More Than Half of Pediatricians Make Diagnostic Errors, Study Says

by Honey Berk Jun 22nd 2010 4:00PM

Maybe it’s time to rethink that age-old “doctor-is-god” stereotype.

Fifty-four percent of pediatricians say they make diagnostic errors at least once or twice per month, according to a new survey of more than 700 pediatricians and pediatric trainees.

The data for trainees was even more striking, with 77 percent admitting they make errors at least once or twice per month. And nearly half of the pediatricians surveyed say their errors harm patients at least once or twice per year.

However, according to Business Week, researchers did not ask the extent of the harm and said they didn’t have enough information to gauge the seriousness of it. But the authors say previous research points to the existence of diagnostic errors in 32 percent of pediatric malpractice claims.

“These are perceptions and much more research has to be done to really delineate how often this happens,” senior study author Dr. Geeta Singhal, of Baylor College of Medicine, tells Business Week.

Diagnostic errors typically include those that are delayed, wrong or missed, Business Week reports. Those detailed in the study involve a range of activities, from prescribing, dispensing and administering medications to surgery- and anesthesia-related activities that occur in the operating room.

The most frequent diagnostic error reported was viral illnesses being misidentified as bacterial illnesses, according to the study — so stop feeling guilty for thinking your child’s last bout with strep throat was just a cold. Other diagnostic errors frequently reported were the misdiagnosis of medication side effects, psychiatric disorders and appendicitis.

Pediatricians surveyed most often cited a failure to gather information through medical history, exam or chart review as the cause of errors. Other causes of misdiagnoses included failure of parents to seek care for their child in a timely manner, failure to follow up on abnormal lab tests and parents ignoring follow-up recommendations, Business Week reports.

Physicians say closer follow up of patients and improved teamwork between practitioners would decrease the likelihood of errors, as would improving access to information through electronic health records and diagnostic decision-support tools, according to the authors.

Singhal tells BusinessWeek that parents who are unsure of a diagnosis should be encouraged to ask for more information or seek a second opinion, since physicians are not always right.

“It’s important to me as a pediatrician and as a mom to empower our patients and our families to ask good questions of their physicians,” Singhal tells the magazine. “If they are not comfortable with the diagnosis, it’s OK to ask the doctor to elaborate more or help them understand better.”

Source:

http://www.parentdish.com/2010/06/22/more-than-half-of-pediatricians-make-diagnostic-errors-study-sa/

Cutaneous Mimickers Of Child Abuse: A Primer For Pediatricians

Mohammed AlJasser¹ and Sultan Al-Khenaizan¹

(1)	Division of Dermatology, Department of Medicine, King Saud Bin Abdulaziz University for Health Sciences and King Fahad National Guard Hospital, King Abdulaziz Medical City, P.O. Box 22490, Riyadh, 11426, Kingdom of Saudi Arabia

Sultan Al-Khenaizan Email: khenaizans@ngha.med.sa

Received: 1 April 2008  Accepted: 26 June 2008  Published online: 26 July 2008

Abstract

The annual incidence of child abuse was estimated to be 2.8 million by the national incidence study conducted in the USA in 1993, which is a two-fold increase compared to 1986. Awareness of child abuse has been increasing since the 1960s. Although most victims of child abuse present with cutaneous lesions, many genuine skin diseases may appear as non-accidental injuries which, if not recognized, may lead to misdiagnosis of child abuse. Here, we review the most common cutaneous mimickers of child abuse in order to increase awareness of these disorders and reduce erroneous diagnosis of child abuse.

Introduction

Child abuse is defined by the Child Abuse Prevention and Treatment Act as a recent act or failure to act that results in death, serious physical, or emotional harm, sexual abuse or exploitation, or imminent risk of serious harm; involves a child; and is carried out by a parent or caregiver who is responsible for the child’s welfare [2]. Child sexual abuse is defined as the employment, use, persuasion, inducement, enticement, or coercion of any child to engage in, or assist any other person to engage in, any sexually explicit conduct or simulation of such conduct for the purpose of producing a visual depiction of such conduct; or the rape, molestation, prostitution, or other form of sexual exploitation of children, or incest with children [2]. Awareness of child abuse has been increasing since the 1960s [39]. The annual incidence of child abuse was estimated to be 2.8 million by the national incidence study conducted in the USA in 1993, which is twofold increase compared to 1986 [1]. In 2006, an estimated 3.6 million children were the subject of an investigation by child protective services agencies [4]. An abused child has approximately a 50% chance of being abused again and has an increased risk of dying if the abuser is not caught and stopped after the first presentation. Such figures indicate that the early diagnosis of child abuse is of great importance [48, 50]. Despite advancements in diagnosing child abuse, mistakes in diagnosis still occur. Because skin lesions are one of the most common presentations of child abuse, the findings of unexplained skin changes are alarming to healthcare workers, and if not correctly identified as cutaneous mimickers of child abuse, a false diagnosis of child abuse may—and do—result [22]. Such misdiagnoses can lead to serious consequences to the child, the family, and the falsely accused [19]. Irrefutable physical findings of sexual abuse occur in less than 10% of all cases [38]. Thus, the medical history, in addition to a thorough medical examination, takes on an importance of enormous proportions in both physical and sexual maltreatment cases [56]. Although skin diseases are the most common mimickers of child abuse, other non-dermatologic conditions (such as osteogenesis imperfecta) may also take on this role. There are many reviews that have tackled the subject of cutaneous manifestation of child abuse, but only few have discussed cutaneous mimickers of child abuse. This review will be limited to the most important cutaneous mimickers of child abuse, which can be classified into mimickers of physical abuse and mimickers of sexual abuse (Table 1). We hope that this review will increase the awareness of healthcare workers of different specialties of these presentations and decrease the incidence of the bitter experience of false accusations of child abuse.

Table 1 Classification of cutaneous mimickers of child abuse

Mimickers of physical abuse	Mimickers of sexual abuse
Linear eruptions	Lichen sclerosus et atrophicus
Inflammatory linear verrucous epidermal nevus	Anogenital warts
Allergic contact dermatitis	Perianal streptococcal cellulitis and streptococcal
Stretch marks	vulvovaginitis
Phytophotodermatitis	Genital herpes zoster
	Vulvitis circumscripta plasmacellularis
Non-linear eruptions	Perianal and vulvar Crohn’s disease
Mongolian spots
Hemangiomas
Henoch-Schönlein Purpura
Urticaria pigmentosa
Dermatitis artefacta
X-linked icthyosis
Bullous impetigo
Congenital blistering diseases
Acquired blistering diseases
Neuroblastoma

Mimickers of physical abuse

Linear eruptions

Because of their linearity, most linear eruptions can raise the suspicion of child abuse as many of them occur particularly in children. Pediatricians should be aware that not all linear skin lesions are externally induced and that genuine skin diseases may present in linear fashion.

Inflammatory linear verrucous epidermal nevus   Inflammatory linear verrucous epidermal nevus (ILVEN) is a relatively rare linear psoriasiform papules and plaques with the majority of cases appearing before the age of 5 years (Fig. 1). This condition is more common in females. It most commonly affects the extremities and occasionally the trunk and is usually unilateral. In addition to its linearity, ILVEN is red and itchy. Misdiagnosis of ILVEN as child abuse has been reported before [53].

Fig. 1 Inflammatory linear verrucous epidermal nevus. Well-defined linear erythematous scaly papules involving the dorsal aspect of the hand

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Allergic contact dermatitis   Allergic contact dermatitis (ACD) is a delayed-type hypersensitivity reaction that is elicited when the skin comes in contact with an allergen to which an individual has previously been sensitized. Acute ACD usually presents with a well-demarcated pruritic eczematous eruption with or without blistering. Lesions are typically limited to the site of contact with the allergen. In children, acute ACD to henna tattoos, commonly applied in festivals and parties, can induce an angry looking linear dermatitis (Fig. 2). The medical history and pattern are usually confirmative. There have been a few reports of ACD misdiagnosed as child abuse [31, 59]. Paraphenylenediamine (PPD) is the culprit allergen, and hair dyes are contraindicated because they contain PPD or cross-reactants.

Fig. 2 Allergic contact dermatitis. Well-defined erythematous angry-looking plaques with vesicles due to henna tattoo

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Stretch marks   Stretch marks are commonly seen in adolescents undergoing rapid linear growth and are seen in many physiological states, including normal puberty and pregnancy; however, they are rarely indicative of endocrine abnormalities [32]. Because of their linearity and appearance, they can be mistaken for physical abuse, particularly whipping marks (Fig. 3) [14, 33]. The atrophic appearance, horizontal orientation, and the classic location on the lower back, abdomen, gluteal region, upper thighs, and breasts differentiate them from non-accidental injuries [33].

Fig. 3 Stretch marks. Reddish, horizontally oriented, atrophic plaques involving the lower back

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Phytophotodermatitis   Phytophotodermatitis refers to sun-induced inflammation and hyperpigmentation due to psoralens, which is commonly found in many plants, including citrus fruits [26]. It is commonly seen in children squeezing oranges and limes in sunny climates during the holidays, and it presents as linear brown burn-like blistering erythema followed by hyperpigmentation (Fig. 4) [26]. The erythema and vesicles, which are commonly linear, can even occur in the shape of hands and thus might be misdiagnosed as inflected burns or hand slaps [12, 26].

Fig. 4 Phytophotodermatitis. Well-demarcated linear dark-brown hyperpigmentation due to psoralens in citrus fruit

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Non-linear eruptions

Mongolian spots   Mongolian spots are ill-defined grey to greenish-bluish patches that are usually present at birth or develop within the first few weeks of life. They commonly involve the lumbosacral area or the inner aspect of buttocks. Because of their color, Mongolian spots can be mistaken for bruises, especially when they are located on atypical sites (Figs. 5 and 6) [47]. Unlike bruises, they are not tender and do not evolve over time [42]. They usually fade in early childhood but can persist indefinitely.

Fig. 5 Mongolian spot. Ill-defined bluish-greenish patch on the upper back

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Fig. 6 Mongolian spot. A bluish-greenish patch involving the right thigh

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Hemangiomas   Hemangiomas are the most common tumors in infancy, with the majority of lesions noticed within the first few weeks of life. They are more common in girls and premature infants and may occur on the skin or mucosal surfaces [46]. They can be superficial, deep, or mixed, with the latter being the most common [23]. Superficial hemangiomas are bright red in color with a finely lobulated surface. Deep hemangiomas are warm blue-purple masses with minimal or no overlying skin changes. Because of their red color and liability to ulcerate, hemangiomas can be mistaken for physical abuse when located on lips (Fig. 7) and for sexual abuse when located on perianal area (Fig. 8). There have been many reports of such occurrences [8, 43, 62].

Fig. 7 Hemangioma. A mixed (superficial and deep) hemangioma on the lower lip

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Fig. 8 Hemangioma. Ill-defined erythematous superficial ulcerating hemangioma involving the perianal area

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Henoch-Schönlein purpura   Henoch–Schönlein purpura (HSP), also know as anaphylactoid purpura or allergic vasculitis, is the most common vasculitic disease in children, with an equal prevalence in boys and girls. It presents as erythematous, urticarial papules that rapidly evolve into palpable purpura. The eruption might be preceded by fever or accompanied by headache, myalgias or arthralgias, and abdominal pain. There is usually a typical symmetrical distribution around the buttocks, extensors of extremities, and distal legs, although any area of the body may be involved, including the face (Fig. 9) [16]. Because HSP presents with edema and erythema, it can be mistaken for child abuse, especially early in its course [10, 16]. Individual lesions usually fade within 5–7 days, but recurrence is possible.

Fig. 9 Henoch–Schönlein purpura. Multiple purpuras symmetrically involving the legs

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Urticaria pigmentosa   Mastocytosis is a spectrum of diseases with tissue mast cell proliferation. It can present at birth or develop any time thereafter. Urticaria pigmentosa (UP), the most common type seen in children, is usually limited to skin involvement. It is characterized by ill-defined tan-brown papules and plaques that urticate on pressure or friction during handling or bathing the child, which is referred to as Darier’s sign (Fig. 10). Lesions may even blister or get bruised and, therefore, can be misdiagnosed as inflected injuries [25, 32]. Urticaria pigmentosa usually resolves or improves spontaneously in late adolescence.

Fig. 10 Urticaria pigmentosa. Multiple ill-defined brown papules and plaques involving the whole back and scalp

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Dermatitis artefacta   Dermatitis artefacta (DA) is a factitious disorder characterized by intentional self-induced skin injury that can take various forms and shapes. Patients usually induce lesions to get emotional and psychological support, escape responsibilities, or collect disability insurance. It is most commonly seen in adolescent girls. The bizarre presentation and unconvincing history may lead to erroneous accusation by the patient or the medical team to family members. A thorough history and examination usually leads to the correct diagnosis. Lesions are usually seen on accessible sites, predominantly on the dominant side of the body, although they may occur anywhere (Fig. 11). Lesions usually have geometric patterns or angulated borders surrounded by completely healthy skin. Histopathology might be useful but is not always revealing. Preventing the patient from inducing lesions, by occlusive dressings or casting, usually leads to healing of the lesions, which is a helpful diagnostic tool to confirm the diagnosis.

Fig. 11 Dermatitis artefacta. Self-induced multiple well-defined, round-to-oval scars on the forearms in an adolescent girl

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X-linked ichthyosis   This is an X-linked recessive disorder (OMIM 308100) caused by steroid sulfatase (STS) deficiency secondary to mutation in the gene encoding STS located on the distal portion of the short arm of the X chromosome. It affects only boys with females being carriers for the disease. Almost 90% of patients present within the first weeks of life with mild erythroderma and generalized peeling with large, translucent scales. Later during infancy, typical large, polygonal, dirty-looking, dark-brown adherent scales develop. The distribution is symmetrical on extremities, trunk, and neck, with a sparing of the palms, soles, and face except for the preauricular area (Fig. 12). Parents of X-linked ichthyosis (XLI) children frequently face blame for uncleanness and negligence by school officials. We had frequent requests for medical reports from parents of children with XLI to prove that their children had a skin disease that gave them the “dirty” appearance. Topical keratolytics can dramatically improve the appearance, and their use should be encouraged.

Fig. 12 X-linked icthyosis. Dirty-looking, dark-brown, polygonal scales on the neck

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Bullous impetigo   Bullous impetigo (BI) is a relatively common, highly contagious, superficial skin infection caused by specific strains of Staphylococcus aureus. It affects young children, most commonly neonates and infants. It usually starts as small vesicles on the face, trunk, buttocks, perineum, or extremities that rapidly enlarge to flaccid bullae which evolve into erosions and crusts that heal without scarring (Fig. 13) [62]. Because of their appearance, BI can be confused with cigarette burns [47, 62]. The variable sizes, the uniphasic appearance, and the typical sites of involvement rule out the latter possibility.

Fig. 13 Bullous impetigo. Crusted erythematous erosions with few flaccid bullae on an erythematous base

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Congenital blistering diseases   Epidermolysis bullosa (EB) is a rare inherited mechanobullous skin disease with a defective loose attachment of the epidermis to the dermis. There are many types and subtypes [63], but all are characterized by easy blistering with minimal friction and trauma [63]. Blisters can be linear and hemorrhagic with a potential for scarring, depending on the type (Fig. 14). Blisters mostly occur on friction-prone areas, mainly on extremities. Because of this appearance, EB can be mistaken for physical abuse [21, 63].

Fig. 14 Epidermolysis bullosa dystrophica. Multiple hemorrhagic bullae and ulcers with hyper- and hypopigmentation

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Acquired blistering diseases   Chronic bullous disease of childhood (CBDC) is a form of linear IgA bullous dermatosis that occurs in children and remits spontaneously around puberty [15]. It is a rare disease, but still considered the most common acquired autoimmune blistering disease in children [15]. It is characterized by annular erythema and blisters forming “clusters of jewels” on genitalia, the lower abdomen, thighs, and periorally (Fig. 15) [15]. Epidermolysis bullosa acquisita (EBA) is a rare, acquired, bullous disease due to autoimmunity to type VII collagen. The disease has been reported mainly in adults but can occur in children. It is characterized by the development of blisters on trauma-prone areas, such as elbows, knees, and dorsa of the hands, which heal with atrophic scarring, milia, and pigmentary changes (Fig. 16). It is usually chronic and refractory to various treatment modalities. Bullous pemphigoid is the most common autoimmune blistering disease in adults, and it may occur rarely in children. The distribution is usually symmetrical and predominates on flexural areas. When any of these diseases occur in children, the blisters can be mistaken for physical and sexual abuse, depending on their location [15]. The latter is more likely when anogenital involvement occurs [44].

Fig. 15 Chronic bullous disease of childhood. Annular bullae forming “clusters of jewels”

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Fig. 16 Epidermolysis bullosa acquisita. Multiple linear erythematous erosions and bullae with hypo- and hyperpigmentation

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Neuroblastoma   Neuroblastoma (NB) is one of the most common solid tumors of early childhood. It arises from precursors of the sympathetic nervous system, most commonly in the adrenal medulla. The tumor metastasizes in about 60% of patients to cortical bone, bone marrow, lymph nodes, and liver [18]. Patients with localized disease are generally asymptomatic, but those with metastasis present with systemic symptoms such as fever and bone pain [61]. Metastasis to periorbital bones results in ecchymotic orbital proptosis known as “raccoon eyes”. Because raccoon eyes is a sign that classically occurs with basal skull fractures, when it happens in a patient with NB, it can be falsely suspected as child abuse [9, 28, 34].

See link for further analysis of child abuse mimickers and references:

http://www.springerlink.com/content/1204527834444356/fulltext.html

Summary

The recognition of child abuse is of great importance, but the avoidance of a false accusation for abuse is even more important. The misdiagnosis of child abuse has serious consequences for the child, the family, and the falsely accused. Therefore, all healthcare providers from different specialties, pediatricians in particular, must be aware of cutaneous child abuse mimickers. Important clues, such as congenital onset and a family history of similar skin diseases, should be carefully searched out. Whenever in doubt, referral to a dermatologist is recommended to rule out any genuine skin disease. Healthcare workers should be encouraged to report conditions mistaken for child abuse to increase awareness and, hopefully, avoidance.

Source:

http://www.springerlink.com/content/1204527834444356/

Caffey Revisited: A Commentary On The Origin Of Shaken Baby Syndrome

C. Alan B. Clemetson, M.D

ABSTRACT

Caffey is often cited as the source of the diagnosis of “shaken
baby syndrome” (SBS). Once the “classic” findings attributed to SBS
are identified, it is rare for a differential diagnosis to be considered.
Caffey focused on radiologic findings, but while he was aware
of the possible diagnosis of scurvy, the radiologic signs of infantile
scurvy may not have had sufficient time to develop. Other findings
in his cases were compatible with scurvy due to toxic histaminemia,
which can cause capillary fragility, retinal petechiae, and subdural
hematoma. Although dietary vitamin C deficiency is very rare today
in our country, both vitamin C deficiency and toxic histaminemia
can accompany systemic infection. Toxic histaminemia may also
occur following immunizations.

Skeletal Findings in Caffey’s Cases

In 1946, John Caffey, a radiologist, described multiple
fractures in the long bones of infants suffering from chronic
subdural hematoma. None of the parents reported any knowledge
of falls or physical injury, but Caffey suspected child abuse to
explain the injuries.
Following this retrospective, radiological study by Caffey, the
diagnosis of “shaken baby syndrome” (SBS—including retinal
petechiae, multiple fractures of the long bones, and subdural
hematomas) evolved and has resulted in many men and women
being convicted of child abuse, all without any meaningful
consideration of a differential diagnosis.
Although Caffey mentioned the word scurvy in the differential
diagnosis of each of the six cases, he stated that none of the infants
showed the typical radiological changes of scurvy: many of the
fractures were in the shafts of the long bones, instead of at the
junctions between the epiphyses and the diaphyses.
The radiologic signs of scurvy, however, are variable. The
most consistent finding used to be elevation and calcification of
the periosteum of the long bones due to subperiosteal hemorrhage,
above and below the fracture sites. In reviewing Caffey’s six
original cases, this finding was present in most of the cases. And,
although osteopenia and contrasting white lines of healing are said
to be characteristic radiological features of classical scurvy,
absence of these findings on radiographs does not rule out a
scorbutic state. The precise time course of increased susceptibility
to fractures and the development of osteopenia and white lines of
healing seen on radiographs is not known. Bones may be
vulnerable to fracture because of proline and lysine hydroxylase
deficiencies affecting chondroblasts and osteoblasts before these
classic radiological signs appear, especially if scurvy develops
rapidly at an early age.

Additional Findings in Caffey’s Case Studies

In addition to the long-bone fractures and subdural hematomas,
other clinical signs consistent with infantile scurvy were evident in
most of Caffey’s six cases:
Case 1. A purulent discharge from the right ear began at age 5
months and persisted for 2 months; a convulsion due to subdural
hemorrhage occurred at 7 months. Spontaneous fracture of the right
radius occurred after nine days in the hospital.
Case 2. Convulsions began at age 1 month. At 7 months, the
infant developed soft, spongy, bleeding gums typical of scurvy, and
retinal petechiae indicative of increased capillary fragility.At age 8
months, he developed signs of subdural hematoma.
Case 3. Multiple fresh hemorrhages were present in both ocular
fundi. Petechiae were also scattered on the abdominal wall, and a
large ecchymosis was seen on the left side of the face.
Case 4. Radiographs showed evidence of epiphyseal separation
at the proximal end of the right humerus, suggestive of scurvy.
Case 5. Subdural hematoma and bone fractures associated with
otitis media were present; black-and-blue spots on the forehead and
face could be interpreted as either traumatic or scorbutic.
Case 6. There was bilateral proptosis due to retrobulbar
hemorrhages consistent with scurvy—akin to the unilateral
proptosis seen in vitamin C-deficient 18 century sailors.
Even with adequate dietary vitamin C intake, infections can
rapidly deplete ascorbic acid stores and increase the blood histamine
level. In cases 1 and 5 above, it is noted that subdural hemorrhages
occurred in the context of ongoing otitis media infections.
Many factors affect vitamin C metabolism, but the most
important is systemic infection. Hess, in his Cutter Lecture at
Harvard Medical School, recognized that infection and vitamin C
deficiency were both related to the development of infantile scurvy.
It was a number of years, however, before he realized that each
affected the other—vitamin C deficiency predisposes to infection,
and infection predisposes to vitamin C deficiency. Blood levels of
vitaminCare also inversely related to blood histamine levels.

Onset of Infantile Scurvy

Infantile scurvy used to occur most commonly after age 7
months, when swollen, bleeding gums were evident, as the lower
incisor teeth had erupted and bacteria could enter the scorbutic
gingival sulcus. In contrast, an earlier onset variant of infantile
scurvy now occurs at 8 to 12 weeks of age. Bleeding gums are rarely
never seen before the eruption of the lower incisor teeth at 7
months, so the diagnosis of scurvy may not be obvious.
The hypothesis that subdural hemorrhages, retinal petechiae,
and spontaneous fractures of the ribs and long bones can occur as an
early variant of scurvy at about 8 to 10 weeks of age has not been
adequately studied, and, therefore, has not been disproven. Unless
and until vitamin C and histamine levels are actually measured in
these infants, who are automatically classified as victims of SBS,

we will not know the truth about causation. Unfortunately, even if
the diagnosis of infantile scurvy is considered, most hospitals do
not have the ability to measure either vitaminCor histamine levels.
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 two countries, respectively.

A Multifactorial Cause?

Infants with the findings attributed to SBS may be affected by a
combination of factors causing generalized capillary fragility,
which in turn affects the capillaries of the bridging veins between
the brain and the dura mater—predisposing to subdural
hematoma—due to inadequate ascorbic acid intake and/or
depletion by infections or multiple immunizations.
The defective formation of fibrous tissue, bone, and dentin that
is known to occur in scurvy results from proline and lysine
hydroxylase deficiencies that affect fibroblasts, chondroblasts,
osteoblasts, and ameloblasts. However, the increased capillary
and venular fragility causing the bleeding associated with scurvy
is due to a many-fold increase in the blood histamine level, as
shown by Clemetson.
The total blood histamine increases exponentially as the
plasma ascorbic acid falls. Majno and Palade have shown that
toxic levels of histamine in the blood cause openings in the tight
junctions between the vascular endothelial cells, leading to
extravasation of blood. Leakage of blood into the tissue slowly
leads to local hemolysis, as evidenced by the yellow color
characteristic of the fluid of old subdural hematomas. Hemolysis
also leads to local ascorbate depletion.
Chatterjee et al. reported increased blood histamine levels
following vaccinations in guinea pigs. This effect would likely be
heightened when six vaccinations are given at the same time at 8
weeks of age, such as is now the custom in most English-speaking
countries. If vitamin C levels are low at the time of vaccination, a
resulting toxic histaminemia may cause further clinical problems.
Arelevant finding by Archie Kalokerinos is that the increased
death rate following vaccination of Aboriginal infants in Australia
was arrested by administering vitamin C at the time of
vaccination—because ascorbic acid “detoxifies” histamine.
Indeed, Chatterjee et al. demonstrated that ascorbic acid is
essential for the detoxification of histamine (in guinea pigs), by
converting it to hydantoin-5-acetic acid, and on to aspartic acid in
vivo. Illustrations of the physiology and pathology of ascorbic acid
and blood histamine have been presented previously.
Other factors that are not given sufficient weight in evaluations
for SBS are the presence of chronic subdural hematomas, often
occurring during or shortly after birth, and the fact that chronic
subdurals are susceptible to rebleeding. Subdural hematomas have
been found using fetal ultrasound in utero, before labor, as reported
by Gunn, and also following normal, spontaneous delivery, as
reported by Chamnavanaki et al. The tendency to rebleed could be
exacerbated by toxic histaminemia through the mechanisms
explained above.

More Research Needed

The effects of various vaccinations, given alone or together, on
whole blood histamine levels and plasma ascorbic acid levels,
should be further studied. Concerted research may increase our
understanding of the toxicity of different vaccines and the effects of
giving single versus multiple, simultaneously administered
vaccines. Their impact on vitamin C, histamine, and clinical
manifestations of deficiency/toxemia must be assessed. It should be
helpful to reduce the number of vaccines given simultaneously or in
rapid succession.
A better understanding of these factors may help prevent
adverse reactions following vaccinations. Dr. Kalokerinos has
shown a clear benefit by providing supplemental vitamin C at the
time of vaccination in some children. Vitamin C is an extremely
safe substance—the only ill effects tend to occur in older children
and adults who suffer from hemosiderosis due to sickle cell disease
or Mediterranean anemia. Iron storage depletes ascorbic acid stores
via oxidation and hydrolysis, and the dehydroascorbic acid so
formed can be harmful. Even then, the toxic effect of vitamin C
may only be mild and temporary in young infants.

Conclusions

The so-called “classic” findings of subdural hematoma and
retinal hemorrhages in infants, without any evidence of major
trauma, do not always automatically equate to a diagnosis of
SBS. As in all other areas of medicine, it is prudent to do a
differential diagnosis.
The findings in the cases that initially established SBS as a
diagnosis were compatible with and even suggestive of infantile
scurvy or toxic histaminemia.

C. Alan B. Clemetson, M.D., is Professor Emeritus, Tulane UniversitySchool of Medicine, New Orleans, La. He may be contacted by e-mail atmegcc2000@yahoo.com.

See Source For References and PDF

http://www.jpands.org/vol11no1/clemetson.pdf

Shaking Wrong Beliefs

By: Dr. F. Edward Yazbak

The medical controversies section of the recent issue of the Journal of American Physicians and Surgeons (1) features three outstanding articles on the more and more controversial subject of shaken baby syndrome (SBS).

Together, these papers contribute immensely to the understanding of this obscure syndrome by debunking assumptions that have been accepted for some time as “proof” of abuse of young and innocent infants:

• That subdural and retinal hemorrhages can only be due to severe shaking and, therefore, must be intentional;
• That the presence of a “fracture or fractures” in the ribs and long bones is “evidence” of inflicted trauma.

The papers are:

• “Shaken Baby Syndrome:” Do Confessions by Alleged Perpetrators Validate the Concept? by Jan E. Leestma, MD, MM. (2)
• Vaccines, Apparent Life-Threatening Events, Barlow’s Disease and Questions about “Shaken Baby Syndrome” by Michael D. Innis, MBBS. (3)
• Caffey Revisited: A Commentary on the Origin of “Shaken Baby Syndrome” by C. Alan B. Clemetson, MD. (4)

Jan Leestma is a former professor at the University of Chicago’s division of biological sciences and the Pritzker School of Medicine (pathology and neurology), and neuropathologist and associate medical director for the Chicago Institute of Neurosurgery and Neuroresearch,

Michael Innis is a hematologist and pathologist, former consultant hematologist at Princess Alexandra Hospital in Australia, and the director of Medisets International.

Alan Clemetson is a professor emeritus at Tulane University School of Medicine in New Orleans, Louisiana.

The credentials and qualifications of these distinguished authors are evidently impeccable.

* * * *

The Leestma paper

“The concept that a certain constellation of findings develops immediately after a baby is shaken, with no impact of the head, is based solely on confessions or admissions by alleged perpetrators”¦. A review of the literature reveals very few cases of admissions of “pure” shaking. Methodologic flaws preclude any definitive conclusions about causation from these cases”¦.

“The studies have been regarded by many as strong support for the theory of SBS. Of prime concern in these papers, however, is the basic issue of the value of a supposed confession in determining a mechanism for injury. With any confession or admission, there is the issue of veracity. Accused individuals are well known to fabricate historical information”¦.

“It should be apparent that from virtually every perspective many flaws exist in the theory that shaking is causative. No case studies have ever been undertaken to probe even a partial list of the potential causes”¦.

“The confessions or admissions of a perpetrator are at best tenuous support for the shaking mechanism for infantile head injury. A critical appraisal of any literature that proposes a causal mechanism of shaking for brain injury must include an investigation of case selection methodology, population or sample size, possible case control issues, data analysis methods, and whether the conclusions reached are justified by the data presented”¦.”

The Innis paper

“Apparent Life-Threatening Events (ALTE), as defined by the National Institutes of Health, encompass all the findings hitherto attributed to open “Shaken Baby Syndrome” (SBS), and may follow routine vaccination. Vaccines may also induce vitamin C deficiency (Barlow’s disease), especially in formula-fed infants or infants whose mothers smoke”¦.

“Shaken Baby Syndrome (SBS) is a collection of findings, not all of which may be present in any individual infant diagnosed to have the condition. Findings include intracranial hemorrhage, retinal hemorrhage, and fractures of the ribs and at the ends of long bones”¦.

“The National Institutes of Health, and its 1986 Health Consensus Development Conference on Infantile Apnea and Home Monitoring, defined “Apparent Life-Threatening Event (ALTE) as an episode that is frightening to the observer and is characterized by some combination of apnea (central or occasionally obstructive), color change (usually cyanotic or pallid but occasionally erythematous or plethoric), marked change in muscle tone (usually marked limpness), and choking and gagging. In some cases, the observer fears that the infant has died. ALTE is not so much a specific diagnosis as a description of an event”¦.

“The current concept of SBS includes intracranial bleeding, usually in the form of a subdural hematoma, which may be acute or chronic; parenchymal injury and/or anoxic changes in the brain; skull fracture (if impact occurred); and retinal hemorrhages. Constant features are subdural and retinal hemorrhages. Various fractures including those of the long bones and ribs are often used to support an impression of child abuse, but it should not be forgotten that Barlow’s disease can resemble “battered baby””¦.

“Animal experiments have demonstrated that administration of vitamin C can counter some of the ill effects of nicotine in newborns. This suggests that mothers who smoke may compromise vitamin C levels in their children”¦.

“One essential function of vitamin C is maintenance of normal connective tissue by the hydroxylation of praline and lysine in procollagen, using the enzyme prolyl hydoxylase with Vitamin C as a cofactor. While vitamin C has numerous other functions, this one maintains the integrity of the blood vessels, bones, and dentine, which is compromised in scurvy, leading to manifestations that might be mistaken for SBS.  Expansion at the ends of the costochondral junctions is highly suspicious for scurvy, and should in itself have raised questions about the diagnosis of SBS.

“Formula feedings are often heated before being given to the infant and heat destroys vitamin C.  Under such circumstances, vitamin C supplements are needed to prevent scurvy”¦.

“As part of the immune response to vaccines, mast cells liberate histamine, causing further widening of the intercellular spaces between the vascular endothelial cells in children who may have subclinical scurvy. Although it has not been established that vaccinations cause vitamin C deficiency, the inverse relationship between histamine and vitamin C levels in the blood would support the hypothesis that vaccinations could lead to vitamin C deficiency, and might explain spontaneous bleeding”¦.

“Post-immunization deaths in aboriginal children in Australia were greatly reduced when Kalokerinos administered vitamin C by IM injection before, and sometimes after, immunizing the child.  Many of these children had the classical signs and symptoms of scurvy.”

The Clemetson paper

“Caffey is often cited as the source of the diagnosis of “shaken baby syndrome” (SBS). Once that “classic” findings attributed to SBS are identified, it is rare for differential diagnosis to be considered”¦

“In 1946, John Caffey, a radiologist, described multiple fractures in the long bones of infants suffering from chronic subdural hematoma. None of the parents reported any knowledge of falls or physical injury, but Caffey suspected child abuse to explain the injuries.

“Following this retrospective, radiologic study by Caffey, the diagnosis of “shaken baby syndrome” (SBS – including retinal petechiae, multiple fractures of the long bones, and subdural hematomas) evolved and has resulted in many men and women being convicted of child abuse, all without any meaningful consideration of a differential diagnosis”¦.

“In addition to the long-bone fractures and subdural hematomas, other clinical signs consistent with infantile scurvy were evident in most of Caffey’s six cases”¦.

“Even with adequate dietary vitamin C intake, infections can rapidly deplete ascorbic acid stores and increase the blood histamine level”¦.

“Many factors affect vitamin C metabolism, but the most important is systemic infection. Hess, in his Cutter Lecture at Harvard Medical School, recognized that infection and vitamin C deficiency were both related to the development of infantile scurvy. It was a number of years, however, before he realized that each affected the other – vitamin C deficiency predisposes to infection, and infection predisposes to vitamin C deficiency. Blood levels of vitamin C are also inversely related to blood histamine levels”¦.

“The hypothesis that subdural hemorrhages, retinal petechiae, and spontaneous fractures of the ribs and long bones can occur as an early variant of scurvy at about 8 to 10 weeks of age has not been adequately studied, and, therefore, has not been disproven. Unless and until vitamin C and histamine levels are actually measured in these infants, who are automatically classified as victims of SBS, we will not know the truth about causation”¦.

The effects of various vaccinations, given alone or together, on whole blood histamine level and plasma ascorbic acid levels, should be further studied.  Concerted research may increase our understanding of the toxicity of different vaccines and the effects of giving single versus multiple, simultaneously administered vaccines. Their impact on vitamin C, histamine, and clinical manifestations of deficiency/toxemia must be assessed. It should be helpful to reduce the number of vaccines given simultaneously or in rapid succession.”

* * * *

In his paper, Leestma summarized the findings of his careful review of the extensive English-language medical literature on child abuse between 1969 and 2001, where he only found 54 cases in which someone had admitted “shaking” the injured infant. (5) In only 11 cases, there was no sign of cranial impact and the infant could have been “free-shaken.” Such a small number of cases obviously did not allow valid statistical analysis.

As mentioned in a previous column (6), a young, scared and disadvantaged parent can literally confess to anything “just to get it over with.” In any other criminal investigation, such “confessions” would not be worth the paper they are written on. In shaken baby trials, they effectively destroy families and put innocent adult caretakers in jail for years.

Innis strongly highlights lessons we should have learned in medical school:

• Take a good history
• Investigate judiciously
• Interpret findings correctly
• Consider all the possibilities in the differential diagnosis
• Reach the diagnosis carefully
• Treat appropriately

Without repeating his now famous challenge, Innis recommended that the diagnosis of SBS not be made until malnutrion, coagulation/hemostatic difficulties, liver dysfunction, gestational, delivery and neonatal factors, and recent vaccinations had been seriously reviewed and found to be non-contributory.

By carefully reviewing every one of Caffey’s original six cases, which had become the bases on which the theory of shaken baby syndrome was built, and by showing that most of them suggested vitamin C deficiency in one way or another, Clementson contributed immensely to the subject. With his very original approach to destroy the cornerstone, he may have brought the whole edifice down.

In a communication to the British Medical Journal on June 27, 2005, Innis said:

“A name change from “˜Shaken Baby Syndrome’ to “˜Kalokerinos-Clemetson Sydrome,’ when haemorrhages, fractures and intracranial lesions follow immunization within 28 days, should be the first step in stopping false allegations against innocent individuals.

“Both [Archie] Kalokerinos and Clemetson have for years been trying to educate the medical profession on the risks of vaccines to some children.

“The witch hunt will be over once the name is changed.”

I can safely add that if this happened, justice would be better served and so would science.

We not only should, we must, recommend that upon detecting retinal and subdural hemorrhages, with or without rib and long bone “fractures”, admitting physicians immediately order blood histamine and serum ascorbate levels, in addition to the usual bleeding and coagulation battery of tests, which should include a PIVKA II test and fibrinogen level, fibrin split products and D Dimer tests. Abnormalities in the liver and kidney function tests should be taken seriously and not discounted as so often happens.

A review of recent vaccinations is also essential. Accessing the VAERS web site is relatively easy and often very informative. Discounting the role of multiple vaccinations without investigating it properly has been evident for years; it should not be permitted any longer.

* * * *

The editor of the Journal of American Physicians and Surgeons should be complimented for publishing these three very important papers in the latest issue.

Reprints of the articles in bundles of 25 to 500 copies are available for those individuals and organizations who wish to distribute them. (7)

Conclusions

Three recent articles in the Journal of American Physicians and Surgeons have helped disperse much of the misinformation about shaken baby syndrome.

Histaminemia and vitamin C deficiency may be responsible for SBS and should be tested in every case in which such diagnosis is suspected.

The role of multiple recent vaccinations in SBS cases should be carefully evaluated before it is discounted.

The Kalokerinos-Clemetson Syndrome is a more appropriate label for cases that present with an apparent life-threatening event soon after vaccinations and where retinal and intracranial hemorrhages and long bones and rib “fractures” are identified.

References

1. The Journal of American Physicians and Surgeons, Vol. 11, No. 1, spring 2006 issue. Also available at http://www.jpands.org/
2. J.E. Leestma. Shaken Baby Syndrome”: Do Confessions by Alleged Perpetrators Validate the Concept? J Am Phys Surg. 2006; 11(1): 14-16.
   Also available at http://www.jpands.org/vol11no1/leestma.pdf
3. M.D. Innis. Vaccines, Apparent Life-Threatening Events, Barlow’s Disease, and Questions about “Shaken Baby Syndrome. J Am Phys Surg. 2006; 11(1): 17-19. Also available at http://www.jpands.org/vol11no1/innis.pdf
4. C.A.B. Clemetson. Caffey Revisited: A Commentary on the Origin of “Shaken Baby Syndrome” J Am Phys Surg. 2006; 11(1): 20-21. Also available at http://www.jpands.org/vol11no1/clemetson.pdf
5. J.E. Leestma. “Case analysis of brain-injured admittedly shaken infants: 54 cases, 1969-2001.” Am J Forensic Med Pathol. September 2005. 26(3): 199-212. Review.
6. F.E. Yazbak. Shaken Baby Syndrome: Pitfalls in Diagnosis and Demographics. Red Flags,February 2006. Available at  http://www.redflagsdaily.com/yazbak/2006_feb17.php
7. http://www.jpands.org/reprints.pdf; A+ Printing Co., 4500 East Speedway, Suite 41, Tucson, AZ 85712.

Source:

http://www.vaccinationnews.com/node/19951

F. Edward Yazbak, MD, FAAP

F. Edward Yazbak, MD, FAAP of Falmouth, Massachusetts, practiced pediatrics and was a school physician in Northern Rhode Island for 34 years. He was formerly the Assistant Clinical Director of the Charles V. Chapin Hospital, a specialized infectious disease hospital and the Director of Pediatrics at the Woonsocket Hospital in Rhode Island. He was also the Pediatric Director of the Child Development Study, the Brown University division of the NINDB Collaborative Study and an assistant member of the Institute of Health Sciences at the University.

Since 1998, Ed has devoted his time to researching vaccine injury and the increased incidence and autoimmune causes of regressive autism focusing on maternal re-vaccination with live viruses.

Ed has been recognized as an expert witness in autism, vaccine injury and Shaken Baby Syndrome litigation and has published extensively on those subjects.

Ed and Maureen, a pediatric nurse practitioner, have four children and twelve grandchildren. Their family like many others has been severely affected by autism.

Source:

http://yazbakarticles.wordpress.com/