HICNet Medical News Digest Sun, 11 Sep 1994 Volume 07 : Issue 42 Today's Topics: [MMWR 1 Sep 94] Minors' Access to Cigarette Machines [MMWR] Interstate Measles Transmission from a Ski Resort [MMWR] Arenavirus Infection [MMWR 9 Sep 94] Hyponatremic Seizures Infants on Bottled Water [MMWR] AIDS Among Racial/Ethnic Minorities [MMWR] Prilocaine Induced Methemogloinemia +------------------------------------------------+ ! ! ! Health Info-Com Network ! ! Medical Newsletter ! +------------------------------------------------+ Editor: David Dodell, D.M.D. 10250 North 92nd Street, Suite 210, Scottsdale, Arizona 85258-4599 USA Telephone +1 (602) 860-1121 FAX +1 (602) 451-1165 Internet: mednews@stat.com Bitnet: ATW1H@ASUACAD Mosaic WWW: http://biomed.nus.sg/MEDNEWS/welcome.html Compilation Copyright 1994 by David Dodell, D.M.D. All rights Reserved. License is hereby granted to republish on electronic media for which no fees are charged, so long as the text of this copyright notice and license are attached intact to any and all republished portion or portions. The Health Info-Com Network Newsletter is distributed biweekly. Articles on a medical nature are welcomed. If you have an article, please contact the editor for information on how to submit it. If you are interested in joining the automated distribution system, please contact the editor. Associate Editors: E. Loren Buhle, Jr. Ph.D. Dept. of Radiation Oncology, Univ of Pennsylvania Tom Whalen, M.D., Robert Wood Johnson Medical School at Camden Douglas B. Hanson, Ph.D., Forsyth Dental Center, Boston, MA Lawrence Lee Miller, B.S. Biological Sciences, UCI Dr K C Lun, National University Hospital, Singapore W. Scott Erdley, MS, RN, SUNY@UB School of Nursing Jack E. Cross, B.S Health Care Admin, 882 Medical Trng Grp, USAF Albert Shar, Ph.D. CIO, Associate Prof, Univ of Penn School of Medicine Martin I. Herman, M.D., LeBonheur Children's Medical Center, Memphis TN Stephen Cristol, M.D., Dept of Ophthalmology, Emory Univ, Atlanta, GA Subscription Requests = mednews@stat.com anonymous ftp = vm1.nodak.edu; directory HICNEWS FAX Delivery = Contact Editor for information ---------------------------------------------------------------------- Date: Sun, 11 Sep 94 07:54:55 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR 1 Sep 94] Minors' Access to Cigarette Machines Message-ID: <9XTHsc1w165w@stat.com> Minors' Access to Cigarette Vending Machines -- Texas The sale of tobacco products to persons aged less than 18 years has been prohibited by law in Texas since September 1989*. This law requires cigarette vending machine owners to post signs on their machines stating the illegality of tobacco product sales to persons aged less than 18 years and that merchants convicted for selling tobacco products to underaged persons be fined a maximum of $500. In August 1991, Arlington, Texas, enacted legislation requiring installation of electronic locking devices on all cigarette vending machines. These devices render the vending machine inoperable until the store owner electronically unlocks the machine on customer request. To assess minors' access to cigarettes through vending machines, in October 1993 the Texas Department of Health conducted a study in Arlington and five neighboring communities. This report summarizes the study findings. In September 1993, the health department obtained a list of business establishments with cigarette vending machines owned by the largest cigarette vending company in the Arlington area. A total of 116 establishments were identified in the study area; 59 (51%) machines were in establishments considered easily accessible to minors (i.e., restaurants, gas stations, motel lobbies, food stores, and recreational facilities). Data were collected for 42 of the 59 sites. Four investigative teams consisted of one adult paired with one minor (aged 15-17 years). One purchase attempt was made at each of the 42 establishments. During each purchase attempt, the adult entered the establishment first and asked for street directions. The adult then observed while the minor entered and attempted to purchase cigarettes from the vending machine. Minors were instructed to answer, if asked, that the cigarettes were for themselves. While attempting to purchase cigarettes from vending machines, no minors were challenged by business owners. Of the 42 attempts, 41 were successful. Of the 41 sites where purchase attempts were successful, 24 (59%) were located within 1/2 mile of a school. Most (35 [83%] of 42) purchase attempts occurred in restaurants; however, cigarettes were bought at every type of establishment where purchases were attempted. Warning signs prohibiting cigarettes sales to minors were posted on vending machines in 32 (76%) establishments. Of the 16 vending machines located in business establisments in the city of Arlington, one was equipped with an electronic locking device. The single unsuccessful purchase attempt occurred at this electronically locked machine. Reported by: JM Gomez, Arlington Police Dept; GJ Flores, SR Tobias, Office of Smoking and Health, CR Allen, MD, Public Health Region 2, PP Huang, MD, Bur of Chronic Disease Prevention and Control, DM Simpson, MD, State Epidemiologist, Texas Dept of Health. Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion; Div of Field Epidemiology, Epidemiology Program Office, CDC. Editorial Note: The findings in this report indicate that, despite laws prohibiting cigarette sales to persons aged less than 18 years, minors readily purchased cigarettes from vending machines in Arlington and five neighboring communities. Although the only failed purchase attempt in this study resulted from a vending machine equipped with a remote-controlled locking device, compliance with legislation requiring these devices has been minimal (1). The finding that only one of 16 vending machines in Arlington was equipped with the device is similar to findings of studies about locking device usage in other areas (1). The findings in this report are subject to at least two limitations. First, data in this report were obtained for only one vending machine company in the Arlington area because the Texas Department of the Treasury does not require vending machine companies to specify the locations of their machines. Second, because of time constraints during the study, data were not collected for 17 establishments considered easily accessible to minors; however, sites included in the analysis probably do not differ from sites that were not included. Approximately 82% of adult smokers report that they first tried a cigarette by age 18 years, and 53% were daily smokers by that age (2). The initiation rate for smoking increases rapidly after age 11 years (3); in Texas, a 1989 survey of 4400 high school students found that 55% of 12-year-olds had already tried cigarette smoking (4). Because vending machine sales are not monitored actively by adults, cigarette vending machines can be an important source for younger adolescents (i.e., aged 12-15 years), who are more likely than older adolescents (i.e., aged 16-18 years) to be refused an over-the-counter cigarette sale (5). Studies indicate that younger adolescent smokers are more likely to buy cigarettes from vending machines than older adolescent smokers (6,7). Unregulated cigarette vending machines may facilitate initiation of smoking among younger adolescents; therefore, more effective regulation of these sales may be an important preventive measure. Prevention of adolescent smoking may be enhanced by the recently enacted Synar Amendment to the Alcohol, Drug Abuse, and Mental Health Administration (ADAMHA) Reorganization Act.** The Synar Amendment requires that states demonstrate effective prohibition of the sale of tobacco products (including cigarettes from vending machines) to persons aged less than 18 years as a condition of receiving full ADAMHA block grants. As a result of this study, the Arlington City Council enacted legislation prohibiting cigarette vending machines in all business establishments that admit persons aged less than 18 years. References 1. Forster JL, Hourigan M, Kelder S. Locking devices on cigarette vending machines: evaluation of a city ordinance. Am J Public Health 1992;82:1217-9. 2. US Department of Health and Human Services. Preventing tobacco use among young people: a report of the Surgeon General. Atlanta: US Department of Health and Human Services, Public Health Service, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1994. 3. Kandel DB, Logan JA. Patterns of drug use from adolescence to young adulthood: I. Periods of risk for initiation, continued use, and discontinuation. Am J Public Health 1984;74:660-6. 4. Texas Department of Health. University of Texas Health Science Center: Texas Tobacco Survey, 1989--a survey of 7th, 8th, 10th, and 12th graders in public schools in Texas. Austin, Texas: Texas Department of Health, 1989. 5. Forster JL, Hourigan M, McGoven P. Availability of cigarettes to underage youth in three communities. Prev Med 1992;21:320-8. 6. Allen KF, Moss AJ, Giovino GA, Shopland DR, Pierce JP. Teenage tobacco use: data estimates from the teenage attitudes and practices survey--United States, 1989. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, NCHS, 1992. (Advance data no. 224). 7. National Automatic Merchandising Association. Findings: study of teenage cigarette smoking and purchase behavior. Chicago: National Automatic Merchandising Association, 1989. * Texas Health and Safety Code, Title 2, Sections 161.081-161.082. ** Public Law 102-321, section 1926. ------------------------------ Date: Sun, 11 Sep 94 07:55:47 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Interstate Measles Transmission from a Ski Resort Message-ID: Interstate Measles Transmission from a Ski Resort -- Colorado, 1994 During April 1-May 25, 1994, a chain of measles transmission began in Breckenridge, Colorado, and extended into nine additional states; a total of 247 measles cases were reported, representing 36% of all U.S. measles cases reported to the National Notifiable Diseases Surveillance System (excluding those reported from U.S. territories) through July 2 (week 26). The source of exposure was unknown but is believed to have been an out-of-state tourist who probably visited Breckenridge during March because 1) no measles cases had previously been reported in Colorado during 1994, and 2) the only common exposure appeared to have been at a ski resort visited by many out-of-state travelers. Persons associated with spread of measles from Breckenridge were predominately school- and college-aged. This report summarizes the investigation of this chain of interstate measles transmission. A total of 15 measles cases with rash onset during April 4-21 occurred in Breckenridge. Persons with measles ranged in age from 16 years to 46 years (median: 27.6 years). All cases met the CDC measles clinical case definition (1); 12 were serologically confirmed. All 15 ill persons either lived in Summit County (Breckenridge) or three neighboring counties (Arapahoe, Chaffee, and Park) or worked in tourism-related services in or near Breckenridge. Twelve of the 15 ill persons are believed to have been exposed to the unidentified source, and three cases resulted from secondary transmission. Two cases occurred among high school students; no further transmission in schools was reported. Interstate transmission of measles occurred through four out-of-state travelers and a Silver Thorn, Colorado, resident--all of whom had visited Breckenridge during March 18-25. All five visitors are believed to have been exposed to the unidentified source. Two persons (a 46-year-old Texas resident [rash onset: April 16] and a 29-year-old Missouri resident [rash onset: April 4]) developed measles on return home but have not been linked to additional cases. The other three persons--an Illinois resident, a Maryland resident, and the Silver Thorn resident--became sources for further transmission. Illinois. A 14-year-old unvaccinated female high school student returned home to Jersey County, Illinois; she developed a rash on April 4. The student was identified as the source of an outbreak involving 51 unvaccinated persons (age range: 1-24 years; median: 18 years; last rash onset: June 3) in her community--which was associated with a Christian Science college in the county. She also was identified as the source of an outbreak involving 156 persons (age range: 4-25 years; median: 15 years; rash onsets: April 17-May 15) at the Christian Science boarding high school she attended in St. Louis County, Missouri. After several unvaccinated persons from other states visited the school during the outbreak, six additional cases occurred. Five persons developed measles on return home (two persons to Maine and one each to California, New York, and Washington); the California patient was the source of exposure for a sibling. No further transmission associated with these six cases is known. Maryland. A 24-year-old woman returned home to Baltimore County, Maryland; she developed a rash on April 4. The woman was the source of exposure for her 56-year-old father, who had rash onset on April 21. Michigan. A 25-year-old Silver Thorn man visited his family in Wayne County, Michigan; he developed rash on April 17. The man was identified as the source of an outbreak involving 12 persons (age range: 9 months-37 years; median: 24 years; rash onsets: April 17- May 18) who were exposed at a wedding and a restaurant. One additional case (rash onset: April 16) was reported in a 12-year-old Chicago resident who had visited Wayne County. No further transmission associated with the Michigan or Chicago cases is known. Reported by: GW Rutherford, III, MD, State Epidemiologist, California State Dept of Health Svcs. RE Hoffman, MD, State Epidemiologist, Colorado Dept of Health. BJ Francis, MD, State Epi-demiologist, Illinois Dept of Public Health. KF Gensheimer, MD, State Epidemiologist, Bur of Health, Maine Dept of Human Svcs. E Israel, MD, State Epidemiologist, Maryland State Dept of Health and Mental Hygiene. KR Wilcox, Jr, MD, State Epidemiologist, Michigan Dept of Public Health. HD Donnell, Jr, MD, State Epidemiologist, Missouri Dept of Health. D Morse, MD, State Epidemiologist, New York State Dept of Health. DM Simpson, MD, State Epidemiologist, Texas Dept of Health. W Lasota, Immunization Program, Washington Dept of Health. National Immunization Program, Office of the Director; Epidemiology Program Office, CDC. Editorial Note: The sustained interstate measles outbreak described in this report demonstrates the ability of measles virus to spread rapidly and widely among a highly mobile population. The dates of rash onset for the five Breckenridge visitors suggest that they had been exposed to measles during the same period the Breckenridge cases were exposed; therefore, exposure to the common, unidentified source--not the Breckenridge cases--probably led to this widespread interstate outbreak. Direct contact of the five visitors with the unidentified source resulted in primary transmission of measles in five other states (222 reported cases), and further contact resulted in secondary transmission in four additional states (six reported cases) before the chain of transmission ended. Factors that may have contributed to this interstate measles outbreak include 1) the timing of the initial exposure during school spring break; 2) exposure of an unvaccinated student who subsequently returned home to a community and school with many susceptible, unvaccinated persons; and 3) special events at the Missouri boarding school that drew susceptible, unvaccinated visitors from other states. Although measles spread from Colorado to nine other states, transmission in six states stopped with the index case or after one additional case. In some of these states, spread may have been limited because the sources were adults whose routine activities may not have involved close contact with groups containing susceptible persons. Only two outbreaks (lllinois/Missouri and Michigan) resulted in substantial numbers of reported cases, and both were associated with contact with large groups (e.g., high school and college populations, wedding guests, and restaurant patrons). The extended outbreak in Illinois and Missouri has been the largest measles outbreak in the United States (excluding territories) in 1994 (2). The primary strategy to prevent measles outbreaks is achieving and sustaining measles vaccination coverage levels of at least 90% for a single dose among all age groups. Efforts are under way to increase measles vaccination coverage among preschool children and implement a recommendation that all school-aged and college-aged persons receive two doses of measles-mumps-rubella vaccine. However, additional strategies may be needed to ensure complete vaccination of adults and to prevent outbreaks in settings where large groups of adults gather (e.g., resorts and restaurants). Large groups that do not routinely accept vaccination will remain potential problems for measles-control programs. To achieve the Childhood Immunization Initiative's goal of eliminating indigenous measles in the United States by 1996 (3), continued efforts to assure rapid detection of measles cases and implementation of control measures are necessary. To define disease transmission patterns more completely, state and local health departments should rapidly investigate and report all suspected measles cases, obtain laboratory confirmation, determine the vaccination status of each suspected case, and determine the source or chain of disease transmission. Identification of measles cases by transmission category (i.e., international importation, linked to an importation, or indigenously acquired) also will be necessary to track progress toward achieving the 1996 elimination goal. References 1. CDC. Case definitions for public health surveillance. MMWR 1990;39(no. RR-13):23. 2. CDC. Outbreak of measles among Christian Science students-- Missouri and Illinois, 1994. MMWR 1994;43:463-5. 3. CDC. Reported vaccine-preventable diseases--United States, 1993, and the Childhood Immunization Initiative. MMWR 1994;43:57-60. ------------------------------ Date: Sun, 11 Sep 94 07:59:01 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Arenavirus Infection Message-ID: <35THsc4w165w@stat.com> Arenavirus Infection -- Connecticut, 1994 On August 20, 1994, the Connecticut Department of Public Health and Addiction Services received a report of a case of acute illness in a virologist suspected to be associated with Sabia virus, a newly described arenavirus. This report presents preliminary findings from the case investigation. On August 19, 1994, the virologist presented to the Tropical Medicine Clinic at Yale-New Haven Hospital with a 4-day history of fever, malaise, backache, stiff neck, and myalgias that he attributed to a recurrence of a Plasmodium vivax infection. On evaluation at the clinic, his temperature was 99.8 F (37.6 C) on antipyretics, and he had a normal physical examination. Laboratory evaluation included a negative malaria smear, a total white blood cell count (WBC) of 2600 cells/cubic millimeter (normal: 4000- 10,000 cells/cubic millimeter), a platelet count of 138,000 cells/cubic millimeter (normal: 150,000-350,000 cells/cubic millimeter), 2+ proteinuria, and alanine aminotransferase (ALT) of 6356 U/L (upper limit normal: 35 U/L). A history of a possible laboratory exposure to Sabia virus was obtained, and the man was hospitalized for prompt treatment with intravenous ribavirin, an antiviral drug that is effective against other arenavirus infections such as Lassa fever (1). On admission, the patient had a temperature of 103 F (39.4 C). Within 24 hours of hospitalization, his total WBC and platelet count had declined to a low of 1400 cells/cubic millimeter and 92,000 cells/cubic millimeter, respectively. His ALT peaked at 128 U/L on the 9th day of hospitalization. No hemorrhagic manifestations of the infection were observed during hospitalization. A diagnosis of Sabia infection was confirmed on acute serum by amplification of a portion of the viral genome by polymerase chain reaction and by isolation of the virus from blood. The patient recovered and was discharged on August 26. On August 8, the virologist was apparently exposed to an aerosol of Sabia virus when a centrifuge bottle developed a crack, and tissue culture supernatant containing the virus leaked into the high-speed centrifuge. At the time of the incident, the virologist was working alone in the biosafety level-3 laboratory (negative pressure with HEPA-filtered exhaust system). He cleaned the spilled material from the centrifuge while wearing a gown, surgical mask, and gloves. Persons who came in contact with the patient or with his biological specimens in the hospital laboratories since onset of his illness were notified and enrolled in a surveillance program. None of these persons have had exposure to the patient that would suggest a high risk for secondary infection. As of August 31, none of the persons under surveillance have reported a febrile illness. Reported by: M Barry, MD, F Bia, MD, M Cullen, MD, L Dembry, MD, S Fischer, MD, D Geller, MD, W Hierholzer, MD, P McPhedran, MD, P Rainey, MD, M Russi, MD, E Snyder, MD, E Wrone, MD, Yale Univ School of Medicine and Yale-New Haven Hospital; JP Gonzalez, MD, R Rico-Hesse, PhD, R Tesh, MD, R Ryder, MD, R Shope, MD, Yale Arbovirus Research Unit, Yale Univ; WP Quinn, MPH, New Haven Health Dept; PD Galbraith, DMD, ML Cartter, MD, JL Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health and Addiction Svcs. A DeMaria, Jr, MD, State Epidemiologist, Massachusetts Dept of Public Health. Div of Field Epidemiology, Epidemiology Program Office; Special Pathogens Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC. Editorial Note: Sabia virus was isolated by scientists in Sau Paulo, Brazil, in 1990 and characterized by scientists in Belem, Brazil, and at the Yale Arbovirus Research Unit (2). Only two cases of Sabia virus infection (both in Brazil) have been reported (2). One was a naturally acquired infection in an agricultural engineer who was probably infected by exposure to an infected rodent (the natural reservoir of other known arenaviruses). The engineer died approximately 2 weeks after becoming ill. The second case was in a laboratory technician who was working with the virus. He had a severe illness characterized by 15 days of fever, chills, malaise, headache, generalized myalgia, sore throat, conjunctivitis, nausea, vomiting, diarrhea, epigastric pain, bleeding gums, and leukopenia. He recovered after hospitalization and treatment with intravenous fluids. Little is known about the modes of transmission of the Sabia virus. Based on the pathogenesis of other arenaviruses, the Sabia virus is not believed to be infectious until the patient exhibits symptoms. Other arenaviruses can be transmitted by needle-stick but do not readily spread from person to person. Persons in casual contact with persons with arenavirus infection are not at risk for disease and do not require medical follow-up. References 1. McCormick JB, King IJ, Webb PA, et al. Lassa fever: effective therapy with ribavirin. N Engl J Med 1986;314:20-6. 2. Coimbra TLM, Nassar ES, Burattini MN, et al. New arenavirus isolated in Brazil. Lancet 1994;343:391-2. ------------------------------ Date: Sun, 11 Sep 94 08:01:07 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR 9 Sep 94] Hyponatremic Seizures Infants on Bottled Water Message-ID: Hyponatremic Seizures Among Infants Fed with Commercial Bottled Drinking Water -- Wisconsin, 1993 In 1993, two infants were treated at a pediatric referral hospital in Wisconsin for hyponatremic seizures caused by water intoxication associated with bottled drinking water. This report summarizes information about these cases and a review of hospitalizations for hyponatremic seizures in this hospital during 1984-1993. Patient 1 In October 1993, a 55-day-old infant was taken by her mother to the emergency department (ED) of a local hospital for evaluation of "eye twitching." During transport, she had onset of generalized, tonic-clonic seizures. Examination at the hospital revealed periorbital and gluteal edema; her serum sodium level was 116 mEq/L (normal: 135-145 mEq/L), and metabolic acidosis was documented by blood gas analysis. Status epilepticus secondary to hyponatremia was diagnosed. Treatment was initiated with intravenous anticonvulsants. Forty-five minutes after onset of seizures, the infant experienced respiratory depression. Following endotracheal intubation, the infant was transported to the children's hospital, where she received intravenous normal saline. Serum sodium subsequently normalized, and metabolic acidosis resolved. The infant was discharged after 5 days and recovered fully. The infant's mother had been buying cow's milk-based infant formula and had been supplementing feedings with several ounces of bottled water for several days. She reported using bottled water as a supplement because the product was inexpensive and because she interpreted the labeling to indicate that the product had been produced specifically for infants and contained nutrients adequate for use as a feeding supplement. The mother later reported to the Food and Drug Administration (FDA) that she had substituted tap water for infant formula during the 24 hours before hospitalization. Patient 2 In December 1993, a 56-day-old infant was transported to the ED at the children's hospital following an apparent brief seizure. He had had mild upper-respiratory tract symptoms for several days but otherwise had been in good health. At the hospital, he appeared alert, healthy, and in no distress. His serum sodium level was 121 mEq/L, and urine specific gravity was less than 1.005. Computed tomography of his head was normal. Seizures secondary to hyponatremia was diagnosed. Treatment with intravenous saline was initiated, and his serum sodium level reached normal limits after 9 hours. He was discharged 24 hours after admission and recovered fully. The infant's mother had supplemented feedings of soy-based formula with bottled drinking water since the onset of symptoms of an upper-respiratory illness. Daily feedings consisted of three bottles of formula and three bottles of drinking water. She believed the water was a safe and economical liquid that would help relieve the upper-respiratory symptoms, and she indicated that she interpreted the bottle label to depict a product specially made for infants. Reported by: RC Bruce, MD, RM Kliegman, MD, Dept of Pediatrics, Medical College of Wisconsin, Milwaukee. Office of Special Nutritionals, Center for Food Safety and Applied Nutrition, Food and Drug Administration. Maternal and Child Health Br, Div of Nutrition, National Center for Chronic Disease Prevention and Health Promotion, CDC. Editorial Note: Manifestations of water intoxication include altered mental status (typically irritability or somnolence), hypothermia, edema, and seizure (1-7). Symptoms are preceded by a rapid decline in serum sodium levels (to less than or equal to 125 mEq/L) and result from an acute overload of solute-free water that increases total body water by 7%-8% or more (8). The rapid decline in serum sodium may result in cellular dysfunction (i.e., abnormal ion gradients and cellular swelling) in the central nervous system. Factors that increase the risk for water intoxication among infants (especially those aged less than 6 months) include immature renal function and the powerful hunger drive of early infancy (1,3,8). Hyponatremic seizures among infants resulting from improper feeding practices and water intoxication were first reported in 1967 (1). The risk for this problem may be increased among infants of parents living in poverty (1-7). This possible increased risk may be associated with a lack of resources to purchase infant formula or oral rehydration solution and a lack of knowledge about the potential dangers of feeding infants solute-free water. The risk for hyponatremia may be particularly increased among infants aged less than 6 months who are vomiting or have diarrhea but who are fed fluids lacking sufficient sodium. However, symptomatic hyponatremia also may occur in infants with no acute medical conditions who are fed excess solute-free water. This problem has been caused most commonly by tap water, given either as supplemental feedings or in overly diluted formula; juices, soda, and tea also have been implicated. Bottled water products marketed specifically for infants may be mistaken by parents and other caregivers as an affordable and appropriate feeding supplement or substitute for infants. In some stores, these products are placed on shelves alongside infant formulas or oral electrolyte solutions. Product packaging may advocate the use of bottled water for mixing with baby foods or juices but also for drinking by infants. Labels also may indicate that the water contains added minerals that babies need, including calcium, magnesium, and potassium. However, the quantity of such minerals--which are often used for flavor enhancement--may be unspecified. These products, generally priced at less than $1 per gallon, are considerably less expensive than infant formula or juices. The physician who reported both cases in Wisconsin reviewed the medical records for all infants aged less than 1 year who had been admitted to the children's hospital during 1984-1993 for diagnosis and/or treatment of hyponatremic seizures; 27 additional cases were identified. All 27 infants had been fed solute-free water in excessive amounts; 25 cases were attributed to dietary water intoxication. No cases were associated with bottled water products. In addition to the two cases described in this report, from August 1993 through January 1994, FDA received reports of three other infants who were hospitalized because of water intoxication. For two of these cases, the reporting physician believed that bottled drinking water was used instead of oral rehydration solution. Because of the reports of bottled water use associated with hyponatremia, FDA has recommended to the International Bottled Water Association that the labels of these products clearly indicate their contents and appropriate uses (e.g., rehydrating infant formula and mixing with juices) and that they should not be used in lieu of infant formula. Several manufacturers have submitted their existing labels for FDA review. Human milk and infant formula provide infants with sufficient quantities of water for growth and for replacement of water lost through the skin, lungs, feces, and urine. Supplemental water generally is not indicated for healthy infants who are not yet receiving solid foods (i.e., breast-fed or formula-fed), except possibly during hot weather for formula-fed infants (9). Physicians and other health-care providers should discourage parents from using water (either tap or bottled) as a supplement for infants aged less than 6 months and should advise parents that children of any age who have diarrhea or vomiting should be given oral rehydration solution instead of solute-free water (10). Parents, guardians, and other child-care providers should be educated about the potential hazard solute-free water poses to the health of infants if used inappropriately. Cases of hyponatremia associated with excessive water intake should be reported to the local health department. References 1. Dugan S, Holliday MA. Water intoxication in two infants following the voluntary ingestion of excessive fluids. Pediatrics 1967;39:418-20. 2. Nickman SL, Buckler JM, Weiner LB. Further experiences with water intoxication. Pediatrics 1968;41:149-51. 3. Crumpacker RW, Kriel RL. Voluntary water intoxication in normal infants. Neurology 1973;23:1251-5. 4. Partridge JC, Payne ML, Leisgang JJ, Randolf JF, Rubenstein JH. Water intoxication secondary to feeding mismanagement: a preventable form of familial seizure disorder in infants. Am J Dis Child 1981;135:38-40. 5. Keating JP, Schears GJ, Dodge PR. Oral water intoxication in infants: an American epidemic. Am J Dis Child 1991;145:985-90. 6. Finberg L. Water intoxication: a prevalent problem in the inner city. Am J Dis Child 1991;145:981-2. 7. Schaeffer AV, Ditchek S. Current social practices leading to water intoxication in infants. Am J Dis Child 1991;145:27-8. 8. Gruskin AB, Baluarte HJ, Prebis JW, Polinsky MS, Morgenstern BZ, Perlman SA. Serum sodium abnormalities in children. Pediatr Clin North Am 1982;29:907-32. 9. Committee on Nutrition, American Academy of Pediatrics. Pediatric nutrition handbook. 3rd ed. Elk Grove Village, Illinois: American Academy of Pediatrics, 1993. 10. CDC. The management of acute diarrhea in children: oral rehydration, maintenance, and nutritional therapy. MMWR 1992;41(no. RR-16). ------------------------------ Date: Sun, 11 Sep 94 08:01:48 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] AIDS Among Racial/Ethnic Minorities Message-ID: AIDS Among Racial/Ethnic Minorities -- United States, 1993 In 1993, local, state, and territorial health departments reported to CDC 58,538 cases of acquired immunodeficiency syndrome (AIDS) among racial/ethnic minorities (Table 1). A total of 38,544 (66%) cases were reported among blacks, 18,888 (32%) among Hispanics, 767 (1%) among Asians/Pacific Islanders, and 339 (1%) among American Indians/Alaskan Natives*. These cases represented 55% of the 106,949 AIDS cases reported in the United States in 1993. Rates of AIDS and modes of human immunodeficiency virus (HIV) exposure varied substantially both among and within minority populations. This report describes these differences and summarizes the epidemiologic characteristics of AIDS cases reported among racial/ethnic minorities during 1993. In 1993, racial/ethnic minorities accounted for 45,039 (51%) of 89,165 AIDS cases reported among adult and adolescent males (aged greater than or equal to 13 years) and 12,696 (75%) of 16,824 cases among adult and adolescent females. Of the 959 cases reported among children (aged less than 13 years), 803 (84%) were among minorities. In 1993, 111 AIDS cases per 100,000 adults and adolescents were reported among racial/ethnic minorities. Rates were highest among blacks and Hispanics (162 and 90, respectively) and lowest among American Indians/Alaskan Natives and Asians/Pacific Islanders (24 and 12, respectively). Blacks are disproportionately affected by the HIV epidemic: the AIDS rate for black females (73) was approximately 15 times greater than that for white females (5), and the rate for black males (266) was nearly five times greater than that for white males (57). AIDS rates for blacks and Hispanics varied substantially by geographic region (Figures 1 and 2).** Rates for both groups were generally highest in the Northeast.*** For blacks, rates were highest in Vermont (445****), New York (379), New Jersey (373), and Florida (366). AIDS rates for blacks were less than the overall adult and adolescent rate (50) in 11 (22%) of the 50 states. For Hispanics, AIDS rates were highest in New York (293), Connecticut (271), Massachusetts (249), and Pennsylvania (246). Rates for Hispanics were less than the overall rate in 26 (52%) of the 50 states. In Arizona, California, Hawaii, Mississippi, New Mexico, Texas, Wyoming, and the District of Columbia, AIDS rates for Hispanics were lower than rates for whites. Among males who were racial/ethnic minorities, the most common modes of HIV exposure were male-male sex (39%) and injecting-drug use (IDU) (38%). Among females, the most common exposures were IDU (47%) and heterosexual contact (37%). However, the distribution of exposures differed substantially by race/ethnicity (Table 2) and geographic location. IDU was the principal HIV exposure among blacks and Hispanics; most (60%) IDU-associated cases among blacks and Hispanics were reported in the Northeast and Puerto Rico. Male-male sex was the primary exposure among Asians/Pacific Islanders and American Indians/Alaskan Natives. The proportion of AIDS cases with no reported risk for HIV infection was greater among racial/ethnic minorities than among whites. In geographic locations outside the Northeast, patterns of HIV exposure among blacks and Hispanics varied substantially. Among black males with AIDS, male-male sex was the most common mode of exposure in the District of Columbia, the U.S. Virgin Islands, and 32 (67%) of 48 states that reported AIDS cases among black males. Among Hispanic males, male-male sex was the most common exposure in the District of Columbia and 34 (71%) of 48 states that reported cases among Hispanic males. Among black females, IDU was the most common exposure in the District of Columbia and 23 (52%) of 44 states that reported AIDS cases among black females, and heterosexual contact was the leading exposure in 20 (45%) states. Among Hispanic females, heterosexual contact was the most common exposure in the District of Columbia, Puerto Rico, and 19 (54%) of 35 states that reported AIDS cases among Hispanic females, and IDU was the leading exposure in 10 (29%) states. Reported by: Local, state, and territorial health depts. Div of HIV/AIDS, National Center for Infectious Diseases, CDC. Editorial Note: Following the 1993 expansion of the AIDS surveillance case definition, the number of AIDS cases reported among racial/ethnic minorities in 1993 increased 135% over that in 1992, while the number among whites increased 114%. The greater increase in cases among racial/ethnic minorities is consistent with trends in the number of AIDS cases reported in previous years, representing a continued increase in the epidemic among certain minority populations. However, because the increase in cases reported in 1993 reflects a transient effect of the expansion of the AIDS surveillance case definition, the number of AIDS cases reported in 1994 is expected to be lower than that in 1993 (1). AIDS surveillance may underestimate the number of AIDS cases reported among certain minority populations because of misclassification of race/ethnicity on medical records, which are the source for AIDS case reports. For example, a study conducted during June 1990-August 1992 that compared self-reported race/ethnicity with that listed on AIDS case reports indicated that AIDS cases among Asians/Pacific Islanders (12 cases), American Indians/Alaskan Natives (14), and Hispanics (249) were underreported by 25%, 21%, and 18%, respectively; in comparison, AIDS cases among whites and blacks were overreported by 4% and 2%, respectively (2). The increase in the number of persons with AIDS has greatly affected death rates for racial/ethnic minorities, particularly young adults. In 1991, among males aged 25-44 years, HIV infection was the leading cause of death for blacks and Hispanics and the sixth leading cause for Asians/Pacific Islanders and American Indians/Alaskan Natives. Among females in this age group, HIV infection was the third leading cause of death for blacks and Hispanics, the seventh for American Indians/Alaskan Natives, and the ninth for Asians/Pacific Islanders. Provisional mortality data for 1992***** indicate that HIV infection was the second leading cause of death among black females aged 25-44 years (3); in 1991, the HIV/AIDS death rate for all black females was approximately 10 times the rate for white females (4). Most AIDS cases classified as having no reported risk for HIV infection will be reclassified into one of the known exposure groups after additional follow-up. A greater proportion of racial/ethnic minorities than whites may be initially classified without an HIV risk because of unrecognized heterosexual transmission, the diagnosis of AIDS at or near death, and language and cultural differences that make risk ascertainment more difficult. Although race and ethnicity are not risk factors for HIV transmission, they are markers for underlying social, economic, and cultural factors and personal behaviors that affect health (5). Socioeconomic status in particular is associated with morbidity and premature mortality (6); unemployment, poverty, and illiteracy are correlated with decreased access to health education, preventive services, and medical care, resulting in an increased risk for disease (5). In 1992, 33% of blacks and 29% of Hispanics lived below the federal poverty level,****** compared with 13% of Asians/ Pacific Islanders and 10% of whites (7). Therefore, the social, economic, and cultural context of HIV infection should be considered when designing and implementing prevention programs for diverse populations. Although IDUs in the Northeast and Puerto Rico accounted for 24% of all AIDS cases reported among racial/ethnic minorities, AIDS rates and modes of HIV exposure varied greatly among minority populations in other areas of the country. HIV serosurveillance studies have demonstrated similar patterns (8). In addition, the incidence of AIDS and the distribution of HIV exposures among Hispanics and Asians/Pacific Islanders vary in relation to their place of birth (9,10). These geographic and racial/ethnic differences are directly related to variations in the prevalence of HIV infection, the type and frequency of behaviors associated with HIV transmission, and the time of introduction of HIV into the specific communities; and indirectly related to the social, economic, and cultural influences within those communities. Because the epidemiology of HIV infection varies considerably by geographic region and among racial/ethnic populations, preventive interventions should be developed at the local level to ensure that they reflect the language, culture, and behavioral norms of the targeted community. CDC is collaborating with local, state, and territorial health departments to establish planning groups composed of community representatives, epidemiologists, behavioral scientists, and other public health practitioners who will participate in the development and implementation of HIV-prevention programs. References 1. CDC. Update: impact of the expanded AIDS surveillance case definition for adolescents and adults on case reporting--United States, 1993. MMWR 1994;43:160-1,167-70. 2. Kelly JJ, Chu SY, Diaz T, Leary LS, Buehler JW. Race/ethnicity misclassification of persons reported with AIDS. Ethn Dis (in press). 3. CDC. Update: mortality attributable to HIV infection among persons aged 25-44 years--United States, 1991 and 1992. MMWR 1993;42:869-72. 4. NCHS. Excess deaths and other mortality measures for the black population, 1979-81 and 1991. Hyattsville, Maryland: US Department of Health and Human Services, Public Health Service, CDC, 1994. 5. National Commission on AIDS. The challenge of HIV/AIDS in communities of color. Washington, DC: National Commission on AIDS, December 1992. 6. Adler NE, Boyce WT, Chesney MA, Folkman S, Syme SL. Socioeconomic inequalities in health. JAMA 1993;269:3140-5. 7. Bureau of the Census. Poverty in the United States, 1992. Washington, DC: US Department of Commerce, Economics and Statistics Administration, Bureau of the Census, September 1993. 8. CDC. National HIV serosurveillance summary: results through 1992. Atlanta: US Department of Health and Human Services, Public Health Service, CDC, November 1993. 9. Diaz T, Buehler JW, Castro KG, Ward JW. AIDS trends among Hispanics in the United States. Am J Public Health 1993;83:504-9. 10. Metler R, Hu DJ, Fleming PL, Ward JW. AIDS among Asians and Pacific Islanders (A/PI) reported in the U.S.A. [Abstract no. PCO325]. Vol 2. Xth International Conference on AIDS/International Conference on STD. Yokohama, Japan, August 10-11, 1994:241. * The racial/ethnic categories used in federal statistics are specified in the Office of Management and Budget's Directive 15, Race and Ethnic Standards for Federal Statistics and Administrative Reporting (1978). ** The numbers of AIDS cases reported among Asians/Pacific Islanders and American Indians/ Alaskan Natives were insufficient to analyze by state. *** New England and Middle Atlantic regions. **** Based on six reported AIDS cases in 1993. ***** Provisional data were available only for blacks and whites without stratification by Hispanic ethnicity. ****** Poverty statistics are based on definitions originated by the Social Security Administration in 1964, subsequently modified by the federal interagency committees in 1969 and 1980, and prescribed by the Office of Management and Budget as the standard to be used by federal agencies for statistical purposes. ------------------------------ Date: Sun, 11 Sep 94 08:02:46 MST From: mednews (HICNet Medical News) To: hicnews Subject: [MMWR] Prilocaine Induced Methemogloinemia Message-ID: Prilocaine-Induced Methemoglobinemia -- Wisconsin, 1993 Methemoglobinemia is an uncommon disorder in which hemoglobin is not oxidized and not capable of binding oxygen. This condition may be associated with exposure to nitrate-contaminated drinking water, aniline dyes, and amide-containing medications. Ortho-toluidine, a metabolite of the anesthetic prilocaine, also can induce this condition (1). During March-August 1993, three Wisconsin women treated by the same oral surgeon developed methemoglobinemia after being injected with a prilocaine-based local anesthetic. The surgeon notified the Division of Health, Wisconsin Department of Health and Social Services, of these cases 1 week after the third case occurred. This report summarizes the case investigations. Case 1. A 22-year-old woman (body weight: 127 lbs [58 kg]) sought care at an emergency department (ED) for dizziness approximately 5 hours after her oral surgeon extracted four wisdom teeth. The oral surgeon had administered anesthetic of 560 mg prilocaine (4.4 mg per pound [9.7 mg/kg] of body weight) by local injection and 90 mg methohexital sodium, 10 mg diazepam, and 6 mg dexamethasone sodium phosphate by intravenous infusion. On examination in the ED, the patient was alert but reported slight dizziness. The emergency physician noted perioral and nailbed cyanosis. Her oral temperature was 99.1 F (37.3 C); pulse, 108/minute; respirations, 20/minute; and blood pressure, 130/90 mmHg. A sample of venous blood was described as brown and indicated a methemoglobin level of 27%. Methemoglobinemia was diagnosed, and treatment was initiated with oxygen; in addition, 100 mg methylene blue was administered intravenously over 5 minutes. Within 1 hour, the patient was discharged. She recovered fully. Case 2. A 33-year-old woman (body weight: 112 lbs [51 kg]) was transported by ambulance from her oral surgeon's office to an ED 4 hours after extraction of four wisdom teeth. Her symptoms included fatigue, cyanosis, and orthostatic hypotension with syncope. The oral surgeon had administered 560 mg prilocaine (5.0 mg per pound [11.0 mg/kg] of body weight) by local injection and 60 mg methohexital sodium, 10 mg diazepam, and 0.025 mg fentanyl intravenously. On examination in the ED, her oral temperature was 98.1 F (36.7 C); pulse, 66/minute; respirations, 12/minute; blood pressure, 122/88 mmHg; and peripheral oxygen saturation, 89%. A venous blood sample revealed a methemoglobin level of 28%. Methemoglobinemia was diagnosed, and she was administered oxygen through a nasal cannula and 100 mg methylene blue intravenously over 5 minutes. One hour after treatment, her methemoglobin level was 2%, and the patient was discharged. She recovered fully. Case 3. A 17-year-old female (body weight: 105 lbs [48 kg]) was transported by ambulance from her oral surgeon's office to an ED after she developed tachycardia, drowsiness, and shakiness while being prepared for extraction of four wisdom teeth. The oral surgeon had administered 480 mg prilocaine (4.6 mg per pound [10.1 mg/kg] of body weight) by local injection and 7.5 mg diazepam, 6 mg dexamethasone sodium phosphate, and 0.025 mg fentanyl intravenously. The patient had been taking an oral contraceptive and, 1 week earlier, her physician had begun treating her with amitriptyline for headaches. In addition, she had a history of exercise-induced asthma and allergies to amoxicillin and cefaclor. On examination in the ED, she was alert and oriented. Her oral temperature was 98.1 F (36.7 C); pulse, 110/minute; respirations, 20/minute; blood pressure, 120/92 mmHg; peripheral oxygen saturation, 89%; and methemoglobin level, 10.7%. Methemoglobinemia was diagnosed, and she was treated with oxygen through a nasal cannula and an intravenous infusion of normal saline. The patient was hospitalized overnight for observation and recovered fully. Reported by: L Knobeloch, PhD, J Goldring, PhD, W LeMay, DDS, H Anderson, MD, Environmental Epidemiologist, Div of Health, Wisconsin Dept of Health and Social Svcs. Editorial Note: Prilocaine is a lidocaine homologue and the only secondary amine local anesthetic that remains in clinical use. Prilocaine is biotransformed by hepatic amidase to aminophenol metabolites (i.e., ortho-toluidine and N-propylalanine), which subsequently can oxidize hemoglobin to methemoglobin. Administration of prilocaine in doses exceeding 400 mg has been associated with methemoglobinemia in adults. Proportionately lower doses may cause this problem in children (1). Methemoglobin levels above 10% may result in clinical anoxia (2), and levels above 60% can cause stupor, coma, and death. The findings in this report indicate that doses of prilocaine only slightly exceeding the recommended therapeutic dose have the potential to cause methemoglobinemia. The manufacturer's package insert for prilocaine recommends a therapeutic dose of 4 mg/lb* (8 mg/kg) for "normal healthy adults," with a maximum dose of 600 mg indicated for persons weighing 150 lbs (68 kg) or more. For persons weighing less than 150 lbs (68 kg), the maximum dose must be accurately adjusted for body weight to reduce the risk for adverse effects. The Food and Drug Administration (FDA) has investigated the incidents in this report and recommends that the manufacturer update the package insert for prilocaine to emphasize the importance of adjusting dosage for body weight, particularly for persons weighing less than 150 lbs (68 kg). During January 1992-September 1993, FDA received nine reports of prilocaine-induced methemoglobinemia. However, methemoglobinemia may be underreported because 1) some persons may develop only mild symptoms that do not require medical care, 2) some cases may not be recognized as prilocaine-induced, and 3) only drug manufacturers are required by law to report these events. Oral surgeons and other health practitioners should use accurate body weight information to calculate safe doses of prilocaine and should know that doses exceeding 4.0 mg per pound (8 mg/kg) of body weight pose a risk to healthy adults. The risk for adverse effects associated with prilocaine use is increased for infants, persons with underlying health problems (i.e., anemia or diseases affecting the respiratory or cardiovascular systems), persons with hereditary deficiencies of glucose-6-phosphate dehydrogenase and methemoglobin reductase, and persons taking other oxidant drugs (e.g., nitrite-containing medications, sulfonamides, antimalarials, or acetaminophen). References 1. Astra Pharmaceutical Products, Inc. Brief summary of prescribing information: Citanest Plain[Registered] and Citanest[Registered] Forte [Package insert]. Westborough, Massachusetts: Astra Pharmaceutical Products, Inc, 1992. 2. National Academy of Sciences. The health effects of nitrate, nitrite, and N-nitroso compounds. Washington, DC: National Academy Press, 1981. ------------------------------ End of HICNet Medical News Digest V07 Issue #42 *********************************************** --- Editor, HICNet Medical Newsletter Internet: david@stat.com FAX: +1 (602) 451-1165 Bitnet : ATW1H@ASUACAD