Retinopathy of prematurity in multiple-gestation pregnancies

Retinopathy of prematurity in multiple-gestation pregnancies.




Blumenfeld LC, Siatkowski RM, Johnson RA, Feuer WJ, Flynn JT

Am J Ophthalmol 1998; 125:197-203.

Abstract
PURPOSE: To determine differences in incidence of retinopathy of prematurity between neonates of multiple-gestation and single-gestation pregnancies and to analyze differences in severity of retinopathy of prematurity among siblings of multiple-gestation pregnancies. METHODS: We reviewed the records of 149 neonates of multiple-gestation pregnancies and 691 single-gestation neonates screened for retinopathy of prematurity at one hospital from January 1, 1992, through December 31, 1995. The peak stage of retinopathy of prematurity was recorded for all infants. The multiple-gestation infants were then separated into concordant and discordant retinopathy of prematurity groups, with discordance defined as a difference of at least 2 stages of retinopathy of prematurity between siblings. Between siblings with discordant retinopathy of prematurity, multiple factors were compared. RESULTS: Retinopathy of prematurity was present in 69 (46%) of the multiple-gestation neonates. Retinopathy of prematurity was present in 312 (45%) of single-birth neonates. The percentage of multiple-gestation neonates with stages 1, 2, or 3 (prethreshold) or threshold retinopathy of prematurity was similar to that of single-gestation neonates. Stage 4 or 5 retinopathy of prematurity did not occur in either group. CONCLUSIONS: There was no significant difference in stage of retinopathy of prematurity between infants of single-gestation pregnancies vs those of multiple-gestation pregnancies. The majority (84%) of infants of multiple-gestation pregnancies had concordant retinopathy of prematurity. In those infants with discordant disease, zygosity and postgestational factors other than lowest serum glucose were not related to severity of retinopathy of prematurity.

MeSH
Adult; Birth Weight; Female; Florida; Gestational Age; Humans; Incidence; Infant, Newborn; Pregnancy; Pregnancy Outcome; Pregnancy, Multiple; Retinopathy of Prematurity; Severity of Illness Index

Author Address
Bascom Palmer Eye Institute, Department of Ophthalmology, Miami, FL 33101, USA.

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The outcome of pregnancies complicated by rubella, 1990-1997

The outcome of pregnancies complicated by rubella, 1990-1997]





Figueroa-Damián R, Ortiz-Ibarra FJ, Arredondo-García JL, Ahued-Ahued JR

Salud Publica Mex ; 41:271-7.

Abstract
OBJECTIVE: To describe the experience of management of pregnant women complicated with rubella and to evaluate the perinatal outcome. MATERIAL AND METHODS: A total of 67 pregnant women with positive IgM test for rubella were studied in the period from January 1st, 1990 to October 31st, 1997. Sixty-six of these women were followed until the end of gestation, in 4 patients an elective abortion was performed and 1 patient had a molar pregnancy. The effects of rubella on gestation and on the product were evaluated in sixty-one of the patients. Anti-rubella IgM was determined at birth and positive infants were subjected to evaluation by echocardiogram, brainstem auditory evoked potentials (BAEP) and ophthalmological study. RESULTS: Mean age of the patients was 24.7 +/- 5.5 years; 28 patients were primigravidae. Pregnancies were normal showing no complications due to the rubella episode. In 35 cases (52.2%), the viral infection occurred during the first trimester of pregnancy, in 23 cases (34.5%) during the second and in 9 (13.3%) during the third. Seventy-one percent of infants born to mothers infected during the first trimester of pregnancy were also infected, and 51.6% developed congenital rubella syndrome. The most frequent manifestations of CRS were: prematurity, low birth weight and alterations of the BAEP. CONCLUSIONS: In Mexico, rubella is still a cause of fetal damage, which shows the need for preventive strategies, such as universal vaccination, to avoid rubella infection during pregnancy.

MeSH
Adolescent; Adult; Female; Gestational Age; Humans; Incidence; Infant, Newborn; Mexico; Pregnancy; Pregnancy Complications, Infectious; Pregnancy Outcome; Rubella

Author Address
Departamento de Infectología, Instituto Nacional de Perinatología (INPer), México.

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Neovascular maculopathy associated with rubella retinopathy

[Neovascular maculopathy associated with rubella retinopathy]




Hirano K, Tanikawa A, Miyake Y

Nippon Ganka Gakkai Zasshi 2000; 104:431-6.

Abstract
BACKGROUND: We report three eyes of two patients with rubella retinopathy which were associated with choroidal neovascularization in the macula. CASES: A 7-year-old girl (case 1) and a 12-year-old girl (case 2) whose mothers had suffered rubella during their pregnancy revealed typical rubella retinopathy in both eyes and neovascular maculopathy in one eye at their initial visit to our clinic. Neovascular maculopathy developed in another eye of case 1 after a follow-up of 10 months. RESULTS: The clinical characteristics indicated that 1. sudden visual loss occurs in children, 2. there is no external trigger such as eye injury, and 3. the visual prognosis appears relatively good. CONCLUSION: Although neovascular maculopathy is rare in pediatric disease, the rubella retinopathy may have the potential to cause neovascular maculopathy.
MeSH
Child; Female; Humans; Macula Lutea; Macular Degeneration; Pregnancy; Pregnancy Complications, Infectious; Prenatal Exposure Delayed Effects; Retinal Diseases; Retinal Neovascularization; Rubella

Author Address
Department of Ophthalmology, Nagoya University School of Medicine, Japan.

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Optical coherence tomography in the management of acute retinopathy of prematurity

Optical coherence tomography in the management of acute retinopathy of prematurity.




Patel CK

Am J Ophthalmol 2006; 141:582-4.

Abstract
PURPOSE: To demonstrate the microscopic changes, in vivo, accompanying stage 4 retinopathy of prematurity. DESIGN: Interventional case study. METHODS: Optical coherence tomography (OCT) of the macula was performed in a baby with presumed stage 4a retinopathy of prematurity (retinopathy of prematurity). The findings were correlated with clinical staging and video indirect ophthalmoscopy. RESULTS: OCT changed the staging of retinopathy of prematurity from 4a to 4b, demonstrated intraretinal edema, and objectively confirmed the clinical impression of disease progression. CONCLUSIONS: OCT could be valuable as a new strategy in the staging and surgical management of retinopathy of prematurity.

MeSH
Acute Disease; Disease Progression; Female; Gestational Age; Humans; Infant, Newborn; Infant, Very Low Birth Weight; Laser Surgery; Ophthalmoscopy; Retina; Retinopathy of Prematurity; Tomography, Optical Coherence

Author Address
Oxford Eye Hospital, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, United Kingdom. ckpatel@btinternet.com

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Perinatal factors associated with retinopathy of prematurity

Perinatal factors associated with retinopathy of prematurity.




Gallo JE, Jacobson L, Broberger U

Acta Paediatr 1993; 82:829-34.

Abstract
The etiology of retinopathy of prematurity appears to be multifactorial. Introduction of new treatments in neonatal care may add new risk factors. We have analyzed the relationship between 42 perinatal factors and the development of retinopathy of prematurity in 78 infants with a birth weight < 1501 g and/or gestational age < 33 weeks. We have also applied a chronological analysis of the maximum and minimum pO2 and pCO2 values. Retinopathy of prematurity was seen in 37 of 78 infants (47.4%). Nineteen factors were found to be related to the development of retinopathy of prematurity. However, when step-wise logistic regression analysis was used, only birth weight, number of days of oxygen therapy and use of beta-blocking agents by the mother before birth were found to be associated with the development of retinopathy of prematurity. The results suggest that medication with beta blockers immediately before birth should be used cautiously.

MeSH
Blood Gas Analysis; Humans; Infant, Newborn; Infant, Premature; Prospective Studies; Retinopathy of Prematurity; Risk Factors

Author Address
Department of Ophthalmology, Huddinge University Hospital, Stockholm, Sweden.

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Persistent rubella infection and rubella-associated arthritis

Persistent rubella infection and rubella-associated arthritis.

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Chantler JK, Ford DK, Tingle AJ

Lancet 1982; 1:1323-5.

Abstract
Rubella virus has been isolated from peripheral blood lymphocytes in six out of seven women with rubella-associated arthritis. The arthritis occurred after natural infection (one case) or immunisation with HPV 77 DES vaccine (six cases) and had been present for up to 6 years. The identification of rubella virus was confirmed by plaque/microfocus reduction in the presence of anti-rubella antiserum, and by immunoprecipitation of rubella virus antigens and their analysis on polyacrylamide gels. These women with rubella virus in their lymphocytes did not have abnormal serum antibody levels, but a standard lymphoproliferative assay showed that they had strong cell-mediated immune responses to rubella virus antigens.

MeSH
Adult; Antibodies, Viral; Antigens, Viral; Arthritis, Infectious; Chronic Disease; Female; Humans; Immunity, Cellular; Lymphocytes; Rubella; Rubella Vaccine; Rubella virus; Time Factors; Vaccines, Attenuated

CAS Registry Number (Substance Name)
0 (Antibodies, Viral), 0 (Antigens, Viral), 0 (Rubella Vaccine), 0 (Vaccines, Attenuated)

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Prevalence of retinopathy of prematurity in premature babies examined during the period 1992-1999, Joinville (SC)

Prevalence of retinopathy of prematurity in premature babies examined during the period 1992-1999, Joinville (SC): evaluation of associated risks--screening.]





Bonotto LB, Moreira AT, Carvalho DS

Arq Bras Oftalmol ; 70:55-61.

Abstract
PURPOSES: To evaluate the prevalence of retinopathy of prematurity in premature babies examined at the "Hospital de Olhos Sadalla Amin Ghanem", coming from the "Maternidade Darcy Vargas" during the period from June 1992 to June 1999. To describe the risk factors that cause a predisposition to develop retinopathy of prematurity in the "Maternidade Darcy Vargas" and criteria to improve screening. METHODS: 286 premature babies were selected in accordance with the predetermined criteria (gestation period less than 37 weeks, first examination at 4-12 week of age, minimum of 3 ophthalmic examinations before being 180 days old and registration at the "Hospital de Olhos Sadalla Amin"). An analysis of the total group of premature babies was carried out, being classified into Group 1 (without retinopathy of prematurity) and Group 2 (with retinopathy of prematurity) and the factors related to presence or not of retinopathy of prematurity in the premature babies were described. In order to evaluate the frequency of retinopathy of prematurity and factors associated with its occurrence, the Chi-Squared or the Fisher Exact tests were used. Margin of error 5%. RESULTS: 228 premature babies did not present sings of retinopathy of prematurity (group 1) and 58 presented signs (group 2). The prevalence of retinopathy of prematurity was 20%, 9% being in stage 1; 7% in stage 2; 4% in stage 3 and 1% in stage 4a. The most involved factors were: birth weight (p<0.0001), oxygen therapy (p<0.0000), birth age (p=0.0006), lung disease (p=0.0041), blood transfusion (p=0.0002), central nervous system alterations (p=0.0259), serious infections (p=0.0278) and Apgar less than 7 in the first minute (p=0.0442). The premature babies that most needed treatment weighed less than 1,399 g and were 33 weeks old. CONCLUSION: According to the data the prevalence of retinopathy of prematurity was 20%. The premature babies' risks of retinopathy of prematurity were concentrated on weight below 1,400 g and age of 33 weeks. Bigger premature babies should be observed when one or more of the following factors are present: oxygen therapy, blood transfusion, lung disease, central nervous system alterations, serious infections and Apgar less than 7 in the first minute.

Author Address
Setor de Ciências da Saúde, Universidade Federal do Paraná, Curitiba, PR, Brazil. ligia@oftalmopediatria.com.br

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Retinopathy following measles, mumps, and rubella vaccination in an immuno-incompetent girl

Retinopathy following measles, mumps, and rubella vaccination in an immuno-incompetent girl.

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Schuil J, van de Putte EM, Zwaan CM, Koole FD, Meire FM

Int Ophthalmol 1998; 22:345-7.

Abstract
We describe a 4-year-old girl with subnormal visual acuity due to a bilateral retinopathy. The child had a history of encephalitis following MMR vaccination. Temporary retinopathy associated with measles, mumps, and rubella (MMR) vaccination has been described. Recently an idiopathic CD4+ T lymphocytopenia in the child was diagnosed. This cellular immunodeficiency supports our hypothesis of measles retinopathy after vaccination of an immuno-deficient child.

MeSH
CD4-Positive T-Lymphocytes; Child, Preschool; Diagnosis, Differential; Female; Humans; Immunoglobulin G; Measles; Measles Vaccine; Measles-Mumps-Rubella Vaccine; Mumps; Mumps Vaccine; Retinal Diseases; Rubella; Rubella Vaccine; T-Lymphocytopenia, Idiopathic CD4-Positive; Vaccines, Combined; Visual Acuity

CAS Registry Number (Substance Name)
0 (Immunoglobulin G), 0 (Measles Vaccine), 0 (Measles-Mumps-Rubella Vaccine), 0 (Mumps Vaccine), 0 (Rubella Vaccine), 0 (Vaccines, Combined)

Author Address
Bartiméus Institute of Visually Impaired Children, Zeist, The Netherlands.

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Retinopathy of prematurity: the life of a lifetime disease.

Retinopathy of prematurity: the life of a lifetime disease.

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Tasman W, Patz A, McNamara JA, Kaiser RS, Trese MT, Smith BT

Am J Ophthalmol 2006; 141:167-74.

Abstract
PURPOSE: To provide information on retrolental fibroplasias (RLF), later known as retinopathy of prematurity. DESIGN: Review of the literature on the subject and a first-person account of what was then RLF by one of the authors (A.P.) who was involved in the earliest days in research regarding RLF. METHODS: MEDLINE search on the topics of RLF and retinopathy of prematurity plus a first-person historic review of original work that dealt with RLF. RESULTS: In 1942, elevated levels of oxygen were thought to play a major role in the development of the disease; at that time, no treatment was available. During the lifetime of this disease, other possible causes have been investigated. These include vitamin E as a prophylaxis against retinopathy of prematurity and the efficacy of light reduction to prevent retinopathy of prematurity. It has been shown that the light reduction does not play a role in reducing the progression of retinopathy of prematurity. Vitamin E studies were inconclusive; some studies show a positive effect and others do not. A major advance occurred with the development of the International Classification of Ophthalmology in 1984, which laid the groundwork for collaborative studies to determine whether cryotherapy of the avascular zone of retina would reduce the incidence of blindness in newborn infants, when compared with control subjects. The study showed that cryotherapy was effective; this was followed by laser photocoagulation when lasers became portable enough to take to the neonatal intensive care unit. At the same time, improved surgical techniques moved from scleral buckling for retinal detachment to vitrectomies (some lens sparing) for more desperate cases that had progressed to stage 4 and stage 5 retinopathy of prematurity. Late changes in adults who were born before any treatment and are now baby boomers ran the gamut from the dragging of the retina in the posterior pole to retinal detachment, cataract, and myopia. CONCLUSION: Retinopathy of prematurity is a lifetime disease for which preventive and better treatment modalities continue to evolve.

MeSH
Animals; Disease Models, Animal; Humans; Hyperoxia; Infant, Newborn; Oxygen; Retinopathy of Prematurity

CAS Registry Number (Substance Name)
7782-44-7 (Oxygen)

Author Address
Department of Ophthalmology, Jefferson Medical College, and Wills Eye Hospital, 840 Walnut Street, Suite 1510, Philadelphia, PA 19107, USA. wst1@ureach.com

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Retinopathy of prematurity in multiple-gestation pregnancies

Retinopathy of prematurity in multiple-gestation pregnancies.




Blumenfeld LC, Siatkowski RM, Johnson RA, Feuer WJ, Flynn JT

Am J Ophthalmol 1998; 125:197-203.

Abstract
PURPOSE: To determine differences in incidence of retinopathy of prematurity between neonates of multiple-gestation and single-gestation pregnancies and to analyze differences in severity of retinopathy of prematurity among siblings of multiple-gestation pregnancies. METHODS: We reviewed the records of 149 neonates of multiple-gestation pregnancies and 691 single-gestation neonates screened for retinopathy of prematurity at one hospital from January 1, 1992, through December 31, 1995. The peak stage of retinopathy of prematurity was recorded for all infants. The multiple-gestation infants were then separated into concordant and discordant retinopathy of prematurity groups, with discordance defined as a difference of at least 2 stages of retinopathy of prematurity between siblings. Between siblings with discordant retinopathy of prematurity, multiple factors were compared. RESULTS: Retinopathy of prematurity was present in 69 (46%) of the multiple-gestation neonates. Retinopathy of prematurity was present in 312 (45%) of single-birth neonates. The percentage of multiple-gestation neonates with stages 1, 2, or 3 (prethreshold) or threshold retinopathy of prematurity was similar to that of single-gestation neonates. Stage 4 or 5 retinopathy of prematurity did not occur in either group. CONCLUSIONS: There was no significant difference in stage of retinopathy of prematurity between infants of single-gestation pregnancies vs those of multiple-gestation pregnancies. The majority (84%) of infants of multiple-gestation pregnancies had concordant retinopathy of prematurity. In those infants with discordant disease, zygosity and postgestational factors other than lowest serum glucose were not related to severity of retinopathy of prematurity.

MeSH
Adult; Birth Weight; Female; Florida; Gestational Age; Humans; Incidence; Infant, Newborn; Pregnancy; Pregnancy Outcome; Pregnancy, Multiple; Retinopathy of Prematurity; Severity of Illness Index

Author Address
Bascom Palmer Eye Institute, Department of Ophthalmology, Miami, FL 33101, USA.

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Rubella-associated arthritis. I. Comparative study of joint manifestations associated with natural rubella infection and RA 27/3 rubella immunisation

Rubella-associated arthritis. I. Comparative study of joint manifestations associated with natural rubella infection and RA 27/3 rubella immunisation.





Tingle AJ, Allen M, Petty RE, Kettyls GD, Chantler JK

Ann Rheum Dis 1986; 45:110-4.

Abstract
Joint manifestations observed during the course of a prospective RA 27/3 rubella immunisation trial were compared with those observed during an intercurrent wild rubella epidemic in an outlying community. Among 44 rubella haemagglutination inhibition (HAI) negative females ranging in age from 17 to 33 years who received rubella vaccine, six (13.6%) developed acute polyarticular arthritis within two to four weeks postvaccine and two (4.5%) had continuing or recurrent arthropathy lasting longer than 18 months. In contrast, among 23 females ranging in age from 11 to 39 years undergoing wild rubella infection, 12 (52.2%) developed acute polyarticular arthritis and seven (30.4%) had recurrent arthropathy 18 months postinfection. Among 23 males ranging in age from 13 to 54 years undergoing wild rubella infection, only two (8.7%) developed acute arthritis and both individuals had continuing joint manifestations 18 months postinfection. Wild rubella infection in adult populations is associated with a higher incidence, increased severity, and more prolonged duration of joint manifestations than is seen after RA 27/3 rubella immunisation.

MeSH
Adolescent; Adult; Arthritis, Infectious; Female; Humans; Joints; Rubella; Rubella Vaccine; Time Factors

CAS Registry Number (Substance Name)
0 (Rubella Vaccine)

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Significance of congenital mixed viral infection in the pathogenesis of retinopathy of prematurity

Significance of congenital mixed viral infection in the pathogenesis of retinopathy of prematurity]



Lozovskaia LS, Okhotnikova IM, Parameĭ OV, Sidorenko EI

Vestn Oftalmol ; 117:15-8.

Abstract
Forty-three infants aged 1-5 months with somatic and neurological diseases, including congenital, 18 of these with retrolental fibroplasia (RF) and 25 without RF were examined. Control group consisted of 36 age-matched infants. Based on identification of viral antigens in urine precipitate cells, mixed viral infection was diagnosed in 100% patients and 16.6% healthy babies. Ophthalmotropic ECHO 11 and 19 viruses were detected in 100% patients with RF, 28% patients without RF, and 10% healthy babies, while rubella virus was identified in 83.3, 60, and 8.3%, respectively. The viruses were detected only in association with other enteroviruses: Coxsakie A, B, and entero 69-71. These viruses detected in infants with RF were as a rule present in their mothers. Maternal anamnesis was in all cases aggravated by high risk indicators of vertical transfer of toxigenic enteroviruses to the fetus. The results indicate that congenital mixed viral infection (association of ophthalmotropic ECHO and rubella viruses with toxigenic Coxsakie and entero 69-71 viruses) is involved in the pathogenesis of RF.

MeSH
Adult; Age Factors; Coxsackievirus Infections; Disease Transmission, Vertical; Enterovirus B, Human; Enterovirus Infections; Female; Humans; Infant; Infant, Newborn; Male; Pregnancy; Pregnancy Complications, Infectious; Retinopathy of Prematurity; Rubella; Virus Diseases

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The prevalence of retinopathy of prematurity in very low birth weight newborn infants

The prevalence of retinopathy of prematurity in very low birth weight newborn infants.





Lermann VL, Fortes Filho JB, Procianoy RS

J Pediatr (Rio J) ; 82:27-32.

Abstract
OBJECTIVE: To evaluate the prevalence of retinopathy of prematurity and the risk factors affecting very low birth weight infants at a neonatal intensive care unit. METHODS: A cross-sectional study investigating all newborn infants with birth weights < or = 1,500 g and/or gestational ages < or = 32 weeks, admitted to the Neonatal ICU at the Hospital de Clínicas de Porto Alegre, from October 2002 to March 2004. Patients underwent indirect binocular ophthalmoscopy of the fundus at six weeks postpartum. Infants who progressed to threshold disease were given laser therapy. RESULTS: One hundred and fourteen newborn infants were studied. Eighty-three patients were not diagnosed with retinopathy of prematurity, 18 had stage I retinopathy of prematurity, seven stage II retinopathy of prematurity and six patients had threshold retinopathy of prematurity. The prevalence of retinopathy of prematurity was 27.2% (95% CI: 19.28-36.32) affecting 31 newborn infants, and the prevalence of retinopathy of prematurity progressing to threshold disease was 5.26% (95% CI: 1.96-11.10), affecting six patients. Retinopathy of prematurity was confirmed in 50% of the patients with weights below 1,000 g and 71.5% of newborn infants born at gestational ages of less than 28 weeks. Gestational age and birth weight were significantly lower among patients with retinopathy of prematurity than among those without. CONCLUSIONS: Although the results of this study demonstrate that the observed prevalence was similar to that described in literature, this ROP frequency remains elevated among very low birth weight infants. The development of retinopathy of prematurity was inversely proportional to weight and gestational age at birth.

MeSH
Apgar Score; Brazil; Epidemiologic Methods; Female; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Infant, Very Low Birth Weight; Intensive Care Units, Neonatal; Male; Ophthalmoscopy; Retinopathy of Prematurity

Author Address
Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil

Significance of congenital mixed viral infection in the pathogenesis of retinopathy of prematurity]

[Significance of congenital mixed viral infection in the pathogenesis of retinopathy of prematurity][Article in Russian]


Lozovskaia LS, Okhotnikova IM, Parameĭ OV, Sidorenko EI.
Forty-three infants aged 1-5 months with somatic and neurological diseases, including congenital, 18 of these with retrolental fibroplasia (RF) and 25 without RF were examined. Control group consisted of 36 age-matched infants. Based on identification of viral antigens in urine precipitate cells, mixed viral infection was diagnosed in 100% patients and 16.6% healthy babies. pOphthalmotropic ECHO 11 and 19 viruses were detected in 100% atients with RF, 28% patients without RF, and 10% healthy babies, while rubella virus was identified in 83.3, 60, and 8.3%, respectively. The viruses were detected only in association with other enteroviruses: Coxsakie A, B, and entero 69-71. These viruses detected in infants with RF were as a rule present in their mothers. Maternal anamnesis was in all cases aggravated by high risk indicators of vertical transfer of toxigenic enteroviruses to the fetus. The results indicate that congenital mixed viral infection (association of ophthalmotropic ECHO and rubella viruses with toxigenic Coxsakie and entero 69-71 viruses) is involved in the pathogenesis of RF.

PMID: 11569172 [PubMed - indexed for MEDLINE]

Congenital Rubella: Retinopathy

Congenital Rubella: Retinopathy



"Salt-and-pepper" retinopathy
This fine speckling of the retina is the commonest ocular manifestation of congenital rubella.
It is called "salt-and-pepper" because there are tiny flecks of dark pigment mixed with fine areas of whitish depigmentation. Usually the pigment alteration is diffuse, but it may be most prominent either around the macula or in the retinal periphery.

These signs reflect diffuse damage to the retinal pigment epithelium (RPE). The good news is that the RPE is never damaged enough to interfere with vision or to cause major abnormalities in the electroretinogram (ERG), the standard objective test used to evaluate outer retinal function. The preservation of vision and a relatively or completely normal ERG allows you to differentiate rubella retinopathy from the hereditary retinal degenerations called retinitis pigmentosa.

Other causes of "salt-and-pepper" retinopathy are congenital syphilis, and toxicities of systemically administered thioridazine, choroquine, and deferoxamine.

Other ophthalmic complications include microphthalmia (small eye), cataract, glaucoma, corneal opacification, and uveitis. Vision is usually quite poor from these problems.

Congenital rubella is a multisystem disorder resulting from exposure of the fetus to maternal rubella during the first trimester of pregnancy. Ophthalmic complications are present in over 70% of patients.

The Global Initiative Vison 2020: The Right to Sight Childhood Blindness

The Global Initiative Vison 2020: The Right to Sight Childhood Blindness
David Yorston, FRCS FRCOphth
David Yorston, Eye Unit of Kikuyu Hospital, PO Box 45, Kikuyu, Kenya;
Top
Blindness in Children Worldwide
The Global Initiative and Childhood Blindness
Corneal Scarring
Congenital Cataract
RETINOPATHY OF PREMATURITY
Conclusion Blindness in Children WorldwideApart from cataract, trachoma and onchocerciasis, which are specific diseases, the Global Initiative has also targeted childhood blindness—blindness from any cause occurring in a person aged 15 or less. Why is this relatively uncommon problem such a high priority?
Childhood blindness is the second largest cause of blind-person years, following cataract. Globally, about 70 million blind person years are caused by childhood blindness. There are about 1.5 million blind children worldwide, and this number appears to be growing. Approximately 500,000 children become blind every year—one every minute—and about half of them die within one or two years of becoming blind. Approximately one third of the total economic cost of blindness is thought to be due to childhood blindness.
A child's eye is not merely a smaller version of an adult eye, and childhood blindness is different compared with adult blindness. Strategies that are effective against adult blindness need to be modified to combat childhood blindness.
Children are the most precious resource of families in developing countries. A blind child is a tragedy for these families. A child whose blindness could have been prevented or cured is an even greater disaster. Approximately 40% of childhood blindness is avoidable.
Corneal scarring after vitamin A deficiency

The different causes of avoidable blindness in children vary with geographical location, and with time. For example, the avoidable causes of childhood blindness in western Europe are very different to the avoidable causes in sub-Saharan Africa. However, even in the very poor countries in Africa, improvements in nutrition and primary health care have meant that blindness from vitamin A deficiency is less common than it was 25 years ago. It must also be expected that severe economic recession, or the destruction of health care systems by war or natural disaster, could lead to the re-emergence of conditions that had previously been controlled.
Top The Global Initiative and Childhood BlindnessThe goal of the Global Initiative is to reduce childhood blindness from its present level of 0.75/1,000 children to 0.4/1,000 children by 2020. To achieve this, three conditions must be controlled. They are:
corneal scarring in children
congenital cataract
RETINOPATHY OF PREMATURITY

Top
Blindness in Children Worldwide
The Global Initiative and Childhood Blindness
Corneal Scarring
Congenital Cataract
Retinopathy of Prematurity
Conclusion Corneal ScarringGreat improvements have already taken place in the prevention of corneal scarring. Primary health care programmes are distributing vitamin A, and immunising against measles. Traditional healers have been trained to avoid harmful practices. The greater availability of primary eye care has enabled children with corneal ulcers to be treated sooner and more effectively. However, despite these changes thousands of children become blind from corneal scarring every year, and many of them die. Goals for 2020 may include the total elimination of measles, and vitamin A deficiency, both of which are achievable targets.
Much of the work that has been done to prevent corneal scarring in children has been carried out by primary health care (PHC) programmes. PHC workers are often unaware of the great impact their services have. In future, prevention of childhood blindness should be a particular and recognised part of PHC.
Healthy eyes in Jamaica

Some children, particularly those with corneal dystrophies such as keratoconus, may benefit from corneal transplants. The role of penetrating keratoplasty in prevention of childhood blindness is unclear, and more research is required.
Top
Blindness in Children Worldwide
The Global Initiative and Childhood Blindness
Corneal Scarring
Congenital Cataract
Retinopathy of Prematurity
Conclusion Congenital CataractThis remains a major cause of blindness in low- and middle-income countries. Some congenital cataract may be preventable. For example, it is estimated that 50,000 children every year are born with cataracts caused by congenital rubella syndrome, which could be prevented by a programme of rubella immunisation. Several high- and middle-income countries have set a goal of eliminating new cases of congenital rubella syndrome by the year 2000. This goal should be extended to cover the rest of the world by 2020.
The results of cataract surgery in children with congenital cataract are frequently poor. The treatment and post-operative care of these patients requires special skills and experience, and expensive equipment. It is likely that outcomes would be improved if all congenital cataracts were operated on in tertiary centres—‘children's eye centres’. Approximately ten million people require one such centre. The centre requires at least one ophthalmologist with a special interest in childhood eye disease; and two low vision therapists, able to monitor visual acuity in young children, treat amblyopia, and manage any residual visual impairment.
There is uncertainty over the best way to manage congenital cataract. The role of intraocular lenses in children under two years of age remains very controversial. Removal of the posterior capsule at the time of initial surgery is the best way of guaranteeing a clear visual axis. However, there is a need for more research to clarify these issues.
Top
Blindness in Children Worldwide
The Global Initiative and Childhood Blindness
Corneal Scarring
Congenital Cataract
Retinopathy of Prematurity
Conclusion Retinopathy of PrematurityRetinopathy of prematurity (ROP) remains an important cause of blindness in children in high- and middle-income countries. In high-income countries, it is known that neonates under 1500g are at risk of ROP. In middle-income countries, the risk factors are much less clearly defined, and ROP may affect babies weighing more than 2000g at birth.
ROP may be partially preventable through improved obstetric and neonatal care and a reduction in the number of premature babies. Babies at risk of ROP must be examined by a trained ophthalmologist. Those with ‘threshold’ ROP disease require peripheral retinal ablation, either with cryotherapy or laser. The treatment of these children is best carried out in specialist children's eye centres, by appropriately trained, and adequately equipped, ophthalmologists.
More research is needed to clarify which babies are at risk of ROP in middle-income countries, in order to develop a clear screening regimen.
Top ConclusionThe goal of reducing childhood blindness by 2020 is achievable. It will require an emphasis on eliminating the causes of childhood blindness at the primary level, and the development of specialist centres for treating congenital cataract, glaucoma, and ROP at the tertiary level. To facilitate the planning of childhood blindness programmes, a table of the estimated needs of a population of ten million people, in different situations, is shown below.
Table
Estimated Needs for a Total Population of Ten Million

Congenital cataract

FootnotesFootnote: Figures included in David Yorston's article on Childhood Blindness have still to be officially ratified by the World Health Organization, but we are advised by WHO that a review and compilation of data presented is underway.
Editor.


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Did Findings Develop in Utero?

Did Findings Develop in Utero?

Patient with retinal pigmentary changes reports childhood cardiac problems and maternal infection with German measles while pregnant.

Mark T. Dunbar, O.D.







A 36-year-old white female presented for her routine eye exam. As part of her history, she reported symptoms of dizziness that she had been experiencing for one week. She said that she felt better after eating. She reported no history of nausea, vomiting, visual aura or migraines.

Her medical history was significant for asthma for which she takes albuterol. She was born with a heart murmur and underwent heart valve surgery at age 4. Also, she reported that her mother had German measles when pregnant with the patient. Ocular history was unremarkable, but she said that at prior exams, several doctors commented on how interesting her eyes are.

Best-corrected visual acuity was 20/20 O.U. at distance and near. Pupils were equal and reactive with no afferent pupillary defect. Motility and confrontational fields were full. The anterior segment exam was unremarkable. IOP measured 15mm Hg O.U.

Dilated fundus exam showed a healthy optic nerve with a small cup and good rim coloration O.U. Each macula was flat with yellowish coloration, and vessels appeared normal O.U. Peripheral clinical findings are shown in figures 1 and 2.




1,2. Dilated fundus exam (O.D. left, O.S. right) revealed unusual pigmentary changes.



Take the Retina Quiz
1. How would you describe the fundus findings?
a. Tigroid fundus.
b. Salt and pepper retinopathy.
c. Bone spicule formation.
d. Choroidal folds.

2. What is the likely diagnosis?
a. Retinitis pigmentosa.
b. Congenital rubella retinopathy.
c. Syphilis retinopathy.
d. Ocular albinism.

3. What is the likely etiology?
a. Autoimmune.
b. Virus.
c. Trauma.
d. Bacterial.

4. What additional testing would be most beneficial?
a. Ocular coherence tomography.
b. Electroretinogram.
c. B-scan ultrasonography.
d. Pachymetry.

5. What do the changes around the optic nerve likely represent?
a. Peripapillary atrophy.
b. Myopic crescent.
c. Angioid streaks.
d. Nonspecific changes to the retinal pigment epithelium.

For answers, see bottom of page.

Discussion
The mother’s history of German measles during her pregnancy is evidence that this patient has congenital rubella pigmentary retinopathy.

Rubella infection affects children and young adults but often goes undetected. It results from an RNA virus of the Togaviridae family.

The systemic and ocular complications that manifest with rubella infection in utero are called congenital rubella syndrome (CRS).1 CRS results from primary maternal infection of rubella during the first trimester of the pregnancy. The fetus is most vulnerable to rubella insult in the first 16 weeks of gestation because specific immunity against the virus is undeveloped during the first two trimesters of pregnancy. The virus transplacentally infects the developing fetus and is disseminated in the bloodstream, inhibiting cell growth.

The World Health Organization encourages member countries to eradicate CRS by 2010.1 New CRS cases have been rare since the introduction of the measles-mumps-rubella (MMR) vaccine in 1969.2 The Centers for Disease Control and Prevention recommends vaccinations at age 12 to 15 months and again at age 4 to 6.3

CRS can lead to multisystemic malformations, resulting in severe morbidity and mortality. Malformations most associated with CRS are auditory (sensorineural deafness), cardiac (patent ductus arteriosus) and neurologic (microcephaly and mental retardation).

CRS also can affect almost all ocular structures. CRS can be diagnosed in the presence of these three common signs, either in isolation or in combination, even with a lack of laboratory evidence:2,4

• Congenital cataracts (also known as rubella cataracts). These usually present as dense, symmetrical and bilateral cataracts. The virus enters the lens prior to development of a lens capsule that would otherwise act as a barrier to the virus. Rubella cataracts most commonly occur at the fetal nuclear level.

• Pigmentary retinopathy. A diffuse disturbance of the retinal pigment epithelium (RPE) often has a “salt-and-pepper” appearance. Pigment deposits may vary from fine, powdery, sprinkled or granular shapes throughout the retina. Persistence of the virus in the RPE often causes progression during childhood. This can lead to subretinal neovascularization and subsequent macular scarring, usually in the second decade of life.

• Congenital glaucoma with buphthalmos. This can occur in approximately 10% of infants diagnosed with CRS.3 Glaucoma also can manifest at a later stage in these patients, possibly due to virus-induced trabeculodysgenesis. Delayed-onset glaucoma is more commonly associated with microphthalmos. These patients have a poor visual prognosis.

Less common ocular complications of CRS include iris atrophy, uveal coloboma, nystagmus, strabismus, corneal haze, optic atrophy and high refractive error.

Ancillary testing for patients with CRS may include optical coherence tomography and fluorescein angiography when there is a high suspicion of choroidal neovascularization, visual field exam as part of a standard glaucoma assessment, and electroretinogram (ERG) to aid in the differential diagnosis of CRS and retinitis pigmentosa (RP), which is similar in appearance. ERG is normal in patients who have CRS but abnormal in those who have RP. Our patient’s ERG was normal.

The severity of ocular complications of CRS varies among patients. Our patient only presented with bilateral pigmentary retinopathy. Small angioid streaks were present around the optic nerve, but we believe these were an incidental finding.

Pigmentary retinopathy is common among congenital infections, such as cytomegalovirus, toxoplasmosis and syphilitic retinopathy. Thus, the diagnosis of CRS requires a positive serological finding or history of maternal measles infection, as in our patient. Our patient also presented with congenital cardiac deficits, one of the systemic complications associated with CRS.

We must closely monitor patients who have CRS for the development of glaucoma. Our patient currently has no risk factors for glaucoma. We plan to monitor her annually. We do not know why she experienced dizziness, but we told her to see her primary-care doctor if her symptoms continue.

Written by Neha Patel, O.D., an optometry resident at Bascom Palmer Eye Institute in Miami.

1. Khandekar R, Al Awaidy S, Ganesh A, Bawikar S. An epidemiological and clinical study of ocular manifestations of congenital rubella syndrome in Omani children. Arch Ophthalmol 2004 Apr;122(4):541-5.
2. Weisinger HS, Pesudovs K. Optical complications in congenital rubella syndrome. Optometry 2002 Jul;73(7):418-24.
3. Watson JC, Hadler SC, Dykewicz CA, et al. Measles, mumps, and rubella—vaccine use and strategies for elimination of measles, rubella, and congenital rubella syndrome and control of mumps: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 1998 May 22;47(RR-8):1-57.
4. Vijayalakshmi P, Kakkar G, Samprathi A, Banushree R. Ocular manifestations of congenital rubella syndrome in a developing country. Indian J Ophthalmol 2002 Dec;50(4):307-11.

Answers: 1) b; 2) b; 3) b; 4) b; 5) c.

Childhood Blindness

Childhood Blindness

As the causes of blindness in children differ from those in adults, different control measures are needed. In low-income countries, high proportions of children are blind from preventable causes, which require community-based interventions. In all regions, children with treatable diseases, principally cataract, can have their sight restored. Childrens’ eyes cannot, however, be considered smaller versions of adults’ eyes, and specific expertise and equipment are required. Unlike adults, children require longterm follow-up after surgery, to manage complications and to prevent amblyopia (‘lazy eyes’). The understanding and involvement of parents is critical. In all regions, children with irreversible visual loss must be assessed for low-vision services, early visual stimulation, rehabilitation or special education, depending on their age and level of residual vision.

Current situation

It has been estimated that there are 1.4 million blind children in the world, 1 million of whom live in Asia and 300 000 in Africa (26). The prevalence ranges from 0.3/1000 children aged 0–15 years in affluent countries to 1.5/1000 children in very poor communities. Although the number of blind children is relatively low, they have a lifetime of blindness ahead, with an estimated 75 million blind-years (number blind × length of life), second only to cataract.
The same report showed that 500 000 children become blind each year (nearly one per minute). Many die in childhood from the underlying cause, such as measles, meningitis, RUBELLA , prematurity, genetic diseases and head injuries. Most blind children are either born blind or become blind before their fifth birthday. Owing to demographic differences, the number of children who are blind per 10 million population varies from approximately 600 in affl uent countries to approximately 6000 in very poor communities. About 40% of the causes of childhood blindness are preventable or treatable.


The causes of childhood blindness vary, but the main avoidable causes are:

corneal scarring in Africa and poorer countries in Asia;
cataract everywhere
glaucoma everywhere;
retinopathy of prematurity in high- and middle-income countries and some cities in Asia;
refractive errors everywhere, but particularly in South-East Asia; and
low vision, which encompasses visual impairment and blindness from untreatable causes, in all regions.
The main causes of blindness in children change over time. As a consequence of child survival programmes (for example, integrated management of childhood illness), corneal scarring due to measles and vitamin A defi ciency is declining in many developing countries, so that the proportion due to cataract is increasing. Retinopathy of prematurity is emerging as an important cause in the middle-income countries of Latin America and eastern Europe and is likely to become an important cause in Asia over the next decade. The prevalence of refractive errors, particularly myopia, is increasing in school-age children, especially in South-East Asia

Achievements
Vitamin A deficiency: There are concerted global efforts to control vitamin A deficiency in children and women of child-bearing age. The United Nations Children’s Fund (UNICEF) has estimated (27) that between 1998 and 2000 about 1 million child deaths were prevented by these global efforts, and the Vitamin A Global Initiative led by UNICEF has set the target of eliminating vitamin A deficiency by the year 2010.
Measles: Measles immunization coverage continues to improve, resulting in a lower incidence of measles and measles-related deaths. In 2004, there were 454 000 deaths from measles, a reduction of 48% from 1999. The Measles Initiative (28), a partnership between the American Red Cross, the United States Centers for Disease Control and Prevention, the United Nations Foundation, UNICEF and WHO, is now focusing on 47 countries, mainly in sub-Saharan Africa where 98% of deaths occur, with the goal of reducing deaths from measles by 90% by 2010 from the estimates for 2000. The WHO Region of the Americas has eliminated measles, and three other regions have set elimination targets. Reducing the prevalence of measles will also reduce the number of children with measles-related corneal ulceration and scarring.
Retinopathy of prematurity: Programmes for detecting and treating severe retinopathy in premature infants at risk are expanding throughout Latin America and eastern Europe and are being established in urban areas in China, India and other Asian countries.
Child eye-care centres: Training in paediatric ophthalmology is becoming more prevalent, and tertiary level child eye-care centres are being set up in low-income countries.
Consumables for children: Low-vision devices suitable for children as well as other consumables are available through resource centres in Hong Kong, China, and Durban, South Africa.
Limitations
inadequate population-based data on the prevalence and causes of blindness in children;
lack of awareness among parents and the community about preventive measures and that the vision of children who are blind can often be improved or maximized;
barriers to accessing services, including lack of awareness, distance, cost, fear and competing demands for scarce resources within the family;
shortage of paediatric eye-care professionals and inadequate opportunities for training in paediatric ophthalmology in most low-income countries;
lack of international exchanges in human resource development for paediatric ophthalmology and insufficiently developed postgraduate curricula for training paediatric ophthalmologists in many industrialized countries;
fragmentation of paediatric eye-care services in many countries, so that children who need specialist expertise are managed by general ophthalmologists; and
inadequate provision of special education for children with irreversible visual loss, particularly in low-income countries.
Aim
to eliminate avoidable causes of blindness in children
Objectives
to promote programmes that reduce corneal scarring and visual loss from vitamin A deficiency and measles and
to implement interventions against harmful traditional practices, neonatal conjunctivitis and eye injuries;
to provide services to treat children with cataract, glaucoma, retinopathy of prematurity and corneal ulcer or scarring;
to provide optical services for children with refractive errors, for instance in school eye-health programmes; and to provide services for children with low vision.
Strategies
Provide comprehensive services for children at all levels of service delivery'
In areas where childhood blindness from preventable diseases is common, increase awareness in the community and encourage primary health care, including specific preventive measures at the primary level, through primary eye care, including:

measles immunization, to prevent corneal scarring;
vitamin A supplementation, nutrition education, food supplementation and fortification of commonly eaten foods with vitamin A, to control vitamin A deficiency;
avoidance of harmful traditional practices, to prevent corneal scarring; ocular prophylaxis of newborns, to prevent neonatal conjunctivitis; and
rubella immunization where congenital rubella is an important cause of mortality or morbidity in children, with strategies appropriate to the setting (e.g. schoolgirls aged 12–13 years).
At the secondary level, strengthen diagnosis and management of less complex cases.
At the tertiary level, provide specialist training and services for the management of surgically remediable visual loss from cataract, congenital glaucoma and corneal scarring, including longterm follow up. Examine premature infants at risk of retinopathy of prematurity, treat those with severe disease and promote oxygen monitoring.
As children with cataract often do not present, or present late, undertake active case finding, particularly for girls.
Provide each child eye-care centre with a well-trained team (e.g. paediatric or child-centred ophthalmologist, optometrist, anaesthetist, counsellor, low-vision therapist, mid-level personnel), appropriate equipment and infrastructure and access to consumables for infants and children (e.g. small spectacle frames, high-power intraocular lenses).
Ensure the availability of ophthalmologists experienced in indirect ophthalmoscopy to identify premature infants in intensive neonatal care who require treatment for retinopathy of prematurity.
Ensure that infants at risk have fundus examinations starting 4–6 weeks after birth and that infants with severe disease are treated immediately by laser or cryotherapy.
Develop low-vision services for children with irreversible visual loss at secondary and tertiary levels.
Promote school eye-health programmes:
for the diagnosis and management of common conditions, such as refractive errors, and trachoma and vitamin A deficiency in endemic areas;
to promote a healthy environment; and
to educate children in looking after their eyes as part of the normal school curriculum.
In areas where significant uncorrected refractive errors affect more than 2% of schoolchildren aged 11–15 years (29).
Ensure that children undergo a simple vision screening examination, ideally as part of the school health programme, with provision of spectacles to those who will benefit.
Ensure that all children in special education establishments are examined by an ophthalmologist and receive medical, surgical, optical or low-vision services to maximize their vision.
Ensure good linkages between eye-care services and those providing education and rehabilitation services for incurably blind children.
Targets
By 2011, each country’s national plan will include the control of blindness in children, with achievable targets.
For disease control:
reduction in the global prevalence of blindness in children from 0.75/1000 to 0.4/1000 by the year 2020;
reduction in corneal scarring caused by vitamin A deficiency, measles, neonatal conjunctivitis and the use of traditional eye remedies;
reduction in the proportion of blindness due to retinopathy of prematurity, particularly in countries where it is responsible for more than 10% of blindness in children; and appropriate management of children with cataract, with immediate, effective optical correction in suitably equipped specialist centres.
For human resource development:
prevention of blindness in children an explicit aim of primary health care programmes and included in all primary eye-care training curricula
personnel in secondary-level eye clinics with knowledge and skills necessary to manage less complex eye conditions in children; and
at least one child eye-care centre with a well-trained team for every 20 million population by the year 2011 and one per 10 million by 2020.
For infrastructure and technology
all child eye-care centres have adequate supplies of consumables for children, e.g. paediatric aphakic spectacles and low-power, small-diameter intraocular lenses; and
secondary-level eye clinics have facilities to provide appropriate spectacles for children with refractive errors.
Indicators
prevalence of childhood blindness;
prevalence of avoidable childhood blindness, by cause
number of child eye-care centres per at least 20 million population (recommended);
from other WHO programmes:
proportion of countries with measles immunization coverage > 80%;
proportion of countries with vitamin A deficiency control programmes or with eliminated vitamin A deficiency, in line with global targets; and
proportion of countries with a policy or immunization programme for rubella.
Trachoma

Trachoma, which is the commonest infectious cause of blindness, is caused by Chlamydia trachomatis. Children who have the active stages of the disease are the reservoir of infection, while blindness, which occurs after repeated episodes of infection, principally affects adults. Boys and girls are equally affected by active infection, while blindness is more common in women. Trachoma is a condition of poverty and is a focal disease, affecting communities that have poor water supplies and sanitation and poor health services. The organism is transmitted from person to person through direct and indirect contact and by flies. Blindness can be prevented by surgery to correct inturning of the upper lid (trichiasis),
while the infection and its transmission can be reduced with surgery, antibiotics, facial cleanliness and environmental change (the SAFE strategy).

Current situation
Trachoma is endemic in 55 countries: Afghanistan, Algeria, Australia, Benin, Brazil, Burkina Faso, Cambodia, Cameroon, Central African Republic, Chad, China, Côte d’Ivoire, Djibouti, Egypt, Eritrea, Ethiopia, Fiji, Gambia, Ghana, Guatemala, Guinea, Guinea-Bissau, India, Islamic Republic of Iran, Iraq, Kenya, Kiribati, Lao People’s Democratic Republic, Libyan Arab Jamahiriya, Malawi, Mali, Mauritania, Mexico, Morocco, Mozambique, Myanmar, Namibia, Nepal, Niger, Nigeria, Oman, Pakistan, Papua New Guinea, Senegal, Solomon Islands, Somalia, Sudan, Togo, Uganda, United Republic of Tanzania, Vanuatu, Vietnam, Yemen, Zambia and Zimbabwe. The estimated number of affected people has fallen from 360 million in 1985 to about 80 million today. Trachoma affects the poorest and most remote rural areas of Africa, Asia, Central and South America, Australia and the Middle East (30). Updated reports on 36 countries are available (31), while 19 endemic countries have not yet reported data.


There are approximately 10.6 million people with inturned eyelashes (entropion trichiasis), for which eyelid surgery is needed to prevent blindness. The majority of these people are women. An estimated 5.9 million adults are irreversibly visually impaired from corneal scarring due to trachoma.

Achievements

At national level, political support for trachoma control has increased continually since 1997, the year the WHO Alliance for the Global Elimination of Blinding Trachoma (GET 2020) was created; intersector collaboration is growing, and use of the SAFE strategy for eliminating the disease is increasing.


GET 2020 is active at the global level. It is a public–private partnership, bringing together WHO, national coordinators, nongovernmental organizations, donors and international experts, with support from the pharmaceutical industry. Launched in 1997, it was endorsed by WHA Resolution 51.11, adopted in 1998. A nongovernmental organization task force, the International Coalition for Trachoma Control, has been working since 2004 within the framework of GET 2020 to improve information exchange with governments and to coordinate the efforts of international nongovernmental organizations in countries. The GET 2020 secretariat is responsible for trachoma within the WHO department focusing on neglected tropical diseases. The WHO GET 2020 secretariat is also coordinating the drawing up of guidelines for certification of elimination of blinding trachoma, as requested by several WHO Member States.

Limitations
Not all countries in which blinding trachoma is suspected to be endemic have undertaken a proper assessment of the epidemiological situation of trachoma.
The WHO SAFE strategy does not yet cover 100% of the populations in trachoma-endemiccountries.
International partners who are members of the WHO GET 2020 Alliance do not implement the entire SAFE strategy, but only certain components.
The available resources for trachoma control are not suffi cient to achieve the ultimate intervention goals in all countries.

Aim
Global elimination of blindness due to trachoma by the year 2020 by applying the WHO-recommended SAFE strategy
Objectives
Integrate the SAFE strategy into primary health care in all communities with blinding trachoma.
Certify the elimination of trachoma in countries, where applicable.
Strategies
Identify districts where blinding trachoma is a public health problem
Provide surgical services with trained and certifi ed medical or paramedical staff at community level to operate on cases of trachomatous trichiasis.
Provide mass antibiotic administration (azithromycin or tetracycline ointment) for populations living in districts where the prevalence of active disease (follicular trachoma) in children aged 1–9 years is above 10%. In districts where the prevalence is below 10% but above 5%, community or family treatment might be required. The treatment interventions must be implemented in association with promotion of personal hygiene, with particular focus on facial cleanliness of children under 10 and improvement of environmental hygiene and sanitation as part of primary health care.
During the 10th Meeting of GET 2020 (31), the following recommendations were adopted to facilitate implementation of the SAFE strategy:
All endemic countries should establish collaboration with the WHO GET 2020 Secretaria
All endemic countries, particularly the more populous countries, should continue to assess the distribution and severity of trachoma, e.g. by rapid assessment
Countries should develop their strategic 5-year national trachoma plans, in collaboration with national and international partners, reflecting the commitment to implement the SAFE strategy; these plans should be integrated into their VISION 2020 national plans (WHA Resolution 56.26).

WHO should design methods and tools for assessing the trachoma burden and for certifying elimination of the disease.
Countries should endeavour to increase coverage of all the components of the SAFE strategy to the highest possible level.
In countries in which active trachoma prevalence has declined to < 5%, rapid assessment might be the most useful tool for identifying communities that need trachoma control activities as a priority in order to eliminate remaining pockets of the disease.
Countries should institute an ongoing audit of the quality of trichiasis surgery on the basis of the WHO guidelines for assessment (32)
Increased intersectoral collaboration should be instituted at national and district levels to ensure comprehensive implementation of all components of the SAFE strategy.
WHO and the international development community should advocate and promote trachoma as a marker of poverty and GET 2020 as a model of a public–private partnership for tackling the problem.
Target

By 2020, all 49 countries where endemic trachoma has been confi rmed should have achieved their ultimate intervention goals. The countries with plans for achieving those goals are shown in table 3
Indicators
number of countries with blinding trachoma as a public health problem;
proportion of endemic communities covered by the SAFE strategy;
recommended, where applicable:
• prevalence of trachomatous entropion trichiasis at district level;
• prevalence of active trachoma in 1–9-year-olds at district level; and
• progress in achieving the ultimate intervention goals.


National data are being used to refi ne ultimate intervention goals and annual intervention objectives in countries. The data are included in WHO information on neglected tropical diseases, in the WHO Global Health Atlas and in the WHO Infobase.

How To Do Pelvic Floor Muscle Exercises (Kegel's)

How To Do Pelvic Floor Muscle Exercises (Kegel's)

Frederick R. Jelovsek MD


Many Women with urinary incontinence can decrease their urinary leakage during coughing, laughing, sneezing, or other activities by exercising the muscles of the pelvic floor. These exercises are often called "Kegel exercises" after the doctor, Arnold Kegel, M.D., who first described them.

To find the muscle you need to exercise, imagine that you have a tampon in your vagina that is falling out and you must tighten your muscle in order to hold it in. The muscle you tighten is the muscle you should exercise. Another way to find the right muscle, the bulbocavernosis muscle, is to sit on the toilet, place one finger in the vagina and contract that muscle around you finger. The muscle you use to tighten around your finger is the muscle you should exercise. Your doctor can help you determine which muscle to contract and make sure you are doing it properly by checking you during a pelvic examination.

Do not make a habit of doing these exercises by starting and stopping your urine flow while voiding! You can teach yourself bad bladder habits and develop voiding difficulty by doing this! Instead, you should practice your exercises at other times. Stopping your urine stream during voiding is taught by others only to help you find the correct muscle to contract .

Pelvic muscle exercises can be done in many different ways. We will give you instructions on how to do the type of exercise described by Dr. Kegel. Since continued vigorous exercise can lead to muscle soreness and fatigue, don't try to start out at maximum exercises all at once. Spread them out over the course of the day. We suggest starting with 25 muscle contractions divided into 3 daily sessions. This should take 5 minutes 3 times a day. You should eventually build up to 20 minutes (100 contractions) 3 times a day. If you do have muscle soreness starting out, try doing the exercises vigorously every other day instead. this will allow your muscle to recover from the fatigue of exercise.

These exercises can be done anywhere and at any time. You may find it helpful to associate an activity with your muscles, such as doing them while stopped at a red light, during a TV commercial, talking on the phone, or doing various household chores such as ironing, washing dishes, cooking, etc. The important think is to get in the habit of doing them!
Initially - Tighten the pelvic floor muscles for count of six and relax for six seconds. Each contraction cycle should last 12 seconds or 5 contractions a minute. Repeat 25 times. Do this 3 times each day - total 75 contractions.

Week 2 - Tighten the pelvic floor muscles for 6 seconds every 12 seconds (5 per minute) for 10 minutes, 50 contractions. Do this 3 times each day - total 150 contractions.

Week 3 - Tighten the pelvic floor muscles for 6 seconds every 12 seconds (5 per minute) for 15 minutes, 75 contractions. Do this 3 times each day - total 225 contractions.

Weeks 4-24 - Tighten the pelvic floor muscles for 6 seconds every 12 seconds (5 per minute) for 20 minutes, 100 contractions. Do this 3 times each day - total 100 contractions.

After 24 months - Continue maintainence at 10 minutes three times a day or 15 minutes twice a day, total of 150 contractions a day.
You may notice some soreness in the pelvic muscles and around the vaginal opening once you start exercising regularly. Do not worry about this - it is only soreness associated with increased muscle activity. The benefits of these exercises will continue ONLY as long as you do them! Use it or lose it! You should expect to have to do these exercises regularly for three months before you notice an improvement in your urine loss. At six months of regular exercise you will get maximum effect.

If at any time you think you are getting headaches, chest discomfort or abdominal muscle discomfort, then you are contracting other muscles in addition to, or instead of the bulbocavernosis muscle. Concentrate on just the perineum, while relaxing all other muscles.



From BackupMD

Pelvic Floor Muscle Training (Kegel Exercises)

Pelvic Floor Muscle Training (Kegel Exercises)
What is pelvic floor muscle training?
Why should I do pelvic floor muscle exercises?
How do you do pelvic floor muscle exercises?
Important Tips for pelvic floor muscle exercises
What are the most common mistakes made during pelvic muscle exercises?
When should I use the pelvic floor muscles?
How can I work this new health habit into my everyday life?


What is pelvic floor muscle training?
It is a daily training program for the muscles that support the uterus, bladder and other pelvic organs. It is also called Kegel exercise or pelvic muscle rehabilitation. This exercise will help your pelvic muscles prevent accidental urine leakage.

Back to Top
Why should I do pelvic floor muscle exercises?
Regular pelvic floor muscle exercises make the muscles that support your pelvic organs stronger and helps you use the muscles more effectively. Women who have a problem with urine leakage have been able to eliminate or greatly improve this problem just by doing pelvic floor muscle exercises each day. Pregnant and postpartum women who do pelvic floor muscle exercises have significantly less urine leakage.

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How do you do pelvic floor muscle exercises?
When you are doing pelvic floor muscle exercises in a way that will build muscle strength you will feel all the muscles drawing inward and upward. A good way to learn the exercise is to pretend that you are trying to avoid passing intestinal gas. Think about the way you tighten (or contract) the muscles to keep the gas from escaping. Bring that same tightening motion forward to the muscles around your vagina. Then move the contraction up your vagina toward the small of you back. Another good way to understand pelvic floor muscle training can be found in thinking about the vagina being able to clasp the penis during intercourse. This is the same upward and inward motion that helps build strong pelvic muscles.

Back to Top
Important Tips for pelvic floor muscle exercises
Each contraction should involve a concentrated effort to get maximum tightening.
Try to contract only the pelvic muscles. (If you feel your abdomen, thighs or buttocks tightening then relax and aim just for the pelvic muscles by using a less intense muscle contraction. If it seems impossible not to tighten the abdomen, thigh, or buttock muscles, then concentrate on full relaxation and try gentle �flicks� of the pelvic muscles, for example, �flick, flick, flick, relax�--working the muscles to higher layers with each flick.)
Be sure to breathe while holding the muscles contracted.
Practice fully relaxing the muscle for at least 10 seconds between each contraction.
Experiment with contracting the muscles in many different positions (standing upright, lying, sitting, on hands and knees, feet together, feet apart).
Back to Top
What are the most common mistakes made during pelvic muscle exercises?
The most serious mistake women make when doing pelvic muscle exercise is to strain down instead of drawing the muscles up and in. Try doing this on purpose once so you can feel what NOT to do: take a breath, hold it, and push down with your abdomen. You can feel a pushing out around your vagina. It is very important to avoid this straining down.

To keep from straining down when you do a pelvic muscle contraction: exhale gently and keep your mouth open each time you tighten your muscles. Remember to breathe. Rest a hand lightly on your abdomen. If you feel your stomach pushing out against your hand, you are straining down. If you cannot avoid straining down, do not continue with the exercise until you check with your nurse to learn how to do it properly.

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When should I use the pelvic floor muscles?
Squeezing the pelvic floor muscles can help you right away to avoid leakage. Practice coordinating contraction of these muscles with an event in which you may be prone to leak urine (i.e., coughing, sneezing, nose-blowing, lifting a heavy object, etc.) You should also contract the muscles when you need to delay going to the toilet.

Back to Top
How can I work this new health habit into my everyday life?
Think about your typical day. Pick a time (about 15 minutes) that you should have time to do pelvic floor muscle training, maybe when you first wake up or maybe during a TV program you almost always watch.
Decide on a way to remind yourself to do pelvic floor muscle training. You might put a note on a mirror you always use in the morning or a sticker on your TV or a special magnet on your refrigerator.
Reward yourself for exercising each time you do it. You might get some special small candies and treat yourself to one each day that you remember. Or you could draw a small flower on your calendar to mark each day you exercise and get yourself a real flower or bouquet when you have drawn 10 or 30 flowers. Any small reward that you know will keep you working on this habit is fine.
Everyone who is making a change like this has lapses. You may forget for several days at a time. Don�t get discouraged and think that you won�t be able to continue the exercise program. When you realize that you have forgotten, just resume the program.
Monitor your progress. You might want to keep a daily diary of whether or not you have had a leaking accident. Over the weeks you should begin to see a decrease in the frequency and amount of unwanted urine loss. Another way to check your progress is to see whether or not you can slow or stop your urine stream when you are going to the bathroom. We recommend that you try this no more than once a week. As your pelvic muscles get stronger you will find that you are able to stop the stream more quickly.
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University of Michigan, School of Nursing.
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Revised: February 07, 2001 .