cratered papillae o blunted papillae o highly rolled o bulbous o knife-edged o scalloped o stippled Consistency: o firm o edematous o hyperplastic o fibrotic Band of gingiva: o amount o quality o location o treatability Bleeding tendency: o sulcus base, lining o gingival margins Suppuration Sinus tract formation Pocket depths Pseudopockets Frena Pain Other pathology Dental Description Defective restorations: o overhangs o open contacts o poor contours Fractured cusps 1 ww.links2success.biz [email protected] 914-303-6464 Caries Deposits: o Type . plaque . calculus . stain . matera alba o Location . supragingival . subgingival o Severity . mild . moderate . severe Wear facets Percussion sensitivity Tooth vitality Attrition, erosion, abrasion Occlusal plane level Occlusion findings Furcations Mobility Fremitus Radiographic findings Film dates Crown:root ratio Amount of bone loss o horizontal; vertical o localized; generalized Root length and shape Overhangs Bulbous crowns Fenestrations Dehiscences Tooth resorption Retained root tips Impacted teeth Root proximities Tilted teeth Radiolucencies/opacities Etiologic factors Local: o plaque o calculus o overhangs 2 ww.links2success.biz [email protected] 914-303-6464 o orthodontic apparatus o open margins o open contacts o improper -
Successful Uterovaginal Anastomosis in an Unusual Presentation Of
JSAFOMS Successful Uterovaginal Anastomosis in an Unusual Presentation10.5005/jp-journals-10032-1056 of Congenital Absence of Cervix CASE REPORT Successful Uterovaginal Anastomosis in an Unusual Presentation of Congenital Absence of Cervix 1Nusrat Mahmud, 2Naushaba Tarannum Mahtab, 3TA Chowdhury, 4Anjan Kumar Deb ABSTRACT Source of support: Nil Cervical agenesis or dysgenesis (fragmentation, fibrous cord Conflict of interest: None and obstruction) is an extremely rare congenital anomaly. Conser vative surgical approach to these patients involves uterovaginal anastomosis, cervical canalization and cervical INTRODUCTION reconstruction. In failed conservative surgery, total hysterec- Primary amenorrhea is defined as absence of menstrua- tomy is the treatment of choice. We report what we believe to be the first successful end-to-end uterovaginal anastomosis of tion by the age of 14 years in the absence of secondary an unusual case of congenital cervical agenesis. A 25-year- sex characteristics or the absence of periods by the age of old female presented complaining of primary amenorrhea 16 years regardless of appearance of secondary sex and primary subfertility for the same duration. At laparoscopy, complete separation between the cervix and the body of the charac ters. In our last study, a series of total 108 cases uterus was found and hanging from surrounding supports. of primary amenorrhea were reviewed. It was found Both ovaries and fallopian tubes were anatomically positioned. that 69.4% were due Müllerian dysgenesis, 19.4% due to There was another muscular tissue of 2 cm in diameter at the gonadal dysgenesis, 2.7% male pseudohermaphroditism pouch of Douglas which was attached with lateral pelvic wall 13 by transverse cervical ligament. -
59. Lateral Facial Clefts
59 LATERAL FACIAL CLEFTS LI OR TRANSVERSE CLEFTS ARE CONSIDERED THE RESULT OF FAILURE OF MESODERM MIGRATION OR MERGING TO OBLITERATE MANDIBULAR THE EMBRYONIC GROOVES BETWEEN THE MAXILLARY AND PROMINENCES TRANSVERSE CLEFTS AS THESE CLEFTS ARE RARE AND ALMOST EVERYBODY HAVING ONE HAS AND REPORTED IT IT IS POSSIBLE TO REVIEW MOST OF THE REPORTED CASES 769 DESCRIBED THE AFTER WHEN NOTE TREATMENT SPECIFIC CASE RECORDINGS IN WHAT MAY SEEM HELTERSKELTER ARRANGEMENT GENERALIZATIONS MAY BE OF VALUE IN 1891 ROSE NOTED FOR LONG THE VERY EXISTENCE OF THIS MACROSROMATOUS DEFORMITY WAS DOUBTED BUT CASES HAVE BEEN RECOGNIZED MORE OR LESS SINCE 1715 WHEN MURALT PICTURED IT FOR THE FIRST TIME ONE OF THE FIRST CASES REPORTED WAS BY VROLIK WHOIN HIS 1849 CLEFTS WORK GAVE SEVERAL ILLUSTRATIONS OF COMMISSURAL AS WELL AS OTHER DEFORMITIES OF THE FACE OTHER CASES WERE REPORTED BY REISSMANN IN 1869 AND MORGAN IN 1882 MACROSTOMIA OR COMMISSURAL HARELIP ACCORDING TO ROSE IS DIAMETER OF WHICH EVIDENCED BY AN INCREASED THE MOUTH MAY VARY IN FROM SLIGHT INCREASE TO CONSIDERABLE DISTANCE CASE RE PORTED BY RYND IN 1862 THE MOUTH OPENING EXTENDED AS FAR AS THE THE LEFT FIRST MOLAR ON THE RIGHT SIDE AND TO THE LAST MOLAR ON IN 1887 SUTTON PUBLISHED THE DRAWING OF CHILD WITH VERY LARGE RED CICATRIX THIS CLEFT THE ANGLES OF WHICH GRADUALLY PASSED INTO SCAR ENDED IN GAPING WOUND OVER THE TEMPORAL REGION EXTEND ING TO THE DURA MATER ROSE ALSO POINTED OUT MACROSROMA IS NOR ONLY ATTENDED BY GREAT DISFIGUREMENT HUT IS ALSO TROU BLESOME FROM THE IMPOSSIBILITY OF THE CHILD RETAINING -
OCSHCN-10G, Medical Eligibility List for Clinical and Case Management Services.Pdf
OCSHCN-10g (01 2019) (Rev 7-15-2017) Office for Children with Special Health Care Needs Medical Eligibility List for Clinical and Case Management Services BODY SYSTEM ELIGIBLE DISEASES/CONDITIONS ICD-10-CM CODES AFFECTED AUTISM SPECTRUM Autistic disorder, current or active state F84.0 Autistic disorder DISORDER (ASD) F84.3 Other childhood disintegrative disorder Autistic disorder, residual state F84.5 Asperger’s Syndrome F84.8 Other pervasive developmental disorder Other specified pervasive developmental disorders, current or active state Other specified pervasive developmental disorders, residual state Unspecified pervasive development disorder, current or active Unspecified pervasive development disorder, residual state CARDIOVASCULAR Cardiac Dysrhythmias I47.0 Ventricular/Arrhythmia SYSTEM I47.1 Supraventricular/Tachycardia I47.2 Ventricular/Tachycardia I47.9 Paroxysmal/Tachycardia I48.0 Paroxysmal atrial fibrillation I48.1 Persistent atrial fibrillationar I48.2 Chronic atrial fibrillation I48.3 Typical atrial flutter I48.4 Atypical atrial flutter I49.0 Ventricular fibrillation and flutter I49.1 Atrial premature depolarization I49.2 Junctional premature depolarization I49.3 Ventricular premature depolarization I49.49 Ectopic beats Extrasystoles Extrasystolic arrhythmias Premature contractions Page 1 of 28 OCSHCN-10g (01 2019) (Rev 7-15-2017) Office for Children with Special Health Care Needs Medical Eligibility List for Clinical and Case Management Services I49.5 Tachycardia-Bradycardia Syndrome CARDIOVASCULAR Chronic pericarditis -
Morphologic Diversity in Human Papillomavirus-Related Oropharyngeal Squamous Cell Carcinoma: Catch Me If You Can! James S Lewis Jr
Modern Pathology (2017) 30, S44–S53 S44 © 2017 USCAP, Inc All rights reserved 0893-3952/17 $32.00 Morphologic diversity in human papillomavirus-related oropharyngeal squamous cell carcinoma: Catch Me If You Can! James S Lewis Jr Department of Pathology, Microbiology, and Immunology; Department of Otolaryngology, Vanderbilt University Medical Center, Nashville, TN, USA As the human papillomavirus (HPV)-related oropharyngeal squamous cell carcinoma epidemic has developed in the past several decades, it has become clear that these tumors have a wide variety of morphologic tumor types and features. For the practicing pathologist, it is critical to have a working knowledge about these in order to make the correct diagnosis, not to confuse them with other lesions, and to counsel clinicians and patients on their significance (or lack of significance) for treatment and outcomes. In particular, there are a number of pitfalls and peculiarities regarding HPV-related tumors and their nodal metastases that can easily result in misclassification and confusion. This article will discuss the various morphologic types and features of HPV- related oropharyngeal carcinomas, specific differential diagnoses when challenging, and, if established, the clinical significance of each finding. Modern Pathology (2017) 30, S44–S53; doi:10.1038/modpathol.2016.152 It is now well-established that human papilloma- Among its many effects on clinical practice, the virus (HPV) is responsible for a large fraction of oropharyngeal HPV epidemic has put pathologists at oropharyngeal squamous cell carcinomas (SCC), the forefront of diagnosis and recognition of these particularly in the United States and Europe.1 Many unique tumors, which are much less clinically have termed the increase in HPV-related orophar- aggressive than conventional head and neck SCC, 7 yngeal SCC as an epidemic.2,3 There are numerous and which are beginning to be managed differently. -
Oral Lesions in Leprosy
Study Oral lesions in leprosy Ana Paula Fucci da Costa, José Augusto da Costa Nery, Maria Leide Wan-del-Rey de Oliveira, Tullia Cuzzi,* Marcia Ramos-e-Silva Departments of Dermatology & *Pathology, HUCFF-UFRJ and School of Medicine, Federal University of Rio de Janeiro, Brazil. Address for correspondence: Marcia Ramos-e-Silva, Rua Sorocaba 464/205, 22271-110, Rio de Janeiro, Brazil. E-mail: [email protected] ABSTRACT Background: Leprotic oral lesions are more common in the lepromatous form of leprosy, indicate a late manifestation, and have a great epidemiological importance as a source of infection. Methods: Patients with leprosy were examined searching for oral lesions. Biopsies of the left buccal mucosa in all patients, and of oral lesions, were performed and were stained with H&E and Wade. Results: Oral lesions were found in 26 patients, 11 lepromatous leprosy, 14 borderline leprosy, and one tuberculoid leprosy. Clinically 5 patients had enanthem of the anterior pillars, 3 of the uvula and 3 of the palate. Two had palatal infiltration. Viable bacilli were found in two lepromatous patients. Biopsies of the buccal mucosa showed no change or a nonspecific inflammatory infiltrate. Oral clinical alterations were present in 69% of the patients; of these 50% showed histopathological features in an area without any lesion. Discussion: Our clinical and histopathological findings corroborate earlier reports that there is a reduced incidence of oral changes, which is probably due to early treatment. The maintenance of oral infection in this area can also lead to and maintain lepra reactions, while they may also act as possible infection sources. -
Cervical and Vaginal Agenesis: a Novel Anomaly
Cervical and Vaginal Agenesis: A Novel Anomaly Case Report Cervical and Vaginal Agenesis: A Novel Anomaly Irum Sohail1, Maria Habib 2 1Professor Obs/Gynae, 2Postgraduate Trainee, Wah Medical College, Wah Cantt Address of Correspondence: Dr. Maria Habib, Postgraduate Trainee, Wah Medical College, Wah Cantt Email: [email protected] Abstract Background: Cervical agenesis with vaginal agenesis is an extremely rare congenital anomaly. This mullerian anomaly occurs in 1 in 80,000-100,000 births. It is classified as type IB in the American Fertility Society Classification of mullerian anomalies. Case report: We report a case presented to POF Hospital, Wah cantt with primary amenorrhea and cyclic lower abdominal pain. She was diagnosed to have cervical agenesis associated with completely absent vagina. Conservative surgical approach to these patients involve uterovaginal anastomosis and cervical reconstruction. Creation of neovagina is necessary in these cases. Due to high failure rate and potential for complications, total hysterectomy with vaginoplasty is the treatment of choice by many authors. Conclusion: A thorough investigation of the patients with primary amenorrhea is necessary and total hysterectomy with vaginoplasty is feasible and should be considered as a first-line treatment option in cases of cervical and vaginal agenesis. Key words: Primary amenorrhea, Cervical agenesis, Vaginal agenesis, Hysterectomy. Introduction The female reproductive organs develop from the Society of Human Reproduction and Embryology fusion of the bilateral paramesonephric (Müllerian) (ESHRE)/European Society for Gynaecological ducts to form the uterus, cervix, and upper two- Endoscopy (ESGE) classification system of female thirds of the vagina.1 The lower third of the vagina genital anomalies is designed for clinical orientation develops from the sinovaginal bulbs of the and it is based on the anatomy of the female urogenital sinus.2 Mullerian duct anomalies (MDAs) genital tract. -
Genetic Syndromes and Genes Involved
ndrom Sy es tic & e G n e e n G e f Connell et al., J Genet Syndr Gene Ther 2013, 4:2 T o Journal of Genetic Syndromes h l e a r n a DOI: 10.4172/2157-7412.1000127 r p u y o J & Gene Therapy ISSN: 2157-7412 Review Article Open Access Genetic Syndromes and Genes Involved in the Development of the Female Reproductive Tract: A Possible Role for Gene Therapy Connell MT1, Owen CM2 and Segars JH3* 1Department of Obstetrics and Gynecology, Truman Medical Center, Kansas City, Missouri 2Department of Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 3Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA Abstract Müllerian and vaginal anomalies are congenital malformations of the female reproductive tract resulting from alterations in the normal developmental pathway of the uterus, cervix, fallopian tubes, and vagina. The most common of the Müllerian anomalies affect the uterus and may adversely impact reproductive outcomes highlighting the importance of gaining understanding of the genetic mechanisms that govern normal and abnormal development of the female reproductive tract. Modern molecular genetics with study of knock out animal models as well as several genetic syndromes featuring abnormalities of the female reproductive tract have identified candidate genes significant to this developmental pathway. Further emphasizing the importance of understanding female reproductive tract development, recent evidence has demonstrated expression of embryologically significant genes in the endometrium of adult mice and humans. This recent work suggests that these genes not only play a role in the proper structural development of the female reproductive tract but also may persist in adults to regulate proper function of the endometrium of the uterus. -
Pathophysiology, Diagnosis, and Management of Pediatric Ascites
INVITED REVIEW Pathophysiology, Diagnosis, and Management of Pediatric Ascites ÃMatthew J. Giefer, ÃKaren F. Murray, and yRichard B. Colletti ABSTRACT pressure of mesenteric capillaries is normally about 20 mmHg. The pediatric population has a number of unique considerations related to Intestinal lymph drains from regional lymphatics and ultimately the diagnosis and treatment of ascites. This review summarizes the physio- combines with hepatic lymph in the thoracic duct. Unlike the logic mechanisms for cirrhotic and noncirrhotic ascites and provides a sinusoidal endothelium, the mesenteric capillary membrane is comprehensive list of reported etiologies stratified by the patient’s age. relatively impermeable to albumin; the concentration of protein Characteristic findings on physical examination, diagnostic imaging, and in mesenteric lymph is only about one-fifth that of plasma, so there abdominal paracentesis are also reviewed, with particular attention to those is a significant osmotic gradient that promotes the return of inter- aspects that are unique to children. Medical and surgical treatments of stitial fluid into the capillary. In the normal adult, the flow of lymph ascites are discussed. Both prompt diagnosis and appropriate management of in the thoracic duct is about 800 to 1000 mL/day (3,4). ascites are required to avoid associated morbidity and mortality. Ascites from portal hypertension occurs when hydrostatic Key Words: diagnosis, etiology, management, pathophysiology, pediatric and osmotic pressures within hepatic and mesenteric capillaries ascites produce a net transfer of fluid from blood vessels to lymphatic vessels at a rate that exceeds the drainage capacity of the lym- (JPGN 2011;52: 503–513) phatics. It is not known whether ascitic fluid is formed predomi- nantly in the liver or in the mesentery. -
The Diseases of Airway-Tracheal Diverticulum: a Review of the Literature
Review Article The diseases of airway-tracheal diverticulum: a review of the literature Asli Tanrivermis Sayit, Muzaffer Elmali, Dilek Saglam, Cetin Celenk Department of Radiology, Faculty of Medicine, Ondokuz Mayis University, Samsun, Turkey Contributions: (I) Conception and design: A Tanrivermis Sayit; (II) Administrative support: M Elmali, C Celenk; (III) Provision of study materials or patients: A Tanrivermis Sayit; (IV) Collection and assembly of data: A Tanrivermis Sayit, D Saglam; (V) Data analysis and interpretation: A Tanrivermis Sayit, M Elmali, C Celenk; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors. Correspondence to: Asli Tanrivermis Sayit. Department of Radiology, Faculty of Medicine, Ondokuz Mayis University, 55139, Atakum/Samsun, Turkey. Email: [email protected]. Abstract: Tracheal diverticulum (DV) is a type of paratracheal air cyst (PTAC) that is often asymptomatic and usually detected incidentally by imaging methods. Tracheal DV are divided into two subgroups: congenital and acquired. Dysphagia, odynophagia, neck pain, hoarseness, hemoptysis, choking, and recurrent episodes of hiccups and burping can also be seen in symptomatic patients. Thin-section multidetector computed tomography (MDCT) is useful for diagnosis of tracheal diverticulum. The relationship between DV and tracheal lumen can be demonstrated by axial, coronal, and sagittal reformat multiplanar images. Bronchoscopy can also be used in diagnosis for tracheal DV. However, the connection between DV and tracheal lumen can not be shown easily with bronchoscopy. Conservative treatment is the preferred treatment in asymptomatic patients. Surgical or conservative treatment can be performed for symptomatic patients, depending on patient age and physical condition. Keywords: Trachea; diverticulum (DV); thorax; multidetector computed tomography; tracheal diseases; chronic obstructive pulmonary disease (CODP) Submitted Sep 17, 2016. -
Congenital Cardiac Surgery ICD9 to ICD10 Crosswalks Page 1 of 4 8
Congenital Cardiac Surgery ICD9 to ICD10 Crosswalks ICD-9 code ICD-9 Descriptor ICD-10 Code ICD-10 Descriptor 164.1 Malignant neoplasm of heart C38.0 Malignant neoplasm of heart 164.1 Malignant neoplasm of heart C45.2 Mesothelioma of pericardium 212.7 Benign neoplasm of heart D15.1 Benign neoplasm of heart 425.11 Hypertrophic obstructive cardiomyopathy I42.1 Obstructive hypertrophic cardiomyopathy 425.18 Other hypertrophic cardiomyopathy I42.2 Other hypertrophic cardiomyopathy 425.3 Endocardial fibroelastosis I42.4 Endocardial fibroelastosis 425.4 Other primary cardiomyopathies I42.0 Dilated cardiomyopathy 425.4 Other primary cardiomyopathies I42.5 Other restrictive cardiomyopathy 425.4 Other primary cardiomyopathies I42.8 Other cardiomyopathies 425.4 Other primary cardiomyopathies I42.9 Cardiomyopathy, unspecified 426.9 Conduction disorder, unspecified I45.9 Conduction disorder, unspecified 745.0 Common truncus Q20.0 Common arterial trunk 745.10 Complete transposition of great vessels Q20.3 Discordant ventriculoarterial connection 745.11 Double outlet right ventricle Q20.1 Double outlet right ventricle 745.12 Corrected transposition of great vessels Q20.5 Discordant atrioventricular connection 745.19 Other transposition of great vessels Q20.2 Double outlet left ventricle 745.19 Other transposition of great vessels Q20.3 Discordant ventriculoarterial connection 745.19 Other transposition of great vessels Q20.8 Other congenital malformations of cardiac chambers and connections 745.2 Tetralogy of fallot Q21.3 Tetralogy of Fallot 745.3 Common -
Reportable BD Tables Apr2019.Pdf
April 2019 Georgia Department of Public Health | Division of Health Protection | Maternal and Child Health Epidemiology Unit Reportable Birth Defects with ICD-10-CM Codes Reportable Birth Defects in Georgia with ICD-10-CM Diagnosis Codes Table D.1 Brain Malformations and Neural Tube Defects ICD-10-CM Diagnosis Codes Birth Defect ICD-10-CM 1. Brain Malformations and Neural Tube Defects Q00-Q05, Q07 Anencephaly Q00.0 Craniorachischisis Q00.1 Iniencephaly Q00.2 Frontal encephalocele Q01.0 Nasofrontal encephalocele Q01.1 Occipital encephalocele Q01.2 Encephalocele of other sites Q01.8 Encephalocele, unspecified Q01.9 Microcephaly Q02 Malformations of aqueduct of Sylvius Q03.0 Atresia of foramina of Magendie and Luschka (including Dandy-Walker) Q03.1 Other congenital hydrocephalus (including obstructive hydrocephaly) Q03.8 Congenital hydrocephalus, unspecified Q03.9 Congenital malformations of corpus callosum Q04.0 Arhinencephaly Q04.1 Holoprosencephaly Q04.2 Other reduction deformities of brain Q04.3 Septo-optic dysplasia of brain Q04.4 Congenital cerebral cyst (porencephaly, schizencephaly) Q04.6 Other specified congenital malformations of brain (including ventriculomegaly) Q04.8 Congenital malformation of brain, unspecified Q04.9 Cervical spina bifida with hydrocephalus Q05.0 Thoracic spina bifida with hydrocephalus Q05.1 Lumbar spina bifida with hydrocephalus Q05.2 Sacral spina bifida with hydrocephalus Q05.3 Unspecified spina bifida with hydrocephalus Q05.4 Cervical spina bifida without hydrocephalus Q05.5 Thoracic spina bifida without