Documentation of Brain-Death Testing Often Incomplete

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]

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