Harold Buttram, MD
Review of the medical-legal issues surrounding court cases of shaken baby syndrome (SBS) reveals that courts frequently rule against defendants based upon a diagnostic triad consisting of (1) retinal hemorrhages, (2) subdural hemorrhages, and (3) diffuse axonal injury. This triad has been conventionally accepted as exclusively diagnostic of SBS. Skeletal fractures, and external bruises, when present, are also used as supportive evidence. However, a significant body of medical literature, largely by pathologists and specialists in the United States and the United Kingdom, suggests that these conditions can, and frequently do, arise from a number of other sources. This evidence is reviewed elsewhere on this website.
There is growing awareness among professionals that many SBS court cases have been based upon superficial diagnostic investigation, resulting in what many believe to be misdiagnoses and, consequently, false accusations and convictions. In my experience, most misdiagnosis occurs due to inadequate investigation in three areas:
(1) subclinical scurvy,
(2) bleeding disorders due to deficiencies in clotting factors (vitamin K, clotting factors II, VII, IX, and X),
(3) brittle bone disease, temporary brittle bone disease, and other conditions wherein spontaneous fractures can occur.
To provide example of the blatant inadequacy of screening and testing in SBS cases in general, a list of the possible diagnoses/contributory causes of death (other than the conventional triad noted above) in the case of baby Alan Yurko has been compiled from reviews of the case by many professionals: autoimmune hemolytic anemia, global malnutrition, retarded development, failure to thrive, subclinical scurvy, rickets, temporary brittle bone disease, vaccine-induced encephalopathy with secondary cerebral edema, brain hemorrhages (I believe this was the primary cause of death but could not prove it), pneumonia, meningitis, hemorrhagic disease of the newborn.
In order to prevent future medical/legal travesty, there is a most urgent need to establish a panel of diagnostic screening tests that, in my opinion, should be made mandatory before entertaining a diagnosis of shaken baby syndrome. Tests corresponding to the three areas listed above will serve as examples:
(1) To rule out subclinical scurvy: plasma ascorbate and serum histamine.
Comment: Contrary to general opinion, vitamin C deficiency is still quite common in the Western World. For example, among people attending a Health Maintenance Organization (HMO) clinic in Tempe, Arizona in 1998, plasma vitamin C was depleted in 30% of cases to between 0.2 and 0.5 mg/100 ml, and below 0.2 mg/100 ml in 6% of cases.1 (If an apparently healthy adult population was deficient, how much more so would be infants with multiple complications, such as prematurity and feeding problems, or those from complicated pregnancies?)1 Based upon both older literature on classical scurvy and more recent publications, we know that vitamin C is necessary for production and maintenance of connective tissue,2 that bleeding from capillaries and spontaneous fractures are characteristic of classical scurvy,3-5 and that subperiosteal bleeding is a common, if not the most common, site of scorbutic bleeding.3-5
The prevalence of subclinical scurvy in at least one population, that of Australian Aborigines, has been well documented by Australian physician, Archivides Kalokerinos.6 It is known that blood leukocyte ascorbic acid concentration is reduced by infection. Even the common cold causes a fifty per cent reduction of the leukocyte ascorbic acid concentration within 24 hours.7 Thus, we see a possible relationship between vaccines and the inducing of subclinical scurvy.
histamine concentration begins to rise when
the plasma ascorbic acid level falls below
normal (1mg/100 ml), and rises exponentially
when it falls below 0.7 mg/100 ml.8 When the
human plasma ascorbic acid level falls below
0.2 mg/100 ml, the whole-blood histamine level
is doubled or quadrupled.8 The whole-blood
(2) To rule out bleeding diatheses due to clotting factor deficiencies (deficiencies in vitamin K, coagulation factors II, VII, IX, and X): prothrombin time, thromboplastin time, fibrinogen level, platelet count, and D dimer test.
Comment: In a medical review of the Alan Yurko case, Michael Innis, MD, Honorary Consultant Haematologist, Princess Alexandra Hospital, Brisbane, Australia, made the following the following observations, most of which are consistent with the particulars of many other shaken-baby cases reviewed by me and others in this field:
“Alan Yurko, DOB September 16, 1997, died 29 November;
“Significant early history:
1. Mother unwell during pregnancy with gestational diabetes and anorexia. Nutritional supplements of vitamins not fully augmented.
2. Infant born after 35 weeks gestation and kept under observation for a week after birth because of respiratory distress. Was placed in an oxyhood and given Ampicillin and Gentamycin.
3. Nose bleed observed by mother and reported to doctor.
“This history is important because a nose bleed alerts a Haematologist to urgently consider the possibility of a Haemorrhagic Disorder occurring in a Newborn and would prompt an immediate investigation of:
1. The prothrombin time
2. The platelet count
3. The fibrinogen level
4. The D Dimer test”
Based on the history of nose bleed and on laboratory tests on baby Alan which confirmed significant liver failure and malnutrition, Dr. Innis made the following statements:
“The low levels of Total Protein, of Albumin, Creatinine and of Cholesterol are frequently seen in malnutrition and malabsorption. Prematurity, respiratory infection, for which the child was given antibiotic therapy, and the prolonged and repeated episodes of apnoea are factors to be considered in liver failure. . .
“The liver is the major site of synthesis of all the coagulation factors, with the exception of Factor VIII. Some of the factors require Vitamin K before they function adequately. Any condition which causes damage to the Liver will affect the coagulation system by interfering with the interaction between Vitamin K and the coagulation factors II, VII, IX, and X. The administration of Vitamin K does not correct the coagulation defect when the liver is severely damaged.10
“Factor XIII does not require Vitamin K but it is particularly susceptible to inactivation by certain drugs of which Penicillin is one.11 (The infant was given ampicillin.) Factor XIII deficiency may be congenital and there is a higher incidence of intracranial haemorrhage than in other inherited bleeding disorders.12 Acquired deficiency of Factor XIII has been demonstrated in subjects with liver disease.”
Laboratory tests done on baby Alan did show elevated prothrombin time, high fibrin split products, an elevated platelet count, and an elevated D dimer test, all of which Dr. Innis interpreted as consistent with liver failure and a serious disorder of the coagulation system.13 Cause of Death was listed as follows:
“Intracranial Haemorrhage and a Bleeding Diathesis following a Coagulopathy resulting from Failure of the Liver to synthesize functional Clotting Factors in adequate amounts.”
(3) When there are fractures, to rule out temporary brittle bone disease: bone densitometry.
Comment: X-rays commonly appear normal in these cases.14,15 Again, plasma ascorbate and serum histamine should be done to rule out spontaneous fractures from subclinical scurvy. Other metabolic causes of weakened bone, such as classical brittle bone disease and rickets, should be also be considered and evaluated.16, 17
Obviously, the panel does not include tests
for vaccine reactions. As noted earlier, no
suitable post-licensing diagnostic protocol
for vaccine reactions has ever been officially
established. There is no basic science in
this area worthy of the name, and this seems
to be no accident, based upon my experiences
at court hearings. There are two important
These tests would hold up in court, which is why an iron curtain of official resistance surrounds them. In my opinion also, within a reasonable degree of medical certainty, vaccines and vaccine reactions very frequently trigger subclinical scurvy and its complications, as well as bleeding complications from deficiencies of clotting factors. Based upon what we can only imagine the post-vaccinal suffering of that small life to exemplify, not to mention the misery his loving family endured, professionals with even the slightest sense of responsibility must not relent in insistence upon measures to prevent such tragedy.
Caveat: The suggested panel is not intended to be comprehensive, but only a starting point for screening purposes where child abuse is suspected. Changes and/or additions are likely as we learn more about these areas. Any further pertinent information will be added to this article.
1. Johnston, CS and MS Thompson. 1998. Vitamin C status of an out-patient population. J. Amer. Col. Nutr. 17:366-370.
2. Stone, N. and A. Meister. 1962. Function of ascorbic acid in the conversion of proline to collagen hydroxyproline. Nature 194:555.
3. Gilman, BB and RC Tanzer. 1932. Subdural hematoma in infantile scurvy. JAMA 99(12):989-991.
4. Hess, AF. Scurvy, Past and Present. 1920. Philadelphia: J. B. Lippincott Co.
5. Behrman, RE, RM Kliegman and HB Jenson, eds. 2000. Nelson Textbook of Pediatrics, 16th Edition. pp 182-183. Philadelphia: W. B. Saunders Company.
6. Kalokerinos, A. 1974. Every Second Child, Australia: Thomas Nelson Limited. (Note: In the 1970s Dr. Kalokerinos made a major contribution to medicine by proving that post-vaccinal death of Aboriginal babies (nearly 50% in some geographic areas), especially if colds or respiratory infections were present, was caused by vaccinal aggravation of a condition he diagnosed as “subclinical scurvy.” By improving diets, giving vitamin Csupplements, and avoiding vaccines during minor respiratory infections, infant deaths in his health district were nearly abolished.
7. Hume R., and E. Weyers. 1973. Changes in the leukocyte ascorbic acid concentration during the common cold. Scot. Med. J. 18:3.
8. Clemetson, CAB. Histamine and ascorbic acid in human blood. 1980. J. Nutr. 110:662-668.
9. Chatterjee, IB, AK Majunder, BK Nandi et al. 1975. Synthesis and some major functions of vitamin C in animals Ann. NY Acad. Sci. 258:24-47.
10. Williams, WJ, E. Beutler, AJ Erslev, and MA Lichman. 2001. Hematology Sixth Edition, pp 1511, 1673. New York: McGraw Hill Publishing Company.
11. Ibid. p 1591.
12. Ibid. p 1629.
13. Innis, MD. 1997. Clinical problem solving – the role of expert laboratory systems. Med. Inform. 22:251-262.
14. Miller, ME. 1999. Temporary brittle bone disease, a true entity? Seminars in Perinatology 23:174-182.
15. Miller, ME and TN Hangartner. 1999. Temporary brittle bone disease associated with decreased fetal movement and osteopenia. Calcified Tissue Intl. 64:137-143.
16. Hiller, HG. 1972. Battered or not – a reappraisal of metaphyseal fragility. Amer. J. Roentgenology,
Radiotherapy & Nuclear Medicine 114:241-246.
17. Behrman, RE et al, eds. (Ref #5) pp 184-187 (rickets), and pp 2128-2130 (brittle bone disease).
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