Diagnosing brain death
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7368.836 (Published 12 October 2002) Cite this as: BMJ 2002;325:836
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Editor:
I read with interest the recent article on diagnosing brain death without a
neurologist (1), and the responses to this issue. I am interested in the
dilemma of performing tests for brain death criteria by competent doctors of high
qualification and of special related subspecialities. Recently so much
debate has arisen in professional circles. In Saudi Arabia a
national committee on brain death met for many sessions and then came up
with recommendations to be followed which helped in settling the argument.
Brain death issues need to be developed in Islamic and Arabic society among all
social leaders, be they lawyers, clergymen and scholars, to tailor
society's need to understand to the scientific evidence concerning the end
of life.
The Saudi committee on brain death in the Saudi centre for organ
transplantation laid down very rigid criteria and procedures to certify
brain death cases.(2)There are courses and workshops to help understanding and define the need
in certain areas of nurses, and doctors' proper handling of the
questions without ill effect or controversy.
The criteria of brain death are circulated to all intensive care units
in Saudi Arabia. The diagnosis of brain death is done by two consultants
simultaneously in two sessions. They may be intensivists, anesthesiologists,
neurologists or neurosurgeons. One confirmatory test either an EEG or
Cerebral angiogram is done, after apnea testing, for the purpose of
organ donation. There is no switching off the ventilation after the
diagnosis, none of the interested parties in the donation will share
in the diagnosis.
The addition of a documentation of brain activity or circulation
confirm without doubt the clinical situation with permanant evidence.
We found in the current practice of critical care a good way to
eliminate the element of doubt which casts itself on such clinical tests and may be affected by human bias and errors.
References
(1) Baumgartner H, Gerstenbrand F. Diagnosing brain death without a
neurologist. BMJ 2002;1471-2
(2) Brain Death Committee National Kidney Foundation, Riyadh
Kingdom of Saudi Arabia; Diagnosis of Brain Death and Policy on Cadaveric
Organ Procurement in KSA. SAUDI KIDNEY DISEASES AND TRANPLANTAION
BULLETIN. Vol. 3, No. 3, 1992
Competing interests: No competing interests
In an interview published in Metro today, October 15, Kaylee Davidson
said “If it wasn’t for organ donors, I wouldn’t be here today”. The
article is yet another plug for organ donation observing that “Kaylee
knows how lucky she was and has become a vociferous campaigner for organ
donation”. The article illustrates another aspect of the therapeutic
nihilism that organ transplantation appears to have fostered, namely that
concerning the evolution of effective treatments for cardiomyopathy.
Fifteen years ago Kaylee was a healthy five month old baby when she
contracted an acute viral illness which caused her to develop
cardiomyopathy. The medical treatment she was given no doubt included
endotracheal intubation, supplemental oxygen, mechanical ventilation,
intravenous fluids and inotropes. Obviously her doctors concluded that
her condition was irreversible and had informed her parents that she would
die if she did not receive a heart transplant. Is that really the case?
Many patients in Kaylee’s position have not been the beneficiary of a
heart transplant and have died but others have recovered spontaneously as
recently reported in the lay press. There is therefore a possibility,
albeit small, that Kaylee might have recovered spontaneously had an organ
donor not been found. Fifteen years later there is much that could be
done that might have allowed her to recover spontaneously, but it is not
being done.
First measures of intramyocardial tissue pH, pCO2, and pO2 are needed
to obtain objective information about the adequacy of oxygen delivery,
uptake and utilisation (1,2). These could be obtained from tonometric
measurements derived from a flat, one-way sensing tonometer applied to the
surface of the heart or in older children and adults from measurements in
the myocardial venous effluent draining into the coronary sinus (3,4,5).
Second management needs to be driven by systemic and regional
measurements of tissue pH rather than by haemodynamic measurements (6). It
would seem very likely that inotropes may be counter productive decreasing
rather than increasing the adequacy of mitochondrial oxidative
phosporylation and returning it the intramyocardial tissue pH to normal
levels. As viral infections release cytokines which may inhibit and/or
uncouple oxidative phosphorylation therapeutic options that should be
considered including increasing the intramyocardial tissue pO2 as high as
60 mmHg and administering monoclonal antibodies directed against TMF
alpha and possibly other cytokines (7,8). Limiting potentially harmful
demands for cAMP synthesis at the expense of the putatively compromised
intramyocardial ATP stores is another therapeutic option to consider. Beta
blockers may exert their myocardial protective effects in this manner. As
beta blockers may also compromise oxygen dispatch from the heart a measure
of the adequacy of systemic tissue oxygenation, best monitored with
measurements of gastric intramucosal pH obtained during the administration
of a proton pump inhibitor or H2 receptor antagonist, is desirable. Other
novel therapeutic options that might be entertained include optimising
the delivery of glucose into myocytes by infusing glucose, insulin and
potassium, improving myocardial tissue oxygenation by increasing
intramyocardial tissue pO2 to 60 mmHg and/or improving capillary blood
flow by isovolaemic haemodilution with Perflubron, inhibiting free
radical generation and/or administering free radical scavengers. Loop
ileostomy and colonic lavage might even be of benefit in those patients
whose low cardiac output causes a gastric intramucosal acidosis that is
highly predictive of a fatal outcome, the associated translocation of
bacterial endotoxin and release of cytokines (9).
1. Fiddian-Green RG. Gastric intramucosal pH, tissue oxygenation and
acid-base balance. Br J Anaesth. 1995 May;74(5):591-606. Review.
2. Fiddian-Green RG. Monitoring of tissue pH: the critical measurement.
Chest. 1999 Dec;116(6):1839-41
3. US patent 5,526,809. Hollow viscous and soild organ tonometry
4. US patnet 5,433,216. Intra-abdominal pressure measurement apparatus and
method
5. US patent 5,415,165. Tonometric catheter combination 4. 5,187,177.
6. Fiddian-Green RG. Haemodynamic and/or tonometric monitoring in cardiac
surgery.
Br J Anaesth. 2000 Jan;84(1):128.
7. Fiddian-Green RG. Mitochondrial considerations
bmj.com/cgi/eletters/325/7367/735/a#26019, 4 Oct 2002
8. Fiddian-Green RG. Intracranial compartment syndrome
bmj.com/cgi/eletters/325/7364/598/a#25555, 16 Sep 2002
9. Fiddian-Green RG. Colonic lavage for severe haemorrhagic shock?
bmj.com/cgi/eletters/325/7366/674/b#25839, 27 Sep 2002
Competing interests: No competing interests
I share Dr Hill's concerns. As mentioned in earlier rapid responses
on the subject I am concerned that for decades the conflict of interest,
inevitably present when one NHS trust is responsible for the management of
both acute intracranial pathology and transplanation, might have fostered
a climate of therapeutic nihilism in the management of acute intracranial
pathology. Of partcular concern to me is the possibility that the
application of arguably more pathophysiologically appropriate monitoring
and management of the intracranial compartment syndrome might allow
persons declared "brain dead" by current criteria to recover.
As we do not know what advances in management of acute intracranial
pathology might be around the corner can any defintion of "brain death"
ever be cast in stone? If not can it ever be appropriate to use a
definition of "brain death" for the purposes of organ harvesting?
1. RAPID RESPONSES
Intracranial compartment syndrome
Richard G Fiddian-Green
bmj.com/cgi/eletters/325/7364/598/a#25555, 16 Sep 2002 2.
2. RAPID RESPONSES
Re: Intracranial compartment syndrome
CELIO LEVYMAN
bmj.com/cgi/eletters/325/7364/598/a#25593, 17 Sep 2002 [Full text]
3. RAPID RESPONSES
Intracranial compartment syndrome
Richard G Fiddian-Green
bmj.com/cgi/eletters/325/7362/454#25977, 3 Oct 2002 [Full text]
Competing interests: No competing interests
I share Dr Hill's concerns. I am particularly concerned that
harvesting organs from persons declared brain dead for transplantation
into recipients might have fostered a climate of therapeutic nihilism in
the management of head injuries. From what I have read there is certainly
much that can be done to improve current management in the NHS simply by
applying accepted practices more efficiently and expertly. There may also
be great potential for improving upon accepted practices by addresing the
management of the intracranial compartment syndrome in a more
pathophysiologically appropriate manner(1,2). In so doing patients once
declared "brain dead" might even be seen to recover.
An additional concern is the conflict of interest that must exist in
any organisation, such as the government or NHS trust, that is responsible
for the management of both patients with head injuries and those waiting
for organ donors.
1. Fiddian-Green RG. Intracranial compartment syndrome
bmj.com/cgi/eletters/325/7364/598/a#25555, 16 Sep 2002
2. CELIO LEVYMAN Re: Intracranial compartment syndrome
bmj.com/cgi/eletters/325/7364/598/a#25593, 17 Sep 2002
Competing interests: No competing interests
Evidence-based versus "established" medical practice
EDITOR - Hutton et al. have listed some of the principles for the
diagnosis of brain stem death which, according to them, are to be
considered established as they have been accepted for many years in the
United Kingdom.1 The authors failed to acknowledge the extensive
discussion carried out on the bmj.com web site during the past 2 years
regarding the pathophysiology of deep coma associated with cephalic
areflexia. In conditions like severe head trauma, intracranial pressure
may be high enough to reduce the blood supply to the whole brain or solely
to the infratentorial structures down to the range of ischaemic penumbra
for several hours or a few days, when the absence of the specific set of
synapse-dependent functions listed in the current protocols may lead to
misdiagnosis of brain or brain stem death in a subset of deeply comatose
patients with cephalic areflexia.2
As repeatedly proposed and never scientifically refuted during the
past 2 years, the apnoea test (performed twice) may exacerbate the brain
damage. Apnoea may induce (I) severe hypotension in up to 39%3, (II)
hypoxia (PaO2<_70mmhg in="in" _133="_133" and="and" iii="iii" further="further" increase="increase" of="of" intracranial="intracranial" pressure="pressure" icp="icp" an="an" unknown="unknown" number2="number2" those="those" so="so" tested="tested" despite="despite" the="the" implementation="implementation" current="current" oxygenation="oxygenation" measures.="measures." after="after" apnoea="apnoea" testing="testing" all="all" patients="patients" show="show" normal="normal" levels="levels" cerebral="cerebral" perfusion="perfusion" paradoxical="paradoxical" association="association" with="with" absent="absent" or="or" extremely="extremely" reduced="reduced" blood="blood" flow.4="flow.4" these="these" results="results" are="are" complete="complete" disagreement="disagreement" demonstration="demonstration" that="that" consistently="consistently" remains="remains" near="near" above="above" level="level" mean="mean" arterial="arterial" non-apnoeic="non-apnoeic" who="who" go="go" on="on" to="to" develop="develop" spontaneous="spontaneous" cardiac="cardiac" arrest.5="arrest.5" such="such" a="a" diametrical="diametrical" divergence="divergence" indicates="indicates" sudden="sudden" permanent="permanent" efflux="efflux" volume="volume" from="from" space="space" as="as" result="result" testing.="testing." irreversibility="irreversibility" condition="condition" may="may" be="be" related="related" tension="tension" forces="forces" involving="involving" luminal="luminal" endothelial="endothelial" surfaces="surfaces" established="established" during="during" period="period" hypercarbia-induced="hypercarbia-induced" hypotension="hypotension" increased="increased" icp.2="icp.2" p="p"/> By contrast, a review of the literature shows that some of even the
most severely head-injured patients (GCS of 3 or 4, with pupils fixed to
light) who are not subjected to apnoea may recover to normal life.2 Early
labelling of these patients as dead (for transplant purposes) during the
past 3 decades has diverted medical researchers away from developing novel
therapeutic resources that could already have saved many thousands of
human lives throughout the world. "Primum non nocere" must be reinstated
as the governing principle in the care of the defenceless comatose and
early apnoeic/hypercarbic insults avoided.
Cicero G Coimbra
Associate Professor
Department of Neurology and Neurosurgery,
Federal University of São Paulo
References:
1. Hutton P, Nightingale P, Ridley S, Short A. Guidelines for United
Kingdom were not described. BMJ 2002; 325: 836.
2. Coimbra CG. Implications of ischemic penumbra for the diagnosis of
brain death. Braz J Med Biol Res 1999; 32:1479-1487.
3. Jeret JS, Benjamin JL. Risk of hypotension during apnea testing.
Arch Neurol 1994; 51:595-599.
4. Obrist WD, Jaggi JL, Langfitt TW, Zimmerman RA. Cessation of CBF
in brain death with normal perfusion pressure. J Cereb Blood Flow Metab
1981;1(suppl 1):S524-S525.
5. Balslev-Jorgensen P, Heilbrun MP, Boysen G, Rosenklint A,
Jorgensen EO. Cerebral perfusion pressure correlated with regional
cerebral blood flow, EEG and aortocervical arteriography in patients with
severe brain disorders progressing to brain death. Eur Neurol 1972;8:207-
212.
Competing interests: No competing interests