Monday, November 30, 2009

Index of MashCan.Org

Index of MashCan.Org

Only the public can inform the public about medical murder


Marked for Murder

Canada's Homegrown Solution

Language Alerts

Robert Latimer: Pin the Tail on the Donkey

What is the Public Interest?

Branded at Birth

Cues and Clues to Murder for Organs

Trillium Gift of Life Network and Your Networth

Nina: Realworld Counterpart

The Pluto Principle

Canadian Justice: What's on the Menu?



Select Topics:

Date: 2008.12.09 01:38
Description: "Only the public can inform the public about medical murder"

Title: Canadian Justice: What's on the Menu?
Date: 2009.11.30 01:12
Description: Warning the public about medical murder and the organ trade in Canada

Title: Marked for Murder
Author: MashCan.Org
Date: 2009.11.30 01:06
Description: Warning the public about medical murder and the organ trade in Canada

Title: Cues and Clues to Murder for Organs
Date: 2009.11.30 01:09
Description: Warning the public about medical murder and the organ trade in Canada

Sunday, November 29, 2009

Medical Secrets Index


Wednesday, November 18, 2009


Run away from the vaccines. . . .

WARNING: Drug Cartel Exposed Creating, Releasing, Injecting, Infecting, and Depopulating Planet with Pandemic H1N1 Swine Flu Viruses and vaccines

AFFIDAVIT OF LEONARD G. HOROWITZ 1. This Affidavit is based on my personal knowledge, except where otherwise stated, and, if called upon to do so, I could and would competently ...

The Affidavit - Dr. Leonard G. Horowitz & Sherri Kane ... 1. This Affidavit is based on my personal knowledge, except where otherwise stated, and, if called upon to do so, I could and would competently ...

WARNING: Drug Cartel Exposed Creating, Releasing, Injecting, Infecting, and Depopulating Planet with Pandemic H1N1 Swine Flu Viruses and Vaccines Los Angeles, CA— World ...

Tuesday, November 17, 2009

Guillain Barre syndrome Facts

Guillain-Barre Syndrome

Frequency of Autonomic Abnormalities in GBS.

Frequency of Autonomic Abnormalities in GBS. Prompt medical procedure ensures fast recovery and fewer complications.

Cases have been seen in patients who have had various viral and bacterial infections including HIV infection, in patients with chronic diseases such as lupus (SLE), Hodgkin lymphoma (and some other malignancies), and in patients who recently had a vaccination (such as for rabies or swine flu).

WARNING: GBS can mimic almost any neurological disease process, including "brain death", effective allowing cover-up of drug induced medical error.

Get the FACTS!

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Searches related to: guillain barre syndrome

guillain barre syndrome paralysis

Wednesday, June 17, 2009

Inconsistencies in the ethical declaration of death


Brain death: resolving inconsistencies in the ethical declaration of death

[La mort
cérébrale : résoudre les contradictions de la
déclaration éthique de la mort]

Christopher James
Doig MD MSc,* Ellen Burgess MD†

first criteria for the determination of brain death were developed in
1968 in part to address concerns that had arisen with the retrieval
of organs for transplantation. Despite over 30 years of application,
some professional and public doubt persists over the validity of the
theoretical construct underlying this method of determining death.
Our review will address historical perspectives on the development of
brain death criteria, and inconsistencies in current clinical

review from selected MEDLINE references
and other published sources.

primary construct of the determination of death is that either
cardiopulmonary or neurological function irreversibly ceases.
However, there is inconsistency in the neurological criteria for
death between jurisdictions, between patient populations, and in the
use of confirmatory tests. These inconsistencies may cause concern in
the public or profession about the validity of the determination of
death by neurological criteria.

transplantation is premised on professional and public acceptance
that the donor is dead. Given that the criteria for brain death or
their application remain variable, we suggest that it is reasonable
to consider a national consensus to address these inconsistencies.
Alternatively, the standard use of confirmatory radiographic testing
prior to the retrieval of organs from donors who meet clinical brain
death criteria should be considered to provide conclusive evidence of
permanent and irreversible loss of brain function.

Objectif : Les
premiers critères de mort cérébrale ont été
formulés en 1968 pour répondre, en partie, aux
inquiétudes soulevées par la recherche d’organes pour
les greffes. Malgré 30 ans d’application, un certain doute
subsiste chez les professionnels et le public sur la validité
de la notion théorique à l’origine de cette façon
de déterminer la mort. Notre revue aborde les perspectives
historiques de la formulation des critères de mort cérébrale
et des contradictions des critères cliniques actuels.

Méthode : La
revue descriptive provient de la consultation de

dans MEDLINE et d’autres sources publiées.
principales :
Le principal concept de la détermination
de la mort est l’arrêt irréversible de la fonction
cardio-pulmonaire ou neurologique. Cependant, il y a des
contradictions dans les critères neurologiques de la mort
entre les pays, entre les populations de patients et dans l’usage
des tests de confirmation. Ces contradictions peuvent inquiéter
le public et la profession médicale sur la validité de
la détermination de la mort par des critères

Conclusion: La
greffe d’organes est fondée sur l’acceptation publique et
professionnelle du fait que le donneur soit décédé.
Étant donné que les critères de mort cérébrale,
ou de leur application, demeurent variables, nous croyons qu’il est
raisonnable d’envisager la formation d’un consensus visant à
traiter de ces contradictions. Autrement, l’utilisation standard
des tests radiographiques confirmatifs, qui précèdent
le prélèvement d’organes de donneurs répondant
aux critères cliniques de mort cérébrale,
devrait être considérée pour fournir la preuve
concluante de la perte permanente et irréversible de la
fonction cérébrale.

From the
Department of Critical Care Medicine and the Office of Medical
Bioethics;* and the Division of Nephrology, Department of Medicine,†
Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada.

correspondence to
: Dr. Christopher James Doig, Rm EG23G,
Foothills Medical Centre, 1403, 29th Street NW, Calgary Alberta T2N
2T9, Canada. E-mail:

Accepted for
publication March 17, 2003.

accepted April 30, 2003.

CAN J ANESTH 2003 / 50: 7 / pp


If one subject
in health law and bioethics can be said to be at once well settled
and persistently unresolved, it is how to determine that death has



retrieval of organs for transplantation obtained from anonymous
‘cadaveric’ (brain dead, or non-heart beating) donors is based on
the moral acceptance of the ‘dead donor rule’: that these
patients are dead.
2,3 The
retrieval of organs from individuals who are brain dead is based on
the premise that permanent cessation of (whole) brain function
equates with death and can be identified by simple bedside clinical
4,5 In
the Uniform Determination of Death Act (UDDA), there are two distinct
definitions for death: "an individual who has sustained either
1) irreversible cessation of circulatory and respiratory function,
and 2) irreversible cessation of all functions of the entire brain,
including the brainstem is dead. A determination of death must be
made in accordance with accepted medical standards."
Below, we address inconsistencies in the
clinical criteria for brain death, and present an opinion that a
reconsideration of a national medical standard is necessary.

1959, Mollaret and Goullon used the term coma dépassé,
"a state beyond coma", to describe a condition from which
they believed recovery was not possi-ble.
In 1965, ‘brain dead’ was used to
describe a patient with a heart beat from whom a kidney was procured
for transplant into a non-related recipient.
In 1968, the Harvard criteria for brain
death were developed as the conclusions of the Ad Hoc Committee of
the Harvard Medical School.
9 All
subsequent criteria for brain death have been founded on this seminal
work. To quote from their original communiqué, "Our
primary purpose is to define irreversible coma as a new criterion for
death. There are two reasons why there is need for a definition: 1)
improvements in resuscitative and supportive measures have led to
increased efforts to save those who are desperately injured.
Sometimes these efforts have only partial success so that the result
is an individual whose heart continues to beat but whose brain is
irreversibly damaged. The burden is great on patients who suffer
permanent loss of intellect, on their families, on the hospitals, and
those in need of hospital beds already occupied by those comatose
patients. 2) Obsolete criteria for the definition of death can lead


controversy in
obtaining organs for transplantation." The ad hoc committee’s
criteria were not based on a physiologic or philosophical
understanding that the brain, and therefore the person, was dead.
Rather, the committee’s recommendations were premised on the
understanding that the coma was irreversible and care was futile "we
are concerned here only with those comatose individuals who have no
discernible central nervous system activity… [and where it is
possible to determine] the characteristics of a permanently
non-functioning brain." The committee identified that function
in the cerebrum including subcortical function (specific examples
presented were thalamic and basal ganglionic mechanisms), and
brainstem must be lost to be consistent with brain death.

The medical
consultants to the President’s Commission for the Study of Ethical
Problems in Medicine and Biomedical and Behavioral Research
subsequently detailed a comprehensive set of clinical circumstances
and a battery of tests to identify brain death:6 “1)
Cessation [of brain function] is recognized when evaluation discloses
findings of (a) and (b): (a) cerebral functions are absent, (b) brain
stem functions are absent. 2) Irreversibility is recognized when
evaluation discloses findings of (a), (b), and (c): (a) the cause of
coma is established and is sufficient to account for the loss of
brain functions, (b) the possibility of any recovery of any brain
function is excluded, (c) cessation of all brain functions persists
for an appropriate period of observation and/or trial of therapy.”
The Uniform Determination of Death Act (UDDA - the United States
Federal Legislation adopted by most State Legislatures which legally
defines death) used the recommendation of the President’s
Commission as the basis for the statute. Though the Commission’s
report does provide detailed criteria on how to diagnose brain death,
the authors did not attempt to provide a conceptual understanding of
why these clinical findings equate with death, or provide evidence
that these tests in fact assess the integrity of whole brain

Bernat provided a
structural framework for the conceptual understanding of the
diagnosis of brain death.10 He argues that the formal
acceptance of ‘brain death’ is dependent on three conditions: 1)
the "permanent cessation and functioning of the whole brain";
2) that future changes in clinical understanding of brain function
and assessment including the use of technology will only slightly
alter the criterion of death, and 3) that the "explicit
formulation" must be consistent with "society’s
traditional" understanding of death. As will be discussed vide
, the UDDA criteria (similar to Canadian criteria) for brain

Doig et al.:

and the accepted
standards of whole brain death enumerated in the policy do not meet
these reasonable criteria of Bernat.

permanent cessation of function

The UDDA criteria
for brain death, and guidelines from other jurisdictions such as
current Canadian standards11 do not test function of the
"entire brain", and there is sound evidence that many
individuals who meet the clinical criteria of brain death continue to
have some cortical, subcortical, or brain stem function. The current
clinical tests for brain death do not assess subcortical function of
structures such as the hypothalamus-pituitary axis. Many patients
diagnosed as brain dead have intact neurohumoral control of
hypothalamic-pituitary function, demonstrate normal hypothalamic
mediated thermoregulatory control, and have intact autonomic
function: they do not have hemodynamic collapse, they have physical
findings such as bowel sounds, and are reported to have autonomic
reflexes (tachycardia and hypertension) at the time of organ
retrieval.12 Thermoregulatory control, maintenance of
normal hypothalamus and pituitary gland function, and intact
autonomic function represent normal subcortical functions
inconsistent with the understanding of ‘permanent cessation of
functioning of the entire brain’. Given that current clinical
testing does not assess subcortical brain function, ‘whole brain
death’ cannot be conclusively identified at the bedside by using
clinical criteria.

One of the
enduring arguments in support of the consistency of the clinical
confirmation of brain death equating with death is that loss of
integrative functions of the cortex and brainstem will rapidly result
in failure of other systems and death of the person - the so called
somatic disintegration hypothesis.13 "That structural
disintegration follows brain death is not a contingent matter; it is
a necessary consequence of the death of the critical system. The
death of the brain is the point beyond which other systems cannot
survive with, or without, mechanical support."14 Shewmon
reviewed 12,200 sources to identify 175 cases of individuals with
brain death reported to have cardiac function persist for a minimum
of one week; 56 cases are reported in detail.15 In
approximately 60% of the 56 cases, cardiac function persisted to one
month. Of the individuals whose cardiac function ceased in this one
month interval, half had cardiac arrest as a result of withdrawal of
ventilatory support. Shewmon’s publication has questioned the
construct of the somatic integration hypothesis. His work was subject
to much criticism in subsequent correspondence,16–19 but
the importance of his work cannot be overlooked given that many
lawmakers and judges have viewed the somatic integration hypothesis
as a cornerstone to the legal basis for brain death equating with


It would be
reasonable to assume that the criteria for the clinical diagnosis of
brain death have remained relatively static over the past three
decades since no new relevant physical examination maneuvers have
been described during this time. This assumption is incorrect. In
1977, Walker published on behalf of a collaborative group from the
National Institute of Neurological Diseases and Strokes, a study
reviewing the then current criteria for cerebral death.20 The
criteria included coma, apnea, dilated pupils, absent motor
responses, and electrocerebral silence on electroencephalogram (EEG).
Four years later, the President’s Commission criteria expanded the
required number of brain stem reflexes that needed to be absent, and
removed the criterion of electrocerebral silence. However, the
Commission still recommended EEG as desirable when objective
documentation was required to confirm clinical findings…
"electrocerebral silence verifies irreversible loss of cortical
functions, except in patients with drug intoxication or hypothermia…
when joined with the clinical findings of absent brainstem functions,
electrocerebral silence confirms the diagnosis." The
Commission’s decision to remove electrocerebral silence as a
necessary confirmatory test remains puzzling given its subsequent
recommendation for its use. Subsequent to the President’s
Commission report there are studies that document the presence of
electrocerebral activity following the declaration of brain
death.21,22 Grigg and colleagues from Loyola University
Medical Centre reported on EEG activity in a consecutive case series
of 56 patients with confirmed clinical ‘brain death’.21
These authors reported that in 11 patients, electrocerebral
silence was not present following the diagnosis of brain death. These
authors used appropriate measures to avoid external interference
(room noises, internal machine noise, muscle activity, or movement
artifact), as a source of observed EEG activity. As well, EEG
interpretations were conservative assuming any observed activity as
artifact unless the observer was without doubt. EEG activity observed
was categorized into low voltage theta or beta activity, alpha like
activity, or sleep-like activity. In one of two patients EEG activity
resembling physiologic sleep persisted at repeat EEG testing 168 hr
following ‘declaration’ of ‘brain death’. The finding of
coordinated EEG activity, such as sleep, is inconsistent with the
presumption of loss of coordinated and integrating whole brain
function and raises doubt about the accuracy of the clinical
diagnosis of brain death.

There remains
considerable international inconsistency in the application of
clinical criteria for the diagnosis of brain death.23 In
North America, the recently published guidelines prepared by expert
opinion of the Canadian Neurocritical Care group differ from the
‘evidence based approach’ of the American Academy of
Neurology.11,24 A recent article reviews the American
criteria.25 For example, the Canadian guidelines do not
require the testing of the oculocephalic reflex, permit a core
temperature as low as 32.2°C during the apnea test, and allow an
interval between examinations as short as two hours, or as long as 24
hr if due to anoxic-ischemic insult. The American criteria do not
specify a necessary interval between assessments but recommend as
reasonable an arbitrary six-hour interval, require a core temperature
of 36.5°C during the apnea test, and do require testing of the
oculocephalic reflex. The criteria used for the diagnosis of brain
death in infants less than one year of age are also different than
the criteria for the diagnosis in adults. In England, this definition
of death has been adopted: "irreversible loss of the capacity
for consciousness, combined with irreversible loss of the capacity to
breathe should be regarded as the definition of death." The
nomenclature in the United Kingdom has been changed from ‘brain
death’ to ‘brain stem death’.26 Takeuchi has
published on other inconsistencies.27 There has been no
coherent cogent pathophysiologic or philosophical explanation to
explain these differences in diagnostic criteria. Perhaps, as
discussed by Wijdicks in the only ‘evidence based’ synthesis of
brain death criteria, the diagnosis of brain death has been
established largely on class III data defined as "evidence
provided by expert opinion, nonrandomized historical controls, or one
or more case reports."24,28 These inconsistencies,
changes in the criteria for ‘brain death’ over time, and lack of
specificity in tests of cortical and subcortical brain function
exemplify the inadequacy and inconsistency of clinical criteria for
confirming "complete cessation of brain function" and
therefore brain death. This raises concern over whether these
criteria are satisfactory.

and the medical profession’s understanding of brain death

There is a
misunderstanding of the concept, definition, and clinical criteria
for the diagnosis of brain death among the health care professions.
Youngner and colleagues performed a multicentre survey of staff
caring for organ donors including physicians responsible for
determining brain death, and medical and


nursing staff
involved in the care of the potential donor/their family.29 Only
64% of physicians and 28% of other staff accurately identified the
clinical criteria for brain death, and/or in case scenarios correctly
categorized patients as dead or alive. Even physicians actively
involved in the identification of brain death were unable to identify
the requisite diagnostic components of brain death, and/or were
unable to apply the criteria correctly.

In a recent
editorial in the Journal Anaesthesia, Young and Matta advocate
for the use of anesthetics during the harvesting of organs from brain
dead organ donors.30 They provided three reasons, of which
two are particularly relevant: 1) the surgical retrieval of organs
from brain dead donors is often associated with hypertension and
tachycardia and this is distressing for operating room personnel to
witness (ostensibly because these findings during operative
procedures are usually an indication of awareness and/or pain); and
2) that the concept of brain death is not well understood and given
the arbitrary nature of the clinical criteria for brain death,
caution is required before assuming anesthesia is not necessary. In
subsequent commentaries,31,32 these authors were chided in
part because "by urging the use of anaesthetic agents, they have
accepted that there are doubts over the state of consciousness in the
brainstem dead individual. It would have been far more appropriate to
suggest reappraisal of the UK brainstem criteria, public debate, or
even more openness and honesty in our discussions with bereaved
relatives. We cannot hope to maintain public confidence merely by
following their ill thought out suggestions."

Although two
physicians with experience and expertise must be responsible for the
declaration of brain death, and a neurologic condition capable of
causing brain death is a mandatory prerequisite to the diagnosis of
brain death, there are reports in the literature of conditions that
mimic brain death or that provide examples of the mistaken diagnosis
of brain death.33–40

Van Norman41
describes three cases (two of which she has apparent immediate
knowledge) involving the determination of brain death. In these three
cases, the patients did not meet the clinical criteria for brain
death, yet were referred for organ retrieval. In two of the cases,
the patient’s had suffered devastating brain injuries, but were
breathing spontaneously. Despite spontaneous respiratory effort,
these patients were certified as brain dead, and proceeded to organ
retrieval. In the second of these two cases, organ retrieval occurred
against the protests of the anesthesiologist who questioned the
diagnosis of brain death, and despite the patient demon

Doig et al.:

hypertension and movement during organ retrieval necessitating the
use of muscle relaxants and general anesthesia. In the third case, a
young woman postvaginal delivery with concomitant pregnancy induced
hypertension suffered generalized seizures, and had clinical and
radiographic evidence (computed tomography findings of coning,
diffuse edema, and occipital lobe infarcts) of a "catastrophic
neurological event". The patient was determined to be brain
dead, and prepared for organ retrieval. One physician subsequently
identified intact brainstem reflexes. A review of this case
determined that the clinical diagnosis of brain death had occurred
after the patient had received iv muscle relaxants, and had a
serum magnesium level of

5.2 mEq·L–1.
In the third case, the mother regained consciousness, and was
discharged home alert and oriented, but with unspecified neurological

Brain death is a
concept often misunderstood by the general public. Sanner performed a
survey about attitudes toward autopsy and organ donation in a sample
size of 1,950 randomly selected individuals.42 Of
respondents, only 62% would donate their organs, and only 39% would
assent to the donation of their rela-tive’s organs. The two
predominant reasons for refusal were the fear of not being dead at
the time of organ retrieval and the uncertainty of the concept of
brain death. Because families misunderstand brain death, many organ
retrieval programs stress the necessity of stating that the patient
is ‘dead’ and not ‘brain dead’, thereby potentially obviating
any family concerns about the status of their loved one.

In summary, the
current clinical criteria for brain death are not consistent with the
stated objective of the outcome "to identify the permanent
cessation of entire brain function". Nor are the clinical
criteria for brain death either universally understood, and/or
correctly applied, and at least in one report, two cases were
presented where the criteria were deliberately misrepresented in an
attempt to retrieve an organ for transplantation. Finally, brain
death is not a concept that is coherent and clearly understood in the
general public.

the criteria for brain death

Is this simply a
pedantic and pedagogical discourse, or is there relevance in
discussing these inconsistencies? As was identified in the seminal
Harvard report, there are two reasons to determine that brain death
has occurred: 1) to support withdrawal of treatment as further
interventions are futile, or 2) for the purposes of solid organ
donation which is now the most common practical reason.

A premature death
from end-stage organ dysfunction is potentially preventable with an
organ transplant.

Unfortunately, the scarcity of
available organs for transplantation is a barrier to saving more
lives. The ethical approach to organ donation dictates that the need
of those requiring organs should not supercede the ethical management
of potential donors.

Society’s acceptance of organ
transplantation, and the willingness to donate organs is dependent on
absolute trust in the process, a process that starts with the
diagnosis of brain death. Therefore, it would seem a reasonable
proposal for a broad based coalition to reexamine the Canadian
criteria to address issues such as the evidence that justifies the
clinical criteria as proposed, the differences between published
criteria and the current application of criteria in Canadian
hospitals including professional training and standards. Such a forum
is planned, and this approach should help ensure public confidence in
the validity of the medical standard, and also address mechanisms to
avoid conflict of interest when organ donation is considered.43

There is an alternative
approach. A lack of blood flow to an organ causes an organ to die.
The brain is considered the organ most sensitive to necrosis from
cessation of blood flow. Lack of blood flow to the entire brain is an
anatomic equivalent to the cessation of brain function. In the
setting of normal arterial pressures, technetium 99
hexamethylpropyleneamineoxime (Tc99-HMPAO) perfusion scanning, or
four-vessel selective cerebral contrast dye angiography can
accurately assess anterior and posterior cerebral circulation (that
is ‘whole brain’ blood flow).44,45 Tc99-HMPAO scanning
is usually performed with dynamic and static imaging. The dynamic
imaging can quickly assess the presence or absence of intracranial
perfusion, whereas static imaging detects any uptake of the tracer by
functioning neurons. Both of these tests provide irrefutable proof of
absent blood flow to the brain, and therefore permanent and
irreversible cessation of brain function. If we cannot resolve the
inconsistencies in the use of current clinical criteria, it may be
reasonable to consider them as a mandatory component of determining
‘whole’ brain death.

organ donation is an important and laudable objective. To do so at
the expense of exploiting society’s most vulnerable cannot be
supported despite the best of intentions. We share the opinion of
Dossetor who states: "ethics dictates the following: organs
should not be procured from bodies where there is life... no measures
should be carried out on the dying person even with family consent,
that are not directed at serving the best interests of the dying
person… Our faith in the supposedly objective diagnosis of brain
death leads us to remove organs from the dead body where the heart is
still beating. We now need to take seriously the question of whether
the criteria to establish brain death are as reliable as we claim
them to be. If they are not as satisfactory as we once thought, the
whole matter should be brought into debate."

Rosenbaum S. Ethical
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2 Bernat JL. Ethical and
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3 Price D. Contemporary
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24 Anonymous. Practice
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29 Youngner SJ, Landefeld
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30 Young P, Matta B.
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31 Turner M. The
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32 Poulton B, Garfield M.
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Doig et al.: DECLARATION

36 Hughes R, McGuire G.
Neurologic disease and the determination of brain death. The
importance of a diagnosis. Crit Care Med 1997; 25: 1923–4.

37 Hassan T, Mumford C.
Guillain-Barre syndrome mistaken for brain stem death. Postgrad Med J
1991; 67: 280–1.

38 Ragosta K. Miller
Fisher syndrome, a brainstem encephalitis, mimics brain death. Clin
Pediatr 1993;

32: 685–7.

39 Ringel RA, Riggs JE,
Brick JF
. Reversible coma with prolonged absence of pupillary and
brainstem reflexes: an unusual response to a hypoxic-ischemic event
in MS. Neurology 1988; 38: 1275–8.

40 Okamoto K, Sugimoto T.
Return of spontaneous respiration in an infant who fulfilled
current criteria to determine brain death. Pediatrics 1995; 96:

41 Van Norman GA. A
matter of life and death. What every anesthesiologist should know
about the medical, legal, and ethical aspects of declaring brain
death. Anesthesiology 1999; 91: 275–87.

42 Sanner M. A
comparison of public attitudes toward autopsy, organ donation, and
anatomic dissection. A Swedish survey. JAMA 1994; 271: 284–8.

43 Shemie S, Doig C,
Belitsky P
. Advancing toward a modern death: the path from severe
brain injury to neurological determination of death. CMAJ 2003; 168:

44 de la Riva A, Gonzalez
FM, Llamas-Elvira JM, et al
. Diagnosis of brain death:
superiority of perfusion studies with 99Tcm-HMPAO
over conventional radionuclide cerebral angiography. Br J Radiol
1992; 65: 289–94.

45 Nau R, Prange HW,
Klingelhofer J, et al
. Results of four technical investigations
in fifty clinically brain dead patients. Intensive Care Med 1992; 18:

46 Dossetor JB. Death
provides renewed life for some, but ethical hazards for transplant
teams (Editorial). Can Med Assoc J 1999; 160: 1590–1.


Sunday, June 14, 2009

West Nile virus (WNV)

For the record, West Nile virus (WNV) can cause severe, potentially fatal neurological illnesses, which include encephalitis, meningitis, Guillain Barre syndrome, and anterior myelitis. WNV season: May through October. A person with WNV-associated acute flaccid paralysis may present with or without fever or mental status changes.

Get the FACTS!

Wednesday, May 13, 2009

Creatine Kinase: Factbites

Creatine Kinase Factbites

Creatine Kinase
(CK) is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

CK is often determined routinely in emergency patients. In addition, it is determined specifically in patients with chest pain and acute renal failure. Normal values are usually between 25 and 200 U/L. This test is not specific for the type of CK that is elevated. In females, total Creatine Kinase should be 10-79 units per liter (U/L).

Elevation of CK is an indication of damage to muscle. It is therefore indicative of injury, rhabdomyolysis, myocardial infarction, myositis, myocarditis, malignant hyperthermia and neuroleptic malignant syndrome.

Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged. CK helps cells make the energy needed to move: may also be tested from the patient's medical record. The CK level usually parallels a disease activity.

In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being.

Muscle wasting is a hallmark of a number of diseases, including cancer, bacterial sepsis, AIDS, diabetes, and end-stage heart, kidney, and obstructive pulmonary disease. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Skeletal muscle atrophy is a common comorbidity of cancer. The progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer. However, a clinical feature of demyelination is muscle weakness without muscle atrophy.

Guillain-Barré syndrome and similar disorders do not produce evidence of muscle inflammation, such as elevation of the CK. Hypokalaemic periodic paralysis has a predilection for thyrotoxicity in some patients. It is associated with a low potassium concentration but it too is associated with a normal creatine kinase level.

Persons with cancer typically have high CK levels.

Metastatic malignant neoplasms cause severe body wasting-cachexia. The hallmark of muscle damage or muscle wasting is elevation of CK concentration. The wasting away of fat and muscle (cachexia) is the most visible hallmark of metastatic cancer.

Elevation of CK may be seen in stroke, extreme shock, or brain tumor(s). A very high creatine kinase value indicates severe muscle fiber breakdown (necrosis). Even in paraneoplastic disorders the serum CK level is typically elevated 8-100 times normal. Persistent or ongoing muscle injury will maintain high CK concentrations.

The hallmark of muscle damage is elevation of creatine kinase ( CK ) concentration, which is also present in all patients with rhabdomyolysis. During episodes of acute muscle breakdown (rhabdomyolysis), CK levels can temporarily go off the scale, topping out at 50,000 to 200,000 U/L.

Other forms of muscle damage, such as from a fall, a car accident, surgery, or a shot, can also increase CK. CK levels usually rise significantly in about 2 to 3 hours or perhaps a little longer (can rise two-fold within six hours) and peak within 24 hours. High CPK levels may be seen in patients who have: Heart attack; Brain injury or stroke.

See also

Creatine kinase test | Encyclopedia of Medicine | Find Articles

Elevated Serum Creatine Kinase

Creatine kinase BB: a new tumor-associated marker

Creatine kinase testing

Abstracts: The diagnostic and prognostic value of pretreatment

Cancer of the Nervous System

Saturday, May 2, 2009

Creatine kinase (CK)

Creatine kinase (CK or CPK) is an enzyme or type of protein found in muscle and brain that leaks out and is released into the bloodstream when muscle is damaged. In normal conditions, there is very little creatine kinase circulating in the blood of the average, healthy human being.

CK is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients. Even in paraneoplastic disorders the serum CK level typically is elevated 8-100 times normal.

Skeletal muscle atrophy is a common comorbidity of cancer. Progression of skeletal muscle atrophy is one of the characteristic features in cancer patients and the progressive depletion of skeletal muscle is a hallmark of many types of advanced cancer.

Guillain-Barré syndromeis a disorder caused by "nerve" inflammation (not muscle inflamation), involving progressive muscle weakness or paralysis. GBS initially does not usually produce evidence of muscle inflammation or waisting such as elevation of Creatine Kinase (CK) concentration. Persons with GBS or clinically similar disorders typically have normal or low CK levels at onset of the disease, unless tissue damage in the brain or elsewhere has already occurred.

To illustrate, a low/normal CK at the time of a patient's admission to hospital would argue favourably against a diagnosis of structural brain damage, or active metastatic cancer.

A clinical feature of demyelination is muscle weakness without muscle atrophy. Persons with Muscular Dystrophy, Guillain-Barré Syndrome and other neuromuscular disorders typically have low creatine kinase levels.

Lyme disease may also cause weakness secondary to peripheral neuropathy but it too does not produce evidence of muscle inflammation such as elevation of the CK.

Creatine Kinase (CK) should typically not be elevated in GBS and if it is, another cause (or underlying disorder) should be suspected.

The highest creatine kinase activities are found in skeletal muscle, myocardium and brain tissue. Significantly increased creatine kinase levels may support a hypothesis of brain death; normal CK levels do NOT.

In females, total Creatine Kinase should be 10-79 units per liter (U/L). CK is the most sensitive enzyme and in the presence of most diseases, levels can be elevated as much as 50 to 100 times the reference level.

narcotic analgesics and laxitives

Coadministration of narcotic analgesics with laxitives may have additive central nervous system (CNS) and gastrointestinal (GI) system effects, and increase the risk of severe constipation or paralytic ileus, including CNS depression.

Migraine headaches

Migraine headaches happen when blood vessels in your head open too wide or close too tight. The most common triggering agents for migraines are alterations in serotonin metabolism (deficiency), diabetic condition, hormonal imbalances, histamine-induced platelet aggregation (blood platelets sticking together), blood sugar imbalances and certain medications.

In women, migraine attacks may also be triggered by hormonal changes during menstruation (periods).

Ameboma, the forgotten granuloma?

Consider a cyst that occupies space and feeds off red blood cells ... giving rise to purulent matter resulting in dessemination and abscess formation. You are encouraged to think critically about what you find here. Do your own research if you still have questions.

Amebiasis is a disease caused by a one-celled parasite called Entamoeba histolytica (ent-a-ME-ba his-to-LI-ti-ka). There are a number of variants.

In the Canada and the United States, amebiasis is most often found in immigrants from developing countries. It also is found in people who have traveled to (or who have come into contact with) developing countries, such as Mexico.

The symptoms often are quite mild and can include loose stools, stomach pain, and stomach cramping. Amebic infection is a severe form of amebiasis associated with stomach pain, bloody stools, and fever. Rarely, E. histolytica invades the liver and forms an abscess. Even less commonly, it spreads to other parts of the body, such as the lungs or brain, and cause abscesses. It may produce symptoms that mimic a number of intestinal disease processes, including cancer.

The infection may mimic space-occupying lesions in CNS, and the infected patient may present with hemiparesis, aphasia or seizures. In such instances, head CT and MRI may reveal ring-enhancing lesion (abscesses) suggestive of brain tumors. Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

Clinical Features:
A wide spectrum, from asymptomatic infection ("luminal amebiasis"), to invasive intestinal amebiasis (dysentery, colitis, appendicitis, toxic megacolon, amebomas), to invasive extraintestinal amebiasis (liver abscess, peritonitis, pleuropulmonary abscess, cutaneous and genital amebic lesions). An ameboma may mimic carcinoma of the colon.

Pleuropulmonary amebiasis is the common and pericardial amebiasis the rare form of thoracic amebiasis. Pleuropulmonary amebiasis is easily confused with other illnesses and is treated as pulmonary TB, bacterial lung abscesses, and carcinoma of the lung, which may exacerbate the condition.

Amebiasis is caused by the protozoan parasite. Protozoan infections include amebiasis, toxoplasmosis, and trypanosomiasis (sleeping sickness). Protozoa can produce malaria, amebiasis, leishmaniasis and trypanosomiasis.

Typically, N fowleri produces primary amebic meningoencephalitis (PAM), which is clinically indistinguishable from acute bacterial meningitis.

The cyst fills with bacteria and pus, and becomes an abscess (chocolate-brown abscess fluid is thought to be highly characteristic of amebic abscess); the earliest amoebic lesions appear as small, yellow mucoid (yellowish exudate) elevations containing necrotic material where the parasite can be found. The center of an amebic abscess, consisting of lysed hepatocytes, erythrocytes, bile and fat, may liquify and this necrotic material (sometimes incorrectely called pus) will range in color from yellowish to reddish brown. If the abscess bursts inside the body, there is a risk of blood poisoning (septicaemia). Septicemia, is a form of sepsis.

The most common signs of amebic infection are alternating diarrhea and constipation(possibly accompanied by blood and excessive mucus) and irregular appetite. Other clinical signs include vomiting, listlessness,weakness, low weightand signs of dehydration (e.g.sunken eyes, thick oral mucus). If the lungs are infected (a condition generally associated with more chronic infections), labored breathing, mouth/nasal discharge and wheezing may also be noted.

In the Canada and the United States, amebiasis is most often found in immigrants from developing countries, such as Mexico. It also is found in people who have traveled to (or who have come into contact with) developing countries and in people who live in institutions that have poor sanitary conditions which pose health issues for travelers.

Ameba only multiplies rapidly if a person is very run down by an immune deficiency, illness or infection. Only virulent amoeba can lyse polymorphonuclear leukocytes (PMNs).

Ameba can spread hematogeneously from a cutaneous, ocular, or pulmonary lesion to the CNS, where vasculitis may also dominate the clinical picture.

An ameboma may simulate an "adenocarcinoma" or another granulomatous process. Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

immigrant doctors

Many immigrant doctors who come to Canada have very low qualifications. Many of them have been exposed to malaria, parasites and unfamiliar infectious diseases, such as amebiasis and also pose public health risks from a variety of emerging infectious diseases.

Mexico is a hotbed for amebic infection (amebiasis ), a source of infectious cysts.
Some doctors may be carriers and not even know it.

WARNING: Parasitic cysts of any origin may mimic primary or metastatic brain tumor(s).

Friday, May 1, 2009

Altered & Falsified Medical Records


Fraudulent addition
to a medical record for the purposes of covering up an incident can be detected by current technology. Expert document examiners will need the original medical record in order to analyze it for tampering. This will enable them to detect differences in ink, look for indentations caused by writing on sheets above the questioned document, and perform chemical analysis of the document. There are clues used
to detect altered records.

Clues to altered records:
  • writing crowded around existing entries

  • changes in slant, pressure

  • uniformity or other differences in handwriting

  • erasure or obliteration

  • use of different pens or typewriters to write one entry

  • misaligned typed notation, impressions or lack of impressions from writing instruments on the following pages

  • ink offsets or lack of offsets on the back side of the preceding page, and

  • additions on different dates written in the same ink, while original entries were written in different ink.

All health care professionals should be aware that falsification of medical records is grounds for criminal indictment.

Case In Point:

The evidence speaks when victims cannot

Altered Medical Records

In Memory of Arlene Berry 1958-2000

“Truth cannot live on a diet of secrets withering within entangled lies” H. Michael Sweeney

The Quest for Medical Truth

Part I

The Arlene Berry Death Coverup

These are the facts:

There are numerous material deficiencies in the related medical record of Arlene Berry which manifest a complete lack of internal consistency ranging from out of sequence records, from the physician s Critical Care note to the nurses Triage to obviously rewritten, altered and falsified medical records seen between N-1 and N-3 of the nurses notes, including the physician’s Lab Report, marked by error, inconsistency, omission, and contradiction that is consistent with telling lies, to the Ventilation Record seen at A-16 and A-17, presenting similarly.

The record at A-6, what I consider to be quite contradictory, documents a “history of metastatic lung cancer” while the record at OP-54 clearly documents “no metastasis” and “mediastinoscopy negative”.

The Ventillation record contains a self-serving entry, ie. “without adversities” relating to patient’s intubation procedure, which took place at 0325 hours on May 24th of 2000, while the record at A-17 documents patient being “suctioned for moderate amounts of coffee ground emesis” at 0330 hours, only five minutes later, which can suggest thoracic injury, or perhaps a severe gastrointestinal problem, or both. That the patient’s Heart Rate soared to 174 bpm during the intubation procedure should be borne in mind. I find this to be very significant in terms of iatrogenic injury.

An example of going a step further, requires a high index for suspicion of iatrogenic injury which may become more readily apparent after following a time course for events, “before and after” , which in this case is marked by hypotension preceded by evidence of hypertension and is evidenced by a documented blood pressure of 162/80 at 0220 hours followed by a lethal drop in blood pressure to 78/70 by 0235 hours that is a hallmark feature of orthostatic hypotension in which BP rises or falls significantly. Another example is a documented BP of 163/117 at 0320 hours that by 0352 hours dropped to 85/52, with much of the record presenting similarly.

N-4 and N-5 present with less than half a page of documentation that is consistent with deliberate omission, such as withholding information.

A-24 and A-25 of the record, what I take to be identical forms, appear to be misaligned when superimposed (one over the other) and held over a light. Further, the print sizes appear to be slightly different and both are marked “Page 1 of 1”, to rule out conformity and consistency. Further, A-14 shows a misaligned margin suggesting a split in the page, or perhaps a cut out, with A-13 and A-27 presenting similarly.

Many of the records contain write-overs, primarily with respect to date and time, suggesting that perhaps the authors were no longer oriented to date and time of events that is consistent with making changes at a later date.

According to the Certificate of Death Arlene Berry died on May 24th of 2000. According to her physician “she died several days later with numerous metastatic lesions to her brain”. However, the medical record for May 23rd and 24th of 2000 tells a very different story, suggestive of a known “resistant bacterium” of the Staph aureus variety with a sepsis-like picture that is consistent with a severe hospital acquired infection or a bacterial meningitis. Further examination of the record reveals evidence of “iatrogenic neglect” (doctor caused negligence) and outright incompetence on the part of the healthcare providers to say the least, that is consistent with substandard care.

There is a complete absence of record with respect to the patient’s blood pressure between 1845 hours on May 23rd and 0040 hours on May 24th of 2000. This can suggest either incompetence or deliberate omission and can also constitute evidence of substandard care. lA-26 of the record documents a BP (blood pressure) of 78/70 at 0235 hours, while N-5 documents a BP of 98/70 at the very same time suggestive of having been copied.

A-16 documents a BP of 163/117 at 0330 hours while N-3 documents a BP of 136/85 at the very same time. The same record documents a BP of 121/81 at 0400 hours, while N-2 documents a BP of 112/57 at the very same time that is also consistent with copious error.

A-24 documents a Heart Rate (HR) of 154 bpm at 0330, while the Ventilation Record documents a HR of 126 bpm at the very same time, a significant difference. The same record documents the mechanical charting of the patients vital signs commencing at 0315 hours on May 24th of 2000. It is interesting to note that the patient’s transfer to the ICU had not taken place until ten minutes later at 0325 hours. I would really like to know how they were able to proceed with the recording of the patient’s vital signs in her absence.

A-4 of the record, what I take to be a Trauma Legend, barely visible in the physician’s notes situated at the lower right hand side of that record there is an obliterated area suggesting a white-out or perhaps an erasure. This to me suggests that was was indeed trauma involved.

A-1 of the record documents “she had a left lung pneumonectomy back in October of 1999”, which is erroneous. A-17 documents the very same error with “removal of left lung in 99”, suggestive of having been copied. The bald truth is that the patient was last seen by the same physician who originally had misdiagnosed her in October of 1999 for which she had the lung removed on January 13th of 2000.

A-3 of the record, what I take to be the physician’s diagnostic chart is a total blank. From that record it seems clear that nothing was entered because nothing was done. The same record was filed out-of-sequence. The emergency record at A-4 was also filed out-of-sequence. Interestingly both of these records were dated using a rubber stamp that is consistent with backdating.

A-1 of the record documents “I was called in later that night because the patient had become obtunded”, while N-6 documents “no response to deep pain” as early as 0030 hours on May 23rd of 2000. N-4 of the record documents that Dr. Jordan was notified of patient condition at 0225 hours, while N-2 documents “attempts to pull away to painful stimuli” at 0400 hours on May 24th, one hour and thirty-five minutes later, after the time the physician claims he was called in. There can be no question that the doctor lied.

There is a complete absence of documentation with respect to the patients bowel routine and urinary elimination pattern for toileting as evidenced at N-10 of the record, with the very same information omitted at OP-53 of the record.

Caveat: There are two precautions on record for what I take to be a warning with respect to “resistant bacteria”. The precaution can be seen more visibly at N-9 of the record under the subheading for “INFECTION CONTROL PRECAUTIONS”, evidenced by a check mark in the box. Notably, the particulars with respect to type of resistant bacterium are omitted. A “resistant bacteria” denotes a very serious infection of the “super-bug” antibiotic resistant variety, usually hospital acquired.

In a letter to the College of Physicians and Surgeons of Ontario dated November 28, 2000, Dr. Jordan writes “discussed the situation with family members and a decision was made to intubate Ms. Berry”, while the Ambulance Call Report documents an unsigned physician order to withdraw life support from an obviously critically ill patient, as evidenced by an obscure and secretive 3.3 Code only to be found in the annals of internal medicine. In acting as aforesaid it seems clear that Dr. Jordan ordered her death.

The record at N-6 documents bilious vomit at 1915 hours following the patient’s admission, as evidenced by “emesis of >> 100 cc yellowish fluid” that is the hallmark of intestinal obstruction that by 0330 documents “moderate amounts of coffee ground emesis” that is consistent with upper gastrointestinal bleeding. Another record documents a “large bloody emesis of reddish brown”, and “orally thick secretions” suggestive of a more significant backup of intestinal material, while the Ambulance Call sheet at A-7 documents an “intracranial bleed” that is inconsistent with the hospital record as a whole. This infers a blatant attempt tp obfuscate the truth.

The record at A-8 and A-9 documents “Medi-Vac team were due to arrive at 0435”, while the Ambulance Call sheet documents the time of the call event for ”call received at 0620” hours, a significant difference.

There are several late dictations and I can count at least three two page documents, all of them questionable seen at A-1, A-2, A-6, A-7, A-8, and A-9, as evidenced by the times and dates upon which they were dictated and transcribed. One of them was dictated in June of 2000, and transcribed in July of 2000, some two months after the patient s death. lThe Cardiac Index falsely documents the patient’s age at “55 years”, she was only 41.

N-7 documents a “stable” condition. Yet the same record documents a complete withdrawal of life support from a critically ill patient as evidenced by a Code 3.3, including a Nature Code 0 that is consistent with No Care.

The Ambulance Call report also documents a “pale, dry and cool” condition that is consistent with clinical manifestations of adrenal insufficiency, or hypovolemic shock. Compare Shock Syndromes in which pallor and cold peripheries suggestive of vaso-constriction all point to circulatory failure.

The same record at N-7 documents pulses X 4 good; head and neck OK; chest OK; abdomen OK; pelvis OK; extremities OK. The “coffee ground emesis” (suggestive of old blood and gastric juices) including the “large bloody emesis of reddish brown” and “ orally thick secretions” (suggestive of a more significant backup from the intestinal tract) associated with abdominal bleeding documented elsewhere on the record were completely omitted from the ambulance call record and substituted for “intracranial bleed”.

According to Dr. Jordan “she was admitted by Dr. Spiller with symptoms suggestive of metastatic CA of the brain”. According to Dr. Spiller ”a question has been raised” with respect to metastatic cancer of the brain. According to the record she was admitted for “vomiting”. Vomiting is not a diagnosis, but rather a symptom of many causes. The buck-passer, let us agree, tries to pass the buck together with all the possible blame for not having the right answer.

Much of the record is illegible. Illegible writing is reckless writing suggestive of callousness, ie no quality in writing, no quality in care. It also explains why many medical records are rewritten, after the fact, but which also affords opportunity for malfeasance to those who would dare skew the record in order to save face.

No autopsy was done. A family request for a formal inquest into the denied. cause of the patient’s death was also denied

Worthy of mention is that there is absolutely nothing in the patient’s blood values to even remotely suggest metastatic cancer, although a leukomoid reaction is a distinct possibility. In fact , everything points to a severe undiagnosed and untreated hospital acquired infection with a sepsis-like picture suggestive of the Toxic Shock Syndrome or staphilococcal meningitis, including evidence of neuroleptic drug involvement.

From the record it seems clear that the healthcare providers failed miserably in their concerted efforts to obfuscate the truth. Not only did they act together, but together with malice and forethought and with intent to defraud the estate of the deceased of any lawful claim they may have had against them (the doctors and nurses) for their part in substandard care and civil wrongdoing. They unwittingly escalated their plot into a criminal conspiracy and criminal wrongdoing of all kinds by their own doings. Perhaps its time they all had their moral codes thoroughly overhauled.

Altered Medical Records
by meverett Wednesday, Aug. 03, 2005 at 6:38 AM

The following Supporting Information is available for this article:

LSU Law Center's
Medical and Public Health Law Site
Articles on Law, Science, and Engineering
Scientific Misconduct: Part 3 - Standards for Scientific Record Keeping

add your comments

falsified medical reports
by Amy Lynne Friday, Sep. 30, 2005 at 9:49 AM

I found this site while trying to research the prevalence of falsified medical documents...

I have experienced the death of a loved one, my 2 year old son, and have discovered false and contradictory statements from the ambulance report, which logically explains the confusion and mis-diagnosis at the hospital where they did not treat my son based on his actual condition or a truthful account of events leading up to his arrival at the hospital.

I do not know how to go about reporting this injustice, as there seems to be nobody who is willing to investigate this. Although the sequence of events in the report is impossible and illogical, and directly related to our son's needless death, our lawyer advises against persuing a lawsuit because the possibility of a small and limited court award does not justify the vast expense involved in the legal process and the possible risk of financial loss in the event that the case is lost.

More people should insist on laying criminal fraud charges in such cases. The main purpose of altering and falsifying medical records is obvious - to "dupe" the injured party or in the case of death his/her estate or next of kin of any lawful claim they may have had. My advice is to go for it.

Detecting Tampering with Medical Records

Articles From IEEE Engineering in Medicine and Biology Magazine
Scientific Misconduct

View the medical record of Arlene Berry

physicians' attitudes: deception

Physicians' attitudes toward using deception to resolve difficult ethical problems

To assess physicians' attitudes toward the use of deception in medicine, JAMA sent a questionnaire to 407 practicing physicians. "One third indicated they would offer incomplete or misleading information to a patient's family if a mistake led to a patient's death." JAMA Vol. 261 No. 20, May 26, 1989