References
opinions Ophthalmol. 1990;108:192-194.
1. Zimmerman TJ. Second
Arch 2.
in
ophthalmic health
care.
Roper WL, Winkenwerder W, Hackbarth GM, Krakauer
H.
Effectiveness in health care: an initiative to evaluate and improve medical practice. N Engl J Med. 1988:1197-1202. 3. Ellwood PM. Outcomes management: a technology of patient experience. N Engl J Med. 1988;318:1549-1556. 4. Fowler FJ Jr, Wennberg JE, Timothy RP, Barry MJ, Mulley AG Jr, Hanley D. Symptom status and quality of life following prostatectomy. JAMA. 1988;259:3018-3022.
Vitamin A
5. Barry MJ, Mulley AG Jr, Fowler FJ Jr, Wennberg JE. Watchful waiting vs immediate transurethral resection for symptomatic prostatism: the importance of patients' preferences. JAMA.
1988;259:3010-3017. 6. Wennberg J, Mulley AG Jr, Hanley D, et al. An assessment of prostatectomy for benign urinary tract obstruction: geographic
variations and the evaluation of medical
outcomes. JAMA.
Deficiency and Xerophthalmia
A deficiency and xerophthalmia Vitamin widely considered be problems of developing countries. than 60 such countries are
to
are Indeed, more recognized by the World Health Organization as suffering from an aggregate 5 million new cases of xerophthalmia, one quarter million resulting in
blindness, every year.1 The true number may be twice
as large: recent data suggest that a significant proportion of measles-associated blindness, the major cause of pediatric blindness in Africa, is secondary to acute decompensation of borderline vitamin A status.2 The mechanism(s) by which vitamin A deficiency results in corneal ulceration and necrosis remains uncertain, but local sepsis appears to be a late and variable complication.3,4
sian peasants, Chinese university students and con¬ scripts, and other nutritionally deprived segments of society during the 19th and early 20th centuries. As the two articles in this issue of the Archives make clear, vitamin A deficiency and xerophthalmia still occur in affluent Western societies. Being uncommon, they are frequently overlooked and the diagnosis is delayed, sometimes with tragic consequences. Most instances of vitamin A deficiency and xe¬ rophthalmia in the United States are the result of bi¬ zarre dietary practices,1415 chronic alcoholism,16 or
lipid malabsorption (particularly cystic fibrosis).17 Night blindness and Bitot's spots are occasionally the presenting manifestation of cystic fibrosis; corneal ulcération unresponsive to antimicrobial therapy in
alcoholic should be considered a consequence of vitamin A deficiency until proven otherwise. Indeed, it may be prudent to obtain baseline vitamin A levels on all chronic alcoholics with corneal ulcers and to initiate vitamin A treatment from the start. It is safe, inexpensive, and if the patient is deficient in vitamin A, highly effective. Management of xerophthalmia is the same every¬ where in the world, regardless of the cause; it requires immediate restitution of normal vitamin A nutriture. Except for rare instances of severe lipid malabsorp¬ tion, oral vitamin A is at least as effective as paren¬ teral therapy, much less expensive, and safer.18 Pa¬ tients should receive 200 000 IU of retinyl palmitate on successive days and a third dose, 1 to 4 weeks later, to "top up" liver stores. Infants receive half these amounts. Night blindness, xerosis, and corneal ulcér¬ ation will begin to respond within 1 to 3 days (and are usually stable in the interim). Although bacterial in¬ fection does not appear to be significant in initiating an
See also pp 350 and 354.
Recent data suggest that vitamin A deficiency also has a profound impact on general morbidity,5 mortality,6-8 growth,8,9 and hematopoiesis.8,10 Even subclinical deficiency may have important implications for survival.11 Pilot studies have indicated that vitamin A supplementation can reduce overall childhood mor¬ tality by one third or more.7 The US Congress, the World Health Organization, and UNICEF have all launched ambitious vitamin A intervention programs
save children's sight and lives. Developing countries do not have a monopoly on vitamin A deficiency. The condition occurs wherever dietary intake or intestinal absorption are inadequate for metabolic demands. Outbreaks of night blindness were common in the Confederate Army of Northern Virginia,12 in Danish orphanages,13 and among Rus-
to
care
1988;259:3027-3030. 7. Roos NP, Wennberg JE, Malenka DJ, et al. Mortality and reoperation after open and transurethral resection of the prostate for benign prostatic hyperplasia. N Engl J Med. 1989;320:1120-1124.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Iowa User on 06/10/2015
xerophthalmic ulcération, it may be prudent to obtain appropriate cultures and provide antibacterial cover¬ age. Topical retinole acid can speed corneal healing19 but generally does not have a significant impact on the clinical outcome, and it does not replace the need for systemic vitamin A, which is vital to other organs. Severe protein-energy malnutrition can interfere
with the storage and mobilization of vitamin A and therefore requires equally prompt attention.20 Surgi¬ cal intervention is generally unwarranted. Ulcération usually begins in the periphery; perforations tend to be plugged by the iris, thereby maintaining the ante¬ rior chamber and providing a source of vascular invasion and healing. Limbus-to-limbus necrosis (keratomalacia) is beyond repair. Severe malabsorption, as in some cases of cystic fi¬ brosis, poses a special challenge. It is probably pru¬ dent to initiate treatment of xerophthalmia with parenteral administration of 100 000 IU of watermiscible retinyl palmitate (50 000 IU for infants) to ensure an adequate dose. Subsequent maintenance of adequate nutriture can often be achieved by large daily oral supplements of 10 000 to 50 000 IU of reti¬ nyl palmitate, the appropriate dose determined by periodically monitoring serum retinol levels. Values within the normal range (40 to 70 Mg/dL, 1.4 to 2.5 µ /L) ensure the absence of even subclinical defi¬ ciency. In some extreme cases, maintenance of normal vitamin A nutriture will require periodic parenteral
therapy.
Oil-miscible vitamin A should never be adminis¬ tered parenterally for treatment or maintenance; it is released slowly, if at all, from the injection site. Vitamin A deficiency is a serious and compelling challenge to health authorities in most developing countries. For those of us fortunate to practice oph¬ thalmology in better-nourished societies, the chal¬ lenge is in maintaining a high level of suspicion for an uncommon, but highly treatable disorder. Alfred Sommer, MD Baltimore, Md This study was supported in part by Cooperative Agreement DAN0045 from the US Agency for International Development and from the Task Force Sight and Life, Basel, Switzerland. Reprint requests to Wilmer Room 120,600 Wolfe St, Baltimore, MD 21209 (Dr Sommer).
References
1. Sommer A, Tarwotjo I, Hussaini G. Incidence, prevalence and scale of blinding malnutrition. Lancet. 1981;1:1407-1408. 2. Foster A, Sommer A. Corneal ulceration, measles and childhood blindness in Tanzania. Br J Ophthalmol. 1987;71:331-343. 3. Sommer A. Nutritional Blindness: Xerophthalmia and Keratomalacia. New York, NY: Oxford University Press Inc; 1982. 4. Sommer A, Green WR, Kenyon KR. Clinical-histopathologic correlation in xerophthalmic ulceration and necrosis. Arch Oph-
thalmol. 1982;100:953-963. 5. Sommer A, Katz J, Tarwotjo I. Increased risk of respiratory disease and diarrhea in children with pre-existing mild vitamin A deficiency. Am J Clin Nutr. 1984;40:1090-1095. 6. Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in mild vitamin A deficiency. Lancet. 1983;2:585-588. 7. Sommer A, Tarwotjo I, Djunaedi E, et al. Impact of vitamin A supplementation on childhood mortality: a randomized con-
trolled community trial. Lancet. 1986;1:1169-1173. 8. Muhilal, Permeisih D, Idjradinata YR, Muherdiyantiningsih, Karyadi D. Vitamin A-fortified monosodium glutamate and health, growth, and survival of children: a controlled field trial. Am J Clin Nutr. 1988;48:1271-1276. 9. West KP, Djunaedi E, Pandji A, Kusdiono, Tarwotjo I, Sommer A, Aceh Study Group. Vitamin A supplementation and growth: a randomized clinical trial. Am J Clin Nutr. 1988;48:1257-1264. 10. Mejia LA, Chew F. Hematological effect of supplementing vitamin A alone and in combination with iron to anemic children. Am J Clin Nutr. In press. 11. Sommer A. New imperatives for an old vitamin (A): the VII EV McCollum International Lecture in Nutrition. J Nutr.
1989;119:96-100.
12. Hicks RJ. Night-blindness in the Confederate Army. Richmond Med J. 1867;3:34-38. 13. Bloch CE. Clinical investigation of xerophthalmia and dystrophy in infants and young children (xerophthalmia et dystrophia alipogenetica). J Hygiene. 1921;19:283-301. 14. Fells P, Bors F. Ocular complications of self-induced vitamin A deficiency. Trans Ophthalmol Soc UK. 1969;89:221-228. 15. Smith RS, Farrell T, Bailey T. Keratomalacia. Surv Ophthal-
mol. 1975;20:213-219. 16. Russell RM, Morrison SA, Smith FR, Oaks EV, Carney EA. Vitamin A reversal of abnormal dark adaptation in cirrhosis: study of effects on the plasma retinol transport system. Ann Intern Med.
1978;88:622-626.
17. Petersen RA, Petersen VS, Robb RM. Vitamin A deficiency with xerophthalmia and night blindness in cystic fibrosis. AJDC.
1968;116:662-665. 18. Sommer A, Muhilal, Tarwotjo I, Djunaedi E, Glover J. Oral versus intramuscular vitamin A in the treatment of xerophthalmia. Lancet. 1980;1:557-559. 19. Sommer A. Treatment of corneal xerophthalmia with topical retinoic acid. Am J Ophthalmol. 1983;95:349-352. 20. Sommer A, Muhilal, Tarwotjo I. Protein deficiency and treatment of xerophthalmia. Arch Ophthalmol. 1982;100:785-787.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Iowa User on 06/10/2015
opinions Ophthalmol. 1990;108:192-194.
1. Zimmerman TJ. Second
Arch 2.
in
ophthalmic health
care.
Roper WL, Winkenwerder W, Hackbarth GM, Krakauer
H.
Effectiveness in health care: an initiative to evaluate and improve medical practice. N Engl J Med. 1988:1197-1202. 3. Ellwood PM. Outcomes management: a technology of patient experience. N Engl J Med. 1988;318:1549-1556. 4. Fowler FJ Jr, Wennberg JE, Timothy RP, Barry MJ, Mulley AG Jr, Hanley D. Symptom status and quality of life following prostatectomy. JAMA. 1988;259:3018-3022.
Vitamin A
5. Barry MJ, Mulley AG Jr, Fowler FJ Jr, Wennberg JE. Watchful waiting vs immediate transurethral resection for symptomatic prostatism: the importance of patients' preferences. JAMA.
1988;259:3010-3017. 6. Wennberg J, Mulley AG Jr, Hanley D, et al. An assessment of prostatectomy for benign urinary tract obstruction: geographic
variations and the evaluation of medical
outcomes. JAMA.
Deficiency and Xerophthalmia
A deficiency and xerophthalmia Vitamin widely considered be problems of developing countries. than 60 such countries are
to
are Indeed, more recognized by the World Health Organization as suffering from an aggregate 5 million new cases of xerophthalmia, one quarter million resulting in
blindness, every year.1 The true number may be twice
as large: recent data suggest that a significant proportion of measles-associated blindness, the major cause of pediatric blindness in Africa, is secondary to acute decompensation of borderline vitamin A status.2 The mechanism(s) by which vitamin A deficiency results in corneal ulceration and necrosis remains uncertain, but local sepsis appears to be a late and variable complication.3,4
sian peasants, Chinese university students and con¬ scripts, and other nutritionally deprived segments of society during the 19th and early 20th centuries. As the two articles in this issue of the Archives make clear, vitamin A deficiency and xerophthalmia still occur in affluent Western societies. Being uncommon, they are frequently overlooked and the diagnosis is delayed, sometimes with tragic consequences. Most instances of vitamin A deficiency and xe¬ rophthalmia in the United States are the result of bi¬ zarre dietary practices,1415 chronic alcoholism,16 or
lipid malabsorption (particularly cystic fibrosis).17 Night blindness and Bitot's spots are occasionally the presenting manifestation of cystic fibrosis; corneal ulcération unresponsive to antimicrobial therapy in
alcoholic should be considered a consequence of vitamin A deficiency until proven otherwise. Indeed, it may be prudent to obtain baseline vitamin A levels on all chronic alcoholics with corneal ulcers and to initiate vitamin A treatment from the start. It is safe, inexpensive, and if the patient is deficient in vitamin A, highly effective. Management of xerophthalmia is the same every¬ where in the world, regardless of the cause; it requires immediate restitution of normal vitamin A nutriture. Except for rare instances of severe lipid malabsorp¬ tion, oral vitamin A is at least as effective as paren¬ teral therapy, much less expensive, and safer.18 Pa¬ tients should receive 200 000 IU of retinyl palmitate on successive days and a third dose, 1 to 4 weeks later, to "top up" liver stores. Infants receive half these amounts. Night blindness, xerosis, and corneal ulcér¬ ation will begin to respond within 1 to 3 days (and are usually stable in the interim). Although bacterial in¬ fection does not appear to be significant in initiating an
See also pp 350 and 354.
Recent data suggest that vitamin A deficiency also has a profound impact on general morbidity,5 mortality,6-8 growth,8,9 and hematopoiesis.8,10 Even subclinical deficiency may have important implications for survival.11 Pilot studies have indicated that vitamin A supplementation can reduce overall childhood mor¬ tality by one third or more.7 The US Congress, the World Health Organization, and UNICEF have all launched ambitious vitamin A intervention programs
save children's sight and lives. Developing countries do not have a monopoly on vitamin A deficiency. The condition occurs wherever dietary intake or intestinal absorption are inadequate for metabolic demands. Outbreaks of night blindness were common in the Confederate Army of Northern Virginia,12 in Danish orphanages,13 and among Rus-
to
care
1988;259:3027-3030. 7. Roos NP, Wennberg JE, Malenka DJ, et al. Mortality and reoperation after open and transurethral resection of the prostate for benign prostatic hyperplasia. N Engl J Med. 1989;320:1120-1124.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Iowa User on 06/10/2015
xerophthalmic ulcération, it may be prudent to obtain appropriate cultures and provide antibacterial cover¬ age. Topical retinole acid can speed corneal healing19 but generally does not have a significant impact on the clinical outcome, and it does not replace the need for systemic vitamin A, which is vital to other organs. Severe protein-energy malnutrition can interfere
with the storage and mobilization of vitamin A and therefore requires equally prompt attention.20 Surgi¬ cal intervention is generally unwarranted. Ulcération usually begins in the periphery; perforations tend to be plugged by the iris, thereby maintaining the ante¬ rior chamber and providing a source of vascular invasion and healing. Limbus-to-limbus necrosis (keratomalacia) is beyond repair. Severe malabsorption, as in some cases of cystic fi¬ brosis, poses a special challenge. It is probably pru¬ dent to initiate treatment of xerophthalmia with parenteral administration of 100 000 IU of watermiscible retinyl palmitate (50 000 IU for infants) to ensure an adequate dose. Subsequent maintenance of adequate nutriture can often be achieved by large daily oral supplements of 10 000 to 50 000 IU of reti¬ nyl palmitate, the appropriate dose determined by periodically monitoring serum retinol levels. Values within the normal range (40 to 70 Mg/dL, 1.4 to 2.5 µ /L) ensure the absence of even subclinical defi¬ ciency. In some extreme cases, maintenance of normal vitamin A nutriture will require periodic parenteral
therapy.
Oil-miscible vitamin A should never be adminis¬ tered parenterally for treatment or maintenance; it is released slowly, if at all, from the injection site. Vitamin A deficiency is a serious and compelling challenge to health authorities in most developing countries. For those of us fortunate to practice oph¬ thalmology in better-nourished societies, the chal¬ lenge is in maintaining a high level of suspicion for an uncommon, but highly treatable disorder. Alfred Sommer, MD Baltimore, Md This study was supported in part by Cooperative Agreement DAN0045 from the US Agency for International Development and from the Task Force Sight and Life, Basel, Switzerland. Reprint requests to Wilmer Room 120,600 Wolfe St, Baltimore, MD 21209 (Dr Sommer).
References
1. Sommer A, Tarwotjo I, Hussaini G. Incidence, prevalence and scale of blinding malnutrition. Lancet. 1981;1:1407-1408. 2. Foster A, Sommer A. Corneal ulceration, measles and childhood blindness in Tanzania. Br J Ophthalmol. 1987;71:331-343. 3. Sommer A. Nutritional Blindness: Xerophthalmia and Keratomalacia. New York, NY: Oxford University Press Inc; 1982. 4. Sommer A, Green WR, Kenyon KR. Clinical-histopathologic correlation in xerophthalmic ulceration and necrosis. Arch Oph-
thalmol. 1982;100:953-963. 5. Sommer A, Katz J, Tarwotjo I. Increased risk of respiratory disease and diarrhea in children with pre-existing mild vitamin A deficiency. Am J Clin Nutr. 1984;40:1090-1095. 6. Sommer A, Tarwotjo I, Hussaini G, Susanto D. Increased mortality in mild vitamin A deficiency. Lancet. 1983;2:585-588. 7. Sommer A, Tarwotjo I, Djunaedi E, et al. Impact of vitamin A supplementation on childhood mortality: a randomized con-
trolled community trial. Lancet. 1986;1:1169-1173. 8. Muhilal, Permeisih D, Idjradinata YR, Muherdiyantiningsih, Karyadi D. Vitamin A-fortified monosodium glutamate and health, growth, and survival of children: a controlled field trial. Am J Clin Nutr. 1988;48:1271-1276. 9. West KP, Djunaedi E, Pandji A, Kusdiono, Tarwotjo I, Sommer A, Aceh Study Group. Vitamin A supplementation and growth: a randomized clinical trial. Am J Clin Nutr. 1988;48:1257-1264. 10. Mejia LA, Chew F. Hematological effect of supplementing vitamin A alone and in combination with iron to anemic children. Am J Clin Nutr. In press. 11. Sommer A. New imperatives for an old vitamin (A): the VII EV McCollum International Lecture in Nutrition. J Nutr.
1989;119:96-100.
12. Hicks RJ. Night-blindness in the Confederate Army. Richmond Med J. 1867;3:34-38. 13. Bloch CE. Clinical investigation of xerophthalmia and dystrophy in infants and young children (xerophthalmia et dystrophia alipogenetica). J Hygiene. 1921;19:283-301. 14. Fells P, Bors F. Ocular complications of self-induced vitamin A deficiency. Trans Ophthalmol Soc UK. 1969;89:221-228. 15. Smith RS, Farrell T, Bailey T. Keratomalacia. Surv Ophthal-
mol. 1975;20:213-219. 16. Russell RM, Morrison SA, Smith FR, Oaks EV, Carney EA. Vitamin A reversal of abnormal dark adaptation in cirrhosis: study of effects on the plasma retinol transport system. Ann Intern Med.
1978;88:622-626.
17. Petersen RA, Petersen VS, Robb RM. Vitamin A deficiency with xerophthalmia and night blindness in cystic fibrosis. AJDC.
1968;116:662-665. 18. Sommer A, Muhilal, Tarwotjo I, Djunaedi E, Glover J. Oral versus intramuscular vitamin A in the treatment of xerophthalmia. Lancet. 1980;1:557-559. 19. Sommer A. Treatment of corneal xerophthalmia with topical retinoic acid. Am J Ophthalmol. 1983;95:349-352. 20. Sommer A, Muhilal, Tarwotjo I. Protein deficiency and treatment of xerophthalmia. Arch Ophthalmol. 1982;100:785-787.
Downloaded From: http://archopht.jamanetwork.com/ by a University of Iowa User on 06/10/2015
