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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

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----------------------------------------------------------------------

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: <[e-mail]>

       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: <[e-mail]>

        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: <[e-mail]>

              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: <[e-mail]>

         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: <[e-mail]>

   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: <[e-mail]>

    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
***********************************************


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