home
***
CD-ROM
|
disk
|
FTP
|
other
***
search
/
Shareware Overload Trio 2
/
Shareware Overload Trio Volume 2 (Chestnut CD-ROM).ISO
/
dir26
/
hicn746.zip
/
HICN746.TXT
< prev
Wrap
Text File
|
1994-10-03
|
93KB
|
1,400 lines
HICNet Medical News Digest Sat, 24 Sep 1994 Volume 07 :
Issue 46
Today's Topics:
[MMWR 16 Sept 94] Inadequately Filtered Drinking Water
[MMWR] Salmonella enteritidis associated with Home Made Ice Cream
Reflections on First International Symposium on Brain Death
+------------------------------------------------+
! !
! 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: Sat, 24 Sep 94 16:07:45 MST
From: mednews@stat.com (HICNet Medical News)
To: hicnews
Subject: [MMWR 16 Sept 94] Inadequately Filtered Drinking Water
Message-ID: <mFJ7sc1w165w@stat.com>
Assessment of Inadequately Filtered
Public Drinking Water -- Washington, D.C.,
December 1993
The risk for waterborne infectious diseases increases when
filtration and other standard water-treatment measures fail. On
December 6, 1993, water-treatment plant operators in the District of
Columbia (DC) began to have difficulty maintaining optimal filter
effectiveness. On December 7, filter performance worsened, and levels
of turbidity (i.e., small suspended particles) exceeded those
permitted by U.S. Environmental Protection Agency (EPA) standards. On
December 8, DC residents were advised to boil water intended for
drinking because of high municipal water turbidity that may have
included microbial contaminants. Although adequate chlorination of the
DC municipal water was maintained throughout the period of increased
turbidity, the parasite Cryptosporidium parvum is highly resistant to
chlorination. Because of the increased risk for infection with this
organism and other enteric pathogens, the DC Commission of Public
Health and CDC conducted four investigations to determine whether
excess cases of diarrheal illness occurred because residents drank
inadequately filtered water. This report describes the results of
these investigations.
The investigations included a random-digit-dialed telephone
survey of DC residents and retrospective reviews of records from two
emergency departments, two nursing homes, and seven hospital
microbiology laboratories. The occurrence of diarrheal illness or
presence of organisms in stool during the 2 weeks before the turbidity
violation (period 1: November 22-December 5) was compared with that
during the 2-3 weeks after the violation was first noted (period 2:
December 6-December 21 or 26). The incubation period for
cryptosporidiosis typically ranges from 2 to 14 days.
Telephone survey. The telephone survey sampled 1197 household
members (0.2% of DC's 600,000 residents) from 462 households in all
22 DC residential ZIP code areas. The percentage of persons who
reported having diarrhea (i.e., three or more loose or watery stools
in a 24-hour period) were similar for period 1 (the reference period)
and period 2 (2.8% versus 3.5%, respectively; relative risk [RR]=1.2;
95% confidence interval [CI]=0.8-1.9). A total of 37% of persons
reported that bottled water was their principal source of drinking
water at home, and 30% reported that bottled water was their primary
source of drinking water both at home and at work. For both periods,
reported use of bottled water was similar for persons with and without
diarrhea.
Hospital emergency department survey. During the two periods,
totals of 2140 (period 1) and 3315 (period 2) persons were evaluated
at two DC hospital emergency departments. Medical records were
reviewed for all persons with diagnoses suggestive of gastrointestinal
illness* (104 and 211 persons for periods 1 and 2, respectively). The
percentage of all persons who had diarrhea recorded in their emergency
department charts was similar for periods 1 and 2 (1.5% versus 2.0%;
RR=1.3; 95% CI=0.9-2.0). For both periods, approximately 70% of
patients with diarrheal illness were DC residents. The percentages of
stool specimens that were positive for enteric pathogens (i.e.,
bacteria, parasites, or rotavirus antigen) were similar for the two
periods. During each period, two stool specimens were examined for
Cryptosporidium: none were positive during period 1, and one was
positive during period 2.
Nursing home survey. Medical records were reviewed for all 443
residents from two selected nursing homes (14% of the 3156 nursing
home beds in DC). During both periods, the mean numbers of bowel
movements per person per day were 1.3. In addition, the daily mean
number of residents with loose or large-volume bowel movements were
similar (27.1 and 27.8 persons for periods 1 and 2), and antidiarrheal
medications were given at the same rate (0.002 doses per person per
day) during both periods.
Microbiology laboratory survey. Data were obtained from
microbiology laboratories of seven (64%) of the 11 DC hospitals.
Although the total number of stool specimens examined for
Cryptosporidium increased from period 1 (32 specimens) to period 2 (54
specimens), the percentage positive was lower--but not statistically
different--for period 2 (12.5% versus 7.4%; RR=0.6; 95% CI=0.2-2.2).
The percentages of stools positive for other pathogens (i.e.,
bacteria, Giardia lamblia, and rotavirus antigen) were similar for
both periods.
Reported by: MN Akhter, MD, Commissioner, ME Levy, MD, District
Epidemiologist, C Mitchell, R Boddie, District of Columbia Commission
of Public Health. N Donegan, B Griffith, M Jones, Washington Hospital
Center; TO Stair, MD, Georgetown Univ Medical Center, Washington, DC.
Epidemiology Br, Div of Parasitic Diseases, National Center for
Infectious Diseases, CDC.
Editorial Note: To ensure safe municipal drinking water supplies,
water-treatment programs employ multiple barriers to prevent
contaminants from reaching the consumer. These barriers include
protection of the watershed, chemical disinfection, and filtration of
surface water supplies such as lakes and rivers. When one of these
barriers is absent or fails, the risk for waterborne disease may
increase. The failure of the filtration process in DC prompted
particular concerns about contamination with and exposure to
Cryptosporidium.
Outbreaks of cryptosporidiosis resulting from surface water
contamination have occurred when turbidity was 0.9-2.0 nephelometric
turbidity units (NTU)**. For example, in a waterborne outbreak in
Milwaukee in 1993, a peak turbidity of 1.7 NTU was associated with
illness in approximately 400,000 persons (1). In DC, the turbidity
levels reached 9.0 NTU.
Because Cryptosporidium is highly resistant to chlorination,
disinfection of water is not a reliable method for preventing exposure
to it. The failure to detect increased rates of illness among
residents of DC probably reflects the absence of, or presence of only
a small number of, oocysts in the water that supplied the municipal
water-treatment plant at the time the filtration failure occurred. In
addition, the investigations in DC did not detect any increase in
diarrheal illness associated with the elevated water turbidity;
however, the sample sizes in these investigations were too small to
rule out low-level transmission of waterborne agents. For example, the
telephone survey probably would not have detected an outbreak
affecting fewer than 12,000 persons.
Cryptosporidium is present in 65%-87% of surface water samples
tested throughout the United States (2,3). However, because current
techniques to detect Cryptosporidium in water are cumbersome, costly,
and insensitive, tests to detect it are not routinely performed by
water utilities. During 1995, EPA plans to collect additional
information about Cryptosporidium and other microorganisms in surface
water used by municipal water-treatment facilities in the United
States and to assess the effectiveness of water-treatment methods for
removing them.***
The early detection of waterborne outbreaks of cryptosporidiosis
is difficult for at least four reasons: 1) many physicians are unaware
that Cryptosporidium can cause watery diarrhea; 2) the symptom complex
often resembles a viral syndrome; 3) clinical laboratories often do
not routinely test for Cryptosporidium when a physician requests a
stool examination for ova and parasites; and 4) few states include
cryptosporidiosis as a reportable disease.
Variations in recommendations regarding the duration of boiling
during boil-water advisories have reflected uncertainty about how long
some organisms can survive. On the basis of a recent literature
review, CDC and EPA recommend that water be rendered microbiologically
safe for drinking by bringing it to a rolling boil for 1 minute; this
will inactivate all major waterborne bacterial pathogens (i.e., Vibrio
cholerae, enterotoxigenic Escherichia coli, Salmonella, Shigella
sonnei, Campylobacter jejuni, Yersinia enterocolitica, and Legionella
pneumophila) and waterborne protozoa (e.g., Cryptosporidium parvum,
Giardia lamblia, and Entamoeba histolytica [4-7]). Although
information about thermal inactivation is incomplete for waterborne
viral pathogens, hepatitis A virus--considered one of the more
heat-resistant waterborne viruses (8)--also is rendered noninfectious
by boiling for 1 minute (9). If viral pathogens are suspected in
drinking water in communities at elevations above 6562 ft (2 km), the
boiling time should be extended to 3 minutes.
References
1. Mac Kenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in
Milwaukee of Cryptosporidium infection transmitted through the public
water supply. N Engl J Med 1994;331:161-7.
2. Rose JB, Gerba CP, Jakubowski W. Survey of potable water supplies
for Cryptosporidium and Giardia. Environmental Science and Technology
1991;25:1393-400.
3. LeChevallier MW, Norton WD, Lee RG. Occurrence of Giardia and
Cryptosporidium spp. in surface water supplies. Appl Environ Microbiol
1991;57:2610-6.
4. Bandres JC, Mathewson JJ, Dupont HL. Heat susceptibility of
bacterial enteropathogens. Arch Intern Med 1988;148:2261-3.
5. Anderson BC. Moist heat inactivation of Cryptosporidium sp. Am J
Public Health 1985;75: 1433-4.
6. Bingham AK, Jarroll EL, Meyer EA. Giardia sp.: physical factors of
excystation in vitro, and excystation vs eosin exclusion as
determinants of viability. Exp Parasitol 1979;47:284-91.
7. Boeck WC. The thermal-death point of the human intestinal protozoan
cysts. Am J Hygiene 1921;1:365-87.
8. Larkin EP. Viruses of vertebrates: thermal resistance. In: Rechcigl
M Jr, ed. CRC handbook of foodborne diseases of biological origin.
Boca Raton, Florida: CRC Press, Inc, 1983:3-24.
9. Krugman S, Giles JP, Hammond J. Hepatitis virus: effect of heat on
the infectivity and anti-genicity of the MS-1 and MS-2 strains. J
Infect Dis 1970;122:432-6.
*Gastroenteritis, diarrhea, nausea, vomiting, gastritis, viral
syndrome, dehydration, and hyperemesis gravidarum.
**The American Waterworks Association encourages water utilities to
maintain turbidity measurements of water as it leaves the treatment
plant at or below 0.1 NTU.
***59 FR 6332.
------------------------------
Date: Sat, 24 Sep 94 16:09:00 MST
From: mednews@stat.com (HICNet Medical News)
To: hicnews
Subject: [MMWR] Salmonella enteritidis associated with Home Made Ice
Cream
Message-ID: <PHJ7sc2w165w@stat.com>
Outbreak of Salmonella enteritidis Associated
with Homemade Ice Cream -- Florida, 1993
On September 7, 1993, the Epidemiology Program of the Duval
County (Florida) Public Health Unit was notified about an outbreak of
acute febrile gastroenteritis among persons who attended a cookout at
a psychiatric treatment hospital in Jacksonville, Florida. This report
summarizes the outbreak investigation.
On September 6, seven children (age range: 7-9 years) and seven
adults (age range: 29-51 years) attended the cookout at the hospital.
A case of gastroenteritis was defined as onset of diarrhea, nausea or
vomiting, abdominal pain, or fever within 72 hours of attending the
cookout. Among the 14 attendees, 12 cases (in five of the children and
all seven adults) were identified. The median incubation period was
14 hours (range: 7-21 hours); the mean duration of illness was 18
hours (range: 8-40 hours). Predominant symptoms were diarrhea (93%),
nausea or vomiting (86%), abdominal pain (86%), and fever (86%). All
ill persons were examined by a physician. Salmonella enteritidis (SE)
(phage type 13a) was isolated from stool of three of the seven
patients from whom specimens were obtained.
Eleven of the 12 ill persons had eaten homemade ice cream served
at the cookout. No other food item was associated with illness.
Testing of a sample of ice cream revealed contamination with SE (phage
type 13a).
The ice cream was prepared at the hospital on September 6 using
a recipe that included six grade A raw eggs. An electric ice cream
churn was used to make the ice cream approximately 3 hours before the
noon meal. The ice cream had been properly cooled, and no
food-handling errors were identified. The person who prepared the ice
cream was not ill before preparation; however, she became ill 13 hours
after eating the ice cream. Her stool specimen was one of the three
stools positive for SE (phage type 13a).
The U.S. Department of Agriculture's (USDA) Animal and Plant
Health Inspection Service attempted to trace the implicated eggs back
to the farm of origin. The hospital purchased eggs from a distributor
in Florida. However, the traceback was terminated because the
implicated eggs from the distributor had been purchased from two
suppliers--one of whom bought and mixed eggs from many different
sources. Current USDA Salmonella regulations limit testing of flocks
to one clearly implicated flock.
Reported by: P Buckner, MPH, D Ferguson, HRS Duval County Public
Health Unit, F Anzalone, MD, D Anzalone, DrPH, College of Health, Univ
of North Florida, Jacksonville; J Taylor, Office of Lab Svcs, WG
Hlady, MD, RS Hopkins, MD, State Epidemiologist, State Health Office,
Florida Dept of Health and Rehabilitative Svcs. Foodborne and
Diarrheal Diseases Br, Div of Bacterial and Mycotic Diseases, National
Center for Infectious Diseases, CDC.
Editorial Note: The outbreak described in this report represents the
fourth SE outbreak in Florida since 1985; this outbreak is the first
in the state to implicate eggs. In the United States, the number of
sporadic and outbreak-associated cases of SE infection has increased
substantially since 1985; much of the increase can be attributed to
consumption of raw or undercooked eggs (1-3). During 1983-1992, the
proportion of reported Salmonella isolates that were SE increased from
8% to 19%. During 1985-1993, a total of 504 SE outbreaks were reported
to CDC and resulted in 18,195 cases, 1978 hospitalizations, and 62
deaths (Table 1). Of the 233 outbreaks for which epidemiologic
evidence was sufficient to implicate a food vehicle, 193 (83%) were
associated with eggs. Of these 193 outbreaks, 14 (7%) were associated
with consumption of homemade ice cream. No outbreaks have been
associated with pasteurized egg products.
After eggs are identified by public health officials as the
cause
of an SE outbreak, USDA attempts to trace the implicated eggs back to
the farm of origin to conduct serologic and microbiologic assessments
of the farm. If SE is detected on the source farm, the eggs are
diverted to pasteurization, or the flocks are destroyed. Under current
regulations, USDA can pursue the traceback only if one farm is
identified as the source. During 1990-1993, the success rate of USDA
tracebacks to the source farm declined from 86% (19/22 outbreaks) in
1990 to 17% (3/21 outbreaks) in 1993. The rate declined primarily
because eggs increasingly have been marketed in shipments containing
eggs from multiple sources.
Although 0.01% of all eggs contain SE and, therefore, pose a
risk
for infection with SE (4), raw or undercooked eggs are consumed
frequently. Based on the Food and Drug Administration (FDA) Food
Safety Survey conducted in 1993, 53% of a nationally representative
sample of 1620 respondents reported ever eating foods containing raw
eggs; of these, 50% had eaten cookie batter, and 36% had eaten ice
cream containing raw eggs (S. Fein, FDA, personal communication,
September 9, 1994). Many persons may eat raw or undercooked eggs
because they are unaware that eggs are a potential source of
Salmonella (3) and that certain foods (e.g., homemade ice cream,
cookie batter, Caesar salad, and hollandaise sauce) contain raw eggs.
Consumers should be informed that eating undercooked eggs may
result in Salmonella infection. In addition, eggs should be
refrigerated to prevent proliferation of Salmonella if present and
should be cooked thoroughly to kill Salmonella. Because most serious
------------------------------------------------------------------------
References
1. St. Louis ME, Morse DL, Potter ME, et al. The emergence of grade
A eggs as a major source of Salmonella enteritidis infections: new
implications for the control of salmonellosis. JAMA 1988;259:2103-7.
2. Mishu B, Koehler J, Lee LA, et al. Outbreaks of Salmonella
enteritidis infections in the United States, 1985-1991. J Infect Dis
1994;169:547-52.
3. Hedberg CW, David MJ, White KE, MacDonald KL, Osterholm MT. Role
of egg consumption in sporadic Salmonella enteritidis and Salmonella
typhimurium infections in Minnesota. J Infect Dis 1993;167:107-11.
4. Mason J, Ebel E. APHIS Salmonella enteritidis Control Program
[Abstract]. In: Snoeyenbos GH, ed. Proceedings of the Symposium on the
Diagnosis and Control of Salmonella. Richmond, Virginia: US Animal
ealth Association, 1992:78.
------------------------------
Date: Sat, 24 Sep 94 16:13:51 MST
From: mednews@stat.com (HICNet Medical News)
To: hicnews
Subject: Reflections on First International Symposium on Brain Death
Message-ID: <sPJ7sc3w165w@stat.com>
REFLECTIONS ON THE FIRST INTERNATIONAL SYMPOSIUM ON BRAIN
DEATH. (Havana, September 22-25, 1992).
By: CALIXTO MACHADO
President of the Organizing Committee
Correspondence: Dr. CALIXTO MACHADO
Instituto de Neurologia y Neurocirugia
29 y D, Vedado, Habana 4
Ciudad de La Habana 10400
Apartado Postal 4268
CUBA
Fax: 53-7-336321
E.mail: braind@.ceniai.cu
Note: If possible, use E.mail to contact me.
The "FIRST INTERNATIONAL SYMPOSIUM ON BRAIN DEATH" was
held at the International Conference Center, Havana, between
September 22 and 25, 1992.
Delegates from twenty-one countries attended this sunny
and Caribbean city to discuss many controversial issues
concerning brain death and other related states. Argentina
provided the biggest delegation (22 attenders).
The Opening Ceremony was highlighted by the performance
of the National Chorus of Cuba. The singing of beautiful
cuban songs prepared the delegates for the words of
welcome given by the Organizing Committee, emphasizing that
even in such a scientific context, there would be
opportunities to discuss human dignity, and life as well as
death.
On the morning of September 22, delegates enjoyed four
striking opening lectures. Like Olympic Gold Medallists,
Earl Walker (U. S. A.), Christopher Pallis (U. K.), Gaetano
Molinari (U. S. A.) and Daniel Wikler (U. S. A.) followed
one another to the rostrum.
In his address "Dead or Alive" Earl Walker presented
much of the basic material derived from the Collaborative
Study of Cerebral Survival sponsored by the National
Institute of Neurological and Communicative Diseases and
Stroke (1). For ages, people had considered life to exist
as long as an individual was breathing. It was later
realized that respiration was a means of maintaining the
heart which circulated the blood. Life was then attributed
to cardio-respiratory action. As long as such activity
maintained the nutritional needs of the brain, the
individual was alive. But, in the middle of this century,
physicians became aware that the brain required much more
energy than other organs and, if its needs were not met, it
would cease to function, while other parts of the body
(requiring less energy) might remain viable and even
regain their activity provided the circulation was
maintained. The result would be a dead brain in a viable
body. Is such a preparation alive or dead? Before
answering that question, one had to establish the general
principles upon which the diagnosis of a dead brain could be
made. The cause of the coma had to be known, so that it
could be remedied, if possible. If the condition was not
remediable, the state of the brain (underlying all sets of
brain-death standards) had to be determined. The clinical
status could be ascertained by standard neurological
examination. Testing was, however, often complicated by
factors such as wounds, which could render it difficult to
carry out or difficult to interpret. Other confirmatory
examinations then had to be relied upon to establish the
death of the brain. But these confirmatory tests had
limitations too, some related to the quality of the
examination (such as electroencephalo-graphy) and others
quantitative aspects (such as isotopic angio-graphy). But
with the recognition of these limitations, the available
yardsticks provide a satisfactory estimate of the state of
the brain. In the rare case in which the clinical and
confirmatory test seem to be at variance, observation of
the subject for a longer period of time provided
clarification of the issue. The validity of these criteria
under such circumstances as infancy, concomitant
intoxications and impaired cardiovascular status had
been questioned. Having established the clinical states
of the subject, the physician usually had no problem in
certifying death. Problem cases required a careful
consideration of medical, religious and legal factors.
The second lecture "Brainstem death. Evolution of the
Concept", proved a detonator for future discussions. Pallis
(2, 3, 4) emphasized that most controversies concerning the
criteria for diagnosing death had sprung from a reluctance
to define death. Discussions about the validity of different
criteria could not meaningfully take place in a
philosophical vacuum. What we did (or did not or did not do)
in the Intensive Care Unit had to flow from explicitly
formulated philosophical premises. "There was only a kind of
human death: the irreversible loss of the capacity for
consciousness, combined with the irreversible loss of the
capacity to breathe (and hence to sustain a spontaneous
beat)". All death, in this perspective, was brainstem death.
But whereas there was only one death there were clearly
several ways of dying. The commonest, by far, was
circulatory arrest. But this only proved lethal if it
persisted for long enough for the brainstem to sustain
irreversible anoxic damage. Circulatory arrest of briefer
duration either had no sequelae, or cause slight, moderate
or severe neurological damage, the most pronounced form of
which was PVS (persistent vegetative state). The death of
the brainstem was nearly always the infratentorial
repercussion of supratentorial events. It implied the death
of the "brain as a whole". A diagnosis of brainstem death
had two fundamental implications. The first, pragmatic, was
that the heart would inevitably stop, within a relative
short period. This was an empirically validated observation,
to which no exception had as yet been recorded. The second,
philosophical, was that quite independently of the cardiac
prognosis an individual with a dead brainstem was already
dead (because irreversible unconscious and irreversible
apnoeic).
The distinctions between "whole brain death" (death of
every neuron in the intracranial cavity) and "brainstem
death" (death of the "brain as a whole") were, both
philosophically and in practice, of minor significance.
There were fundamental differences, however, between both
of these concepts and the various "higher brain"
formulations currently being proposed and discussed mainly
by philosophers (5, 6, 7). Their views implied that an
individual might be declared dead even if still breathing.
We would undoubtedly lose public support for transplantation
(and rightly so) if such a proposition were ever seriously
put forward.
Gaetano Molinari (U. S. A.) was the third on the
scene. He emphasized that: "still prohibiting unanimity
among physicians worldwide were only some unfortunate but
persisting choices of words". Terms like brain death (BD),
whole brain death, brainstem death, neocortical death served
only to confuse a basic issue, namely, that heartbeat, blood
pressure, and even body temperature had lost significance as
evidence of life in modern intensive care units. In
situations in which spontaneous respirations had stopped
but heartbeat persisted, death must be pronounced
"neurologically". Comparing the "whole brain" and "brain as
a whole" formulations of death, he stated that the only
situation in which the British Criteria (8) might declare
persons dead while the cerebrum retained functional capacity
was the possibility and demonstration in three cases in the
American Study (1), and subsequently by others (9), of
apnoeic coma with absent cephalic reflexes due to primary
brainstem lesions (suggesting death) while
electroencephalograms might indicate some residual
biological activity (10).
The fourth speaker in this marathon was Daniel
Wikler, presenting some remarks on "The Philosophical
Considerations on Death". Wikler was included as a
philosopher, on the professional staff of the President's
Commission for the Study of Ethical Problems in Medicine and
Biomedical and Behavioral Research (11). He asked: "Should
we consider a further revision in the definition of death,
one which would define death as permanent loss of
consciousness? This change would permit physicians to
pronounce dead patients in a PVS. Today we lack the ability
to diagnose this condition with certainty, so a further
change in the law would be unwise. Nevertheless, we might
wish to be prepared for the day when physicians acquire the
ability to diagnose PVS with certainty, at least for some
types of patient. Should such patients be considered dead
or alive?
A thought experiment suggested the need for a further
redefinition. Suppose that, at some future date, doctors
became capable of maintaining function in severed heads and
decapitated bodies. One poor man, careless in his use of an
electric saw, suffers a complete decapitation. His head is
carried in an ambulance to the Head Hospital; his body is
carried to the Body Hospital in the next town. Since no one
can be in two places at once, we must ask: Where is the
patient? Is he in the Body Hospital or the Head Hospital?
All of us would answer, if we had to make a choice, that he
was in the Head Hospital. Now, to continue the story,
suppose that the head dies, but that the patient's body
continues to live. Is he alive or dead? We cannot say he is
alive, since that would imply that at the time his head died
he magically switched his location to the Body Hospital.
Therefore we must say: he died. At this point in the story,
we have his living body, in the Body Hospital, but the
patient is not alive. But this is what we have with a
patient in PVS; and therefore we ought to say that such a
patient is not alive either. In the future, however, we will
have to address the problem of those patients who remain in
an unconscious state for many years. As an issue in
bioethics, the definition of death has been put to rest, but
it has not yet expired. In this remarkable lecture Daniel
wikler introduced the Symposium to the concept of "higher
brain formulations of death" (5, 6, 7).
The lunch break was taken up in further discussion:
three lunch panels were presented: "Famous Trial Cases" (in
relation to BD and persistent vegetative state) was
moderated by Gaetano Molinari; "Persistent Vegetative State
(PVS)" by R. Firshing (Germany) and "Do not Resuscitate
Orders", by Daniel Wikler and Stuart Youngner (U. S. A.).
The afternoon of Tuesday, September 22, proved an
interesting session in which brain death criteria in
different countries were compared. We presented the "Cuban
Criteria for Brain Death Diagnosis" (12, 13). These involved
a sequential approach for brain death diagnosis, using
multi-modality evoked potentials (MEPs) and
electroretinography (ERG) as a key step. When reviewing
literature it was clear that most sets of criteria had not
presented considering such a sequential approach. MEPs and
ERG were not usually included as confirmatory tests. The
combination of of both a sequential approach, and the
application of a test battery comprising MEPs and ERG,
could overcome the difficulties posed by conditions
traditionally considered as excluding a diagnosis of brain
death, and could facilitate clinical practice, in
establishing a precise and early diagnosis of BD, which was
also fundamental for organ transplantation (14).
Christopher Pallis again took the rostrum (he was
always expected by the auditorium) and presented the U. K.
code (8). The majority of the delegates thought that he had
been a member of the Commission that had drawn up the U.
K.Code, but we were to learn from him that although the U.
K.Code had a brainstem orientation in its concept of
death, his own contributions in this field had been due to
personal interest and commitment. Pallis stressed that the
main emphasis of the U. K. code was the all important
question of "context". Unless strict preconditions had been
fulfilled, and certain conditions specifically excluded, a
diagnosis of brain death could not even considered. He
likened the picture to a patient having to pass through two
tight sieved, before been tested for brain death.
This point had seldom been grasped by those criticizing
the code. The scheme outlined was scientifically sound and
clinically easy to use. Terminological problems remained
however. The memorandum produced by the Conference of
Medical Royal Colleges and their Faculties was entitled "The
Diagnosis of Brain Death" (8). The document stated, however,
that it was the "permanent functional death of the brainstem
that constituted death". This is unexceptionable, if taken
to mean that death of the brainstem prevented any kind of
meaningful functioning of the "brain as a whole". The title
of the document remained, however, open to misunderstanding.
A different view concerning the U. K. code (8) was
presented by a german delegate, Dr. R. Firsching, a close
collaborator of R. A. Frowein's. In Germany, death of the
entire brain was required and brainstem death alone had not
in general been accepted as death of the individual.
Firsching emphasized that as recommended by the
"Bundersfrztekammer" in Germany, prerequisites for the
declaration of brain death were a primary or secondary brain
lesion and the exclusion of drug effects, hypothermia or
endocrine disorders.
After the association of apnoeic coma and cranial nerve
arreflexia had been confirmed (in cases of primary
supratentorial lesions) four options were available: (1) a
waiting period of 12 hours; (2) electrocortical silence as
revealed by EEG; (3) step wise abolition of brainstem
auditory evoked potentials in sequential investigations; (4)
the demonstration of intracerebral circulatory arrest,
either by angiography or by transcranial Doppler sonography.
In primary infratentorial lesions cortical function might be
preserved by hours or days. The demonstration of
electrocortical silence by EEG was therefore mandatory.
An interesting paper was then presented by a group of
colleagues from Argentina. A retrospective analysis of 630
potential donors showed that their average age was 31.
There was a net predominance of males (71,4 %). Head injury
(46,65 %) and cerebrovascular diseases (44,6 %) were the
most common aetiologies among the potential donors. Consent
for organ donation was obtained in 58 % of the cases.
Preliminary results from a prospective study on BD,
were then presented by neurologists from the National
Institute of Neurology and Neurosurgery, in Mexico.
A warm evening proved a pleasant background to the
"Welcome Party". There was plenty of cuban music, rum and
friendship.
The morning of September 23, began with interesting
presentations on: "Neurophysiological Tests and other
Confirmatory Techniques in Brain Death and Related States"
and "Legal Considerations on Brain Death and Related
States".
I presented a paper on the "Early Diagnosis of Brain
Death Using Multi-modality Evoked Potentials (MEPs) and
Electroretinography (ERG)" (14, 15, 16, 17). MEPs and ERG
were highly resistant to factors such as: drug intoxication,
barbiturate narcosis, the use of anaesthetics, hypothermia,
and so on. They had been shown to be reliable in the
Intensive Care Unit environment. Considered as single tests,
they had their limitations and they had been not routinely
included as confirmatory tests for the diagnosis of BD. We
applied a battery of tests (including MEPs and ERG) to
thirty brain-dead patients. For brain stem auditory
evoked potentials (BAEPs), three patterns of abnormality
were observed: (1) no identifiable waves (73.34 %); (2) an
isolated bilateral wave I (16.66 %) and (3) an isolated
unilateral wave I (10 %). For short latency somatosensory
evoked potentials (SSEPs) a characteristic pattern was
found: absence of N20 and later responses in the
scalp-cephalic record with preservation of all or some of
the so-called subcortical components in the rest of the
derivations. An interesting dissociation appeared in which
some SSEP components were still present in neck-cephalic
and spine while absent in scalp-non cephalic leads.
Our data further suggested that all components after P13-N13
(recorded with restricted filter bandpass) also recognized
two or multiple distinct generator sources. Rostral
generators were probably located in the brainstem and/or
thalamus, but a significant part of these SSEP components
seemed to be generated at the lowest part of the medulla
oblongata (dorsal column nuclei) and/or at the level of the
upper cervical spine.
Visual evoked potentials (VEPs) and the ERG were
elicited and recorded simultaneously, using cephalic and
non-cephalic references. In all cases in which a
non-cephalic reference was used the ERG did not change
(either in latency or in morphology) while the VEP channel
showed no response. In only two cases (using the VEP
derivation with a non-cephalic reference) was it possible
to record waves that indicated a spread of the ERG to the
occipital area. These results suggested that although
contamination of the VEP recordings by the possible spread
of the electroretinogram to the occipital area might occur,
when using a non-cephalic reference it was easy to confirm
the absence of a true cortical visual response in
brain-dead patients.
It was suggested that the test battery we proposed
would permit the assessment of several sensory pathways,
in brain-dead patients, thereby considerably
increasing diagnostic reliability. Taking into account that
these techniques are highly resistant to hypothermia, drug
·
(continued next message)
------------------------------------------------------------------------
@FROM :david@STAT.COM
· (Continued from last message)
intoxication, the use of anesthetics, etc., resort to this
battery as confirmatory tests might considerably diminish
the time of observation needed to establish a definitive
diagnosis of BD. This was of course a fundamental
prerequisite to organ transplantation. MEPs and ERG were
considered as confirmatory tests in the Cuban Criteria for
Brain Death Diagnosis (12).
R. Firsching from Germany continued the session,
presenting an interesting paper about "Evoked Potentials and
Brainstem Reflexes in BD". In Germany registration of brain
stem auditory evoked potentials (BAEPs) had been
recommended as a confirmatory test of brain death under
certain conditions. The author's group investigated 100
patients who exhibited apnoeic coma and cranial nerve
arreflexia after primary brain lesions and who finally met
all the criteria of brain death. BAEPs, somatosensory (SEP)
and visual evoked potentials (VEP) and, in addition,
transcranial magnetic (TmgMEP) and electric (TelMEP) motor
evoked potentials were registered. In no patient with
apnoeic coma and cranial nerve arreflexia could preserve
BAEPs, SEP, VEP or TmgMEP or TelMEP. Brainstem reflexes were
also abolished with the exception of seven cases with a
preserved R1 response of the blink reflex immediately after
apnoea had been documented. Registration of evoked
potentials as a confirmatory test added safety to the
diagnosis of brain death, as they were particularly
resistant to drugs. They proved practicable for the
declaration of brain death in one third of our patients.
Brain stem reflexes required further research.
Hilmar Prange, also from Germany, continued the session
with some remarks concerning the reliability of several
technical investigations for the confirmation of BD. Fifty
consecutive patients with suspected brain death were
included in his study dedicated to evaluate the reliability
of different diagnostic techniques. The techniques employed
comprised clinical examination, apnoea testing, EEG,
extracranial Doppler ultrasonography (ECD), brainstem
acoustic evoked potentials (BAEP) and arterial digital
subtraction angiography (DSA). In 39 cases these were no
discrepancies in the results of the different techniques
used to confirm brain death. With the remaining 11
patients the findings were not exactly concordant or, at
least, permitted varying interpretations. For example, in
six cases doubts existed as to whether or not the EEG
was isoelectric. In four patients BAEP findings were
compatible with brain death two to three days before
intracranial circulatory arrest was documented. Finally, in
two patients with isoelectric EEG and absent BAEP,
arterial DSA showed residual cerebral flow. The
significance of the mentioned technique for brain death
diagnosis was discussed in the light of their conceptual
differences implicit in the term brain death.
A beautiful lady from Chile, then proved that women
were to be respected in neurophysiology. Nelly Chiofallo had
worked with Professor Earl Walker during the seventies in
an International Commission on Brain Death. She emphasized
that when since clinical criteria were only partially
realized and there was not total certainty concerning
suspected brain death, certain non-invasive
electrophysiological tests could provide objective evidence
as to whether or not the cerebrum was active. Monitoring EEG
and computer-average Evoked Potentials (EP) were among
these confirmatory methods. EEG methodology was highly
important in relation to both false negatives or false
positives findings. (The author's experience with corpses
was reported). Dr. Chiofalo presented 132 brain-dead
patients studied by EEG, in a three year period, taking
into consideration: age-sex distribution, primary
diagnosis, consciousness state on admission, time elapsed
until respiratory arrest, time elapsed from isoelectric EEG
to asystole, etc. She also discussed the utility of
topographic brain mapping in a controversial paedriatic
case. Minimal EEG activity in few channels were related to
artifacts. Mapping-histograms defined the presence of true
bioelectrical activity.
Flying thousand of miles, A. Erbengy came from Turkey
to the Pearl of the Antilles (Cuba). He stressed that
although the determination of brain death was
fundamentally a clinical diagnosis, conditions that might
interfere with diagnostic accuracy required assessment by
at least one ancillary test. In his institution (Hacettepe
University Medical School) they had found that brain stem
auditory evoked potentials (BAEPs) was the most reliable
technique. They had also performed radionuclide
angiography and brain perfusion studies, whenever they had
felt it was necessary. More than 150 brain-dead patients had
been studied by BAEPs and 30 by radionuclide angiography
and brain perfusion. A highly significant correlation was
found among BAEPs and radionuclide study results. None of
the patients with absent BAEPs had showed cerebral
perfusion. BAEP records, with or without radionuclide
studies, had been found to be very reliable adjunct to
a clinical diagnosis of brain death. Besides the
determination of brain death, radionuclide studies also
provided valuable information on the current status of the
organs to be used as grafts in organ transplantation
(kidneys, liver, heart, etc.)
The chairman of this session, Arnold Starr (U. S. A.),
had in 1976 reported original data in 1976 about the use of
auditory brainstem responses in brain death (18). He now
presented a nice lecture entitled "Averaged evoked brain
potentials and brain death". The averaging of electrical
events in the brain (time-locked to sensory events) revealed
a sequence of components reflecting activity at different
levels of the pathway from receptor to cerebral cortex. The
generators of these components varied, and examples that had
been defined included activity in nerve fibers at points of
an impedance change or activity in neuronal clusters. In
comatose patients, the pattern of potential loss could be
used to define the level of brain dysfunction. Brain death
had been equated with the loss of central brain or brainstem
activity while receptor function could be preserved. Among
theoretical problems engendered by these assumptions was the
fact that averaging required synchrony of brain activity
time-locked to the sensory stimuli. Pathological processes
might lead to a loss of this synchrony. Thus even though the
brain was viable, averaged evoked potentials might be
absent. A pathological process might result in the loss of
function of nerve fiber pathways sparing neurons. Averaged
evoked potentials would be absent in this scenario, since
the neurons would not be receiving input yet the brain would
be viable. Compromised receptor function might impair
sensory pathway responses in a viable brain. Alternative
activation of sensory pathways had to be developed for this
situation as it had to be developed with peripheral nerve
stimulation for somatosensory evoked potentials.
The lunch break proved not only a moment to enjoy
cuban food. Three equally attractive lunch panels reported.
As a final game for the World Crown in Chess, Christopher
Pallis (U. K.) and Earl Walker (U. S. A.) moderated a
discussion on the "Brain as a Whole and Whole Brain
formulations of death on neurological grounds". Stuart
Youngner (U. S. A.) chaired a group of discussion of: The
"Higher Brain Formulations of Death". Meanwhile R. Dierkens
(Belgium) was accompanied by enthusiastic delegates wanting
to discuss "Medical Decisions in Terminal Cases".
From Oslo, Marianne Forsman, an interesting nordic
lady, presented some remarks about the effect of nimodipine
on cerebral flow and cerebrospinal fluid pressure after
cardiac arrest. Fifty-one patients were included in a blind
randomized study to evaluated whether the Ca-blocker
nimodipine could influence cerebral blood flow (CBF) or
cerebrospinal fluid pressure (CSFP) during the cerebral
hypoperfusion period that followed resuscitation from
cardiac arrest and to determined whether changes in CBF
correlated with neurologic outcome. CBF (measured 1 to 4
hours after arrest with the use of intravenous 133Xe) was
significantly greater with nimodipine than with placebo,
There was no clinical evidence of seriously increased CSFP
in any patient in either group during the first 48 hours.
Mean arterial pressure was significantly lower, and
antiarrhythmic drugs were used significantly less frequently
in the nimodipine group than in the placebo group.
Twelve patients in each group eventually regained
consciousness. There was no significant difference in
neurologic status between the two groups at any point, and
no positive correlation between CBF in the hypoperfusion
period and neurologic outcome.
From my group, Dr. Orlando Garcia presented the results
of a study dealing with heart rate variability (HRV) in coma
and brain death. Thirty-three comatose patients were studied
serially by HRV and Glasgow Coma Scale (GCS), as were 40
normal subjects to document our normative data. HRV values
were considered for different GCS scores. For GCS from 7 to
9, the HRV achieved its maximum values. We considered these
in relation to a functional disconnection of the defense
hypothalamic area with a normal functioning brainstem, such
results apparently not been previously reported in the
literature. HRV showed a significant tendency to decrease
with low GCS values (3-6). For high GCS scores (10-15), the
HRV also showed a significant tendency to decrease. With
these results a non-lineal correlation between HRV and GCS
was defined. Fourteen brain-dead patients were also studied
and were found to present the lowest values for HRV
(significantly different from normals). During the atropine
test no significant changes in the HRV were found for
brain-dead patients.
An enthusiastic group of neurologists and neurosurgeons
from the Neurological Center of the French Hospital in
Buenos Aires, (Argentina) presented three papers dealing
with the application of neurophysiological techniques to
study brain-dead patients. They described a patient
diagnosed as brain dead who had preservation of the spinal
(somatosensory) evoked potential at L5-S1. These results
might be used to explain the finding of the Lazarus's Sign
in brain death. In another paper, they described a series of
30 patients, studied by multi-modality evoked potentials and
EEG, finding patterns which confirmed absence of cerebral
function. All cases showed a electrocerebral silence, except
three patients, who showed preservation of rudimentary but
recordable EEG. They discussed the possible mechanisms of
EEG preservation in such patients, in relation to the
intracranial pathology and to the timing of the EEG study in
relation to the clinical evolution, since brain death was
established. The colleagues from Argentina were in fact
defending the "brain as a whole" (brainstem death)
formulation of death. The third paper consisted in the
presentation of a patient who developed a cardiac arrest
during a study of the brainstem auditory evoked potential.
Several changes in evoked responses were noted, that
confirmed the diagnosis of brain death.
The session devoted to discuss the "Legal
Considerations on Brain Death and Related States" was
chaired by Professor R. Dierkens, President of the World
Association of Medical Law. Dierkens emphasized that the
wishes of the patient had to be considered, but in a
context in which the medical opinion was also important. The
deontological code in Belgium proposed the cessation of
treatment when the clinical diagnosis was hopeless. The
Catholic Church in this country had also proposed to
discontinue treatments progressively in terminal patients,
but without abandoning nurse care, pain relief and
psychological support.
From my group, Dr. Jesus Parets, a young lawyer,
continued with "Legal Considerations on Brain Death
Diagnosis and the Moment of its Occurrence" . The old Civil
Code in Cuba (1942) had stated that "death was diagnosed by
physicians confirming an irreversible cessation of
cardio-respiratory functions". In 1985 a new Civil Code
altered this, starting that "death is diagnosed by
physicians in relation to criteria defined by the Ministry
of Public Health". This view defended a position in which
the relevant criteria were not included in any law. New
criteria could thus be included at any time. The Ministry of
Public Health had then organized a national commission which
every year reviewed and updated the criteria to be applied
in our country. A ministerial resolution had validated the
use and application of the "Cuban Criteria for Brain Death
Diagnosis" (19).
DONAR (the Spanish for to donate) is an organization
from Santa Fe, Argentina. Its President, Dr. Pedro Zukas,
emphasized that "Time is too short for egoism". Dr. Zukas
read a paper whose main author was Dr. Cesar Rey Leyes
(Argentina). Article 103 of the Argentinean Civil Code
emphasized that death made it impossible to have human
rights. The diagnosis of death was accepted in relation to
medical criteria, but this had to be done independently of
any decision concerning organ transplantation. The
patient's relatives could give or refuse permission
regarding organ donation. The law had to facilitate medical
development, and not impede it.
A controversial session (Bioethical Considerations on
Brain Death and Related States) began in the morning of
thursday 24. It was chaired by Daniel Wikler and Stuart
Youngner (U. S. A.)
An expected lecture was presented by the chairman,
Daniel Wikler: "Why Brain-dead Patients are Dead? The
President's Commission Explanations After One Decade".
Daniel Wikler's presentation was a discussion of the
definition of death provided by the President's Commission
for the study of Ethical Problems in Medicine and Biomedical
and Behavioral Research (11). This commission had been
appointed in 1979, by the President of the United States. It
had produced eleven reports which had proven influential in
American and international bioethics. The President's
Commission report addressed three topics: (a) What concept
of death should be used? (b) What legal statute should be
adopted? (c) How should brain death be diagnosed? However,
only (a) was the official product of the Commission. The
statute had been written in collaboration with the American
Medical Association and the American Bar Association (among
others). It gave a legal definition of death as either
whole-brain death or cardio-respiratory death. The
Commission's report provided (c) as a public service in an
Appendix (not endorsed by the Commission itself) its
recommendations on diagnosing death. These had been
formulated by an expert panel, including Dr. Walker and Dr.
Molinari. In its comments on the concept of death (a), the
Commission had argued that patients who suffered whole-brain
death should be viewed as dead. The primary reason was that
the brain (and in particular the brainstem) was the
integrator of the body's major organ systems. Without this
integration, the Commission reasoned, continued functioning
of the patient's major organ systems (in an ICU) did not
constitute organismic life. The Commission rejected a
"cortical-death" definition, pointing out that such a
definition of death would seem to endorse the burial of a
patient with a spontaneously beating heart. The Commission's
findings had resulted in a change in the definition of death
in nearly every one of the states in the U. S. A. (where
defining death is a matter of state, rather than federal,
law). Philosophers, however, had questioned the logic of the
Commission's central argument, pointing out that the major
organ systems in a well-maintained brain-dead patient,
interacted so as to sustain the main non-cognitive bodily
functions.
Dr. Stuart Youngner (Associate Professor of Medicine,
Psychiatry and Biomedical Ethics at the Case Western Reserve
University School of Medicine and Director of the Clinical
Ethics Program of the University Hospitals of Cleveland)
presented a paper on "Brain Death and Organ Transplantation:
Confusion and Its Consequences" (20). He argued that despite
the rapid and widespread embrace of so-called "brain death"
in the United States, confusion about its meaning and
implications remained a problem. He gave several examples
of evidence of this confusion. First, the criterion of brain
death, i.e the irreversible loss of all brain function, was
accepted for practical reasons (without a wide agreement on
exactly why patients who had lost all brain function were
dead). The practical reasons were: (1) in the hands of a
competent neurologist, neurosurgeon, or critical care
physician, brain death was a relatively easy diagnosis to
make; and (2) that once the diagnosis of brain death had
been made the prognosis was certain that the patient would
never regain consciousness and would develop asystole within
a short time, despite continued aggressive intervention.
The diagnostic certainty and uniformly dismal cardiac
prognosis for brain-dead patients facilitated the acceptance
of policies aimed at treatment withdrawal and organ
retrieval.
A study by Youngner and his colleagues (20) at Case
Western Reserve University had, however, indicated that
physicians and nurses working in critical care and operating
room settings accepted brain death for different reasons.
Some thought brain-dead patients were dead because they
would never wake up again. Others accepted them as dead
because they had lost the integrating functions of the
brainstem. Still others indicated that they did not really
believe the patients were dead, saying that the patients
were "going to die very soon despite aggressive treatment"
or that their "quality of life was unacceptable."
Further evidence of confusion was the stubborn
persistence of the term "brain death" itself. Health
professionals consistently referred to patients who had lost
all brain function as brain-dead (rather than, simply dead).
It is also common to hear them say that the brain-dead
patient "died" after life support had been removed. Of
course you can not die if you are already dead. The
persistence of term brain death may well reflect an
inevitable conflict between reason (which told us that
brain-dead patients were dead) and emotions. The latter
were stimulated by the many signs of "life" still shown in
brain-dead patients. These were of particular concern to
nurses who took care of brain-dead patients. Intensive Care
Unit nurses reported feelings of discomfort at calling
patients "dead" who require aggressive treatment (including
·
(continued next message)
------------------------------------------------------------------------
@FROM :david@STAT.COM
· (Continued from last message)
resuscitative efforts if the "dead" patient develop a
cardiac arrests) at a time when clearly living and conscious
patients, in the same unit, fell into the "do not
resuscitate" category. In the operating theater, nurses
sometimes felt that the patient's spirit was in the room
during organ retrieval surgery, and only departed when the
ventilator was turned off and the patient came to complete
rest. These examples of confusion were inevitable when we
were willing to call patients dead when so much life
persisted. This confusion pointed not only to the need for
more ongoing education about brain death, but also for wide
debate and consensus among various elements of society
(including not only doctors, but the legal and religious
communities, and especially the lay public) before policies
are implemented and enforced. To do otherwise was to foment
distrust and suspicion of medical science, perhaps
undermining the worthwhile goal of saving more lives by
getting more persons to donate their organs.
Dr. E. Bochiardo from DONAR (Argentina) presented a
paper "Brain Death", in which he emphasized that until some
time ago the determination of death was relatively easy:
confirming the irreversible absence of cardio-respiratory
function. In the sixties, the development of reanimation and
other intensive care techniques, forced physicians to
confront the concept of brain death. A man had to be
considered dead when his brain functions disappeared. He
considered that the decision (made by patient's relatives)
to donate organs was a transcendental and admirable token.
The results of an interesting survey were then
presented by Dr. Eduardo Fermin, a delegate of the Cuban
group. The subject of the survey was related to the
decisions and feelings of the physician, who had to decide
what to do in a brain-dead patient, when transplantation was
not envisaged. The survey described to the attitudes of 50
specialists in intensive care medicine. This survey was
anonymous, assessing the concepts of life and death,
euthanasia, as well as the methods used in the process of
diagnosing brain death. Many interesting results had arisen:
for example, the confusion about methods and criteria for
diagnosing death, concerns about the legal protection of
physicians, doubts about when to turn-off the respirator,
mistakes in the concepts of BD and euthanasia, etc. Many
physicians had expressed religious opinions in this
context.
Two cuban specialists in psychiatry (Drs. Jose A.
Hernandez and Carlos M. Notario) ended this session
presenting a paper entitled: "Attention to
Near-Death-Patients". They appreciated the classic study of
Dr. Klubler-Ross and particularly her description of the
psychological stages in dying persons. They paid attention
to the medical custom which sought to prolong, in all
possible ways, the life of hopelessly ill patients, while
accepting that medical procedures should be directed to
relieve the pain of the dying and allowing a decorous death.
They stated that their purpose was to stimulate a discussion
about this subject in our country and to exchange opinions
with foreign experts, but always keeping their patients in
the forefront of their minds.
Three interesting lunch panels joined delegates with
providing food for thought. "Near-death Experiences" was
chaired by the Reverend Douglas Lynn (Canada), "Organ
Marketing" by Dr. Raul Herrera (Cuba) and "Transplant
Alternatives" by Dr. Noel Gonzalez (Cuba).
"Brain Death in Children" is always a controversial
subject. This session was chaired by Dr. Kimio Sainio from
Finland. He opened the session with a study of the patients
with suspected brain death seen in the Children's University
Hospital of Helsinki, during a ten year period (1983-1992).
The study correlated clinical, neuroradiological and EEG
data. A total of 36 patients were studied, ranging in age
from 0 days to 11 years (mean = 1.9). Brain death was
diagnosed in 21 patients. The diagnosis was confirmed in
three patients by cerebral angiography and in four patients
by colour flow Doppler ultrasound examinations. The EEG was
inactive in 19 patients. Two patients showed minimal EEG
activity two to five days before brain death was confirmed.
The diagnosis of BD was not confirmed in 15 patients. Five
of these cases had either flat or burst-suppression EEGs.
Four of them died and one survived with major neurological
sequelae. The inactivity of the EEG was due to
barbiturate medication in two patients; both survived with
major neurological sequelae. Both EEG and Doppler
examinations were compatible with brain death, while
clinically some brainstem function persisted in these two
cases; both developed asystole within 24 hours. Of the
remaining 6 patients, five died and one survived, a child
who had inactive EEG at t 7