The inherent dishonesty of Rupert Anthony Risdon

Risdon, in the court room, states in Burridge that the bridging veins had sheared due to rotational acceleration deceleration injury (new phrase for shaken baby) - he is then cross examined on just how many veins there are, where they are and what they connect to - what does Rupert do ... does he properly explain to the court what it is he means and back it up with his knowledge and experience, no he suddenly, because he hasn't a fucking clue what he's talking about, decides to use a get out of jail free card and state he isn't an anatomist so he doesn't know. Readers of this blog need to ask themselves the following questions about this latest in a long line of lies.

• Why doesn't Rupert know how many veins there are given he testifies about them?
• Why did Rupert lie about the fact he wasn't an anatomist having taught people anatomy for years? 
• Having told the lie, why, given everyone had his CV, wasn't he cross examined further on that clearly false and misleading statement?
• How is it he is able to give evidence in cases of RADI, having claimed he is clueless about the anatomy of the human brain?
• How is it he is able to conduct post mortems with no clue about human anatomy (stated by him on oath)?
• Why is it that everyone is so stupid as to never question the claims of these so called experts?
• Is Rupert the ultimate fake - the wannabe doctor who actually is not qualified at all?
• Would Rupert's evidence have been any better if the questions were about photosynthesis? 

Rupert Anthony Risdon "Reader in morbid anatomy" ONLY WHEN IT SUITS APPARENTLY!

R-V-BURRIDGE

RISDON CV

Undergraduate Education

State Scholarship (Botany & Zoology) - June 1957

                                                      Student at Charing Cross Hospital Medical School October 1957 - March 1962

Qualifications

MB BS (London) April 1962

MRCS (England) March 1962

LRCP (London) March 1962

Primary MRCPath (Haematology & Histopathology)

April 1965

Final MRCPath (Morbid Anatomy & Histopathology)

June 1968

MD (London) June 1972

FRCPath February 1980

Diploma of Medical Jurisprudence (Pathology)

December 1993

Previous Appointments

July 1962 - December 1962   House Physician to Professor H E de

Wardener at Fulham Hospital, London

January 1963 - June 1963      House Surgeon to Mr H L Cochrane at

Fulham Hospital

July 1963 - June 1964              Senior House Officer in Pathology at

Charing Cross Hospital, London

July 1964 - June 1965              Registrar in Pathology at Charing Cross

Hospital, London

July 1965 - December 1965   Registrar in Haematology at Charing

Cross Hospital, London

January 1966 - March 1969   Lecturer in Histopathology at Charing

Cross Hospital, London

April 1969 - June 1971              Lecturer in Morbid Anatomy, Great

Ormond Street Hospital for Children, London

June 1971 - December 1975   Senior Lecturer in Histopathology (with

Consultant status), Great Ormond Street Hospital for Children, London

January 1976 - December 1976            Consultant Pathologist at Addenbrooke's

Hospital, Cambridge

January 1977 - September 1985 Reader in Morbid Anatomy, The Royal

London Hospital Medical College, London

October 1985 - March 2004 Professor of Histopathology, Great

Ormond Street Hospital for Children, London

Shaken Baby - COL4A1 - and there you have it - an answer to the triad

http://keran-henderson-innocent.blogspot.com/2009/09/ehlers-danlos-syndrome-mistaken-for.html



When to consider genetic testing for COL4A1
gene?


At present COL4A1disorder is probably largely underestimated
for several reasons. First it is a newly identified
disorder. Second its clinical expression is extremely variable
with ages of onset varying from antenatal period
until late adulthood (Table 1). In addition there is variability
in the severity of the symptoms and the clinical
phenotypes and there are asymptomatic forms. Some
combinations of neurological and/or extra-neurological
symptoms are however highly suggestive and should
prompt genetic testing in clinical practice.
(1) First, any deep intracerebral hemorrhage of unknown
cause particularly when involving children or young
adults (<50–60 years of age) and if associated with
diffuse white matter abnormalities on brain MRI
suggestive of a diffusesmall vessel disease of the brain.
(2) Second, any intracerebral hemorrhage of unknown
cause in the presence of one of the cardinal extraneurological
symptoms of the disorder in the patient
or in a family member. These indicative manifestations
include retinal arteriolar tortuosities, retinal
hemorrhage, congenital or juvenile cataract, Axenfeld–
Rieger syndrome, chronic hematuria and
muscle cramps with elevated serum creatine
phosphokinase levels.
(3) Third, any bilateral and symmetrical leukoencephalopathy
of unknown cause in the presence of one of
the cardinal extra-neurological symptoms of the disorder
in the patient or a family member (see above).
(4) Fourth, any intracranial aneurysm if associated with a
diffuse small vessel disease of the brain in the
absence of any hypertension and particularly in
younger patients.
(5) And finally any infantile hemiparesis and/or porencephaly
of unknown cause.


More prospective studies are needed to better define the
whole phenotypic characteristics of the disorder. Meanwhile
the key element in clinical practice is to perform in
each suspected patient a comprehensive multisystem
exploration including neurological, extra-neurological
(ophthalmological and renal especially), vascular and
extravascular investigations. In addition it is also crucial
to look carefully for any suggestive family history.

Evidence points to increased risk of IVH with early cord clamping

Read the document, absorb the evidence and then ask yourselves why it is that in every alleged case of shaking an obstetrician has not been called to give evidence - the reason is that everyone is trying to either prove that shaking did or it didn't happen, losing sight of the science - is it just conceivable that the "old bleeds" alleged by the prosecution "experts" to be a "first shake" to be found at Post Mortem are the direct result of the widespread medical practice of early cord clamping? Certainly there is more evidence based medicine that this has occurred than a parent/carer has shaken the baby, which is nothing more than speculation and given that there has been no follow up of the babies who did suffer a bleed, who can say if the bleeding didn't just continue? Certainly Rees Burridge's head continued to swell from birth, something was going on he went from the 50th centile to the 98th centile pre final collapse - given that this practice would now appear to carry significant risk to the baby after it has been born, perhaps the RCPCH would like to comment?????


http://www.rcog.org.uk/files/rcog-corp/uploaded-files/SACPaper14ClampingUmbilicalCord09.pdf


5. Opinion
● Evidence suggests that immediate cord clamping reduces placental transfusion and thus lowers
neonatal haemoglobin. For term infants, this leads to less jaundice and phototherapy at birth,
and to lower iron stores in the first few months of life. For preterm infants it increases the
need for transfusion. The risk of an ultrasound diagnosis of intraventricular haemorrhage is
also increased, but the long term significance of this is not yet known.
● The impact on other substantive outcomes for the woman and the infant remains unclear, after
both term and preterm birth, and should be evaluated in randomised trials.
● Owing to the influence of gravity on placental transfusion, sensible advice is that while the
cord is intact the baby should not be lifted more than 20 cm above the introitus at a vaginal
birth or more than 10 cm above the uterus at caesarean section. The effects of placing the
baby with cord intact on the woman’s abdomen following a vaginal birth, or on her thighs
following a caesarean birth are unclear and should be evaluated in randomised trials.
● Although administration of intramuscular uterotonic drugs before cord clamping may not
have a substantive effect on placental transfusion, this merits further research to confirm
whether there is a clinically relevant effect on either volume or flow.
● Techniques for care and early stabilisation of the newborn with the cord intact should be
developed and evaluated.
Therefore, large randomised trials comparing the effects of alternative strategies for cord clamping are
needed, with assessment of substantive outcomes and long-term follow-up for both mother and baby.

And now the research backs up my theory ......

EDS/Hypermobility.

R-V-Wainwright
R-V-Gibbs

And many more ....

There are none so blind as those that don't see
Or those who lie for the fat fee!

If only they had all done their homework as specified in the Kennedy Review, to which Risdon contributed!




http://www.ncbi.nlm.nih.gov/pubmed/21157337

Curr Opin Neurol. 2010 Dec 13. [Epub ahead of print]

Clinical spectrum of type IV collagen (COL4A1) mutations: a novel genetic multisystem disease.

Vahedi K, Alamowitch S.

aDepartment of Neurology, Lariboisière Hospital, France bDepartment of Neurology, Tenon Hospital, APHP, France cUniversité Pierre et Marie Curie, Paris, France.

Abstract

PURPOSE OF REVIEW: This review dsecribes the clinical spectrum of a newly identified disorder related to COL4A1 gene mutations. COL4A1 encodes type IV collagen α1 chain, a crucial component of nearly all basement membrane including vasculature, renal glomerule and ocular structures.

RECENT FINDINGS: The human phenotypes are extremely variable between patients and between families, with disease onset as early as in the fetal period. COL4A1 mutations are responsible for a wide range of abnormalities affecting mainly the brain and the retinal vasculature, the anterior and posterior ocular structures and the renal glomerules. In the brain, intracerebral hemorrhage is the most frequent phenotype. It affects mainly young adults, children and more typically neonates. Mutated patients develop a diffuse small vessel disease of the brain as shown by a diffuse leukoencephalopathy on MRI. In the eye, patients may have retinal arteriolar tortuosities and retinal hemorrhages or anterior segment dysgenesis. Other phenotypes include intracranial aneurysms, porencephaly, infantile hemiparesis, muscle cramps, optic nerve dysgenesis and secondary glaucoma. There is in addition a specific phenotype called HANAC with constant nephropathy, muscle cramps and frequent intracranial aneurysms.

SUMMARY: COL4A1 disorder is probably largely underestimated because of its multisystem and variable phenotype. In addition the whole spectrum of the phenotype is not yet known and there are many asymptomatic patients.

PMID: 21157337 [PubMed - as supplied by publisher]

SDH, anaemia, Early cord clamping the missing link?

Early cord clamping in the Western world became learnt medicine and has been carried out as a procedure as a matter of course.

I am not a doctor, so I will cite the evidence, peer reviewed research instead and the readers can draw their own conclusions.

It stands to reason that anaemia can and does cause bleeding, is it possible that the SDH seen in so many newborn infants is a direct result of early cord clamping, giving a viable alternative to alleged shaking, especially given how many times the yet to be adequately medically explained OLD hypoxic ischemic damage we see at PM in so many cases.

It would provide an answer to why it is that SDH is being found on MRI in so many neonates, even those born by elective cesarean - the common denominator across the board is early cord clamping, a practice that the WHO no longer supports having conducted a review of all the available literature.



http://apps.who.int/rhl/reviews/CD004074sp.pdf


http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)61410-0/fulltext

http://www.ispub.com/journal/the_internet_journal_of_pediatrics_and_neonatology/volume_11_number_2_10/article/analysis-of-clinical-course-in-term-patients-with-early-and-delayed-umbilical-cord-clamping-after-birth.html

Rupert Anthony Risdon, it's the final countdown ......

General Medical Council

Fitness to Practise Panel

Session beginning 2 – 23 December 2010

General Medical Council, 350 Euston Road, London NW1 3JN

New case of impairment by reason of misconduct and deficient professional performance.

Dr Mohmed Saeed Sulema (Freddie) PATEL

The Panel will inquire into the following allegation against
Mohmed Saeed Sulema Patel, MB ChB 1974 University of Zambia:

“That being registered under the Medical Act 1983 (as amended):

'1.           Between January 2002 and June 2009, you were working full-time, in private practice, and you were on Home Office Register of Forensic Pathologists (“the Register”); during this period you undertook post mortems, upon instructions from Her Majesty’s Coroner for Inner North London, and at the request of the Metropolitan Police Service, until October 2004; Admitted and found proved

'2.           On 21 January 2002, on the instructions of Her Majesty’s Coroner for Inner North London, and at the request of the Metropolitan Police, you carried out a special or forensic post mortem examination on Ms. E; Admitted and found proved

'3.           In the course of the post mortem examination, referred to in Paragraph 2. above, you did not:

a.            swab the ‘red full-set bite mark’ on the front part of the
upper right thigh for possible DNA analysis, Admitted and found proved

b.            dissect the body to look for areas of counter-pressure bruising on the back of the body;

'4.           On 28 January 2002, you carried out a partial second post mortem examination on Ms. E; Admitted and found proved

'5.           In your first post mortem report, dated 31 January 2002, you recorded:

a.            As ‘Marks of Treatment’: a pinched nose, bluish bruise at the tip; and minor healing abrasions on right wrist and below left knee, and, Admitted and found proved

b.            As ‘Marks of Recent Injury’:

i.              A sagittal scalp laceration 2” on occiput midline, with
full skin thickness at the upper end, with associated bruising and sub-cutaneous contusion, Admitted and found proved

ii.             A diffuse erythema on the left shoulder blade area and on the front of the right upper arm, Admitted and found proved

iii.            A full-set bite mark on the front part of the upper right thigh, and, Admitted and found proved

c.             That there were no ‘Marks of Violence’ found; Admitted and found proved

'6.           In your first post mortem report you concluded that:

a.            The injuries to the liver are characteristic of vigorous CPR, Admitted and found proved

b.            The bruised tip of the nose is consistent with mouth-to-mouth resuscitation, Admitted and found proved

c.             The ‘Cause of Death: 1a: Coronary Heart Disease’; Admitted and found proved

'7.           In your first post mortem report:

a.            You omitted to make reference to the absence of petechiae, Admitted and found proved

b.            You omitted to make reference to the distribution of hypostasis, Admitted and found proved

c.             You did not adequately comment on other possible causes of the ‘Marks of Injury’, which you had identified, or their possible significance, in terms of the mode of Ms. E’s death, Admitted and found proved

d.            In your ‘Addendum’ you did not explain your comment ‘No additional marks of violence’; Admitted and found proved

'8.           In the ‘Conclusions’ of your first post mortem report, or elsewhere in the report, you did not:

a.            Adequately explain your comment ‘no significant marks of violence, of assault or forceful restraint’, Admitted and found proved

b.            Comment on the possibility that the scalp laceration might be ‘a mark of violence’, Admitted and found proved

c.             Comment on whether the sustaining of the scalp blunt force injury which resulted in the scalp laceration could also possibly have caused Ms. E to become unconscious, Admitted and found proved

d.            Adequately comment on the circumstances in which the so called ‘classic signs of asphyxia’, including petechiae, may be absent, Admitted and found proved

e.            Raise or comment on the possibility that the liver injury was caused by someone pushing hard with a hand or knee in the abdominal regions whilst on top of Ms. E; Admitted and found proved

'9.           In your second post mortem report, dated 10 February 2002, having been asked by the Police, to consider an asphyxial mode of death, based on new evidence provided to you, you:

a.            Did not comment on whether the sustaining of the scalphead injury could possibly have caused Ms. E to become unconscious, Admitted and found proved

b.            Did not adequately comment on the fact that the ‘classic signs of asphyxia’, including petechiae, may be absent in where there has been no significant counter resistance, for example, where a victim may have been rendered unconscious beforehand, Admitted and found proved

c.             Did not comment on the possibility that the liver injury was caused by pushing hard with a hand or knee in the abdominal regions by someone on top of Ms. E; Admitted and found proved

'10.        In your third post mortem report, dated 7 April 2003, having been asked by the CPS to expand on asphyxia as a possible mode of death, you:

a.            Did not comment on whether the sustaining of the scalp wound could possibly have caused  Ms. E to become unconscious, Admitted and found proved

b.            Concluded that ‘there were no signs of asphyxia and death was due to natural cause, which was the preponderant evidence’, Admitted and found proved

c.             Concluded that ‘The pinched – nose bruise and liver injury with perimortem internal bleeding suggested an association with first aid resuscitation’; Admitted and found proved

'11.        Your conclusions, in the above post mortem reports, as to cause or mode of  Ms. E’s death:

a.            Were made without proper consideration of the following available (and/or obtainable) evidence, namely,

i.           The location of the deceased's naked body in a locked room within the flat of a man recently arrested by the police,

ii.          The position and state of undress of the deceased's body and the location of her clothing,

iii.         The evidence of recent sexual activity,

iv.         The presence and position of blood staining on the wall adjacent to the bed,

v.          The presence and location of blood staining on the deceased's clothing and her bedding,

vi.         The nature and extent of the deceased's external and internal injuries,

vii.       The deceased's personal history,

viii.      The presence of a bucket of warm water next to the deceased's body,

ix.         The statement of a witness ‘S’, provided to you before the preparation of the second and third post mortem reports,

b.            Were made without any adequate consideration of other possible modes of Ms. E’s death, including, asphyxia;

'12.        Your conduct as set out in paragraphs 3., 5., 6., 7., 8., 9., 10. and 11. was:

i.           Irresponsible,

ii.          Not of the standard expected of a competent forensic pathologist when undertaking and reporting on special or forensic post mortem examination,

iii.         Liable to bring the medical profession into disrepute;

'13.        On 20 February 2006, you signed a ‘Protocol for Home Office Registered Forensic Pathologist’ (“the Protocol”); Admitted and found proved

 

'14.        Paragraph 1 of the Protocol stipulated that: ‘the signing agreement to this of The Protocol wasis a requisite of being on the Home Office Register of Forensic Pathologists.’; Admitted and found proved

'15.        Paragraph 3 of the Protocol stipulated that the forensic pathologist must: ‘Work in a Group Practice’, as defined by ‘Annex GPD’ of 'The Protocol'; Admitted and found proved

'16.        From 20 September 2006 you were not working in a ‘Group Practice’ and you therefore did not satisfy the requirements for being on the Register, as required by the Protocol; Admitted and found proved

'17.        In a Curriculum Vitae [CV] provided to the GMC in 2009 you stated:

a.            You were a Home Office Pathologist between 1988-2009, and, Admitted and found proved

b.            As a ‘Current Appointment’: ‘Home Office South Eastern Group Practice with Professor Vanezis, Dr. Heath and Dr. Rouse -2006-2009’;

'18.        In a further CV provided to the GMC, in August 2010, you represented that:

a.            you were a Home Office registered forensic pathologist between 1988-2009, Admitted and found proved

b.            you were had been in a Group Practice described as ‘Home Office South Eastern Group Practice with Professor Vanezis, Dr. Heath and Dr. Rouse.’; Admitted and found proved

'19.        In the course of GMC Fitness to Practise proceedings, in
August 2010, you gave evidence that:

a.             you were a Home Office registered forensic pathologist between 1988-2009, Admitted and found proved

b.            you were in a Group Practice described as ‘Home Office South Eastern Group Practice with Professor Vanezis, Dr. Heath and Dr. Rouse’ and ‘remained there from 2004 to 2009’;

'20.        Your conduct as set out in paragraphs 17.a., 18.a. and 19.a. was:

a.            Misleading,

b.            Liable to bring the profession into disrepute;

'21.        Your conduct as set in paragraphs 17.b., 18.b. and 19.b. was:

a.            Dishonest,

b.            Liable to bring the profession into disrepute;

“And that in relation to the facts alleged your fitness to practise is impaired by reason of your,

i.              misconduct,

ii.             deficient professional performance.

The Panel will be Chaired by Ms Vickie Isaac,

LLB

PACA David Southall a failed JR and the documents contained within

"The early bird catches the worm"

I am a very good chess player, fact. I also have the benefit of having been bought up in the military, which means strategy is key when planning any campaign.

When I first found out that Davey and crew were trying to JR my position on the GMC working group, I put my pending resignation from said group on hold, in order to get my hands on the application before the court, because my experience has taught me that I am dealing with people who suffer from impulsive behaviours along with predictable patterns of behaviour. What that equates to is they always screw up and allow me access to documents that I would not otherwise be able to obtain. When the content of the JR landed, I was not disappointed.

So the below, which formed part of the defunct JR (there are some other gems in there) was yet another nugget to add to an armoury of evidence. Because of course you can just bombard the GMC and get an investigation under way ... Not and further still my complaint, which I can prove, went into the GMC on October 3rd 2009, long before any announcement of any working party at the GMC.

You don't have to be a rocket scientist to work out what PACA is really about and you don't have to be a rocket scientist to see that Risdon is a liar, lies to his colleagues, lies to the court, lies on his CV!

Click on image for full view.

So thank you PACA and Davey, for making my life so much easier by constantly and predictably following a course of action that shore up my claims. Top Tip David, when trying to anonymise a document, make sure you put a marker pen through the bit that says "The top forensic paediatric pathologist in the UK" and a Top Tip to Rupert, when writing about me in the BMJ, wouldn't it be prudent, if not necessary to declare a conflict of interest ... Oh sorry, that would require a degree of integrity and honesty!!!

And now the end is near .... as the song goes

Bring it on, because I dropped all my evidence in the laps of some very influential media people and they loved it, so much so that they, based on the EVIDENCE, not "vexatious complaints", have decided to not only blow this, but to do it in such a way as to make sure it can't happen again - There's going to be a little wait, but hey that's what you have to do to ensure that the T's are crossed and the i's dotted. Something the so called "experts" need to learn.

This time there is no rock to hide under, this time the public get to know what really goes on in our so called criminal justice system!

Michael Burridge unsafe conviction, along with many more Meadow is going to look like the tooth fairy by the time this is over.

On the subject of Burridge, 98 Centile for Rees's head, his brain so watery that it attracted comment from all the experts, uhhhhhhm, oooh let's see shall we, couldn't have been hydrocephalus could it????? You know, that condition that can cause the triad ............

Remember I only post some of the evidence .... the rest, well that's gone where I should have taken it months ago.

R-V-Burridge The myths vs the facts Rupert Risdon

29. We turn to the post mortem findings and to Professor Anthony Risdon who spent much of his career as a senior Paediatric Pathologist at Great Ormond Street, with a particular interest in sudden death in infants in their first year of life. Since his retirement from the NHS in 2004, he has practised as a forensic pathologist and, in that capacity, on 5 October 2006, conducted a post mortem examination on the body of Rees Burridge .


Yes well that's what the Judges believed and based their findings on .......

Time to turn it up now ... 

R-V-Burridge The myths vs the facts

Further, the combination of the recent subdural haemorrhage at different separate sites, together with hypoxic ischaemic brain injury, was (according to Dr Stoodley) most likely due to an episode of head trauma. As to timing, the acute blood could not date back to the time of Rees's delivery nor, given its appearance, was it likely to be related to his birth and he had, in any event, been delivered by caesarean section and so had not undergone the pressures of a vaginal delivery. The appearances meant that it was possible, although very unlikely, that the relevant event was severe accidental head trauma, but, again, there was no such history in Rees's case.

http://medicalmisdiagnosisresearch.wordpress.com/2010/03/28/intracranial-hemorrhage-from-normal-birth/

Although most of the asymptomatic SDHs seen at MR imaging and US were in neonates delivered vaginally, 18% (4 of 22) of our neonates delivered by cesareanbirth also had SDH. Most infants with SDH delivered by cesarean birth (75%) had a trial of labor with oxytocin administration before the cesarean delivery. Thissupports the proposal that SDH may be related to labor. Presumably, the neonate experienced labor during oxytocin administration before the decision for cesareandelivery.

CONCLUSION

SDH is a common result of parturition and may be seen after vaginal and cesarean delivery. MR imaging is more sensitive than US for the detection of SDH. The hemorrhages seen in asymptomatic term neonates are limited in size and location. SDH after 1 month of age is unlikely to be birth-related.