Available for Review
Summary Review of Maternal Prenatal Timeline of Events and Observations
As reported during a phone interview with the mother, she reported that she had had intractable nausea and vomiting during the first trimester of her pregnancy during which she lost 10 lbs, but did subsequently gain 40 lbs in the latter two trimesters.
Hospital Labor, Delivery, and Newborn Records,
This was the mother’s first pregnancy, with birth at 40.2 weeks gestation. She was 31 years old. Her blood type was O positive.
Uncomplicated delivery was accomplished with pitocin drip augmentation and epidural anesthesia. The mother was also given 2 grams of intravenous ampicillin. Birth took place with nuchal arm presentation (arm came out adjacent to neck).
By phone consultation with the mother, she reported that her perineum “ripped” as the baby’s head emerged (in spite of a preceding episiotomy.)
The baby’s weight was 7 lbs and 10 ozs (75 percentile), length 51.0 cm (75 percentile), head circumference 36.0 cm (95 percentile). APGARS were 9/9. Newborn P.E. was normal.
Hepatitis B vaccine was administered on day-of-birth. (NOTE: On the next day, Feb. 17th, according to mother’s notes, Amanda was brought in to her from the nursery screaming, as “she was bothering the other babies in the nursery,” suggestive of an encephalalitic reaction to the hepatitis B vaccine, something rarely recognized for its true nature. There was no note of vitamin K administration in the records.)
Routine newborn screening blood tests were acceptable, as were CBCs. Bilirubin levels reached a peak of 13.95 on February 18th and dropped to 12.18 on the 19th. On
Hearing test was “nonpass” for the right ear on initial testing but was “pass” with repeat testing.
The baby was placed on combination of breast and formula feedings. At times mother had to pump her milk, as the baby was having difficulty in sucking, (a problem which continued following hospital discharge).
Amanda was discharged with her mother on
Pediatric Outpatient Visits, Westshore Primary Care Associates
The following vaccines were administered:
DTaP, Aventis Pasteur, lot # C2554AA.
Comvax, Merck, lot # 1415F (Hib and Hep B).
IPV, Aventis Pasteur, lot # 20547.
Rotateq, Merck, lot # 1238F.
PCV7 1, Wyeth/Lederle, lot # B056532 (pneumoccoal vaccine)
The following vaccines were administered:
DTaP, Aventis Pasteur, lot # C2605AA.
Comvax, Merck, lot # 1244F, (Hib and Hep B).
IPV, Aventis Pasteur, lot # 20872.
Rotateq, Merck, lot # 0031?
PCV7 1, Wyeth/Lederle, lot # B086548.
Per my phone call with mother on May 19th, 2009, both father and his sister had been previously diagnosed with Moyamoya disease. (The father and his sister are half Japanese). On the morning of
(NOTE: As reviewed in the clinical discussion below, Moyamoya disease is a poorly understood occlusive disease involving large intracranial arteries, especially the distal internal carotid artery and the stem of the middle and anterior cerebral arteries. Vascular inflammation is absent. The lenticulostriate arteries develop a rich collateral circulation around the occlusive lesion, which gives the impression of a “puff of smoke” (Moyamoya in Japanese) on conventional x-ray angiography. The disease occurs mainly in Asian children or young adults, but the appearance may be identical in adults who have atherosclerosis. Breakdown of dilated lenticulostriate arteries may produce parenchymal hemorrhage, and progressive occlusion of large surface arteries can occur, producing large-artery distribution strokes.
Based on these descriptions of Moyamoya disease, Amanda’s father may have been experiencing transient ischemic attacks (TIAs) during the series of mishaps that occurred on June 29th, with his stumbling over and destroying a coffee table at 2:00 pm and dropping Amanda a little later (3:15 pm).
The following notes were dictated by
HISTORY OF PRESENT ILLNESS: This is a 4 month old brought in by
PHYSICAL EXAMINATION: Significant for an obvious left parietal (scalp) hematoma as well as diffuse right head swelling and a full anterior fontanelle. The rest of the HEENT exam was essentially normal. Pupils were noted to be 8 mm bilaterally and unresponsive. Breath sounds were clear. Normal S1, S2. No murmur. There was a mild contusion noted on the right chest. There were no marks noted on the abdomen, which was soft. There were no obvious injuries to any of the extremities. (NOTE: Dr. Petrack’s Emergency Department report at
(Repeated) attempts were made to get blood but were unsuccessful. After the patient was stabilized, she had a head CT, which showed diffuse edema but no focal neurological lesion. The baby was then brought back to the Emergency Dept. Transport was arranged with Rainbow Babies and Children. The neck was stabilized with a collar, and the baby was transported to Rainbow for definitive care.
Bone window images show a fracture line in the calvarium on the left extending from the middle cranial fossa on the left to the parietal region. There is associated soft tissue swelling over the fracture line. An additional fracture is seen extending laterally on the right from the sagittal suture to the parietal region. The fractures do not appear to be depressed. Soft tissue swelling is also noted over the fractures on the right.
There is a low density area in the left posterior parietal region measuring 1.7 X 1.4 cm. There is no evidence of mass effect. This may represent an area of remote infarct.
There is linear increased density adjacent to the falx anteriorly, and there is increased density in the posterior aspect of the occipital horns. In addition, there is an area of subtle increased density in the left parietal lobe. The findings indicate both extra axial bleeding anteriorly, as well as interventricular blood and an area of parenchymal hemorrhage. There is no epidural or subdural hematoma adjacent to the bilateral skull fracture lines.
University Hospitals of
Discharge summary dictated by Paul G. Smith, D.O:
“UNIVERSITY HOSPITALS OF
Date of death,
ADMISSION DIAGNOSIS: Full arrest.
FINAL DIAGNOSIS: Full arrest, non-accidental head trauma.
This is a 4-month-old infant who was brought in by helicopter from
CT scan of abdomen and pelvis showed no abnormalities.
CT of cervical spine with reconstructions:
“Showed transverse lucencies on the right knee. Antero-lateral mass of c (cervical) 5, and on the left in the anteromedial mass of c (cervical) 6 suggests possible minimally displaced acute fractures. No subluxation is evident.”
“Scalp hematomas are evident and the largest is in the right apex.
Right frontal and bilateral parietal fractures are present. The right frontal parietal fracture is depressed by less than 5 mm. There are scattered parenchymal hyperdensities in bifrontal apex. There is a larger area of hyperdensity in the left parietal region. There is interventricular hemorrhage in the atria bilaterally. Extra axial hyperdensity is seen in a thin layer in the right frontal distribution. Hperdensity is also demonstrated in the anterior interhemispheric fissure.
There is diffuse loss of gray-white differentiation, and there is diffuse sulcal effacement. Basal cisterns are not evident. The third and fourth ventricles are not well demonstrated.
Multiple skull fractures. Bilateral cephalhematoma. intraparenchymal, subdural, subarachnoid, and intraventricular hemorrhage.
Diffuse loss of sulci and cisterns as well as gray-white differentiation consistent with global edema. Downward herniation cannot be excluded.”
Portable AP chest: interpreted as normal with normal-appearing bones.
Portable AP abdomen: normal.
“Admitting Diagnosis: SHAKEN INFANT SYNDROME
Principle Diagnosis: SHAKEN INFANT SYNDROME
Other diagnosis: FX C5 VERTEBRA, CLOSED
Other Diag. COMPRESSION OF BRAIN
Other Diag. CL SKULL VLT FX-COMA NOS
Other Diag. FX C6 VERTEBRA-CLOSED
Other Diag. RETINAL HEMORRHAGE
Other Diag. CARDIAC DYSRHYTHMIAS NEC
Other Diag. CONTUSION OF THIGH
Other Diag. CONTUSION OF ABDOMINAL WALL
Other Diag. CONTUSION OF CHEST WALL
Other Diag. BATTER BY FATHER/STEPFTH
Other Diag. OTHER FALL
Heart Donor Resection,
Heart: 38 gram heart with vascular congestion and biventricular mural thrombi, atrial septal defect.
Autopsy, performed on
“The following is the report of autopsy to the best of my knowledge and belief. This person was a female, single, aged 4 months 14 days of the Causasian race with medium complexion, had brown eyes, brown hair, absent teeth, was 25 inches in height, weighing 17 pounds, a native of Middleburg Heights, Ohio with an occupation of infant.
“Marks and Wounds:
“Contusions of face, right thorax, left shoulder, and left arm.
Contusions of right thorax.
Abrasions of abdomen.
Evidence of recent therapy.
1. Blunt impacts to head
A. Contusion of right submandibular face.
B. Contusions (two) of right and left scalp.
C. Fractures (three) of parietal bones and occipital bone.
D. Epidural and subdural hematomas with extensions along cervical and thoracic spinal cord.
E. Cerebral and cerebellar subarachnoid hemorrhages.
F. Intraventricular hemorrhages.
G. Lacerated contusion of the left parieto-occipital cerebrum, right occipital cerebrum, and right cerebellum.
H. Diffuse cerebral edema.
I. Bilateral retinal hemorrhages.
II. Remote blunt impact to head.
A. Remote subdural hemorrhage.
B. Remote left parietal and left occipital cerebral contusion.
III. Blunt impact to neck, trunk, and left upper extremity.
A. Abrasions of anterolateral left abdomen.
B. Cutaneous contusions of right thorax, left shoulder, and left upper arm.
C. Subcutaneous contusions of cervical and thoracic paraspinal soft tissues.
D. Healing fracture calluses of lateral right third through sixth ribs. and lateral left third and fourth ribs.
E. Pulmonary hemosiderosis.
IV. Therapeutic procedures.
A. Indwelling nasogastric catheter, endotracheal tube, intravascular catheter, and intraosseous catheter.
B. Puncture wounds of extremities.
C. Patient identification bracelet.
D. Postmortem organ donation of heart.
(Comment: Brain weight was 770 grams, markedly elevated in comparison with normal weight of 595 grams for a 4-month-old-girl. This extreme brain swelling can be attributed to the accidental fall described in the medical history and does not in any way selectively imply inflicted abuse.)
Cause of death: Blunt impacts to head with skull and brain injuries.
(Signed by pathologist, Joseph A. Felo, D.O., and coroner Elizabeth K. Balraj, M.D.)
Toxicology Report: Assays from liver, urine, and vitreous humor were negative for prescription drugs, opiates, cocaine, salicylates, acetaminophen, glucose, ketones, and volatile chemicals.
Laboratory at Bonfils Reports (
“38 gram heart with vascular congestion and biventricular mural throbi, atrial septal defect.”
Relevant Pathology (Microscopic) Reports
“MUSCULOSKELETAL: Nodular fracture calluses are in the lateral right 3rd through 6th ribs and the lateral left 3rd and 4th ribs. No other fractures or abnormalities are noted.
“HEAD/BRAIN: The frontal scalp shows no evidence of contusions or galeal hemorrhages. The frontal bone is intact and no fractures are palpable with the facial skeleton. The sutures are open and the anterior fontanelle is soft and flat. The dura is smooth and glistening. There is faint golden brown staining of the subdural surface of the left cerebral convexity and the bilateral posterior cranial fossa. A 3 cm X 2.5 cm X 2.5 cm dark brown-dark red concavity is in the parasagittal convexity surface of the left parietal and left occipital cerebrum. The leptomeninges are thin and transparent. The frontal and temporal cerebral hemisphere subarachnoid space does not contain any hemorrhage. The cerebrum presents normal convolutions with diffuse flattening of the gyri and narrowing of the sulci. There is no evidence of subfalcial, uncal, or cerebellar tonsillar herniation present. The major cerebral arteries are normally developed and show no congenital anomalies. The roots of the cranial nerves are unremarkable. No hemorrhages are along the optic nerve sheaths. The brain is fixed in formalin prior to further sectioning. After two days of formalin fixation, serial coronal sections through the cerebral hemispheres show a mostly normal cortical ribbon and underlying white matter. The concave lesion within the left parietal and left occipital cerebrum focally extends to the posterior horn of the left lateral ventricle. The cerebral tissue adjacent to the cerebral hemisphere show a grossly normal cortical ribbon and underlying white matter. The basal ganglia and diencephalons show no gross abnormalities. Serial coronal sections through the brainstem and sagittal sections through the cerebellum show mostly normal cerebral structures. There are focal punctate hemorrhages through the left anterior mid brain. The ventricular system is symmetrical with hemorrhages in the third and fourth ventricles. Serial cross sections through the spinal cord with attached dura show epidural and subdural hemorrhages with no focal lesions within the spinal cord parenchyma.
“DURA: Acute extravasation of blood within dural stroma. Hemosiderin-laden macrophages within dural stroma and within thin fibroblastic subdural membrane.
“BRAIN: Acute extravasation of blood with mild hemosiderin-laden macrophages with cerebral and cerebellar leptomeninges. Irregular cerebral defect with acute hemorrhages on irregular margins and with adjacent neuropil. Organizing cerebral infarction with destruction of cerebral gyrus, acute and organizing hemorrhage with fibrocapillary proliferation and prominent hemosiderin-laden macrophages, and marginal reactive gliosis.
“SPINAL CORD: Acute and early organizing epidural hemorrhage. Acute subdural hemorrhage.”
Eyes: There are no microscopic eye reports.
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Clinical Discussion, Part I: Shaken Baby Syndrome and Lethal
Since “shaken infant syndrome” (SIS) was designated as the primary diagnosis at the University of Cleveland Hospitals (more commonly referred to as “shaken baby syndrome,” (SBS), it is necessary to address and dismiss this diagnosis while at the same time showing the potential lethality of minor falls, (LMF).
Origin of the Shaken Baby Syndrome (SBS)
Working with the U.S. Department of Transportation, an Oxford-trained neurosurgeon, AK Ommaya devised an experiment to measure the amount of rotational acceleration required to reach the threshold of brain injury with adult Rhesus monkeys as subjects. As reviewed by R Uscinski:
“A contoured fiberglass chair was built, mounted on wheels, and placed on tracks with a piston behind it. The monkeys were strapped into the chair with their heads free to rotate in such a way that there would be no impact. The piston then impacted the chair, simulating a rear-end motor vehicle collision. The experiment was photographed with a high-speed camera, allowing calculations of generated rotational accelerations. Ommaya was able to demonstrate that a rotational acceleration of 40,000 radians/second (squared) was sufficient to produce intracranial injury in 19 of the animals, with 11 of them also demonstrating neck injuries. Then, using the scaling parameters, he estimated that less rotational acceleration would be required to produce concussion in the larger human brain, perhaps on the order of 6,000 to 7,000 radians/second (squared),”(1)
Calculations were based on the same laws as described in classical Newtonian physics, as applied to movements of planetary bodies, that force is the product of mass and acceleration.
Ommaya’s experiments were published in the Journal of the American Medical Association in 1968.(2) In 1971 Guthkelch reported on the first diagnosed case of SBS in which he hypothesized that subdural hematomas could be caused by manually shaking an infant without the head impacting on any surface.(3) One year later Caffey alluded to the parent-infant stress syndrome, with manual shaking causing intracranial injury in the form of subdural hematoma and cerebral contusion of infants.(4) Two additional papers published by Caffey over the next two years emphasized shaking as a means of inflicting intracranial bleeding in children.(5,6) It is important to note that each of these four papers referred to Ommaya’s publication of 1968 as justification for this concept.
After publication of these four papers, the term Shaken Baby Syndrome became widely accepted as a clinical diagnosis for inflicted (nonaccidental) head injury in infants in which findings of subdural (brain) hemorrhages and/or retinal hemorrhages became accepted as exclusively diagnostic of SBS in the absence of known major accidental injury and remains so today in hospital emergency rooms.
SBS Theory - Irreconcilable with the Weakness of the Human Infant’s Neck
From its origins, the SBS has been based on the assumption that a parent or caretaker, becoming irritated over a baby’s prolonged fussiness and crying, loses self-control and, grasping the infant by the chest or heels, shakes the infant with such violence that any onlooker would recognize it as excessive and dangerous. It is true that shaking does sometimes take place when an infant collapses and stops breathing, which is a common presentation in these cases. In such situations a panicky parent, usually untrained in resuscitation, picks up an infant and (not knowing what else to do) mildly shakes an infant that has just gone into respiratory arrest. However, these instances do not in any sense constitute SBS.
As pointed out in the Uscinski report,(1) the brain and head of an infant is nearly seven times larger and heavier than that of a monkey. In addition, monkeys are known to be incredibly strong, approximately four times stronger than humans. There would be no comparison, therefore, between the neck muscle strength of an adult monkey and that of an infant, barely able to hold up his or her head by age six months. With these facts in mind, consider the following:
‘Most SBS cases in the
‘11 of the 19 monkeys (over 50 percent) in the Ommaya experiments had neck as well as brain injuries.
‘Although human brain injuries may occur in rear-end vehicle collisions, whiplash injuries to the neck comprise an overwhelming majority of adult injuries, in which ligaments and muscles are torn, resulting in destabilization of the cervical (neck) vertebral column. Since infants have only rudimentary neck muscles and connective tissues as cushions, the full impact of shaking would fall on the highly vulnerable cervical spinal cord near the base of the brain, which almost certainly would be fatal.
‘In view of these considerations, one would expect a far greater incidence as well as severity of neck and cervical spinal cord injuries in infants than took place in the monkeys, and yet this type of injury has not been documented in any SBS case to date. In view of these facts, the Shaken Baby Syndrome theory defies both reason and common observation. As a simple statement, it is physiologically impossible. Most of the relevant scientific references on this subject can be accessed at http://www.sbsreferences.com/.
Reflecting these considerations, F.A. Bandak, Ph.D., (a biomechanical research scientist and research professor in the Department of Neurology with the Uniformed Services University of the Health Sciences, U.S.A., and a former director of head injury research at the National Highway Traffic Safety Administration, U.S.A.) wrote in a paper published in 2005:
“Forceful shaking can severely injure or kill an infant. This is because the cervical spine would be severely injured and not because subdural hematomas would be caused by high head rotational accelerations. We have determined that an infant head subjected to the rotational velocity and acceleration called for in the SBS literature, would experience forces on the infant neck far exceeding the limits for structural failure of the cervical spine. Furthermore, shaking cervical spine injury can occur at much lower levels of head velocity and acceleration than those reported for the SBS.(8)
Perhaps the most definitive statements on this issue come from three bioengineers, Chris Van Ee, PhD,(9) Kenneth L Monson, PhD,(10) and Kirk L Thibault, PhD,(11) each of whom offered “Accepted Findings Will Assist Court” documents in defense of a specific Arizona SBS case. As these reports are now within the public domain, they are offered here for educational purposes. Sections are chosen from the Chris Van Ee report as generally consistent with the conclusions of the other two doctors. (These can be found as exhibits 14A, (9) 14B, (10) and 14C, (11) on http://www.sbsreferences.com/.)
“Scientific testing has shown that head acceleration levels from anterior/posterior human shaking of a normal 0- to 2-year-old child in the sagittal plane results in head acceleration and force levels that are much lower than those which are associated with traumatic head injury. Repeated testing of this hypothetical has shown that the head accelerations associated with shaking are far below the level associated with injury, and there is no quality data to support the SBS brain injury mechanism. Thus shaking, even if done in a fit of anger, is not expected to result in head dynamics sufficient to cause direct intracerebral trauma.
“Human shaking (id) may cause lethal brain stem and cervical spine injuries in a 0-to-2-year-old child, as the forces necessary for these injuries are well below the level needed for fatal brain injuries and are consistent with the forces that can be produced in shaking. Put another way, these neck injuries would be expected in any hypothetical-superhuman strength case of SBS where superhuman dynamics resulted in head accelerations leading to intracerebral trauma (if SBS were valid, which it is not).
“If a 0- to 2-year-old child accidentally falls from a height of six fee and impacts head-first on a hard surface such as carpeted cement, the sudden impact has the potential to generate sufficient head acceleration to cause fatal intracerebral injuries. Whether any given fall is fatal depends on a host of variables and the fall mechanics which are different in each accident, but the potential head dynamics that result from a 6-foot high fall could far exceed the tolerance associated with fatal head injury.
“Intentionally impacting a 0- to 2-year-old child’s head against a hard surface could easily cause fatal brain injuries that would mimic those of a fall, and today’s science cannot distinguish accidental from non-accidental impacts of falls of similar magnitude, barring extraordinary signs, e.g….grip marks or eye-witness accounts.
“The foregoing findings are based on principles universally accepted within my field and concern scientific subject matters that I am willing to testify on in this case. The findings are overwhelmingly supported by the following reference list of biomechanical tests and studies……” (9)
Members of the one and only scientific specialty who, by reasons of their many years of background with the U.S. Highway Department, can be considered experts in the biomechanics of head and neck whiplash injuries, universally reject the shaken baby syndrome. In contrast, their work does confirm the potential lethality of minor falls to infants and children.
The following abstracts are provided as examples showing that the shaken baby syndrome (SBS) has been discredited, while lethal minor falls (LMF) have been confirmed:
The Shaken Baby Syndrome: A Clinical, Pathological, and Biomechanical Study.
Duhaime, AC, Gennarelli, TA, Thibault, LE, Margulies, SS et al, Journal of Neurology, 1987; 66:409-415.
Abstract: Because a history of shaking is often lacking in the so-called “shaken baby syndrome,” the diagnosis is usually based on a constellation of clinical and radiographic findings. Forty-eight cases of infants and young children with this diagnosis between 1978 and 1985 at the Children’s
Models of 1-month-old infants with various neck and skull parameters were instrumented with accelerometers and shaken and impacted against padded or unpadded surfaces. Angular accelerations for shakes were smaller than those for impacts by a factor of 50. All shakes fell below injury thresholds established for subhuman primates scaled for the same brain mass, while impacts spanned concussion, subdural hematoma, and diffuse axonal injury ranges. It was concluded that severe head injuries commonly diagnosed as shaking injuries require impact to occur and that shaking alone in an otherwise normal baby is unlikely to cause the shaken baby syndrome.
Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants.
Abstract: Object: Rotational loading conditions have been shown to produce subdural hemorrhage and diffuse axonal injury. No experimental data are available to compare the rotational response of the head of any infant during accidental and inflicted head injuries. The authors sought to compare rotational deceleration sustained by the head among free falls, from different heights onto different surfaces with those sustained during shaking and inflicted impact.
Methods: An anthropomorphic surrogate of a 1.5 month-old human infant was constructed and used to simulate falls from 0.3 meter (1 feet), 0.9 m (3 ft), and 1.5 m (5 ft), as well as vigorous shaking and inflicted head impact. During falls, the surrogate experienced occipital contact against a concrete surface, carpet pad, or foam mattress. For shakes, investigators repeatedly shook the surrogate in an anteroposterior plane; inflicted impact was defined as the terminal portion of a vigorous shake, in which the surrogate’s occiput made contact with a rigid or padded surface. Rotational velocity was recorded directly and the maximum (peak-peak) change in angular velocity…and peak angular acceleration…were calculated……..
Conclusions: Vigorous shakes of this infant model produced rotational responses similar to those resulting from minor falls, but inflicted impacts produced responses that were significantly higher than even a 1.5-m fall onto concrete. Because larger accelerations are associated with an increasing likelihood of injury, the findings indicate tht inflicted impacts against hard surfaces are more likely to be associated with inertial brain injuries than falls from a height of less than 1.5 m or from shaking.
Abstract: Physicians disagree on several issues regarding head injury in infants and children, including the potential lethality of a short-distance fall, a lucid interval in an ultimately fatal head injury, and the specificity of retinal hemorrhage for inflicted trauma.
There is scant objective evidence to resolve these questions, and more information is needed. The objective of this study was to determine whether there are witnessed or investigated short-distance fall that were concluded to be accidental. The author reviewed the January 1, 1988 through June 30, 1999 United States Consumer Product Safety Commission database for head injury associated with use of playground equipment. The author obtained and reviewed the primary source data, hospital and emergency medical services’ records, law enforcement reports, and coroner or medical examiner records) for all fatalities involving a fall.
The results revealed 18 fall-related injury fatalities in the database. The youngest child was 12 months old, the oldest 13 years. The falls were from 0.6 to 3 meters (2-10 feet). A noncaretaker witnessed 12 of the 18, and 12 had a lucid interval. Four of the six children whom funduscopic examination was documented in the medical record had bilateral retinal hemorrhage. The author concludes that an infant or child may suffer a fatal head injury from a fall of less than 3 meters (10 feet). The injury may be associated with a lucid interval and bilateral retinal hemorrhage.
Denton, S, and Mileusnic, D, Delayed sudden death in an infant following an accidental fall; A case report with review of the literature, American Journal of Forensic Medicine and Pathology, 2003; 24(4):371-376.
Abstract: Several controversies exist regarding ultimately lethal head injuries in small children. Death from short falls, timing of head injury, lucid intervals, presence of diffuse axonal injury (DAI), and subdural hematoma (SDH) as marker of DAI are the most recent controversial topics of debate in this evolving field of study. aIn this area of debate we present a case of delayed death from a witnessed fall backwards off a bed in a 9-month-old black child who struck his head on a concrete floor and was independently witnessed as “healthy” for 72 hours postfall until he was discovered dead in bed. Grandmother, babysitter, and mother all independently corroborated under police investigation that the child “acted and behaved normally” after the fall until death. Autopsy showed a linear nondisplaced parietal skull fracture, diastasis of adjacent occipital suture, subgaleal hemorrhage with evidence of aging, small posterior clotting, subdural hemorrhage, marked cerebral edema, and a small tear of the midsuperior body of the corpus callosum consistent with focal axonal injury. No DAI was seen, and there were no retinal hemorrhages. All other causes of death were excluded upon thorough police and medical examiner investigation..…..
Hall, JR, Reyes, HM, Horvat, M et al, The mortality of childhood falls, Journal of Trauma, 1989; 29(9):1273-1275
Abstract: Falls accounted for 5.9% of the childhood deaths due to trauma in a review of the medical examiner’s files in a large urban county. Falls represented the seventh leading cause of traumatic death in all children 15 years or younger, but the third leading cause of death in children 1 to 4 years old. The mean age of those with accidental falls was 2.3 years, which is markedly younger than that seen in hospital admission series, suggesting that infants are much more likely to die from a fall than older children. Forty one percent of the deaths occurred from “minor” falls such as falls from furniture or while playing; 50% were falls from one story or greater; the remainder were falls down stairs…..…
An 11-month old infant was witnessed to fall backwards from a sitting position, the head striking a carpeted floor. The infant immediately cried, vomited and exhibited some seizure-like activity including tongue-biting and curling of the right hand. Three hours later a large acute left frontal subdural hematoma was removed surgically. [my addition: see forum in retinal hemorrhages topic: Retinal Hemorrhage Forum]
As noted above in the clinical history, Amanda’s head injury occurred when the father tripped on a blanket which had dropped to the floor in a bedroom, at which time he was holding Amanda outstretched in his hands, resulting in her being dropped and landing head-first onto a thinly carpeted concrete floor in their home.
As described in some detail by the mother, the father was accustomed to carrying Amanda in this way (holding her outstretched with the palms of his hands). The father being 6 ft and 5 inches in height, and commonly holding Amanda at his mid-chest level, the fall would have been 4 ½ to 4 ¾ feet. For these reasons, it is feasible and likely that this unfortunate accident was the source of Amanda’s head injuries as well as the external bruises described clinically following hospitalizations as well as at autopsy.
Also, considering the father’s 2:00 pm phone call to the mother on June 29th, that he had fallen over and destroyed a coffee table, this is an indication that, on the afternoon of June 29th, he was experiencing transient ischemic attacks (TIAs) from Moyamoya disease, resulting in impaired neuromuscular control of which he may not have been aware, and which may have been a major factor in his dropping Amanda later that afternoon.
Clinical Discussion, Part II: Moyamoya Disease
As reviewed in Harrison’s Principles of Internal Medicine, 16th Edition, page 2379, under a section entitled “LESS COMMON CAUSES OF STROKE,” Moyamoya disease is discussed as follows:
“Moyamoya disease is a poorly understood occlusive disease involving large intracranial arteries, especially the distal internal carotid artery and the stem of the middle and anterior cerebral arteries. Vascular inflammation is absent. The lenticulostriate arteries develop a rich collateral circulation around the occlusive lesion, which gives the impression of a “puff of smoke” (Moyamoya in Japanese) on conventional x-ray angiography. Other collaterals include transdural anastomoses between the cortical surface branches of the meningeal and scalp arteries. The disease occurs mainly in Asian children or young adults, but the appearance may be identical in adults who have atherosclerosis. The etiology of the childhood form is unkown. Because of the occurrence of intracranial hemorrhage from rupture of the transdural and pial anastomotic channels, anticoagulaton is risky. Breakdown of dilated lenticulostriate arteries may produce parenchymal hemorrhage, and progressive occlusion of large surface arteries can occur, producing large-artery distrubition strokes. Bypass of extracranial carotid arteries to the dura or MCAs may prevent stroke and hemorrhage.”
(COMMENT: Both Amanda’s father and his sister, who are half Japanese, have been diagnosed with Moyamoya disease and therefore susceptible to brain hemorrhage as well transient ischemic attacks, which includes the possibility of transient loss of muscle control. This is corroborated by the father’s medical history of recurrent bouts of ataxia and losses of mental stability. It is plausible that, during the afternoon of June 29th, when the father accidentally stumbled over and destroyed a coffee table around 2:00 pm and a little later dropped Amanda, that he was experiencing transient ischemic attacks from Moyamoya disease.)
Clinical Discussion, Part III: The Enigma of the Brain, Cerebellar, and Dural Hemosiderin
As noted on page 8, pathology slides from the autopsy revealed hemosiderin-laden macrophages in the lepto meninges of both brain and cerebellum, as well as dural stroma. As reviewed in Forensic Pathology, by Vincent J and Dominick DiMaio, 2001, CRC Press, page 167, brain hemorrhages are divided into acute, subacute, and chronic phases. The acute phases manifest themselves clinically within 72 hours of injury, subacute between 3 days and 2-3 weeks, and the chronic phase within 3-4 weeks. About 3 days following an acute hemorrhage, the red blood cells begin lysing or breaking up, gradually releasing their iron. The iron in turn is gradually scavenged by macrophage cells and carried out of the clot area in the form of hemosiderin, a process which becomes prominent within two to three weeks following the acute hemorrhage, but which may persist for pronged periods. What then was the source of the hemosiderin? For answers, we must return to the prenatal and birth records.
Since the accidental dropping of Amanda had occurred on June 29, 2007 and her being declared dead the next day (June 30), the time was too short for the appearance of hemosiderin which, by definition, would not begin to appear until the commencement of the subacute phase 72 hours following injury. What then was the source?
It will be recalled that the mother’s weight was 118 lbs in an early stage of pregnancy, so that her frame was relatively slight. It was her first pregnancy with an unstretched uterus, and she was 31 years old. Another risk factor occurred at birth with a “nuchal hand and arm,” which presented adjacent to the neck at birth but which, earlier and higher in the birth canal, may have impeded descent of the head. In addition, the head was excessively enlarged with circumference of 36 cm (95 percentile). The combination of the obstructive arm presentation with an unusually enlarged (95 percentile) head may well have posed a significant fetal head/maternal pelvic disproportion posing a major risk factor for significant fetal brain hemorrhage, according to standard pediatric texts. For this reason it is a near certainty that birth trauma was the source of hemosiderin demonstrated on pathology slides. [my addition: see multiple topics in forums on birth trauma: RH Forum Birth Trauma, SDH Forum ICH in Vaginal Birth, Skull Fxs Forum Birth Trauma, Skull Fxs Forum Birth Injury, and TBI Forum ICH Birth Trauma]
Clinical Discussion, Part IV: The Rib Fractures:
The autopsy report cited healing callus fractures of lateral ribs 3 to 6 on the right and healing callus fractures of lateral ribs 3 to 4 on the left, the timing of which would also be in perfect accord with birth trauma in a 4-month-old baby. (As reviewed in the Forensic Pathology text by Vincent DiMaio and Dominick DiMaio, second edition, 2001, page 115, a callus is usually visible in two weeks following fracture in children. The bone is consolidated in 4 to 6 weeks, though it usually takes 2 to 3 months to heal solidly.)
Following the now-discredited theory of shaken baby syndrome (SBS), the second major area involving charges of inflicted child abuse is that of multiple fractures in infants, while in the view of this observer, findings attributed to inflicted trauma are almost always due to metabolic bone disease. This opinion is based on two highly definable differences between the two. First, with metabolic bone disease bone fractures are rarely separated, misplaced, or misaligned, nor are there internal chest injuries when rib fractures are involved. This was entirely the case with the 30 cases of infants with multiple fractures that I reviewed, with the exception of one infant with a pleural effusion. With traumatic fractures, in contrast, whether accidental or from inflicted abuse, there is a high percentage of severed, misplaced, and/or misaligned bone fragments. This is especially true for traumatic rib fractures in children which are accompanied by a high percentage of internal chest injuries and significant rate of fatalities. This is reflected in a 1990 study by Garcia who reported on a series of 33 children brought into a trauma treatment center with rib fractures, all brought about by blunt trauma. Nearly 70 percent were from auto accidents, 21.2 from child abuse, and 9.1 percent from falls. 72 percent of the children with three rib fractures had internal chest injuries such as lung punctures or tears and/or injuries to other internal chest organs. With four or more rib fractures there were 100 percent internal chest injuries. Mortality was 42 percent.(12)
A second differential sign is the relative absence of pain in fractures from metabolic bone disease, while traumatic fractures are usually very painful. This difference is explained because metabolic fractures usually involve only the bone which has no pain fibers, while traumatic fractures will almost always involve surrounding connective tissues, which are abundantly supplied with pain fibers. In a majority of cases that I have reviewed, as was true in the present case, there were seldom any office notes indicating signs of discomfort or distress when examined during routine pediatric visits, fractures not being recognized until later when swelling or lack of movement was noted in an arm or leg or from incidental X-rays, as in the present case.
1. Child abuse.
2. Osteogenesis imperfecta.
3. Preterm birth.
4. Rickets (vitamin D deficiency).
6. Copper deficiency.
7. Fractures secondary to demineralization from paralysis.
8. Other rare conditions that mimic child-abuse fractures (including prolonged administration of glucocorticoids, cancer medications, or prostaglandins.)
9. Hypothesized conditions presented in multiple cases referring to the “temporary brittle bone disease.”
As reviewed with the mother by phone call inquiring into possible sources of vitamin D, she had very little exposure to sunlight during her pregnancy, the first trimester of which was troubled with intractable nausea and vomiting, the last two trimesters taking place during fall and winter times in a northern state. She took Flinstone vitamins irregularly. She drank only skim milk, which would be lacking in the fat-soluble vitamin D. She did eat eggs but avoided sea food because of concern about mercury.
Among this list of differential diagnoses, vitamin D-deficient rickets stands as a prominent possibility, with birth trauma again playing a secondary role.
During a two-day conference held by the National Institute of Health (14)(October 9-10, 2003) it was announced that there is a reemergence of vitamin-D deficient rickets and an alarming prevalence of low circulating levels of vitamin D in the USA, leading to an increased incidence of infant fractures, especially when premature.
In a study conducted at the Pittsburgh Graduate School of Public Health, (15)(2007) serum 25-hydroxy vitamin D was measured at 4-21 week gestation and predelivery in 200 white and 200 black pregnant women and in cord blood of their neonates. Over 90 percent of women used prenatal vitamins. Results showed that black and white pregnant women and neonates residing in the northern US are at high risk of vitamin D insufficiency, even when mothers are compliant with prenatal vitamins. Causes of the reemergence include reduction in milk intake, (milk allergies, lactose intolerance, reduction in vitamin D-containing fats, and increased use of sun screens, which prevent sun rays from generating vitamin D precursors from skin oils).
A nutritional rickets has also been described with normal circulating 25-hydroxy vitamin D attributed to dietary calcium deficiency in infants. Elevated parathormone (PTH) levels are generally found in these cases. (16) Amanda’s intractable reflux problems almost certainly would have contributed to calcium deficiency as well of deficiencies in other minerals and vitamins.
A “Yeasty” Baby and Gastroesophageal Reflux
The mother did attempt breast-feedings supplemented with formula but ultimately abandoned breast feedings, primarily because of the infant’s difficulty in sucking. Under normal circumstances, breast-feeding establishes a prevalence of highly beneficial and protective Lactobacillus bifidis in the infant’s intestinal flora, but the mother was administered 2 grams of ampicillin intravenously during her labor with Amanda, which would have largely eliminated the L. bifidis. This in turn would have opened the way for yeast infestations, later manifesting as cradle cap, “yeasty” neck folds, and intestinal yeast overgrowth, the true source of the intractable colic and reflux problems. These in turn in all likelihood would have led to unrecognized nutrient mineral and vitamin deficiencies including calcium, magnesium, zinc, and vitamins A, C, and D.
The Bruising Issues
As noted in the clinical history, there was no record of prophylactic vitamin K administration in Amanda’s hospital newborn records either by mouth or by injection, which is recommended for prevention of Hemorrhagic Disease of the Newborn. Furthermore, Amanda’s intractable reflux problems along with routine vaccines administered on June 19th, known to cause oxidative stresses on the body,(17) might well have brought about terminal clinical scurvy as a contributory source of the bruising noted on the autopsy report.
As reviewed above in the clinical history, the examining doctor at the emergency department of
Summary and Conclusions
As reviewed in some detail above, there are plausible alternate explanations for each and every pathologic autopsy finding in the case of Amanda Sadowsky, other than the hospital and autopsy conclusions of inflicted child abuse. Almost certainly the fatal brain damage resulted from an accidental lethal minor fall. Almost certainly the rib fractures and residual brain, cerebellar, and dural hemosiderin were the results of birth trauma in combination with congenital rickets from vitamin D deficiency. The skull fractures could have also originated from birth trauma and reinjured or expanded from the accidental fall. None of these possibilities were mentioned in the hospital records nor in the autopsy report.
If there is still any validity in the time-honored principle of “considered innocent until proven guilty,” the gross deficiencies in establishing a differential diagnosis of other possible sources for the findings, as listed above, in both the hospital and autopsy reports, should more than vindicate the father of intentionally injuring his daughter.
Harold E Buttram, MD
(1) Uscinski R. The Shaken Baby Syndrome. J Amer Phys Surg, Fall, 2004; 9(3):76-77.
(2) Ommaya AK. Whiplash injury and brain damage. JAMA, 1968; 204:75-79.
(3) Guthkelch A. Infantile subdural haematoma and its relationship to whiplash injuries. BMJ, 19712(759):430-431. http://www.pubmedcentral.nih.gov/articlerender.fegi?artid=1796151
(4) Caffey J. The parent-infant traumatic stress syndrome. Am J Roentgen, 1972;114:217-228.
(5) Caffey J. On the theory and practice of shaking infants. Am J Dis Child, 1972; 24:161-169.
(6) Caffey J. The whiplash shaken infant syndrome: Manual shaking by the extremities with whiplash-induced intracranial and intraocular pleadings, link with residual permanent brain damage and mental retardation. Pediatrics, 1974; 54:396-403.
(7) As “Shepardized” from 3001131 via Lexus and Westlaw.
(8) Bandak FA. Shaken Baby Syndrome: A biomechanics analysis of injury mechanisms, Forensic Science Intern,
(9) See Exhibit 14A, accessible on http://www.sbsreferences.com/.
(10) See Exhibit 14B, accessible on http://www.sbsreferences.com/.
(11) See Exhibit 14C, accessible on http://www.sbsreferences.com/.
. Bone, 2003; 33:466-474.
(12) Garcia, V., Gotschall, C., Eichelberger, M., Bowman, L. Rib fractures in children: a marker of severe trauma, Journal of Trauma. 1990; 30(6):695-700.
(13) Jenny, C, Committee on Child Abuse and Neglect, Evaaluating infants and young children with multiple fractures, Pediatrics, 2006; 118(3): 1299-1303.
(14) National Institute of Health (NIH) conference on vitamin D,
(15) Bodnar, LM, Simhan, HN, Powers, RW et al, High prevalence of vitamin D insufficiency in black and white pregnant women residing in the Northern United States and their neonates. Journal of Nutrition, 2007; 137: 447-452.
(16) DeLucia, M.C.,
(17) Blaylock, R.L., The danger of excessive vaccination during brain development: The case for a link to autism spectrum disorder, Medical Veritas, 2008; 5(1): 1727-1741.
I just received notification that it did get published after all, although I'm not sure quite when.
For a link to the full text article on the Medical Veritas site, please go to the forums under the Rib Fractures topic located here: Medical Veritas Report on Amanda
I had the honor to meet Dr. Buttram at the conference and he agreed to allow me to publish our picture. What an amazing presence this man commands at his advancing age and yet he's so down-to-earth for all his education, skill, and knowledge.
Dr. Buttram is a retired family-practitioner medical doctor. He has authored three books to date and co-authored many papers. To learn more about him or to order one of his books, visit these websites:
Official website: http://sbswebinfo.com/dr-harold-buttram_279.html
and here: http://www.woodmed.com/WhoIsDrB.htm.