|
By Alison McCook
NEW YORK (Reuters Health) Sept 09 –
Criteria for assessing brain death are not
applied consistently, at least judging by the documentation of the
clinical tests used in such cases, US researchers report. This is a
critically important issue, study author Dr. J. Peter Gruen, from
the University of Southern California in Los Angeles, told Reuters
Health. When standard criteria are not followed, the "great fear" is
that a patient may be declared brain dead when he or she may not be,
he said.
Specific guidelines for establishing complete
loss of brain function have been established for decades, Dr. Gruen
noted. These include a battery of tests that target different parts
of the brain, and no single test is adequate in determining brain
death, he cautioned.
However, not all physicians agree on how many
criteria are required when diagnosing brain death, Dr. Gruen said.
In addition, physicians often disagree on how to proceed if a
patient meets all but one or two of the criteria.
To determine what methods different physicians
use to establish brain death, Dr. Gruen and his colleagues reviewed
121 notes about brain death in the records of 58 patients evaluated
during 1 year at a major medical center. The findings are published
in the September issue of Neurosurgery.
The investigators found that physicians were
most likely to perform simple tests when diagnosing brain death,
such as pupillary responses and gag reflexes. However, they note,
only 66% of patients' motor reactions were tested, and their corneal
reflexes only 57% of the time.
The researchers found that some patients were
declared brain dead when it appeared that their physicians had not
performed all the tests needed to examine the entire brain. "I was
unpleasantly surprised to find that a significant number of people
were declared brain dead when there were parts of the brain that
were not evaluated," Dr. Gruen noted
Dr. Gruen explained that
there is a lot of pressure on physicians to declare a patient brain
dead when donor organs are in such short supply. "The concern is
that a corner is going to be cut on the donor side of this."
In their paper, the investigators suggest that
"hospitals may need to increase quality assurance activities with
respect to declarations of brain death." They also recommend
physician education to "improve awareness of uniform brain death
declaration guidelines."
Neurosurgery 2002;51:731-736.
Hyperbaric
Oxygenation prevented brain injury induced by hypoxia-ischemia in a
neonatal rat model.
Calvert J, Yin W, Patel M, Badr A, Mychaskiw
G, Parent A, Zhang J.
Department of Neurosurgery,
University of Mississippi Medical Center,
39216, Jackson, MS,
USA
The occurrence of hypoxia-ischemia (HI) during
early fetal or neonatal stages of an individual leads to the
damaging of immature neurons resulting in behavioral and
psychological dysfunctions, such as motor or learning disabilities,
cerebral palsy, epilepsy or even death. No effective treatment is
currently available and this study is the first to use hyperbaric
oxygen (HBO) as a treatment for neonatal HI. Herein, we sought out
to determine if HBO is able to offer neuroprotectivity against an HI
insult. Seven-day-old rat pups were subjected to unilateral carotid
artery ligation followed by 2.5 h of hypoxia (8% O(2) at 37 degrees
C). HBO treatment was administered by placing pups in a chamber (3
ATA for 1 h) 1 h after hypoxia exposure. Brain injury was assessed
based on ipsilateral hemispheric weight divided by contralateral
hemispheric weight, light microscopy, and EM. Sensorimotor
functional tests were administered at 5 weeks after hypoxia
exposure. After HI, the ipsilateral hemisphere was 52.65 and 57.64%
(P<0.001) of the contralateral hemisphere at 2 and 6 weeks,
respectively. In HBO treated groups, the ipsilateral hemisphere was
77.77 and 84.19% (P<0.001) at 2 and 6 weeks.
There was much less atrophy and apoptosis in
HBO treated animals under light or electron microscopy. Sensorimotor
function was also improved by HBO at 5 weeks after hypoxia exposure
(Chi-square, P<0.050). The results suggest that HBO is able to
attenuate the effects of HI on the neonatal brain by reducing then
progression of neuronal injury and increasing sensorimotor function.
[Brain Res 2002 Sep 27;951(1):1]
PMID:
12231450
Hyperbaric
Oxygenation prevented brain injury induced by hypoxia-ischemia in a
neonatal rat model.
Calvert J, Yin W, Patel M, Badr A, Mychaskiw
G, Parent A, Zhang J.
Department of Neurosurgery,
University of Mississippi Medical Center,
39216, Jackson, MS,
USA
The occurrence of hypoxia-ischemia (HI) during
early fetal or neonatal stages of an individual leads to the
damaging of immature neurons resulting in behavioral and
psychological dysfunctions, such as motor or learning disabilities,
cerebral palsy, epilepsy or even death. No effective treatment is
currently available and this study is the first to use hyperbaric
oxygen (HBO) as a treatment for neonatal HI. Herein, we sought out
to determine if HBO is able to offer neuroprotectivity against an HI
insult. Seven-day-old rat pups were subjected to unilateral carotid
artery ligation followed by 2.5 h of hypoxia (8% O(2) at 37 degrees
C). HBO treatment was administered by placing pups in a chamber (3
ATA for 1 h) 1 h after hypoxia exposure. Brain injury was assessed
based on ipsilateral hemispheric weight divided by contralateral
hemispheric weight, light microscopy, and EM. Sensorimotor
functional tests were administered at 5 weeks after hypoxia
exposure. After HI, the ipsilateral hemisphere was 52.65 and 57.64%
(P<0.001) of the contralateral hemisphere at 2 and 6 weeks,
respectively. In HBO treated groups, the ipsilateral hemisphere was
77.77 and 84.19% (P<0.001) at 2 and 6 weeks.
There was much less atrophy and apoptosis in
HBO treated animals under light or electron microscopy. Sensorimotor
function was also improved by HBO at 5 weeks after hypoxia exposure
(Chi-square, P<0.050). The results suggest that HBO is able to
attenuate the effects of HI on the neonatal brain by reducing then
progression of neuronal injury and increasing sensorimotor function.
[Brain Res 2002 Sep
27;951(1):1] |