The Shaken Baby Syndrome Myth
renamed "Abusive Head Trauma" or "Non-Accidental Injury"



* SBS began as an unproven theory and medical opinions, now discredited by biomechanical engineering studies
* No DIFFERENTIAL DIAGNOSIS done to eliminate other causes, abuse assumed without evidence
* Shaken Baby diagnostic symptoms not caused by shaking
* Child protective agencies snatch children, destroy families based on medical accusations without proof of wrong-doing
*Poor or deceptive police investigations, falsified reports, perjured testimony threaten legal rights, due process
* Prosecutors seek "victory", over justice; defense attorneys guilty of ineffective counsel, ignorance, lack of effort
* Care-takers threatened, manipulated, in order to force plea bargains, false confessions
* A fractured criminal justice system--a big piece for the rich, a small piece for the poor, and none for alleged SBS cases.



Related websites/ important people and projects ShakenBabySyndrome/Vaccines/YurkoProject
"Shaken Baby Syndrome or Vaccine Induced Encephalitis-- Are Parents Being Falsely Accused?" by Dr Harold Buttram, with Christina England (WEBSITE)
Evidence Based Medicine and Social Investigation:
EBMSI conferences, resources and information Articles and Reports
VacTruth: Jeffry Aufderheide; The SBS conection and other dangerous or deadly side effects of vaccination true, suppressed history of the smallpox vaccine fraud and other books:
Patrick Jordan
Sue Luttner, must-read articles and information on Shaken Baby Syndrome: her resources link
The Amanda Truth Project: Amanda's mother speaks out at symposium
Tonya Sadowsky


Online book with search engine:
Scurvy-Past and Present
(produces symptoms that may be misdiagnosed as SBS/AHT or other conditions)

World Literature: SBS-related Articles

Infantile Scurvy

Möller-Barlow disease

Also known as:
Barlow's disease
Barlow’s syndrome
Cheadle-Möller-Barlow syndrome
Moeller's disease

Associated persons:
Sir Thomas Barlow
Walter Butler Cheadle
Julius Otto Ludwig Möller

A diseases of childhood caused by malnutrition with lack of vitamin C - ascorbic acid, and characterized by gingival lesions, haemorrhage, arthralgia, loss of appetite, listlessness, and other symptoms similar to those seen in adult scurvy. Ocular findings may include exophthalmos and conjunctival hemorrhage. Most common in bottle-fed children, rare in breast-feeding children. Usually occurs between 6 and 12 months of age. When associated with cutaneous ecchymoses and submucosal gingicval lesions, the condition simulates infantile scurvy. The course is similar to that of scurvy in adults.

The term Barlow's disease was introduced by Johann Otto Leonhardt Heubner (1843-1926); L. Conitzer named it Möller-Barlow disease.


* J. O. L. Moeller:
Über akute Rachitis.
Königsberger medicinische Jahrbücher, 1859, 1: 377-379.
Königsberger medicinische Jahrbücher, 1862, 3: 135.

* W. B. Cheadle:
Scurvy and purpura.
British Medical Journal, London, 1872, 2: 520-522.

Three cases of scurvy supervening on rickets in young children.
Lancet, London, 1878, 2: 685.
In this article Cheadle distinguished scurvy from rickets.

Infantile scurvy.
With Frederick John Poynton (1869-1943). London, 1909.

* T. Barlow:
On cases described as "acute rickets" which are probably a combination of scurvy and rickets, the scurvy being an essential, and the rickets a variable, element.
Medico-Chirurgical Transactions, London, 1883, 66: 159-220.

* O. Heubner:
Über skorbutartige Erkrankungen rachitischer Säuglinge (Barlowsche Krankheit).
Jahrbuch für Kinderheilkunde, Berlin NF, 1892, 35: 351.

* L. Conitzer:
Zwei Fälle von Moeller-Barlowscher Krankheit.
Münchener medizinische Wochenschrift, 1894, 11: 203.
Vitamin C and Eye Health
Book Series Nutrition and Health

Book Handbook of Nutrition and Ophthalmology
Publisher Humana Press
DOI 10.1007/978-1-59259-979-0
Copyright 2007
ISBN 978-1-58829-196-7 (Print) 978-1-59259-979-0 (Online)
DOI 10.1007/978-1-59259-979-0_9
Pages 371-390
Subject Collection Chemistry and Materials Science
SpringerLink Date Thursday, December 06, 2007

Richard D. Semba
9. Vitamin C and Eye Health
Vitamin C is a water-soluble vitamin that is essential for the biosynthesis of collagen, carnitine, and catecholamines. It serves as a strong antioxidant and protects proteins, lipids, and DNA from oxidative damage. The eye contains the highest concentrations of vitamin C found in the human body. Vitamin C is important to eye health because of its role in protecting the proteins of the crystalline lens from oxidation, in serving as a free radical scavenger in the retina, and in promoting wound healing in the cornea. Scurvy, the classic syndrome of vitamin C deficiency, includes some findings of ophthalmological importance, including vascular abnormalities of the conjunctiva, dry eyes, and hemorrhages of the conjunctiva, orbit, anterior chamber, and retina. Vitamin C may become increasingly important to ocular health with demographic changes such as increasing life span and a larger aging population, and with the continued depletion of the stratospheric ozone layer (1).

September/October 2007

Nutritional Deficiencies
As the number of bariatric procedures in the US rises, clinicians must be aware of the ocular manifestations of vitamin deficiencies and their treatment.
By Ginny Kullman, MD; Jeffrey L. Bennett, MD, PhD; Naresh Mandava, MD; and Malik Y. Kahook, MD

A recent study determined that the prevalence of vitamin C deficiency in the US is 14% among males and 10% among females.19 The deficiency occurs in severely malnourished individuals, drug and alcohol abusers, and those living in poverty. Scurvy results from low levels of ascorbic acid, largely due to impaired collagen synthesis, which depends on ascorbate. Symptoms can occur as early as 3 months after deficient intake. Ocular involvement is primarily due to hemorrhages caused by increased capillary fragility. Proptosis secondary to orbital hemorrhage occurs in 10% of cases of infantile scurvy but is rarely seen in adults.20 Petechiae or larger hemorrhages can occur in the conjunctiva, eyelids, orbit, anterior chamber, vitreous, and other ocular structures. Despite the high concentration of ascorbic acid in the crystalline lens, cataracts are not common. There are no known visual field defects that are classically associated with scurvy. Treatment entails the oral replacement of vitamin C with 100 mg four times a day for 10 to 14 days, followed by a maintenance dose of at least 60 mg per day until the recommended dietary allowance (approximately 120 mg per day, depending on the person's sex and age) is resumed.21

Volume 57, Issue 2, Pages 358-359 (August 2007)

Scurvy in children

Warren R. Heymann, MD

Dialogues in Dermatology, a monthly audio program from the American Academy of Dermatology, contains discussions between dermatologists on timely topics. Commentaries from Dialogues Editor-in-Chief Warren R. Heymann, MD, are provided after each discussion as a topic summary and are provided here as a special service to readers of the Journal of the American Academy of Dermatology.

Based on the dialogue “Nutritional deficiency” between Albert C. Yan, MD, and Jacqueline Junkins-Hopkins, MD

The statements and opinions expressed in this commentary are those of the Editor-in-Chief of Dialogues in Dermatology.

PII: S0190-9622(07)00542-7


© 2007 American Academy of Dermatology, Inc. Published by Elsevier Inc All rights reserved.

Journal of the American Academy of Dermatology : Scurvy in ...
Subperiosteal hemorrhage, a characteristic of infantile scurvy, ... Ocular problems include conjunctival and retinal hemorrhages and optic nerve atrophy. ...

Ocular manifestations of systemic disease.
Current Opinion in Ophthalmology. 10(6):429-430, December 1999.
Emmett T. Cunningham Jr, MD, PhD, MPH
Pediatrics International
Volume 46 Issue 6 Page 753-755, December 2004
Could Vitamin C deficiency have a role in shaken baby syndrome?
* Eva Lai-Wah Fung and
* Edmund Anthony Severn Nelson
*Department of Paediatrics, The Chinese University of Hong Kong, China
Correspondence: ELW Fung, MBChB, MRCP, Department of Paediatrics, The Chinese University of Hong Kong, 6/F, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong, China.
Email:  "If you investigate the last 25 years of Hepatitis B, the disease, you will find or put together a chapter on the promotion of fear about the disease in the male gay community of America. Leading to? Large numbers of gay men getting vaccinations against Hep B. Leading, in turn, to false positive HIV tests. Leading to the administration of killer, cell-destroying drugs."


Volume 24, Issue 14, 24 March 2006, Pages 2685–2691

Adverse events after hepatitis A B combination vaccine, "In May 2001, the U.S. Food and Drug Administration (FDA) approved Hepatitis A Inactivated and Hepatitis B Recombinant Vaccine (HEPAB) for immunization of adults. From May 2001 to September 2003, the Vaccine Adverse Event Reporting System (VAERS) received 305 reports of adverse events after HEPAB. Many events were similar to those reported after the monovalent hepatitis A and B vaccines. Non-serious events included constitutional symptoms and local reactions. Serious events included neurologic, hepatobiliary, and dermatologic conditions..." (Hep B)
Leading Experts Investigate Shaken Baby Syndrome
ScienceDaily (Apr. 10, 2008) — Shaken Baby Syndrome (SBS), also known as childhood neurotrauma or inflicted traumatic brain injury, is the leading cause of death from childhood maltreatment. Unlike many types of child abuse, the action that causes SBS is known, occurs quickly, and is, theoretically, largely preventable. An international symposium sponsored by the National Center on Shaken Baby Syndrome examined how to establish the incidence of inflicted traumatic brain injury in young children and explored issues of definitions, passive versus active surveillance, study designs, proxy measures, statistical issues and prevention. Key findings are published in a Special Supplement to the April 2008 issue of the American Journal of Preventive Medicine.

SBS is a form of intentional injury to infants and children caused by violent shaking with or without associated contact with a hard surface. The mortality rate of victims of this intentional brain injury is about 25%, while survivors do very poorly. In a recent Canadian study, investigators found that after 10 years only 7% of the survivors were reported as "normal," 12% were in a coma or vegetative state, 60% had a moderate or greater degree of disability and 85% would require ongoing multidisciplinary care for the rest of their lives.

Guest Editors Robert M. Reece, Desmond K. Runyan, and Ronald G. Barr and an international group of authors significantly contribute to the increasing visibility of violence against children in general and child maltreatment in particular. They state that although prevention has been a highly desired but elusive goal in the field of child abuse, the apparent potential for prevention of inflicted childhood neurotrauma in particular through universal educational initiatives, both in North America and potentially around the world, has contributed considerable urgency to the importance of addressing these challenges. The symposium participants who convened to address these measurement issues were very cognizant of these challenges.

Presentations addressed two main themes: (1) the adequacy of current and/or projected systems for measuring the incidence of shaken baby syndrome; and (2) a review of available strategies for evaluating the effectiveness of primary programs for its prevention in large jurisdictions.

Reece addressed the complex issue of nomenclature variants and how they might (or might not) be integrated. Runyan described the challenges and emerging evidence concerning rates of the caregiving risk behavior of shaking. Keenan, Minns and Trent described their experiences with active and passive surveillance systems. Bennett described the countrywide Canadian Pediatric Surveillance Program, and Ryan described the design and proposed use of the Department of Defense Birth and Infant Health Registry to measure inflicted childhood neurotrauma.

To assess strategies for evaluating the effectiveness of prevention programs in large jurisdictions, Rivara presented the strengths, weaknesses, and potential pitfalls of available designs applicable at a jurisdictional level, and Shapiro discussed whether case control designs used successfully in disease prevention research could be applied to SBS. Finally, Ellingson, Leventhal, and Weiss described comparative rates derived from retrospective passive surveillance data sets to those derived from prospective active surveillance studies, and Runyan, Berger and Barr provide an integrative proposal for the "ideal system" to measure inflicted neurotrauma incidence.

Writing in the supplement, Guest Editors Ronald G. Barr, University of British Columbia, Vancouver, and Child & Family Research Institute, and Desmond K. Runyan, The University of North Caroline, Chapel Hill, state, " is apparent that there is a 'bad news/good news' storyline emerging here. While the challenges to measuring inflicted injury are real and considerable, it is equally clear that considerable progress has been made and that reliable and valid measurement appears feasible and obtainable. Substantive work continues to be done toward providing reasonable measures that will be informative both about the nature and scope of inflicted neurotrauma in infants and about the possibility that prevention programs will be able to be demonstrated to be effective (or not) on the basis of empiric measurements. It is none too soon."

These articles appear in a Special Supplement to the American Journal of Preventive Medicine, Volume 34, Issue 4 (April 2008), Supplement 1, published by Elsevier.

The Symposium was supported by the Doris Duke Charitable Foundation of New York and the Centers for Disease Control and Prevention (CDC). The Supplement was supported by the Division of Violence Prevention, National Center for Injury Prevention and Control (NCIPC) at the CDC, Atlanta.
ScienceDaily (Jan. 8, 2008) — Each year in the United States, one thousand infants die after being shaken. An equal number of cases result in brain damage. Many people who are guilty of this type of abuse go free due to a lack of evidence; others are wrongly suspected of a crime that they did not commit. Researchers in forensic medicine at the University of Oslo are learning more about these brain injuries by shaking a very advanced doll.

Each year around the world, thousands of infants die after being vaccinated with dangerous vaccines. An equal number of cases result in brain damage. All doctors who are guilty of this type of medical abuse due to lack of information go free due to a lack of published evidence, while caretakers are suspected of a crime they did not commit. A small, courageous group of researchers in forensic and other fields of medicine risk their reputations and livelihoods trying to educate people more about these brain injuries by gathering and providing evidence about these injuries by proving that shaking alone can not cause the cascade of effects seen in babies claimed to have been the victims of shaking by caretakers.

“Cases involving the concealed killing of infants do come up. Still, it is extremely difficult to get a conviction in a court of law,” confirms post-doctoral researcher Arne Stray-Pedersen from the Institute of Forensic Medicine at the University of Oslo, Norway. He is one of Norway’s leading forensic experts in cases of possible child abuse. Now, he is focusing on the trauma that occurs when an infant is violently shaken.

Cases involving the concealed killing of these infants come up constantly. Still, it is extremely difficult to get a conviction based on the real crime. Instead, nearly all accused caretakers are convicted in a court of law without evidence of violence, and are based on the symptoms themselves because leading testifying so-called "forensic experts" have accepted long held theories based originally on junk science, assumption and speculation without questioning recent scientific evidence to the contrary by focusing on the conditions found in these infants without evidence that they have been "violently shaken" since no such incidents have ever been documented be any reliable source and linked to the symptoms directly.
Being shaken is enormously traumatic. The head moves so much that the brain can be destroyed. The same types of injuries occur during car accidents or when vehicles are put under hard breaking.
Of course, if a baby was indeed shaken violently, they might be enormous trauma, but injuries likened "being dropped from a 2-story-window" would also include severe trauma to the neck and spine at the same time, and would usually require an impact of equal force which would manifest in external signs almost never seen in so-called "Shaken Babies".

“The syndrome that occurs when a baby cries too much is called, “Be Quiet Now!”
Supposed experts in the vast and lucrative industry that has grown up around the "shaken baby" phenomena that has only surfaced in recent decades have subjectively created a new "syndrome" they refer to as "Be Quiet Now" since caretakers are imagined to violently shake babies in response to what is admitted as "inconsolable crying". Other experts have another explanation--that babies crying "inconsolably" are already in the throws of vaccine-induced encephalitis which produces a characteristic "inconsolable high-pitched cry" and suffering from a swelling brain and capilary fragility leading to subdural hematomas, brain hemorrhages, and bleeding in and behind the eyes, resulting in retinal and subconjunctival hemorrhages, which may soon lead to vomiting, unconsciousness, seizures and apnea incidents which they may or may not survive, at which point any normal caretaker may try to "shake" the baby awake or to see if there is any response before attempting infant CPR or calling 911 in absolute terror. Of course there may always be isolated cases in which this terrible crying pushes a desperate caretaker over the edge into a mindless act of abuse, but abused and battered babies have external signs of trauma and are easy to spot--although abnormal bruising and broken bones are also signs of capillary fragility and coagulation disorders brought on by infection or vaccine-induced vitamin C deficiencies and corresponding responses of increasing blood histamine levels.

One in three is so injured that he or she dies. “A third of the babies survive with serious complications such as physical paralysis, blindness, and serious mental handicaps.”
Statistically, one third of these babies die from their shots, and one third survive with serious complications such as physical paralysis, blindness and serious mental handicaps. The last third seem unharmed at first, but research indicates that these youngsters are overrepresented in the statistics for ADHD (Attention-Deficit Hperactivity Disorder). In fact, 25% of all school children have now been labled as "learning disabled" in some way. As a long time teacher, I've observed and worked with these children in classrooms for many years and know the nightmare of their existence first hand.

The last third seem unharmed at first, but research indicates that these youngsters are overrepresented in the statistics for ADHD (Attention-Deficit Hyperactivity Disorder).

In Norway every year, 15 babies are violently shaken by their parents. “Norway has fewer cases than other places in the world. In the U.S.A., there are one thousand deaths a year.”
According to sources in Norway, "15 babies are violently shaken by their parents every year." No one has ever produced a reliable witness, videocam or other solid evidence of this claim, but if the cascade of symptoms historically associated with "classical" SBS are seen, it is assumed so, make this argument completely circular, sounding something like this--"If the symptoms exist, therefore the violence must have taken place, since the symptoms themselves are proof." Nice logic, also indicating that Americans don't love their children as much as Norwegions do, suggesting some kind of national predilection for abuse in the US. Perhaps the real problem is the geographical location...or might it be a racial bias? Maybe it's something in the air? Could smog and road rage be driving American parents into baby-battering frenzies that Norwegion parents are spared? ...or do they just possess better Aryan genetic material? Hitler thought so.

Or could it be something else, say, related to the fact that Norway reports a drop in "pure" SIDS rates, however, at the same time there is a corresponding rise in supposedly "non-SIDS" and "borderline SIDS" cases (, making the infant death rate the same as before when added together. Could they be playing a "name game" by changing the diagnostic criteria to tweak the stats? Has that ever happened historically? You bet. After the polio vaccine went into mass production, the "powers-that-be" in their infinite wisdom slyly chose to eliminate all cases of "aseptic meningitis" from the polio numbers, which had previously been included, giving rise to a dramatic drop in numbers. However, adding the two groups together painted a very different picture. The same with the WHO smallpox eradictation campaign. They declared smallpox to have been wiped from the earch by their efforts while the 1986 edition of Encyclopedia Britannica admitted the vaccine was discontinued because the shot was found to be "more dangerous than the disease". But to continue the illusion of success, when further outbreaks in vaccinated individuals manifested, they were suddenly victims of MONKEYPOX. Same symptoms. Same disease. Different name. When vast profits and incomprehensible levels of liability threaten, reason flies out the window.

That means that an American baby is killed by shaking once every eight hours. In per capita terms, that is three times more than in Norway.

The Brain Swells Up

A baby’s head is proportionally larger than the head of an adult. The muscles in the neck are underdeveloped. When the upper body is pulled, the head follows after and begins a pendulum-like movement.

“The brain is floating in brain fluid. Nerve fibres lead from the brain down to the spine. With a hard enough jerk, the brain can move around and the nerve fibres can snap. Doctors call this Diffuse Axonal Injury (DAI).”

With a hard enough jerk to cause brain damage, the likelihood of damage to the neck and spinal structures are also probable. Diffuse Axonal Injury caused by shaking is a THEORY, which means it hasn't been proven definitively. There are other theories to explain what is seen in some of these cases which have credibility.

After the nerve fibres have snapped, the brain swells up. The infant then dies because blood circulation is cut off to the brain. Shaking can also lead to bleeding behind the eye and under the membrane around the brain.

When MRI (magnetic resonance imaging) and CAT (computerised axial tomography) scans are taken of an abused baby’s brain, nerve damage appears as small white dots.

It is also not uncommon for a shaken baby to have bruises around the temple and injuries on other parts of its body—most likely because the baby struck something during the abuse.

Parents often offer their own explanations for an infant’s injuries. They might say that the baby has fallen from its bath or that they have accidentally dropped the baby down a flight of stairs.

“If one were to believe the parent’s explanation for the injuries, it would have to be more dangerous to fall from the baby bath than from a height of three meters. Thus, we cannot take all of the parents’ explanations at face value,” Arne Stray-Pedersen points out.

Legally Difficult

Far from all cases are reported to and investigated by the police. Just a handful of cases are handled by the justice system.

“It is a problematic and difficult task. We unfortunately don’t have good enough measurements to differentiate between injuries due to abuse, accidents, and congenital defects. There are no witnesses when an abuser injures an innocent child, and we have neither video nor other evidence that can be used in court,” explains Arne Stray-Pedersen.

In the interest of improving forensic evidence, Stray-Pedersen has just acquired a technologically advanced doll. This doll will be used to learn more about the connection between shaking and damage in an infant’s brain.

The €19 000 doll is actually designed as an automobile crash test dummy. Although it is already filled with advanced instrumentation, researchers at SINTEF will put in extra equipment so that forensic researchers can measure the stress on the brain from shaking or from the head striking a hard surface or object.

Shaking causes a baby’s head to accelerate quickly. The doll’s head accelerates in three directions.

Under acceleration, the stress on an infant’s head can be compared to the worst stress experienced by the pilot of a fighter jet. While shaking can equal ten times the force of gravity (10 G), a fighter pilot can only stand a force of 9 G for a short time before passing out. In an automobile collision at 70 kilometres per hour, the brain is subjected to the force of only a few G.

American Disagreement

Not everyone is in agreement about the connection between shaking and brain damage.

In 2005, the American researcher Faris A. Bandak published an article about shaking babies in the journal Forensic Science International. He believes that the head of a baby would fall off before the first bleeding occurred. Today, Bandak is the most called witness in American shaken baby cases, in spite of the many dissenting articles published by other American researchers.

Norwegian defence attorneys also cite his research.

“As expert witnesses, we must relate to Bandak as a scientist even if we believe that his conclusions are incorrect. The only way to attack his testimony is to show his errors. From reconstruction and educated guesses, we hope that we can now develop a model with satisfactory data from the laboratory. Abuse cases must not be allowed to fail due to lack of forensic evidence. We hope that our research can increase the likelihood of more correct judgements and fewer dismissals, “ says Arne Stray-Pedersen in an interview with the University of Oslo’s research magazine Apollon.

“Aggressive Parents”

To investigate injuries caused by shaking and blunt force trauma, ten people will be chosen to play “aggressive parents.” When the doll is shaken, researchers will be able to measure what happens when a baby is violently shaken and then compare those injuries with falls from various heights.

Arne Stray-Pedersen works with— among others— the Oslo police department, senior researcher Frode Risland of SINTEF, Professor Per Holck at the University of Oslo’s Department of Anatomy, and Professor Torleiv Ole Rognum, who led the forensic team in the Norwegian identification group in Thailand after the Tsunami disaster in December of 2004.

Following the drop in SIDS rate in Norway after 1989, the share of pure SIDS in proportion to the total population of sudden unexpected deaths in infancy and early childhood has decreased. The increasing proportion of non-SIDS and borderline SIDS cases presents a challenge to improve the quality of the investigation in cases of sudden death in infancy and early childhood.

Gardner HB. Immunizations, retinal and subdural hemorrhages: are
they related? 2005;64:663-664.Med Hypothesis

Gardner has observed that the age of onset of the diagnosis of
so-called “shaken baby syndrome” is significantly later in Japan
(peaking at 7 to 9 months) than in the United States (peaking at 2 to
4 months). Is this because Japanese infants are abused at a later age
than American infants, or is there another explanation? Gardner
noted that these ages correspond to the standard ages when
vaccinations have been given in the tw ocountries,respectively.

15. Yawata, Makoto (1994), “Japan’s troubles with measles-mumps-rubella vaccine”, Lancet 343:105-106, 8 January 1994.

6. Iwasa, A., Ishida, S., Akama, K. (1985), “Swelling of the brain caused by pertussis vaccine: its quantitative determination and the responsible factors in the vaccine”, Japan J. Med. Sci. Biol. 38:53-65.

Endotoxins in commercial vaccines. Applied and Environmental Microbiology 36:445-449. Gilmartin RC, Chien LT. 1977.
Endotoxins and disease mechanisms. Annual Review of Medicine 38:417-432. Munoz JJ. 1985.

Page 148 DPT shots. Injection of DT into children aged 2 to 5 years (a control group) did not increase the dermal response to histamine, but this population was not age-matched to that given DPT. It is not clear that these findings have any relationship to the occurrence of anaphylaxis after injection of DPT. A 45-year-old male volunteer who was hyperimmunized with pertussis vaccine (eight shots of 2.4 NIH [National Institutes of Health] protective units each) to produce anti-pertussis immune globulin died of progressive renal failure secondary to a chronic diffuse vasculitis (Bishop et al., 1966). No etiology was proven for the vasculitis, but the case raises the possibility that an Arthus-type reaction was initiated by an antigen in the vaccine. The extraordinary hyperimmunization makes it impossible to extrapolate to possible responses to standard immunization practices. Evidence from Studies in Animals Pertussis vaccine is said to act as an adjuvant in the formation of skinsensitizing, IgE-like antibody in mice and rats (Clausen et al., 1970; Munoz and Bergman, 1977). At least two substances in the DPT vaccine, PT protein and endotoxin, are believed to have the potential for such an adjuvant effect (Munoz and Bergman, 1977; Tada et al., 1972). Injection of B. pertussis vaccine has been shown to facilitate the induction of anaphylactic shock in the rat and mouse but not in the hamster, guinea pig, rabbit, or dog (Arora et al., 1970; Chang and Gottshall, 1974; Csaba and Muszbek, 1972; Munoz et al., 1987). Injection of pertussis vaccine (0.1 ml/mouse, roughly 200 times the human dose) increased the susceptibility of mice to the lethal effects of various bacterial endotoxins injected subsequently (Kind, 1958). The increased endotoxin sensitivity was not present 1 or 3 days after administration of pertussis vaccine but was pronounced after 5 to 20 days. Steinman and colleagues (1982) have developed a mouse model in which they can regularly induce a lethal shock-like syndrome by injection of 3 x 1010 heat-killed B. pertussis into mice sensitized by repeated injections of 1 mg of bovine serum albumin. Only mouse strains with certain histocompatibility (H-2) genotypes are susceptible, which is compatible with an immunologic basis for the reaction. PT is required for induction of this toxicity (Steinman et al., 1985), and immunization with PT antigens protects the mice against the reaction (Oksenberg et al., 1989). Pretreatment of the mice with histamine H1 receptor antagonists also protected the mice; this result is compatible with an allergic-immunologic basis for the reaction, but it does not prove such, since other actions of the antagonists are possible (Peroutka et al., 1987). Relatively large doses of pertussis vaccine and sensitizing antigen are used in this model compared with injections given to

Page 149 humans; a particular immunizing schedule and certain mouse strains are required. Thus, the relevance of this reaction to that in infants is speculative. Munoz and colleagues (1987) and Wiedmeier and colleagues (1987) have described data suggesting that this reaction represents anaphylaxis and not encephalopathy, as some had hypothesized. The development of the reaction was unrelated to the capacity of PT to act as a toxin through its characteristic activity of ribosylation of key cellular proteins (Wiedmeier et al., 1987). Endotoxin Commercial DPT vaccines across the world have been reported to contain bacterial endotoxin, usually in concentrations of about l to 10 µg/ml (Geier et al., 1978; Ibsen et al., 1988). There was a direct correlation between endotoxin content and the percentage of DPT vaccine recipients who developed fever (Baraff et al., 1989), and it has been questioned whether the endotoxin in DPT vaccine might be responsible, at least in part, for immunologic reactions or encephalopathy. Animal studies have been cited in support of this hypothesis, for example, those showing that endotoxin or DPT vaccine can induce an increase in the permeability of cerebral blood vessels, which might predispose an individual to brain damage (Amiel, 1976; Bergman et al., 1978; Eckman et al., 1958). However, the use of animals to explore this hypothesis is complicated by the fact that different species respond differently to different endotoxins. Moreover, endotoxins from different bacteria cannot be compared on the basis of weight since weight does not accurately reflect biologic activity (Chaby et al., 1979). In short, data do not exist at present to indicate that the endotoxin present in DPT vaccines plays a role in the anaphylaxis associated with injection of DPT. Nor do data exist to support a role for endotoxin in the other immunologic reactions or in the encephalopathies that have been suspected sequelae of DPT immunization. Summary The body of evidence concerning the possible relation between vaccination with DPT or its pertussis component and anaphylaxis includes a number of case reports, case series, studies in animals, and one controlled epidemiologic study. Anaphylaxis is rare in infants in the absence of an obvious exciting cause. Rates of anaphylaxis estimated from two reports (Osvath et al., 1979; Pollock and Morris, 1983) have been approximately 2 per 100,000 injections. The clinical presentation of cases with rapid onset after injection of vaccine and (in two cases) autopsy findings suggest that anaphylaxis can be caused by DPT injection.

Toxicology notes on some vaccine ingredients:

2-phenoloxyethanol contains phenol which has the ability to inhibit phagocyte activity, meaning it is toxic to all cells. It can disable the immune system's primary response mechanism. It can cause systemic poisoning, headache, shock, weakness, convulsions, kidney damage, cardiac or kidney failure, death.

The ethylene oxide component is an irritant causing dermatitis, burns, blisters, eczema. Animal studies have demonstrated that it can cause cancer in female mice. In 1978, the EPA issued "a rebuttal presumption against registration of ethylene oxide for pesticide applications...on the basis of mutagenicity and testicular effects." Editor's note: But they can inject it into infants and babies! [The quote is from: Marshall Sittig, Handbook of Toxic and Hazardous Chemicals and Carcinogens, 2nd Ed. (Park Ridge, NJ: Noyes Publications, 1985): 433f.]

hemorrhage, retinal

Retinal hemorrhage means bleeding onto the surface of the retina (visual receptor of the eye) caused by rupture of the tiny blood vessels that lie on the surface of the retina. Retinal hemorrhage indicates increased pressure within the skull. This may result from head trauma and bleeding, whether accidental or intentional (child abuse). It was once believed to be pathognomonic of so-called shaken baby syndrome, but this is no longer thought to be true by the forensic pathology community.

"Specially or decisively characteristic of a disease; indicating with certainty a disease; as, a pathognomonic symptom." (Webster, 1913)

Simply put, a finding is "pathognomonic" if it is so distinctive it makes the diagnosis obvious taken by itself. One might say, for example, that the classic rash of fifth disease is pathognomonic.

Encyclopedia Index -> S -> shaken baby syndrome | Search
shaken baby syndrome

Shaken baby syndrome is a term that has been applied to cases in which brain hemorrhage (subdural hematoma) and bleeding within the eyes (retinal hemorrhages) have been found in suspected cases of child abuse. The mechanism of these injuries was believed to be violent shaking of the child's shoulders so that the head whipped back and forth with enough force to cause tearing of blood vessels between the brain and its covering (dura mater); subsequent bleeding in the space between the dura and the brain causes increased pressure within the skull, which in turn caused bleeding from the tiny blood vessels that lie on the surface of the retina. The finding of retinal hemorrhages alone has led to charges of child abuse based on suspected shaken baby syndrome.

This concept has been called into question by forensic pathologists, many of whom question whether the syndrome as originally formulated actually exists. They base this conclusion on several points. They believe that pure shaking alone cannot generate sufficient force to cause the observed injuries without also damaging the cervical spinal cord, but cervical cord injuries are not found at autopsy. They also report finding evidence of blunt trauma to the head (fine skull fractures missed with plain x-rays or CT scans) in many if not all such suspected cases, trauma that would cause both the subdural hematomas and the retinal hemorrhages. That is, the child was abused, but shaking alone did not cause the retinal hemorrhages. Next, there are other explanations for retinal hemorrhages, including resuscitation efforts. And finally, retinal hemorrhages reported to be present by the examinations of pediatricians and even ophthalmologists are actually only present about half the time at autopsy.

So "shaken baby syndrome" may not be a real entity as formerly thought. This does not mean at all that children are not abused by beatings, and does not mean that retinal hemorrhages are not found in such cases. It does call into question the concept of basing prosecution of suspected child abuse solely on a finding of retinal hemorrhages.

Munch Med Wochenschr. 1968 Mar 1;110(9):535-40.Links
[Still existing infantile scurvy. Case report on Möller-Barlow's disease]
[Article in German]

Scherzer E. Arch Fr Pediatr. 1982 Aug-Sep;39(7):453-4.Links
[Iconographic rubric: infantile scurvy]
[Article in French]

Bachy A, Hendrickx E, Vandercam J, Gérard P, Dochain J.

Pediatr Radiol. 1976 Aug 20;4(4):251-3.Links
Neonatal scurvy: report of a case.
Hirsch M, Mogle P, Barkli Y.

An Esp Pediatr. 1991 Mar;34(3):243-6.Links
[Radiologic diagnosis of Möller-Barlow disease (scurvy). Apropos of a case]
[Article in Spanish]

Burches Greus E, Lecuona López C, Ardit Lucas J, Aguilar Bacallado F, García Vicent C, Tomás Ratés C, Alvarez Angel V, Donderis Folgado P.

Servicio de Pediatría, Hospital General Universitario de Valencia.

Ryoikibetsu Shokogun Shirizu. 1998;(21 Pt 2):405-7.Links
[Scurvy, Möller-Barlow disease]
[Article in Japanese]

Mase K.
Department of Internal Medicine, Sanyo Hospital.

East Mediterr Health J. 2001 Nov;7(6):1070-2.Links
Perifollicular purpura must not be forgotten in scurvy: case reports.
Shamsaddini S, Shakibi MR, Atapoor J.

Kerman University of Medical Sciences Kerman Darman Hospital, Kerman, Islamic Republic of Iran.

Ann Dermatol Venereol. 2000 May;127(5):510-2.
[Scurvy presenting with ecchymotic purpura and hemorrhagic ulcers of the lower limbs]
[Article in French]

Boulinguez S, Bouyssou-Gauthier M, De Vençay P, Bedane C, Bonnetblanc J.

Service de Dermatologie, CHU Dupuytren, 87042 Limoges Cedex.

INTRODUCTION: The risk of vitamin C deficiency is underestimated in industrialized countries and is only disclosed in rare cases of severe scurvy. CASE REPORT: We report three cases of scurvy presenting with ecchymotic purpura and hemorrhagic ulcerations of the lower limbs. Vitamin C supplementation led to rapid improvement of the skin lesions. DISCUSSION: Clinical diagnosis of low-grade deficiency can be difficult. Biological diagnosis requires special care in sample taking and transport.

Turk J Pediatr. 1998 Apr-Jun;40(2):249-53.Links
Scurvy. A case report.
Yilmaz S, Karademir S, Ertan U, Kuyucu S, Hallioglu O, Ocal B, Mavis N.

Department of Pediatrics, Dr. Sami Ulus Children's Hospital, Ankara, Turkey.

An 18-month-old girl presented with irritability, epistaxis, spongy appearance of the gums perifollicular papules with follicular hyperkeratosis, ecchymosis, painful swollen knees and scorbutic rosary. Her diet consisted mainly of wheat flour. X-ray of the knees showed findings compatible with scurvy. Ascorbic acid level was below 0.003 g/L. Ascorbic acid therapy resulted in a dramatic clinical improvement. Scurvy is an uncommon disease in our society today. It is important to recognize the signs and symptoms of scurvy because it is easily treated with vitamin C replacement.

Int J Dermatol. 2007 Feb;46(2):194-8.
Scurvy in a 10-month-old boy.
Larralde M, Santos Muñoz A, Boggio P, Di Gruccio V, Weis I, Schygiel A.
Pediatric Dermatology Division and Pediatric Department, Ramos Mejía Hospital, Buenos Aires, Argentina.

We report a 10-month-old boy with inflammatory and necrotic gingival lesions, fever, irritability, and pseudoparalysis of the legs. Laboratory examinations revealed moderate anemia and skeletal X-rays showed osteopenia, scorbutic rosary at the costochondral junctions, and "corner sign" on the proximal metaphyses of the femora. The boy had been fed only with diluted cow's milk. He had never taken solid food, vitamin C, or iron complement. Seventy-two hours after starting oral vitamin C supplementation, there was significant improvement in the patient's gingival lesions and general health. The clinical presentation and laboratory and imaging findings, together with the dramatic response to ascorbic acid intake, allowed us to confirm the diagnosis of infantile scurvy. Scurvy, a dietary disease due to the deficient intake of vitamin C, is uncommon in the pediatric population. In an infant who has never received vitamin C, the combination of gingival lesions, pseudoparalysis, and irritability strongly suggests a diagnosis of scurvy. The clinical picture, together with the laboratory data, radiological studies, and therapeutic response to vitamin C administration, confirmed the diagnosis.

Pediatrics. 2001 Apr;107(4):E46.

Comment in:
Pediatrics. 2001 Apr;107(4):E45.

Severe nutritional deficiencies in toddlers resulting from health food milk alternatives.
Carvalho NF, Kenney RD, Carrington PH, Hall DE.

Scottish Rite Pediatric and Adolescent Consultants, Childrens Healthcare of Atlanta, Atlanta, Georgia 30342-1600, USA.

It is widely appreciated that health food beverages are not appropriate for infants. Because of continued growth, children beyond infancy remain susceptible to nutritional disorders. We report on 2 cases of severe nutritional deficiency caused by consumption of health food beverages. In both cases, the parents were well-educated, appeared conscientious, and their children received regular medical care. Diagnoses were delayed by a low index of suspicion. In addition, nutritional deficiencies are uncommon in the United States and as a result, US physicians may be unfamiliar with their clinical features. Case 1, a 22-month-old male child, was admitted with severe kwashiorkor. He was breastfed until 13 months of age. Because of a history of chronic eczema and perceived milk intolerance, he was started on a rice beverage after weaning. On average, he consumed 1.5 L of this drink daily. Intake of solid foods was very poor. As this rice beverage, which was fallaciously referred to as rice milk, is extremely low in protein content, the resulting daily protein intake of 0.3 g/kg/day was only 25% of the recommended dietary allowance. In contrast, caloric intake was 72% of the recommended energy intake, so the dietary protein to energy ratio was very low. A photograph of the patient after admission illustrates the typical features of kwashiorkor: generalized edema, hyperpigmented and hypopigmented skin lesions, abdominal distention, irritability, and thin, sparse hair. Because of fluid retention, the weight was on the 10th percentile and he had a rotund sugar baby appearance. Laboratory evaluation was remarkable for a serum albumin of 1.0 g/dL (10 g/L), urea nitrogen <0.5 mg/dL (<0.2 mmol/L), and a normocytic anemia with marked anisocytosis. Evaluation for other causes of hypoalbuminemia was negative. Therapy for kwashiorkor was instituted, including gradual refeeding, initially via a nasogastric tube because of severe anorexia. Supplements of potassium, phosphorus, multivitamins, zinc, and folic acid were provided. The patient responded dramatically to refeeding with a rising serum albumin and total resolution of the edema within 3 weeks. At follow-up 1 year later he continued to do well on a regular diet supplemented with a milk-based pediatric nutritional supplement. The mortality of kwashiorkor remains high, because of complications such as infection (kwashiorkor impairs cellular immune defenses) and electrolyte imbalances with ongoing diarrhea. Children in industrialized countries have developed kwashiorkor resulting from the use of a nondairy creamer as a milk alternative, but we were unable to find previous reports of kwashiorkor caused by a health food milk alternative. We suspect that cases have been overlooked. Case 2, a 17-month-old black male, was diagnosed with rickets. He was full-term at birth and was breastfed until 10 months of age, when he was weaned to a soy health food beverage, which was not fortified with vitamin D or calcium. Intake of solid foods was good, but included no animal products. Total daily caloric intake was 114% of the recommended dietary allowance. Dietary vitamin D intake was essentially absent because of the lack of vitamin D-fortified milk. The patient lived in a sunny, warm climate, but because of parental career demands, he had limited sun exposure. His dark complexion further reduced ultraviolet light-induced endogenous skin synthesis of vitamin D. The patient grew and developed normally until after his 9-month check-up, when he had an almost complete growth arrest of both height and weight. The parents reported regression in gross motor milestones. On admission the patient was unable to crawl or roll over. He could maintain a sitting position precariously when so placed. Conversely, his language, fine motor-adaptive, and personal-social skills were well-preserved. Generalized hypotonia, weakness, and decreased muscle bulk were present. Clinical features of rickets present on examination included: frontal bossing, an obvious rachitic rosary (photographed), genu varus, flaring of the wrists, and lumbar kyphoscoliosis. The serum alkaline phosphatase was markedly elevated (1879 U/L), phosphorus was low (1.7 mg/dL), and calcium was low normal (8.9 mg/dL). The 25-hydroxy-vitamin D level was low (7.7 pg/mL) and the parathyroid hormone level was markedly elevated (114 pg/mL). The published radiographs are diagnostic of advanced rickets, showing diffuse osteopenia, frayed metaphyses, widened epiphyseal plates, and a pathologic fracture of the ulna. The patient was treated with ergocalciferol and calcium supplements. The published growth chart demonstrates the dramatic response to therapy. Gross motor milestones were fully regained within 6 months. The prominent neuromuscular manifestations shown by this patient serve as a reminder that rickets should be considered in the differential diagnosis of motor delay. (ABSTRACT TRUNCATED)

Am J Clin Dermatol. 2007;8(2):103-6.Links
Infantile scurvy: an old diagnosis revisited with a modern dietary twist.
Burk CJ, Molodow R.

Pediatric Dermatology, University of Miami, Miami, Florida 33125, USA.

Ascorbic acid (vitamin C) is necessary for the formation of collagen, reducing free radicals, and aiding in iron absorption. Scurvy, a disease of dietary ascorbic acid deficiency, is uncommon today. Indeed, implementation of dietary recommendations largely eradicated infantile scurvy in the US in the early 1900s. We present a case of an otherwise healthy 2-year-old Caucasian girl who presented with refusal to walk secondary to pain in her lower extremities, generalized irritability, sleep disturbance, and malaise. The girl's parents described feeding the patient an organic diet recommended by the Church of Scientology that included a boiled mixture of organic whole milk, barley, and corn syrup devoid of fruits and vegetables. Physical examination revealed pale, bloated skin with edematous, violaceous gums and loosening of a few of her teeth. Dermatologic findings included xerosis, multiple scattered ecchymoses of the extremities, and perifollicular hemorrhage. Laboratory and radiographic evaluation confirmed the diagnosis of scurvy. The patient showed dramatic improvement after only 3 days of treatment with oral ascorbic acid and significant dietary modification. In this case report, we revisit the old diagnosis of scurvy with a modern dietary twist secondary to religious practices. This case highlights the importance of taking a detailed dietary history when evaluating diseases involving the skin.

Rev Clin Esp. 1996 Aug;196(8):570.Links
[Vitamin C deficiency and hemorrhagic syndrome]
[Article in Spanish]

Rodríguez Cuartero A.

Pediatrics. 2001 Sep;108(3):E55.
An orange a day keeps the doctor away: scurvy in the year 2000.
Weinstein M, Babyn P, Zlotkin S.

Department of Paediatrics, Hospital for Sick Children and University of Toronto, Toronto, Canada.

Scurvy has been known since ancient times, but the discovery of the link between the dietary deficiency of ascorbic acid and scurvy has dramatically reduced its incidence over the past half-century. Sporadic reports of scurvy still occur, primarily in elderly, isolated individuals with alcoholism. The incidence of scurvy in the pediatric population is very uncommon, and it is usually seen in children with severely restricted diets attributable to psychiatric or developmental problems. The condition is characterized by perifollicular petechiae and bruising, gingival inflammation and bleeding, and, in children, bone disease. We describe a case of scurvy in a 9-year-old developmentally delayed girl who had a diet markedly deficient in vitamin C resulting from extremely limited food preferences. She presented with debilitating bone pain, inflammatory gingival disease, perifollicular hyperkeratosis, and purpura. Severe hypertension without another apparent secondary cause was also present, which has been previously undescribed. The signs of scurvy and hypertension resolved after treatment with vitamin C. The diagnosis of scurvy is made on clinical and radiographic grounds, and may be supported by finding reduced levels of vitamin C in serum or buffy-coat leukocytes. The response to vitamin C is dramatic. Clinicians should be aware of this potentially fatal but easily curable condition that is still occasionally encountered among children.

Radiologic diagnosis of Moller-Barlow disease (scurvy). Apropos of a case]
An Esp Pediatr. 1991 Mar;34(3):243-6. Spanish. No abstract available.

Scherzer E.
[Still existing infantile scurvy. Case report on Moller-Barlow's disease]
Munch Med Wochenschr. 1968 Mar 1;110(9):535-40. German. No abstract available.

Kleiner HJ.
No Abstract [Clinical aspects of scurvy]
Dtsch Gesundheitsw. 1971 Nov 4;26(45):2133-5. German. No abstract available.

Wechsler B, Gatfosse M, Cabane J, Mouthon JM, Godeau P.

Abstract [A case of purpura, or the return to natural diseases]
Sem Hop. 1984 Jan 12;60(1):21-4. French.

Chaudhry SI, Newell EL, Lewis RR, Black MM.

No Abstract Scurvy: a forgotten disease.
Clin Exp Dermatol. 2005 Nov;30(6):735-6. No abstract available.

Gabay C, Voskuyl AE, Cadiot G, Mignon M, Kahn MF.

Abstract A case of scurvy presenting with cutaneous and articular signs.
Clin Rheumatol. 1993 Jun;12(2):278-80.

Heymann WR.
Abstract Scurvy in children.
J Am Acad Dermatol. 2007 Aug;57(2):358-9. Review.
Salvi A, Coppini A, Lazzaroni G, Manganoni A.
Abstract A case of vascular purpura with scurvy.
Recenti Prog Med. 1992 Nov;83(11):652-3.

Kasa RM.
Abstract Vitamin C: from scurvy to the common cold.
Am J Med Technol. 1983 Jan;49(1):23-6. Review.

Nienhuis AW.
No Abstract Vitamin C and iron.
N Engl J Med. 1981 Jan 15;304(3):170-1. No abstract available.

Vairo G, Salustri A, Trambaiolo P, D'Amore F.
Abstract Scurvy mimicking systemic vasculitis.
Minerva Med. 2002 Apr;93(2):145-50. English, Italian.

Touyz LZ.
Abstract Vitamin C, oral scurvy and periodontal disease.
S Afr Med J. 1984 May 26;65(21):838-42. Review.

Khonsari H, Grandiere-Perez L, Caumes E.
Abstract [Scurvy, a re-emerging disease]
Rev Med Interne. 2005 Nov;26(11):885-90. Review. French.

Weinstein M, Babyn P, Zlotkin S.
Free Full Text An orange a day keeps the doctor away: scurvy in the year 2000.
Pediatrics. 2001 Sep;108(3):E55.

Gomez-Carrasco JA, Lopez-Herce Cid J, Bernabe de Frutos C, Ripalda-Crespo MJ, Garcia de Frias JE.
No Abstract Scurvy in adolescence.
J Pediatr Gastroenterol Nutr. 1994 Jul;19(1):118-20. No abstract available.

Monks G, Juracek L, Weigand D, Magro C, Cornelison R, Crowson AN.
No Abstract A case of scurvy in an autistic boy.
J Drugs Dermatol. 2002 Jul;1(1):67-9. No abstract available.
Pediatria (Napoli). 1983 Jun-Sep;91(2-3):251-60.Links
[Clinico-radiologic studies of a case of scurvy in an infant]
[Article in Italian]

Tolone C, Santinelli R, Salvi V, Toraldo R, Di Lena C, D'Avanzo M.
Zhonghua Fang She Xue Za Zhi. 1987 Apr;21(2):69-74.
[X-ray manifestations of scurvy and its pathological basis (report of 70 cases)]
[Article in Chinese]

Wang YZ.
Am J Dis Child. 1979 Mar;133(3):323-4.
Radiological case of the month. Scurvy: almost historic, but not quite.
Young LW, Schiliro G, Russo A.

Brickley M, Ives R.
Abstract Skeletal manifestations of infantile scurvy.
Am J Phys Anthropol. 2006 Feb;129(2):163-72.

Ramar S, Sivaramakrishnan V, Manoharan K.
Related Articles, Links
Abstract Scurvy--a forgotten disease.
Arch Phys Med Rehabil. 1993 Jan;74(1):92-5.

De DC, Bhattacharyya AK.
Related Articles, Links
No Abstract Scurvy: report of a case with atypical radiological features.
Indian J Pediatr. 1968 Jan;35(240):34-5. No abstract available.

Monatsschr Kinderheilkd. 1984 Apr;132(4):240-1.
[Infantile scurvy]
[Article in German]

von Mühlendahl KE.

Infantile scurvy, today a rare disease, can be diagnosed either by recognition of a characteristic constellation of clinical features, or on the correct interpretation of nearly pathognomonic radiological signs. Dystrophy, recurrent infections, fever, anemia, hemorrhagic effusions, hematuria, tenderness of the legs, pseudo-paralysis and "frog position" and costochondral swelling or angulation are frequent signs. Radiologically, thickening of the epiphyseal plate ("scurvy line") and subepiphyseal rarefication , general osteoporosis and subperiostal hemorrhage are important diagnostic clues.

Arch Pediatr Adolesc Med. 2001 May;155(5):607-8.Click here to read Links
Special feature: picture of the month. Infantile scurvy.
Riepe FG, Eichmann D, Oppermann HC, Schmitt HJ, Tunnessen WW Jr.

Department of Pediatrics, Christian Albrechts University Kiel, Germany.

Med J Aust. 1970 Jan 24;1(4):187.Links
Scurvy amongst central Australian Aboriginal children.
Kirke DK, Vorbach EA, Newman DM.

Pediatr Ann. 1983 Dec;12(12):894-903.Links
The battered child syndrome: pitfalls in radiological diagnosis.
Radkowski MA.

An Esp Pediatr. 1991 Mar;34(3):243-6.Links
[Radiologic diagnosis of Möller-Barlow disease (scurvy). Apropos of a case]
[Article in Spanish]

Burches Greus E, Lecuona López C, Ardit Lucas J, Aguilar Bacallado F, García Vicent C, Tomás Ratés C, Alvarez Angel Donderis Folgado P.

Servicio de Pediatría, Hospital General Universitario de Valencia. Z Arztl Fortbild (Jena). 1966 Nov 15;60(21):1221-3.Links
[Möller-Barlow disease in twins. A contribution to infantile scurvy]
[Article in German]

Hagedorn C.

Int Z Vitaminforsch Beih. 1957;27(3):265-74.Links
[Möller-Barlow's disease, scurvy (vitamin C deficiency) in infants.]
[Article in German]


: Pediatr Int. 2002 Feb;44(1):37-42.Click here to read Links

Comment in:
Pediatr Int. 2003 Apr;45(2):220.
Pediatr Int. 2003 Dec;45(6):758.

Unexplained subdural hematoma in young children: is it always child abuse?
Fung EL, Sung RY, Nelson EA, Poon WS.

Department of Paediatrics, Faculty of Medicine, 6/F Clinical Science Building, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong.

BACKGROUND: In the published reports of the developed society, subdural hematoma and/or retinal hemorrhages, in the absence of documented history of major trauma, should be considered diagnostic of child abuse. Many people used the above criteria for diagnosis, but subsequently found that retinal hemorrhages were more common in non-accidental injuries (NAI). To what extent is the proposed pathognomonic association between unexplained subdural hematoma/retinal hemorrhages and child abuse a self-fulfilling prophecy? METHODS: Clinical details of nine children under 2 years with unexplained subdural hematoma admitted to Prince of Wales Hospital between 1995 and 1998 were reviewed. RESULTS: Four had no other physical signs of injury, five had retinal hemorrhages and one had multiple bruises over the body. Following multidisciplinary case conferences for seven children, a diagnosis of NAI was concluded in four cases, but in no case could the abuser be definitely identified. Clinical outcome was poor with seven children showing either profound disability (n = 5) or evidence of developmental delay (n = 2). CONCLUSION: In this series, NAI were not established in three of the seven cases. Did we underdiagnose child abuse in these cases? Despite a magnitude of opinion to the contrary, the issue of whether "trivial" head injury can cause subdural hemorrhages and/or retinal hemorrhages is yet unresolved. Clearly much more information on this very sensitive and serious issue is required and these data should be collected with an open mind.
Thromb Diath Haemorrh Suppl. 1968;30:145-5.Links

[Vitamin C deficiency--scurvy and Moeller-Barlow's disease]
[Article in German]

Winckelmann G.

: Eur J Pediatr. 2004 Jul;163(7):420-1. Epub 2004 Apr 9.Click here to read Links
An infant with methylmalonic aciduria and homocystinuria (cblC) presenting with retinal haemorrhages and subdural haematoma mimicking non-accidental injury.
Francis PJ, Calver DM, Barnfield P, Turner C, Dalton RN, Champion MP.

Eye Department, Guys Hospital, London, UK.

J R Soc Med. 2000 Nov;93(11):591-2.Click here to read Click here to read Links
Hermansky-Pudlak syndrome presenting with subdural haematoma and retinal haemorrhages in infancy.
Russell-Eggitt IM, Thompson DA, Khair K, Liesner R, Hann IM.

Department of Ophthalmology, Great Ormond Street Hospital for Children, Great Ormond Street, London WC1N 3JH, UK.

Clin Pediatr (Phila). 1966 Apr;5(4):230-7.Links
A "pseudo" battered child.
Berant M, Jacobs J.
: Thromb Diath Haemorrh Suppl. 1968;30:145-5.Links
[Vitamin C deficiency--scurvy and Moeller-Barlow's disease]
[Article in German]

Winckelmann G.

Thromb Diath Haemorrh Suppl. 1968;30:145-5.Links
[Vitamin C deficiency--scurvy and Moeller-Barlow's disease]
[Article in German]

Winckelmann G.

PMID: 4269136 [PubMed - indexed for MEDLINE]

1: Dtsch Zahnarztl Z. 1968 Dec;23(12):1422-4.Links
[On cases of infantile scurvy (Moeller-Barlow's disease) and of scorbutoid diseases (mixed forms) in infants]
[Article in German]

Spier JP. Br Med J (Clin Res Ed). 1983 Dec 17;287(6408):1862-3.Click here to read Links
Infantile scurvy: the centenary of Barlow's disease.
Evans PR.

Personal Name as Subject:
Barlow T

Med Arts Sci. 1967 Jan-Apr;21(1):9-22.Links
The incidence of infantile scurvy. A problem of yesteryear and today.
Vyhmeister IB.

Spier JP.
No Abstract [On cases of infantile scurvy (Moeller-Barlow's disease) and of scorbutoid diseases (mixed forms) in infants]
Dtsch Zahnarztl Z. 1968 Dec;23(12):1422-4. German. No abstract available.

No Abstract [Moeller-Barlow's disease, infantile scurvy; review with 2 case reports.]
Ugeskr Laeger. 1954 Aug 23;116(34):1223-8. Danish. No abstract available.

Meinecke R, Bannert N, Schmerse G.
No Abstract [Moeller-Barlow's disease. Clinical picture and surgical treatment of extremly dislocated femoral epiphyses]
Z Orthop Ihre Grenzgeb. 1970 Sep;108(2):286-93. German. No abstract available.

Evans PR.
Free in PMC Infantile scurvy: the centenary of Barlow's disease.
Br Med J (Clin Res Ed). 1983 Dec 17;287(6408):1862-3. No abstract available.

Falconer DT.
No Abstract Scurvy presenting with oral symptoms. A case report.
Br Dent J. 1979 May 15;146(10):313-4. No abstract available.

Scherzer E.
No Abstract [Still existing infantile scurvy. Case report on Moller-Barlow's disease]
Munch Med Wochenschr. 1968 Mar 1;110(9):535-40. German. No abstract available.

No Abstract [Infantile scurvy, Barlow's disease.]
Pol Przegl Radiol. 1956 Jul-Aug;20(4):217-22. Polish. No abstract available.

Clemetson CA.
Abstract Barlow's disease.
Med Hypotheses. 2002 Jul;59(1):52-6.

No Abstract [Moller-Barlow's disease, scurvy (vitamin C deficiency) in infants.]
Int Z Vitaminforsch Beih. 1957;27(3):265-74. German. No abstract available.

Winckelmann G.
No Abstract [Vitamin C deficiency--scurvy and Moeller-Barlow's disease]
Thromb Diath Haemorrh Suppl. 1968;30:145-5. German. No abstract available.

Blancher G.
No Abstract [Treatment of infantile scurvy or Barlow's disease]
Cah Coll Med Hop Paris. 1968 Feb;9(2):188-94. French. No abstract available.

Schimke E, Seidel H, Grunbaum EG, Bornert D.
No Abstract [Clinical, laboratory diagnostic, electrophonocardiographic, and roentgenologic studies with consideration of the ACTH test in Moller-Barlow's disease and acropachy of the dog. I. Moller-Barlow's disease]
Wien Tierarztl Monatsschr. 1967 Oct;54(10):650-63. German. No abstract available.

Related Articles, Links
Chir Organi Mov. 1964;53:112-59. Italian. No abstract available.
PMID: 14214242 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract [Severe scurvy (Moeller-Barlow disease) associated with a bone disorder.]
Istanbul Tip Fak Mecmuasi. 1959;22:186-208. Turkish. No abstract available.
PMID: 13839814 [PubMed - indexed for MEDLINE]
Rowland RW.
Related Articles, Links
Abstract Necrotizing ulcerative gingivitis.
Ann Periodontol. 1999 Dec;4(1):65-73; discussion 78. Review.
PMID: 10863376 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract [Barlow's disease in Bogota.]
Rev Colomb Pediatr Pueric. 1950 Apr;9(4):120-9. Undetermined Language. No abstract available.
PMID: 15430734 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract [Case of Barlow's disease with epiphyseal detachment.]
Arch Fr Pediatr. 1950;7(6):588-90. Undetermined Language. No abstract available.
PMID: 14790839 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract [Barlow's disease.]
Dia Med. 1954 Jun 24;26(42):1110-3. Spanish. No abstract available.
PMID: 13191224 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract Acute gingivitis and dermatitis of scorbutic origin.
Oral Surg Oral Med Oral Pathol. 1963 Feb;16:236-45. No abstract available.
PMID: 13972954 [PubMed - indexed for MEDLINE]
Schmidt LJ, Davis CC.
Related Articles, Links
No Abstract Acute necrotizing ulcerative gingivitis: clinical features, etiology and treatment.
Dent Hyg (Chic). 1984 Jan;58(1):20-4. No abstract available.
PMID: 6585327 [PubMed - indexed for MEDLINE]

1: Pol Przegl Radiol. 1956 Jul-Aug;20(4):217-22.Links
[Infantile scurvy, Barlow's disease.]
[Article in Polish]


PMID: 13388806 [PubMed - indexed for MEDLINE]

: Cah Coll Med Hop Paris. 1968 Feb;9(2):188-94.Links
[Treatment of infantile scurvy or Barlow's disease]
[Article in French]

Blancher G.

PMID: 5745278 [PubMed - indexed for MEDLINE]

1: Pediatr Radiol. 1976 Feb 13;4(2):122-3.Links
Epiphyseo-metaphyseal cupping following infantile scurvy.
Sprogue PL.

A five year old girl presented with short femora, cupped distal metaphyses and flexion deformity of the knees suggesting previous epiphyseo-metaphyseal damage. The aetiology was suggested by finding a history of previous infantile scurvy with separated distal femoral epiphyses. The rarity of this complication and possible contributing factors are discussed.

PMID: 967570 [PubMed - indexed for MEDLINE]

1: Indian Pediatr. 1999 Oct;36(10):1067.Links
Scurvy persists in the current era.
Paul DK, Lahiri M, Garai TB, Chatterjee MK.

PMID: 10745326 [PubMed - indexed for MEDLINE]

1: Pol Przegl Radiol. 1956 Jul-Aug;20(4):217-22.Links
[Infantile scurvy, Barlow's disease.]
[Article in Polish]


PMID: 13388806 [PubMed - indexed for MEDLINE]


Mase K.
Related Articles, Links
No Abstract [Scurvy, Moller-Barlow disease]
Ryoikibetsu Shokogun Shirizu. 1998;(21 Pt 2):405-7. Review. Japanese. No abstract available.
PMID: 9833527 [PubMed - indexed for MEDLINE]
Burches Greus E, Lecuona Lopez C, Ardit Lucas J, Aguilar Bacallado F, Garcia Vicent C, Tomas Rates C, Alvarez Angel V, Donderis Folgado P.
Related Articles, Links
No Abstract [Radiologic diagnosis of Moller-Barlow disease (scurvy). Apropos of a case]
An Esp Pediatr. 1991 Mar;34(3):243-6. Spanish. No abstract available.
PMID: 2064156 [PubMed - indexed for MEDLINE]
Stolyhwo-Suchanek A, Sloma-Walejko B, Zawistowska E.
Related Articles, Links
No Abstract [Moller-Barlow disease and Jaksch-Hayem anemia in 2 infants from twin pregnancies]
Pediatr Pol. 1968 Nov;43(11):1399-402. Polish. No abstract available.
PMID: 5710791 [PubMed - indexed for MEDLINE]
Hagedorn C.
Related Articles, Links
No Abstract [Moller-Barlow disease in twins. A contribution to infantile scurvy]
Z Arztl Fortbild (Jena). 1966 Nov 15;60(21):1221-3. German. No abstract available.
PMID: 5990877 [PubMed - indexed for MEDLINE]
Brunelli G, Mariotti A.
Related Articles, Links
No Abstract [Contribution to the knowledge of Moller-Barlow disease]
Clin Pediatr (Bologna). 1966 Feb;48(2):65-72. Italian. No abstract available.
PMID: 5955612 [PubMed - indexed for MEDLINE]
Related Articles, Links
No Abstract [Case of Moller-Barlow disease.]
Orv Hetil. 1953 Nov 22;94(47):1311-2. Undetermined Language. No abstract available.
PMID: 13133445 [PubMed - indexed for MEDLINE]

1: Am J Phys Anthropol. 2006 Feb;129(2):163-72.
Skeletal manifestations of infantile scurvy.
Brickley M, Ives R.

Institute of Archaeology and Antiquity, School of Historical Studies, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

Recent investigations of human skeletal material from the historic St. Martin's cemetery, England, found a range of abnormal lesions in six infants that are almost certainly related to scurvy. Porous and proliferative bone lesions affecting the cranial bones and scapulae were found, and this paper presents images obtained using both macroscopic and scanning electron microscope examination of the lesions. Previous work on infantile scurvy (Ortner et al., 1997-2001) relied heavily on changes at the sphenoid, which is often missing in archaeological bone, so the identification of changes attributable to scurvy on other cranial bones and the scapulae is encouraging. The ability to recognize changes related to scurvy on a range of bones will ensure an enhanced potential for recognition of this disease in future research involving archaeological bone. Research on historical documents from Birmingham dating to the eighteenth and nineteenth centuries, combined with the probable cases of scurvy identified, supports the view that the paucity of cases of infantile scurvy from the archaeological record reflects a lack of understanding and recognition of bone manifestations, rather than a lack of occurrence in this period. Changes linked to scurvy were only found in infants from the poorer sections of the community from St. Martin's, and this is almost certainly linked to patterns of food consumption and may be related to shortages of potatoes, due to blight, experienced during this period.

PMID: 16323179 [PubMed - indexed for MEDLINE]

1: Istanbul Tip Fak Mecmuasi. 1959;22:186-208. Related Articles, Links

[Severe scurvy (Moeller-Barlow disease) associated with a bone disorder.]

[Article in Turkish]

TUMAY SB. (photos)

Vol. 155 No. 5, May 2001 TABLE OF CONTENTS
• Online Features

Special Feature

Picture of the Month

Felix G. Riepe, MD; Dirk Eichmann, MD; Hans C. Oppermann, MD; Heniz J. Schmitt, MD; Walter W. Tunnessen, Jr, MD
From the Departments of Pediatrics (Drs Riepe, Eichmann, and Schmitt) and Diagnostic Radiology (Dr Opperman), Faculty of Medicine, Christian Albrechts University Kiel, Kiel, Germany; and the American Board of Pediatrics, Chapel Hill, NC (Dr Tunnessen).

Arch Pediatr Adolesc Med. 2001;155:607-608.

A 15-MONTH-OLD boy had a history of unexplained bleeding from his gums for several weeks and fever for 2 days. He had been fed only cow's milk and oatmeal since age 4 months. On physical examination he had almost no spontaneous movement. His legs were held in a "frog leg" position (Figure 1), were swollen along the long bones, and were tender to palpation. His skin was dry and pale. Hemorrhages of the gingiva were obvious as were 2 blood-filled cysts of the lower canine teeth (Figure 2). The tympanic membranes were hyperemic, and evidence of middle-ear fluid was present. Palpable prominence of the costochondral junctions of the chest wall was noted.

Figure 1.

Figure 2.

The results of laboratory examinations revealed a normal white blood cell count, a hemoglobin level of 76 g/L, and a platelet count of 334 x 109/L. The serum calcium, phosphorous, copper, and alkaline phosphatase levels were normal. Thyroid stimulating hormone, triiodothyronine, and thyroxine levels were also normal. The serum level of vitamin D was normal, but vitamin C levels were low, 28 µmol/L (reference range, 45-108 µmol/L). Chest x-ray film showed a scorbutic rosary at the costochondral junctions with a "corner" sign noted in the proximal metaphysis of the humerus. Lower extremity radiographs demonstrated abnormalities (Figure 3).

Figure 3.

Denouement and Discussion: Infantile Scurvy

Figure 1. The infant initiated little spontaneous movement and held his legs slightly flexed and abducted.

Figure 2. The gingiva are spongy and bleeding with blood-filled cysts in both lower canine teeth.

Figure 3. A radiograph of the right lower extremity demonstrates osteoporosis with a "corner" sign at the distal femur and rings of ossification around the proximal tibia epiphysis and distal femoral epiphysis.

Infantile scurvy (Moeller-Barlow disease) is rarely reported in developed countries except in association with global malnutrition.1, 2, 3 The rarity of occurrence is responsible for the frequent delayed recognition of this disorder. A deficiency of vitamin C (ascorbic acid) is responsible for the manifestations of scurvy. Vitamin C is a cofactor for numerous enzymes that are critical to several body functions. The most common manifestations of scurvy are due to the decreased production and increased fragility of collagen, a result of faulty hydroxylation of proline and lysine in forming a precise triple-helical collagen structure.4, 5 Vitamin C also plays a number of roles in hematopoiesis, including the promotion of iron absorption and as a cofactor for the conversion of folic acid to folinic acid. Humans cannot synthesize vitamin C and must rely on intestinal absorption from ingested nutrients.


Most cases of scurvy are seen between ages 6 and 24 months. Neonatal scurvy is rare, except in infants of mothers with extreme hypovitaminosis C.6, 7 Breast milk contains sufficient amounts of vitamin C unless the mother's diet is deficient in this vitamin.8 The first clinical manifestations of scurvy are often associated with acute febrile illnesses that seem to increase the need for vitamin C.

Initial manifestations of scurvy are vague and include irritability, decreased appetite, and delayed development. As effects of vitamin C deficiency progress, affected children lie still with little movement because of generalized tenderness, most apparent in bones as a result of subperiosteal hemorrhages. Swelling may be noted along the shafts of long bones. Pseudoparalysis may be apparent as a result of the bone pain. Infants often hold their legs in a "frog leg" position and dislike being handled, often refusing to walk.

Gingival hemorrhages may occur along with spongy, hemorrhagic swellings of the mucous membranes overlaying teeth. Petechial hemorrhages may occur in the skin spontaneously or, more commonly, below the site of tourniquet application, the Rumpel-Leede sign, as a manifestation of capillary fragility. Swelling may be palpated along the costochondral junctions of the rib cage, resembling the rosary seen in rickets.


Changes in the long bones, particularly around the knee, are most diagnostic of scurvy. The earliest finding is generalized demineralization with a ground-glass appearance to the bones. The cortex is thinned. A white line, so-called Fränkel sign, is apparent at the ends of metaphyses, representing widening of the provisional zones of calcification and its increased density. The epiphyseal centers show central rarefaction and are also surrounded by a white line of calcification, referred to as the Wimberger ring or halo-ossification center. Transverse bands of diminished density adjacent to the Fränkel sign are known as scurvy lines. Lateral metaphyseal spurs (corner sign) between the provisional zone of calcification and the cortex are the result of metaphyseal infarctions. The corner sign is more pathognomonic of scurvy than the other bony findings. Irregular calcification and widening of the costochondral junctions results in the scorbutic rosary. Periosteal hemorrhages cannot be detected on radiography in scurvy until they become calcified during healing.


Bleeding manifestations and bone pain may suggest acute leukemia. Bone pain and refusal to walk may lead to consideration of osteomyelitis, septic arthritis, and rheumatic disorders.

The diagnosis of scurvy is based on a combination of clinical and radiographic findings. A dietary history compatible with insufficient intake of vitamin C should be present. Accurate laboratory measurement of vitamin C levels is difficult because of the instability of vitamin C.

Healing occurs rapidly with the oral administration of 100 to 200 mg/d of vitamin C. As healing occurs, the intake of vitamin C may be reduced to 50 mg/d until complete clinical and radiologic resolution has taken place.9


Accepted for publication January 14, 2000.

Reprints: Felix G. Riepe, MD, Klinikum der Christian-Albrechts Universitit, Klinik far Allgemeine Pädiatrie, Schwanenweg 20, 24105 Kiel, Germany.


1. Yilmaz S, Karademir S, Ertan U, et al. Scurvy: a case report. Turk J Pediatr. 1998;40:249-253. ISI | PUBMED
2. Najera-Martinez P, Rodriquez-Collado A, Gorian-Maldonado E. Scurvy: a study of 13 cases. Bol Med Hosp Infant Mex. 1992;49:280-285. PUBMED
3. Young LW, Schiliro G, Russo A. Radiological case of the month: scurvy: almost historic, but not quite. AJDC. 1979;133:323-324.
4. Gershoff SN. Vitamin C (ascorbic acid): new roles, new requirements? Nutr Rev. 1993;51:313-326. ISI | PUBMED
5. Halliwell B. Ascorbic acid: hype, hoax, or healer [editorial]? Am J Clin Nutr. 1997;65:1891-1892. FREE FULL TEXT
6. Clow CL, Laberge C, Scriver CR. Neonatal hypertyrosinemia and evidence for deficiency of ascorbic acid in arctic and subarctic peoples. CMAJ. 1975;113:624-626. ABSTRACT
7. Gómez DB, Warmann S, Scholl S, Glüer S. Neonatal scurvy [in German]. Monatsschr Kinderheilkd. 1999;147:570-572. FULL TEXT
8. Macy IG. Composition of human colostrum and milk. AJDC. 1949;78:589-594.
9. Moran JR, Greene HL. The B vitamins and vitamin C in human nutrition. AJDC. 1979;133:308-314.



Vitamin C Deficiency and Depletion in the United States: The Third National Health and Nutrition Examination Survey, 1988 to 1994
Hampl et al.
Am. J. Public Health 2004;94:870-875.

Radiological case of the month: scurvy: almost historic, but not quite.

Ryoikibetsu Shokogun Shirizu. 1998;(21 Pt 2):405-7.Links
[Scurvy, Möller-Barlow disease]
[Article in Japanese]

Mase K.

Department of Internal Medicine, Sanyo Hospital.

Skeletal Radiol. 1987;16(1):67-9.Links
Case report 406: Scurvy.
Boeve WJ, Martijn A.

Scurvy Signs

In 1914, Alfred Hess, a pediatrician practicing at the Hebrew Asylum in New York, observed an increase in scurvy among the infants at the asylum. This increase in scurvy coincided with the introduction of pasteurized milk and exclusion of orange juice from the infants’ diet. Modifying the infants’ diet, with the provision of raw milk or orange juice or potatoes, Hess reversed the scurvy and effected a cure. Hess had demonstrated that pasteurization results in the loss of vitamin C. He recommended the provision of fresh fruit or vegetable juice for the prevention of scurvy in infants fed on heated formulas. This practice of supplementing the diet of infants receiving heated formulas with fresh fruit or vegetable juices eventually led to the eradication of infantile scurvy in the United States.

The human body lacks the ability to synthesize and make vitamin C and therefore depends on exogenous dietary sources to meet vitamin C needs. Consumption of fruits and vegetables or diets fortified with vitamin C are essential to avoid ascorbic acid deficiency. Even though scurvy is uncommon, it still occurs and can affect adults and children who have chronic dietary vitamin C deficiency.
Pathophysiology: Scurvy is caused by a prolonged deficiency of vitamin C intake that results in defective collagen synthesis, tissue repair, and synthesis of lipids and proteins. It functions both as a reducing agent and as an antioxidant and is required for many physiologic functions, including metabolism of iron and folic acid, resistance to infection, and integrity of blood vessels.

The clinical manifestations of scurvy are primarily due to abnormal collagen synthesis resulting from a lack of vitamin C. Vitamin C is a cofactor required for the function of several hydroxylases. The absence of vitamin C reduces the function of prolyl hydroxylase, which is required to form hydroxyproline, an amino acid found in collagen but rarely found in other proteins. The presence of hydroxyproline in collagen stabilizes the collagen triple-helix structure by forming interstrand hydrogen bonds. Collagen lacking hydroxyproline is more fragile and contributes to the clinical manifestations of scurvy, including purpura due to vessel wall fragility. In addition, osteoid matrix formation is defective and bone resorption is increased in persons with vitamin C deficiency.


* Symptoms of scurvy develop after 3 months of severe or total vitamin C deficiency.

* Patients may complain of weakness, fatigue, shortness of breath, and aching limbs. Left untreated scurvy progresses, with potentially fatal complications, including cerebral hemorrhage or hemopericardium.

* Infantile scurvy is uncommon before age 7 months, and clinical and radiographic manifestations rarely occur in infants younger than 3 months. Early clinical manifestations consist of pallor, irritability, and poor weight gain.

* In advanced infantile scurvy, the major clinical manifestation is extreme pain and tenderness of the arms and, particularly, the legs. The baby is miserable and tends to remain in a characteristic immobilized posture from subperiosteal pain, with semiflexion of the hips and the knees, as described by Thomas Barlow in 1884. The body is both wasted and edematous, and petechiae and ecchymoses are commonly present.


* Symptoms and signs of scurvy may be remembered by the 4 Hs: hemorrhage, hyperkeratosis, hypochondriasis, and hematologic abnormalities. Patients may be miserable, irritable, depressed, resentful, and full of aches and pains. The body is both wasted and edematous, and petechiae and ecchymoses are commonly present.

* The earliest signs are found on the skin, often on the shins, after 3 months of severe or total vitamin C deprivation. Perifollicular hyperkeratotic papules are surrounded by hemorrhagic halos. The central hairs are twisted like corkscrews, and they may become fragmented. The posterior parts of the legs develop purpura that may coalesce.

* Soft, spongy swelling of the gums and gingival interdental papillae is followed by gingival hemorrhage, which is accentuated by coexistent poor oral hygiene and periodontal disease. Disrupted tooth formation and loosening of teeth may result in permanent defects of dentition.

* Ocular features include those of Sjögren's syndrome, subconjunctival hemorrhage, and bleeding within the optic nerve sheath. Funduscopic changes include cotton wool spots and flame-shaped hemorrhages.

* Bleeding into the joints causes exquisitely painful hemarthroses. Subperiosteal hemorrhage may be palpable, especially along the distal portions of the femurs and the proximal parts of the tibias of infants. In advanced cases, clinically detectable beading may be present at the costochondral junctions of the ribs. This finding is known as the scorbutic rosary (Costochondral beading). Bleeding into the femoral sheaths may cause femoral neuropathies, and bleeding into the muscles of the arms and the legs may cause woody edema.

* Heart complications include cardiac enlargement, ECG changes (reversible ST-segment and T-wave changes), hemopericardium, and sudden death.

* Anemia develops in 75% of patients, resulting from blood loss into tissue, coexistent dietary deficiencies (folate deficiency), altered absorption and metabolism of iron and folate, gastrointestinal blood loss, and intravascular hemolysis. The anemia is most often characterized as normochromic and normocytic. Vitamin C enhances iron absorption by reducing dietary iron from the ferric form to the ferrous form. Thus, vitamin C deficiency may reduce the availability of intracellular iron. Vitamin C is also necessary to convert folic acid to its active metabolite, folinic acid.

* Other problems include increased redness and swelling in recently healed wounds and the failure of new wounds to heal.


* Scurvy is caused by a prolonged deficiency of vitamin C intake.

* Most animals can convert gluconate into ascorbate. Primates, including humans, and guinea pigs as well as a few other species cannot convert gluconate into ascorbate and, therefore, require exogenous ascorbic acid, otherwise known as vitamin C. Humans obtain 90% of their intake of vitamin C from fruits and vegetables, and cooking these sources decreases vitamin C content 20-40%. The US Food and Drug Administration recommends a daily dietary allowance of vitamin C of 75 mg for women and 90 mg for men.

* The total body pool of vitamin C is approximately 1500 mg. The absorbed vitamin is found ubiquitously in body tissues, with the highest concentrations in glandular tissue and the lowest concentrations in muscle and stored fat. Ascorbic acid is metabolized in the liver by oxidation and sulfation. The renal threshold for excretion by the kidney in urine is approximately 1.4 mg/100 mL plasma. Excess amounts of ascorbic acid are excreted unchanged or as metabolites. When body tissue or plasma concentrations of vitamin C are low, excretion of the vitamin is decreased. Scurvy occurs after vitamin C has been eliminated from the diet for at least 3 months and when the body pool falls below 350 mg.

* Initial symptoms are nonspecific and include the following:

o Loss of appetite

o Peevishness

o Poor weight gain

o Diarrhea

o Tachypnea

o Fever

* Specific symptoms include the following:

o Irritability

o Pain and tenderness of the legs

o Pseudoparalysis

o Swelling over the long bones

o Hemorrhage


* The infant is apprehensive, anxious, and progressively irritable. Upon handling and changing of diapers, severe tenderness over the thighs is present. The excruciating pain results in pseudoparalysis. The infant assumes the frog leg posture (ie, keeping hips and knees slightly flexed and externally rotated) for comfort.

* Hemorrhages of the gums usually involve the tissue around the upper incisors. The gums have a bluish-purple hue and feel spongy. Gum hemorrhage occurs only if teeth have erupted.

* Subperiosteal hemorrhage is a typical finding of infantile scurvy. The lower ends of the femur and tibia are the most frequently involved sites. The subperiosteal hemorrhage is often palpable and tender in the acute phase.

* Petechial hemorrhage of the skin and mucous membranes can occur. Rarely, hematuria, hematochezia, and melena are noted.

* Proptosis of the eyeball secondary to orbital hemorrhage is a sign of scurvy.

* Costochondral beading or scorbutic rosary is a common finding. The scorbutic rosary is distinguished from rickety rosary (which is knobby and nodular) by being more angular and having a step-off at the costochondral junction. The sternum is typically depressed.

* Low-grade fever, anemia, and poor wound healing are signs of scurvy.

* Hyperkeratosis, corkscrew hair, and sicca syndrome are typically observed in adult scurvy but rarely occur in infantile scurvy.

4.6 Scurvy, clinical aspects

A pronounced lack of vitamin C results in a clinical disease known as scurvy. Haemorrhagic problems and bone abnormalities are the most characteristic and recognizable features of this disease. When a diet is chronically deficient in vitamin C (less than 10 mg/day) the first signs may be expected to appear after 3 to 6 months (half life of vitamin C is about 18 days). This explain why scurvy only appeared on board ships during long sea voyages. The patient first complains of general debility of slow onset, irritability, weight loss and vague muscular and joint pain. Sometimes the first symptom is stiffness in the calves, due to local haemorrhages. Because of the pain in the legs, children may present with pseudoparalysis. In many cases they spontaneously adopt an antalgic posture, with endorotation and bent knees and hips. This is usually seen in babies born prematurely when they reach about 6-12 months of age if they have been fed deficient artificial food. Splinter haemorrhages beneath the fingernails may occur, as in endocarditis. Haemorrhages around the eyes, ears, neck and on the roof of the mouth may occur. are very suggestive of scurvy. Spontaneous bleeding may occur anywhere in the body, including bleeding leading to palpable subperiosteal haemorrhages. Hyperkeratotic hair follicles and perifollicular petechiae (scorbutic purpura) are quasi pathognomonic. Old scars break open. New wounds do not heal or heal poorly. The gums become swollen, purple and spongy and bleed easily. Often there will be secondary infection. In advanced scurvy, teeth fall out spontaneously. Endochondral bone development ceases because osteoblasts no longer produce osteoid. A fibrous area is formed between diaphysis and epiphysis. The costochondral junctions enlarge. This is clinically palpable as a scorbutic rosary (not to be confused with rachitic rosary). Other symptoms include femoral neuropathy and oedema of the legs. Microcytic hypochromic anaemia may develop, which only improves after administration of vitamin C. If other deficiencies are simultaneously present (e.g. folic acid), the anaemia may be macrocytic.

4.8 Scurvy, diagnosis

The vitamin C content in peripheral blood can be measured in specialized laboratories. A level of less than 11 µmol/litre is diagnostic for scurvy. Measurement in leukocytes is more precise. The urinary excretion after administration of a test dose of vitamin C can also be measured. A capillary fragility test will be positive. When this is measured using the sphygmomanometer, it is called the Hess capillary test. The regular haemostasis parameters (platelets, coagulation times) are normal. On X-rays of the legs, a ‘ground-glass’ appearance of the epiphysis is often described.
verview :

Scurvy is the term for clinical deficiency of vitamin C (ascorbic acid). Although encountered less often today than in the past, it still occurs and mild cases may go unrecognized.

Patients at risk for vitamin C deficiency:

(1) infants

(2) adults > 55 years of age, especially males

(3) refugees or displaced persons

(4) malnutrition

(5) heavy cigarette smokers

(6) abnormal diets devoid of vegetables and vitamins

Clinical features of scurvy - bleeding tendency:

(1) petechiae

(2) purpura

(3) ecchymoses

(4) subperiosteal hemorrhage

(5) bleeding gums

(6) intracranial hemorrhage, which may be fatal

(7) conjunctival hemorrhages

Clinical features of scurvy - oral:

(1) gingival swelling and gingivitis

(2) loose or missing teeth

(3) scurvy buds on the gingiva

Clinical features of scurvy - skeletal changes in children:

(1) bowing of long bones in the lower extremities

(2) scorbutic rosary (depression of sternum with projection of the ends of the ribs)

(3) tender or aching limbs

Clinical features of scurvy - other:

(1) anemia

(2) hyperkeratosis

(3) abnormal wound healing

(4) poor localization of bacterial infections

(5) fatigue or weakness

The diagnosis of scurvy involves both of the following:

(1) the presence of clinical features in a person with a risk factor for vitamin C deficiency

(2) low blood levels of vitamin C, or clinical response to ascorbic acid replacement


Cotran RS, Kumar V, et al (editors). Robbins Pathologic Basis of Disease, 5th Edition. WB Saunders Company. 1994. pages 423-425.

Sauberlich HE. Laboratory Tests for the Assessment of Nutritional Status, Second Edition. CRC Press. 1999. pages 12-13.

Pediatrics International
Vol. 46 Issue 6 Page 753 December 2004
Could Vitamin C deficiency have a role in shaken baby syndrome?
Eva Lai-Wah Fung, Edmund Anthony Severn Nelson
Department of Paediatrics, The Chinese University of Hong Kong, China

Correspondence: ELW Fung, MBChB, MRCP, Department of Paediatrics, The Chinese University of Hong Kong, 6/F, Clinical Sciences Building, Prince of Wales Hospital, Shatin, Hong Kong, China. Email:;jsessionid=G4ZTvgT9HBWv1h2LQL2BLrggVmxpT25pqjZKqCYJ3f1rkm7qR2Ts!-170133123!181195628!8091!-1

Scurvy in a 10-month-old boy.

Case report
International Journal of Dermatology. 46(2):194-198, February 2007.
Larralde, Margarita PhD, MD; Munoz, Andrea Santos MD; Boggio, Paula MD; Di Gruccio, Vanesa MD; Weis, Isaac MD; Schygiel, Adolfo MD

We report a 10-month-old boy with inflammatory and necrotic gingival lesions, fever, irritability, and pseudoparalysis of the legs. Laboratory examinations revealed moderate anemia and skeletal X-rays showed osteopenia, scorbutic rosary at the costochondral junctions, and "corner sign" on the proximal metaphyses of the femora. The boy had been fed only with diluted cow's milk. He had never taken solid food, vitamin C, or iron complement. Seventy-two hours after starting oral vitamin C supplementation, there was significant improvement in the patient's gingival lesions and general health. The clinical presentation and laboratory and imaging findings, together with the dramatic response to ascorbic acid intake, allowed us to confirm the diagnosis of infantile scurvy.

Scurvy, a dietary disease due to the deficient intake of vitamin C, is uncommon in the pediatric population. In an infant who has never received vitamin C, the combination of gingival lesions, pseudoparalysis, and irritability strongly suggests a diagnosis of scurvy. The clinical picture, together with the laboratory data, radiological studies, and therapeutic response to vitamin C administration, confirmed the diagnosis.

Copyright (C) 2007 Blackwell Publishing Ltd.


Shaken Babies

by Archie Kalokerinos, MD
RMB 218ZA Bournes Lane
Tamworth, NSW, 2340, Australia
Ph. 011 61 2 67608166
Fax. 015 61 2 67608344

Shaken Baby Syndrome was originally defined to include
1. Fractures
2. Bruising
3. Haemorrhages
a) Intracranial
b) Retinal
c) Elsewhere
4. Other injuries not explained by a clear and witnessed (by so-called ‘reliable witnesses’) history of accidental injury. That is; what is regarded as ‘nonaccidental injury’ (NAI).

It was later defined by intracranial and/or retinal haemorrhages alone.
Then it was claimed that gentle shaking alone could initiate the problem.

Later still, the definition was extended to include some cases of the ‘Sudden Infant Death Syndrome’. Reasons for this included the idea that shaking a baby could upset the brain stem and result in cessation of breathing. Support for this was generated by the fact that, sometimes in the brain stem ‘diffuse axonal injury’ is found, and cervical spinal ‘injuries’, such as haemorrhages, are sometimes found during autopsies. Note that diffuse axonal injury does not necessarily mean that an inflicted injury is always the cause. The term is misleading because cerebral anoxia can result in similar pathology – and this, obviously, is not always precipitated by inflicted injuries.

When so-called ‘diffuse axonal injury’ was added to the list of ‘baddies,’ paediatricians and forensic scientists became totally overcome by what they saw as the ultimate crime - someone loosing control, grasping an infant firmly around the chest, and shaking it violently for several seconds. Animated videos were produced to demonstrate how the brain moved inside the skull and ‘tore’ the axons apart. Animal experiments were performed and the results appeared to support the shaking hypothesis. The matter was therefore declared closed. Those who were accused appeared to have no defence. In America several individuals are on death row.

But, like so many other aspects of medicine, it was not simple. There are reasons to believe that shaking is not always the cause of the pathologies found. That is: there are explanations that do not involve inflicted trauma.
A true ‘whodunit’ detective story

The search began some years ago when I was asked to investigate one particular shaken baby case. There was a mountain of paperwork. To make matters difficult, I was not involved in the case until a Thursday and the long trial was due to end a few days later.

At the time I was also investigating another case. Deep within myself I sensed that I was missing something, but I could not determine what it was. This obsessed me, it bothered me, and I could not rest. Then suddenly, it appeared like a gift from heaven. In both cases there were ‘fractures’ of the costochondral junctions—caused, according to the prosecutors, when the infants were roughly gripped around the chest. These, I realised, were not inflicted injuries. They were similar to the changes that occur in the costochondral junctions in scurvy!

All this happened on the Friday night. Excited, almost beyond measure, I faxed the information to the lawyers. On the Monday I contacted them by phone. But that is where I came down to earth. A ‘confession’ had been extracted—as part of a ‘plea bargain’. The case was closed.

However, I was not closed. With the help of Dr. Ian Dettman, an extremely extensive literature search, and my own clinical experience, I was able to piece together a picture that was remarkable in its clarity and significance. Words and terms that previously had no meaning to me now became a part of me. I had, from the medical libraries of the world unearthed a treasure of medical knowledge and understanding. And to think that it had been there, documented by many medical researchers, for many years. It was also exploding in size every day.

I was left to wonder why so many of my colleagues could not see the glitter of the gems that so obviously confronted me.


Because of the complexities of the issues, it is best to initially consider, separately, the various pathologies found:
1. Bruises
2. Haemorrhages, including intracranial, and retinal haemorrhages
3. Fractures.

There are some important common causes and features in each of these pathologies. However, because of differences in physiology and biochemistry, responses and, therefore, pathologies, will vary in many ways according to which organ is involved. For example, a haemorrhage in the brain, can progress towards complications that cannot occur in a skin haemorrhage.

The fundamental cause of all the pathologies
There is an increased utilization of Vitamin C precipitated (mostly) by endotoxin or other bacterial toxins. This, in turn, results in two pathologies:
1. Due to Vitamin C deficiency
2. Due to endotoxaemia.

Usually there is a combination of these two factors, with special complications that can occur in the brain because of its unique physiology. Taking this one step further, one can then move on to understand how:
1. Vitamin C deficiency can, in itself, cause haemorrhages.
2. Vitamin C deficiency can, in itself, cause spontaneous fractures.
3. Endotoxin can in itself, cause coagulation/bleeding disorders.
4. Endotoxin uses vast quantities of Vitamin C while being ‘detoxified’ (involving free radical reactions).

Endotoxin can specifically target the brain by:
1. specifically, and selectively, damaging the endothelial linings of cerebral blood vessels
2. breaking the blood-brain barrier
3. seeping into the cerebral tissue
4. causing anoxia by a direct effect on the respiratory centre
5. initiating a rapid series of biochemical disturbances, including free radical reactions, leading to an extremely rapid onset of cerebral oedema—with a host of possible complications
6. causing coagulation/bleeding disturbances.

Lacroix, Brain Pathol 1998 Oct:8(4):625-40 states:
" …a direct role of endotoxin on specific cell populations of the central nervous system, which is likely to be responsible for the transcription of proinflammatory cytokines, first within accessible structures from the blood vessels and thereafter through scattered cells."

Mayer, Medicina (B Aires) 1998;58(4):377-85, states:
" Lipopolysaccharide affects the permeability of the blood-brain barrier…"

The cerebral capillaries are particularly sensitive to endotoxin damage. Because of this the cerebral circulation can quickly cease—either in a localised area, or totally. Because the respiratory centre is damaged, respiration may cease—either forever, or for a period. This has the same effect as anoxia due to cardiac or respiratory arrest. In other words, there is no need to have cardiac or respiratory arrest for the initiation of cerebral oedema, although cardiac and/or respiratory arrest may sometimes occur. Failure to understand this is the reason why, in some very high profile cases, the prosecution has attempted to add an element involving suffocation, even though no evidence existed.

Thus, there can be two separate, but sometimes related, mechanisms responsible. Both involve a breakdown of the blood-brain barrier. The first involves a direct effect of endotoxin on the respiratory centre. The second involves a breakdown of cerebral circulation and, indirectly, a cessation of function of the respiratory centre.

The rapid effects of hypoxia on certain blood coagulation factors and fibrinolysis is well known. A coagulation/bleeding disorder follows on from this. Immediately, one can understand that there are features in the developing pathology of so-called ‘shaken babies’ that are similar to what is found following obvious cerebral trauma—for example, disseminated intravascular coagulopathy complicating cerebral trauma.

How does one separate the ‘spontaneous’ causes (via endotoxin/ excessive vitamin C utilization) from somewhat similar pathologies found in trauma?
The answer lies in:
1. the case history – sometimes a difficult issue
2. the presence of pathologies (outside the brain, such as scurvy type bone changes) suggestive of increased utilization of Vitamin C
3. factors that can lead to, or cause, endotoxaemia.

It is known that requirement for Vitamin C may vary from one individual to another by a factor of 1,000 - or even more. Furthermore, there are many conditions that may respond to Vitamin C only when this is administered, in a large dose, by injection.

Dr Sherry Lewin, in Vitamin C. Its Molecular Biology and Medical Potential, pages 182-183, states:
"It follows that the variation in vitamin C requirements by different individuals allowing for the various parameters noted, is of the order of a hundred – to a thousand fold…the range is likely to lie between the very approximate limits of 0.2 to 10 g daily."
Scurvy can occur when an infant is supplemented with the recommended daily allowance of Vitamin C – or more.

Hess, page 228-229, states:
"We have met two cases of recurrences in infants, one of which is of particular interest as it happened in spite of giving lemon juice in the intervening period…It improved, but during the winter had bronchitis, otitis, enteritis, and later furunculosis. In spite of the fact that it had been receiving an antiscorbutic for almost this entire period it developed scurvy once more."

This matches my own experience – infants, under my care, developed scurvy (usually following infections) despite being supplemented with more than the recommended daily allowances of Vitamin C. The use of Vitamin C, administered by injection, was a dramatic ‘discovery’ by myself in 1967 – or so I thought, because I later found that other practitioners, in other parts of the world, had beaten me to it by many years.

Endotoxin is often the precipitating factor for an increased utilization/need for Vitamin C. Furthermore, an intramuscular or intravenous injection of Vitamin C can almost instantly ‘detoxify’ endotoxin; and free radical reactions, set in train, are quickly quenched.

There is no standard, typical, presentation of scurvy. Certainly, some presentations have been highlighted, but the absence of all the signs of typical scurvy does not negate a diagnosis.
Furthermore because of:
1. The administration of antibiotics.
2. The administration of vaccines
3. Failure to exclusively breast-feed
4. The role played by endotoxin
infantile scurvy is presenting at an earlier age than it did 75-100 years ago
And the mode of presentation and the nature of the pathologies, are different, in many respects, to what is usually described in the literature as ‘classical’ infantile scurvy.

Present-day infantile scurvy is mainly a mixture of scurvy and endotoxaemia. Scurvy and endotoxaemia cause haemorrhages by different mechanism, although the two, more often than not, combine.

From a purist’s point of view, scurvy is a disease caused by Vitamin C deficiency and affecting collagen formation. Certainly, Vitamin C is necessary for more than one of the stages involved in the synthesis of the complex triple helix that is a feature of the four types of collagen.

Faulty collagen formation—the feature of scurvy. This affects many tissues, including bone and blood vessels. The result is:
1. Bruises and haemorrhages.
2. Some complex bone pathologies that, to the uninitiated, look like trauma-induced fractures.

Bruises and haemorrhages can occur anywhere – including:
1. Subdural.
2. Other intracranial areas
3. Retina
4. Spine.
5. Skin.
There is no typical area for bruising and haemorrhaging. And there is no typical distribution.

Bone pathologies include:
1. Periosteal elevations with underlying haemorrhages that quickly ossify in a manner similar to ossification that occurs in haemorrhages that surround fracture sites.
2. Epiphyseal disorders, primarily due to breakdown of collagen formation, complicated by haemorrhages. There may be separation of the epiphyses – resulting in ‘pathological’ fractures.
3. Weakening of bone structure, due to faulty collagen formation.

A ‘favourite’ site for epiphyseal changes is the costochondral junctions—the so-called ‘scorbutic rosary’, or ‘beading’. This, in individual cases, may involve only one, or several ribs. The areas involved quickly heal with callus formation. The bone pathologies can occur in any bone, in one bone (or area of a bone) at a particular time, and in another area at a different time. This ‘reinforces’ the impression that an infant has been physically abused on multiple occasions. One overseas case that I am investigating at the moment had 32 ‘fractures’ of various ages.

The fractures may be painless and not detected by a clinical examination. Much depends on how quickly the scorbutic process proceeds. Relatively slow onset of a scorbutic bone pathology may not present with signs typical of inflicted injury (pain or tenderness). Yet, X-rays may show many fractures. The so-called ‘frog-leg posture’, with pain and tenderness (due to haemorrhages) does exist. However, mechanisms involved are complex, and the posture can present, together with pain and tenderness, without haemorrhages – and be relieved quickly, and dramatically, in a matter of minutes, by administering Vitamin C by injection.

I do not understand the mechanisms involved. But there is a striking resemblance to some of the features found in acute poliomyelitis. Because of the dramatic response to injections of Vitamin C I suspect that endotoxin is involved.

It is necessary to highlight several details.

1. Coagulation factors are not fully understood – despite the presence of an enormous amount of knowledge that has been instrumental in the saving of many lives.
2. Standard coagulation profiles may be normal but the patient may bleed to death.
3. Extensive coagulation profiles may reveal a problem not revealed by standard profiles.
4. Platelet function tests should always be a part of extensive profiles despite known difficulties that exist with infants..
5. In typical scurvy, standard coagulation profiles can be normal.
6. In typical scurvy, capillary fragility tests are abnormal.
7. Endotoxaemia (a ‘cause’ of scurvy) can disturb coagulation/bleeding factors and result in bleeding.
8. In shaken baby cases a diagnosis of ‘shaking’ is usually made at an early stage, and it is then not considered necessary to search for signs of endotoxaemia, or anything else.
9. Strangely, cost has been advanced as a reason for failure to thoroughly investigate.
10. One ‘authority’ demanded that I produce retinal haemorrhages ‘with retinal haemorrhages due to scurvy written all over them’ [my words]. What he really asked for were features of scurvy-induced retinal haemorrhages that differentiated them from other retinal haemorrhages. This was quite absurd. Retinal haemorrhages due to scurvy can occur anywhere in the retina. They are, simply, haemorrhages, and have no specific features – unless one uses technologies like electron microscope studies.
11. It is of interest to note that during autopsies on SIDS cases liquid (uncoagulated blood) is sometimes found. This demonstrates the presence of a coagulation disturbance – confirmed by extremely high D-dimer levels.
12. Platelet functions may be abnormal in some cases of scurvy, but it is difficult to separate scurvy and endotoxin as causes. The two interact together in many cases.

Sushkevick et al, Vopr Pitan, 1969 Sept-Oct;28(5):23-7. state:
" Experiments were staged on 25 healthy and 38 guinea pigs with vitamin C deficiency. The blood platelets count, their adhesiveness, thrombocytogram, factor X111 activity, thrombotic test, bleeding time and the volume of blood lost were determination the 18-22nd day of keeping the animals on a scorbutogenic diet, parallel with analogous determinations in controls. In animals suffering from C-avitaminosis the number of blood platelets dropped, thrombocytograms demonstrated a decrement of mature forms of blood platelets and an increase in degenerative forms. This was attended by reduced adhesiveness of blood platelets and factor X111 activity and also by deranged structure and properties of the fibrin clot. Hence, disrupted formation of full-fledged thrombocyte plugs and fibrin clots with impaired vessels which in scurvy have reduced mechanical strength, this resulting in lengthening of the bleeding time and in increased volume of blood lost."

This does not mean that every case of infantile scurvy presents with all these features. However, it is a very significant report. Obviously, coagulation factors should be intensely investigated in all shaken baby cases. The extreme example of haemorrhage complicating a viral infection is seen in Ebola fever. With an extremely short time of presentation, most patients ‘bleed from everywhere’. I never cease to wonder why intravenous Vitamin C is not used to treat this awful disease—and used early.

The use of italics for the word ‘injury’ is deliberate because the pathology involved is not always caused by an ‘inflicted injury’.
Kaur et al, J Clin Pathol. 1999;52::203-209, state:
" Conclusions – Axonal bulbs staining positively for _APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilatory support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone."

Rosomoff et al, Crit Care Med, 1996, Feb;24(2 Suppl):S48-56, state:
"Severe traumatic brain injuries are extremely heterogenous. At least seven of the secondary derangements in that have been identified as occurring after most traumatic brain injuries also occur after cardiac arrest."

Geddes et al, Neuropathol Appl Neurobiol 2000 Apr:26(2):105-16, state:
"The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of traumatic axonal injury or diffuse axonal injury is likely to be of limited use for medicolegal purposes."

Little more needs to be said about this except to state that, in many cases, diffuse axonal injury is presented as clear evidence of shaking. The animated video showing how the brain is supposed to move inside the skull when a baby is shaken, and ‘tear’ the axons apart, certainly impresses the judge and the jury. The effect of that video is, indeed, dramatic. Attempting to counter that, even with extensive references from the best medical literature, is difficult—particularly when the video is presented by authorities with impeccable qualifications.

Endotoxins can have extremely rapid actions – and, often, this is virtually instantaneous. Although, in this paper, I refer to ‘endotoxin’, other toxins of bacterial origin can have somewhat similar actions. It is possible to estimate the amount of endotoxin in blood and CSF – during life and during an autopsy. Endotoxin can specifically ‘target’ the brain via mechanisms involving specific sensitivity of the cerebral capillaries to endotoxic damage. This allows endotoxin to seep into the brain tissue. Cerebral anoxia can follow. Anoxia can, of course, by itself cause a breakdown of the blood-brain barrier. Free radical reactions are immediately initiated and accelerate violently. The result is cerebral haemorrhage, retinal haemorrhage and/or cerebral oedema that can begin and accelerate with dramatic rapidity.

How to look for endotoxaemia

1. Can be measured directly.
2. Look for ‘toxic’ strains of intestinal bacteria.
3. The administration of vaccines can result in changes in the nature of intestinal bacteria and excessive endotoxin formation.
4. The administration of antibiotics can result in excessive endotoxin formation.
5. Failure to exclusively breast-feed has already been mentioned.
6. Culture blood and CSF, during life and during the autopsy. Cultures should include viral cultures, which can, by indirect mechanisms result in excessive endotoxin production by gut bacteria.
7. Check for otitis media – which is sometimes associated with endotoxaemia. In the Australian Nanny case there was no sign of otitis media when the baby was first admitted to hospital following the final collapse. Yet during the autopsy , a few days later, ‘muco-purulent’ material was found in both middle ears.
8. Check liver and kidney functions – which can be disturbed by endotoxin.
9. Check liver and kidney histology – including electron microscope studies.
10. Electron microscope studies of several parts of the gastrointestinal tract may show signs of endotoxin damage or abnormal adhesion of bacteria to the gut wall.
11. Electron microscope, and light microscope, studies of blood vessels (including capillaries in the brain) may reveal signs of endotoxin damage.
* Note that it is not necessary to have a raised leucocyte count to have raised levels of endotoxin.


I would like to avoid this subject but cannot do so.
It is not a matter of whether vaccines should or should not be used.
It is a matter of – "Is there a role for vaccines in the pathogenesis of the Shaken Baby Syndrome?"

In several cases (probably a significant number) the final collapse followed within a very short period of a vaccine administration. In the Sally Clarke case, this happened with her two babies. She refused to have her third baby (born after she was charged) vaccinated.

There is no doubt, in my mind (and this is based on long experience) that despite advice to the contrary it is not wise to administer vaccines to sick infants—including infants with ‘colds’. This is because, with infections (including ‘colds’), endotoxin is likely to be produced in the gut in excessive amounts, and liver detoxification processes are likely to be stressed. Immediately, some practitioners are going to state that in many situations some infants ‘always have colds’. This applies particularly to groups such as Australian Aborigines. The answer to that is to supplement, first, with Vitamin C and zinc. Risks will then be reduced enormously (but not completely).

Mechanisms involved with vaccine administration include excessive endotoxin formation. Knowing this allows one to follow the remainder of the pathway towards the development of the pathologies found in so-called ‘shaken babies’.

There are several aspects to this:

1. Infants are said to have been ‘healthy and normal’ before the final collapse despite a long history of medical problems, such as repeated infections and the administration of multiple courses of antibiotics.
2. Many infants were hospitalised several times before the final collapse.
One infant, for example, was on an intravenous drip for several days, for what was called (by specialists) ‘a trivial illness’.
3. The inappropriate administration of medications.
One case, being investigated at the moment, was given (inappropriately) frequent doses of promethazine.

Parry EW. Inflamm Res 1996 Jul;45(7):354-6, states:
" The three drugs (dexamethasone, promethazine and nordihydroguauaretic acid) have the ability to inhibit powerfully the synthesis of tumour necrosis factor-alpha in response to lipopolysaccharide [endotoxin] …it is proposed that
the three drugs act by impairing the hepatic mechanism which normally removes portal vein-borne endogenous lipopolysaccharide leading to systemic distribution of lipopolysaccharide."

One problem, demonstrated here, is that many practitioners are too busy and cannot find the time to study everything. I have a ‘bone to pick’ with this issue, because, for 30 years I have been trying to interest my colleagues about the potential dangers involved when antihistamines are administered to infants. The response has been one of extreme hostility.

With shaken babies this is done in several ways:

1. By ‘declaring’ that certain pathologies are ‘diagnostic’, when there are serious doubts about the logic involved.
2. By accepting that ‘convictions’ are certain evidence of guilt, and the features found in these cases are therefore diagnostic of the shaken baby syndrome.
3. By the process of ‘plea bargaining’ – where it is made clear to the defendant that to plead innocent will result in a charge of murder and a long jail term (or even execution), and a guilty plea will result in a lesser charge (such as involuntary manslaughter) and a short sentence.
4. Many of those charged have limited financial resources and cannot afford good lawyers.
5. Publishing what are called ‘position papers’ and ‘a consensus’, that generates an impression of ‘finality’. That is; the matter is settled and there is no need to examine it further.
6. By deliberately withholding important information from the defence in order to strengthen the case for the prosecution.

The ‘Australian Nanny’ (Louise Sullivan) case was one of the first where lack of knowledge (and an absolute determination to achieve a conviction) generated disturbing responses. It was felt that Louise had ‘killed’ the child, but lacking was an important piece of evidence. The prosecution could not understand what initiated the rapid onset of cerebral oedema. It was, of course, cerebral anoxia, caused by endotoxin, but the prosecution did not know this. So it was deduced that Louise not only shook the infant but suffocated it as well.

In order to win a conviction, it was decided that if Louise was 'psychologically softened' first, then hit with an invented piece of evidence, she would ‘confess.' I will not detail how the ‘softening’ was carried out—but it was not nice. Then Scotland Yard said to Louise, "We have re-examined the lungs and can prove that you suffocated the infant as well as shook it. Plead guilty to a lesser charge of involuntary manslaughter and your sentence will be light. Plead innocent and you will be charged with murder and spend many years in jail." Louise accepted the plea in order to save her sanity. She was allowed to go home.

I then asked to see the reports of the lung examination. Clearly stated was: "The lungs are normal. No evidence of anoxia." Unfortunately, that ‘little’ detail was omitted from the book that was later written about the case.

The recently finalised Sally Clarke case (England) demonstrated the existence of the strange psychology involved in the last (number 6) factor, in a dramatic manner—after Sally had spent more than 3 years in jail for ‘killing’ two of her babies.

The first died, and an autopsy resulted in a diagnosis of ‘cot death’. Later, a second baby died, and the authorities claimed that this was because it was ‘shaken’. Then the first death was ‘reconsidered’ and the authorities said that this, also, was ‘shaken’. Paediatrician, Professor Sir Roy Meadow, stated that the likelihood of having two cot deaths in one family were one in 73 million. This certainly impressed the court. Then the Home Office Pathologist, Dr Alan Williams, withheld vital evidence from the court. This concerned the fact that cultures were taken from the blood and CSF from the second baby—and these showed that the baby was ‘riddled with potentially lethal organisms’ (staph. aureus).

After more than 3 years, Sally’s husband was finally able to obtain the full medical records to which the defence had previously been denied access. And a ‘proper statistician’ showed that the chances of having two cot deaths in one family could be as low as one hundred to one. Sally was freed.

Now the two ‘experts’ who gave false/wrong evidence are in real trouble. The question that should be asked is - Why did the eminent doctors behave in such a fashion? It appears that they were hell-bent on achieving a prosecution and cared little about how this was achieved.

In another case an eminent paediatrician was asked to comment about a detail in my report to the court, where I stated that the infant concerned ‘had endotoxaemia’. He declared something to the effect that this could not be so because ‘the infant was not sick’. Some time later he was asked why he did not transfer the infant to another hospital (as recommended by an ophthalmologist) in order to have the retinas photographed for evidence. He answered with something like ‘We could not, because he was too sick’.

I have no doubt that this ‘shaken baby’ business will eventually be recorded as one of the worst pages in the history of paediatrics. And the saddest part of it all concerns the fact that, while important doctors are busy collecting ‘evidence’ for the prosecution, vital issues that can save many lives are being not only ignored but destroyed with intense hostility.

During one trial, the prosecution stated that infantile scurvy was no longer seen. I replied with ‘Yes it is. But it is not called ‘scurvy’ it is called the ‘shaken baby syndrome’.

Failure to properly consider the case history.
Usually, the prosecution attributes all problems suffered by an infant previous to the final collapse as caused by abuse. For example, if an infant has ‘colic’ this is diagnosed as being due to abuse. Crying is also considered to be due to abuse. Of particular concern is the tendency to disregard concern expressed by parents, and then claim that the parents were negligent. Frequent admissions to hospital (for infections or undiagnosed problems), and frequent examinations by doctors (including paediatricians) are usually, in retrospect, after the final collapse, left unexplained or considered to be part of the chronic abuse syndrome.

If a premature infant, while still in hospital after birth, develops intracranial haemorrhages or periosteal haemorrhages the diagnosis is usually considered to be ‘a normal risk that all premature babies are exposed to’. However, if one of these infants is diagnosed with one or more of these disorders soon after being allowed home the chances are that someone will be charged with abuse. Radiologists report the presence of periosteal elevations in premature infants as ‘a normal variant’. Mechanisms responsible are rarely considered.

When the findings, either before or after death, cannot be explained by a carer, this is regarded as ‘an inconsistency’ consistent with abuse. It is considered by authorities to be a diagnostic feature of abuse.

In many ways this is like the ‘witch hunts’ of old.

Because of knowledge that is now available, prosecutors (including doctors) who provide evidence suggestive of guilt, without considering the factors stated in this lecture, possibly, later, may be charged with criminal negligence. Furthermore, the issues involved are extremely complex. No single doctor can possibly claim to be an ‘authority’ on every aspect of every factor involved in the genesis of the pathologies found in shaken babies. However, sufficient knowledge exists to enable one to at least cast serious doubt on the inflicted trauma hypothesis of the pathologies found in some so-called ‘shaken babies’.

For those of you who want to investigate the subject of shaken babies in greater detail I suggest that you connect onto PubMed, and Google. Type in endotoxin, vitamin C, blood-brain barrier, coagulation/bleeding disorders, platelets, Factor X111, axonal injury, shaken babies, collagen, and free radicals. Be prepared to spend a few years doing so, because there is an enormous amount of literature available.

I do not doubt that it is possible to shake a baby to death. However, in the 35 cases I have extensively investigated, there were substantial reasons to conclude that shaking was not the cause of the pathologies found.

Dianne Jacobs Thompson  Est. 2007
Also (alternative medicine featuring drugless cancer treatments)
Author publication: NEXUS MAGAZINE "Seawater--A Safe Blood Plasma Substitute?"