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JOM        Volume 27, Number 3, 2012                                        Synthesis Paper                1



Malnutrition, Liver Dysfunction,
Subdural and Retinal Haemorrhages
and Encephalopathy in Children
Resulting from a Deficiency or
Abnormality of Vitamins C, D and K


Michael D. Innis, MBBS, DTM&H, FRCPA, FRCPath1,2
1. Retired Haematologist, Princess Alexandra Hospital, Brisbane
2. Wurtulla , Queensland, Australia 4575, Tel: 011-61-07-5493-2826, Email: micinnis@bigpond.com



Abstract Subdural and retinal haemorrhages, encephalopathy, bruises and fractures in children
have hitherto been attributed to shaken baby syndrome, non-accidental injury, abusive head trauma
or inflicted brain injury. The purpose of this investigation is to explore another possible explanation.
Since vitamin K and other nutrients are necessary for the integrity of both the coagulation of blood
and the mineralization of bone, and since a deficiency of this vitamin is known to cause haemor-
rhagic disease of the new born and fractures in children with cystic fibrosis and biliary atresia, it
seems appropriate to investigate the status of vitamin K and other essential nutrients in children
alleged to have suffered non-accidental injuries. It was found that all three children reported here
had a prolonged prothrombin time with evidence of liver dysfunction and malabsorption/malnu-
trition as shown by abnormality of the liver enzymes and a reduced level of serum albumin. It is
concluded that subdural and retinal haemorrhages, encephalopathy, bruises and fractures in children
which have hitherto been attributed to shaken baby syndrome, non-accidental injury, abusive head
trauma or inflicted brain injury may also be due to a metabolic disorder resulting from a deficiency
or abnormality of vitamin K and other essential nutrients such as vitamins C and D following
malnutrition/malabsorption or liver dysfunction.

Introduction                                           a violent impact of the skull against a hard
    In the mid 20th century following the              object was the most probable cause of this
publication of a report by an American radi-           type of fracture.4 The SBS became known as
ologist on fractures and haemorrhages in in-           “the shaken–impact syndrome.”
fants1 a neurosurgeon in England suggested                 Retinal haemorrhages seen in these chil-
that the cause of the lesions was violent shak-        dren were claimed to be conclusive proof of
ing of the infant by an adult2 and this claim          abuse and ophthalmologists added “acceler-
was echoed by the radiologist3 and given the           ation-deceleration of the head as it is vio-
name “shaken baby syndrome” (SBS).                     lently rotated by the abuser as the cause of
    When it was realized that skull fractures          the retinal hemorrhages.”5
could not be explained by shaking, a profes-               Throughout academia the current teach-
sor of paediatrics in England suggested that           ing is that it is the combined “triad” of sub-
2     Journal of Orthomolecular Medicine Vol 27, No 3, 2012




    dural and retinal haemorrhage with brain          1. Haemoglobin: decreased
    damage, as well as the characteristics of each    2. Prothrombin Time (PT): increased
    of these components that allow a recon-           3. Albumin: decreased
    struction of the mechanism of injury, and         4. Total protein: decreased
    assessment of the degree of force employed.       5. Aspartate aminotransferase (AST or SGOT):
    The application of rotational acceleration        increased
    and deceleration forces to the infant’s head      6. Alanine aminotransferase (ALT or SGPT):
    causes the brain to rotate in the skull. Abrupt   increased
    deceleration, it is claimed, allows continu-      7.Gamma-glutamyl transpeptidase (GTT):
    ing brain rotation until bridging veins are       increased
    stretched and ruptured, causing a thin layer
    of subdural haemorrhage on the surface of         Case #1
    the brain.6-17                                        The mother was found to be anaemic
         Maguire et al17 claim that their review,     and was prescribed iron therapy during her
    the largest of its kind, offers for the first     pregnancy. The infant was born by a normal
    time, a valid “statistical probability of in-     vaginal delivery and had Apgar scores of 9
    flicted brain injury” (IBI) when certain key      and 10. His birth weight was 8 lbs 15 oz. He
    factors are present.                              had a congenital right hydrocele.
         One of the “key factors” upon which
    they base their opinion, retinal haemor-              Laboratory investigations performed the
    rhages, is known to be associated with raised     day after birth showed:
    intracranial pressure from any cause as in        1. White blood count: 31.5 x 109/L (reference
    Terson’s syndrome18 and following vitamin         range: 4.0-10.8 x 109/L)
    K deficiency.19,20                                2. Lymphocytes: 6.6 x 109/L (reference range:
         Apnoea, also, is rated high in their list    0.7-4.2 x 109/L)
    of statistical markers of IBI and is claimed      3. Monocytes: 1.9 x 109/L (reference range:
    to be a crucial distinguishing feature. Ap-       0.5-0.8 x 109/L)
    noea is a feature of the condition known as       4. Basophils: 0.5 x 109/L (reference range: 0.0-
    an apparent life threatening event (ALTE),        0.2 x 109/L)
    which can be caused by prematurity, gas-          5. Granulocytes: 21.5 x 109/L (reference range:
    tro-oesophageal reflux, cardiac arrhythmia,       2.4-7.9 x 109/L)
    laryngomalacia, trachiomalacia, infection,        6. Eosinophils: 1.0 x 109/L (reference range:
    metabolic disorders and seizure and has been      0.0-0.7 x 109/L)
    reported by Ghosh et al as “Shaken baby
    syndrome masquerading as an apparent life              The infant was formula fed and his prog-
    threatening event.21 Bruises, rib, spinal and     ress appeared to be satisfactory. His weight
    limb fractures not “satisfactorily explained”     steadily increased to 16 lb 11oz at the age of
    have been attributed to physical abuse by         four months. There was, however, little or no
    the perpetrator, but Clemetson22 has shown        change in the lymphocytosis and monocyto-
    that the clinical findings “were compatible       sis which had been recorded at birth. Over
    with and even suggestive of infantile scurvy      the course of the next year the child suffered
    or toxic histaminaemia” and “bruises of the       several bouts of fever, cough and lethargy for
    thigh and even fractures of the femur have        which he was treated with antibiotics.
    been recorded as arising from the gentle act           At the age of two years his mother’s
    of diapering a scorbutic infant.”23               partner who was looking after him went to
         The following cases demonstrate the          prepare a bath and left the room. He heard
    clinical features of the metabolic disorder,      a thud and on returning to the room found
    which is invariably associated with some or       the child on the floor apnoeic and having a
    all of the following biochemical markers of       seizure. The EMS was called and when they
    malnutrition and/or liver disease:                arrived they found him listless and floppy.
Metabolic Disorders Involving Vitamins C, D and K      3



He was intubated and taken to the local              and vomiting. She was admitted to hospi-
hospital.                                            tal where a diagnosis of gastroenteritis was
    Physical examination showed he had               made, and she was treated and discharged
numerous bruises about the front of his neck         after a stay of three days.
and others scattered about his body. A com-              When six weeks old and being fed by
puterised tomography (CT) scan showed                the father she suddenly stopped breathing,
cerebral oedema consistent with cerebral             her eyes rolled back, her body stiffened and
anoxia and an ophthalmoscopic examina-               she became cyanosed. En route to hospital
tion showed bilateral retinal haemorrhages.          she was observed to have a seizure.
A skeletal X-Ray showed a metaphyseal                    A CT scan was read as negative. The in-
fracture of the left distal humerus and a            fant was discharged home after a stay of three
periosteal reaction of the left ulnar and left       days under observation. A diagnosis of seizure
scapular.                                            disorder and anaemia was made when her he-
                                                     moglobin level was found to be 8.4 g/dL.
Laboratory investigations showed:                        At 3 pm that same day she had another
1. PT: 18.7 seconds (reference range: 10.8-          seizure and was returned to hospital where
13.7 seconds)                                        it was found she was apnoeic, hypotonic and
2. INR:1.43 (reference range: 0.9-1.1)               unresponsive with a bulging anterior fon-
3. Haemoglobin: 11.0 g/dL (reference range:          tanel. She was immediately intubated and
13.4-16.7 g/dL)                                      oxygenated while other investigations were
4. Lymphocytes: 6.2 x 109/L (reference range:        carried out.
0.7-4.2 x 109/L)
5. Monocytes:0.9 x 109/L (reference range:           Laboratory investigations showed:
0.5-0.8 x 109/L)                                     1. PT: 20.0 seconds (reference range: 11-13
6. Granulocytes: 8.5 x 109/L (reference range:       seconds)
2.4-7.9 x 109/L)                                     2. APTT: 100.0 seconds (reference range: 25-
                                                     36 seconds)
    Toxic granulation and atypical lympho-           3. Fibrinogen: 34 mg/dL (reference range:
cytes present. The child died soon after ad-         200-400 mg/dL)
mission and his organs were harvested for            4. ALT: 107 U/L (reference range: 4-40 U/L)
donation. At the autopsy a small subdural            5. AST: 131 U/L (reference range: 5-40 U/L)
hematoma was found. Death was attributed             6. GGT: 143 U/L (reference range: 7-37 U/L)
to homicide.                                         7. Alkaline Phosphatase: 274 U/L (reference
                                                     range: 115-450 U/L)
Case #2                                              8. Calcium: 8.9 mg/dL (reference range:
     The 24-year-old mother had an unevent-          8-11 mg/dL)
ful pregnancy followed by premature rupture          9. Phosphorus: 2.0 mg/dL (reference range:
of the membranes, a temperature of 100°F,            4-6 mg/dL)	
oligohydramnios and failure of labour to             10. Albumin: 3.0 g/dL (reference range: 3.2-4.8)
progress. A caesarean section was performed
and an 8 lb 5 oz female infant was delivered             A CT Scan of the head showed “blood
and breathed and cried spontaneously. The            within the subarachnoid or subdural space
infant was initially breast fed and was given        consistent with recent head trauma.” A heal-
an injection of 1 mg vitamin K before being          ing fracture of the posterior seventh rib was
discharged home.                                     present. The child died shortly after admis-
     At home the baby was formula fed on             sion.
Enfamil by the father when the mother re-                The autopsy report noted the following:
turned to work. The infant’s progress was            A purple contusion and ecchymosis below
satisfactory until, at the age of three weeks,       the right ear, the scalp tissues were swol-
she suddenly developed a bout of diarrhoea           len and nine separate contusions were scat-
4     Journal of Orthomolecular Medicine Vol 27, No 3, 2012




    tered near the midline of the back; subdural        The mother called 911 and the child was ad-
    hemorrhages were present over both cere-            mitted to hospital where a cranial CT scan
    bral convexities and the brain diffusely and        showed a combination of acute subdural and
    symmetrically swollen; and a callus was seen        subaracnoid haemorrhage. Ophthalmoscope
    on the left eighth rib and the body of the          examination was not reported.
    vertebra T10 has a recent fracture without
    evidence of healing. The cause of death was         Laboratory investigations showed:
    attributed to blunt head trauma.                    1. PT: 19.1 seconds (reference range: 14.6-16.9
                                                        seconds)
    Case #3	                                            2. AST: 79 U/L (reference range: 15-37 U/L)
         The pregnancy was complicated by dis-          3. Serum protein: 5.2 g/dL (reference range:
    cordant growth of twins and the perinatolo-         5.4-7.0 g/dL)
    gist recommended the pregnancy be termi-
    nated at 32 weeks gestation.                        The child died shortly after admission. Death
         The neonatal record noted that the pre-        was attributed to non-accidental injury.
    sentation was vertex and the delivery nor-
    mal. The infant cried spontaneously, but was        Discussion
    “dusky” and was transferred to the neonatal              All three cases had an apparent life-
    intensive care unit where assisted respiration      threatening event (ALTE). One case had the
    was instituted and continued for several days.      classical “triad” of subdural and retinal haem-
    He was discharged after a stay of five weeks.       orrhages with encephalopathy, and all three
                                                        cases had the associated laboratory findings
    The discharge summary noted:                        of increased PT indicative of vitamin K de-
    1. Prematurity: 32-week small for gestational age   ficiency, anaemia indicative of vitamin D
    2.Respiratory distress: requiring additional        deficiency24 and reduced serum albumin in-
    oxygen therapy                                      dicative of a nutritional deficiency including
    3. Suspected sepsis                                 vitamin C deficiency. Increased AST signi-
    4. Necrotizing entrocolitis: associated with        fied disordered liver function. These are the
    bloody stools necessitating antibiotic thera-       essential clinical and laboratory features of
    py and a blood transfusion                          the metabolic disorder.
    5. Hyperbilirubinaemia                                   Vitamin K, a fat soluble vitamin, is a co-
    6. Feeding problems                                 factor for an enzymatic conversion of glu-
    7. Thrombocytopaenia                                tamic acid to gamma-carboxyglutamic acid
    8. Anaemia of prematurity                           by gamma-glutamyl-carboxylase, a process
                                                        essential for both the clotting of blood and
         Hepatitis B vaccine was administered           the mineralization of bone.25 Vitamin D,
    the day before his discharge. There was no          also a fat soluble vitamin, is necessary for the
    mention of him being given vitamin K either         stimulation of osteoblastic activity and the
    by mouth or by injection.                           formation of bone matrix while vitamin C is
         His progress appeared to be satisfactory       essential for the synthesis of collagen which
    and he was immunized with DTaP, Polio               is the principal component of the skin, blood
    (IPV), Hemophilus Influenza, and Prevnar.           vessels, bone matrix, dentine and a deficien-
    He developed thrush and was treated with            cy causes skin lesions, dental problems, frac-
    an oral medication. Following his vaccina-          tures and haemorrhages in scurvy.26
    tion, the parents noticed a change in that he            The level of vitamin C in the blood was
    appeared to be more irritable and the mother,       not determined in these children, but the
    thinking he was hungry, placed him down on          fact that there was evidence of malabsorp-
    a pillow and went to warm a bottle of milk          tion/malnutrition suggests that a deficiency
    for him. On returning she found him gasping         was possible.
    for breath and he was limp and unresponsive.             The subdural and retinal haemorrhages,
Metabolic Disorders Involving Vitamins C, D and K               5



encephalopathy, bruises and fractures in chil-        stating: “There is no evidence of cerebral
dren which have hitherto been attributed to           trauma or ‘Shaken Baby Syndrome’ despite
SBS, non-accidental injury, abusive head              the radiological and clinical findings of sub-
trauma or IBI are, it is suggested, the result        dural haemorrhage and retinal haemorrhag-
of a metabolic disorder involving essential           es.” Referring to the use of orthodox medical
nutrients including vitamins C, K and D.              evidence, at the retrial of a woman whose
     While the ALTE was the initial overt             life sentence was overturned having served
manifestation of the disorder it is clear that        three years for the alleged murder of a child
malabsorption and liver disease preceded              in her care, Lord Justice Toulson30 said: “To-
and caused the ALTE.                                  day’s orthodoxy may become tomorrow’s out
     In Case #1 the blood tests suggest con-          dated learning.”
genital infectious mononucleosis or cyto-
megalovirus infection. Either would account           Conclusion
for the severe coagulopathy precipitated by               The contemporary notions of retinal and
hepatic failure as shown by the alteration in         intracerebral haemorrhage being caused by
the PT, the serum protein level and liver en-         rotation and slamming  the head of the in-
zymes. Congenital infectious mononucleosis            fant against a hard object is not validated by
is known to be associated with other con-             science. When one considers the evidence of
genital defects,27 and this child had a con-          nutritional deficiencies and liver dysfunction
genital hydrocele.                                    in all three cases shown here, it is entirely
     The CT scan of the head showed evi-              conceivable that a metabolic disorder involv-
dence of cerebral oedema, and an ophthal-             ing vitamins C, K and D may be the main
moscopic examination showed retinal hae-              cause of the bruising, bleeding and fractures
morrhages together with a metaphyseal                 seen in these children.
fracture of the medial left distal humerus,
and a periosteal reaction of the left ulnar           Competing Interests
and left scapular mistakenly suggested non-               The author has given evidence for the
accidental injury to the attending physicians,        defence in courts in England, United States
whereas vitamin K and C deficiency would              of America and Australia, and has received
account for all the lesions.                          payment for these services
     In Case #2 the cause of the liver fail-
ure, as shown by the liver function tests, was        References
probably the result of the infection which            1.	 Caffey J: Multiple fractures in the long bones of
caused the diarrhoea and vomiting. Malnu-                 infants suffering from chronic subdural hemato-
                                                          ma. Am J Roentgenol, 1946; 56: 163-173.
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         rics, 2001; 108: 206-210.                                 26.	 Heird WC: Vitamin deficiencies and excesses. Nel-
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         the shaken baby syndrome: four types of inflicted              irishtimes.com/newspaper/ireland/2009/0717/
         brain injury predominate BMJ, 2004; 328: 766.                  1224250848594.html].
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Innis

  • 1. JOM Volume 27, Number 3, 2012 Synthesis Paper 1 Malnutrition, Liver Dysfunction, Subdural and Retinal Haemorrhages and Encephalopathy in Children Resulting from a Deficiency or Abnormality of Vitamins C, D and K Michael D. Innis, MBBS, DTM&H, FRCPA, FRCPath1,2 1. Retired Haematologist, Princess Alexandra Hospital, Brisbane 2. Wurtulla , Queensland, Australia 4575, Tel: 011-61-07-5493-2826, Email: micinnis@bigpond.com Abstract Subdural and retinal haemorrhages, encephalopathy, bruises and fractures in children have hitherto been attributed to shaken baby syndrome, non-accidental injury, abusive head trauma or inflicted brain injury. The purpose of this investigation is to explore another possible explanation. Since vitamin K and other nutrients are necessary for the integrity of both the coagulation of blood and the mineralization of bone, and since a deficiency of this vitamin is known to cause haemor- rhagic disease of the new born and fractures in children with cystic fibrosis and biliary atresia, it seems appropriate to investigate the status of vitamin K and other essential nutrients in children alleged to have suffered non-accidental injuries. It was found that all three children reported here had a prolonged prothrombin time with evidence of liver dysfunction and malabsorption/malnu- trition as shown by abnormality of the liver enzymes and a reduced level of serum albumin. It is concluded that subdural and retinal haemorrhages, encephalopathy, bruises and fractures in children which have hitherto been attributed to shaken baby syndrome, non-accidental injury, abusive head trauma or inflicted brain injury may also be due to a metabolic disorder resulting from a deficiency or abnormality of vitamin K and other essential nutrients such as vitamins C and D following malnutrition/malabsorption or liver dysfunction. Introduction a violent impact of the skull against a hard In the mid 20th century following the object was the most probable cause of this publication of a report by an American radi- type of fracture.4 The SBS became known as ologist on fractures and haemorrhages in in- “the shaken–impact syndrome.” fants1 a neurosurgeon in England suggested Retinal haemorrhages seen in these chil- that the cause of the lesions was violent shak- dren were claimed to be conclusive proof of ing of the infant by an adult2 and this claim abuse and ophthalmologists added “acceler- was echoed by the radiologist3 and given the ation-deceleration of the head as it is vio- name “shaken baby syndrome” (SBS). lently rotated by the abuser as the cause of When it was realized that skull fractures the retinal hemorrhages.”5 could not be explained by shaking, a profes- Throughout academia the current teach- sor of paediatrics in England suggested that ing is that it is the combined “triad” of sub-
  • 2. 2 Journal of Orthomolecular Medicine Vol 27, No 3, 2012 dural and retinal haemorrhage with brain 1. Haemoglobin: decreased damage, as well as the characteristics of each 2. Prothrombin Time (PT): increased of these components that allow a recon- 3. Albumin: decreased struction of the mechanism of injury, and 4. Total protein: decreased assessment of the degree of force employed. 5. Aspartate aminotransferase (AST or SGOT): The application of rotational acceleration increased and deceleration forces to the infant’s head 6. Alanine aminotransferase (ALT or SGPT): causes the brain to rotate in the skull. Abrupt increased deceleration, it is claimed, allows continu- 7.Gamma-glutamyl transpeptidase (GTT): ing brain rotation until bridging veins are increased stretched and ruptured, causing a thin layer of subdural haemorrhage on the surface of Case #1 the brain.6-17 The mother was found to be anaemic Maguire et al17 claim that their review, and was prescribed iron therapy during her the largest of its kind, offers for the first pregnancy. The infant was born by a normal time, a valid “statistical probability of in- vaginal delivery and had Apgar scores of 9 flicted brain injury” (IBI) when certain key and 10. His birth weight was 8 lbs 15 oz. He factors are present. had a congenital right hydrocele. One of the “key factors” upon which they base their opinion, retinal haemor- Laboratory investigations performed the rhages, is known to be associated with raised day after birth showed: intracranial pressure from any cause as in 1. White blood count: 31.5 x 109/L (reference Terson’s syndrome18 and following vitamin range: 4.0-10.8 x 109/L) K deficiency.19,20 2. Lymphocytes: 6.6 x 109/L (reference range: Apnoea, also, is rated high in their list 0.7-4.2 x 109/L) of statistical markers of IBI and is claimed 3. Monocytes: 1.9 x 109/L (reference range: to be a crucial distinguishing feature. Ap- 0.5-0.8 x 109/L) noea is a feature of the condition known as 4. Basophils: 0.5 x 109/L (reference range: 0.0- an apparent life threatening event (ALTE), 0.2 x 109/L) which can be caused by prematurity, gas- 5. Granulocytes: 21.5 x 109/L (reference range: tro-oesophageal reflux, cardiac arrhythmia, 2.4-7.9 x 109/L) laryngomalacia, trachiomalacia, infection, 6. Eosinophils: 1.0 x 109/L (reference range: metabolic disorders and seizure and has been 0.0-0.7 x 109/L) reported by Ghosh et al as “Shaken baby syndrome masquerading as an apparent life The infant was formula fed and his prog- threatening event.21 Bruises, rib, spinal and ress appeared to be satisfactory. His weight limb fractures not “satisfactorily explained” steadily increased to 16 lb 11oz at the age of have been attributed to physical abuse by four months. There was, however, little or no the perpetrator, but Clemetson22 has shown change in the lymphocytosis and monocyto- that the clinical findings “were compatible sis which had been recorded at birth. Over with and even suggestive of infantile scurvy the course of the next year the child suffered or toxic histaminaemia” and “bruises of the several bouts of fever, cough and lethargy for thigh and even fractures of the femur have which he was treated with antibiotics. been recorded as arising from the gentle act At the age of two years his mother’s of diapering a scorbutic infant.”23 partner who was looking after him went to The following cases demonstrate the prepare a bath and left the room. He heard clinical features of the metabolic disorder, a thud and on returning to the room found which is invariably associated with some or the child on the floor apnoeic and having a all of the following biochemical markers of seizure. The EMS was called and when they malnutrition and/or liver disease: arrived they found him listless and floppy.
  • 3. Metabolic Disorders Involving Vitamins C, D and K 3 He was intubated and taken to the local and vomiting. She was admitted to hospi- hospital. tal where a diagnosis of gastroenteritis was Physical examination showed he had made, and she was treated and discharged numerous bruises about the front of his neck after a stay of three days. and others scattered about his body. A com- When six weeks old and being fed by puterised tomography (CT) scan showed the father she suddenly stopped breathing, cerebral oedema consistent with cerebral her eyes rolled back, her body stiffened and anoxia and an ophthalmoscopic examina- she became cyanosed. En route to hospital tion showed bilateral retinal haemorrhages. she was observed to have a seizure. A skeletal X-Ray showed a metaphyseal A CT scan was read as negative. The in- fracture of the left distal humerus and a fant was discharged home after a stay of three periosteal reaction of the left ulnar and left days under observation. A diagnosis of seizure scapular. disorder and anaemia was made when her he- moglobin level was found to be 8.4 g/dL. Laboratory investigations showed: At 3 pm that same day she had another 1. PT: 18.7 seconds (reference range: 10.8- seizure and was returned to hospital where 13.7 seconds) it was found she was apnoeic, hypotonic and 2. INR:1.43 (reference range: 0.9-1.1) unresponsive with a bulging anterior fon- 3. Haemoglobin: 11.0 g/dL (reference range: tanel. She was immediately intubated and 13.4-16.7 g/dL) oxygenated while other investigations were 4. Lymphocytes: 6.2 x 109/L (reference range: carried out. 0.7-4.2 x 109/L) 5. Monocytes:0.9 x 109/L (reference range: Laboratory investigations showed: 0.5-0.8 x 109/L) 1. PT: 20.0 seconds (reference range: 11-13 6. Granulocytes: 8.5 x 109/L (reference range: seconds) 2.4-7.9 x 109/L) 2. APTT: 100.0 seconds (reference range: 25- 36 seconds) Toxic granulation and atypical lympho- 3. Fibrinogen: 34 mg/dL (reference range: cytes present. The child died soon after ad- 200-400 mg/dL) mission and his organs were harvested for 4. ALT: 107 U/L (reference range: 4-40 U/L) donation. At the autopsy a small subdural 5. AST: 131 U/L (reference range: 5-40 U/L) hematoma was found. Death was attributed 6. GGT: 143 U/L (reference range: 7-37 U/L) to homicide. 7. Alkaline Phosphatase: 274 U/L (reference range: 115-450 U/L) Case #2 8. Calcium: 8.9 mg/dL (reference range: The 24-year-old mother had an unevent- 8-11 mg/dL) ful pregnancy followed by premature rupture 9. Phosphorus: 2.0 mg/dL (reference range: of the membranes, a temperature of 100°F, 4-6 mg/dL) oligohydramnios and failure of labour to 10. Albumin: 3.0 g/dL (reference range: 3.2-4.8) progress. A caesarean section was performed and an 8 lb 5 oz female infant was delivered A CT Scan of the head showed “blood and breathed and cried spontaneously. The within the subarachnoid or subdural space infant was initially breast fed and was given consistent with recent head trauma.” A heal- an injection of 1 mg vitamin K before being ing fracture of the posterior seventh rib was discharged home. present. The child died shortly after admis- At home the baby was formula fed on sion. Enfamil by the father when the mother re- The autopsy report noted the following: turned to work. The infant’s progress was A purple contusion and ecchymosis below satisfactory until, at the age of three weeks, the right ear, the scalp tissues were swol- she suddenly developed a bout of diarrhoea len and nine separate contusions were scat-
  • 4. 4 Journal of Orthomolecular Medicine Vol 27, No 3, 2012 tered near the midline of the back; subdural The mother called 911 and the child was ad- hemorrhages were present over both cere- mitted to hospital where a cranial CT scan bral convexities and the brain diffusely and showed a combination of acute subdural and symmetrically swollen; and a callus was seen subaracnoid haemorrhage. Ophthalmoscope on the left eighth rib and the body of the examination was not reported. vertebra T10 has a recent fracture without evidence of healing. The cause of death was Laboratory investigations showed: attributed to blunt head trauma. 1. PT: 19.1 seconds (reference range: 14.6-16.9 seconds) Case #3 2. AST: 79 U/L (reference range: 15-37 U/L) The pregnancy was complicated by dis- 3. Serum protein: 5.2 g/dL (reference range: cordant growth of twins and the perinatolo- 5.4-7.0 g/dL) gist recommended the pregnancy be termi- nated at 32 weeks gestation. The child died shortly after admission. Death The neonatal record noted that the pre- was attributed to non-accidental injury. sentation was vertex and the delivery nor- mal. The infant cried spontaneously, but was Discussion “dusky” and was transferred to the neonatal All three cases had an apparent life- intensive care unit where assisted respiration threatening event (ALTE). One case had the was instituted and continued for several days. classical “triad” of subdural and retinal haem- He was discharged after a stay of five weeks. orrhages with encephalopathy, and all three cases had the associated laboratory findings The discharge summary noted: of increased PT indicative of vitamin K de- 1. Prematurity: 32-week small for gestational age ficiency, anaemia indicative of vitamin D 2.Respiratory distress: requiring additional deficiency24 and reduced serum albumin in- oxygen therapy dicative of a nutritional deficiency including 3. Suspected sepsis vitamin C deficiency. Increased AST signi- 4. Necrotizing entrocolitis: associated with fied disordered liver function. These are the bloody stools necessitating antibiotic thera- essential clinical and laboratory features of py and a blood transfusion the metabolic disorder. 5. Hyperbilirubinaemia Vitamin K, a fat soluble vitamin, is a co- 6. Feeding problems factor for an enzymatic conversion of glu- 7. Thrombocytopaenia tamic acid to gamma-carboxyglutamic acid 8. Anaemia of prematurity by gamma-glutamyl-carboxylase, a process essential for both the clotting of blood and Hepatitis B vaccine was administered the mineralization of bone.25 Vitamin D, the day before his discharge. There was no also a fat soluble vitamin, is necessary for the mention of him being given vitamin K either stimulation of osteoblastic activity and the by mouth or by injection. formation of bone matrix while vitamin C is His progress appeared to be satisfactory essential for the synthesis of collagen which and he was immunized with DTaP, Polio is the principal component of the skin, blood (IPV), Hemophilus Influenza, and Prevnar. vessels, bone matrix, dentine and a deficien- He developed thrush and was treated with cy causes skin lesions, dental problems, frac- an oral medication. Following his vaccina- tures and haemorrhages in scurvy.26 tion, the parents noticed a change in that he The level of vitamin C in the blood was appeared to be more irritable and the mother, not determined in these children, but the thinking he was hungry, placed him down on fact that there was evidence of malabsorp- a pillow and went to warm a bottle of milk tion/malnutrition suggests that a deficiency for him. On returning she found him gasping was possible. for breath and he was limp and unresponsive. The subdural and retinal haemorrhages,
  • 5. Metabolic Disorders Involving Vitamins C, D and K 5 encephalopathy, bruises and fractures in chil- stating: “There is no evidence of cerebral dren which have hitherto been attributed to trauma or ‘Shaken Baby Syndrome’ despite SBS, non-accidental injury, abusive head the radiological and clinical findings of sub- trauma or IBI are, it is suggested, the result dural haemorrhage and retinal haemorrhag- of a metabolic disorder involving essential es.” Referring to the use of orthodox medical nutrients including vitamins C, K and D. evidence, at the retrial of a woman whose While the ALTE was the initial overt life sentence was overturned having served manifestation of the disorder it is clear that three years for the alleged murder of a child malabsorption and liver disease preceded in her care, Lord Justice Toulson30 said: “To- and caused the ALTE. day’s orthodoxy may become tomorrow’s out In Case #1 the blood tests suggest con- dated learning.” genital infectious mononucleosis or cyto- megalovirus infection. Either would account Conclusion for the severe coagulopathy precipitated by The contemporary notions of retinal and hepatic failure as shown by the alteration in intracerebral haemorrhage being caused by the PT, the serum protein level and liver en- rotation and slamming  the head of the in- zymes. Congenital infectious mononucleosis fant against a hard object is not validated by is known to be associated with other con- science. When one considers the evidence of genital defects,27 and this child had a con- nutritional deficiencies and liver dysfunction genital hydrocele. in all three cases shown here, it is entirely The CT scan of the head showed evi- conceivable that a metabolic disorder involv- dence of cerebral oedema, and an ophthal- ing vitamins C, K and D may be the main moscopic examination showed retinal hae- cause of the bruising, bleeding and fractures morrhages together with a metaphyseal seen in these children. fracture of the medial left distal humerus, and a periosteal reaction of the left ulnar Competing Interests and left scapular mistakenly suggested non- The author has given evidence for the accidental injury to the attending physicians, defence in courts in England, United States whereas vitamin K and C deficiency would of America and Australia, and has received account for all the lesions. payment for these services In Case #2 the cause of the liver fail- ure, as shown by the liver function tests, was References probably the result of the infection which 1. Caffey J: Multiple fractures in the long bones of caused the diarrhoea and vomiting. Malnu- infants suffering from chronic subdural hemato- ma. Am J Roentgenol, 1946; 56: 163-173. trition is evidenced by the reduced levels of 2. Guthkelch AN: Infantile subdural haematoma calcium, phosphorus and albumin. and its relationship to whiplash injuries. Br Med In Case #3 immaturity of the liver from J, 1971; 2: 430-431. premature birth was most likely the event 3. Caffey J: The whiplash shaken infant syndrome: which initiated the metabolic disorder, but manual shaking by the extremities with whiplash- induced intracranial and intraocular bleedings, there is also the possibility that his vaccina- linked with residual permanent brain damage and tion may have contributed to the metabolic mental retardation. Pediatrics, 1974; 54: 396-403. disorder as reported by Kalokerinos.28 4. David TJ: Shaken baby (shaken impact) syn- In the light of what is now known, the drome: non-accidental injury in infancy. J R Soc diagnoses SBS, abusive head trauma, IBI or Med, 1999; 92: 556-561. 5. Adams G, Ainsworth J, Butler L, et al: Update non-accidental head trauma, are unaccept- from the ophthalmology child abuse working able if nutritional deficiencies have not spe- party: royal college ophthalmologists. Eye, 2004; cifically been excluded. 18: 795-798. In a recent case the Dublin city coro- 6. American Academy of Pediatrics: Committee on ner,29 ignoring the opinions of the specialists Child Abuse and Neglect. Shaken baby syndrome: rotational cranial injuries-technical report. Pediat- involved, recorded death by natural causes
  • 6. 6 Journal of Orthomolecular Medicine Vol 27, No 3, 2012 rics, 2001; 108: 206-210. 26. Heird WC: Vitamin deficiencies and excesses. Nel- 7. Hoskote A, Richards P, Anslow P, et al: Subdural son Textbook of Pediatrics. 17th ed. In. eds. Behrman haematoma and non-accidental injury in children. RE, Kliegman RM, Jenson HB Philadelphia, PA. Child’s Nerv Syst, 2002; 18: 311-317. W.B. Saunders Company. 2004;177-190. 8. Duhaime AC, Christian CW, Rorke LB, et al: 27. Goldberg  GN, Fulginiti  VA, Ray  CG, et al: In Non-accidental head injury in infants – the utero Epstein-Barr virus (infectious mononucleo- shaken baby syndrome. N Engl J Med, 1998; 338: sis) infection.  JAMA, 1981;246:1579–1581. 1822-1829. 28. Kalokerinos A: Every Second Child. New Canaan, 9. Joint Statement on Shaken Baby Syndrome. Pae- CT. Keats Publishing, Inc. 1981. diatr Child Health, 2001;6:663-667. 29. Duncan P: Parents given apology over their baby’s 10. Minns RA, Busuttil A: Patterns of presentation of death. Irishtimes, 2009;July 7. Retrieved from:[www. the shaken baby syndrome: four types of inflicted irishtimes.com/newspaper/ireland/2009/0717/ brain injury predominate BMJ, 2004; 328: 766.  1224250848594.html]. 11. Harding B, Risdon RA, Krous HF: Shaken baby 30. Lewis P, Dodd V: Babysitter freed from jail after syndrome. BMJ, 2004; 328: 720-721. court orders retrial on murder charge. The Guard- 12. Green MA: A practical approach to suspicious ian, 2008; May 2. Retrieved from: [www.guard- death in infancy – a personal view. J Clin Pathol, ian.co.uk/uk/2008/may/02/ukcrime.law]. 1998; 51: 561-563. 13. Reece RM: The evidence base for shaken baby syndrome: Response to editorial from 106 doc- tors. BMJ, 2004; 328: 1316-1317. 14. Alexander RC, Sato Y, Smith W, et al: Incidence of impact trauma with cranial injuries ascribed to shaking. Am J Dis Child, 1990; 144: 724-726 15. Protocol for the investigation of sudden and un- expected deaths in children under 2 years of age [Memorandum No 631].Ontario, Canada. Minis- try of the Solicitor General and Correctional Services. 1995. 16. Kempe CH, Silverman FN, Steele BF, et al: The battered child syndrome. JAMA, 1962; 181: 17- 24. 17. Maguire S, Pickerd N, Farewell D, et al: Which clinical features distinguish inflicted from non- inflicted brain injury? A systematic review. Arch Dis Child, 2009; 94: 860-867. 18. Terson LL: Lesions of the fundus associated with brain hemorrhage. Arch Neural Psychiatry, 1939; 42: 664. 19. Rutty GN, Smith CM, Malia RG.: Late form hemorrhaagic disease of the newborn. A fatal case report with illustrations of investigations that may assist in avoiding the mistaken diagnosis of child abuse. Amer J Forensic Med Pathol, 1999; 20: 48-51. 20. Innis MD. Vitamin K deficiency disease. J Or- thomol Med, 2008; 23: 15-20. 21. Ray M, Ghosh D, Malhi P,et al: Shaken baby syn- drome masquerading as apparent life threatening event. Indian J Pediatr, 2005; 72: 85. 22. Clemetson CAB: Caffey revisited. A Commen- tary on the origin of “Shaken Baby Syndrome.” JPandS, 2006; 11: 20-21. 23. Clemetson CAB: Vitamin C, (Volume I of 3-vol- ume set). Boca Raton, Florida. CRC Press. 1989; 215-221. 24. Wharton BA, Bishop NJ: Rickets seminar. Lancet, 2003; 362: 1389-1400. 25. Vermeer C, Knapen MHJ, Schurgers LJ: Vitamin K and metabolic bone disease. J Clin Path, 1998; 51: 424-426.