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Section IV. Analysis of the Medical Examiner’s Autopsy Report and His Court Testimony in the Case of Baby Alan
A. General appearance [click]
B. Microscopic examination of the heart and liver function tests [click]
C. Subdural hemorrhage, brain [click]
D. Subdural hemorrhage, spinal cord [click]
E. Bleeding in the brain [click]
F. Meningitis [click]
G. Diffuse axonal injury [click]
H. Retinal hemorrhage [click]
I. Pneumonia and lung hemorrhage [click]
J. Rib fracture [click]
K. Superficial bruise and contusions [click]
Conclusions [click]

References [click]

Dr. Shashi B. Gore, the Chief Medical Examiner of District Nine Orlando, Florida performed the autopsy on Alan Ream Yurko (case number: MEH-1064-97) at 10:15 AM on November 29, 1997 in Orlando [28]. The main objective of this autopsy was to establish the cause(s) of death. He stated that Baby Alan died because of bleeding in the brain resulting from shaking of the baby by his father, Alan Yurko. My review of Dr. Gore’s autopsy report indicates that it lacks the accuracy and the expected minimum scientific detail to make it reliable and useful to answer the questions about the cause(s) of death. In addition, he did not provide the medical evidence in his report and his court testimony in February of 1999 to support his conclusion that baby Alan died of “Shaken Baby Syndrome.” The following is a list of medical evidence that supports my assessment.

IV-A. General appearance
Dr. Gore stated that “Alan’s body is that of a 2 months old white male infant and appears to be of that age. The build and nourishment are average. The height of the body is 22 inches. The weight of the body is 9 lbs. The circumference of the head is 22 cm.”

The medical evidence related to this case contradicts Gore’s statements that the baby had average build and nourishment at the time of autopsy, and that his head circumference was 22 cm. Baby Alan was born on 9/16/1997, and his age on November 29th was about 2 and a half months. His head circumference measurements on October 1 and November 11/1997 were 33.3 and 37.5 cm, respectively (Table 4). It is very obvious that Gore’s measurement of 22 cm for the circumference of Alan’s head was wrong.

Furthermore, the baby had diabetes at the time of admission to Princeton Hospital on November 24th, as described above (III). Dehydration, polyurea, weight loss, and wasting are symptoms and complications of diabetes mellitus. His weight on November 24th was 10.05 pounds, and during his stay in the hospital, despite treatment with a relatively high volume of fluid IV, he lost 1.05 lb (10% of his weight) in five days. Alan received 725.8 mL of fluid and red blood cells during the first twenty-four hours in the hospital, and his output during this period was 786 mL of fluid. Net output was 60.2 mL. Again, he was suffering from dehydration in spite of being treated with adequate amount of fluid by IV infusion in the hospital (Table 6, Table 7, Table 13).

Also, he was treated with antidiuretic hormone (DDAVP) on November 28th to prevent dehydration (Table 13). Additionally, his average serum creatinine value on November 24 was 0.45 mg/dL (75% of low normal value), and dropped to 0.2 mg/dL (33% of low normal) on November 27th (Table 12). Low creatinine is an indicator of low muscle mass and wasting disease. Moreover, Dr. Douglas Radford Shanklin found that the fatty tissue of baby Alan was mostly pink and granular, which is an abnormal metabolic state that is consistent with poor development [D4].

IV-B. Microscopic examination of the heart and liver function tests
Dr. Gore stated on page 9 of his autopsy report that “The myocardium shows no evidence of inflammation, interstitial or replacement type fibrosis. There is no necrosis of myocytes and no evidence of ischemic change. The microvasculature shows no areas of thickening or perivascular fibrosis. There are no atypical changes present. No inflammation is noted”.

Gore’s description of the histology of Alan’s heart, stated above, contradicts his statement in court in February of 1999 as well as his findings presented on page 5 of his autopsy report. He stated in court that Translife removed the heart with other organs prior to performing the autopsy [13]. He described in his report that “when the chest and the abdominal cavities are opened it is noted that the heart, the liver with gallbladder, spleen, pancreas, mesenteric lymph nodes and parts of the small intestine are surgically absent as a result of organ harvesting by Translife” [28]. This indicates that he did not have the chance to examine the heart grossly and to take samples for pathological evaluation. He also confirmed this issue in his court testimony in February of 1999. He stated that the liver, spleen, pancreas, heart and partial small intestine were donated [13].

Moreover, blood analysis of November 24, 1997 showed that the baby had a very high LDH level of 2411 IU/L (1148% of normal), and this indicates damage in the cardiac muscle. The other indicators of cardiac problems are dysrhythmia, hypokalemia, and diabetes, which are observed in this case. Also, the serum levels of liver enzymes were elevated (Table 12). These findings contradict the statements made by the examiner in his court testimony that the heart and the liver were normal and did not contribute to the cause of illness and death.

IV-C. Subdural hemorrhage, brain
Dr. Gore stated that subdural hemorrhage was seen prominently on the right cerebral hemisphere, and that this hemorrhage was in liquid as well as in clotted form. There was also subdural hemorrhage on the left cerebral hemisphere posteriorly, and this hemorrhage was relatively less prominent as compared to the right. The dura mater of the cortex of the cerebral hemispheres showed thickened and slightly clotted blood adherent to the dura mater. At places, the thickness of this clotted material was between 2-3 mm.

The description of the nature of the clot and bleeding, stated above, indicate that the blood was released from the blood vessels in a continuous fashion during the five days prior to autopsy, or, more precisely, in three stages. The thickened clotted blood that adhered to the dura mater represents the first stage of blood release, the clotted blood represents the second stage, and the blood in the liquid form represents the third stage, which is the most recent. Dr. Gary Steven Pearl, the state witness, examined the blood clot and observed the proliferation of fibroblasts in layers. Based on this observation, he estimated the age of the oldest portion of the subdural hematoma to be two to five days [13]. I also examined the H & E stained tissue section of the meninges and observed the proliferation of fibroblasts in the blood clot in the subdural space and in the clot attached to the dura matter. I also observed fresh blood in the subdural space.

Furthermore, the CT brain scan taken at 7:50 PM on November 24th showed the subdural hematoma present only on the right side of the brain, and no bleeding was seen on the left. This means that the bleeding on the left occurred after 7:50 pm on November 24th. These facts contradict Dr. Gore’s conclusion that the hemorrhage occurred in minutes, or even in a few seconds, due to vigorous shaking of the head.

Also, the medical evidence indicates that the subdural hemorrhage resulted from damage to the blood vessel wall due to the excessive use of heparin, and from severe hypoxia due to severe anemia, hypotension, apnea, and metabolic alkalosis induced by excessive treatment with sodium bicarbonate (III and (Table 6, Table 7 and Table 11). The facts in the following list support my assessment:

1) The baby was treated with high doses of heparin (219 IU/kg per hour) on November 24th and 25th which is 8.8 times the recommended doses for infants. Treatment with such doses of heparin usually leads to bleeding in and individual already suffering from anemia, hypotension, and hypoxia.

2) The platelet count was reduced by 30% following the treatment with heparin, due to clot formation induced by heparin.

3) The fibrinogen split product and prothrombin time were found to be elevated on November 24th, but returning to normal on November 26th. These changes coincide with the use of heparin on November 24th and cessation of heparin treatment on the 26th.

4) The blood vessels of the meninges were swollen, as reported by Drs. Pearl and Shanklin in their court testimony. This indicates that these blood vessels were damaged as a result of hypoxia, metabolic changes, and/or inflammation [13].

5) The brain was edematous. Fluid was released from the blood vessels because of damage to their wall from hypoxia, inflammation, hypotension, and the excessive use of sodium bicarbonate.

6) Hemorrhage was also observed in the lungs and the subdura of the spinal cord. This shows that the damage in the blood vessels was not limited to the brain, and resulted from metabolic changes and inflammation that affected many sites.

7) The subdural hemorrhage observed in the left side of the brain on November 29th, that was absent on November 24th at 7:50 PM, also indicates that the subdural bleeding and the bleeding in the brain occurred in the hospital.

IV-D. Subdural hemorrhage, spinal cord
Dr. Gore stated that “when the spinal cord is traced downward through the lumbar and sacral regions it is noted that there is a small quantity of hemorrhage in the subdural space of the spinal cord representing the areas of the lower thoracic, lumber and sacral regions”.

Dr. Gore stated that the bleeding was present only in the subdural space of the lower thoracic, lumber, and the sacral regions of the spinal cord. There was no bleeding found in the cervical and upper thoracic portions of the spinal cord. Gore’s observation indicates that the bleeding in these regions of the spinal cord occurred independently of the bleeding that occurred in the brain. The blood did not come down from the brain through the spinal canal. This fact is also supported by the observations of two pathologists: Dr. Shanklin observed a fresh hemorrhage (6-12 hours old) in the subdural space of the spinal cord. And Dr. Pearl indicated that there was a spinal cord injury, that blood vessels were swollen and nerve cells damaged. I also examined the H & E stained tissue section of the spinal cord and found a fresh hemorrhage in the subdural space. Dr. Gore and other physicians examined the entire vertebral column of the baby, and they did not find any injury caused by trauma. These observations indicate that the bleeding occurring in the subdural space resulted from damage in the blood vessels due to hypoxia and from the treatment with excessive doses of heparin.

IV-E. Bleeding in the brain
Dr. Gore stated that serial-cut sections of the brain did not show any internal hemorrhage in the brain parenchyma grossly. The two sections which were stained with H & E stain showed appearance of very minute parenchymal hemorrhages. The cerebellum showed normal appearance, and one section showed evidence of shearing type injury with multiple foci of minute hemorrhages. He also stated that the brain appeared very edematous, shiny and fluffy. Differentiation of the cortex and medulla appeared poor. The ventricles were slightly reduced in size and the cerebrospinal fluid appeared clear.

The information described above indicates that the hemorrhage in the brain was very minor and only microscopic. It also shows that the brain was edematous. The edema fluid leaks into the extracellular space either through damaged capillary endothelial cells that have lost their barrier function or through newly formed capillaries that have not established barriers. Fluid in the brain increases the intracranial pressure (ICP) and this pressure causes brain damage. ICP causes either focal or diffuse flattening of the cortical gyri, sometimes associated with compressed or distorted ventricles. Relatively rigid dural folds form the flax cerebri and the tentorium cerebelli partitions in the cranial vault. Localized expansion of the brain causes it to be displaced in relation to these portions, producing brain herniations [11]. On section, the white matter may appear soft and gelatinous, and the peripheral layer of gray matter is widened. The ventricles are usually compressed. Microscopically, there is considerable widening of the interfibrillar spaces of the brain, which gives a loose appearance to the white and gray matter. Swelling of the neural and glial cells may also be present [11, p. 87-88].

In baby Alan’s case, the brain edema was severe and diffused. The ICP pressure reduced ventricle size and made the differentiation between the cortex and medulla appear poor. The ICP in this case is certainly capable of causing damage to the tiny blood vessels in the brain that were damaged by hypoxia. It seems that Dr. Gore overlooked these established medical facts and incorrectly stated that the minor bleeding observed in the brain was caused by shaking the baby.

IV-F. Meningitis
Meningitis is an inflammation of the meninges and the subarachnoid space. Infectious meningitis can be broadly classified as acute pyogenic meningitis (usually bacterial), acute lymphocytic meningitis (generally viral), and chronic meningitis, which may be bacterial or fungal [11, p. 1378]. The changes in tissues that are usually observed in cases of acute meningitis include: congestion of the blood vessels, swollen blood vessels, edema, presence of inflammatory cells in tissues (neutrophils and/or lymphocytes), hemorrhage, and degeneration and necrosis of brain cells. These changes were observed in baby Alan’s brain, as described by the state and the defense expert witnesses [13], and they confirm that Alan had meningitis. I also examined H & E stained tissue section of the meninges and observed the infiltration of the middle arachnoid membrane with lymphocytes and macrophages.

Dr. Douglas Shanklin examined the meninges, finding the blood vessels distended and the meninges tremendously thickened, perhaps to eight or ten times normal. Also present were hundreds of inflammatory cells (acute and chronic inflammatory cells). He also observed damaged nerve cells in the brain, and inflammatory cells in the walls of the blood vessels. Dr. Gary Pearl also observed swollen blood vessels and chronic inflammatory cells in the meninges. In addition, he found damaged neurons in the cerebellar dentate nucleus. Also, cerebral edema was confirmed by Dr. Gore.

The changes in tissues described above, with the presence of fever (105.8 F) and an elevated white blood cell count (20, 900/µL) that were observed on November 24th (Table 12), indicate that the baby suffered from acute meningitis. However, the severity of the acute inflammation in tissue was reduced by the treatment with high therapeutic doses of antibiotics. On November 24th, baby Alan was treated with three types of antibiotics to fight bacterial infections. These included 20 mg gentamicin, 300 mg rocephin, and 222 mg Claforan (Table 6, Table 7). Treatment with the antibiotics reduced blood white blood cell count from 20, 900 to 13, 600 /µL, and body temperature from 105.8 F to 99.8 F. The antibiotics also caused a significant reduction in number of neutrophils in the inflamed tissues.

It seems that Dr. Gore overlooked the medical facts described above when he stated that baby Alan did not suffer from meningitis. He stated that “I examined the meninges in this case and found no evidence of meningitis”. However, there is no description of a microscopic examination of the meninges in his report. Also, he did not examine the cerebrospinal fluid (CSF) at the time of autopsy to check for the presence of inflammatory cells. He stated in court that he did not examine the CSF because it was mixed with blood [13]. However, he stated in his autopsy report that the CSF fluid was clear. He reported that serial cut sections of the brain did not show any internal hemorrhage in the brain parenchyma grossly. “The ventricles are slightly reduced in size and the cerebrospinal fluid appears clear” [28].

IV-G. Diffuse axonal injury
Dr. Gore stated that baby Alan died as a result of vigorous shaking which caused diffuse axonal injury. He also claimed that diffuse axonal injury is a characteristic lesion of Shaken Baby Syndrome. I have two problems with Gore’s conclusions: 1) Gore did not present any evidence in his autopsy report or in court that he found an axonal injury in this case; and 2) axonal injuries indistinguishable from those observed in cases of head trauma can occur as a result of edema, hypoxia, hypoglycemia, cardiac arrest, and other causes. In this case, the child was suffering from brain edema, hypoxia, and cardiac arrest, and no head injury due to trauma was found. However, Gore overlooked these medical facts and based his conclusions on a theory only. Below are data that support my assessment.

1) Dr. Gore did not provide any evidence to show that he found diffuse axonal injury in Alan’s brain. Below are Mr. Barrett’s (defense attorney) questions related to the axonal injury, and Gore’s answers. These are taken from Gore’s court testimony in February of 1999 related to this case [13].
Barrett: Are there any of the slides we could look at to show us this diffuse
axonal injury?
Gore: Well, diffuse axonal injury is nothing but minute petechial hemorrhage
and these we can not show you.

Barrett: These are injuries to the axons which are parts of the nerves, correct?
Gore: Right.

Barrett: Are there any slides you have that you examined that you could show us
that will show us this diffuse axonal injuries you said you saw in this
case?
Gore: No.

Barrett: And again, nowhere in your report do you mention anything, about diffuse
axonal injury, correct?
Gore: Correct.

2) Below is a description of the findings of six studies that show axonal injury present in the brain in cases of edema, hypoxia, cardiac arrest, which are observed in Alan’s case. As noted, axonal injury due to brain trauma cannot be differentiated from axonal injury resulting from other causes. Therefore, all the causes that lead to an axonal injury should be considered prior to stating that this axonal injury was caused by a shaking force, especially in cases with no evidence of trauma.

Study # 1
Extensive neurohistological examination was undertaken in 13 patients in whom coma was attributed to hypoglycemia. It had revealed varying degrees of widely distributed neuronal necrosis. In five of these cases, there was also evidence that the intracranial pressure had been high, with internal herniation. It was concluded that a significant amount of axonal injury found in these 13 cases can be attributed to hypoglycemia per se, although the amount and distribution of the axonal damage is altered in the presence of increased intracranial pressure. However, in some cases, axonal damage is seen in the absence of an elevated intracranial pressure, and in one case its distribution closely mimicked that seen in microscopical diffuse traumatic axonal injury. This further demonstrates that not all axonal pathology is caused by trauma [29].

Study #2
The brains of 17 individuals who died of cardio-respiratory arrest, and 12 of status epilepticus were evaluated microscopically to check for axonal damage. Axonal damage was seen in 9/17 and 7/12 of the cases, respectively. In most of these cases, there was also evidence of elevated intracranial pressure (ICP). It is concluded that the great majority of axonal damage identified in cases dying after cardiac arrest and status epilepticus can be attributed to increased ICP and the vascular complications of internal herniation. However, in some cases, axonal damage was seen in the absence of an elevated ICP, although its amount and distribution were different from diffuse axonal injury [30].

Study # 3
Sections from 28 brains showing evidence of cerebral hypoxia with no history of head injury, four with a history of head trauma but no evidence of hypoxic change, and eight with a history of head trauma and hypoxic change were evaluated by immunohistochemistry staining. Axonal damage was found in seven of eight cases of head injury and hypoxic changes and 12 of 28 cases of hypoxia without history of head injury. The role of hypoxia, increased intracranial pressure, edema, shift effects, and ventilatory support in the formation of axonal bulbs should be considered. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone [31].

Study # 4
Brain tissue sections from 67 individuals who died due to trauma-induced focal cortical hemorrhage without dural involvement and 51 cases of non-traumatic death due to cerebral hypoxia/ischemia were evaluated by immunohistochemical staining to determine the reliability of axonal injury (AI) as a marker of traumatic insult. Investigations of the pons in theses cases revealed that cases of non-traumatic death due to cerebral hypoxia/ischemia (n = 51) demonstrated AI with the same frequency as in the trauma group, although the expression tended to be less pronounced. The investigations were based primarily upon immunohistochemical demonstration of antibodies targeted to beta-amyloid precursor protein (beta-APP) in the pons as a marker of AI. The results of this study confirm that beta-APP expression in the pons is a reliable indicator of AI, but does not discriminate between (a) injuries caused by traumatic strain or shearing mechanisms and (b) secondary damage due to cerebral hypoxia/ischemia or edema. Therefore, positive differentiation of the type of biomechanical event based on this criterion alone is not possible [32].

Study # 5
Beta-amyloid precursor protein (beta-APP) was used to detect axonal injury (AI) in the brain of individuals who died of nonmissile closed-head injury (n = 119), gunshot injury (n = 30), cerebral ischemia/hypoxia (n = 51), brain death caused by mechanical trauma (n =14), and nonmechanical injury (n = 18). AI was observed in 65% to 100% of cases of closed-head injury, fatal cerebral ischemia/hypoxia, and brain death, with a survival time of more than 3 h. A statistically significant difference between traumatically and nontraumatically induced (nondisruptive) AI was not found [33].

Study # 6
Brain tissues of 14 children who lacked skull fracture and allegedly died of Shaken Baby Syndrome (SBS), and 7 children who died of non-traumatic hypoxic ischemic encephalopathy (HIE) were evaluated using immunohistochemical stains. Swollen axons were present in 11 of 14 cases of SBS and in 6 of 7 cases of HIE [34].

IV-H. Retinal hemorrhage
Dr. Ben Guedes examined baby Alan at the time of the baby’s admission to Princeton Hospital on November 24th and found that Alan’s corneas were cloudy. Dr. Douglas Shanklin evaluated the H & E stained tissue section of the right eye microscopically and observed the presence of numerous inflammatory cells that are consistent with a long-standing chronic inflammation. Drs. Shanklin, Pearl, and Gore examined the H & E stained tissue sections of the retina of the eyes microscopically and observed very minor bleeding in the retina of the right eye only. Dr. Pearl stated that the bleeding in the retina was not significant. It did not impact his evaluation of this case [13].

My evaluation of baby Alan’s case revealed the presence of many risk factors that usually lead to bleeding in the retina. These include:
1) diabetes, as explained in this report (III), and retinal hemorrhage (inner retina, superficial nerve fiber layer, and preretinal hemorrhage) is commonly described in patients suffering from diabetes [7].
2) hypoxia, as a result of severe anemia; apnea; hypotension; metabolic and respiratory acidosis; and metabolic alkalosis (from the excessive treatment with sodium bicarbonate in the hospital). Hypoxia causes damage in the small blood vessels wall that leads to bleeding.
3) probable infection in the right eye, as indicated by the corneal edema (his corneas were cloudy) and the presence of inflammatory cells in the retina of the right eye, as described above.

Dr. Gore presented the minor bleeding in the retina of the right eye as evidence in court to support his claim that baby Alan died as a result of vigorous shaking. It is very hard to believe that Gore overlooked the medical evidence described above that provides explanation for the factual causes of the minor bleeding observed in the retina of right eye. His duty as a medical examiner is to evaluate the medical evidence that explains the causes of injuries in this case. I believe that he did not follow the standard medical protocol in this case as required by his job and the law.

IV-I. Pneumonia and lung hemorrhage
Dr. James Edward Hannah, radiologist, evaluated baby Alan’s chest x-ray taken on November 24, 1997, and he observed that the lungs were infiltrated. This means that the lungs were filled with fluids, inflammatory cells, and debris. These are signs of pneumonia. In addition, the presence of fever (105.8 F) and the elevated white blood cells counts (20, 900/µL) observed on November 24th (Table 12) indicated that the baby suffered from acute bacterial infection.

On November 29th, Dr. Gore examined the lungs grossly and found that both lungs were congested and contained irregular areas of hemorrhagic appearance. Serial cutting sections of both lungs showed irregular areas of hemorrhages. He also examined the H & E stained tissue sections of the lungs microscopically and observed the presence of red blood cells and clumps of inflammatory cells in the alveolar sacs. The inflammatory cell infiltrates are scattered throughout one section. He stated that this picture appears to be somewhat similar to interstitial pneumonitis. Dr. Douglas Shanklin also examined the H & E stained tissue sections of the lungs and observed inflammatory cells (white blood cells) present in the alveoli and in the structure of the lung. He also found the bronchioles filled with inflammatory cells. He identified this condition as pneumonia and said that the infection was much older than 75 hours. Furthermore, I examined the H & E stained tissue section of the lung and observed thickening of the interstitial septa, bronchioles filled with inflammatory cells, and multifocal areas of fresh hemorrhage.

The histopathology and the radiology findings described above, and the elevated body temperature (105.8 F) and white blood cell count (20, 900/µL) indicate that the baby suffered from acute pneumonia. However, the severity of the acute inflammation in tissue was reduced by the treatment with high therapeutic doses of antibiotics. On November 24th, baby Alan was treated with three types of antibiotics IV to fight bacterial infections that included 20 mg gentamicin, 300 mg rocephin, and 222 mg Claforan (Table 6, Table 7). The treatment with antibiotics reduced the blood white blood cell count from 20, 900 to 13, 600 /µL and the body temperature from 105.8 F to 99.8 F. The treatment with antibiotics also caused a significant reduction in the number of neutrophils in the inflamed tissue. It misled Gore to believe that the lesions in the lungs on November 24th were minor and not significant.

The pathological changes observed in the lungs have two significant clinical points. 1) Alan had acute pneumonia, which caused hypoxia and respiratory acidosis; and 2) the hemorrhage in the lungs indicates that the baby was suffering from a bleeding condition that affected many organs, and that this bleeding was not caused by trauma. Bleeding was also observed in the subdural area of the spinal cord, and the examination of the vertebral column revealed no injuries due to trauma, as described in section IV-D of this report.

These clinical findings support my conclusions that the bleeding in tissues in this case was caused by treatment with excessive doses of heparin and sodium bicarbonate, and by hypoxia.

IV-J. Rib fracture
Dr. Robert Scott Mahan and Dr. James Edward Hannah, radiologists, read the chest x-rays of baby Alan taken on November 24 and 25, 1997 and found only one fractured rib (rib #6). They gave the time for this fracture between weeks and several months. Dr. Gore stated that he observed during his autopsy irregular swelling of the left ribs #5, 6, 7 and 10; that these sites appeared as globular masses of cartilaginous tissue, and that cut sections of these masses showed normal appearance of the cartilage. He further stated that these masses probably resulted from healing fractures of the ribs, and that these fractures occurred between one and four weeks. He also stated that x-rays were taken and confirmed the presence and positions of these healing fractures, and that multiple sections were taken for histopathological study [28]. However, Gore did not present in his report or in court any information describing his histology and radiology findings of these fractured ribs. He showed only photographs of these ribs in his court testimony.

Gore further stated that the cut sections of these masses showed normal appearance of cartilage. The calluses of healing bone usually contain calcium and not simply normal cartilage. This indicates that the masses of cartilage observed by Gore in ribs # 5, 7, and 10 do not represent healing fractures of these ribs. This assessment is supported by the fact that two radiologists read the chest x-rays taken on November 24th/25th and saw only one rib fracture (rib #6). It is also supported by Gore’s statement in court describing the process of healing in a rib fracture. He stated that the healing process in a rib usually starts with initial swelling of the rib and then gradual calcium deposition in the fracture sites [13]. I am puzzled by the fact that Gore did not show the x-ray film of these fractured ribs in court, but showed only photographs. He stated that he took the x-rays and samples for pathology to confirm the presence and positions of these healing fractures. It seems reasonable that he be asked to explain his reason for not presenting the evidence that supports his claim.

Review of the medical literature reveals cases in which rib fractures that occurred during labor were missed during initial examination of the baby. Below is brief description of these cases.
Case # 1
A large weight (3912 g) for gestational age female neonate was delivered vaginally with the use of vacuum extraction. The neonate was breathing quietly, with no respiratory tract distress. A chest radiograph was obtained and showed minimally displaced fractures of ribs 4, through 8 posteriorly on the right side. The lungs, heart, and other skeletal structures were normal [35].
Case # 2
A large weight (4205 g) for gestational age, term male neonate was delivered vaginally with the use of vacuum extraction to assist delivery. A chest radiograph showed nondisplaced fractures of ribs 6 through 8 posteriorly on the right side. The baby had normal lungs and mediastinum [35].
Case # 3
A 37-year-old diabetic woman spontaneously went into labor at 38 weeks of gestation. She delivered a 3300g baby with the assistance of vacuum extraction. Physical examination did not detect any abnormality. At about 9 hours after delivery, the nurse noticed the child having rapid respirations. Examination by a resident physician revealed mild respiratory distress with tachypnea and tachycardia. Crepitus was palpable over the left posterolateral chest. No skin changes suggestive of trauma were found. Chest x-ray examination revealed five fractured ribs over the left posterolateral chest area. There is no evidence of pneumothorax or other skeletal trauma. Over the next 36 hours, the child experienced progressively less tachypnea and gradual disappearance of the crepitus. Full skeletal survey failed to show evidence of osteogenesis imperfecta or any other abnormality of bone mineralization [36].
Case # 4
Chest radiograph of a 4905-gm female delivered by midforceps after right shoulder dystocia. On the 11th day, a prominent mass was noted in the right midclavicular region. Radiograph reveals a right midclavicular fracture with slight superior angulation and incidental fractures of left ribs #5 & 6.

Moreover, Fanaroff et al, explained the mechanism of rib injuries during labor as follows: Rib injury is initiated when the anterior shoulder is impacted behind the symphysis pubis, with the other shoulder attempting to descend into the posterior compartment of the pelvis. This results in compression forces on the fetal arm and thorax, leading to spontaneous rib fractures on the same side as the posterior shoulder [10]. They also stated that the specific clinical manifestations of ribs injuries are often absent, making diagnosis difficult [10].

The four cases with rib fracture described above were born at term or close to term, and they had better health than baby Alan. Alan was born five weeks premature and had respiratory distress and jaundice. His mother was suffering from gestational diabetes and had chronic oligohydramnios. Skeletal and facial deformities in a fetus are some of the risks associated with oligohydramnios pregnancy. Furthermore, pregnancy in diabetics is usually associated with a higher incidence of congenital anomalies (6 to 12 percent vs. 2 to 3 percent in non diabetics) [7]. These data point out the high possibility that Alan’s rib # 6 was fractured during labor.

The prosecutor brought the issue that the rib fracture did not occur during birth, because it was not seen in the x-ray films taken on 9/16-18, 1997. Alan was born on 9/16/97. A rib fracture occurring during labor would have been two days old on 9/18, and it takes at least 7 days for the calluses to form and to show on the x-rays. Cumming reported that when a fracture is discovered in a newborn infant, it is important to decide whether it occurred at birth or after birth. Calcification around the fracture site gives a useful estimate of the age of the fracture. We reviewed films of 23 patients with fractures resulting from delivery. These fractures occurred at three different sites: the clavicle, the humerus, and the femur. Calcification could be seen as early as seven days after birth and was absent for as long as 11 days after birth [37].

IV-K. Superficial bruise and contusions
Dr. Ben Guedes examined baby Alan at the time of admission to the Princeton Hospital on November 24, 1997 to check for injuries resulting from trauma. He found only a small, reddish, linear bruise under the right eye, as described in section III-A of this report. Dr. Robert Gold, pediatric ophthalmologist, also examined the baby on November 24th and observed only a slight bruise under the right lower eyelid. No other injuries to suggest trauma were found by other physicians and nurses who examined baby Alan during his five days in the hospital. Furthermore, on November 29th, Dr. Gore examined the body during his autopsy to check for injuries caused by trauma and found no evidence of injuries caused by trauma, except for the small bruise under the right lower eyelid described above, and two minor contusions on the right and the left temporal areas.

Dr. Gore stated in court that the bruise under the right eye was about five days old, and the minor contusions about 24 hours old. This means that these contusions occurred no later than November 28th, and that it happened in the hospital. The baby was admitted on November 24, 1997. Also, the baby’s mother explained in court that the bruise under the right eyelid described above was caused by an octagon baby bottle. The baby’s four year-old sister was giving the bottle to her father and accidentally hit the baby in the eye area [13]

In court, Dr. Gore showed three photographs of the bruise under the eyelid and the two minor contusions, and he spent time describing these minor superficial injuries. These actions on Gore’s part are quite troubling, because he knew very well that these minor injuries had nothing to do with the causes of baby Alan’s illness and death. He stated that the two minor contusions occurred at about 24 hours prior to autopsy. This means that they occurred in the hospital and have no impact on this case. Furthermore, he did not ask the parents of the baby for an explanation of the minor bruise under the right eyelid. His presentation of the three photographs of these minor injuries in the court did not serve any medical objectives, but certainly confused the jury by making them think that a physical force was used. He mentioned that these injuries were caused by blunt force. I believe that Gore’s approach is not scientifically and professionally justified, and that he should be asked to explain his actions.

Conclusions
Dr. Shashi Gore conducted the medicolegal examination of the body of Alan Ream Yurko Pursuant to Florida Statutes Chapter 406 and 732.9185. The main purpose of his examination was to discover the cause(s) of injuries and death. This task can be accomplished only by evaluating all medical evidence related to the case, as presented in this report (I-IV). I believe that the medical examiner did not meet his obligation as required by his job and the law as shown by the evidence described above (IV). Below is a summary of the medical evidence showing that Gore’s actions and conclusions are not supported by medical facts, and that he did not meet his obligation as medical examiner in this case.

1. Gore did not review the case history of baby Alan’s mother during her pregnancy with Alan. She suffered from several medical problems (gestational diabetes, oligohydramnios, anemia, infections). Her illness caused health problems in the fetus, as described in section I of this report, which made the baby more susceptible to develop adverse reactions to vaccines. Alan developed an infection and diabetes after receiving six vaccines, which led to his cardiac arrest on November 24, 1997.
2. Gore did not review the case history of baby Alan from birth to the time of his cardiac arrest on November 24, 1997. Alan was born five weeks premature and suffered from Respiratory Distress Syndrome, jaundice, hypoglycemia, anemia, and growth retardation (section II). His illness made him more susceptible to develop adverse reactions to vaccines. Alan developed an infection and diabetes, which led to his cardiac arrest on November 24, 1997
3. Gore did not evaluate the impact of vaccines given to Alan on his health (Table 5). The studies presented in section II of this report clearly show that these vaccines caused very serious adverse reactions in premature infants such as apnea, cardiac problem, and respiratory infections. Baby Alan developed diabetes, which was the result of an infection and complications of vaccination. This led to his cardiac arrest on November 24, 1997.
4. Gore overlooked the evidence that showed baby Alan had diabetes on November 24, 1997, which led to his cardiac arrest and apnea due to hypokalemia. Also, the level of serum LDH was high, and this indicates Alan suffered from cardiomyopathy.
5. Gore overlooked the evidence that showed Alan had bacterial infections, as indicated by elevated white blood cell count, body temperature, and his response to treatment with antibiotics.
6. Gore overlooked the evidence that indicated Alan was treated with high doses of three types of antibiotics, and his infections responded well to this treatment (Table 6, Table 7. Also, he did not consider the influence of this treatment on the pathological changes in tissues and on his autopsy findings on November 29, 1997.
7. Gore overlooked the evidence that showed Alan was treated with excessive doses of sodium bicarbonate and heparin that caused hypoxia and bleeding in the brain, spinal cord, and lungs. Also, the baby suffered from anemia and hypotension, which are risk factors for bleeding in individuals treated with heparin.
8. Gore overlooked the evidence that baby Alan had bleeding in the brain, spinal cord, and lungs. This indicates that his problem was caused by metabolic changes and cardiovascular disturbance.
9. Gore did not consider the clinical data that showed Alan suffered from anemia, clotting problem, and infections.
10. Gore stated that the liver, heart, and organs other than the brain did not contribute to the cause of illness and death. The clinical data presented in this report shows that the baby suffered from diabetes, and had problems in liver and heart.
11. Gore stated that baby Alan had an average build and nourishment, but the clinical data presented in this report shows that the baby was losing weight and suffering from dehydration.
12. Gore’s measurement for the head circumference of 22 cm on November 29th was obviously wrong. It was 37.5 cm at eighteen days prior to this date (Table 4).
13. Gore described the histology of the heart in his autopsy report; but the evidence showed that the heart was donated prior to autopsy, and therefore he did not have the chance to examine it. This indicates that his work is suffering from very serious problems. It seems that he got cases mixed up with each other. The level of serum LDH, hypokalemia, and dysrhythmia indicate that the heart was not normal.
14. Gore overlooked the evidence that showed the subdural hemorrhage was found only on the right side of the brain on November 24, 1997. Finding bleeding on the left side on November 29th indicates that the bleeding did not happen in minutes or a few seconds, as he claimed in his court testimony in February of 1999.
15. Gore overlooked the facts that the brain was edematous and that edema increased the intracranial pressure and caused axonal injury and brain damage.
16. Gore claimed that he observed an axonal injury in the brain but he did not provide any evidence that supported his claim. There is no description of an axonal injury presented in his report or in court. He said that we couldn’t show you the axonal injury in the brain! He needs to be asked to explain his reason.
17. Gore stated in court that the cerebrospinal fluid (CSF) was mixed with blood, but the information presented in his report shows that the CSF was clear. He reported that serial cut sections of the brain did not show any internal hemorrhage in the brain parenchyma grossly. The ventricles were slightly reduced in size and the cerebrospinal fluid appeared clear [28].
18. Gore stated that Alan had no meningitis, but the evidence presented in this report showed otherwise (III, IV). Alan suffered from meningitis, as indicated by the presence of swelling blood vessels, congestion, edema, and infiltration of tissue with inflammatory cells.
19. Gore claimed that axonal injury is a characteristic lesion of Shaken Baby Syndrome, but the published literature described in this section (IV) of this report shows that axonal injuries occurred in cases of brain edema, hypoxia, and cardiac arrest.
20. Gore presented the minor bleeding in the retinal of the right eye as evidence that baby Alan died as a result of “Shaken Baby Syndrome,” and he did not investigate the factual causes that led to bleeding in the retina as presented in this section (IV).
21. Gore did not provide x-ray findings to prove that Alan had fracture in ribs 5, 7, and 10. Also he did not search the medical literature to find out if rib fractures can occur during labor as presented in this report (IV-J).
22. Gore showed in court photographs of a minor contusion in the temporal areas of the head that occurred in the hospital at about one day prior to autopsy, and had no relation to the cause of death in this case. I believe that he did this to influence the jury’s thinking that physical force was used in this case.
23. Gore showed in court a photograph of a minor bruise under the right eyelid, which has no relation to the cause of death in this case this case. He did not make any attempt to speak with the baby’s parents or to seek their explanation for the cause of this insignificant minor injury. I believe that he was acting desperately to find any injury caused by trauma in this case to influence the jury’s thinking that physical force was used in this case.

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References

[1] Medical records of Francine Ream (1997). Florida Hospital, Orlando Florida.
[2] Medical records of Francine Ream (1997). Birthing Cottage of Winter Park,
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[28] Shashi B. Gore, MD, MPH, autopsy report for Alan Ream-Yurko (sic), case # MEH-1064-97, 1997. Office of The Medical Examiner, District Nine, 1401 Lucerne Terrace, Orlando, Florida 32806-2014.
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[34] Shannon P, Smith CR, Deck J, Ang LC, Ho M, Becker L. Axonal injury and the neuropathology of Shaken Baby Syndrome. Acta Neuropathol (Berl).
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